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Q: how to get the parent element id in JQuery or Javascript i have un ordered list of html elements from the list on clicking any of the list i want to get the parent ul tag id. <ul id="123"> <li> <li>test1</li> <a href="#" onclick="validate()"/> </li> </li> ........ ........ </ul> function validate(){ var test=$(this).parent().parent().attr('id'); alert(test); } above validate function test variable result should ul tag id that is 123. A: First problem is that your function validate() dont know what this refers to, so you need to add it like validate(this); Then we can do it like this. function validate(obj) { var test = $(obj).closest("ul").attr('id'); alert(test); } Also, you should not really have <li> as a child of another <li> use something like this structure. <ul id="123"> <li> <a href="#" onclick="validate(this)">test1</a> <ul id="456"> <li> <a href="#" onclick="validate(this)">test2</a> </li> </ul> </li> </ul> function validate(obj) { var test = $(obj).closest("ul").attr('id'); alert(test); } <script src="https://cdnjs.cloudflare.com/ajax/libs/jquery/3.3.1/jquery.min.js"></script> <ul id="123"> <li> <a href="#" onclick="validate(this)">test1</a> <ul id="456"> <li> <a href="#" onclick="validate(this)">test2</a> </li> </ul> </li> </ul>

Q: Button Click event not firing for dynamically created button I have created dynamic controls on DropdownList's SelectedIndexChanged event. Button is one of those controls. I have also assigned event to that button but debugger is not coming on that click event. Following is my code. protected void Page_Load(object sender, EventArgs e) { try { token = Session["LoginToken"].ToString(); if (!IsPostBack) { BindData(); fsSearch.Visible = false; btnDownload.Visible = false; } else { foreach (HtmlTableRow row in (HtmlTableRowCollection)Session["dynamicControls"]) { tblSearch.Rows.Add(row); } } } catch { } } private void BindData() { ddlReportName.DataSource = svcCommon.GetReports(token, out message); ddlReportName.DataValueField = "Key"; ddlReportName.DataTextField = "Value"; ddlReportName.DataBind(); ddlReportName.Items.Insert(0, "--Select--"); } protected void ddlReportName_SelectedIndexChanged(object sender, EventArgs e) { try { string[] reportInfo = ddlReportName.SelectedValue.Split('|'); Session["dynamicControls"] = null; tblSearch.Rows.Clear(); HtmlTableRow row = new HtmlTableRow(); HtmlTableCell cellFieldNameLbl = new HtmlTableCell(); HtmlTableCell cellFieldNameDdl = new HtmlTableCell(); HtmlTableCell cellOperatorLbl = new HtmlTableCell(); HtmlTableCell cellOperatorDdl = new HtmlTableCell(); HtmlTableCell cellValueLbl = new HtmlTableCell(); HtmlTableCell cellValueTxt = new HtmlTableCell(); HtmlTableCell cellOperatorRbtn = new HtmlTableCell(); HtmlTableCell cellAddMoreFilter = new HtmlTableCell(); Button btnAddMore = new Button(); DropDownList ddlColumn = new DropDownList(); DropDownList ddlOperator = new DropDownList(); TextBox txtValue = new TextBox(); RadioButtonList rbtnOperator = new RadioButtonList(); List<string> filterValues = svcCommon.GetSearchColumns(Convert.ToInt64(reportInfo[0]), token, out message); fsSearch.Visible = btnDownload.Visible = filterValues.Count > 0 ? true : false; ddlColumn.ID = "_ddlColumn0"; ddlOperator.ID = "_ddlOperator0"; txtValue.ID = "_txtValue0"; rbtnOperator.ID = "_rbtnOperator0"; btnAddMore.ID = "_btnAddMore0"; rbtnOperator.Items.Add("AND"); rbtnOperator.Items.Add("OR"); rbtnOperator.RepeatDirection = RepeatDirection.Horizontal; btnAddMore.Text = "Add More"; btnAddMore.Click +=btnAddMore_Click; ddlColumn.DataSource = filterValues; ddlColumn.DataBind(); ddlOperator.DataSource = new List<string>() { "Equal", "Not Equal", "Less Than", "Less Than Or Equal", "Greater Than", "Greater Than Or Equal", "Start With", "Not Start With", "End With", "Not End With", "Contains", "Not Contains", "Between", "Not Between", "In", "Not In" }; ddlOperator.DataBind(); cellFieldNameLbl.InnerText = "Field Name:"; cellFieldNameDdl.Controls.Add(ddlColumn); cellOperatorLbl.InnerText = "Operator"; cellOperatorDdl.Controls.Add(ddlOperator); cellValueLbl.InnerText = "Value"; cellValueTxt.Controls.Add(txtValue); cellOperatorRbtn.Controls.Add(rbtnOperator); cellAddMoreFilter.Controls.Add(btnAddMore); row.Cells.Add(cellFieldNameLbl); row.Cells.Add(cellFieldNameDdl); row.Cells.Add(cellOperatorLbl); row.Cells.Add(cellOperatorDdl); row.Cells.Add(cellValueLbl); row.Cells.Add(cellValueTxt); row.Cells.Add(cellOperatorRbtn); row.Cells.Add(cellAddMoreFilter); tblSearch.Rows.Add(row); Session["dynamicControls"] = tblSearch.Rows; } catch (Exception ex) { } } protected void btnAddMore_Click(object sender, EventArgs e) { try { } catch { } } A: The problem with dynamically created controls in asp.net webforms is that they aren't automatically added to the viewstate, so the postback event won't happen. This should help you to understand adding controls dynamically, and managing them via the viewstate http://forums.asp.net/t/1900207.aspx?Creating+buttons+dynamically Alternatively, a much easier way to manage this is to have the buttons on the page but not visible, then in the selected_index_changed event, just switch the visibility to true. A: I hadn't enough time to try so many thing. The thing I did is stored the container on which dynamic controls are added into Session and on Page_Init event I have bound event and it is working fine now. :)

A list of all the animated features I have watched, taking into consideration not only overall movie but animation style/technique, and sentimental value. Sometimes I feel conflicted on which to put first… technique > overall movie? Sentimental > technique? Sentimental > overall movie? Or backwards?

Did Voyager Get It Too Easy? 23 posts in this topic Voyager, for a ship alone, always looked pristine. After every battle there was minor damage in that they never lost a nacelle (a la Relaint in Khan) or a major bulkhead. Would you have liked to have seen them struggle a bit more in the last seasons like in Year of Hell or the Equinox? A half dead crew struggling for survival years away from home really tugs at the heart strings. A blind Tuvok, a dead Seven: now that would have been drama. Never have I ever laughed or felt like crying at Voyager. I feel the actors were capable of more but the circumstances and the stories just never opened up the floodgates. Voyager was essentially a flying hotel throughout with lovely lighting and immaculate carpets. They always briefly got into trouble but you always new they would get out of it. Imagine if in season 4, a big chunk of Voyager was lost forever. That would have put a spin on the show making it darker and more dangerous. Voyager should have got home by the skin of their teeth and no more, with a heavy price to pay. Share this post Link to post Share on other sites Guest Ktrek I agree here Prometheus! I would have liked the show more if it had been a little more realistic. I know it's not generally good to kill your stars off but it sure adds to realism and heavy drama that the fans won't forget. Voyager coming through virtually unscathed is unrealistic for sure. I wish I had liked Voyager more than I do. I'm hoping that when it's released on DVD that I will look at the show differently. Ktrek Share this post Link to post Share on other sites All right on the money prometheus. Generously speaking, I would say there were perhaps 20 noteworthy episodes in all. Here is the stickler though, I will, most likely, buy every season! I'm insane for Trek! I'm hoping that when it's released on DVD that I will look at the show differently. Share this post Link to post Share on other sites Everyone in the Delta Quadrent ended up hating the Voyager crew. They were always interfering with active wars and getting caught in the middle of them. But the Engineering staff always managed to make the ship look brand new. A little hard to believe, eh? Share this post Link to post Share on other sites They had to ration food becausethe replicators supposedly used lots of power. I mean, that was how they tried to inject suffering into the show. How much power does a flippin replicater use anyway? I think having to eat Neelix's poo-poo eggs and stuff was a load of hoey. The amount of power used in phasers and lifts and stuff ,not to mention when Voyager kept getting taken over by aliens, would have made the power used replicating a bowl of soup negligible. And i thought dilithium crystals went on for ever? Share this post Link to post Share on other sites I don't think they had it easy at all..It seemed that just because the ship was always proper that we assume it was easy for them. The mental anguish alone ( Am I being over dramatic) was enough to cuz un-ease..True, Janeway did float over Prime Directive enough. Share this post Link to post Share on other sites I agree Voyager should have been the most dangorous show, yet compared to DS9 and TNG Voyager was a joy ride most of the time. I also feel kind of the same way about Enterprise. The NX-01 is the only Human ship out as far as it is, they don't have shields, they don't have good weapons, transporters are still a new thing, ect... In TOS and even in TNG people got killed all the time. It made sense because they were doing very dangourous things. Enterprise however just isn't neer as scary as it should be. It's still a good show, I just think they should make it a bit darker. Share this post Link to post Share on other sites I never thought of that, but it's true, Prometheus! IF they had a tiny little scratch on them, and it was always gone by the next episode (or scene for that matter). Also, TNG had more people die than VOY, I think, and they were in safe federation space half the time...I don't think I'd be happy-smilie-face if members of the crew died, but I think I'd have been happy-understanding if they had. (I don't handle death too well, though. I was even sad when Seska died and man did she annoy me) Link to post Share on other sites I think people are neglecting the logicstics of Voyager.... think about all the knowledge the people have gained in the late (what was it, 23rd century) Picard and Kirk (not to mention Archer) all survived terrible fates in their quadrant. Although that Voyager was lost, they had the spirit and determinition of kicking it through the Delta Quadrant. I believe that they made terrific allies that helped them through the way and made some daring mission tasks. Share this post Link to post Share on other sites I do agree that Voyager had it a little easy. I mean they were a great crew, but in the time they spent in the Delta quadrant we should have seen more damage to the ship. At least they could have left damage for an episode or two until they could find a friendly race or a place to put in to dock to make the repairs. Share this post Link to post Share on other sites Watching Year of Hell on rerun and it is by far one of the best episodes of Voyager. THAT should have been what the pilot was like. The named Anorax is a bit funny though. Like jackets. We needed a darker more dramatic realistic series called Voyager. Even the name could have been better. Voyager is a bit blah. They might as well have called it Challenger or something. Storylines, for example, where a crew member has Cancer and knows he or she is going to die without ever getting to say goodbye to their loved ones. An episode where the crew are so hungry and working so hard to keep the ship going that they are bad tempered and fight. Maybe fly on the wall style like they did with Galactica ... Share this post Link to post Share on other sites ... or they should have just gone the whole cheesy hog and had a concussed Janeway wake up (bun and all) in the Badlands with her First Officer helping her up saying "are you all right mamn" and her croaking "I had the stangest dream ..." [ouch]

Classic International Cruises Classic International Cruises was a British-Australian owned shipping company operating five luxury cruise ships, most notably their flagship, the rebuilt ocean liner MS Athena. The company only operated cruise ships that are former ocean liners, the classic ships of their day (hence the company's name). History Classic International Cruises was seemingly founded in 1985, with the purchase of the MV Funchal as the Arcalia Shipping Company Ltd, which eventually became Classic International. They operated the one ship until 1994, when they bought the Princess Danae. The Princess Danae entered service with an all-white hull and a sailing ship logo on her funnel. Funchal was given a yellow and blue striped funnel and a white hull, but by 2000 her livery was changed to what now all Classic International ships have. Since 2000 they have purchased 3 ships, Arion, Athena and Princess Daphne, the near-identical sister of Princess Danae. With their main headquarters in Lisbon, Portugal, the company also has several branches based in Paris, France, Piraeus, Greece, Neutral Bay, Australia, Stockholm, Sweden, and London, England. Due to unpaid bills by the line, the company's four ships, Princess Danae, Princess Daphne, Athena & Arion have all been arrested, the only ship not arrested is the Funchal which is laid up pending refurbishment for SOLAS. On 20 December 2012, it was resolved to place the company into liquidation. In the beginning of 2013, the recently created cruise company Portuscale Cruises, led by the Portuguese entrepreneur Rui Alegre, bought Princess Danae, Athena, Arion and Funchal, assuming as well the liabilities of Classic International Cruises. Ships References Category:Defunct companies based in London Category:Defunct cruise lines Category:Defunct shipping companies of Australia Category:Defunct shipping companies of the United Kingdom

2019 IL App (3d) 170185 Opinion filed July 11, 2019 _____________________________________________________________________________ IN THE APPELLATE COURT OF ILLINOIS THIRD DISTRICT 2019 THE PEOPLE OF THE STATE OF ) Appeal from the Circuit Court ILLINOIS, ) of the 10th Judicial Circuit, ) Peoria County, Illinois. Plaintiff-Appellee, ) ) Appeal No. 3-17-0185 v. ) Circuit No. 16-CF-264 ) WILLIAM GRANT, ) The Honorable ) John P. Vespa, Defendant-Appellant. ) Judge, presiding. ____________________________________________________________________________ JUSTICE CARTER delivered the judgment of the court, with opinion. Presiding Justice Schmidt and Justice Lytton concurred in the judgment and opinion. _____________________________________________________________________________ OPINION ¶1 After a jury trial, defendant, William Grant, was convicted of home invasion (720 ILCS 5/19-6(a)(1) (West 2016)) and was sentenced to 24 years in prison. Defendant appeals his conviction and sentence, arguing that the trial court erred in (1) granting the State’s midtrial request to remove the lone African American juror from the jury for cause and (2) considering a fact inherent in the crime of which defendant was convicted as a factor in aggravation in defendant’s sentencing. We affirm the trial court’s judgment. ¶2 I. BACKGROUND ¶3 In April 2016, defendant, who is African American, was charged with home invasion (two counts), attempted aggravated criminal sexual assault, and certain other related offenses for allegedly breaking into a home in Peoria, Illinois, and attempting to sexually assault a person who was staying at the residence. Four months later, in August 2016, defendant’s case proceeded to a jury trial. The jury was selected with one African American juror, Juror B., on the jury. ¶4 Following opening statements, outside the presence of the jury, the trial court noted that two of the jurors were starting to fall asleep. The trial court stated: “Okay. I’m gonna make a record of this then too. It’s 10:00 in the morning. At 9:40, less than one half an hour of—of time being on the—being in the jury box I noticed a juror starting to nod off, starting to fall asleep, and I told the lawyers about it, indicated which juror it is, and it is Juror [B.]. And I see his eyelids going more and more towards closing, and as—as that’s happening, his head starts lowering. That whole thing is only maybe five seconds, and I cannot say that he ever fell asleep. And, in fact, I don’t think he did ever fall asleep, but I’m thinking at 9:30 in the morning he’s like that, it worries me then about his ability to stay awake the entire morning. And by the way, the juror sitting right in front [Juror C.] was doing the same thing, but nowhere near as much as [Juror B.] so I’m gonna be keeping my eye on—on both of them.” ¶5 After the testimony of the State’s first witness, the alleged victim of the attempted sexual assault, the trial court took a recess. Outside the presence of the jury, the prosecutor informed the trial court that he had asked a victim witness advocate who was employed by the Peoria County -2-  State’s Attorney’s Office to watch Juror B. during the victim’s testimony. According to the prosecutor, the advocate indicated that Juror B. was sleeping for a large and significant portion of the victim’s testimony. The trial court stated that it had been “keeping an eye” on Juror B. during the testimony but it had not noticed him sleeping. The advocate told the trial court that Juror B. was nodding off and that he had lowered his head down and jolted awake during the testimony. The advocate stated further that Juror B.’s tablet had slid off his lap onto the floor two or three times and had attracted the attention of other jurors. Defendant’s attorney indicated that he did not see Juror B.’s conduct because he was paying attention to the witness and commented that, before the trial court considered removing Juror B., it was important for the court to actually establish that Juror B. was sleeping. The trial court stated repeatedly that it had complete faith in the advocate’s credibility and noted that there easily could have been times where Juror B. had done what the advocate claimed but the trial court had not seen it because the trial court was watching the witness testify a lot of the time and was also watching the lawyers and all of the jurors. The trial court checked to see if the courtroom security cameras had recorded the complained-of conduct but was told that the security cameras did not record the jurors. After some further discussion, the trial court found that Juror B. had been sleeping. ¶6 On the State’s motion and over defendant’s objection, the trial court dismissed Juror B. from the jury for cause. Defendant moved for a mistrial, and the trial court denied that request. In denying defendant’s request for a mistrial, the trial court stated that, based upon its own observations coupled with the observations of the advocate, it had concluded that Juror B. was sleeping and that it had removed Juror B. from the jury for that reason. ¶7 Defendant reminded the trial court that Juror C. had been falling asleep as well. The trial court commented that Juror C. “was only doing the eyelids getting heavy thing, nowhere near the -3-  extent that [Juror B.] was doing” but stated that it was worried about Juror C. and that it was going to instruct the jurors that they should all stay awake. When the jury was brought back into the courtroom, the trial court instructed the jurors that it expected the jurors to stay away during the trial. The trial then proceeded, and defendant was eventually found guilty of home invasion. 1 ¶8 A presentence investigation report (PSI) was ordered, and the case was scheduled for a sentencing hearing. Prior to the sentencing hearing, defendant filed two posttrial motions. One motion was filed by defense counsel; the other was filed by defendant pro se. In the motions, defendant (defendant and defense counsel) argued, among other things, that defendant was denied a fair trial when the trial court granted the State’s motion to remove the lone African American juror from the jury and that the trial court applied a double standard in doing so. After a hearing, the trial court denied defendant’s posttrial motions. In doing so, the trial court commented on Juror B. falling asleep during the trial and stated that there was a big difference in what the court had observed between Juror B. and any other juror. ¶9 Defendant’s PSI showed that defendant was 48 years old and had a lengthy criminal history that spanned over 30 years. Defendant had seven prior felony convictions—four for the Class 4 felony offense of failing to register or to report address change as a sex offender (1998, 2000, 2000, 2002), one for the Class 3 felony offense of failing to report address change as a sex offender (2009), one for the Class 2 felony offense of aggravated domestic battery (2006), and one for the Class X felony offense of aggravated criminal sexual assault (1987). Defendant also had approximately 18 prior misdemeanor convictions (not including traffic offenses), many of which were for resisting a police officer or correctional employee. 1 Defendant was actually found guilty of two counts of home invasion. A mistrial was declared on a remaining charge because the jury was unable to reach a verdict on that charge. -4- ¶ 10 A sentencing hearing was held in December 2016. During the sentencing hearing, the State recommended to the trial court that defendant be sentenced to the maximum sentence of 30 years in prison because of defendant’s criminal record; the circumstances of the offense (breaking into a person’s home, holding a knife to a woman’s throat in her own bedroom, and demanding that the woman take her clothes off); the need to deter others from committing the same offense; and the need to protect the community from defendant. In addition, the State suggested to the trial court that defendant’s conduct had threatened serious harm in that the victim awoke to find defendant on top of her and that defendant had held a knife to the victim’s throat in her own bedroom. Defense counsel argued that, while defendant had a number of previous convictions, his record did not warrant the harsh sentence advocated by the State and asked the court to consider a sentence in the lower portion of the sentencing range. Defense counsel pointed out to the court that five of defendant’s seven prior felony convictions were for registration offenses, that defendant’s prior Class X felony conviction was for an offense that took place a long time ago, and that defendant had already been punished for his prior offenses. Defense counsel also noted that defendant had obtained his General Education Development certificate, had a significant work history, and had struggled through some difficulties in his life. ¶ 11 After listening to the arguments of the attorneys, the trial court announced its sentencing decision. The trial court stated that it found three factors in aggravation: (1) that “defendant’s conduct caused or threatened serious harm with the holding [of] the knife to the throat *** of the victim in this case,” (2) that defendant had a history of prior criminal activity, and (3) that the sentence was necessary to deter others from committing the same crime. The trial court commented further about defendant’s criminal history, stating: -5-  “Seven prior felonies is a lot to overlook, to be asked to overlook even if only figuratively asked that. Seven prior felonies. One is a [sic] aggravated criminal sexual assault, a Class X. Another is aggravated domestic battery, Class 2. The others are failures to report. I count failures to report. The legislature counts them and insists that I count them. This [‘]only failures to report,[’] what do you mean only I would say? Definitely do not rise to the level of an aggravated domestic battery or a [sic] aggravated criminal sexual assault.” The trial court ultimately sentenced defendant to 24 years in prison. 2 ¶ 12 Defendant filed a motion to reconsider sentence and argued that the sentence imposed upon him was excessive. A hearing was later held on the motion. When defense counsel finished his argument on the motion and before the State responded, the trial court commented: “Sentencing range was six to 30 years. Day-for-day good time applies. I did not have the option of probation. Defendant had seven prior felony convictions, just for everybody’s information.” After the State made its argument on the motion, the trial court announced its ruling—that it was denying defendant’s motion to reconsider sentence. In doing so, the trial court stated: “I said what I said between the two lawyers speaking for a reason, laying out a foundation for my ruling which is to deny the Motion to Reconsider the Sentence. Six-to-30-year range and you get 24 when you’ve got seven prior felonies. And the situation I’ve [sic] presented with on file 16 CF 264, the one that the sentencing was about, looking at my trial notes, and 24 is a fine sentence that I can easily defend. So Motion to Reconsider is denied.” 2 The trial court imposed sentence on defendant on only one of the two home invasion convictions (count I) and did not impose sentence upon defendant for the other home invasion conviction (count II). -6- ¶ 13 Defendant appealed. ¶ 14 II. ANALYSIS ¶ 15 A. Midtrial Removal of Juror for Cause ¶ 16 As his first point of contention on appeal, defendant argues that the trial court erred in granting the State’s midtrial request to remove the lone African American juror from the jury for cause. Defendant asserts first that the disparate treatment of the lone African American juror amounted to unconstitutional discrimination that denied defendant equal protection of the law because the African American juror (Juror B.) was treated differently than the other similarly situated juror (Juror C.) who was not African American. Second, defendant asserts that he was denied due process of law when the trial court granted the State undue, outsized influence over the composition of the jury during defendant’s trial by granting the State’s request to remove Juror B. from the jury for cause without any factual support and without conducting an inquiry. According to defendant, there was no independent evidence to support a finding that Juror B. had fallen asleep or that he had missed any testimony. Defendant also claims that the trial court did not recognize that it had the discretion to reopen voir dire and conduct an independent investigation of the State’s allegation of juror misconduct. Instead, defendant maintains, the trial court essentially delegated its authority to the State and merely adopted the State’s victim witness advocate’s representations that Juror B. had fallen asleep during the testimony, even though those representations were contrary to the trial court’s own observations. For all of the reasons stated, defendant asks that we reverse his conviction and that we remand this case for further proceedings, presumably a new trial. ¶ 17 The State argues first that defendant has forfeited this claim of error on appeal by failing to specifically raise it in the trial court. In the alternative, the State argues that the trial court’s -7-  ruling was proper and should be upheld. As for defendant’s equal protection claim, the State asserts that the trial court’s ruling did not deprive defendant of equal protection of the law because Juror B. and Juror C. were not similarly situated, as the trial court noted that Juror B.’s conduct was far worse than Juror C.’s. Thus, the State contends that Juror B. was properly dismissed for race-neutral reasons—because he was falling asleep during the presentation of the evidence. As for defendant’s due process claim, the State asserts that defendant’s claim should be rejected because it is based upon unsubstantiated statements and selective quotes from the record. According to the State, a fair reading of the record shows that the trial court exercised its discretion and made a finding, which is entitled to deference on appeal, that Juror B. was sleeping during the trial. Thus, the State contends, defendant was not deprived of due process of the law. For all of the reasons set forth, the State asks that we affirm the trial court’s judgment. ¶ 18 In reply, defendant asserts that he sufficiently raised this claim of error in the trial court to prevent the issue from being forfeited on appeal. Alternatively, defendant asserts that this court should reach the issue, nevertheless, as a matter of second-prong plain error. ¶ 19 We need not address plain error because we agree with defendant that he properly preserved this claim of error for appellate review. See People v. Lovejoy, 235 Ill. 2d 97, 148 (2009) (stating that the issue raised by a litigant on appeal does not have to be identical to the objection raised at trial and that a court will not find that a claim has been forfeited when it is clear that the trial court had the opportunity to review essentially that same claim). Even though defendant may not have specifically referred to equal protection or due process, he raised essentially the same claims in the trial court when he argued that the trial court erred in granting the State’s request to remove Juror B. for cause, that the trial court applied an unfair double standard, and that he was deprived of a fair trial as a result of the trial court’s ruling. We find, -8-  therefore, that the forfeiture rule does not apply, and we will now address the merits of defendant’s first claim of error. ¶ 20 The question of whether a defendant was denied equal protection or due process by the trial court is a question of law that is subject to de novo review on appeal. See People v. Hollins, 366 Ill. App. 3d 533, 538 (2006) (stating that because an equal protection claim is a constitutional question, the standard of review on appeal is de novo); People v. Williams, 2013 IL App (1st) 111116, ¶ 75 (stating that whether a defendant’s due process rights have been denied is an issue of law that is subject to de novo review on appeal). The equal protection clause of the fourteenth amendment to the United States Constitution prohibits the exclusion of any individual juror from a jury on account of his or her race. See U.S. Const., amend. XIV; Powers v. Ohio, 499 U.S. 400, 404 (1991); Hollins, 366 Ill. App. at 538. Although a defendant has no right to a jury composed in whole or in part of persons of his own race, he does have the right to be tried by a jury whose members are selected using nondiscriminatory criteria. Powers, 499 U.S. at 404. Because the fourteenth amendment protects an accused throughout the proceedings used to bring him to justice, the State may not draw up its jury lists pursuant to neutral procedures but then resort to discrimination in other parts of the selection process. Id. at 409. An equal protection claim arises when a charge is made that similarly situated individuals were treated differently without a rational relationship to a legitimate State purpose. Kaltsas v. City of North Chicago, 160 Ill. App. 3d 302, 305-06 (1987). To establish a claim of racial discrimination in jury selection, a purpose to discriminate must be present, “which may be proven by systematic exclusion of eligible jury persons of the proscribed race or by unequal application of the law to such an extent as to show intentional discrimination.” Akins v. Texas, 325 U.S. 398, 403-04 (1945). The burden is on the defendant to establish discrimination. Id. at 400. -9- ¶ 21 The due process clauses of the United States and Illinois Constitutions protect individuals from the deprivation of life, liberty, or property without due process of law. U.S. Const., amend. XIV; Ill. Const. 1970, art. I, § 2; People v. One 1998 GMC, 2011 IL 110236, ¶ 21; People v. Pollard, 2016 IL App (5th) 130514, ¶ 29. Under the case law, there are two distinct branches of due process analysis: substantive due process and procedural due process. Pollard, 2016 IL App (5th) 130514, ¶ 29. When a violation of substantive due process is alleged, such as in the present case, the appropriate inquiry is whether the individual has been subjected to the arbitrary exercise of the powers of government, unrestrained by the established principles of private rights and distributive justice. Id. Substantive due process requires, among other things, that there be an overall balance—a level playing field—between the prosecution and the defense in a criminal trial. See United States v. Harbin, 250 F.3d 532, 540 (7th Cir. 2001); Tyson v. Trigg, 50 F.3d 436, 441 (7th Cir. 1995); In re Detention of Kortte, 317 Ill. App. 3d 111, 115-16 (2000). Substantive due process, however, does not mandate that the rights or advantages granted to the prosecution and the defense be in absolute symmetry at every stage of a criminal proceeding, only that the overall total balance between each side be designed to achieve the goal of a fair trial. See Harbin, 250 F.3d at 540; Tyson, 50 F.3d at 441. Nevertheless, a shift at just one stage of a criminal trial as to the rights or advantages granted to each side might so skew the balance of rights or advantages in favor of the prosecution that it deprives the defendant of the right to a fair trial. See Harbin, 250 F.3d at 540; Tyson, 50 F.3d at 441. ¶ 22 After having reviewed the record in the present case, we find that the trial court did not deprive defendant of equal protection or due process by granting the State’s midtrial request to remove Juror B. from the jury for cause. The record clearly shows that a race-neutral reason existed for the removal of Juror B.—Juror B. had fallen asleep during the presentation of the - 10 -  evidence. Although defendant points to Juror C. as a similarly situated juror who was not removed, the record abundantly shows that Juror B. and Juror C. were not similarly situated. In fact, the trial court specifically noted that Juror C.’s level of “nodding off” was nowhere near as bad as Juror B.’s. Furthermore, we are not persuaded by defendant’s suggestion that the trial court failed to conduct a proper inquiry as to whether Juror B. had fallen asleep during the first witness’s testimony. The trial court obtained input from the State, the defendant’s attorney, and the victim advocate; checked to determine whether the jurors’ actions had been recorded by the security cameras; and considered its own observations before ultimately making a specific finding that Juror B. had fallen asleep during the testimony of the witness. Contrary to defendant’s assertion on appeal, there is no indication that the trial court was unaware of its ability to inquire further into the factual circumstances surrounding Juror B.’s conduct during the trial if the trial court chose to do so. Moreover, the facts in the present case do not in any way indicate that the trial court gave the State an improper, unfair, or outsized amount of control over the composition of the jury at any time during the course of the trial. Rather, the facts show that the trial court was required to make a difficult decision and to remove a juror for cause after that juror had fallen asleep during an important part of the trial. We, therefore, find defendant’s argument on this issue to be without merit. ¶ 23 In reaching that conclusion, we note that we are not persuaded that a different result is mandated by the decisions in Harbin (cited above) or People v. Brown, 2013 IL App (2d) 111228—the two main cases cited by defendant in support of his argument on this issue. Both Harbin and Brown involved the prosecutions’ midtrial use of a peremptory challenge (see Harbin, 250 F.3d at 537; Brown, 2013 IL App (2d) 111228, ¶ 1), which is not the situation before the court in the present case. Indeed, in both of those cases, the courts recognized, - 11 -  although somewhat implicitly, that the result might have been different if the juror at issue had been removed for cause, rather than pursuant to a peremptory challenge. See Harbin, 250 F.3d at 539; Brown, 2013 IL App (2d) 111228, ¶ 31. ¶ 24 B. Possible Consideration of an Improper Factor in Sentencing ¶ 25 As his second point of contention on appeal, defendant argues that the trial court erred in considering a fact inherent in the crime of which defendant was convicted as a factor in aggravation in defendant’s sentencing. More specifically, defendant asserts that the trial court improperly found that the threat of force underlying the incident was a factor in aggravation at sentencing (that the conduct caused or threatened serious harm), even though that fact was an element of the offense of home invasion. Defendant acknowledges that he did not properly preserve that claim of error for appellate review but asks that this court review the error, nevertheless, under the second prong of the plain error doctrine. For all of the reasons stated, defendant asks that we vacate his sentence and remand this case for a new sentencing hearing. ¶ 26 The State argues that the trial court did not commit plain error in sentencing defendant in this case and that defendant’s sentence was appropriate based upon the offense and defendant’s criminal history. In support of that argument, the State asserts first that even though the trial court mentioned the allegedly improper factor in sentencing defendant, a remand for resentencing is not required because the record clearly shows that the trial court did not give significant weight to the improper factor. Second and in the alternative, the State asserts that although consideration of that factor would be improper in some circumstances, it was not improper under the circumstances of the present case where the trial court considered the factor when it was considering the nature and circumstances of the offense and the degree of harm. For - 12 -  all the reasons set forth, the State asks that we honor defendant’s forfeiture of this issue and that we affirm defendant’s sentence. ¶ 27 The plain error doctrine is a very limited and narrow exception to the forfeiture or procedural default rule that allows a reviewing court to consider unpreserved error if either one of the following two circumstances is present: (1) a clear or obvious error occurred and the evidence in the case was so closely balanced that the error alone threatened to tip the scales of justice against the defendant, regardless of the seriousness of the error, or (2) a clear or obvious error occurred and the error was so serious that it affected the fairness of the defendant’s trial and challenged the integrity of the judicial process, regardless of the closeness of the evidence. People v. Walker, 232 Ill. 2d 113, 124 (2009); People v. Piatkowski, 225 Ill. 2d 551, 565 (2007); People v. Herron, 215 Ill. 2d 167, 177-87 (2005); Ill. S. Ct. R. 615(a) (eff. Jan. 1, 1967). Under either prong of the plain error doctrine, the burden of persuasion is on the defendant. Walker, 232 Ill. 2d at 124. If the defendant fails to satisfy that burden, the forfeiture or procedural default of the issue must be honored. Id. The first step in any plain error analysis is to determine whether an error occurred. Id. at 124-25. To do so, a reviewing court must conduct a substantive review of the issue. Id. at 125. ¶ 28 Whether the trial court relied on an improper factor in sentencing a defendant is a question of law that is subject to de novo review on appeal. People v. Abdelhadi, 2012 IL App (2d) 111053, ¶ 8. In general, although a trial court has broad discretion when imposing a sentence, it may not consider a factor that is inherent in the offense of which defendant has been convicted as an aggravating factor in sentencing defendant for that offense. Id. ¶ 9; People v. Phelps, 211 Ill. 2d 1, 11-12 (2004). Doing so would constitute an improper double enhancement. See Phelps, 211 Ill. 2d at 12. The rule prohibiting such double enhancements is based on the - 13 -  rationale that the legislature obviously already considered the factors inherent in the offense when setting the range of penalties for that offense and that it would be improper, therefore, to consider those factors once again as a justification for imposing a greater penalty. Id. The defendant bears the burden to establish that a sentence was based on an improper consideration. Abdelhadi, 2012 IL App (2d) 111053, ¶ 9. On appeal, a reviewing court will not vacate a sentence that was based upon an improper factor and remand for resentencing if the reviewing court can determine from the record that the weight placed on the improperly considered aggravating factor was so insignificant that it did not lead to a greater sentence. See People v. Heider, 231 Ill. 2d 1, 21 (2008). ¶ 29 In the present case, we need not determine whether the trial court improperly considered a factor inherent in home invasion when it sentenced defendant for that offense because we find that, even if the trial court did so, defendant’s sentence should still be affirmed because the record clearly shows that the trial court gave insignificant weight to that allegedly improper factor. 3 Although the trial court mentioned the factor as being one of the three factors it was considering in aggravation, it is clear from the trial court’s comments, especially those that the trial court made in denying defendant’s motion to reconsider sentence, that the trial court’s focus on the aggravating factors in sentencing was upon defendant’s criminal history and his prior 3 Although the State agreed that the trial court considered a factor inherent in the offense, we make no such determination in this case because we have found it unnecessary to do so. We have made no ruling upon whether the threat of force, which may be an element of home invasion depending on how the offense is charged, is the same as the factor in aggravation—that defendant’s conduct caused or threatened serious harm. While not a determinative factor in our decision in this case, we note that our supreme court has indicated that it is permissible for a trial court to consider the force employed and the physical manner in which a victim’s death was brought about (but not the end result—the fact of the victim’s death) in applying the statutory aggravating factor that defendant’s conduct caused serious harm to the victim when sentencing a defendant for voluntary manslaughter, an offense in which serious bodily harm was implicit in the offense. See People v. Saldivar, 113 Ill. 2d 256, 271 (1986). - 14 -  felony convictions. We, therefore, reject defendant’s argument on this issue and uphold the sentence imposed. ¶ 30 III. CONCLUSION ¶ 31 For the foregoing reasons, we affirm the judgment of the circuit court of Peoria County. ¶ 32 Affirmed. - 15 -  No. 3-17-0185 Cite as: People v. Grant, 2019 IL App (3d) 170185 Decision Under Review: Appeal from the Circuit Court of Peoria County, No. 16-CF-264; the Hon. John P. Vespa, Judge, presiding. Attorneys James E. Chadd, Peter A. Carusona, and Matthew Lemke, of for State Appellate Defender’s Office, of Ottawa, for appellant. Appellant: Attorneys Jerry Brady, State’s Attorney, of Peoria (Patrick Delfino, for Thomas D. Arado, and Richard T. Leonard, of State’s Attorneys Appellee: Appellate Prosecutor’s Office, of counsel), for the People. - 16 - 

Sunday, October 13, 2013 Guy Delisle: Graphic Novels you must read! A package arrived from Lahore via TCS on my birthday. Sent by Maleeha Azeem. It was longish and fat … and I thought the girl must be really mad to send me Sugar-Free Laddoos, Barfees, & Gulab Jamuns from Nirala (and I thought again, for the hundredth time, "Why the fuck have they closed their shop in Karachi?"). I hurried to open it and put the contents into the fridge … and, lo and behold, there were two gifts inside. Worth a lot more than the Sugar-Free stuff. There was a box of 100 Comic Magazine Covers and a book: "Jerusalem" by Guy Delisle. The cards were a thrill to view quickly and be put aside to view again at leisure. But Delisle! I had to start reading it right away. The first page had this, of course. I had liked this French-Canadian cartoonist when I read his "Burma Chronicles", mainly because it went back to a land that I had visited three times in my early shipping days. It has changed an awful lot, since then, though the people still seem to be as aggravated as ever if they are in uniform. I remembered how, in 1959, I had put my pass down at the main desk to go out, once. A very, very drunken guardsman had pulled out a cocked gun and pointed it a couple of inches from my head because he felt that the paper made a noise while he was sleeping. He was shaking wildly and said my body can be taken back to the ship when he was through, swearing in Burmese. Trembling, Stanley Fernandes (a Second Engineer who was with me) and I pleaded with him and apologised as profusely as one does when facing death. Fifteen minutes of standing there, with a gun at your head is a terrible experience, let me tell you. Finally the guard agreed, took all the money we had, and let us go out. Photo by Luigi Novi Guy Delisle draws simple things wonderfully well! Take a look at this mess/mass of wires … … that reminded me of Karachi, as did the sketch of a plug point inside the house. So does this: Right on! It reminds you of how close to our home Burma is! (It's called Myanmar, now, by many countries except US and a couple of others who do not recognize it's Government and insist on calling it Burma.) The trip to Burma with his wife who works at Doctors Without Frontiers shows you their life for a few months in that country, introducing you to its people, their customs, their religion, the repression that takes place there, and much more that could remind you of our own military rule. ••••• So getting to read Jerusalem was essential! Once again, I thought how amazing these people are. Away from us, they think very much the same way as we do, give or take a few points. I am not sure if we can find Mullas who would be anything like the anti-Zionist Jews, apart from the 'seven kids', their 'fashions', and the 'variations' among their personal beliefs that make everyone else a kaafir. The Arabs, naturally, are even more like us.Which is why we like them? Don't we? The buses and the clothes. Wow. The books takes us into their places that are strictly Jewish, strictly Arab, and includes the mistreatment of the Arabs by the Israelis (which is plenty!), and offers you a run down of the city that is (was?) a home to Jews, Christians, and Muslims. The book also suggests, as most Muslims do, that the Second Mosque is in Jerusalem. There was no mosque at the Meraaj (Isra' in the Qur'an) of The Prophet at Jerusalem, of course. It was built much later. The Second Mosque, as you may know, is never named in the Qur'an. It just states that it is the furthest mosque. Also the Qur'an says that the First and Second Mosques will have Peace … something that this Mosque has never really had. The First Mosque is the Kaaba and the Second Mosque is the Masjid Al Nabvi — both known for Peace!!! This statement is now accepted by a few scholars. You can go to Google or YouTube and find a video from Mohammad Sheikh about this. The priests there, too, have a sacrifice of animals, and seem to love blood! No wonder there's so much killing of humans in both parts because this must allow them to get over the feelings I and many others have about killing. When I was 10 years old a Mulla came to do the sacrifice at our downstair neighbour's house. He gathered all the children and said that the way to do this is to look straight at the animals eyes … "and that will help you kill kaafirs in a Jihad without fearing." I wonder how many kids are taught this at Madressahs. The Jerusalem book was superb and I learnt a lot more about the Jews despite having read many of their writings. My paternal side of the family that came from Turkey used to be Jews three generations before they migrated to India with Babar, who brought Kazi Kidvah with him to be the head of his court. I was most amused to find out about the Messianic Jews. (Read the book and you'd be surprised, too.) Now I am waiting to read "Pyongyang" - a slightly older book by Guy Delisle - and learn more about Korea. words of wisdom Three passions, simple but overwhelmingly strong, have governed my life: the longing for love, the search for knowledge, and unbearable pity for the suffering of mankind.These passions, like great winds, have blown me hither and thither, in a wayward course, over a deep ocean of anguish, reaching to the very verge of despair. I have sought love, first, because it brings ecstasy - ecstasy so great that I would often have scrificed all the rest of life for a few hours of this joy. I have sought it, next, because it relieves loneliness - that terrible loneliness in which one shivering consciousness looks over the rim of the world into the cold unfathomable lifeless abyss. I have sought it, finally, because in the union of love I have seen, in a mystic miniature, the prefiguring vision of the heaven that the saints and poets have imagined. This is what I sought and, though it might seem too good for human life, this is what - at last - I have found. With equal passion I have sought knowledge. I have wished to understand the hearts of men. I have wished to know why the stars shine. And I have tried to apprehend the Pythagorean power by which number holds sway above the flux. A little of this, but not much, I have achieved. Love and knowledge, so far as they were possible, led upward toward the heavens. But always pity brought me to earth. Echoes of cries of pain reverberate in my heart. Children in famine, victims tortured by oppressors, helpless old people a hated burden to their sons, and the whole world of loneliness, poverty, and pain make a mockery of what human life should be. I long to alleviate the evil, but I cannot, and I too suffer. This has been my life. I have found it worth living, and would gladly live it again if the chance were offered me.Bertrand Russell The smart way to keep people passive and obedient is to strictly limit the spectrum of acceptable opinion, but allow very lively debate within that spectrum - even encourage the more critical and dissident views. That gives people the sense that there's free thinking going on, while all the time the presuppositions of the system are being reinforced by the limits put on the range of the debate.Noam Chomsky Few people are capable of expressing with equanimity opinions which differ from the prejudices of their social environment. Most people are even incapable of forming such opinions.Albert Einstein Each century seems to take on a particular character as we view it in retrospect. How will the 20th Century be remembered? My guess is that this dramatic span of 100 years will ultimately be marked not by computers or the Internet, but by the drive toward individual freedom, the breaking of human barriers of prejudice, and the opening of society to include all people.John S. Spong DESIDERATA Go placidly amid the noise and haste, and remember what peace there may be in silence. As far as possible without surrender be on good terms with all persons. Speak your truth quietly and clearly; and listen to others, even the dull and the ignorant; they too have their story. Avoid loud and aggressive persons, they are vexations to the spirit. If you compare yourself with others, you may become vain and bitter; for always there will be greater and lesser persons than yourself. Enjoy your achievements as well as your plans. Keep interested in your own career, however humble; it is a real possession in the changing fortunes of time. Exercise caution in your business affairs; for the world is full of trickery. But let this not blind you to what virtue there is; many persons strive for high ideals; and everywhere life is full of heroism. Be yourself. Especially, do not feign affection. Neither be cynical about love; for in the face of all aridity and disenchantment it is as perennial as the grass. Take kindly the counsel of the years, gracefully surrendering the things of youth. Nurture strength of spirit to shield you in sudden misfortune. But do not distress yourself with dark imaginings. Many fears are born of fatigue and loneliness. Beyond a wholesome discipline, be gentle with yourself. You are a child of the universe, no less than the trees and the stars; you have a right to be here. And whether or not it is clear to you, no doubt the universe is unfolding as it should. Therefore be at peace with God, whatever you conceive Him to be, and whatever your labors and aspirations, in the noisy confusion of life keep peace with your soul. With all its sham, drudgery, and broken dreams, it is still a beautiful world. Be cheerful. Strive to be happy.Max Ehrmann

Skander Zaïdi Skander Zaïdi (born 23 April 1997) is a Tunisian handball player for Al Mudhar and the Tunisian national team. He participated at the 2017 World Men's Handball Championship. References Category:1997 births Category:Living people Category:Tunisian male handball players

The Department of Labor released the numbers for last week’s unemployment filings. 3.28 million for the country. For The New York Times, Quocktrung Bui and Justin Wolfers show the numbers relative to the past and a breakdown by state: This downturn is different because it’s a direct result of relatively synchronized government directives that forced millions of stores, schools and government offices to close. It’s as if an economic umpire had blown the whistle to signal the end of playing time, forcing competitors from the economic playing field to recuperate. The result is an unusual downturn in which the first round of job losses will be intensely concentrated into just a few weeks. You can find the recent data here.

The present invention relates to a gantry for acquiring projection data, which is an important component of an X-ray computer tomography apparatus. FIG. 1 shows external appearance of a conventional gantry. The gantry 100 has a box-like shape having a cylindrical hole (hereinafter referred to as a view field) 121 in the central portion thereof. A subject is inserted in the view field 121, when photographed. The cover 111 of the gantry 100 has an air intake 115 and an air outlet 116 to cool the interior of the gantry. FIGS. 2 and 3 are front and side views of the interior of the gantry, respectively. The gantry has a rotation ring 101, on which an X-ray tube and an X-ray detector are mounted in an arrangement such that they are opposite to each other with the subject lying therebetween. The rotation ring 101 is rotatably supported by a ring frame 103. A motor 104 for rotating the rotation ring 101 is mounted on the ring frame 103. The ring frame 103 is supported by two main posts 106 via tilt mechanisms 110. The main post 106 is mounted on a stand base 107 at right angles, as shown in FIG. 4. The gantry 100 contains electric members 105, for example, a control board and a power source. As well known, the standard scan time at present is a second for a rotation. In the near future, a direct drive system, which directly drives the rotation ring (rotor) 101 by a stator coil, will be the mainstream of the driver of a gantry. Such high-speed rotations of the unbalanced rotation ring 101 cause the main posts 106 to vibrate violently. To suppress the vibration, the main posts 106 must be thick. For this reason, the gantry is inevitably large and heavy. Further, if the top end of the main post 106 is displaced 0.5 mm, a tumor or a bone smaller than 0.5 mm cannot be observed, and a ring-like artifact may be produced. An object of the present invention is to provide a gantry of a compact X-ray computer tomography apparatus having a high damping property. A gantry of an X-ray computer tomography apparatus comprises a base, two main posts mounted on the base at right angles, a ring frame tiltably supported by the two main posts, a rotation ring rotatably supported by the ring frame, an X-ray tube mounted on the rotation ring, and an X-ray detector mounted on the rotation ring, opposing to the X-ray tube. The props obliquely abut on the main posts to reinforce them. Since the main posts are reinforced by the props, the vibration due to high-speed rotations of the rotation ring can be effectively suppressed. Moreover, since the main posts need not be thick, the gantry can be compact. Additional objects and advantages of the invention will be set forth in the description which follows, and in part will be obvious from the description, or may be learned by practice of the invention. The objects and advantages of the invention may be realized and obtained by means of the instrumentalities and combinations particularly pointed out hereinafter.

Initial coin offerings are the latest fad for many emerging cryptocurrency companies and projects. From the recently completed Lisk, Waves and Mycelium coin offerings to the historic crowd sale by the DAO — which was subsequently hacked for about $60 million — to Bitland, Project Decorum, Elastic Project and a good number more sales, the trend is clear. Cryptocurrency organizations are viewing their initial coin offerings as an opportunity to build capital and to provide a near-seamless method to distribute a percentage of their digital coins in exchange for a vested interest or stake in the organization. The stake in the corporation will naturally vary from offering to offering. ICOs are similar to initial public offerings issued by corporations: They are essentially the first sale of stock in the form of an organization's cryptocurrency. ICOs can be bought with fiat currency or with another digital currency at a set exchange rate. Unlike what may be found in a typical IPO — especially the most popular ones such as last year's Ferrari, First Data and FitBit IPOs — an ICO lets people of all classes and ethnicities participate because of the low barrier to entry. Further, the sale occurs online, so it's borderless. The entire phenomenon is an interesting mechanism carried out by cryptocurrency developers who have recognized the potential of digital currency and decentralizing technology. However, most if not all cryptocurrency varieties now emerge with esoteric blockchain-based features, capabilities and/or applications. Therefore, coin offerings are also pigeonholed by existing within a niche sector: anything blockchain-based. Sure, there are many ways you can subdivide or subcategorize cryptocurrencies. However, the resounding and important question is: Can every blockchain-based project to emerge produce something innovative and of future value? Ethereum's offering in the summer of 2014 is a strong, if not paramount, example. The coin sale's immediate aftermath was a bumpy road. With a supply of 72,524,960 ether (abbreviated ETH), Ethereum's market capitalization opened at around $180 million before plummeting to $42 million to finally moving up to $122 million — all within the first week and a half. No one then could have known how the cryptocurrency would become worth more than $1 billion market capitalization — rivaling the world's most valuable cryptocurrency, the one that kindled it all in 2009. But Ethereum offered, and continues to offer, a unique platform within the blockchain space. It incorporates smart contract capability with other emerging features and it allows developers to build applications on top of its blockchain layer. It is an innovative platform that offers and inspires innovation in a wide array of use cases, via products and services that can be based off of the Ethereum's blockchain. It has also spawned some of the most successful crowd sales of recent: the DAO, Augur and DigixGlobal. Yet, great ideas — whether an autonomous, crowdfunding organization (the DAO), a decentralized prediction market (Augur) or an asset-tokenization to apply to physical assets (DigixGlobal) — are not a dime a dozen. Not every token sale or ICO will turn out like Ethereum's. Therefore, ICOs may just serve to dilute the appeal of cryptocurrencies and reduce esteem so critical to the success of emerging technologies. Put another way: The greater quantity of ICOs, the greater the risk of creating a stale investment environment. From a practical investment perspective, whether every cryptocurrency will reach heights set by current giants in the space is something to consider as well. In an article on prospective shifts in computing paradigms published by the nonprofit Institute for Ethics and Emerging Technologies, a nonprofit based in Connecticut, Melanie Swan described: " … a continuously connected seamless physical-world multidevice computing layer, with a blockchain technology overlay for payments, and not just payments, but micropayments, decentralized exchange, token earning and spending, digital asset invocation and transfer, and smart contract issuance and execution; all as the economic layer the web never had." The "connected world" paradigm envisioned above is the beautifully envisioned endgame. Initial coin offerings thus stand at the starting point. Therefore, they should be gauged by two practical factors: Is the technology useful? In other words, does the use case purport to help move toward something beyond the current computing paradigm or what is currently in the market?; How well has the organization moved to achieve its outlined objectives? Only so many companies or teams will innovate and only some will endure. The more projects funded — and that ultimately fail — the worse the result for the general advancement of the industry. Sure, it will not stall the ecosystem; however, it may compound doubt within an already often misunderstood area of technology. The cryptocurrency ecosystem operates on the fringes of tradition, with coin offerings announced, talked about and carried out largely via online forums and without regulation. The entire phenomenon is high-risk and should be treated as such. Steer clear of anything that appears too good to be true, devoid of any clear value proposition and with a lack of transparency in design, leadership and direction. Exercise caution, and do research and a speculative analysis of the value proposition being claimed in coin offerings. Analysis on whether the technology being offered is something that advances or will help advance the current computing paradigm is necessary. Perhaps, in the end, skepticism around every new ICO is a positive sentiment. The wonder is whether too much of one thing will begin to strain the investment environment, especially if promising projects like the ones mentioned fizzle out with no return — and if probability stands true, they wouldn't be the first, nor the last. Brandon Kostinuk is the communications lead at the Vanbex Group, a professional services firm that provides consultation and marketing services to clients in the digital currency and blockchain space. He can be reached at [email protected].

DROID3 Poses Again, This Time With Keyboard Showing The DROID3 made a surprise public appearance this morning and apparently wasn’t done. A lot of of us were wondering how its keyboard would look under what appears to be a much thinner top piece. I think it’s safe to say that we now know. Five rows of fun, with an HDMI port just below it on the side. Slap a stock Google Experience on this phone with a 4″ qHD screen and you could have yourselves a major player here.

Q: find the particular solution of the semi linear equation given the data u(1,y)= ln(y^(-1/2)) semi linear equation the general solution to that equation (general solution) Given the data that u(1,y)=ln(y^(-1/2)) what would the right method be to go from the general solution to the particular solution given the data? particular solution A: This is the continuation of Find the general solution of $x^3u_x-u_y=e^{2u}$ to which a boundary condition is now added. The general solution is $$y-\frac12 e^{-2u}=f(y-\frac{1}{2x^2}) \tag 1$$ and the condition is : $$u(1,y)=\ln(y^{-1/2})=-\frac12\ln(y)$$ $e^{-2u}=e^{\ln(y)}=y\quad$ that we put into $(1)$ with $x=1$ : $$y-\frac12 y=f(y-\frac{1}{2}) $$ $$\frac12 y=f(y-\frac{1}{2})$$ Let $\quad X=y-\frac{1}{2} \quad\implies\quad y=X+\frac12$ $$\frac12 (X+\frac12)=f(X)$$ Now the function $f$ is determined : $$f(X)=\frac12X +\frac14$$ We put it into $(1)$ where $X=y-\frac{1}{2x^2}$ $$y-\frac12 e^{-2u}= \frac12(y-\frac{1}{2x^2}) +\frac14$$ $$e^{-2u}= y+\frac{1}{2x^2} -\frac12$$ $$-2u= \ln\left(y+\frac{1}{2x^2} -\frac12\right)$$ The particular solution satisfying the specified condition is : $$u=-\frac12\ln\left(y+\frac{1}{2x^2} -\frac12\right)$$

Sağlıklı Beslenme Piramidi Menü Planlaması Yaparken Dikkat Edilmesi Gereken Hususlar Hizmet verilen grubun yaşı ve cinsiyetine göre besin ögesi gereksinimleri Besin çeşitliliğinin olması ve besinlerin kalitesi Hizmet verilen kişi ya da grupların özel durumları, fiziksel aktivite düzeyleri ve beslenme alışkanlıkları Mutfak harcamalarına ayrılan bütçe Yemek yiyen günlük kişi sayısı Mutfaktaki araç ve gereçler Mutfaktaki personel sayısı Bulunan bölgenin iklimi ve coğrafi özellikleri Neden Menü Planlaması Yapılmalı? Yeterli ve dengeli beslenmeyi sağlaması Yemek artıkları oluşmasının önüne geçmesi Biyolojik olarak doyum sağladığı gibi psikolojik olarak da doyum sağlaması Maliyeti kontrol altında tutması Yemek yapan kişinin, aile bireylerinin, restoran çalışanlarının ve yönetimin huzurlu olması Satın alma konusunda kolaylıklar sunması Toplu beslenmede başarı Menü Planlaması ile Sabah Kahvaltısında Dikkat Edilmesi Gerekenler Kahvaltıda her gün peynir, süt, yumurta gibi besinlerden en az birisi mutlaka olmalıdır. Kahvaltılık temel yiyecek olarak yumurta, peynir, yağ-reçel ve zeytin kullanılır. Kahvaltıda içeceğin yanında temel yiyeceklerden en az 2 tanesi kesinlikle olmalıdır. Yumurta haftada 2 defa listede olabilir. Kahvaltılık temel içecekler; süt, çay, ve taze sıkılmış meyve sulardır. Süt, haftada en az 2 defa listede yer almalıdır. Yağ ve reçel kahvaltılık tek çeşittir. Ayrı olarak değerlendirilmemelidir. Kahvaltının monotonluğunu engellemek için peynir olarak; beyaz, kaşar ve tulum kullanılabilir. Aynı şekilde zeytin ve reçel çeşitliliğine de yer verilebilir. Menü Planlaması ile Öğle ve Akşam Yemeklerinde Dikkat Edilmesi Gerekenler Yemekler arasında renk, tat, şekil ve kıvam uyumu olmalıdır. Yemekler, birinci, ikinci ve üçüncü grup şeklinde en az 3 kapta bulunmalıdır. Etli sebze yemekleriyle birlikte zeytinyağlı sebze yemekleri ve dolmaların yanında da pilav, makarna gibi yemekler verilmemelidir. Pilavın, böreğin ve makarnanın yanında tatlı olmamalıdır. Zeytinyağlı sebze yemekleriyle birlikte salata verilmemelidir. Genel olarak çorba, akşam yemeklerinde, kuru baklagiller ise öğle yemeklerinde yer almalıdır. Yemek Gruplarının Oluşturulması Birinci Yemek Grubu : Menü planlama yapılırken ilk olarak et, yumurta, kuru baklagiller grubundan yemeklerin belirlenmesi gerekir. Her çeşit etli yemek, balık, yumurtalı yemekler, etli sebze yemekleri ve dolmalar ana yemek olarak seçilir. Bu gruptaki besinleri barındıran çorbalar ise birinci yemek sayılır. : Menü planlama yapılırken ilk olarak et, yumurta, kuru baklagiller grubundan yemeklerin belirlenmesi gerekir. Her çeşit etli yemek, balık, yumurtalı yemekler, etli sebze yemekleri ve dolmalar ana yemek olarak seçilir. Bu gruptaki besinleri barındıran çorbalar ise birinci yemek sayılır. İkinci Yemek Grubu : Bu grup, ilk gruba göre değişmekle birlikte tahıl ve sebze yemeklerinden seçilir. Ana yemek et, yumurta, tahıl, balık, tavuk gibi bol proteinli besinlerden oluşuyorsa, ikinci yemek sebzelerden yapılabilir. Eğer ana yemek etli sebze ise, ikinci yemeğin makarna ve börek gibi karbonhidrat açısından zengin olan yemeklerden yapılması gerekir. : Bu grup, ilk gruba göre değişmekle birlikte tahıl ve sebze yemeklerinden seçilir. Ana yemek et, yumurta, tahıl, balık, tavuk gibi bol proteinli besinlerden oluşuyorsa, ikinci yemek sebzelerden yapılabilir. Eğer ana yemek etli sebze ise, ikinci yemeğin makarna ve börek gibi karbonhidrat açısından zengin olan yemeklerden yapılması gerekir. Üçüncü Yemek Grubu: Üçüncü yemek grubu da birinci ve ikinci gruba göre değişiklik gösterir. Öğünde sebze yemeği yoksa, üçüncü yemek olarak salata ya da meyve verilir. Menü planlaması ile süt grubuna yer verilmemişse, yoğurt, cacık ve ayran üçüncü yemek grubuna eklenebilir. İkinci yemek tahıllardan oluşmuşsa, bu grupta ise hamur tatlısına yer verilebilir. Bir Günlük Menü Planlama Örneği Sabah Peynirli Omlet Domates Siyah Zeytin Çay Öğle Orman Kebabı Pilav Yoğurt Akşam Erzincan Çorbası Izgara Tavuk Zeytinyağlı Pırasa Çikolatalı Puding Menü planlama ve yöntemi hakkında bilgiler vermeye devam ediyoruz. En yaygın günlük menü listesi, 3 ana öğünde her besin grubundan yeterli miktarlar ile hazırlanır. Yemek gruplarını ise şunlardır:

Taking the pulse: medical student workforce intentions and the impact of debt. To define what factors are important to medical students as they make decisions about where they will live, work and train after graduation, and to explore the effects of student debt A mixed quantitative-qualitative questionnaire to all 5th and 6th year medical students residing in New Zealand in 2008. Questions related to students' perspectives of the workforce, debt, and workforce intentions. 372 medical students completed the survey (55% response rate from those in NZ at the time of the survey). Fifty-two percent of students planned to leave New Zealand at the start of PGY2 or 3. The average debt was $75,752. Thirty-six percent said their debt would influence their choice of vocation, 39% their choice of location of work in New Zealand and 64% their choice of locality of work in the world. Twenty-six percent and 25% believed that they would be valued by the hospital management and government respectively. Students most commonly cited financial incentives to work overseas and to locum. Strategies to counter emigration trends in the New Zealand health workforce need an holistic approach. Debt levels need to be countered, and the perceived lack of value of graduates needs to be rectified.

Serum and wound drain ropivacaine concentrations after wound infiltration in joint arthroplasty. Ropivacaine blood and drain levels were measured in 20 hip and 15 total knee arthroplasties after intraoperative wound infiltration with 150 to 200 mL (360-400 mg) of ropivacaine, followed by a 48-hour intra-articular pain pump infusion of 1000 mg (knees) and 300 mg (hips) commencing 12 hours postoperatively. Concentrations were below 2 microg/mL over the first 12 hours before the pain pump increased levels. Peak total ropivacaine concentration ranged from 0.65 to 4.36 microg/mL with the pain pump. The high infiltration doses produced levels below or within the safe threshold of 1 to 3 microg/mL. Pain pump infusion produced some C(max) levels above 3.0 microg/mL, but there was no clinical evidence of toxicity. Wound drain amounts (0.53-26.69 mg) indicate reinfusion should be safe, although further study is needed to confirm this.

Highlands row over armed police POLICE officers are now regularly carrying firearms while supporting colleagues on normal duties in the Highlands, in a major departure from the established approach to policing. POLICE officers are now regularly carrying firearms while supporting colleagues on normal duties in the Highlands, in a major departure from the established approach to policing. QUESTIONS: John Finnie is raising the issue with Police Scotland. Custom byline text: David Ross Highland CorrespondenT The Highlands and Islands MSP who discovered the move, which followed the creation of a single police force last year, is to raise the issue in Holyrood and with the Chief Constable of Police Scotland Stephen House. John Finnie, the Independent MSP for the Highlands and Islands who was a police officer and a full-time elected official of the Scottish Police Federation (SPF), said it was a "worrying development". Officers can be armed when keeping a watching brief on customers dispersing from night clubs in the early hours of the morning, it has emerged. Mr Finnie, who was also a ­parliamentary liaison officer to Justice Secretary Kenny MacAskill until he left the SNP in 2012 in protest at the party's ­decision to end its long-standing opposition to Nato membership, said: "There was an armed response vehicle (ARV) in the old Northern Constabulary force area. But then the firearms were stored in locked gun-safe in the boot of the vehicle and could only be removed from the safe on the authorisation of a senior officer. "But I am now reliably informed that, since the advent of Police Scotland, officers deployed in the ARV wear a side-arm all the time." He said these officers were routinely deployed policing the major trunk roads and on occasion support other operational officers on non-firearm-related police ­business. This included supporting officers at the time when the nightclubs are closing and people disperse. "So, you have armed uniformed officers on the streets of the ­Highlands for what is routine police business of monitoring crowds leaving licensed premises," he said. He added that given his background in the police and the federation, he recognised and accepted the need for a risk assessment of every situation. However, he could not understand how any meaningful assessment could identify a routine need for guns. "I understand this is uniform practice across Scotland. But the routine deployment of armed ­officers in the Highlands, even in small numbers, is a very worrying development." He said he was dismayed at Police Scotland's failure to recognise the unique nature of policing in the Highlands and Islands. "I will write the chief constable reminding him the Highlands and Islands is the safest place in UK because of public support - and co-operation could be threatened by police appearing militarised and unapproachable. I also intend raising this matter at the Parliament's Police Committee." When asked whether officers could be wearing side-arms while supervising the departure of late-night revellers, Chief Inspector Charles Armstrong said: "All officers within specialist services, which includes armed policing, are deployed in support of their colleagues in territorial divisions. "They have their part to play in keeping people safe and that includes addressing concerns within communities and responding to calls. I can confirm armed-response officers within Police Scotland are routinely armed and have been since April 1, 2013." Police Scotland was criticised when it cracked down on saunas in Edinburgh that sold sex. The practice had been tolerated for health and safety reasons under Lothians Police, but Strathclyde took a tougher approach on its patch and critics said it was this tougher policy that appeared to be adopted under the new national force. Commenting & Moderation We moderate all comments on HeraldScotland on either a pre-moderated or post-moderated basis. If you're a relatively new user then your comments will be reviewed before publication and if we know you well and trust you then your comments will be subject to moderation only if other users or the moderators believe you've broken the rules

Field of the Invention The present invention relates to an image processing device, an image processing method, and a program. Description of the Related Art Recently, technology referred to as augmented reality (AR) has been drawing attention whereby an image obtained by imaging a real space and modified through a specific process is presented to a user. In the AR technology, useful information on an object in a real space shown in an input image may be inserted into the image to be output as an output image, for example. That is, in the AR technology, typically, a large part of the image presented to the user shows the real space, and some part of the image may be processed in accordance with an application purpose. Such a characteristic is in contrast to virtual reality in which an entire (or a large part) of the output image is composed using computer graphics (CG). By using the AR technology, for example, advantages such as easy understanding of a situation of the real space by a user or work support based on the output image may be provided. Further, in the AR technology, in addition to the technique involving inserting useful information on an object in a real space into an image obtained by imaging a real space, there is also a technique of presenting to a user useful information on an object in a real space in a superimposing manner on a visual field of a user who is viewing the real space. In this technique, the useful information on an object in the real space is presented to the user by being optically composited with the visual field of the user who is viewing the real space by using a half mirror and the like. Also in the case of using such AR technology, for example, advantages such as easy understanding of a situation of the real space by a user or work support may be provided. In the AR technology, in order to present really useful information to the user, it is important that a computer accurately understands the situation of the real space. Therefore, technology aimed to understand the situation of the real space, which serves as a basis of the AR technology, has been developed. For example, Japanese Patent Application Laid-Open No. 2008-304268 discloses a method of dynamically generating an environment map representing a three-dimensional positions of objects existing in a real space by applying technology referred to as simultaneous localization and mapping (SLAM) capable of simultaneously estimating a position and posture of a camera and a position of a feature point shown in an image of the camera. Note that, a basic principle of the SLAM technology using a monocular camera is disclosed in “Real-Time Simultaneous Localization and Mapping with a Single Camera” (Andrew J. Davison, Proceedings of the 9th IEEE International Conference on Computer Vision Volume 2, 2003, pp. 1403-1410).

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UA researchers put the bite on mosquitoes January 15, 2008 By Flinn Foundation [Source: Deborah Daun, BIO5 Institute] – Few things sting like a mosquito’s bite–especially if that bite carries a disease such as malaria, yellow fever, Dengue fever, or West Nile virus. But if a team of University of Arizona (UA) life sciences researchers has their way, one day mosquito bites may prove deadly to the mosquitoes as well.“Our goal is to turn the female mosquito’s blood meal into the last meal she ever eats,” explains project leader Roger L. Miesfeld, a professor of biochemistry and molecular and cellular biology in the UA College of Science and a member of BIO5 and the Arizona Cancer Center. Other UA researchers involved with the project include Patricia Y. Scaraffia, Guanhong Tan, Jun Isoe, BIO5 member Vicki H. Wysocki, and the late Michael A. Wells. These researchers have discovered that one particular mosquito species, Aedes aegypti, has a surprisingly complex metabolic pathway, one that requires its members to excrete toxic nitrogen after gorging on human blood. If the mosquitoes fail to do so, they’ll also fail to lay eggs–and will likely sicken and die. Scaraffia, a research assistant professor in UA’s department of biochemistry and molecular biophysics, and the other members of the team are publishing their findings in the January 15, 2008 issue of the Proceedings of the National Academy of Sciences. The research was funded by the National Institutes of Health. Miesfeld and his colleagues are seeking a molecule that is harmless to humans, but that will gum up the works of mosquito metabolism, forcing the mosquitoes to hang onto the nitrogen. Such a molecule would kill both the mosquitoes and their would-be progeny–thus slowing the spread of disease. Once found, this molecule–and similar molecules aimed at other mosquito species–could be developed into an insecticide and sprayed in places where mosquitoes congregate, such as around water and on mosquito netting. The researchers envision one day also developing an oral insecticide–a mosquito-slaying pill that members of a community with a high instance of, say, yellow fever or malaria might take in order to reduce the mosquito population. The pill wouldn’t be a vaccine; if someone who took it were then bitten by a disease-carrying mosquito, they would still become infected. However, the mosquito would ingest the insecticide, along with the human blood, causing her to bear fewer young and possibly die before she could bite anyone else. “The whole community would essentially become one big mosquito trap,” Miesfeld explains, and over time, mosquito populations and disease rates would both decline. “It would be a group effort that in the long run could have a huge impact.” In a world where both mosquitoes and the diseases they carry are becoming increasingly resistant to known insecticides and medicines, finding new ways to fight them is crucial. “This would be one more weapon in our arsenal against diseases that kill millions of people a year,” Miesfeld says.

Mechalarum Page-a-Day: Page 6 - Bugs Although I do not have the privilege of calling myself a professional software developer, I've spent enough time around them (two decades and change) to know what goes into building digital products. Namely, it's impossible to create anything technological without countless iterations, and in some cases you create more bugs than you fix. Additionally, your program or device is almost guaranteed to display the most embarrassing of those bugs on Big Demo Day. In some science fiction worlds, technology is effortlessly integrated into everyday life. Not in the Citadel! The difficulty in perfecting technology is, in fact, essential to the story. Life ain't perfect, and neither are widgets.

1. Introduction {#sec0005} =============== Hydatid bone disease is caused by the *Echinococcus granulosus worm*. This zoonosis is endemic in the Mediterranean, Middle East, Asia, Africa and many South American countries, and it is a major public health and economic problem in the Patagonian region of Argentina. Osseous involvement accounts for 0.5 %--4 % of cases in humans. The spine (35 %) and the pelvis (21 %) are the most commonly involved skeletal sites, followed by the long bones, especially the femur (16 %) \[[@bib0005]\]. The location of the disease in the humerus is infrequent. Epidemiological research in some regions has shown: 3 cases of hydatidosis of the humerus between 1971 and 2010 in Serbia, 1 case between 2010 and 2017 in Kazagistan, and no cases have been reported in Spain between 1989 and 2017 \[[@bib0005]\]. Out of 329 cases of hydatidosis reported between 2005 and 2016, only one case of hydatidosis in the humerus was reported in Turkey \[[@bib0010]\]. There is no consensus as regards the medical treatment of hydatidosis in the humerus. Local procedures such as partial resection, curettage, and bone grafting or filling with cement PMMC POLIMETILMETACRILATO were indicated. More severe or extended cases, or where complications such as pathological fractures have occurred, require mega prosthesis or massive allograft for reconstruction \[[@bib0015],[@bib0020]\]. Another radical option is the limb ablation, but the rescue surgery often has better results and is more easily tolerated by the patient, than complete limb amputation, both emotionally and socially \[[@bib0025],[@bib0030]\]. The use of allografts, alloprosthetic composites and prosthetic replacements to reconstruct the proximal humerus after tumor resection and associated complications, have been well described \[[@bib0035]\]. However, the affections of the entire humerus and the recurrences present a challenge of treatment for the reconstruction and rescue of the limb \[[@bib0040]\]. No reports of hydatid disease in the entire humerus have been found in the bibliography. This research presents one case of primary hydatid bone disease affecting the entire humerus, which was treated with radical resection and total endoprosthesis of the humerus. This work has been reported in line with the SCARE criteria \[[@bib0045]\], and it has been performed in a private academic hospital. Informed consent was obtained from the patient included in the study, and the institutional Ethical Committee approved the retrospective medical chart review [Fig. 1](#fig0005){ref-type="fig"}.Fig. 1An AP x-rays showing humeral shaft fracture. B MRI showing total humerus compromise.Fig. 1 Case. A 24-year-old patient derived from another center with a diagnosis of delayed healing of left humerus diaphyseal fracture (non-dominant side) with four months of evolution. He had been treated with a brace. At the moment of admission, he had pain and limited motion of his shoulder and elbow. Anteroposterior and lateral radiological images of the humerus showed a line of oblique fracture in the distal third of the diaphysis, and heterogeneous osteolytic and multiloculated images along the entire humerus. The MRI showed pathological images that compromised the entire diaphysis of the humerus and soft tissues at the expansive fracture site, with thinning of the cortical bones. It was decided to perform a biopsy, which resulted in hydatid cysts. The wound of the puncture evolved with the secretion of the hydatids prolonging its healing. Surgical treatment was planned in order to save the limb, given the aggressiveness and expansion of the lesions. Treatment. Oncological resection of the humerus and total replacement of the same with a non-conventional prosthesis designed for the patient was indicated. The surgery was performed using an anteromedial approach extended to the entire diaphysis, achieving total resection. The macroscopic anatomy showed involvement of the entire humerus, including the proximal and distal end with fistulas and vesicles with parasites. The prosthesis at its proximal end consisted of a unipolar head with provisions to attach abductors [Fig. 2](#fig0010){ref-type="fig"}.Fig. 2A--C macroscopic humeral image with proximal, distal, and shaft hydatidosis.Fig. 2 Soft tissue reconstruction was achieved by suturing the divided tendons, i.e., tendons of the rotator cuff, pectoralis major, subscapularis, latissimus dorsi, and teres major, and extensors and flexors in the elbow to the prosthesis. The arm was placed in a sling for six weeks, and the first ROM exercises are started at the elbow. Passive ROM exercises of the shoulder started at four weeks, followed by active exercises at three months and eight weeks after the operation. The patient was also treated with albendazole (15 mg/kg/ d orally) before the operation for one month and after the operation for six months as adjuvant therapy. Result: After two years of follow-up, the patient was pain-free with a range of elbow mobility of 15--90° of flexion-extension, with 0° of pronosupination, and wrist and hand with a full range of motion. At his shoulder he had 30° of anterior flexion, rot ext of 10° and internal rot at the gluteal level. No local or general disease recurrences were observed. The patient could perform only administrative tasks. The ASES score was 58.33 and Mayo elbow was 65, Quick Dash was 42.3. At present, the patient does not perform tasks or effort with the affected upper limb but can use the hand and the elbow [Fig. 3](#fig0015){ref-type="fig"}, [Fig. 4](#fig0020){ref-type="fig"}.Fig. 3A, B total humerus prosthesis. C postoperative X-rays.Fig. 3Fig. 4Histopatology showing hydatid cysts.Fig. 4 2. Discussion {#sec0010} ============= Hydatidosis is an endemic disease in different areas of the planet. The primary form in the bones is rare; the humerus has hardly been reported. There is scant information on severe cases with involvement of the entire humerus, including both epiphyses. The information published following our literature review is case reports with local treatment (curettage), most of them without prolonged follow-up. Surgery is usually the first treatment option. There have been reports of local resections and osteosynthesis, but we believe that in this particular case is not feasible. Curettage in the humerus has been proposed, but multiple local recurrences have been reported \[[@bib0050]\], as well as the need for multiple reoperations due to local recurrences and loosening of osteosynthesis in fractures. In addition, short follow-ups or lack thereof are reported \[[@bib0055], [@bib0060], [@bib0065]\]. The use of drugs, such as albendazole also seems to be controversial. In an epidemiological study of 17 patients diagnosed with hydatidosis, eight were found with bone involvement, two patients in the spine, 3 in the pelvis, and only 1 in the humerus and 1 in the tibia. None received albendazole, and no treatment or evolution was reported \[[@bib0070]\]. The only real curative procedure seems to be a radical excision. However, it was only possible in 16 percent of the cases \[[@bib0070]\]: when the axial bone-spine, the pelvic bone or the femur are affected. In many cases, combined therapies based on surgery and antiparasitic drugs are used. However, it is known that the cure is difficult, and recurrence is frequent. We have not identified information on humerus hydatidosis that involves all the bone and its treatment with total resection of the humerus with an endoprosthesis. The radical resection as salvage of the entire humerus is a challenge. The options are the allograft and the halo prostheses. For both procedures, functional expectations are scarce mainly at shoulder level, functioning as spacers, and to preserve the function of the wrist and hand. In addition to other general complications such as infections and loosening. Regarding the total endoprostheses, they present functional complications in the shoulder and elbow. There is little experience with tumors, and they are considered a reasonable option in terms of elbow and hand preservation \[[@bib0075]\]. Another problem is usually the migration and dislocations of the prosthesis \[[@bib0080]\]. Natarajan et al· reported the use of a customized megaprosthesis for the reconstruction of bone defects secondary to hydatid bone resection in 3 patients, with excellent results and without recurrences. However, this study had a brief follow-up, which underestimates the likelihood of recurrent infection or loosening of the implant, which complicates prosthetic reconstruction \[[@bib0040]\]. Many authors have reported on the limited active ROM of the shoulder after the proximal humeral and THERs \[[@bib0085],[@bib0090]\]. Careful soft tissue reconstruction with reattachment of the rotator cuff tendons did not seem to improve the results. Despite the poor movement at the shoulder, patients had excellent manual dexterity and functional use of their hands. The use of tubes and vascular graft for the capsular reconstruction and for the reattachment of the soft tissue in addition to tendon transfers has not shown better results in terms of joint mobility \[[@bib0085],[@bib0095]\]. In the present case, the functional result was not good at the level of the shoulder but functional in the wrist, hand, and elbow, and without recurrence of the disease until the last follow-up. It was planned with that objective. Recently, techniques with better shoulder results have been reported \[[@bib0085]\]. These authors used a fully expandable humerus prosthesis in a girl with osteosarcoma. We did not find reports about massive allograft reconstruction in the humerus. Until the last follow-up of our patient, we did not find glenohumeral subluxation. Marulanda et al. observed no shoulder dislocations in their series of 16 patients with proximal humeral replacement reconstructed with an aortograft mesh. They found that the sleeve created by the aortograft allows for mechanical restraint and facilitates soft tissue reconstruction after tumor resection \[[@bib0100]\]. Puri and Gulia reported a similar experience with no observation of shoulder dislocations in their series of 20 patients with total humeral \[[@bib0105]\]. 3. Conclusions {#sec0015} ============== The cases of hydatidosis in the humerus are infrequent; the management is not standardized, the local resection plus graft and osteosynthesis conserving the bone has shown complications and recurrences. To aim for healing, a radical procedure is necessary with resections and reconstructions with prostheses. Although functional results may be limited, the preservation of the limbs and the function of the hand and wrist are feasible. Funding {#sec0020} ======= We did not receive any funding. Ethical approval {#sec0025} ================ The institutional Ethical Committee approved the retrospective medical chart review. Consent {#sec0030} ======= Informed consent was obtained from the patient included in the study, and the institutional Ethical Committee approved the retrospective medical chart review. Author's contribution {#sec0035} ===================== Juan Martin Patiño and Alejandro Jose Ramos Vertiz contributed to study design, data collection, data interpretation, and writing. Registration of research studies {#sec0040} ================================ This manuscript is not a human study, but a case report. Guarantor {#sec0045} ========= Juan Martin Patiño. Provenance and peer review {#sec0050} ========================== Not commissioned, externally peer-reviewed. Declaration of Competing Interest ================================= We do not have conflicts of interest to declare. This article did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

<!-- ! Licensed to the Apache Software Foundation (ASF) under one ! or more contributor license agreements. See the NOTICE file ! distributed with this work for additional information ! regarding copyright ownership. The ASF licenses this file ! to you under the Apache License, Version 2.0 (the ! "License"); you may not use this file except in compliance ! with the License. You may obtain a copy of the License at ! ! http://www.apache.org/licenses/LICENSE-2.0 ! ! Unless required by applicable law or agreed to in writing, ! software distributed under the License is distributed on an ! "AS IS" BASIS, WITHOUT WARRANTIES OR CONDITIONS OF ANY ! KIND, either express or implied. See the License for the ! specific language governing permissions and limitations ! under the License. !--> ## <a id="ComparisonFunctions">Comparison Functions</a> ## ### greatest ### * Syntax: greatest(numeric_value1, numeric_value2, ...) * Computes the greatest value among arguments. * Arguments: * `numeric_value1`: a `tinyint`/`smallint`/`integer`/`bigint`/`float`/`double` value, * `numeric_value2`: a `tinyint`/`smallint`/`integer`/`bigint`/`float`/`double` value, * .... * Return Value: * the greatest values among arguments. The returning type is decided by the item type with the highest order in the numeric type promotion order (`tinyint`-> `smallint`->`integer`->`bigint`->`float`->`double`) among items. * `null` if any argument is a `missing` value or `null` value, * any other non-numeric input value will cause a type error. * Example: { "v1": greatest(1, 2, 3), "v2": greatest(float("0.5"), double("-0.5"), 5000) }; * The expected result is: { "v1": 3, "v2": 5000.0 } ### least ### * Syntax: least(numeric_value1, numeric_value2, ...) * Computes the least value among arguments. * Arguments: * `numeric_value1`: a `tinyint`/`smallint`/`integer`/`bigint`/`float`/`double` value, * `numeric_value2`: a `tinyint`/`smallint`/`integer`/`bigint`/`float`/`double` value, * .... * Return Value: * the least values among arguments. The returning type is decided by the item type with the highest order in the numeric type promotion order (`tinyint`-> `smallint`->`integer`->`bigint`->`float`->`double`) among items. * `null` if any argument is a `missing` value or `null` value, * any other non-numeric input value will cause a type error. * Example: { "v1": least(1, 2, 3), "v2": least(float("0.5"), double("-0.5"), 5000) }; * The expected result is: { "v1": 1, "v2": -0.5 }

Knee morphometric and alignment measurements with MR imaging in young adults with central cartilage lesions of the patella and trochlea. The goal of this study was to assess whether common measurements of patellar and trochlear morphology and patellar alignment are associated with central cartilage lesions of the patella and trochlea using magnetic resonance imaging (MRI). The MRI examinations of 58 patients (38 women, 20 men; mean age, 28.59 years [range: 19-35 years]) with central cartilage lesions of the patella and trochlea were retrospectively compared to those obtained in 102 control subjects (57 women, 45 men; mean age, 27.05 years [range: 20-35 years]). Patients had Modified Noyes Classification grade IIA, IIB or III cartilage defects whereas control subjects had normal MRI examination of the knee as determined by two radiologists. Patellar measurements of facet asymmetry, patellar tilt, lateral patellofemoral angle, Insall-Salvati ratio, and patellotrochlear cartilage overlap were performed in patients and control subjects along with trochlear measurements of the trochlear depth and width, and sulcal angle. Multivariate logistic regression adjusted for age and body mass index was used to assess associations. The ratio of the lengths of the medial to lateral facets of the patella (OR=2.7×10-3; P<0.001), angle of the median eminence of the patella (OR=1.05; P=0.040), lateral patellofemoral angle (OR=0.91; P=0.048), Insall-Salvati ratio (OR=364.4; P<0.001) and edema in the superolateral aspect of Hoffa's fat pad (OR=6.52; P<0.001) were significantly associated with central cartilage lesions of the patella and trochlea. Central cartilage lesions of the patellofemoral joint are associated with patellar and trochlear morphology, and patellar alignment.

package au.edu.wehi.idsv.visualisation; import au.edu.wehi.idsv.visualisation.TrackedBuffer.NamedTrackedBuffer; import htsjdk.samtools.util.CloserUtil; import java.io.File; import java.io.FileOutputStream; import java.io.IOException; import java.lang.ref.WeakReference; import java.nio.charset.StandardCharsets; import java.time.LocalDateTime; import java.util.ArrayList; import java.util.Collections; import java.util.List; /** * Tracks intermediate buffer sizes for memory tracking purposes. * @author Daniel Cameron * */ public class BufferTracker { private final List<WeakReference<TrackedBuffer>> bufferObjects = Collections.synchronizedList(new ArrayList<WeakReference<TrackedBuffer>>()); private final File output; private final float writeIntervalInSeconds; private volatile Worker worker = null; /** * Tracking * @param owner owning object. If the owning object is garbage collected, tracking stops * @param output output file * @param writeIntervalInSeconds interval between */ public BufferTracker(File output, float writeIntervalInSeconds) { this.output = output; this.writeIntervalInSeconds = writeIntervalInSeconds; } public void start() { worker = new Worker(); worker.setName("BufferTracker"); worker.setDaemon(true); worker.start(); } public void stop() { if (worker == null) return; Worker currentWorker = worker; worker = null; currentWorker.interrupt(); } public synchronized void register(String context, TrackedBuffer obj) { obj.setTrackedBufferContext(context); bufferObjects.add(new WeakReference<TrackedBuffer>(obj)); } private synchronized String getCsvRows() { StringBuilder sb = new StringBuilder(); String timestamp = LocalDateTime.now().toString(); for (WeakReference<TrackedBuffer> wr : bufferObjects) { TrackedBuffer buffer = wr.get(); if (buffer != null) { for (NamedTrackedBuffer bufferSize : buffer.currentTrackedBufferSizes()) { sb.append(timestamp); sb.append(','); sb.append(bufferSize.name); sb.append(','); sb.append(Long.toString(bufferSize.size)); sb.append('\n'); } } } return sb.toString(); } private void append() { FileOutputStream os = null; String str = getCsvRows(); if (!str.isEmpty()) { try { os = new FileOutputStream(output, true); os.write(str.getBytes(StandardCharsets.UTF_8)); os.flush(); os.close(); os = null; } catch (IOException e) { } finally { CloserUtil.close(os); } } } private class Worker extends Thread { @Override public void run() { while (true) { try { Thread.sleep((long)(writeIntervalInSeconds * 1000)); append(); } catch (InterruptedException e) { } finally { if (worker != this) { return; } } } } } }

(CNN) Washington Mayor Muriel Bowser on Wednesday declared a state of emergency and a public health emergency as the nation's capital looks to mitigate the spread of the novel coronavirus. The move -- which will help free up resources and funding -- came alongside news of six new cases in Washington, bringing the total number to 10. "While this is an administrative action, largely, it will give me more authority to implement and fund the measures that we need to monitor and respond to Covid-19 in our community," Bowser told reporters. The announcement came just hours after the World Health Organization declared the coronavirus a pandemic with more than 1,200 cases in the US and growing clusters of the disease forcing many Americans to change their daily lives. In Washington, this includes the suspension of visitor tours in the US Capitol, according to a Capitol official. Additionally, a city health advisory published earlier Wednesday recommended that "non-essential mass gatherings, including conferences and conventions, be postponed or canceled" through the end of the month. Read More

Backpack frames have traditionally been rigid structures to which a pack is secured. Traditional backpack frames distribute the load of the pack to the wearer's hips and bring the pack in contact with the wearer's back. This construction has been unsatisfactory as it is uncomfortable for the wearer to have the pack in contact with his or her back. The close proximity of the pack to the wearer's back prevents air from circulating in the area and cooling the wearer. Additionally, the contents of the pack may exert pressure on the wearer's back causing additional discomfort for the wearer. Another difficulty with these prior backpack frames is that they are generally complex in structure and expensive to manufacture. Since these frames are generally constructed of materials that are permanently secured together, the frame cannot be reduced in size for storage or flattened for easier transport or storage. It is therefore an object of my invention to provide a backpack frame that may be easily assembled and disassembled in the field without special tools, that may be easily flattened for storage or transport, and that, when applied to the back of a wearer, will avoid any hard surface contact with the body while at the same time distributing the weight of the pack to the wearer's hips.

“Intensify forward fire power!” - Admiral Piett, Return of the Jedi Establish galactic control with prizes from the Quarter 1 Tournament Kit for Star Wars™: Armada! Quarterly Tournament Kits provide prizes for a local game store to award to players for competing in their events and a new kit will be released each quarter with refreshed prizes to invigorate participation. Contact your local game store today to see if they are hosting any tournament kit events and join in on the fun! What Prizes are in the Star Wars: Armada Quarter 1 Tournament Kit? Core Prize Card - 16 copies of the alternate art card “Turbolaser Reroute Circuits” - a favorite upgrade of Admirals who are willing to risk lowering their defenses for a little more punch. Elite Prize Card - 2 copies of the alternate art card “TIE Interceptor”. When you want a squadron that exists simply to destroy an enemy squadron, look no further than the TIE Interceptor. Elite Prize Item - 2 sets of 5 acrylic Engineering Tokens. Our team of engineers have been working hard to bring these to you and they’re finally here! An additional copy of each prize card is included for the organizer to keep or award, at their discretion. What Can I Expect at a Tournament Kit Event? Every Star Wars: Armada Tournament Kit comes with an optional outline for a tournament that your retailer may choose to follow. If your local retailer announces they are hosting a Fleet Patrol event, you can expect to play two matches of Star Wars: Armada. If you do well in the competition, you will be eligible to earn some cool prizes, as detailed in the Event Outline below. Retailers can also choose to create their own tournaments and special events, such as demo days, charity events, or alternate play formats in order to support their gaming community. If this is the case, they may have different plans on how they would like to award these prizes. Make sure you contact your local game store to see what kind of event they are hosting! Be a Part of the Growing Star Wars: Armada Community Each quarter, there will be a new set of tournament kits for our Organized Play supported games! Keep your eyes out for the contents of the next kit and make sure that your local game store has ordered theirs for the season! Note: The alternate art cards in this kit are produced via FFG's In-House Manufacturing and may appear slightly different in color and texture from the game's other cards.

Is Coinbase going to solve the thorny challenges of proof-of-stake (PoS) blockchain governance or centralize those systems even further? That’s the question experts in the space are pondering with the recent announcement that Coinbase Custody will offer staking support for Maker, Tezos and Cosmos. The move means institutional investors will be able to vote on blockchain governance matters directly through their Coinbase accounts. “We’re hoping to bring online, frankly, the majority of institutional investors,” Coinbase Custody CEO Sam McIngvale told CoinDesk. “We’re growing these three assets under custody and hoping to see an increased turnout of these votes.” That this is possible is because blockchains like Cosmos, Tezos and Maker use staking to guide their networks. Staking relies on participants essentially buying into the blockchain’s decision-making council. In addition to backing their votes with deposits – staking their claim with real assets – in Tezos and Cosmos stakers can also earn token rewards for fueling the network’s growth. But, in turn, these networks are beginning to face the same challenge democracies have grappled with for centuries: How do we incentivize voting? Lessons from Maker This Coinbase Custody addition was driven by institutional demand, since few PoS token holders so far are actually participating in governance. According to Becker, nearly 10 percent of Maker tokens were involved in a recent vote to hike fees related to ethereum-pegged stablecoin loans. While cryptocurrency researcher David Hoffman estimated only 0.58 percent of unique wallets holding Maker participated, Becker told CoinDesk the turnout was high among institutional holders that are able to vote. Indeed, he said the most recent fee-raising proposal had the highest turnout to date with 61 voters. For many institutional holders, Becker argued, compliance requirements can still complicate the logistics of using tokens to vote. “If you’re an institution and you represent third-party investors,” Becker explained, “you do need third-party custody as extra protection, to make sure those assets are looked after in a safe manner.” That’s where the recent move by Coinbase comes in. On one hand, a Coinbase voting interface could boost turnout by being convenient for the largest Maker holders, including Polychain Capital (founded by Coinbase’s first employee), 1confirmation (founded by an early Coinbase employee) and Andreessen Horowitz’s crypto fund (co-managed by a Coinbase board member). On the other, Tezos holder and veteran crypto investor Meltem Demirors tweeted that Coinbase Custody could become a “wallet-driven proxy voting platform that influences, gathers, aggregates, and reports on user behavior.” In response, Coinbase’s McIngvale said the custody solution is a business-to-business tool for institutions, not individuals. So there is scant “user behavior” to track. Plus, he said there aren’t currently any plans to analyze or utilize voting data, adding: “We are here to provide support, pure infrastructure and services to enable our clients to participate in these networks however they want to. What they’re doing is not really our business. In fact, our business is to protect their anonymity as best we can, and the security of their funds.” McIngvale said the exchange already custodies roughly 4 percent of Maker tokens, less than the 6 percent Andreessen Horowitz owns by itself. Meanwhile, the Maker Foundation, which employs MakerDAO COO Steven Becker, owns more than 22 percent of the total Maker supply and only sells these tokens to institutions that previous holders like Polychain deem to be committed to participating in governance, according to Becker. Tendermint Inc director Zaki Manian, co-creator of the Cosmos ecosystem, told CoinDesk each of the three PoS assets Coinbase Custody will support requires a unique approach to governance options based on whether the systems automate changes, like Tezos, or merely show sentiment, like Cosmos. Either way, governance is often inseparable from politics. “If a big validator [staker] votes for something early, it gives that proposal a lot more legitimacy,” Manian said, adding: “I have a thesis that they [Coinbase Custody] are going to have a hard time keeping them [stakers] because … custody is designed not to be a nimble business and staking has to be a nimble business.” So far, staking votes have appeared to revolve around money rather than infrastructure. Comparable to semi-automated Maker votes about stability fees for stablecoin loans, the first Cosmos vote was an affirmative move toward inflation. “It’s going to be interesting because part of the dynamics of proof-of-stake is how frequently do people just vote to give themselves more money?” Manian said. Binance wants in Coinbase is hardly the only giant entering the game of stakes. On April 3, Binance’s custody provider Trust Wallet also announced plans to support Tezos staking features by the end of Q2 2019. Unlike institution-centric Coinbase Custody, retail-friendly Trust Wallet will create delegation features on the mobile wallet first, then potentially add voting options down the road. “We’re already talking to the Cosmos people to bring that [staking] technology to them,” Trust Wallet founder Viktor Radchenko told CoinDesk. “It’s going to be all open source so that any community, like Maker, who would like to come in and have this functionality will be able to do it.” Radchenko said he believes custody providers and wallets should offer simplified interfaces for users “to be involved in the blockchain itself” when it comes to PoS governance. From Manian’s perspective, exchange competition will benefit stakers and token buyers. “Binance and Coinbase are both going real hard on bringing these features to various customer bases,” he said. Additionally, Manian said the “elephant in the room” is whether exchanges like Binance and Coinbase will offer governance derivatives – the ability to buy votes without owning the underlying assets – to retain institutional stakers as the competition heats up. So far no exchange has announced any intention to offer such derivatives. To the contrary, Radchenko said that token holders and issuers may be too preoccupied with voting dynamics these days, given how nascent the technology is. “We plan to bring that functionality [voting] a little bit later just because there’s less usage [than staking],” Trust Wallet’s Radchenko said. “Governance features will come a little bit later, maybe not even this year.” As for the value Coinbase aims to offer institutional players, McIngvale said: “We’ll work with our clients to figure out how to grow their impact as they start to participate in more and more governance processes.” UPDATE (April 17, 13:40 UTC): Added clarifying information about how staking operates for the Tezos, Maker and Cosmos blockchain networks. Coinbase image via Shutterstock

The specific aims of the project are (1) to determine the types of impairments of emotional expression and perception that are found in autism, and (2) to investigate the neuropsychological bases of these impairments. Measures will be taken on three groups of subjects: autistic children ranging from 6 to 18 years of age, and developmentally-matched normal and mentally retarded children. These three groups will be compared in terms of their ability to perceptually discriminate and categorize facial expressions, and in terms of their spontaneous expression of various emotions. Measures of spontaneous emotional behavior will be taken in both a controlled laboratory setting and in naturalistic school situations. Parents will also provide information about their child's emotional behavior in a questionnaire The above measures will be used to investigate whether individual differences in affective and social ability are related to specific patterns of frontal and parietal lobe functioning. Electroencephalographic (EEG) recordings of right and left frontal and parietal activity will be taken in response to a variety of affective and cognitive stimuli. EEG will be subjected to power spectrum analysis to yield measures of alpha band power frequency (8-13 Hz). Measures of right and left parietal and frontal integrated alpha will be used to infer differential cortical activation during affective and cognitive processing. Comparisons of patterns of brain activity will be made among autistic, and matched mentally retarded and normal subjects. Specific predictions regarding the pattern of brain dysfunction expected in autistic subjects are based on current neuropsychological models of emotion. The long term objectives of the research program are to shed light on the neuropsychological bases of early infantile autism and to use this information to develop more effective diagnostic and treatment methods for autistic persons.

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Hymenobacter gelipurpurascens Hymenobacter gelipurpurascens is a bacterium from the genus of Hymenobacter which has been isolated from soil from Alberta in Canada. References External links Type strain of Hymenobacter gelipurpurascens at BacDive - the Bacterial Diversity Metadatabase Category:Flavobacteria Category:Bacteria described in 2006

Editor’s note: The following is from the chapter “Introduction to Strategy” of the book Deep Green Resistance: A Strategy to Save the Planet. This book is now available for free online. by Aric McBay I do not wish to kill nor to be killed, but I can foresee circumstances in which both these things would be by me unavoidable. We preserve the so-called peace of our community by deeds of petty violence every day. Look at the policeman’s billy and handcuffs! Look at the jail! Look at the gallows! Look at the chaplain of the regiment! We are hoping only to live safely on the outskirts of this provisional army. So we defend ourselves and our hen-roosts, and maintain slavery. —Henry David Thoreau, “A Plea for Captain John Brown” Anarchist Michael Albert, in his memoir Remembering Tomorrow: From SDS to Life after Capitalism, writes, “In seeking social change, one of the biggest problems I have encountered is that activists have been insufficiently strategic.” While it’s true, he notes, that various progressive movements “did just sometimes enact bad strategy,” in his experience they “often had no strategy at all.”1 It would be an understatement to say that this inheritance is a huge problem for resistance groups. There are plenty of possible ways to explain it. Because we sometimes don’t articulate a clear strategy because we’re outnumbered and overrun with crises or immediate emergencies, so that we can never focus on long-term planning. Or because our groups are fractured, and devising a strategy requires a level of practical agreement that we can’t muster. Or it can be because we’re not fighting to win. Or because many of us don’t understand the difference between a strategy and a goal or a wish. Or because we don’t teach ourselves and others to think in strategic terms. Or because people are acting like dissidents instead of resisters. Or because our so-called strategy often boils down to asking someone else to do something for us. Or because we’re just not trying hard enough. One major reason that resistance strategy is underdeveloped is because thinkers and planners who do articulate strategies are often attacked for doing so. People can always find something to disagree with. That’s especially true when any one strategy is expected to solve all problems or address all causes claimed by progressives. If a movement depends more on ideological purity than it does on accomplishments, it’s easy for internal sectarian arguments to take priority over getting things done. It’s easier to attack resistance strategists in a burst of horizontal hostility than it is to get things together and attack those in power. The good news is that we can learn from a few resistance groups with successful and well-articulated strategies. The study of strategy itself has been extensive for centuries. The fundamentals of strategy are foundational for military officers, as they must be for resistance cadres and leaders. PRINCIPLES OF WAR AND STRATEGY The US Army’s field manual entitled Operations introduces nine “Principles of War.” The authors emphasize that these are “not a checklist” and do not apply the same way in every situation. Instead, they are characteristic of successful operations and, when used in the study of historical conflicts, are “powerful tools for analysis.” The nine “core concepts” are: Objective. “Direct every military operation toward a clearly defined, decisive, and attainable objective.” A clear goal is a prerequisite to selecting a strategy. It is also something that many resistance groups lack. The second and third requirements—that the objective be both decisive and attainable—are worth underlining. A decisive objective is one that will have a clear impact on the larger strategy and struggle. There is no point in going after one of questionable or little value. And, obviously, the objective itself must be attainable, because otherwise efforts toward that operation objective are a waste of time, energy, and risk. Offensive. “Seize, retain, and exploit the initiative.” To seize the initiative is to determine the course of battle, the place, and the nature of conflict. To give up or lose the initiative is to allow the enemy to determine those things. Too often resistance groups, especially those based on lobbying or demands, give up the initiative to those in power. Seizing the initiative positions the fight on our terms, forcing them to react to us. Operations that seize the initiative are typically offensive in nature. Mass. “Concentrate the effects of combat power at the decisive place and time.” Where the field manual says “combat power,” we can say “force” more generally. When Confederate General Nathan Bedford Forrest summed up his military theory as “get there first with the most,” this is what he was talking about. We must engage those in power where we are strong and they are weak. We must strike when we have overwhelming force, and maneuver instead of engaging when we are outmatched. We have limited numbers and limited force, so we have to use that when and where it will be most effective. Economy of Force. “Allocate minimum essential combat power to secondary efforts.” In order to achieve superiority of force in decisive operations, it’s usually necessary to divert people and resources from less urgent or decisive operations. Economy of force requires that all personnel are performing important tasks, regardless of whether they are engaged in decisive operations or not. Maneuver. “Place the enemy in a disadvantageous position through the flexible application of combat power.” This hinges on mobility and flexibility, which are essential for asymmetric conflict. The fewer a group’s numbers, the more mobile and agile it must be. This may mean concentrating forces, it may mean dispersing them, it may mean moving them, or it may mean hiding them. This is necessary to keep the enemy off balance and make that group’s actions unpredictable. Unity of Command. “For every objective, ensure unity of effort under one responsible commander.” This is where some streams of anarchist culture come up against millennia of strategic advice. We’ve already discussed this under decision making and elsewhere, but it’s worth repeating. No strategy can be implemented by consensus under dangerous or emergency circumstances. Participatory decision making is not compatible with high-risk or urgent operations. That’s why the anarchist columns in the Spanish Civil War had officers even though they despised rulers. A group may arrive at a strategy by any decision-making method it desires, but when it comes to implementation, a hierarchy is required to undertake more serious action. Security. “Never permit the enemy to acquire an unexpected advantage.” When fighting in a panopticon, this principle becomes even more important. Security is a cornerstone of strategy as well as of organization. Surprise. “Strike the enemy at a time or place or in a manner for which they are unprepared.” This is key to asymmetric conflict—and again, not especially compatible with a open or participatory decision-making structures. Resistance movements are almost always outnumbered, which means they have to use surprise and swiftness to strike and accomplish their objective before those in power can marshal an overpowering response. Simplicity. “Prepare clear, uncomplicated plans and clear, concise orders to ensure thorough understanding.” The plan must be clear and direct so that everyone understands it. The simpler a plan is, the more reliably it can be implemented by multiple cooperating groups. Many of these basic principles fall into conflict with the favored actions of dissidents. Protest marches, petitions, letter writing, and so on often lack a decisive or attainable objective, give the initiative to those in power, fail to concentrate force at a decisive juncture, put excessive resources into secondary efforts, limit maneuvering ability, lack unified command for the objective (such as there is), have mixed implementation of security, and typically offer no surprise. They are, however, simple plans, if that’s any consolation. In fact, these strategic principles might as well come from a different dimension as far as most (liberal) protest actions are concerned. That’s because the military strategist has the same broad objective as the radical strategist: to use the decisive application of force to accomplish a task. Neither strategist is under the illusion that the opponent is going to correct a “mistake” if this enemy gets enough information or that success can occur by simple persuasion without the backing of political force. Furthermore, both are able to clearly identify their enemy. If you identify with those in power, you’ll never be able to fight back. An oppositional culture has an identity that is distinct from that of those in power; this is a defining element of cultures of resistance. Without a clear knowledge of who your adversary is, you either end up fighting everyone (in classic horizontal hostility) or no one, and, in either case, your struggle cannot succeed.

Q: Prestashop - Layered Navigation is Empty I'm working on a prestashop site and facing some problem with the layered navigation. It appears for the top level categories but when I click on any of the sub categories, it goes to blank. There is nothing to filter on. It should atleast display a Price filter. And yes I do have products in the category with different prices so a price filter should appear. In my header.tpl file I have {if isset($left_column_size) && !empty($left_column_size)} <div id="left_column" class="column col-xs-12 col-sm-{$left_column_size|intval}">{$HOOK_LEFT_COLUMN}</div> {/if} Which hides the left column when I don't have anything in my layered navigation. I want to diagnose why I don't have anything in my layered navigation. A: To display the filter(s) in all categories you have to configure a blocklayered 'template' with all categories of your shop. I'll post a screenshot to better understating :) Enter in the module configuration, then click on "Add new template" Then on 'check all' After that configure your filters (in the bottom of page) as you wish. Save, now the filters will display in all categories. ;)

Q: How to send WM_ENTERSIZEMOVE? I have the following code called on WM_MOVE procedure TForm15.WMMove(var Message: TMessage); begin if( (((TWMMove(Message).XPos + Self.Width >= Form14.Left) and (TWMMove(Message).XPos <= Form14.Left)) or ((TWMMove(Message).XPos <= Form14.Left + Form14.Width) and (TWMMove(Message).XPos >= Form14.Left))) and (((TWMMove(Message).YPos + Self.Height >= Form14.Top) and (TWMMove(Message).YPos <= Form14.Top)) or ((TWMMove(Message).YPos <= Form14.Top + Form14.Height) and (TWMMove(Message).YPos >= Form14.Top)))) then begin Self.DragKind := dkDock; end else Self.DragKind := dkDrag; end; It's probably the ugliest if statement you've seen in your life,but that's not the question. :) It's supposed to change DragKind if the current form(Self) is somewhere inside the mainForm(Form14). However,When It sets DragKind to dkDock ,it doesn't make the currentForm(Self) dockable unless the user stops moving the form and start moving it again,so I'm trying to do the following: If the result from the statement above is non zero and dkDock is set then Send the following messages to the form: WM_EXITSIZEMOVE //stop moving the form WM_ENTERSIZEMOVE //start movement again However,I don't know how to do it: SendMessage(Self.Handle,WM_EXITSIZEMOVE,?,?); I tried using random parameters(1,1) ,but no effect.Maybe that's not the right way? A: It looks like those two messages are notifications - directly sending them probably doesn't do anything. As Raymond Chen once said (horribly paraphrased), directly sending these messages and expecting action is like trying to refill your gas tank by moving the needle in the gauge. WM_SIZING and WM_MOVING are messages that you can use to monitor a user changing a window's size and position, and block further changes. From MSDN: lParam Pointer to a RECT structure with the current position of the window, in screen coordinates. To change the position of the drag rectangle, an application must change the members of this structure. So you can change the members to force the window to remain in a single position.

Open-air preparation of cross-linked CO2-responsive polymer vesicles by enzyme-assisted photoinitiated polymerization-induced self-assembly. The large-scale preparation of block copolymer nano-objects with tunable and reversible carbon dioxide (CO2) responsiveness is a challenging goal in the polymer community. Herein, an open-air strategy via enzyme-assisted photoinitiated polymerization-induced self-assembly (photo-PISA) in water is developed for preparing cross-linked CO2-responsive vesicles at high solids contents. The CO2 responsiveness of these vesicles can be controlled by changing the composition of the core-forming block. Finally, inorganic/organic hybrid vesicles are prepared by mixing CO2-responsive vesicles with silica (SiO2) nanoparticles, and the amount of SiO2 nanoparticles can be further increased by treating with CO2.

Thihapate Thihapate was a royal, official and military title. Royalty Thihapate of Sagaing: King of Sagaing (r. 1352−64) Thihapate of Yamethin: governor of Yamethin (r. 1330s−40s) Governors Thihapate of Tagaung: governor of Tagaung (r. 1367−1400), also known as Nga Nauk Hsan Thihapate of Mogaung: sawbwa of Mohnyin−Mogaung (r. 1442−50) Generals Ne Myo Thihapate: Early Konbaung period general Category:Burmese royal titles

We had a cross-country move and Tony made sure we knew what was happening every step of the way! The move was tough enough by itself, but it would have been even harder without Tony’s help. Thanks for the wonderful support Tony! Howard Hampton and Karen Staehling-Hampton – Purchased and Sold in Bothell – 2006 We were glad to be referred to you thank you for your efforts in finding our ideal home! Once we gave an outline of requirements for what we wanted in a home, you went to work trying to locate it. With the low inventory, it took some time. However, you were very flexible and accommodating to our time schedule, so we could quickly see any potential contender. Once we did find the perfect home, we appreciate that you were on it, so we could pull the trigger and secure the home. You were very much hands on when it came to the finalizing, making sure everyone involved was on pace to get this purchase wrapped up. Thank you! Kevin Hazelwood and Asfira Usmanova – Purchased in Woodinville – 2013

/* [auto_generated] boost/numeric/odeint/util/ublas_wrapper.hpp [begin_description] Resizing for ublas::vector and ublas::matrix [end_description] Copyright 2011-2013 Mario Mulansky Copyright 2011-2013 Karsten Ahnert Distributed under the Boost Software License, Version 1.0. (See accompanying file LICENSE_1_0.txt or copy at http://www.boost.org/LICENSE_1_0.txt) */ #ifndef BOOST_NUMERIC_ODEINT_UTIL_UBLAS_WRAPPER_HPP_INCLUDED #define BOOST_NUMERIC_ODEINT_UTIL_UBLAS_WRAPPER_HPP_INCLUDED #include <boost/type_traits/integral_constant.hpp> #include <boost/numeric/ublas/vector.hpp> #include <boost/numeric/ublas/matrix.hpp> #include <boost/numeric/ublas/lu.hpp> #include <boost/numeric/ublas/vector_expression.hpp> #include <boost/numeric/ublas/matrix_expression.hpp> #include <boost/numeric/odeint/algebra/vector_space_algebra.hpp> #include <boost/numeric/odeint/algebra/default_operations.hpp> #include <boost/numeric/odeint/util/is_resizeable.hpp> #include <boost/numeric/odeint/util/state_wrapper.hpp> /* extend ublas by a few operations */ /* map norm_inf onto reduce( v , default_operations::maximum ) */ namespace boost { namespace numeric { namespace odeint { template< typename T , typename A > struct vector_space_norm_inf< boost::numeric::ublas::vector<T,A> > { typedef T result_type; result_type operator()( const boost::numeric::ublas::vector<T,A> &x ) const { return boost::numeric::ublas::norm_inf( x ); } }; template< class T , class L , class A > struct vector_space_norm_inf< boost::numeric::ublas::matrix<T,L,A> > { typedef T result_type; result_type operator()( const boost::numeric::ublas::matrix<T,L,A> &x ) const { return boost::numeric::ublas::norm_inf( x ); } }; } } } /* additional operations: * abs( v ) * v / w * a + v */ namespace boost { namespace numeric { namespace ublas { // elementwise abs - calculates absolute values of the elements template<class T> struct scalar_abs: public scalar_unary_functor<T> { typedef typename scalar_unary_functor<T>::value_type value_type; typedef typename scalar_unary_functor<T>::argument_type argument_type; typedef typename scalar_unary_functor<T>::result_type result_type; static BOOST_UBLAS_INLINE result_type apply (argument_type t) { using std::abs; return abs (t); } }; // (abs v) [i] = abs (v [i]) template<class E> BOOST_UBLAS_INLINE typename vector_unary_traits<E, scalar_abs<typename E::value_type> >::result_type abs (const vector_expression<E> &e) { typedef typename vector_unary_traits<E, scalar_abs<typename E::value_type> >::expression_type expression_type; return expression_type (e ()); } // (abs m) [i] = abs (m [i]) template<class E> BOOST_UBLAS_INLINE typename matrix_unary1_traits<E, scalar_abs<typename E::value_type> >::result_type abs (const matrix_expression<E> &e) { typedef typename matrix_unary1_traits<E, scalar_abs<typename E::value_type> >::expression_type expression_type; return expression_type (e ()); } // elementwise division (v1 / v2) [i] = v1 [i] / v2 [i] template<class E1, class E2> BOOST_UBLAS_INLINE typename vector_binary_traits<E1, E2, scalar_divides<typename E1::value_type, typename E2::value_type> >::result_type operator / (const vector_expression<E1> &e1, const vector_expression<E2> &e2) { typedef typename vector_binary_traits<E1, E2, scalar_divides<typename E1::value_type, typename E2::value_type> >::expression_type expression_type; return expression_type (e1 (), e2 ()); } // elementwise division (m1 / m2) [i] = m1 [i] / m2 [i] template<class E1, class E2> BOOST_UBLAS_INLINE typename matrix_binary_traits<E1, E2, scalar_divides<typename E1::value_type, typename E2::value_type> >::result_type operator / (const matrix_expression<E1> &e1, const matrix_expression<E2> &e2) { typedef typename matrix_binary_traits<E1, E2, scalar_divides<typename E1::value_type, typename E2::value_type> >::expression_type expression_type; return expression_type (e1 (), e2 ()); } // addition with scalar // (t + v) [i] = t + v [i] template<class T1, class E2> BOOST_UBLAS_INLINE typename enable_if< is_convertible<T1, typename E2::value_type >, typename vector_binary_scalar1_traits<const T1, E2, scalar_plus<T1, typename E2::value_type> >::result_type >::type operator + (const T1 &e1, const vector_expression<E2> &e2) { typedef typename vector_binary_scalar1_traits<const T1, E2, scalar_plus<T1, typename E2::value_type> >::expression_type expression_type; return expression_type (e1, e2 ()); } // addition with scalar // (t + m) [i] = t + m [i] template<class T1, class E2> BOOST_UBLAS_INLINE typename enable_if< is_convertible<T1, typename E2::value_type >, typename matrix_binary_scalar1_traits<const T1, E2, scalar_plus<T1, typename E2::value_type> >::result_type >::type operator + (const T1 &e1, const matrix_expression<E2> &e2) { typedef typename matrix_binary_scalar1_traits<const T1, E2, scalar_plus<T1, typename E2::value_type> >::expression_type expression_type; return expression_type (e1, e2 ()); } } } } /* add resize functionality */ namespace boost { namespace numeric { namespace odeint { /* * resizeable specialization for boost::numeric::ublas::vector */ template< class T , class A > struct is_resizeable< boost::numeric::ublas::vector< T , A > > { typedef boost::true_type type; const static bool value = type::value; }; /* * resizeable specialization for boost::numeric::ublas::matrix */ template< class T , class L , class A > struct is_resizeable< boost::numeric::ublas::matrix< T , L , A > > { typedef boost::true_type type; const static bool value = type::value; }; /* * resizeable specialization for boost::numeric::ublas::permutation_matrix */ template< class T , class A > struct is_resizeable< boost::numeric::ublas::permutation_matrix< T , A > > { typedef boost::true_type type; const static bool value = type::value; }; // specialization for ublas::matrix // same size and resize specialization for matrix-matrix resizing template< class T , class L , class A , class T2 , class L2 , class A2 > struct same_size_impl< boost::numeric::ublas::matrix< T , L , A > , boost::numeric::ublas::matrix< T2 , L2 , A2 > > { static bool same_size( const boost::numeric::ublas::matrix< T , L , A > &m1 , const boost::numeric::ublas::matrix< T2 , L2 , A2 > &m2 ) { return ( ( m1.size1() == m2.size1() ) && ( m1.size2() == m2.size2() ) ); } }; template< class T , class L , class A , class T2 , class L2 , class A2 > struct resize_impl< boost::numeric::ublas::matrix< T , L , A > , boost::numeric::ublas::matrix< T2 , L2 , A2 > > { static void resize( boost::numeric::ublas::matrix< T , L , A > &m1 , const boost::numeric::ublas::matrix< T2 , L2 , A2 > &m2 ) { m1.resize( m2.size1() , m2.size2() ); } }; // same size and resize specialization for matrix-vector resizing template< class T , class L , class A , class T_V , class A_V > struct same_size_impl< boost::numeric::ublas::matrix< T , L , A > , boost::numeric::ublas::vector< T_V , A_V > > { static bool same_size( const boost::numeric::ublas::matrix< T , L , A > &m , const boost::numeric::ublas::vector< T_V , A_V > &v ) { return ( ( m.size1() == v.size() ) && ( m.size2() == v.size() ) ); } }; template< class T , class L , class A , class T_V , class A_V > struct resize_impl< boost::numeric::ublas::matrix< T , L , A > , boost::numeric::ublas::vector< T_V , A_V > > { static void resize( boost::numeric::ublas::matrix< T , L , A > &m , const boost::numeric::ublas::vector< T_V , A_V > &v ) { m.resize( v.size() , v.size() ); } }; // specialization for ublas::permutation_matrix // same size and resize specialization for matrix-vector resizing template< class T , class A , class T_V , class A_V > struct same_size_impl< boost::numeric::ublas::permutation_matrix< T , A > , boost::numeric::ublas::vector< T_V , A_V > > { static bool same_size( const boost::numeric::ublas::permutation_matrix< T , A > &m , const boost::numeric::ublas::vector< T_V , A_V > &v ) { return ( m.size() == v.size() ); // && ( m.size2() == v.size() ) ); } }; template< class T , class A , class T_V , class A_V > struct resize_impl< boost::numeric::ublas::vector< T_V , A_V > , boost::numeric::ublas::permutation_matrix< T , A > > { static void resize( const boost::numeric::ublas::vector< T_V , A_V > &v, boost::numeric::ublas::permutation_matrix< T , A > &m ) { m.resize( v.size() , v.size() ); } }; template< class T , class A > struct state_wrapper< boost::numeric::ublas::permutation_matrix< T , A > > // with resizing { typedef boost::numeric::ublas::permutation_matrix< T , A > state_type; typedef state_wrapper< state_type > state_wrapper_type; state_type m_v; state_wrapper() : m_v( 1 ) // permutation matrix constructor requires a size, choose 1 as default { } }; } } } #endif // BOOST_NUMERIC_ODEINT_UTIL_UBLAS_WRAPPER_HPP_INCLUDED

High resolution analysis of functional determinants on human tissue-type plasminogen activator. Sixty-four variants of human tissue-type plasminogen activator (tPA) were produced using recombinant DNA techniques. Charged residues were converted to alanine in clusters of from one to four changes per variant; these clusters spanned all the domains of the molecule. The variants were expressed by mammalian cells and were analyzed for a variety of properties. Variants of tPA were found that had reduced activity with respect to each tested property; in a few cases increased activity was observed. Analysis of these effects prompted the following conclusions: 1) charged residues in the nonprotease domains are less involved in fibrin stimulation of tPA activity than those in the protease domain, and it is possible to increase the fibrin specificity (i.e. the stimulation of tPA activity by fibrin compared to fibrinogen) by mutations at several sites in the protease domain; 2) the difference in enzymatic activity between the one- and two-chain forms of tPA can be increased by mutations at several sites on the protease domain; 3) binding of tPA to lysine-Sepharose was affected only by mutations to kringle-2, whereas binding to fibrin was affected most by mutations in the other domains; 4) clot lysis was influenced by mutations in all domains except kringle-2; 5) sensitivity to plasminogen activator inhibitor-1 seems to reside exclusively in the region surrounding residue 300. A model of the tPA protease domain has been used to map some of the critical residues and regions.

Le continent africain maintient les avancées réalisées depuis 2000 en matière de mobilisation des ressources intérieures, les recettes fiscales étant restées stables en 2016 selon l’édition 2018 des Statistiques des recettes publiques en Afrique, une étude réalisée conjointement par l’OCDE (Organisation de coopération et de développement économiques), le Forum sur l’administration fiscale en Afrique (ATAF) et l’Union africaine (UA). D’après les données internationalement comparables concernant les 21 pays couverts par ce rapport, « le ratio moyen impôts/PIB s’est établi à 18,2 % en 2016, au même niveau qu’en 2015, ce qui représente une nette amélioration par rapport au chiffre de 13,1 % enregistré en 2000 », explique l’OCDE dans un communiqué publié le 31 octobre. Le ratio impôts/PIB varie « considérablement » d’un pays à l’autre La troisième édition des Statistiques des recettes publiques en Afrique, lancée officiellement à Paris à l’occasion du 18e Forum économique international sur l’Afrique, montre toutefois que le ratio impôts/PIB varie considérablement d’un pays à l’autre au sein du continent africain, de 7,6 % en République démocratique du Congo à 29,4 % en Tunisie en 2016. Six pays – l’Afrique du Sud, Maurice, le Maroc, le Sénégal, le Togo et la Tunisie – affichent des ratios impôts/PIB supérieurs ou égaux à 20 % pour l’année 2016. En comparaison, le ratio moyen impôts/PIB était en 2016 de 22,7 % dans les pays d’Amérique latine et des Caraïbes et de 34,3 % dans les pays de l’OCDE, poursuit le communiqué. La publication fait ainsi apparaître des tendances contrastées. « Entre 2015 et 2016, les recettes fiscales rapportées au PIB ont augmenté dans 11 des pays couverts et diminué dans dix d’entre eux. C’est le Botswana qui a enregistré la plus forte hausse (1,3 point de pourcentage), suivi du Mali (1,2 point de pourcentage). C’est en République démocratique du Congo et au Niger en revanche que les baisses les plus sensibles (de plus de 2,0 points de pourcentage) ont été observées. Les variations des ratios impôts/PIB sont principalement dues à des facteurs économiques. Le déclin des prix du pétrole, conjugué à un ralentissement de l’activité des compagnies minières et pétrolières, est à l’origine du repli des recettes fiscales constaté en République démocratique du Congo et au Niger alors qu’au Botswana, les recettes ont été dopées par une forte expansion des ventes de diamants. Au Mali en revanche, le mouvement ascendant des recettes fiscales, exprimées en pourcentage du PIB, s’explique pour partie par le renforcement de l’administration fiscale », souligne l’OCDE. La contribution de la fiscalité des revenus s’accroît Les économies africaines dépendent beaucoup de la fiscalité des biens et des services, qui procure 54,6 % des recettes fiscales totales si l’on se réfère à la moyenne des 21 pays africains concernés par cette publication. La taxe sur la valeur ajoutée (TVA) à elle seule représente 29,3 % des recettes fiscales encaissées. Cependant, « la contribution de la fiscalité des revenus s’accroît : les recettes provenant des impôts sur les revenus et les bénéfices représente 34,3 % des recettes fiscales totales à l’échelle du continent africain en 2016 et elle a été le principal moteur de la croissance des recettes fiscales depuis 2000, celles-ci étant passées de 2,6 % du PIB à 6,2 % du PIB entre 2000 et 2016. Les recettes fiscales tirées de l’impôt sur les bénéfices des sociétés ont progressé de 1,4 point de pourcentage pendant cette période pour atteindre 2,8 % du PIB tandis que les recettes tirées de l’impôt sur le revenu des personnes physiques ont été portées de 2,1 % à 3,00 % du PIB en 2016, un record historique », souligne le rapport. La publication contient également des données relatives aux recettes non fiscales, dont le déclin se poursuit en moyenne en 2016 dans les 21 pays couverts par l’étude, mais qui demeurent une source importante de recettes pour certains pays. Les recettes non fiscales, qui englobent des recettes tirées de ressources naturelles et des dons, ont excédé 5 % du PIB dans neuf des 21 pays couverts par la publication. L’OCDE souligne que les Statistiques des recettes publiques en Afrique est un volet important de la Stratégie de l’UA pour l’harmonisation des statistiques en Afrique. « L’édition 2018 contient un chapitre spécial dédié à cette stratégie, décrivant la démarche suivie pour mettre en place un système statistique efficace qui embrasse le développement et l’intégration de l’Afrique sur le plan politique, économique, social, environnemental et culturel », conclut le communiqué. N.B.

Flute Musical Instrument For Cake Yes, musical instruments also have a family just like we do. They are grouped together to form a family depending on the sounds that they produce. Let us introduce you to the most common members of a. Evanston Police Department officers on Tuesday morning responded to a report of a theft in the 800 block of Davis Street in downtown Evanston. A 46-year-old Evanston resident came to the EPD. Rock Progressivo Italiano definition aka "RPI" "So it’s an established fact that in Italy during the period between 1971-1974, a music movement existed where bands would challenge each other to see who could be the most imaginative, who could create the album for the ages. Learning the Music. Listen to other flute players to get a sense of the range of possibilities. You can also get ideas from listening to pipers, fiddlers, whistle players, Students of Stephanie Bailey’s Physics 6B course are donating the instruments they made for their final project to a small school in the Philippines. (Photos by Carolyn Lagattuta) Asia Stautz (Crown, Find flute in Western Cape! View Gumtree Free Online Classified Ads for flute in Western Cape and more. (CNN)– I keep my hands hovering in the space. Around a dozen keen members — and 150 part-time – form the basis of this music chapter; designing, building and re-purposing instruments to suit ambi. Clarinet Quartets, Quintets and Larger Ensemble Music (Updated 2 November 2018) This page has sheet music (scores) for clarinet quartets, quintets, and larger clarinet ensembles.It includes both collections and individual pieces. (CNN)– I keep my hands hovering in the space. Around a dozen keen members — and 150 part-time – form the basis of this music chapter; designing, building and re-purposing instruments to suit ambi. Howe also pursued his interest in the construction of antique woodwind instruments, particularly the oboe, which he had studied as a student. Over the past two decades, he has conducted research and p. A lot of instruments have happy new homes as of Tuesday afternoon. Music for Everyone, the Lancaster-based nonprofit with a mission of cultivating the power of music, distributed instruments to local. (AP) – Never discount the value of a good music teacher. Music for fiddle player and Tiny. This teacher, though, was open-minded and they tried different instruments until they came up with a violi. Howe also pursued his interest in the construction of antique woodwind instruments, particularly the oboe, which he had studied as a student. Over the past two decades, he has conducted research and p. The initiative invites people to donate their gently used musical instruments, for distribution to music programs at Newark and New York City public schools, as well as community music programs. The d. 16th, 17th 18th and 19th Century (1800s) musical instruments, Military and Civilian, along with pictures and pricing. Brooklyn Daily Eagle A new program allowing patrons to borrow musical instruments at Brooklyn Public Library is an overnight sensation. The library officially launched the Musical Instrument Lending L. Where others see trash, Donnie Badgett sees guitars, drums and other instruments. Beyond the door of an unassuming. like N. The sousaphone (US: / ˈ s uː z ə f oʊ n /) is a brass instrument in the same family as the more widely known tuba.Created around 1893 by J.W. Pepper at the direction of American bandleader John Philip Sousa (after whom the instrument was then named), it was designed to be easier to play than the concert tuba while standing or marching, as well as to carry the sound of the instrument above. *** Musician Jokes *** Welcome to the Worlds Largest Collection of Musician Jokes. No instrument, musician or music style is sacred here. Special thanks to Sheldon Wong of Mountain Group Audio and Rick Rosen of the Rick Rosen Marketing Group for helping to get this whole thing started.and to all who have contributed. Pink Elephants On Parade Orchestra Small humans, big art: Free classical for kids in Littleton The Littleton Symphony Orchestra’s. Henry Mancini’s “Pink Pant. The show will feature a mix ofGreat Deals Cd Classical Music Jan 01, 2017 · The 10 Best Classical Releases of 2016: Every year I publish a ‘Best of the Year’ list. The 10 Best Classical RecordingsHymns Of Faith Review We provide free desk, exam, and review copies of many books to professors who are adopting or have adopted one of our texts for their which involved using improvisational approaches through musical instruments, songs and rhythmic cues to target social communication, or non-music intervention, a structurally-matched, play-based inter. Cecilio violins are handcrafted instruments and are tested at our factory. Prior to shipping each instrument is inspected by skilled technicians at our Los Angeles distribution center. Rockabye How To Dance Just Dance Now Published by Ubisoft Game credits. Developed by Ubisoft Paris Studio Ubisoft Pune Studio Massive Entertainment, a Ubisoft Studio. Just Dance Now Active The prize for the best march was awarded to the Co-operative Funeralcare Band. The prize for the best soloist was awarded to Andy Enzor of the Reg Vardy Band. The first modern humans in Europe were playing musical instruments and showing artistic creativity as early as 40,000 years ago, according to new research from Oxford and Tübingen universities. The re. Branding themselves as "Jazz From the East Bay," 510Jazz, named for their home base area code, is a fascinating collective of regional session musicians and world-class vocalists performing Sergio Mendes and Quincy Jones-influenced arrangements of spirited original bossa nova flavored tunes. People who make music out of carrots. The World Carrot Museum has discovered several groups of people who make, and then play, musical instruments from Carrots (and other vegetables and fruit). and drill holes in them to create musical instruments. Not only do they create musical instruments from almost all vegetables that are stiff, they also play music themselves. They have been playing mu. I hope you have found this site to be useful. If you have any corrections, additions, or comments, please contact me.Please note that I am not able to respond to all requests. Black Truffle present the release of Ichida, the first release from the duo of two important, yet often underappreciated musicians, Eiko Ishibashi and Darin Gray.Ishibashi is a singer-songwriter, keyboardist, drummer, and multi-instrumentalist, known in Japan both for her own elaborately conceptual solo albums and for her frequent collaborations with figures such as Jim O’Rourke, Merzbow. Students of Stephanie Bailey’s Physics 6B course are donating the instruments they made for their final project to a small school in the Philippines. (Photos by Carolyn Lagattuta) Asia Stautz (Crown, At the same time, we learn of traditional instruments from all over that are unlike any we’ve seen before. Here are some more in a continuing series on strange and wonderful musical instruments. 1. Wh.

HYPERREFLECTIVE RETINAL SPOTS AND VISUAL FUNCTION AFTER ANTI-VASCULAR ENDOTHELIAL GROWTH FACTOR TREATMENT IN CENTER-INVOLVING DIABETIC MACULAR EDEMA. To assess and correlate early modifications in hyperreflective retinal spots (HRS), retinal sensitivity (RS), fixation stability, and best-corrected visual acuity (BCVA) after anti-vascular endothelial growth factor treatment in naive center-involving diabetic macular edema. Cross-sectional comparative case-control series. Twenty diabetic patients underwent 3 consecutive intravitreal anti-vascular endothelial growth factor injections in the study eye (20 fellow eyes served as control), full ophthalmologic examination including spectral domain optical coherence tomography (Retinascan RS-3000; Nidek, Gamagori, Japan), and microperimetry (MP1; Nidek) at baseline (Visit-V1), 1 month after each injection (V2, V3, V4), and at 6 months (V5). Central retinal thickness, inner and outer retinal thickness, number of HRS, BCVA, RS, and bivariate contour ellipse area were evaluated by analysis of variance test with Bonferroni post hoc test. Correlation analyses were performed by Spearman correlation. In treated eyes, central retinal thickness and inner retinal thickness significantly decreased at V2, V3, V4 versus V1 (P < 0.03 at least for all); the mean number of HRS significantly decreased in both inner and outer retina at all follow-up visits versus V1 (P < 0.008 at least for all); mean RS and bivariate contour ellipse area remained statistically unchanged during the follow-up; BCVA significantly improved at V3, V4, and V5 versus V1 (P = 0.009 at least for all). In fellow eyes, central retinal thickness, HRS, RS, and BCVA did not change at any follow-up. The number of HRS correlated inversely with RS, directly with bivariate contour ellipse area, and not significantly with BCVA. A significant decrease in HRS in the retina after anti-vascular endothelial growth factor treatment is documented. A decrease in HRS correlates with functional parameters, specifically RS. New parameters may be used for treatment evaluation in center-involving diabetic macular edema.

[Predicting the risk of recurrence of duodenal ulcer after vagotomy]. The author suggests a multifactor program for decoding the variant of the course of the postoperative period in patients with duodenal ulcer. It was tested in 199 patients. Three groups of patients with a favourable prognosis, an uncertain prognosis, and with a high risk of recurrent ulcer were distinguished. An individual therapeutic program with consideration for the risk group allows the incidence of postoperative recurrence of ulcer to be reduced by more than three times.

« pas de souci » ou « pas de soucis » ? – orthographe « Il n’y a pas de souci, je peux le faire. Pas de soucis aujourd’hui. » Les expressions commençant par « pas de » posent souvent problème : faut-il mettre le mot qui suit au singulier ou au pluriel ? Un exemple très utilisé dans le langage de tous les jours est « pas de souci ». Alors faut-il écrire « pas de souci » ou « pas de soucis » ? Voici la règle pour ne plus hésiter. Faut-il écrire « pas de souci » ou « pas de soucis » ? La règle : après « pas de », on peut écrire le nom qui suit au singulier ou au pluriel. On écrira « pas de souci » sans « s » s’il s’agit d’un souci particulier, du sentiment d’inquiétude. « Souci » (ou tout autre nom) sera également au singulier après « pas de » s’il décrit une réalité abstraite, non dénombrable. En revanche, on peut parler de plusieurs soucis à la fois. Dans ce cas, on écrira « pas de soucis » dans le sens « il n’y a pas de problèmes » avec l’idée qu’il pourrait y en avoir plusieurs. Exemples : Pas de souci pour sortir ce soir. Je n’ai pas de soucis ce mois-ci. Attention toutefois, selon l’Académie française, l’usage de « pas de souci » (au singulier ou au pluriel) est erroné malgré son adoption large dans la société. Ne l’utilisez donc pas dans vos écritures formelles : On entend trop souvent dire il n’y a pas de souci, ou, simplement, pas de souci, pour marquer l’adhésion, le consentement à ce qui est proposé ou demandé, ou encore pour rassurer, apaiser quelqu’un, Souci étant pris à tort pour « difficulté », « objection ». Selon les cas, on répondra simplement oui, ou bien l’on dira Cela ne pose pas de difficulté, ne fait aucune difficulté, ou bien Ne vous inquiétez pas, Rassurez-vous. Par ailleurs, on voit que les occurrences dans la littérature française de « pas de souci » sans « s » sont plus nombreuses que « pas de soucis » : En conclusion, l’écriture de « pas de souci » peut se faire avec ou sans « s » à la fin. Tout dépend du sens que l’on souhaite donner à notre propos et de la réalité que représente « souci ». N’hésitez pas à parcourir les autres articles pour pouvoir écrire français sans soucis. Vous pouvez aussi partager l’article et laisser un commentaire.

The secular trend in the incidence of hemorrhagic stroke in the region of Osijek, Eastern Croatia in the period 1988-2000--a hospital based study. The purpose of the study was to establish the possible environmental influences in the observed peculiar rising and falling oscillations in the numbers of hemorrhagic stroke (HS) in Eastern Croatia (region of Osijek) during the last thirteen-years' period (1988-2000). In this period 1,222 HS were registered and treated. A constant increase in the incidence of HS was observed, from 60 (in 1988) to 139 (in 1998), with an average annual proportion of 16.5% of all stroke cases. A sharp increase in proportion of HS in total stroke incidence was recorded during the war in Croatia (1991-1995), with a peak incidence of 27.4% in 1993. Typical hypertensive intracerebral hemorrhage (ICH) was the most common (57.1%), atypical ICH occurred in 26.4%, subarachnoid hemorrhage (SAH) in 16.5%. Analysis of the annual number of hypertensive-ICH and SAH disclosed peculiar rising and falling oscillations. These variations were in correlation with heavy living conditions. During the war-period the SAH incidence sharply rose. Immediately after the war it suddenly decreased. The authors named this phenomenon a "pool depletion", supposing the relatively stable proportion of the bearers of aneurysms in population. The observed variations seem to be the consequence of the war stress and other negative psychosocial and economic factors in post-war period, which increases the risk for SAH and typical hypertensive-ICH through complex pathophysiological mechanisms.

Q: Progression bar sync javascript to server time? I have an object which contains some data about progression of a bar but it keeps stopping at 99% and won't continue, i believe its because client time is not going to be the same as server time accurately enough to do it. So i don't know how to solve it. These 2 timers are created server side and sent to the client. myOjb[i].end: 1374805587 //seconds since epoch for when 100% is made myObj[i].strt: 1374805527 //seconds since epoch when it started The function that is calculating the percentage : function clocker() { var now = new Date().getTime() / 1000; for (var i in myObj) { if (myObj[i].end > now) { var remain = myObj[i].end - now; var per = (now - myObj[i].strt) / (myObj[i].end - myBuildings[i].strt) * 100; var per = fix_percentage(per); // stops > 100 and < 0 returns int if true myObj[i].percentage = Math.ceil(per); console.log(myObj[i].percentage); //reaches 99 max if (myObj[i].percentage > 99) { console.log('test'); //never occurs return false; } break; } else { continue; } } setTimeout(clocker, 1000); } function fix_percentage(per){ if(per>100)per=100; if(per<0)per = 0; return Math.round(per); } How could i sync the two together so the timing is more accurate ? A: Edit: Original answer was based on a bad assumption. I think what is happening is that essentially your block setting the percent to 100 might be getting skipped. This would happen if on one iteration, the value of per was < 99.5 but > 88.5. In this case, the rounded per would have a value of 99. Then, one second later when the function gets called again, the outer if block would not be entered due to myObj[i].end > now being false. The following code will make sure that if time expires and the myObj[i].percentage is < 100 because of the above scenario, it will be set to 100 and return like the other if block does. if (myObj[i].end > now) { var remain = myObj[i].end - now; var per = (now - myObj[i].strt) / (myObj[i].end - myBuildings[i].strt) * 100; var per = fix_percentage(per); // stops > 100 and < 0 returns int if true myObj[i].percentage = Math.ceil(per); console.log(myObj[i].percentage); //reaches 99 max if (myObj[i].percentage > 99) { console.log('test'); //never occurs return false; } break; } else if ( (now >= myObj[i].end) && (myObj[i].percentage < 100) ) { console.log('Time expired, but percentage not set to 100') myObj[i].percentage = 100; return false; } else { continue; }

The comprehensive sexual assault assessment tool. The Comprehensive Sexual Assault Assessment Tool (CSAAT) was developed for collection of data about the victims and offenders in cases of rape and sexual assault. The CSAAT provides a systematic guide for victim assessment, evidence documentation, and initial treatment. Use of the CSAAT facilitates collection of investigative data about the victim and the offender that are critical components of victim interviews and crime investigations, as well as victim forensic data. The CSAAT can be used by health care professionals who care for the victims of sexual assault. The tool reflects the major concepts of the Roy Adaptation Model and was designed as a victim evaluation report for clinical and forensic purposes. The CSAAT can also be used to compile agency statistics, as part of the training for sexual assault nurse examiners, and to collect research data. A case study involving two victims illustrates the importance of evidence collection and use of the Federal Bureau of Investigation's Combined DNA Index System (CODIS) for linking victims by offender DNA.

Heretofore, a lot of biodegradable resins and biodegradable compositions, containing, as main components, biodegradable resins such as polylactic acid and fatty acid polyester as well as natural materials such as starch, have hitherto been proposed, and processed biodegradable articles using these biodegradable resins and biodegradable compositions have been provided. For example, JP-A-Hei07-17571 (Patent Document 1) discloses a biodegradable buffer material which contains starch as a main component, and is obtained by adding vegetable fibers and/or protein, followed by blow molding. JP-A-2005-119708 (Patent Document 2) discloses a biodegradable resin composition obtained by blending starch and polyol, monosaccharide or oligosaccharide, and protein. JP-A-Hei05-320401 (Patent Document 3) discloses a biodegradable molded article obtained by blending wheat flour, starch and cellulose, followed by foaming and further firing. However, when natural materials such as starch are used, the resultant product often has poor water resistance and tends to have poor strength. Therefore, JP-A-Hei05-278738 (Patent Document 4) and JP-A-Hei05-57833 (Patent Document 5) and JP-A-2002-355932 (Patent Document 6) each discloses a method of coating the surface of a processed article molded from a biodegradable composition with a water-resistant resin. However, according to this method, coating must be conducted again, resulting in increase of the number of steps. On the other hand, JP-A-Hei06-248040 (Patent Document 7) discloses, as a biodegradable composition having improved impact resistance and improved heat resistance, a composition composed of phenols, sugar and starch. This composition is obtained by applying formation of a resin by the reaction between phenols and sugar. JP-A-2004-137726 (Patent Document 8) discloses a composition for a biodegradable gravel product, which is composed of starch and tannin or polyphenol and, furthermore, protein and a crushed mineral powder, and a divalent metal powder having the chelate mordanting effect with tannin or polyphenol. However, this composition is obtained by supporting a condensation compound of a metal salt and a polyphenol on starch and also contains a divalent metal salt, and therefore it is not suitable for applications such as tablewares. Also, tannins and polyphenols used herein are condensed tannins such as persimmon tannin, tea tannin and bark tannin, and are suitable for use as a substitute of gravel, but are not suitable for processed articles such as tablewares because condensed tannins and divalent metal salts are used and therefore the strength becomes too higher. Furthermore, since the metal salts are used, metals thereof remain after decomposition and thus it is considered that an adverse influence may be exerted on the environment. JP-A-2005-23262 (Patent Document 9) discloses a biodegradable composition using main materials obtained by finely dividing 100% natural materials, for example, grains such as maize, dietary fibers such as weeds, and sugar cane, and natural binders such as persimmon tannin and konjac powder. However, a specific composition ratio is unclear and also it is unclear whether or not the product is actually produced. Since this composition is composed only of natural materials such as cereals, quality of the resultant molded article is not maintained and the molded article is not suitable for use as an industrial product. Furthermore, translation of PCT application No. 9-500924 (Patent Document 10) discloses a biodegradable composition containing starch, protein, cellulose, phenol and tannin, and tall oil or wax. However, this composition contains tall oil or wax, there is a fear of ooze of wax or the like. Therefore, the composition is suitable for production of woodworks. However, when applied to processed articles such as tablewares, there is a possibility that problems for safety may arise. Patent Document 1: JP-A-Hei07-17571 Patent Document 2: JP-A-2005-119708 Patent Document 3: JP-A-Hei05-320401 Patent Document 4: JP-A-Hei05-278738 Patent Document 5: JP-A-Hei05-57833 Patent Document 6: JP-A-2002-355932 Patent Document 7: JP-A-Hei06-248040 Patent Document 8: JP-A-2004-137726 Patent Document 9: JP-A-2005-23262 Patent Document 10: Translation of PCT application No. 9-500924

1. Field One embodiment of the invention relates to a panel attachment assembly and method for fixing, to a housing, a cover panel for covering, for example, a liquid crystal display panel. It also relates to a telephone with a liquid crystal display panel and a cover panel for covering the liquid crystal display panel. 2. Description of the Related Art Office or home telephones incorporate a display for displaying, for example, a telephone number, calendar, time, and dialing/incoming states. Displays have a liquid crystal display panel fitted in a housing, a rectangular opening formed in the upper surface of the housing, and a transparent cover panel held in the opening by a holding frame (see, for example, Jpn. Pat. Appln. KOKAI Publication No. 2000-305477). The opening is defined by four edges and positioned at an easily viewable position on the upper surface of the housing. The holding frame holds the outer periphery of the cover panel and is fitted in the opening. As a result, the cover panel faces the display surface of the liquid crystal display panel. The display surface can be seen from the outside of the telephone via the cover panel. In the conventional display, the edges defining the opening are provided on the upper surface of the housing, therefore the size of the cover panel may be limited, or the outward design of the telephone may be limited. In view of this, in recent years, it has been attempted to extend the opening of the housing so as to open at a corner defined by the upper surface and a side surface of the housing, and to expose an end face of the cover panel through the extended opening. This structure can enhance the flexibility in design of the display. When the end face of the cover panel is exposed to the outside through the opening, the outer periphery of the cover panel cannot be held by a holding frame. In this case, to fix the cover panel to the housing, it is possible, for example, to adhere an end of the cover panel to the housing by an adhesive, or to provide an engagement claw on the back surface of the cover panel and engage the claw with the housing. However, the fixing method of adhering the cover panel to the housing requires the process of coating an adhesive on the cover panel or housing, which increases the manufacturing cost of the display. Furthermore, once the cover panel is adhered to the housing, it cannot easily be exchanged for another. In addition, since the cover panel is made transparent so that the display surface of the liquid crystal display panel can be seen from the outside of the telephone, the adhesive or engagement claw will be seen from the outside through the transparent cover panel. This is not preferable in outward appearance. Moreover, since the engagement claw projects from the back surface of the cover panel, it is difficult to make the entire back surface flat. As a result, if it has come to be necessary to mask a certain area on the back surface of the cover panel, the back surface cannot be subjected to coating or printing since the engagement claw is in the way. Therefore, to mask the cover panel, it is necessary to interpose a dedicated masking sheet or decoration sheet between the cover panel and housing, which inevitably increases the number of required components and accordingly the manufacturing cost.

Introduction {#s0005} ============ All living organisms require exogenous foods/nutrients for producing energy in the form of ATP, which is needed for numerous cellular functions. Most of the cellular energy is efficiently produced in specialized organelles mitochondria by oxidative phosphorylation. In addition to energy production, mitochondria play an important role in other cellular functions such as fatty acid oxidation, anti-oxidant defense, intermediary metabolism including ammonia and glutamate detoxification, synthesis of heme and steroids, cell death process, and autophagy [@bib1]. Recent reports showed that mitochondria also undergo constant morphological changes with fusion and fission, following the exposure to toxic agents and/or under pathological conditions [@bib2], [@bib3]. After decreased glucose supply like during fasting or inefficient oxidative phosphorylation in certain disease states, the mitochondrial fat oxidation pathway becomes important in providing an alternative source of energy (e.g., ketone bodies) [@bib1]. Without these energy supply mechanisms due to suppressed mitochondrial function (i.e., mitochondrial dysfunction), living cells would die or become susceptible to cell death processes (necrosis and apoptosis). In fact, it is well-established that mitochondrial function in different tissues is significantly suppressed in numerous medical disorders such as metabolic syndrome including obesity/diabetes, cardiovascular disorders, ischemia reperfusion injury (I/R)^1^ and cancer as well as many neurological disorders like Alzheimer\'s disease and Parkinson\'s disease [@bib4], [@bib5], [@bib6], [@bib7], [@bib8], [@bib9], [@bib10], [@bib11], [@bib12], although etiological causes of each disease are different. Hepatic mitochondrial abnormalities are observed in both alcoholic fatty liver disease (AFLD) [@bib4], [@bib5], [@bib6], nonalcoholic fatty liver disease (NAFLD) [@bib7], [@bib8], [@bib9] and acute liver injury. As a result, it is conceivable to observe decreased ATP levels and increased fat accumulation (micro-vesicular and macro-vesicular steatosis) in the liver under these conditions. Continued mitochondrial dysfunction with increased oxidative stress also sensitizes the hepatocytes to subsequent necrosis and/or apoptosis of hepatocytes, which likely lead to activation of resident liver macrophage (i.e., Kupffer cells) and recruitment of infiltrating immune cells into the liver with elevated levels of hepatic inflammation (steatohepatitis) and pro-inflammatory cytokines/chemokines [@bib13], [@bib14], [@bib15]. Consequently, hepatic stellate cells can be activated and transformed into myofibroblast-like cells, producing pro-fibrotic cytokines such as transforming growth factor-beta and platelet derived growth factor, leading to hepatic fibrosis/cirrhosis and cancer. These sequential events can be observed in both AFLD [@bib13], [@bib14], [@bib15] and NAFLD [@bib16], [@bib17]. In addition, acute or sub-chronic exposure to various hepatotoxic compounds, including clinically-used drugs, such as acetaminophen (APAP) [@bib18], [@bib19], [@bib20], a major ingredient of Tylenol^®^, an anti-breast cancer agent tamoxifen [@bib21], an anti-retroviral drug zidovudine (AZT) [@bib22] and antidepressants [@bib23], can cause mitochondrial dysfunction, contributing to liver injury with or without fat accumulation, depending on the injurious agent, as extensively reviewed [@bib24], [@bib25], [@bib26]. These hepatotoxic agents and pathological conditions are known to elevate the levels of reactive oxygen and nitrogen species (ROS/RNS) and nitroxidative stress through the suppression of the mitochondrial electron transport chain (ETC) and induction/activation of NADPH oxidase, cytochrome P450 isozymes including ethanol-inducible P450-2E1 (CYP2E1) and CYP4A, xanthine oxidase, and inducible nitric oxide synthase (iNOS). Although increased nitroxidative stress can oxidatively damage mitochondrial DNA and lipids, the majority of insults can also take place at the protein levels through different forms of post-translational modification (PTM) [@bib26], [@bib27]. Because of the newly-emerging information on redox-related protein modifications, we briefly describe five major forms of PTM and functional consequences of some modified mitochondrial proteins in the experimental models of the AFLD, NAFLD and acute liver injury ([Fig. 1](#f0005){ref-type="fig"}). In addition, we highlight potential roles of CYP2E1 in promoting various PTMs. Post-translational modifications of mitochondrial proteins {#s0010} ========================================================== Oxidation of mitochondrial proteins {#s0015} ----------------------------------- Under normal conditions, transiently elevated ROS is known to be involved in cellular signaling pathways [@bib28], [@bib29] and mitochondrial functions are correctly maintained through proper redox balance. However, chronic and/or binge alcohol, high fat diets, tobacco smoking, or certain hepatotoxic drugs can directly damage the mitochondrial ETC, producing greater amounts of ROS leaked from the ETS [@bib24], [@bib25], [@bib26], [@bib27]. Without proper counter-balance by various cellular anti-oxidants, the persistent imbalance in cellular redox states result in decreased levels of mitochondrial antioxidants including mitochondrial glutathione (mtGSH), which serves as a critical determinant between toxic damage and cellular protection [@bib30]. When the cellular defense system is overwhelmed, greater amounts of ROS and RNS remain elevated, ultimately leading to increased nitroxidative stress. It is well-established that many amino acids such as cysteine (Cys), methionine (Met), histidine (His), proline (Pro), lysine (Lys), tyrosine (Tyr), phenylalanine (Phe), threonine (Thr) and tryptophan (Trp) in most proteins can also be redox regulated. As recently reviewed [@bib26], [@bib27], Cys residue(s) can be oxidatively modified in many forms \[sulfenic acid, disulfide, sulfinic/sulfonic acids, NO- or peroxynitrite-dependent *S*-nitrosylation, NO-independent ADP-ribosylation, mixed disulfide formation between Cys residues and glutathione (glutathionylation), cysteine (cystathionylation), succinic acid, myristic acid [@bib31] or palmitic acid (Cys-palmitoylation) [@bib32] prior to membrane attachment or cellular trafficking\]. Since the sensitive methods to detect redox-regulated Cys residues in cellular proteins were extensively described in our previous reviews [@bib26], [@bib33], we will only highlight the functional consequences of oxidative modification of Cys residues in some proteins. If one of these amino acids serves as the active site or is located near the active site of certain enzymes, it is highly likely that oxidative modifications of these amino acids can result in their inactivation, as shown by the oxidation and/or *S*-nitrosylation of Cys residues including the active site Cys in the mitochondrial aldehyde dehydrogenase (ALDH2) [@bib34] and 3-keto-acyl CoA-thiolase (thiolase) [@bib34] in binge alcohol-exposed rodents. In fact, mass-spectral analysis revealed that more than 87 mitochondrial and 60 cytosolic proteins were oxidatively-modified in alcohol-exposed rodents [@bib34], [@bib35]. The rates of protein oxidation in CYP2E1-containing E47-HepG2 hepatoma cells [@bib36] exhibited a dose- and time- dependent pattern in response to alcohol as well as the presence of CYP2E1 [@bib37]. Similar numbers of oxidatively-modified mitochondrial proteins were also identified by mass-spectral analysis in mice with I/R injury [@bib38] and rats exposed to 3,4-methylenedioxymethamphetamine (MDMA) [@bib39]. The number of oxidatively-modified mitochondrial proteins we characterized may represent a small fraction of the estimated number of 1100--1400 total mitochondrial proteins [@bib40], [@bib41]. However, we believe that the actual number of oxidized proteins could be significantly higher than the proteins originally reported [@bib34], [@bib38], [@bib39], because of the technical limitations in the identification and purification of oxidized proteins and detection methods, especially for those proteins expressed in low abundance, as previously discussed [@bib26], [@bib33]. In the case of oxidative inactivation of mitochondrial ALDH2 through active site Cys modification [@bib42], immunoblot analysis of the immunoaffinity purified ALDH2 proteins by using the specific antibody against ALDH2 or *S*-NO-Cys was performed [@bib34]. Protein detection using the anti-ALDH2 antibody revealed that similar levels of ALDH2 (54 kDa) were observed in all 3 mitochondrial samples \[i.e., mitochondria from control rats, mitochondria from alcohol-exposed rats, and dithiothreitol (DTT)-treated mitochondria from alcohol-exposed rats\]. However, one specific immunoreactive band with the anti-*S*-NO-Cys antibody was detected only in mitochondria from alcohol-exposed rats. Furthermore, the significantly decreased ALDH2 activity in ethanol-exposed rats was fully restored by DDT treatment [@bib34]. Similar results of *S*-nitrosylation and inactivation of ALDH2 were also observed in rat hepatoma H4IIE-C3 cells exposed to NO donors such as *S*-nitrosoglutathione (GSNO), *S*-nitroso-*N*-acetylpenicillamine, and 3-morpholino-sydnonimine, respectively [@bib43]. These results indicate that ALDH2 and other ALDH isozymes, which contain the highly conserved active site Cys residue, can be reversibly modulated by *S*-nitrosylation under increased nitroxidative stress, as reviewed [@bib42]. Other PTMs of Cys and other amino acid residues in ALDH2 protein are summarized ([Fig. 2](#f0010){ref-type="fig"}). Oxidative modification and suppression of ALDH2 in alcohol-exposed rodents were consistently observed by other groups [@bib44], [@bib45]. In fact, these phenomena could explain the decreased levels of ALDH2 activity in alcoholic individuals, as discussed [@bib34], [@bib42]. Oxidative modification and inactivation of ALDH2 were also observed after exposure to MDMA [@bib39] or I/R injury [@bib38], resulting in the accumulation of lipid peroxidation products, which are metabolized by ALDH2 [@bib46]. Similar modifications and inactivation of active site Cys residues in thiolase and possibly other enzymes in the β-oxidation pathway of fatty acids are likely to lead to fat accumulation observed in alcohol-exposed rodents [@bib34], in MDMA-exposed rats [@bib39] as well as in mouse liver following I/R injury [@bib38]. Furthermore, oxidative modification of the active site Cys residue of peroxiredoxin 1 (Prx1) and inactivation was observed in alcohol-exposed mice [@bib47]. Since Prx1 was determined to be localized on the cytosolic side of the endoplasmic reticulum (ER) and interacts with CYP2E1 [@bib47], it is likely that this oxidative inactivation of Prx1 contributes to increased ROS production and fatty liver following alcohol exposure. Based on the conserved redox-sensitive Cys residues among the multiple isoforms [@bib47], [@bib48], [@bib49], many Prx enzymes could be also oxidatively-modified and inactivated, contributing to elevated levels of oxidative stress. Furthermore, the activities of NAD^+^- or NADP^+^-dependent isocitrate dehydrogenases (ICDH) are known to be oxidatively-modified and inactivated in experimental models exposed to hydrogen peroxide, menadione, nitric oxide, or alcohol [@bib50], [@bib51], [@bib52], [@bib53]. Oxidative inactivation of ICDH enzymes would increase oxidative stress since they are important in the regulation of mitochondrial redox balance and cellular defense through providing NADPH for the regeneration of reduced GSH [@bib50]. Mass-spectral analysis confirmed that Cys305 and Cys387 of NADP^+^-ICDH were *S*-nitrosylated, resulting in its inactivation in alcohol-exposed animals [@bib53]. By the same logic, it is expected that many other enzymes that contain active site Cys residue would likely undergo similar types of redox-related modifications and become inactivated, as reviewed [@bib26], [@bib33]. For instance, it was reported that a DNA repair enzyme O^6^-methylguanine-DNA-methyltransferase which contains redox-sensitive Cys in its active site can be inactivated through *S*-nitrosylation [@bib54], resulting in increased levels of oxidative DNA modifications, which can contribute to carcinogenesis. It is also possible that redox regulation can indirectly affect the patterns of gene expression by modulating the conserved Cys residues in proteins involved in the cell signaling pathways like many protein phosphatases (see the Section "Phosphorylation of mitochondrial proteins") or directly affecting many redox-sensitive transcription factors such as nuclear factor-kappa B (NF-κB), nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and hypoxia-inducible factor-1 (HIF-1), as recently reviewed [@bib55]. The modulation of transcription factors can either be harmful or beneficial. For instance, NF-κB, a critical transcription factor in inflammation and innate immune regulation, can be activated by alcohol [@bib56] and other toxic agents such as lipopolysaccharide (LPS) [@bib57]. NF-κB can be activated through proteasomal degradation of the inhibitor protein (I-κB) of the NF-κB after its phosphorylation by I-κB kinase. Consequently, NF-κB activation leads to the transcriptional initiation of many pro-inflammatory cytokines, chemokines and pro-oxidant proteins such as TNF-α, IL-12, monocyte chemotactic protein-1, macrophage inflammatory protein-2, cyclooxygenase-2 and iNOS [@bib55], [@bib56], [@bib57]. Chronic or acute alcohol exposure and other hepatotoxic agents can also activate HIF-1α in mice and rats [@bib57], [@bib58], [@bib59], [@bib60], [@bib61]. However, activation of HIF-1α, which is co-localized with CYP2E1 in centrilobular areas, seems to contribute to CYP2E1-dependent oxidative stress and liver toxicity, as recently suggested in chronic and acute alcohol exposure [@bib59], [@bib60], [@bib61]. In contrast, a cell-protective transcription factor Nrf2 can be activated under increased oxidative stress in AFLD and NAFLD [@bib62], [@bib63], [@bib64], [@bib65]. Increased oxidative stress activates Nrf2 through oxidative modifications of redox-sensitive Cys residues of the regulatory binding protein Kelch-like ECH-associated protein 1 (Keap1), leading to ubiquitin-dependent degradation of Keap1, promoting Nrf2 translocation into the nucleus for transcriptional activation of its downstream targets, as reviewed [@bib66]. Activation of Nrf2 with its down-stream target proteins, including glutamate cysteine ligase, heme oxygenase-1, quinone reductase, and thioredoxin reductase, provides anti-oxidant defense against increased oxidative stress caused by alcohol exposure [@bib62]. As described thus far, oxidative modifications of Cys residues in many cellular proteins are associated with inactivation or suppression of the activity of modified target proteins. However, redox modification of Cys, especially the mixed disulfide formation, such as *S*-glutathionylation, can also be considered as a protective mechanism in some cases. For instance, reversible oxidation of Cys residues of mitochondrial NADH-dependent ubiquinone oxidoreductase (complex I), ALDH2, and Prx3 seem to be protective, despite temporary inactivation, against further tissue damage from irreversible hyper-oxidation of Cys to Cys-sulfinic acid (Cys-SO~2~) and Cys-sulfonic acid (Cys-SO~3~) followed by proteolytic degradation [@bib67], [@bib68], as in the case of I/R injury [@bib69], [@bib70], [@bib71], [@bib72]. It is known that Cys-glutathionylation of mixed disulfide groups can create a functional cycle consisting of the forward reaction (glutathione S-transferase P) and the reverse reaction (glutaredoxin system) [@bib67], [@bib73], [@bib74]. Furthermore, some Cys residues can be modified through adduct formation with carbonyl compounds, including lipid peroxide 4-hydroxy-2-nonenal (4-HNE) and reactive metabolites of APAP. However, Cys residues in the adducts with reactive metabolites or lipid peroxides cannot be restored even in the presence of a strong reducing agent DTT and thus are considered irreversible, as discussed [@bib26], [@bib33]. The functional implications of some examples of these adducts are described later (see "Section Electrophilic adduct formation of mitochondrial proteins"). Nitration of many mitochondrial proteins {#s0020} ---------------------------------------- It is well-established that the physiological levels of NO produced by endothelial NOS (eNOS) and neuronal NOS (nNOS) are relatively small and can act as a signaling molecule within the cell or interact with surrounding cells [@bib27], [@bib75], [@bib76]. However, many toxic agents such as alcohol, APAP and LPS can induce iNOS, which produces greater amounts of NO, likely leading to nitrosative/nitrative stress [@bib27], [@bib75], [@bib76], [@bib77]. In this case, NO can interact with ROS to produce a potently toxic peroxynitrite, which can nitrate Tyr residues to generate 3-nitroTyr (3-NT) or *S*-nitrosylate Cys residues of many proteins [@bib77]. These two PTMs can lead to alterations of both protein structure and function, contributing to increased cell and tissue injury. Protein nitration may occur in various cell compartments. Although the concentration of mtGSH is similar to that of cytosolic GSH (5--10 mM), it represents a small fraction of the total cellular GSH [@bib30]. Because mitochondria are a major source of ROS/RNS as previously mentioned, they can be very vulnerable to nitroxidative damage [@bib27]. Indeed, mitochondrial DNA is extremely sensitive to oxidative/nitrative damage due to (A) its location closer to the inner mitochondrial membrane; (B) the relatively low amount of histone, anti-oxidant enzymes, and mtGSH, and (C) the low levels of polyamines and DNA repair enzymes [@bib78], [@bib79]. In support of the view of mitochondrial sensitivity to nitration, it has been reported that the turn-over rates of rat liver mitochondria proteins were markedly decreased from few days to hours as a result of proteolytic degradation following exposure to nitrating conditions [@bib80], [@bib81]. Interestingly, mitochondrial DNA encodes 13 polypeptides all of which are members of the 4 mitochondrial ETC proteins, namely Complexes I, III, IV, and V [@bib82], [@bib83]. Taken together, mitochondrial DNA mutation and/or deletion may lead to abnormal expression or deletion of some of the ETC components, contributing to mitochondrial respiratory dysfunction and more leakage of ROS/RNS. Consequently, mitochondrial damage or dysfunction due to oxidative/nitrative protein modifications can be expected in various pathological conditions or following exposure to some toxic agents such as alcohol, high fat, MDMA, and APAP [@bib18], [@bib19], [@bib20], [@bib21], [@bib22], [@bib23], [@bib24], [@bib84], [@bib85]. Nitration of mitochondrial proteins and their functional roles in fatty liver disease and/or acute liver injury have been extensively reviewed recently [@bib27]. For instance, NO-dependent inhibition of the mitochondrial respiration was monitored in both AFLD and NAFLD [@bib86], [@bib87], [@bib88], [@bib89], [@bib90]. Since protein nitration is one of the emerging research topics in acute tissue injury, we specifically focused on this PTM in promoting mitochondrial dysfunction and acute hepatotoxicty. We used APAP as a well-established model agent for acute drug-induced liver injury (DILI) to study the functional role of nitrated mitochondrial proteins and the mechanisms of mitochondrial dysfunction and hepatotoxicity. APAP was first shown to induce and promote mitochondrial protein nitration and that peroxynitrite can cause mitochondrial DNA damage by Cover et al. [@bib18]. Hepatic necrosis highly correlated with the areas of nitrated proteins [@bib91]. Direct evidence for a critical role of peroxynitrite in APAP-mediating hepatic injury has been provided with the seminal work by Knight et al. [@bib92]. This study showed that the protective effects of GSH were mainly due to the restoration of cellular GSH levels for efficient scavenging of peroxynitrite, thus providing direct evidence of the central role of peroxynitrite in APAP-induced liver injury. CYP2E1, one of the main enzymes involved in APAP metabolism, seems to play a critical role in APAP-induced protein nitration and liver injury [@bib93]. Based on these results, we hypothesized that CYP2E1-dependent nitration of many mitochondrial proteins is important in promoting mitochondrial dysfunction and liver injury. In fact, after immunoaffinity purification followed by mass-spectral analysis, we demonstrated that more than 70 mitochondrial proteins and 30 cytosolic proteins were nitrated in APAP-exposed mice [@bib94]. These results are in line with another recent report [@bib95]. The identified nitrated proteins are involved in cellular energy production, fat metabolism, intermediary metabolism, urea cycle, chaperone activity, and anti-oxidant defense. To further determine the functional roles of protein nitration, we mainly focused on the five selected mitochondrial enzymes, namely SOD2, Gpx, ATP synthase, ALDH2 and thiolase. We specifically studied the presence of nitration and activity change in each of these five enzymes at 2 h after exposure to a toxic dose of APAP in the presence or absence of the co-treatment with an anti-oxidant *N*-acetyl-cysteine (NAC) [@bib94]. Treatment with NAC completely protected the liver from the APAP-induced necrotic injury measured by increased serum transaminase activities and liver histology. Furthermore, NAC ameliorated the inactivation of the five critical enzymes via preventing Tyr nitration, as evidenced by immunoprecipitation with a specific antibody to each protein followed by immunoblot with anti-3-NT antibody. Thus, protein nitration serves as one of the critical causal factors in APAP-induced acute liver damage usually observed at later time points. Indeed, the suppressed activities of anti-oxidant enzymes such as SOD2 and Gpx would certainly interfere with the cellular anti-oxidant abilities. Suppressed ATP synthase activity would lead to decreased ATP production, interfering with vital cell functions and ultimately causing necrosis. Furthermore, inactivation of thiolase likely leads to the inhibition of the β-oxidation of fatty acids with increased hepatic fat accumulation or inefficient supply of an alternative energy (e.g., ketone bodies produced from fat degradation). Furthermore, suppressed ALDH2 would lead to the accumulation of toxic, reactive aldehydes and lipid peroxidation, as previously mentioned in the oxidation section [@bib42]. Based on our results, we expect similar results of mitochondrial dysfunction and tissue injury with other conditions such as I/R injury [@bib38] and LPS treatment [@bib96], which caused extensive protein nitration. It is important to mention that the inactivation of many nitrated proteins can result from the nitration of Tyr residue in the active site, leading to interference of the protein's catalytic activity. However, it is still possible that nitration of other Tyr residues may cause a conformational change in the target protein and thus block the accessibility of ATP or substrates for example, as previously discussed [@bib27]. However, it would be prudent to double-check the function of each nitrated protein, since nitration can also increase the activity of some proteins such as glutathions S-transferase (GST), heat shock protein 90 (HSP90), and protein phosphatase type 2 \[PP2\], or exert no effects at all as reported with transferrin [@bib27]. Although most reported results mainly focused on Tyr nitration, nitration of Trp residues in proteins was also reported [@bib97]. However, there have been fewer reports about Trp nitration and functional consequence than those of Tyr nitration, since Trp is much less abundant than Tyr and that Trp is usually buried inside the protein core with less surface exposure for nitration. Nonetheless, excellent reports discussed the occurrence of Trp nitration that may cause functional alterations in detail [@bib97], [@bib98], [@bib99]. The effects of peroxynitrite on nitration of Tyr or Trp and *S*-nitrosylation of Cys likely depend on cellular status of antioxidants, various microenvironments including surface exposure, peptide loop structure, local charge groups, and the presence of competing amino acids nearby (e.g., Cys near the potentially-nitrated Trp or Tyr), as suggested [@bib98]. Phosphorylation of mitochondrial proteins {#s0025} ----------------------------------------- Many cellular proteins can be regulated by reversible cycles of phosphorylation and dephosphorylation by protein kinases and phosphatases, respectively. It is well-established that many exogenous agents such as alcohol, smoking, high fat, and APAP can modulate many different classes of protein kinases including cAMP-dependent protein kinases (PKA), PI3K/AKT/mTOR (PKB), protein kinase C isoforms (PKC), calcium-calmodulin-dependent protein kinases, stress activated mitogen-activated protein kinases (MAPKs) including c-Jun N-terminal protein kinase (JNK) and p38 kinase (p38K), and receptor-mediated tyrosine kinases. These kinases can work together synergistically or antagonize each other's activities. In fact, crosstalk between different classes of protein kinases becomes complicated, contributing to different outcomes, depending on their inducibility, tissue distribution, subcellular localization or translocation to another compartment, cellular environment, treatment agent, and activity status of phosphoprotein phosphatase, as recently reviewed [@bib100], [@bib101], [@bib102], [@bib103], [@bib104], [@bib105]. For instance, concurrent activation of PKC-delta isoform along with stress activated protein kinases generally enhances cell death [@bib106], [@bib107], [@bib108], although some exceptions exist. In contrast, activation of PI3K/Akt and extracellular signal regulated protein kinase (ERK) is generally known to support cell survival and proliferation. However, we briefly describe the redox-mediated regulation of stress activated MAPKs and AMP-activated protein kinase (AMPK) in this review, based on their involvement in mitochondrial homeostasis, intermediary metabolism for steatosis and liver injury. Under increased nitroxidative stress, stress-activated MAPKs can be stimulated partly through inhibition of phosphoprotein phosphatases. For instance, the highly-conserved active site Cys residue of phosphoprotein phosphatases including MAPK phosphatases [@bib103], [@bib104], [@bib105] can be oxidatively-modified and inactivated by the mechanisms described earlier ("Section of Oxidation of mitochondrial proteins"). This redox-related activation of MAPKs is similar to that of Akt activation through oxidative inactivation of the essential Cys residue of its binding partner lipid phosphatase and tensin homolog (PTEN) [@bib109]. The inactivation of MAPK-phosphatases leads to activation of various stress-activated JNK and p38K [@bib104], [@bib105]. In fact, acute exposure to many hepatotoxic agents including alcohol [@bib110], [@bib111], APAP [@bib112], [@bib113], [@bib114], [@bib115], [@bib116], arachidonic acid [@bib117], 4-HNE and carbon tetrachloride [@bib118], palmitic acid [@bib119], and troglitazone [@bib120] significantly activated JNK (p-JNK) and/or p38K (p-p38K), contributing to toxicity in a variety of cells. Pretreatment with a specific inhibitor of CYP2E1 blocked metabolic activation of some hepatotoxic agents, which are CYP2E1 substrates [@bib110], [@bib111], [@bib112], [@bib113], [@bib114], [@bib115], [@bib116], [@bib117], [@bib118], and prevented JNK activation. Taken together, CYP2E1 is critically involved in JNK activation and cell death caused by those hepatotoxic CYP2E1 substrates. In addition, activation of JNK was positively related to high fat diet-induced insulin resistance and metabolic syndrome [@bib119], [@bib121], [@bib122], [@bib123]. A recent study also showed that sustained JNK activation led to phosphorylation at Ser-46 of sirtuin 1, NAD^+^-dependent deacetylase in cytosol (described later), followed by ubiquitin-dependent degradation, contributing to fat accumulation in obese mice [@bib124]. Furthermore, persistent activation of JNK and/or p38K is positively associated with various liver diseases such as steatohepatitis and I/R injury [@bib122], [@bib123], [@bib124], [@bib125], suggesting the clinical importance of JNK and p38K in human disease states, as reviewed [@bib126]. Experiments with gene deletion technology and anti-sense oligonucleotides were conducted to determine the role of JNK1 versus JNK2 in hepatotoxicity. For instance, both JNK1 and JNK2 seem to be important in alcohol-induced fatty liver injury [@bib111], while JNK1 seems critical in hepatotoxicity caused by co-treatment of pyrazole and TNFα [@bib127]. In contrast, JNK2 plays a dominant role in APAP-induced acute liver injury since *JNK2-null* mice are resistant to acute hepatotoxicity [@bib113], suggesting that this area needs further clarification. Several reports on the redox-related activation of the JNK and/or p38K or their upstream kinases such as mitogen activated protein kinase kinase (M2K) and mitogen activated protein kinase kinase kinase (M3K), as reviewed [@bib128]. However, the number and identity of the mitochondrial and cytosolic proteins, that are phosphorylated by active p-JNK and/or p-p38K, need to be investigated. Our results showed that pro-apoptotic Bax in the cytosol can be phosphorylated (activated) by p-JNK and/or p-p38K, resulting in its conformational change with exposure of the C-terminal membrane domain. These events were followed by translocation of the activated Bax to mitochondria, leading to changes in mitochondrial permeability transition (MPT) and apoptosis of cultured hepatoma cells [@bib129]. The importance of phosphorylation was further confirmed using site-directed mutagenesis of potential amino acids for phosphorylation followed by functional analysis. Our results revealed that Thr167 of Bax was phosphorylated before it was translocated to mitochondria to stimulate mitochondria-dependent apoptosis [@bib129]. In addition, activated p-JNK is known to translocate to mitochondria to initiate MPT change and damage following exposure to hepatotoxic agents including APAP [@bib115], [@bib116], [@bib130], [@bib131]. Since JNK does not contain the canonical mitochondrial leader sequence [@bib132], it would be interesting to identify the mechanism(s) by which activated p-JNK is transported into mitochondria and then phosphorylates mitochondrial matrix proteins such as ALDH2 in CCl4-exposed rats [@bib133]. One of the potential mechanisms of JNK translocation to mitochondria could be through its interaction with a scaffold protein Sab [@bib116], [@bib134] or Bcl-XL [@bib130] on the mitochondrial outer membrane before it gets transported into mitochondria. When the active p-JNK is translocated to mitochondria, it can phosphorylate many mitochondrial proteins such as ATP synthase β subunit, α-KGDH, PDH E1α and β subunits, which were phosphorylated by the recombinant JNK, as shown in an in vitro study using bioenergetically competent mitochondria [@bib135]. However, the identities and physiological roles of numerous mitochondrial proteins phosphorylated by p-JNK (e.g., JNK-specific phosphoproteomes) need to be determined in animal models and human disease states in the future. Regulatory mechanism of AMP-dependent protein kinase (AMPK) by alcohol and other non-alcoholic substances, including high fat diet has become an important research topic, since AMPK serves as a key sensor and/regulator of metabolic syndrome and many cellular processes [@bib136]. In fact, the redox sensitive AMPK can be paradoxically regulated by activation or suppression. For instance, AMPK can be activated by hydrogen peroxide and mitochondria-derived ROS since its activation can be prevented by pretreatment with antioxidants such as NAC or GSH-ethyl ester [@bib101]. AMPK activation by hydrogen peroxide was tightly associated with the elevated levels of AMP with concurrent depletion of ATP. Recent results showed that AMPK can be also activated in an AMP-independent manner. Regardless of AMP dependency, AMPK activation under oxidative stress or by chemical activators such as metformin and AICAR can lead to increased cell survival signal by promoting autophagy to remove damaged mitochondria and to stimulate mitochondrial energetics [@bib101]. In contrast, AMPK can be suppressed by alcohol [@bib137] or other agents such as high fat diet [@bib138] and APAP [@bib139]. Inactivation of AMPK is known to be associated with AFLD and NAFLD or acute liver injury, as reviewed [@bib13]. Acetylation of mitochondrial proteins {#s0030} ------------------------------------- Reversible protein acetylation and deacetylation, catalyzed by acetyltransferases and deacetylases, respectively, represent another form of PTMs, although functional roles of many acetylated proteins are still unclear and need further investigations. In fact, acetylation on *N*-ε-Lys residues in proteins becomes an important research area through epigenetic regulation of many genes involved in normal cellular growth and physiology by acetylated histones and other chromatin associated proteins [@bib140]. A large scale proteomics study revealed that approximately 20% of mitochondrial proteins and 44% of NAD^+^-dependent mitochondrial dehydrogenases are acetylated under physiological conditions [@bib141]. The number of acetylated proteins can be significantly increased in experimental models of pathological conditions or following exposure to hepatotoxic agents, possibly resulting from redox-mediated suppression of deacetylases, as shown in alcohol-exposed [@bib142], [@bib143], [@bib144], [@bib145] or high-fat exposed rodents [@bib146], [@bib147], [@bib148]. For instance, chronic and binge alcohol exposure suppressed the activities or decreased levels of various isoforms of sirtuin, Zn and NAD^+^-dependent deacetylases, involved in cellular aging, lipid metabolism, and anti-oxidant defense. Because of NAD^+^-dependence, the activities of sirtuins can be suppressed by the redox change (e.g., a decreased NAD^+^/NADH ratio) following alcohol metabolism via alcohol dehydrogenase (ADH) and low *K*~m~ ALDH2, both of which use NAD^+^ as a cofactor for their activities. Earlier reports also showed that chronic alcohol exposure suppressed the activities and protein amounts of sirtuin 1, 3 and 5 isoforms [@bib142], [@bib143], [@bib144], [@bib145], [@bib149], [@bib150], in a CYP2E1-independent manner [@bib144]. In addition, the activities of sirtuin isoforms can be allosterically suppressed through thiol-specific modification of Cys280 in the Zn binding site with 4-HNE adduct formation, as demonstrated [@bib151]. Consequently, the levels of acetylated proteins were significantly elevated in alcohol-exposed rodents. Some of the acetylated proteins, that are deacetylated by sirtuin isoforms, are several transcription factors involved in the regulation of lipid metabolism and cell apoptosis such as sterol regulated element binding protein (SREBP), peroxisomal proliferator activated receptor gamma coactivator-1 (PGC-1), forkhead box protein O1 (FoxO1), NF-κB and p53 [@bib142], [@bib143], [@bib144], [@bib149]. Acetylation of these transcription factors is a well-established cause for fat accumulation and altered cell proliferation in the liver. For instance, alcohol-related suppression of sirtuin 1 increased the levels of acetylated SREBP-1 and PGC-1α with functional activation and suppression, respectively, resulting in alcoholic fatty liver [@bib142]. By using immunoprecipitation with anti-Ac-Lys antibody followed by mass spectral analysis, 91 acetylated mitochondrial proteins were recently identified in alcohol exposed mice [@bib152]. Some of the acetylated mitochondrial proteins are ALDH2, ATP synthase, Gpx, and thiolase, suggesting that these acetylated mitochondrial proteins likely contribute to their functional alterations and fat accumulation [@bib152]. Another report further indicated that alcohol treatment elevated the number of acetylated proteins as well as propionylated protein in mitochondria and nuclear fractions with little changes in cytosolic and microsomal fractions through suppression of sirtuin activities [@bib153]. However, in this study, alcohol-exposure did not seem to change the protein levels of sirtuin 3, 4, and 5. The reasons for dissimilar results on sirtuin levels, observed in different laboratories, are unknown, but could be due to distinct ethanol dose, time course, environment, or animal strains, and warrants further investigation. In addition, high fat feeding can suppress the activities of mitochondrial sirtuin 3 and other isoforms, thus increasing the number of acetylated proteins. However, the mechanism(s) by which high fat decreased levels of sirtuin isoforms is poorly understood. The levels of hyper-acetylated proteins are markedly increased in mice deficient of mitochondrial sirtuin 3 [@bib147], [@bib154], [@bib155]. For instance, acetylation of long-chain fatty acyl-CoA dehydrogenase, one of the four enzymes involved in the mitochondrial fat oxidation pathway, causes its inactivation, leading to fat accumulation [@bib154], [@bib155]. In contrast, activation of sirtuins by small molecule polyphenols including resveratrol [@bib156] and green tea extracts [@bib157] can reduce the number of acetylated proteins, including PGC-1α, which contributes to increased fat oxidation and insulin sensitivity with improved outcome against metabolic syndrome. Therefore, sirtuin 3 and its isoforms, involved in fat metabolism and aging process, become important therapeutic targets in managing metabolic syndrome and cellular senescence in the liver and other tissues. As mentioned earlier, key mitochondrial proteins in regulating the fatty acid metabolism are acetylated and that the number of acetylated proteins can be significantly increased through suppression of the mitochondrial deacetylase sirtuin 3 and other sirtuin isoforms by alcohol [@bib142], [@bib143], [@bib144], [@bib145], [@bib149], [@bib150], [@bib151], [@bib152], [@bib153], high fat [@bib148], and other conditions [@bib154], [@bib155]. Compared to numerous reports on the regulation of deacetylase proteins including mitochondrial sirtuin 3, the expression and properties of the mitochondrial acetyltransferase enzyme(s) have been less characterized although acetylation sites in many mitochondrial proteins have been recently reported [@bib158]. In addition, other studies indicated that protein acetylation can take place nonenzymatically in the presence of low levels of acetyl-CoA [@bib159] or acetyl-phosphate and acetyl-adenylate [@bib160]. These reports indicate that the characteristics of acetyltransferase(s) are poorly understood and need further studies, although the GCN5 family seems to be the prototype of (histone) acetyltransferases [@bib161]. Electrophilic adduct formation of mitochondrial proteins {#s0035} -------------------------------------------------------- It is well-established that excessive alcohol intake and many potentially toxic compounds can suppress low *K*~m~ mitochondrial ALDH2 activity in rodents and humans through various PTMs of the active site Cys residue and other redox-sensitive amino acids, as reviewed [@bib26], [@bib27], [@bib42], resulting in the accumulation of toxic acetaldehyde and other lipid aldehydes. Consequently, cellular macromolecules including mitochondrial proteins [@bib162], [@bib163] and DNA [@bib164] are subjected to modification by these toxic aldehydes, leading to mitochondrial dysfunction and oral and gastrointestinal tract cancers [@bib165]. Chronic alcohol drinking and/or smoking or high fat can also cause mitochondrial damage with increased nitroxidative stress and lipid peroxidation products such as 4-HNE, 4-oxonon-2-enal \[4-ONE\], malondialdehyde (MDA), and acrolein (ACR) [@bib166], [@bib167], [@bib168]. In addition, many potentially toxic drugs can produce reactive metabolites, which can induce mitochondrial dysfunction and acute liver injury [@bib18], [@bib19], [@bib20], [@bib21], [@bib24]. For instance, APAP metabolism produces *N*-acetyl-*p*-benzoquinone imine (NAPQI) while the metabolism of potentially hepatotoxic troglitazone generates reactive quinolone-like metabolites. Other drugs such as halothane, tienilic acid, and dihydralazine can produce reactive metabolites, which promote hepatotoxicity. The underlying mechanisms of these idiosyncratic toxicities by these agents could be due to interactions between highly reactive electrophilic intermediates with various mitochondrial proteins, leading to mitochondrial dysfunction and tissue damage including DILI. They can also damage membrane integrity and alter calcium homeostasis between endoplasmic reticulum and mitochondria, leading to hepatotoxicity. Furthermore, these protein adducts can serve as a neo-antigen of hapten--carrier conjugate proteins to activate immune responses and to facilitate infiltration of neutrophils into the liver to promote inflammation [@bib18], [@bib19], [@bib20], [@bib21], [@bib24], [@bib166], [@bib167], [@bib168]. Recent results showed that highly-reactive lipid peroxides including 4-HNE and 4-ONE, despite their extremely short half-lives, can suppress the activities of many mitochondrial proteins likely through adduct formation with a few amino acids such as Cys, His, Arg, and Lys of target proteins [@bib168]. For instance, earlier reports showed that acetaldehyde and 4-HNE produced by alcohol intake interact with mitochondrial proteins, including cytochrome C oxidase (complex IV), leading to its inactivation, mitochondrial dysfunction and liver injury [@bib169], [@bib170], [@bib171], [@bib172]. By using mass-spectrometry, Petersen and colleagues recently determined the specific amino acids that are modified by 4-HNE. They showed that the active site Cys301 of ALDH2 [@bib173] and Cys280 in the critical Zn binding site of sirtuin 3 [@bib151] were covalently modified with 4-HNE, leading to their inactivation. In addition, many other proteins such as protein disulfide isomerase [@bib174] and Grp78 [@bib175] in the ER, gamma-glutamyl-cysteine synthase (GCS) [@bib176], ERK [@bib177], PTEN [@bib178], or AMPK [@bib179] in cytosol could also be inactivated through interaction with 4-HNE, likely leading to ER stress, GSH depletion and alteration of the cell signaling pathways frequently observed in alcohol-fed models and humans. Unlike mixed disulfide bonds of Cys such as *S*-nitrosylation and *S*-glutathionylation, the protein adducts with reactive carbonyls including 4-HNE, 4-ONE, MGO and ACR cannot be reversed by the presence of reducing agents such as DTT, GSH and ascorbate, as recently reviewed [@bib28]. Therefore, these protein adducts may exist for an extended time period unless they are removed by cellular proteolytic enzymes or phagocytic macrophages. Furthermore, HNE-protein adducts can induce immune cell activation of hepatic macrophage Kupffer cells and/or infiltration of neutrophils into the liver, producing inflammatory cytokines and activation of stellate cells, leading to advanced liver disease, as reported in alcoholic liver injury [@bib166], [@bib167], [@bib168], [@bib180]. In fact, the average levels of MDA- and HNE-protein adducts in 50 alcoholic cirrhosis patients were significantly higher than those in a similar number of patients with nonalcoholic cirrhosis or healthy individuals [@bib180]. In contrast, no differences in the levels of ACR- and MGO-protein adducts were found among different groups. Furthermore, the average levels of MDA and HNE-adducts were higher in 51 alcoholic patients with advanced liver disease with fibrosis/cirrhosis than 23 fatty liver disease or 30 healthy control people, suggesting that MDA- and HNE-protein adducts likely served as antigens or activators of immune responses in advanced alcoholic liver disease. The ethanol-induced CYP2E1 was partly responsible for the production of 37 kD-acetaldehyde protein adducts [@bib181] while 4-HNE protein adduct could be produced in CYP2E1-independent manner, although CYP2E1 seems to at least play a permissive role [@bib182]. In case of high-fat fed rodents, the total number of the reports on HNE-protein adducts in the livers of NAFLD seems relatively small compared to those in AFLD, although the identities of HNE-protein adducts were reported in extra-hepatic tissues such as heart [@bib183], [@bib184]. Mass spectral analysis revealed 39 unique lipoxidation sites in 27 mitochondrial proteins. These lipid peroxide-modified mitochondrial proteins include: pyruvate dehydrogenase, malate dehydrogenase, ICDH, methylmalonate-semialdehyde dehydrogenase, long chain fatty acyl-CoA dehydrogenase, NADH-dependent ubiquinone oxidoreductase (complex I), succinate dehydrogenase (complex II), ubiquinone-cytochrome bc1 oxidoreductase (complex III), cytochrome c oxidase (complex IV), ATP synthase (complex V), and others [@bib184]. Although the activities of each HNE-modified protein were not determined in this study, it is reasonable to assume that the functional activities of some of the modified proteins could be suppressed. We also believe similar types of lipid peroxide adducts present in the liver of high-fat exposed rodents (and humans), due to the elevated levels of oxidative stress and lipid peroxides including 4-HNE [@bib185], as comparable to the alcoholic fatty liver [@bib170], [@bib171], [@bib172]. In fact, ALDH2 activity in the heart was significantly inhibited in high fat-exposed diabetic mice [@bib186]. Further characterization revealed that ALDH2 was inactivated through 4-HNE adduct formation, as evidenced by immunodetection of 4-HNE adduct in the immunoprecipitated ALDH2 with the anti-ALDH2 antibody [@bib186]. The levels of cardiomyocyte hypertrophy and dysfunction in high fat-exposed mice were inversely correlated with the ALDH2 activity, suggesting a causal role of ALDH2 in diabetic cardiomyopathy. These results are consistent with the cardioprotective role of ALDH2 which can be activated by small molecule activators [@bib42], [@bib187] or over-expression by genetic modulation [@bib188], [@bib189]. In addition to lipid peroxide-related protein adducts, recent data suggest that sugar moiety-related protein adduct such as advanced glycation end products (AGEs) can be produced by high fat or excessive alcohol exposure or under pathological states such as diabetes, cardiovascular diseases and Alzheimer\'s disease, as recently reviewed [@bib190], [@bib191], [@bib192], [@bib193]. Elevated levels of cross-linked AGEs in many tissues can up-regulate the expression of the receptor for AGEs (RAGE), which activates NADPH oxidase, leading to increased oxidative stress, insulin resistance, and inflammation with disruption of normal cell signaling pathways. These pro-oxidative events with accumulated proteins contribute to acute injury and/or persistent chronic disease states in many tissues [@bib190], [@bib191], [@bib192], [@bib193]. For instance, chronic alcohol exposure elevated the levels of acetaldehyde-derived AGE (AA-AGE) and HNE-protein adducts in the livers of rats and humans while their elevated levels disappeared after alcohol abstinence. The immunostaining intensities of AA-AGE and HNE-adducts positively correlated with the severity of alcoholic liver disease [@bib193]. Furthermore, AA-AGE but not *N*-ethyllysine (NEL) caused apoptosis of rat hepatocytes, suggesting an important role of AA-AGE in alcohol-induced hepatotoxicity and fatty liver injury [@bib193]. Similar results of elevated production of AGE and its plasma levels in cirrhotic patients compared to those in healthy individuals were previously reported [@bib194]. High fat feeding also elevated the levels of AGEs and RAGE in many tissues, including kidneys, hearts and epididymal fat in an aldose reductase-dependent manner [@bib195]. In a mouse model of NASH caused by high fat western diet or choline-deficient diet, AGEs induced TNFα-cleavage enzyme in an NADPH oxidase-dependent manner and stimulated fibrogenic activity via decreasing the levels of sirtuin 1 and tissue inhibitor of metalloproteinase 3 (TIMP3) [@bib196]. The significantly lower levels of sirtuin 1 and TIMP3 were also observed in livers from NASH patients than those of healthy individuals, suggesting a role of AGE adducts in promoting inflammatory responses. Another report recently indicated that several mitochondrial proteins in aged rats were modified with AGEs, thus their activities inactivated. These AGE-modified proteins were: complexes I and V, catalase, ALDH2, medium chain acyl Co-A dehydrogenase, keto-acyl CoA dehydrogenase, and others, leading to decreased ETC, anti-oxidant defense and urea cycle in aged animals [@bib197]. In addition to liver injury, AA-AGE but not NEL stimulated death of neuronal cells [@bib198], suggesting an important role of AA-AGE in neuronal cell death. Consistent with this report, elevated amounts of AGE-albumin adduct, produced by activated microglial cells, were found in alcohol-exposed rat brains and post-mortem brains from human alcoholic individuals compared to those of healthy normal counterparts [@bib199]. Increased oxidative stress can produce AGE-albumin adduct, which elevates the level of RAGE and activates JNK- and p38K-mediated death of neuronal cells. These results are in agreement with the increased expression of RAGE in the brains of alcohol-exposed rats and humans [@bib200]. Consistently, the elevated amounts of AGE-albumin, which was confirmed by mass-spectral analysis [@bib201], were found in the brains of Alzheimer's disease patients than those of the healthy individuals [@bib202]. Inhibition of AGE-albumin production or blockade of RAGE by a chemical antagonist or a specific antibody to RAGE efficiently prevented alcohol-induced brain damage [@bib199], suggesting an important role of AGE-protein adducts in promoting neurodegeneration. Based on these recent results [@bib199], [@bib200], [@bib201], [@bib202], it would be of interest to study the role of AGE-protein adducts in promoting organ damage in the peripheral tissues such as the liver and heart. Translational research with mitochondrial-targeted antioxidants {#s0040} =============================================================== As described above, the increased nitroxidative stress in AFLD and NAFLD or after exposure to hepatotoxic agents can stimulate multiple PTMs, including the hydroxyethyl-adducts observed in alcohol-exposed rats [@bib203] and individuals [@bib204] ([Fig. 3](#f0015){ref-type="fig"}). All these PTMs of cellular proteins are likely to contribute to increased ER stress and mitochondrial dysfunction, leading to energy depletion, fat accumulation, altered metabolism, inflammation and necrotic/apoptotic tissue damage ([Fig. 3](#f0015){ref-type="fig"}). Since elevated nitroxidative stress is a critical contributing factor for acute and chronic liver diseases, beneficial effects of many anti-oxidants from natural and synthetic origins have been tested in experimental model systems. These anti-oxidant agents include: [l]{.smallcaps}-arginine, small molecule metabolites (e.g., GSH-ethyl ester and NAC), natural antioxidants \[e.g., vitamins C, E, co-enzyme Q10, alpha-lipoic acid, fish oil containing n-3 fatty acids, betaine and *S*-adenosyl-methionine (SAMe)\], and herbal molecules and polyphenols (curcumin, esculetin, sulforaphane, resveratrol, epigallocatechin-3-gallate, caffeic acid phenethyl ester, and many others) [@bib205], [@bib206], [@bib207], [@bib208], [@bib209], [@bib210], [@bib211]. Some of these antioxidants, contained in many fruits and vegetables, show beneficial effects on obesity, NAFLD and liver injury [@bib205], [@bib206], [@bib207], [@bib208] while other antioxidants are potentially neuroprotective. Recent reports showed that naturally occurring antioxidants such as SAMe and betaine preserved mitochondrial function and proteome in the animal models of AFLD [@bib212], [@bib213], [@bib214] as well as NAFLD [@bib215], [@bib216], [@bib217], partly through blockade of the ROS/RNS production with restoring the physiological levels of SAMe, *S*-adenosyl-homocysteine and GSH. Nonetheless, the list of these antioxidants with therapeutic potential is exponentially growing and will reduce the oxidative burden in various pathophysiological conditions including fatty liver disease. One of the main problems with some of the natural antioxidants is to guarantee good manufacturing quality control \[e.g., a constant amount of the active component(s) with acceptable levels of impure materials\]. Other problems can be low solubility, poor bioavailability and little mitochondrial transport [@bib208], [@bib209], [@bib210], [@bib211]. To overcome these problems, many compounds with better mitochondrial targeting properties have been synthesized to prevent or treat mitochondrial dysfunction in many pathological conditions [@bib211], [@bib218], [@bib219], [@bib220], [@bib221], [@bib222], [@bib223], [@bib224], [@bib225]. For instance, to accomplish better mitochondrial transport, Szeto and Schiller developed a series of small, cell-permeable, mitochondria targeted antioxidant peptides (Szeto--Schiller or SS-tetrapeptide) that protect mitochondria from oxidative damage [@bib220]. These peptide antioxidants represent a novel approach with targeted delivery of antioxidants to the inner mitochondrial membrane. The structural motif of these SS-peptides centers on alternating aromatic residues and basic amino acids (aromatic-cationic peptides) that can scavenge hydrogen peroxide and peroxynitrite while they inhibit lipid peroxidation. Their antioxidant activities can be attributed to the tyrosine or dimethyltyrosine residue with inhibition of mitochondrial permeability transition and cytochrome c release, thus preventing oxidant-induced cell death. Because these peptides can accumulate \>1000-fold in the inner mitochondrial membrane, they prevent oxidative cell death with EC~50~ in the \~nM range. Similarly, the analogs of SOD-catalase mimetics also showed beneficial effects on many tissues including the liver and brain [@bib221]. In contrast to the SS-peptides or peptide-mimetics, a small molecule triphenyl phosphonium (TPP^+^, a cell permeable lipophilic cation) has been developed to conjugate with various drugs and antioxidants to enhance the transport of target molecules to reduce oxidative stress and damage, as reviewed [@bib222], [@bib223]. The results with mitochondria-targeted ubiquinone (MitoQ) or mitochondria-targeted carboxy-proxyl (Mito-CP) so far have shown promising results in preventing mitochondrial abnormalities and nitroxidative tissue injury in various disease models including Friedreich Ataxia fibroblasts [@bib224], diabetic nephropathy [@bib225], cisplatin-induced renal toxicity [@bib226] and cocaine-induced cardiac dysfunction [@bib227]. In addition, the protective effects of MitoQ and Mito-CP were clearly demonstrated in a mouse model of hepatic I/R injury [@bib228]. In a dose-dependent manner, these mitochondria-targeted compounds blocked the early and delayed nitroxidative stress responses (e.g., HNE/carbonyl adducts, malondialdehyde, 8-OHdG, and 3-nitrotyrosine formation), mitochondrial dysfunction and histopathological signs of liver injury as well as delayed inflammatory cell infiltration and cell death [@bib228]. Consistently, mitoQ was shown to be protective against micro- and macro-vesicular steatosis in AFLD [@bib229] without affecting the levels of CYP2E1 and ALDH2 as well as ethanol-induced mitochondrial respiratory abnormality. The effects of mitoQ were rather mediated through the suppression of ROS/RNS production and their down-stream targets such as protein nitration and HIF-1α stabilization [@bib229]. These promising results from different laboratories suggest that mitochondria-targeted antioxidants are more effective against elevated nitroxidative stress than untargeted natural antioxidants. Because of the recent development of these antioxidant agents and clinical testing [@bib230], [@bib231], we expect approval of some of these beneficial agents in treating mitochondrial dysfunction-related organ damage and hence preventing the health deterioration. Conclusion and future research opportunities {#s0045} ============================================ We have thus far briefly described five major types of PTMs that promote mitochondrial dysfunction, fat accumulation, inflammation and hepatic injury in alcoholic and nonalcoholic substances ([Fig. 1](#f0005){ref-type="fig"}). Although several PTMs in many mitochondrial proteins were identified in different disease states or under increased nitroxidative stress, it is quite possible that many proteins can be modified by multiple PTMs simultaneously. Therefore, it seems difficult to clearly demonstrate the deleterious effect of each single PTM and which PTM plays a critical role in causing mitochondrial dysfunction and tissue damage. In addition, it is challenging to identify the modified amino acid(s) and their roles in activity changes. It is also still unknown what other proteins, especially those expressed in low amounts in a particular tissue, are modified by different PTMs following exposure to a potentially toxic agent. Furthermore, mitochondrial functions can be altered by other types of PTM such as methylation, O-linked glycosylation (Ser or Thr), N-linked glycosylation (Asn), sumoylation, and ubiquitin conjugation. The identities of the proteins modified by these PTMs and their roles in mitochondrial dysfunction, fat accumulation and tissue injury need to be studied in the future. Finally, the patterns of PTM and their functional roles in other extra-hepatic tissues such as brain, heart, pancreas, adipose tissue and intestine need to be investigated. For instance, binge alcohol exposure [@bib232], [@bib233], [@bib234], [@bib235], [@bib236], [@bib237], [@bib238], [@bib239] and nonalcoholic substances including fructose [@bib240], [@bib241], [@bib242] are known to promote gut leakiness, contributing to more severe inflammatory liver disease. In the case of binge alcohol-induced gut leakiness, CYP2E1-mediated increased oxidative stress plays an important role, since treatment with an antioxidant NAC or a CYP2E1 inhibitor chlormethiazole significantly prevented gut leakiness and liver injury. In addition, Cyp2e1-null mice were resistant to alcohol-mediated gut leakiness, which was clearly observed in the corresponding wild-type mice [@bib238]. It is of interest whether gut leakiness caused by nonalcoholic substances also depends on CYP2E1-mediated oxidative stress. Despite numerous reports on gut leakiness caused by alcohol and fructose [@bib232], [@bib233], [@bib234], [@bib235], [@bib236], [@bib237], [@bib238], [@bib239], [@bib240], [@bib241], [@bib242], the functional roles of redox-regulated PTMs on many intestinal proteins are still poorly understood. Therefore, characterization of the modified proteins and their functional consequences in intestinal epithelial tissues and other tissues are not only good for basic mechanistic studies in understanding tissue--tissue interactions but also provide future translational and clinical research opportunities. This research was supported by the Intramural Program Fund at the National Institute on Alcohol Abuse and Alcoholism. The authors thank Dr. Klaus Gawrisch for his support. The authors do not have any conflict of interest. {#f0005} ![Multiple PTM of ALDH2 protein, contributing to its inactivation. Different types of PTM on ALDH2 are illustrated. Most PTMs led to the suppression of ALDH2 activity, although phosphorylation of ALDH2 by the PKCε isoform was shown to stimulate the ALDH2 activity, as recently reviewed [@bib42]. The suppressed activities of ALDH2 and other isozymes, all of which share the 100%-conserved active site Cys residue, likely contribute to increased levels of toxic and carcinogenic acetaldehyde (AcAH) and lipid peroxides (MDA and 4-HNE) following exposure to ethanol, high fat and other toxic compounds. ER stress, mitochondrial dysfunction and tissue injury can be observed in acute and sub-chronic cases. Long-term chronic suppression of ALDH2 and other isozymes can also contribute to fibrosis, cirrhosis and carcinogenesis. The negative sign represents the inactivation of ALDH2 and other isozymes.](gr2){#f0010} ![Overlapping PTMs between AFLD and NAFLD. Overlapping PTMs commonly observed in both AFLD and NAFLD are illustrated. However, acetaldehyde--protein adduct (AA--adduct) [@bib171], [@bib181], NEL-adduct [@bib193], AA-AGE-adduct [@bib193], and hydroxyethyl-adduct [@bib203], [@bib204] seem uniquely observed in AFLD. These PTMs observed in AFLD and NAFLD are likely to suppress the functions of the target proteins, contributing to altered cell signaling, ER stress, mitochondrial dysfunction, fat accumulation and inflammatory tissue injury.](gr3){#f0015}

Stylonurella Stylonurella is a genus of prehistoric eurypterid. It is classified within the Parastylonuridae family and contains three species, S. arnoldi and S. beecheri from the Devonian of Pennsylvania, United States and S. spinipes from the Silurian of Kip Burn, Scotland. Description Stylonurella was a small stylonuroid, possessing a subquadrate prosoma with approximately the same length as width. The midsection was slightly constricted and the eyes were parallel and anteriorly located in the anterior half of the carapace. The metastoma and first two appendages are unknown, the third and fourth prosomal legs are very short and the last two walking legs are very long. The metasoma is very narrow. Classification Though one of the earliest described stylonurines, described shortly after the description of Stylonurus itself, it has no close relations to that genus. Indeed, there are numerous and apparent differences. For instance, the eyes of Stylonurus are located on the posterior half of the carapace and those of Stylonurella are on the anterior half. Furthermore, there are noticeable differences between Stylonurella and its closest relative, Parastylonurus, for instance the widely different shapes of the carapaces (quadrate in Stylonurella and subrounded in Parastylonurus). Species Stylonurella contains three valid species, with other named species now seen as invalid or as part of other genera. Stylonurella? arnoldi Ehlers, 1935 - Pennsylvania, USA (Devonian) Stylonurella? beecheri Hall, 1884 - Pennsylvania, USA (Devonian) Stylonurella spinipes Page, 1859 - Kip Burn, Scotland (Silurian) Invalid or reassigned species are listed below: "Stylonurella" logani Woodward, 1872 - Kip Burn, Scotland (Silurian), synonym of S. spinipes. "Stylonurella" modestus Clarke & Ruedemann, 1912 - New York, USA (Ordovician), a pseudofossil. "Stylonurella" otisius Clarke, 1907 - Eastern USA (Silurian), reclassified as a species of Clarkeipterus. "Stylonurella" ruedemanni Størmer, 1934 - Ringerike, Norway (Silurian), reclassified as a species of Kiaeropterus. See also List of eurypterids References Category:Stylonuroidea Category:Silurian arthropods of Europe Category:Silurian eurypterids Category:Eurypterids of Europe Category:Devonian eurypterids Category:Eurypterids of North America

Concealing spoilers is all in a day's work for Marvel-movie stars 'Ant-Man' stars Michael Douglas, Evangeline Lilly and Paul Rudd say that when it comes to plot spoilers, silence is golden in the Marvel Cinematic Universe. (June 29) AP

--- abstract: | We express the averages of products of characteristic polynomials for random matrix ensembles associated with compact symmetric spaces in terms of Jack polynomials or Heckman and Opdam’s Jacobi polynomials depending on the root system of the space. We also give explicit expressions for the asymptotic behavior of these averages in the limit as the matrix size goes to infinity. [**MSC-class**]{}: primary 15A52; secondary 33C52, 05E05.\ [**Keywords**]{}: characteristic polynomial, random matrix, Jacobi polynomial, Jack polynomial, Macdonald polynomial, compact symmetric space. author: - '<span style="font-variant:small-caps;">Sho MATSUMOTO</span> [^1]' title: '**Moments of characteristic polynomials for compact symmetric spaces and Jack polynomials**' --- Introduction ============ In recent years, there has been considerable interest in the averages of the characteristic polynomials of random matrices. This work is motivated by the connection with Riemann zeta functions and $L$-functions identified by Keating and Snaith [@KS_zetafunctions; @KS_Lfunctions]. The averages of the characteristic polynomials in the cases of compact classical groups and Hermitian matrix ensembles have already calculated, see [@Mehta] and references in [@BG]. In these studies, Bump and Gamburd [@BG] obtain simple proofs for the cases corresponding to compact classical groups by using symmetric polynomial theory. Our aim in this note is to use their technique to calculate averages of the characteristic polynomials for random matrix ensembles associated with compact symmetric spaces. We deal with the compact symmetric spaces $G/K$ classified by Cartan, where $G$ is a compact subgroup in $GL(N,{\mathbb{C}})$ for some positive integer $N$, and $K$ is a closed subgroup of $G$. Assume $G/K$ is realized as a subspace $S$ in $G$, i.e., $S \simeq G/K$, and the probability measure $\dd M$ on $S$ is then induced from $G/K$. We call the probability space $(S, \dd M)$ the random matrix ensemble associated with $G/K$. For example, $U(n)/O(n)$ is the symmetric space with a restricted root system of type A, and is realized by $S=\{M \in U(n) \ | \ M = \trans{M} \}$. Here $\trans{M}$ stands for the transposed matrix of $M$ while $U(n)$ and $O(n)$ denote the unitary and orthogonal group of matrices or order $n$ respectively. The induced measure $\dd M$ on $S$ satisfies the invariance $\dd (H M \trans{H})= \dd M$ for any $H \in U(n)$. This random matrix ensemble $(S, \dd M)$ is well known as the circular orthogonal ensemble (COE for short), see e.g. [@Dyson; @Mehta]. We also consider the classical compact Lie groups $U(n)$, $SO(n)$, and $Sp(2n)$. Regarding these groups as symmetric spaces, the random matrix space $S$ is just the group itself with its Haar measure. The compact symmetric spaces studied by Cartan are divided into A and BC type main branches according to their root systems. There are three symmetric spaces of type A, with their corresponding matrix ensembles called circular orthogonal, unitary, and symplectic ensembles. For these ensembles, the probability density functions (p.d.f.) for the eigenvalues are proportional to $$\Delta^{{\mathrm{Jack}}}(\bz;2/\beta)= \prod_{1 \le i<j \le n} |z_i -z_j|^{\beta},$$ with $\beta=1,2,4$, where $\bz =(z_1,\dots, z_n)$, with $|z_i|=1$, denotes the sequence of eigenvalues of the random matrix. We will express the average of the product of characteristic polynomials $\det(I+ xM)$ for a random matrix $M$ as a Jack polynomial ([@Mac Chapter VI-10]) of a rectangular-shaped Young diagram. Jack polynomials are orthogonal with respect to the weight function $\Delta^{{\mathrm{Jack}}}$. Our theorems are obtained in a simple algebraic way, and contain results given in [@KS_zetafunctions]. For compact symmetric spaces of type BC root systems, the corresponding p.d.f. is given by $$\Delta^{{\mathrm{HO}}}(\bz;k_1,k_2,k_3) = \prod_{1 \le i <j \le n} |1-z_i z_j^{-1}|^{2k_3} |1-z_i z_j|^{2k_3} \cdot \prod_{1 \le j \le n} |1-z_j|^{2k_1} |1-z_j^2|^{2k_2}.$$ Here the $k_i$’s denote multiplicities of roots in the root systems of the symmetric spaces. For example, the p.d.f. induced from the symmetric space $SO(4n+2)/(SO(4n+2) \cap Sp(4n+2))$ is proportional to $\Delta^{{\mathrm{HO}}}(\bz;2, \frac{1}{2},2)$. For this class of compact symmetric spaces, Opdam and Heckman’s Jacobi polynomials ([@Diejen; @Heckman]), which are orthogonal with respect to $\Delta^{{\mathrm{HO}}}$, will play the same role as Jack polynomials for type A cases. Namely, we will express the average of the product of characteristic polynomials $\det(I+ xM)$ as the Jacobi polynomial of a rectangular-shaped diagram. This paper is organized as follows: Our main results, which are expressions for the averages of products of characteristic polynomials, will be given §6. As described above, the symmetric spaces corresponding to the two root systems, type A and BC, will be discussed separately. For type A spaces, we use Jack polynomial theory. These discussions can be generalized to Macdonald polynomials. Thus, after preparations in §2, we give some generalized identities involving Macdonald polynomials and a generalization of the weight function $\Delta^{{\mathrm{Jack}}}$ in §3 and §4. In particular, we obtain $q$-analogues of Keating and Snaith’s formulas [@KS_zetafunctions] for the moments of characteristic polynomials and a generalization of the strong Szegö limit theorem for Toeplitz determinants. These identities are reduced to characteristic polynomial expressions for symmetric spaces of the A type root system in §6.1 - §6.3. On the other hand, for type BC spaces, we employ Opdam and Heckman’s Jacobi polynomials. We review the definition and several properties of these polynomials in §5, while in §6.4 - §6.12 we apply them to obtain expressions for the products of characteristic polynomials of random matrix ensembles associated with symmetric spaces of type BC. Basic Properties of Macdonald symmetric functions ================================================= We recall the definition of Macdonald symmetric functions, see [@Mac Chapter VI] for details. Let $\lambda$ be a partition, i.e., $\lambda=(\lambda_1,\lambda_2,\dots)$ is a weakly decreasing ordered sequence of non-negative integers with finitely many non-zero entries. Denote by $\ell(\lambda)$ the number of non-zero $\lambda_j$ and by $|\lambda|$ the sum of all $\lambda_j$. These values $\ell(\lambda)$ and $|\lambda|$ are called the length and weight of $\lambda$ respectively. We identify $\lambda$ with the associated Young diagram $\{(i,j) \in {\mathbb{Z}}^2 \ | \ 1 \le j \le \lambda_i \}$. The conjugate partition $\lambda'=(\lambda'_1,\lambda'_2,\dots)$ is determined by the transpose of the Young diagram $\lambda$. It is sometimes convenient to write this partition in the form $\lambda=(1^{m_1} 2^{m_2} \cdots )$, where $m_i=m_i(\lambda)$ is the multiplicity of $i$ in $\lambda$ and is given by $m_i=\lambda'_i-\lambda'_{i+1}$. For two partitions $\lambda$ and $\mu$, we write $\lambda \subset \mu$ if $\lambda_i \le \mu_i$ for all $i$. In particular, the notation $\lambda \subset (m^n)$ means that $\lambda$ satisfies $\lambda_1 \le m$ and $\lambda_1' \le n$. The dominance ordering associated with the root system of type A is defined as follows: for two partitions $\lambda=(\lambda_1,\lambda_2,\dots)$ and $\mu=(\mu_1,\mu_2,\dots)$, $$\mu \le_{{\mathrm{A}}} \lambda \qquad \Leftrightarrow \qquad |\lambda|=|\mu| \quad \text{and} \quad \mu_1 + \cdots+\mu_i \le \lambda_1+ \cdots +\lambda_i \quad \text{for all $i \ge 1$}.$$ Let $q$ and $t$ be real numbers such that both $|q|<1$ and $|t|<1$. Put $F={\mathbb{Q}}(q,t)$ and ${\mathbb{T}}^n=\{\bz =(z_1,\dots,z_n) \ | \ |z_i|=1 \ (1 \le i \le n)\}$. Denote by $F[x_1,\dots,x_n]^{{\mathfrak{S}}_n}$ the algebra of symmetric polynomials in variables $x_1,\dots,x_n$. Define an inner product on $F[x_1,\dots,x_n]^{{\mathfrak{S}}_n}$ by $$\langle f, g \rangle_{\Delta^{{\mathrm{Mac}}}} = \frac{1}{n!} \int_{{\mathbb{T}}^n} f(\bz) g(\bz^{-1}) \Delta^{{\mathrm{Mac}}}(\bz;q,t) \dd \bz$$ with $$\Delta^{{\mathrm{Mac}}}(\bz;q,t)= \prod_{1 \le i<j \le n} \Bigg| \frac{(z_i z_j^{-1};q)_\infty}{(t z_i z_j^{-1};q)_\infty} \Bigg|^2,$$ where $\bz^{-1}=(z_1^{-1},\dots,z_n^{-1})$ and $(a;q)_\infty= \prod_{r=0}^\infty(1-aq^r)$. Here $\dd \bz$ is the normalized Haar measure on ${\mathbb{T}}^n$. For a partition $\lambda$ of length $\ell(\lambda) \le n$, put $$\label{eq:monomialA} m_{\lambda}^{{\mathrm{A}}} (x_1,\dots,x_n) = \sum_{\nu=(\nu_1,\dots,\nu_n) \in {\mathfrak{S}}_n \lambda} x_1^{\nu_1} \cdots x_n^{\nu_n},$$ where the sum runs over the ${\mathfrak{S}}_n$-orbit ${\mathfrak{S}}_n \lambda = \{ (\lambda_{\sigma(1)},\dots, \lambda_{\sigma(n)}) \ | \ \sigma \in {\mathfrak{S}}_n\}$. Here we add the suffix “A” because ${\mathfrak{S}}_n$ is the Weyl group of type A. Then Macdonald polynomials (of type A) $P_\lambda^{{\mathrm{Mac}}}=P_{\lambda}^{{\mathrm{Mac}}}(x_1,\dots,x_n;q,t) \in F[x_1,\dots,x_n]^{{\mathfrak{S}}_n}$ are characterized by the following conditions: $$P_{\lambda}^{{\mathrm{Mac}}} = m_{\lambda}^{{\mathrm{A}}} + \sum_{\mu <_{{\mathrm{A}}} \lambda} u_{\lambda \mu} m_{\mu}^{{\mathrm{A}}} \quad \text{with $u_{\lambda\mu} \in F$}, \qquad\qquad \langle P_{\lambda}^{{\mathrm{Mac}}}, P_{\mu}^{{\mathrm{Mac}}} \rangle_{\Delta^{{\mathrm{Mac}}}}=0 \quad \text{if $\lambda \not=\mu$}.$$ Denote by $\Lambda_F$ the $F$-algebra of symmetric functions in infinitely many variables $\bx=(x_1,x_2,\dots)$. That is, an element $f =f(\bx) \in \Lambda_F$ is determined by the sequence $(f_n)_{n \ge 0}$ of polynomials $f_n$ in $F[x_1,\dots,x_n]^{{\mathfrak{S}}_n}$, where these polynomials satisfy $\sup_{n \ge 0} \deg (f_n) < \infty$ and $f_m(x_1,\dots,x_n,0,\dots,0)=f_n(x_1,\dots,x_n)$ for any $m \ge n$, see [@Mac Chapter I-2]. Macdonald polynomials satisfy the stability property $$P^{{\mathrm{Mac}}}_\lambda(x_1,\dots,x_n,x_{n+1};q,t) \Big|_{x_{n+1}=0} = P^{{\mathrm{Mac}}}_\lambda(x_1,\dots,x_n;q,t)$$ for any partition $\lambda$ of length $\ell(\lambda) \le n$, and therefore for all partitions $\lambda$, [*Macdonald functions*]{} $P_{\lambda}^{{\mathrm{Mac}}}(\bx ;q,t)$ can be defined. For each square $s=(i,j)$ of the diagram $\lambda$, let $$a(s)=\lambda_i-j, \qquad a'(s)=j-1, \qquad l(s)= \lambda'_j-i, \qquad l'(s)= i-1.$$ These numbers are called the arm-length, arm-colength, leg-length, and leg-colength respectively. Put $$c_{\lambda}(q,t)= \prod_{s \in \lambda} (1-q^{a(s)}t^{l(s)+1}), \qquad c_{\lambda}'(q,t)= \prod_{s \in \lambda} (1-q^{a(s)+1} t^{l(s)}).$$ Note that $c_{\lambda}(q,t)= c'_{\lambda'}(t,q)$. Defining the $Q$-function by $Q_{\lambda}(\bx;q,t)= c_{\lambda}(q,t) c'_{\lambda}(q,t)^{-1} P_\lambda(\bx;q,t)$, we have the dual Cauchy identity [@Mac Chapter VI (5.4)] $$\begin{aligned} & \sum_{\lambda} P_\lambda(\bx;q,t) P_{\lambda'}(\by;t,q)= \sum_{\lambda} Q_\lambda(\bx;q,t) Q_{\lambda'}(\by;t,q) \label{EqDualCauchy} \\ =& \prod_{i\ge 1} \prod_{j\ge 1} (1+x_i y_j) =\exp \(\sum_{k=1}^\infty \frac{(-1)^{k-1}}{k}p_k(\bx)p_k(\by) \), \notag \end{aligned}$$ where $\by=(y_1,y_2,\dots)$. Here $p_k$ is the power-sum function $p_k(\bx)=x_1^k+x_2^k+ \cdots$. We define the generalized factorial $(a)_{\lambda}^{(q,t)}$ by $$(a)_{\lambda}^{(q,t)} = \prod_{s \in \lambda} (t^{l'(s)} - q^{a'(s)} a).$$ Let $u$ be an indeterminate and define the homomorphism $\epsilon_{u,t}$ from $\Lambda_F$ to $F$ by $$\label{EqSpecialPowerSum} \epsilon_{u,t}(p_r) = \frac{1-u^r}{1-t^r} \qquad \text{for all $r \ge 1$}.$$ In particular, we have $\epsilon_{t^n,t}(f)= f(1,t,t^2,\dots, t^{n-1})$ for any $f \in \Lambda_F$. Then we have ([@Mac Chapter VI (6.17)]) $$\label{EqSpecialMac} \epsilon_{u,t}(P_{\lambda}^{{\mathrm{Mac}}})= \frac{(u)_{\lambda}^{(q,t)}}{c_{\lambda}(q,t)}.$$ Finally, the following orthogonality property is satisfied for any two partitions $\lambda$ and $\mu$ of length $\le n$: $$\label{EqOrthogonality} \langle P_{\lambda}^{{\mathrm{Mac}}}, Q_{\mu}^{{\mathrm{Mac}}} \rangle_{\Delta^{{\mathrm{Mac}}}}= \delta_{\lambda \mu} \langle 1,1 \rangle_{\Delta^{{\mathrm{Mac}}}} \prod_{s \in \lambda} \frac{1-q^{a'(s)}t^{n-l'(s)}}{1-q^{a'(s)+1}t^{n-l'(s)-1}}.$$ Averages with respect to $\Delta^{{\mathrm{Mac}}}(\bz;q,t)$ {#sectionMacAverage} =========================================================== As in the previous section, we assume $q$ and $t$ are real numbers in the interval $(-1,1)$. For a Laurent polynomial $f$ in variables $z_1,\dots,z_n$, we define $$\langle f \rangle_{n}^{(q,t)} = \frac{\int_{{\mathbb{T}}^n} f(\bz) \Delta^{{\mathrm{Mac}}}(\bz;q,t) \dd \bz} {\int_{{\mathbb{T}}^n} \Delta^{{\mathrm{Mac}}}(\bz;q,t) \dd \bz}.$$ In this section, we calculate averages of the products of the polynomial $$\Psi^{{\mathrm{A}}}(\bz;\eta)= \prod_{j=1}^n (1+ \eta z_j), \qquad \eta \in {\mathbb{C}}$$ with respect to $\langle \cdot \rangle_{n}^{(q,t)}$. Denoting the eigenvalues of a unitary matrix $M$ by $z_1,\dots,z_n$, the polynomial $\Psi^{{\mathrm{A}}}(\bz;\eta)$ is the characteristic polynomial $\det(I+\eta M)$. The following theorems will induce averages of the products of characteristic polynomials for random matrix ensembles associated with type A root systems, see §\[sectionCBEq\] and §\[subsectionA\] - §\[subsectionAII\] below. \[ThmAverageMac\] Let $K$ and $L$ be positive integers. Let $\eta_1,\dots, \eta_{L+K}$ be complex numbers such that $\eta_j \not=0 \ ( 1\le j \le L)$. Then we have $$\left\langle \prod_{l=1}^L \Psi^{{\mathrm{A}}}(\bz^{-1};\eta_l^{-1}) \cdot \prod_{k=1}^K \Psi^{{\mathrm{A}}}(\bz;\eta_{L+k}) \right\rangle_{n}^{(q,t)} = (\eta_1 \cdots \eta_L)^{-n} \cdot P_{(n^L)}^{{\mathrm{Mac}}} (\eta_1, \dots, \eta_{L+K};t,q).$$ By the dual Cauchy identity , we have $$\begin{aligned} & \prod_{l=1}^L \Psi^{{\mathrm{A}}}(\bz^{-1};\eta_l^{-1}) \cdot \prod_{k=1}^K \Psi^{{\mathrm{A}}}(\bz;\eta_{L+k}) = \prod_{l=1}^L \eta_l^{-n} \cdot (z_1 \cdots z_n)^{-L} \cdot \prod_{k=1}^{L+K} \prod_{j=1}^n (1+\eta_k z_j) \\ =& \prod_{l=1}^L \eta_l^{-n} \cdot (z_1 \cdots z_n)^{-L} \sum_{\lambda} Q_{\lambda}^{{\mathrm{Mac}}}(\eta_1,\dots,\eta_{L+K};t,q) Q_{\lambda'}^{{\mathrm{Mac}}}(\bz;q,t).\end{aligned}$$ Therefore, since $P_{(L^n)}^{{\mathrm{Mac}}}(\bz;q,t)=(z_1\cdots z_n)^L$ ([@Mac Chapter VI (4.17)]), we see that $$\begin{aligned} \left\langle \prod_{l=1}^L \Psi^{{\mathrm{A}}}(\bz^{-1};\eta_l^{-1}) \cdot \prod_{k=1}^K \Psi^{{\mathrm{A}}}(\bz;\eta_{L+k}) \right\rangle_{n}^{(q,t)} =& \prod_{l=1}^L \eta_l^{-n} \sum_{\lambda} Q_{\lambda}^{{\mathrm{Mac}}}(\eta_1,\dots,\eta_{L+K};t,q) \frac{\langle Q_{\lambda'}^{{\mathrm{Mac}}}, P_{(L^n)}^{{\mathrm{Mac}}} \rangle_{ \Delta^{{\mathrm{Mac}}} } } {\langle 1, 1 \rangle_{\Delta^{{\mathrm{Mac}}} } } \\ =& \prod_{l=1}^L \eta_l^{-n} \cdot Q_{(n^L)}^{{\mathrm{Mac}}}(\eta_1,\dots,\eta_{L+K};t,q) \prod_{s \in (L^n)} \frac{1-q^{a'(s)}t^{n-l'(s)}}{1-q^{a'(s)+1}t^{n-l'(s)-1}}\end{aligned}$$ by the orthogonality property . It is easy to check that $$\prod_{s \in (L^n)} \frac{1-q^{a'(s)}t^{n-l'(s)}}{1-q^{a'(s)+1}t^{n-l'(s)-1}} =\frac{c_{(L^n)}(q,t)}{c'_{(L^n)}(q,t)}= \frac{c'_{(n^L)}(t,q)}{c_{(n^L)}(t,q)},$$ and so we obtain the claim. It may be noted that the present proof of Theorem \[ThmAverageMac\] is similar to the corresponding one in [@BG]. \[CorMomentValue\] For each positive integer $k$ and $\xi \in {\mathbb{T}}$, we have $$\left\langle \prod_{i=0}^{k-1} | \Psi^{{\mathrm{A}}}(\bz; q^{i+1/2} \xi )|^2 \right\rangle_{n}^{(q,t)} = \prod_{i=0}^{k-1} \prod_{j=0}^{n-1} \frac{1-q^{k+i+1} t^j}{1-q^{i+1} t^j}.$$ Set $L=K=k$ and $\overline{\eta_i}^{-1} =\eta_{i+k} =q^{i-1/2} \xi \ (1 \le i \le k)$ in Theorem \[ThmAverageMac\]. Then we have $$\begin{aligned} \left\langle \prod_{i=0}^{k-1} | \Psi^{{\mathrm{A}}}(\bz;q^{i+1/2} \xi)|^2 \right\rangle_{n}^{(q,t)} =& \prod_{i=0}^{k-1} q^{(i+1/2)n} \cdot P_{(n^k)} (q^{-k+1/2}, q^{-k+3/2}, \dots, q^{-1/2}, q^{1/2}, \cdots, q^{k-1/2};t,q) \\ =& q^{n k^2/2} \cdot q^{(-k+1/2)kn} P_{(n^k)}(1,q,\cdots, q^{2k-1};t,q) \\ =& q^{-n k(k-1)/2} \epsilon_{q^{2k},q} (P_{(n^k)}(\cdot;t,q)). \end{aligned}$$ From expression , the right-hand side of the above expression equals $$q^{-n k(k-1)/2} \frac{(q^{2k})_{(n^k)}^{(t,q)}}{c_{(n^k)}(t,q)} =q^{-n k(k-1)/2} \prod_{i=1}^k \prod_{j=1}^n \frac{q^{i-1}-t^{j-1} q^{2k}}{1-t^{n-j}q^{k-i+1}} = \prod_{j=0}^{n-1} \prod_{i=1}^k \frac{1-t^{j} q^{2k-i+1}}{1-t^j q^{k-i+1}},$$ and the result follows. Kaneko [@Kaneko2] defines the multivariable $q$-hypergeometric function associated with Macdonald polynomials by $${_2 \Phi_1}^{(q,t)}(a,b;c;x_1,\dots,x_n)= \sum_\lambda \frac{ (a)_{\lambda}^{(q,t)} (b)_{\lambda}^{(q,t)}}{(c)_{\lambda}^{(q,t)}} \frac{P^{{\mathrm{Mac}}}_{\lambda}(x_1,\dots,x_n;q,t)}{c'_{\lambda}(q,t)},$$ where $\lambda$ runs over all partitions of length $\ell(\lambda) \le n$. The $q$-shifted moment $\left\langle \prod_{i=0}^{k-1} | \Psi^{{\mathrm{A}}}(\bz;q^{i+1/2} \xi )|^2 \right\rangle_{n}^{(q,t)}$ given in Corollary \[CorMomentValue\] can also be expressed as a special value of the generalized $q$-hypergeometric function ${_2 \Phi_1}^{(q,t)}$ as follows: \[PropMomentHypergeometric\] For any complex number with $|\eta|<1$ and real number $u$, $$\left\langle \prod_{j=1}^n \left| \frac{(\eta z_j;q)_\infty}{(\eta z_j u; q)_{\infty}} \right|^2 \right\rangle_{n}^{(q,t)} = {_2 \Phi_1}^{(q,t)}(u^{-1},u^{-1} ;q t^{n-1}; (u|\eta|)^2, (u|\eta|)^2 t,\dots, (u|\eta|)^2t^{n-1}).$$ In particular, letting $u=q^k$ and $\eta=q^{1/2}\xi$ with $\xi \in {\mathbb{T}}$, we have $$\left\langle \prod_{i=0}^{k-1} | \Psi^{{\mathrm{A}}}(\bz;q^{i+1/2} \xi)|^2 \right\rangle_{n}^{(q,t)} = {_2 \Phi_1}^{(q,t)}(q^{-k},q^{-k} ;q t^{n-1}; q^{2k+1}, q^{2k+1}t , \dots, q^{2k+1} t^{n-1}).$$ A simple calculation gives $$\prod_{j=1}^n \frac{(\eta z_j;q)_\infty}{(\eta z_j u; q)_{\infty}} = \exp \(\sum_{k=1}^\infty \frac{(-1)^{k-1}}{k} \frac{1-u^k}{1-q^k} p_{k}(-\eta z_1, \dots, -\eta z_n) \).$$ From expressions and , we have $$\prod_{j=1}^n \frac{(\eta z_j;q)_\infty}{(\eta z_j u; q)_{\infty}} = \sum_{\lambda} (-\eta)^{|\lambda|} \epsilon_{u,q}(Q^{{\mathrm{Mac}}}_{\lambda'}(\cdot;t,q)) Q^{{\mathrm{Mac}}}_{\lambda}(\bz;q,t) = \sum_{\lambda} (-\eta)^{|\lambda|} \epsilon_{u,q}(P^{{\mathrm{Mac}}}_{\lambda'}(\cdot;t,q)) P^{{\mathrm{Mac}}}_{\lambda}(\bz;q,t).$$ Thus we have $$\prod_{j=1}^n \left| \frac{(\eta z_j;q)_\infty}{(\eta z_j u; q)_{\infty}} \right|^2 = \sum_{\lambda, \mu} (-\eta)^{|\lambda|} (-\overline{\eta})^{|\mu|} \epsilon_{u,q}(P^{{\mathrm{Mac}}}_{\lambda'}(\cdot;t,q)) \epsilon_{u,q}(Q^{{\mathrm{Mac}}}_{\mu'}(\cdot;t,q)) P^{{\mathrm{Mac}}}_{\lambda}(\bz;q,t) Q^{{\mathrm{Mac}}}_{\mu}(\bz^{-1};q,t).$$ The average is given by $$\begin{aligned} \left\langle \prod_{j=1}^n \left| \frac{(\eta z_j;q)_\infty}{(\eta z_j u; q)_{\infty}} \right|^2 \right\rangle_{n}^{(q,t)} =& \sum_{\lambda} |\eta|^{2|\lambda|} \epsilon_{u,q}(P^{{\mathrm{Mac}}}_{\lambda'}(\cdot;t,q)) \epsilon_{u,q}(Q^{{\mathrm{Mac}}}_{\lambda'}(\cdot;t,q)) \frac{ \langle P^{{\mathrm{Mac}}}_{\lambda}, Q^{{\mathrm{Mac}}}_{\lambda} \rangle_{\Delta^{{\mathrm{Mac}}}} } {\langle 1, 1 \rangle_{\Delta^{{\mathrm{Mac}}}} } \\ =& \sum_{\lambda} |\eta|^{2|\lambda|} \frac{\{(u)_{\lambda'}^{(t,q)}\}^2}{c_{\lambda'}(t,q) c'_{\lambda'}(t,q)} \prod_{s \in \lambda} \frac{1-q^{a'(s)}t^{n-l'(s)}}{1-q^{a'(s)+1}t^{n-l'(s)-1}}\end{aligned}$$ by expression and the orthogonality property . It is easy to check that $$\begin{aligned} &(u)_{\lambda'}^{(t,q)} =(-u)^{|\lambda|} (u^{-1})_{\lambda}^{(q,t)}, \qquad c_{\lambda'}(t,q) c'_{\lambda'}(t,q)= c_{\lambda}(q,t) c'_{\lambda}(q,t), \\ &\prod_{s \in \lambda} \frac{1-q^{a'(s)}t^{n-l'(s)}}{1-q^{a'(s)+1}t^{n-l'(s)-1}} = \prod_{s \in \lambda} \frac{t^{l'(s)}-q^{a'(s)}t^{n}}{t^{l'(s)} -q^{a'(s)+1}t^{n-1}} = \frac{(t^n)_{\lambda}^{(q,t)}}{(q t^{n-1})_{\lambda}^{(q,t)}}.\end{aligned}$$ Finally, we obtain $$\left\langle \prod_{j=1}^n \left| \frac{(\eta z_j;q)_\infty}{(\eta z_j u; q)_{\infty}} \right|^2 \right\rangle_{n}^{(q,t)} = \sum_{\lambda} (u|\eta|)^{2|\lambda|} \frac{\{(u^{-1})_{\lambda}^{(q,t)}\}^2}{(q t^{n-1})_{\lambda}^{(q,t)}} \frac{P^{{\mathrm{Mac}}}_{\lambda}(1,t,\dots,t^{n-1};q,t)}{c'_{\lambda}(q,t)},$$ which equals ${_2 \Phi_1}^{(q,t)}(u^{-1},u^{-1} ;q t^{n-1}; (u|\eta|)^2,\dots, (u|\eta|)^2t^{n-1})$. Now we derive the asymptotic behavior of the moment of $|\Psi(\bz;\eta)|$ when $|\eta| < 1$ in the limit as $n \to \infty$. The following theorem is a generalization of the well-known strong Szegö limit theorem as stated in §\[subsectionCBEJack\] below. \[Thm:SzegoMacdonald\] Let $\phi(z)=\exp(\sum_{k \in {\mathbb{Z}}} c(k) z^k)$ be a function on ${\mathbb{T}}$ and assume $$\label{Eq:AssumptionSzego} \sum_{k \in {\mathbb{Z}}} |c(k)|< \infty \qquad \text{and} \qquad \sum_{k \in {\mathbb{Z}}} |k| |c(k)|^2 < \infty.$$ Then we have $$\lim_{n \to \infty} e^{-n c(0)} \left\langle \prod_{j=1}^n \phi(z_j) \right\rangle_n^{(q,t)} = \exp \( \sum_{k=1}^\infty kc(k)c(-k) \frac{1-q^k}{1-t^k} \).$$ First we see that $$\begin{aligned} & \prod_{j=1}^n \phi(z_j)= e^{n c(0)} \prod_{k=1}^\infty \exp(c(k) p_k(\bz)) \exp(c(-k) \overline{p_k(\bz)}) \\ =& e^{n c(0)} \prod_{k=1}^\infty \( \sum_{a=0}^\infty \frac{c(k)^{a}}{a!} p_{(k^{a})}(\bz) \) \( \sum_{b=0}^\infty \frac{c(-k)^{b}}{b!} \overline{p_{(k^{b})}(\bz)} \) \\ =& e^{n c(0)} \sum_{(1^{a_1} 2^{a_2} \cdots )} \sum_{(1^{b_1} 2^{b_2} \cdots )} \( \prod_{k=1}^\infty \frac{c(k)^{a_k}c(-k)^{b_k}}{a_k! \, b_k!} \) p_{(1^{a_1}2^{a_2} \cdots )}(\bz)\overline{p_{(1^{b_1}2^{b_2} \cdots )}(\bz)},\end{aligned}$$ where both $(1^{a_1}2^{a_2} \cdots )$ and $(1^{b_1}2^{b_2} \cdots )$ run over all partitions. Therefore we have $$e^{-n c(0)} \left\langle \prod_{j=1}^n \phi(z_j) \right\rangle_n^{(q,t)} = \sum_{(1^{a_1} 2^{a_2} \cdots )} \sum_{(1^{b_1} 2^{b_2} \cdots )} \( \prod_{k=1}^\infty \frac{c(k)^{a_k}}{a_k!} \frac{c(-k)^{b_k}}{b_k!} \) \frac{ \langle p_{(1^{a_1} 2^{a_2} \cdots )}, p_{(1^{b_1} 2^{b_2} \cdots )} \rangle_{\Delta^{{\mathrm{Mac}}}} } { \langle 1, 1 \rangle_{\Delta^{{\mathrm{Mac}}}} }.$$ We recall the asymptotic behavior $$\frac{ \langle p_{(1^{a_1} 2^{a_2} \cdots )}, p_{(1^{b_1} 2^{b_2} \cdots )} \rangle_{\Delta^{{\mathrm{Mac}}}} } { \langle 1, 1 \rangle_{\Delta^{{\mathrm{Mac}}}} } \qquad \longrightarrow \qquad \prod_{k=1}^\infty \delta_{a_k b_k} k^{a_k} a_k! \( \frac{1-q^k}{1-t^k}\)^{a_k}$$ in the limit as $n \to \infty$, see [@Mac Chapter VI (9.9) and (1.5)]. It follows from this that $$\begin{aligned} &\lim_{n \to \infty} e^{-n c(0)} \left\langle \prod_{j=1}^n \phi(z_j) \right\rangle_n^{(q,t)} = \sum_{(1^{a_1} 2^{a_2} \cdots )} \prod_{k=1}^\infty \frac{(k c(k) c(-k))^{a_k}}{a_k!} \(\frac{1-q^k}{1-t^k}\)^{a_k} \\ =& \prod_{k=1}^\infty \( \sum_{a=0}^\infty \frac{(k c(k) c(-k)\frac{1-q^k}{1-t^k})^{a}}{a!}\) = \exp \( \sum_{k=1}^\infty k c(k) c(-k) \frac{1-q^k}{1-t^k}\).\end{aligned}$$ Here $\sum_{k=1}^\infty k c(k) c(-k) \frac{1-q^k}{1-t^k}$ converges absolutely by the second assumption in and the Cauchy-Schwarz inequality, because $| \frac{1-q^k}{1-t^k}| \le \frac{1+|q|^k}{1-|t|^{k}} \le 1+|q|$. Note that the present proof is similar to the corresponding one in [@BD]. The result in [@BD] is the special case of Theorem \[Thm:SzegoMacdonald\] with $q=t$. As an example of this theorem, the asymptotic behavior of the moment of $|\Psi^{{\mathrm{A}}}(\bz;\eta)|$ is given as follows. A further asymptotic result is given by Corollary \[AsymMomentQ\] below. \[ExampleMomentLimit\] Let $\gamma \in {\mathbb{R}}$ and let $\eta$ be a complex number such that $|\eta| < 1$. Then we have $$\lim_{n \to \infty} \left\langle |\Psi^{{\mathrm{A}}}(\bz;\eta)|^{2\gamma} \right\rangle_n^{(q,t)} = \( \frac{(q |\eta|^2;t)_{\infty}}{(|\eta|^2;t)_{\infty}} \)^{\gamma^2}.$$ This result is obtained by applying Theorem \[Thm:SzegoMacdonald\] to $\phi(z)= |1+\eta z|^{2\gamma}$. Then the Fourier coefficients of $\log \phi$ are $c(k)=(-1)^{k-1} \eta^k \gamma/k$ and $c(-k)=(-1)^{k-1} \overline{\eta}^k \gamma/k$ for $k >0$, and $c(0)=0$. Circular ensembles and its $q$-analogue {#sectionCBEq} ======================================= Special case: $t=q^{\beta/2}$ ----------------------------- In this subsection, we examine the results of the last section for the special case $t=q^{\beta/2}$ with $\beta>0$, i.e., we consider the weight function $\Delta^{{\mathrm{Mac}}}(\bz;q,q^{\beta/2})$. Denote by $\langle \cdot \rangle_{n,\beta}^q$ the corresponding average. Define the $q$-gamma function (see e.g. [@AAR (10.3.3)]) by $$\Gamma_q(x)= (1-q)^{1-x} \frac{(q;q)_\infty}{(q^x;q)_{\infty}}.$$ \[ThmMomentGamma\] Let $\beta$ be a positive real number. For a positive integer $k$ and $\xi \in {\mathbb{T}}$, we have $$\begin{aligned} \left\langle \prod_{i=1}^k | \Psi(\bz;q^{i-1/2}\xi )|^2 \right\rangle_{n,\beta}^q =& \prod_{i=0}^{k-1} \frac{\Gamma_t(\frac{2}{\beta}(i+1)) \Gamma_t(n+\frac{2}{\beta}(k+i+1))} {\Gamma_t(\frac{2}{\beta}(k+i+1)) \Gamma_t(n+\frac{2}{\beta}(i+1))} \qquad \text{(with $t=q^{\beta/2}$)} \label{eqCBEmomentQ} \\ =& \prod_{j=0}^{n-1} \frac{\Gamma_q (\frac{\beta}{2}j +2k+1) \Gamma_q(\frac{\beta}{2} j+1)} {\Gamma_q(\frac{\beta}{2}j+k+1)^2}. \notag\end{aligned}$$ The claim follows immediately from Corollary \[CorMomentValue\] and the functional equation $\Gamma_q(1+x) = \frac{1-q^x}{1-q} \Gamma_q(x)$. Consider now the asymptotic behavior of this average in the limit as $n \to \infty$. Put $[n]_q = (1-q^n)/(1-q)$. \[AsymMomentQ\] For a positive integer $k$ and $\xi \in {\mathbb{T}}$, it holds that $$\label{eqCBEmomentLimit} \lim_{n \to \infty} ([n]_t)^{-2k^2/\beta} \left\langle \prod_{i=1}^k | \Psi(\bz;q^{i-1/2}\xi )|^2 \right\rangle_{n,\beta}^q = \prod_{i=0}^{k-1} \frac{\Gamma_t(\frac{2}{\beta}(i+1))} {\Gamma_t(\frac{2}{\beta}(k+i+1))} \qquad \text{with $t=q^{\beta/2}$}.$$ Verify that $$\label{eq:GammaQasym} \lim_{n \to \infty} \frac{\Gamma_t(n+a)}{\Gamma_t(n) ([n]_t)^a} =1$$ for any constant $a$. Then the claim is clear from expression . \[ExFq\] Denote by ${\mathcal{F}}_\beta^q(k)$ the right-hand side of equation . Then we obtain $$\begin{aligned} {\mathcal{F}}_{1}^q(k) =& \prod_{j=0}^{k-1} \frac{[2j+1]_{q^{\frac{1}{2}}} !}{[2k+2j+1]_{q^{\frac{1}{2}}}!}, \label{eqf1q} \\ {\mathcal{F}}_{2}^q(k) =& \prod_{j=0}^{k-1} \frac{[j]_{q} !}{[j+k]_q!}, \label{eqf2q} \\ {\mathcal{F}}_{4}^q(2k) =& \frac{([2]_q)^{2k^2}}{[2k-1]_q !!} \prod_{j=1}^{2k-1} \frac{[j]_q!}{[2j]_q!}. \label{eqf4q}\end{aligned}$$ Here $[n]_q!=[n]_q [n-1]_q \cdots [1]_q$ and $[2k-1]_q!! = [2k-1]_q [2k-3]_q \cdots [3]_q [1]_q$. Equalities and are trivial because $\Gamma_q(n+1)=[n]_q!$. We check relation . By definition, we have $${\mathcal{F}}_4^q(2k)= \prod_{i=0}^{2k-1} \frac{\Gamma_{q^2}(\frac{1}{2}(i+1))} {\Gamma_{q^2}(k+\frac{1}{2}(i+1))} = \prod_{p=0}^{k-1} \frac{\Gamma_{q^2} (p+\frac{1}{2}) \Gamma_{q^2}(p+1)} {\Gamma_{q^2} (k+p+\frac{1}{2}) \Gamma_{q^2}(k+p+1)}.$$ Using the $q$-analogue of the Legendre duplication formula (see e.g. [@AAR Theorem 10.3.5(a)]) $$\Gamma_q(2x) \Gamma_{q^2}(1/2) = (1+q)^{2x-1} \Gamma_{q^2}(x) \Gamma_{q^2}(x+1/2),$$ we have $${\mathcal{F}}_4^q(2k)= \prod_{p=0}^{k-1} \frac{(1+q)^{2k} \Gamma_q(2p+1)}{\Gamma_q(2k+2p+1)}= ([2]_q)^{2k^2} \prod_{p=0}^{k-1} \frac{[2p]_q! }{[2k+2p]_q !}.$$ Expression can then be proven by induction on $n$. Circular $\beta$-ensembles and Jack polynomials {#subsectionCBEJack} ----------------------------------------------- We take the limit as $q \to 1$ of the results of the previous subsection. Recall the formula $$\lim_{q \to 1} \frac{(q^a x;q)_{\infty}}{(x;q)_{\infty}} =(1-x)^{-a}$$ for $|x|<1$ and $a \in {\mathbb{R}}$, see [@AAR Theorem 10.2.4] for example. Then we have $$\lim_{q \to 1} \Delta^{{\mathrm{Mac}}}(\bz;q,q^{\beta/2}) = \prod_{1 \le i<j \le n} |z_i-z_j|^\beta =: \Delta^{{\mathrm{Jack}}}(\bz;2/\beta),$$ which is a constant times the p.d.f. for Dyson’s circular $\beta$-ensembles (see §6). Denote by $\langle \cdot \rangle_{n,\beta}$ the corresponding average, i.e., for a function $f$ on ${\mathbb{T}}^n$ define $$\langle f \rangle_{n,\beta} = \lim_{q \to 1} \langle f \rangle_{n,\beta}^q = \frac{\int_{{\mathbb{T}}^n} f(\bz) \prod_{1 \le i<j \le n} |z_i-z_j|^\beta \dd \bz} {\int_{{\mathbb{T}}^n} \prod_{1 \le i<j \le n} |z_i-z_j|^\beta \dd \bz}.$$ Let $\alpha >0$. The Jack polynomial $P^{{\mathrm{Jack}}}_\lambda(x_1,\dots,x_n;\alpha)$ for each partition $\lambda$ is defined by the limit approached by the corresponding Macdonald polynomial, $$P^{{\mathrm{Jack}}}_\lambda(x_1,\dots,x_n;\alpha) = \lim_{q \to 1} P^{{\mathrm{Mac}}}_\lambda(x_1,\dots,x_n;q,q^{1/\alpha}),$$ see [@Mac Chapter VI-10] for detail. Jack polynomials are orthogonal polynomials with respect to the weight function $\Delta^{{\mathrm{Jack}}}(\bz;\alpha)$. In particular, $s_{\lambda}(x_1,\dots,x_n)=P^{{\mathrm{Jack}}}_\lambda(x_1,\dots,x_n;1)$ are called Schur polynomials, and are irreducible characters of $U(n)$ associated with $\lambda$. From the theorems in the last section, we have the following: from Theorem \[ThmAverageMac\], we see that $$\label{AverageProductA} \left\langle \prod_{l=1}^L \Psi^{{\mathrm{A}}}(\bz^{-1};\eta_l^{-1}) \cdot \prod_{k=1}^K \Psi^{{\mathrm{A}}}(\bz;\eta_{L+k}) \right\rangle_{n,\beta} = (\eta_1 \cdots \eta_L)^{-n} \cdot P_{(n^L)}^{{\mathrm{Jack}}} (\eta_1, \dots, \eta_{L+K};\beta/2).$$ For a positive real number $\gamma$ and complex number $\eta$ with $|\eta|<1$, we have from Proposition \[PropMomentHypergeometric\] that $$\label{MomentHypergeometricJack} \left\langle |\Psi(\bz;\eta)|^{2\gamma} \right\rangle_{n, {\mathrm{C}\beta\mathrm{E}_{}}} = {_2 F_1}^{(2/\beta)}(-\gamma, -\gamma; \frac{\beta}{2}(n-1)+1; |\eta|^2, \dots, |\eta|^2),$$ where ${_2 F_1}^{(\alpha)}(a,b; c; x_1,\dots,x_n)$ is the hypergeometric function associated with Jack polynomials [@Kaneko1] defined by $${_2 F_1}^{(\alpha)}(a,b; c; x_1,\dots,x_n)= \sum_{\lambda} \frac{[a]^{(\alpha)}_\lambda [b]^{(\alpha)}_\lambda}{[c]^{(\alpha)}_\lambda} \frac{\alpha^{|\lambda|} P_\lambda^{{\mathrm{Jack}}}(x_1,\dots,x_n;\alpha)}{c'_\lambda(\alpha)}$$ with $$[u]_\lambda^{(\alpha)}=\prod_{s \in \lambda} (u-l'(s)/\alpha +a'(s)), \qquad \text{and} \qquad c'_\lambda(\alpha)= \prod_{s \in \lambda}(\alpha(a(s)+1)+l(s)).$$ For a positive integer $k$, and $\xi \in {\mathbb{T}}$, by Theorem \[ThmMomentGamma\] and Corollary \[AsymMomentQ\] it holds that $$\label{MomentAsymptoticA} \left\langle | \Psi^{{\mathrm{A}}}(\bz;\xi )|^{2k} \right\rangle_{n,\beta} = \prod_{i=0}^{k-1} \frac{\Gamma(\frac{2}{\beta}(i+1)) \Gamma(n+\frac{2}{\beta}(k+i+1))} {\Gamma(\frac{2}{\beta}(k+i+1)) \Gamma(n+\frac{2}{\beta}(i+1))} \sim \prod_{i=0}^{k-1} \frac{\Gamma(\frac{2}{\beta}(i+1)) } {\Gamma(\frac{2}{\beta}(k+i+1))} \cdot n^{2k^2/\beta}$$ in the limit as $n \to \infty$. For a function $\phi(z)=\exp(\sum_{k \in {\mathbb{Z}}} c(k) z^k)$ on ${\mathbb{T}}$ satisfying inequalities , by Theorem \[Thm:SzegoMacdonald\] it holds that $$\label{eq:SzegoJack} \lim_{n \to \infty} e^{-n c(0)} \left\langle \prod_{j=1}^n \phi(z_j) \right\rangle_{n, \beta} = \exp \( \frac{2}{\beta}\sum_{k=1}^\infty kc(k)c(-k) \).$$ In particular, for $\gamma \in {\mathbb{R}}$ and a complex number $\eta$ such that $|\eta|< 1$, we have $$\lim_{n \to \infty} \left\langle |\Psi^{{\mathrm{A}}}(\bz;\eta)|^{2\gamma} \right\rangle_{n,\beta} = (1-|\eta|^2)^{-2 \gamma^2/\beta}.$$ Several observations may be made concerning the above identities: equation is obtained by verifying the limits $$\lim_{t \to 1} \frac{(q^a)_\lambda^{(q,t)}}{(1-t)^{|\lambda|}} =\alpha^{|\lambda|} [a]_\lambda^{(\alpha)}, \qquad \lim_{t \to 1} \frac{c'_\lambda(q,t)}{(1-t)^{|\lambda|}} =c'_\lambda(\alpha),$$ with $q=t^\alpha$. The expression for the moment is obtained in [@FK] using a different proof, which employs a Selberg type integral evaluation. Equation is also obtained in [@KS_zetafunctions] essentially by the Selberg integral evaluation. When $\beta=2$, equation presents the strong Szegö limit theorem for a Toeplitz determinant. Indeed, the average of the left-hand side of is then equal to the Toeplitz determinant $\det(d_{i-j})_{1 \le i,j \le n}$ of $\phi$, where $d_i$ are Fourier coefficients of $\phi$. Equation with general $\beta>0$ is seen in [@Johansson1; @Johansson2], but it may be noted that the present proof, employing symmetric function theory, is straightforward. This expression is applied in [@Hyper] in order to observe an asymptotic behavior for Toeplitz ‘hyperdeterminants’. Jacobi polynomials due to Heckman and Opdam =========================================== The results obtained in §\[sectionMacAverage\] and §\[sectionCBEq\] will be applied to random matrix polynomials from symmetric spaces of the type A root system in the next section. In order to evaluate the corresponding polynomials of the BC type root system, we here recall Heckman and Opdam’s Jacobi polynomials and give some identities corresponding to and . The dominance ordering associated with the root system of type BC is defined as follows: for two partitions $\lambda=(\lambda_1,\lambda_2,\dots)$ and $\mu=(\mu_1,\mu_2,\dots)$, $$\mu \le \lambda \qquad \Leftrightarrow \qquad \mu_1 + \cdots+\mu_i \le \lambda_1+ \cdots +\lambda_i \quad \text{for all $i \ge 1$}.$$ Let ${\mathbb{C}}[\bx^{\pm 1}] = {\mathbb{C}}[x_1^{\pm 1}, \dots, x_n^{\pm 1}]$ be the ring of all Laurent polynomials in $n$ variables $\bx=(x_1,\dots,x_n)$. The Weyl group $W={\mathbb{Z}}_2 \wr {\mathfrak{S}}_n = {\mathbb{Z}}_2^n \rtimes {\mathfrak{S}}_n$ of type $BC_n$ acts naturally on ${\mathbb{Z}}^n$ and ${\mathbb{C}}[\bx^{\pm 1}]$, respectively. Denote by ${\mathbb{C}}[\bx^{\pm 1}]^W$ the subring of all $W$-invariants in ${\mathbb{C}}[\bx^{\pm 1}]$. Let $\Delta^{{\mathrm{HO}}}(\bz;k_1,k_2,k_3)$ be a function on ${\mathbb{T}}^n$ defined by $$\Delta^{{\mathrm{HO}}}(\bz;k_1,k_2,k_3) = \prod_{1 \le i < j \le n} |1-z_i z_j^{-1}|^{2 k_3} |1-z_i z_j|^{2 k_3} \cdot \prod_{1 \le j \le n} |1-z_j|^{2k_1} |1-z_j^2|^{2k_2}.$$ Here we assume $k_1$, $k_2$, and $k_3$ are real numbers such that $$k_1+k_2>-1/2, \quad k_2 > -1/2, \quad k_3 \ge 0.$$ Define an inner product on ${\mathbb{C}}[\bx^{\pm 1}]^W$ by $$\langle f,g \rangle_{\Delta^{{\mathrm{HO}}}} = \frac{1}{2^n n!} \int_{{\mathbb{T}}^n} f(\bz) g(\bz^{-1}) \Delta^{{\mathrm{HO}}}(\bz;k_1,k_2,k_3) \dd \bz.$$ For each partition $\mu$, we let $$m^{{\mathrm{BC}}}_{\mu}(\bx)=\sum_{\nu \in W \mu} x_1^{\nu_1} \cdots x_n^{\nu_n},$$ where $W\mu$ is the $W$-orbit of $\mu$ (cf. ). These polynomials form a ${\mathbb{C}}$-basis of ${\mathbb{C}}[\bx^{\pm 1}]^W$. Then, there exists a unique family of polynomials $P^{{\mathrm{HO}}}_{\lambda}= P^{{\mathrm{HO}}}_{\lambda}(\bx;k_1,k_2,k_3) \in {\mathbb{C}}[\bx^{\pm 1}]^W$ ($\lambda$ are partitions such that $\ell(\lambda) \le n$) satisfying two conditions: $$P^{{\mathrm{HO}}}_{\lambda}(\bx)= m_{\lambda}^{{\mathrm{BC}}}(\bx)+ \sum_{\mu: \mu < \lambda} u_{\lambda \mu} m^{{\mathrm{BC}}}_{\mu}(\bx), \quad \text{with $u_{\lambda \mu} \in {\mathbb{C}}$}, \qquad\qquad \langle P^{{\mathrm{HO}}}_{\lambda}, P_{\mu}^{{\mathrm{HO}}} \rangle_{\Delta^{{\mathrm{HO}}}} = 0 \quad \text{if $\lambda \not= \mu$}.$$ The Laurent polynomials $P_{\lambda}$ are known as Jacobi polynomials associated with the root system of type $BC_n$ due to Heckman and Opdam, see e.g. [@Diejen; @Heckman; @Mimachi]. They can be seen as BC-analogues of Jack polynomials. For a function $f$ on ${\mathbb{T}}^n$, we denote by $\langle f \rangle_{n}^{k_1,k_2,k_3}$ the mean value of $f$ with respect to the weight function $\Delta^{{\mathrm{HO}}}(\bz;k_1,k_2,k_3)$: $$\langle f \rangle_{n}^{k_1,k_2,k_3} = \frac{\int_{{\mathbb{T}}^n} f(\bz) \Delta^{{\mathrm{HO}}}(\bz;k_1,k_2,k_3)\dd \bz}{ \int_{{\mathbb{T}}^n} \Delta^{{\mathrm{HO}}}(\bz;k_1,k_2,k_3)\dd \bz}.$$ From the three parameters $k_1,k_2,k_3$, we define new parameters $$\tilde{k}_1 = k_1/k_3, \qquad \tilde{k}_2=(k_2+1)/k_3-1, \qquad \tilde{k}_3=1/k_3.$$ Put $$\Psi^{{\mathrm{BC}}}(\bz;x)= \prod_{j=1}^n(1+x z_j)(1+x z_j^{-1}).$$ \[Thm:MainTheorem\] The following relation holds $$\label{eq:MainEq} \left\langle \Psi^{{\mathrm{BC}}}(\bz;x_1)\Psi^{{\mathrm{BC}}}(\bz;x_2) \cdots \Psi^{{\mathrm{BC}}}(\bz;x_m) \right\rangle_{n}^{k_1,k_2,k_3} = (x_1 \cdots x_m)^n P^{{\mathrm{HO}}}_{(n^m)}(x_1,\dots,x_m;\tilde{k}_1,\tilde{k}_2,\tilde{k}_3).$$ In order to prove this, we need the following dual Cauchy identity obtained by Mimachi [@Mimachi]. \[Thm:Mimachi\] Let $\bx=(x_1,\dots, x_n)$ and $\by=(y_1,\dots, y_m)$ be sequences of indeterminates. Jacobi polynomials $P^{{\mathrm{HO}}}_{\lambda}$ satisfy the equality $$\prod_{i=1}^n \prod_{j=1}^m (x_i+x_i^{-1} - y_j - y_j^{-1}) = \sum_{\lambda \subset (m^n)} (-1)^{|\tilde{\lambda}|} P^{{\mathrm{HO}}}_{\lambda}(\bx;k_1,k_2,k_3) P^{{\mathrm{HO}}}_{\tilde{\lambda}}(\by;\tilde{k}_1,\tilde{k}_2,\tilde{k}_3),$$ where $\tilde{\lambda}=(n-\lambda_m', n-\lambda_{m-1}', \dots, n-\lambda_1')$. We see that $$\Psi^{{\mathrm{BC}}}(\bz;x_1) \Psi^{{\mathrm{BC}}}(\bz;x_2) \cdots \Psi^{{\mathrm{BC}}}(\bz;x_m) = (x_1 \cdots x_m)^n \prod_{i=1}^m \prod_{j=1}^n (x_i + x_i^{-1} + z_j + z_j^{-1}).$$ Using Proposition \[Thm:Mimachi\] we have $$\begin{aligned} & \left\langle \Psi^{{\mathrm{BC}}}(\bz;x_1)\Psi^{{\mathrm{BC}}}(\bz;x_2) \cdots \Psi^{{\mathrm{BC}}}(\bz;x_m) \right\rangle_{n}^{k_1,k_2,k_3} \\ = & (x_1 \cdots x_m)^n \sum_{\lambda \subset (m^n)} P^{{\mathrm{HO}}}_{\tilde{\lambda}}(x_1,\dots, x_m;\tilde{k}_1,\tilde{k}_2,\tilde{k}_3) \langle P^{{\mathrm{HO}}}_{\lambda}(\bz;k_1,k_2,k_3) \rangle_{n}^{k_1,k_2,k_3}.\end{aligned}$$ By the orthogonality relation for Jacobi polynomials, we have $$\langle P^{{\mathrm{HO}}}_{\lambda}(\bz;k_1,k_2,k_3) \rangle_{n}^{k_1,k_2,k_3} = \begin{cases} 1, & \text{if $\lambda = (0)$}, \\ 0, & \text{otherwise}, \end{cases}$$ and we thus obtain the theorem. Using Theorem 2.1 in [@Mimachi], we derive a more general form of equation including a Macdonald-Koornwinder polynomial. \[Thm:Main2\] Let $${\mathcal{F}}(m;k_1,k_2,k_3)= \prod_{j=0}^{m-1} \frac{\sqrt{\pi}}{2^{k_1 +2 k_2+j k_3-1} \Gamma(k_1+k_2+\frac{1}{2}+j k_3)}.$$ The $m$-th moment of $\Psi^{{\mathrm{BC}}}(\bz;1)$ is given by $$\left\langle \Psi^{{\mathrm{BC}}}(\bz;1)^m \right\rangle_{n}^{k_1,k_2,k_3} = {\mathcal{F}}(m;\tilde{k}_1,\tilde{k}_2,\tilde{k}_3) \cdot \prod_{j=0}^{m-1} \frac{\Gamma(n+ \tilde{k}_1+2\tilde{k}_2+j \tilde{k}_3 ) \Gamma(n+ \tilde{k}_1+\tilde{k}_2+\frac{1}{2}+j \tilde{k}_3 )} {\Gamma(n+ \frac{\tilde{k}_1}{2}+\tilde{k}_2+\frac{j \tilde{k}_3}{2} ) \Gamma(n+ \frac{\tilde{k}_1}{2}+\tilde{k}_2+\frac{1+j \tilde{k}_3}{2} )}.$$ By Theorem \[Thm:MainTheorem\] we have $$\label{eq:MTspecial} \left\langle \Psi^{{\mathrm{BC}}}(\bz;1)^m \right\rangle_{n}^{k_1,k_2,k_3} = P^{{\mathrm{HO}}}_{(n^m)}(1^m;\tilde{k}_1,\tilde{k}_2,\tilde{k}_3).$$ The special case $P_{\lambda}^{{\mathrm{HO}}}(1,1,\dots,1;k_1,k_2,k_3)$ is known and is given as follows (see e.g. [@Diejen] [^2]): for a partition $\lambda$ of length $\le m$, $$\begin{aligned} P^{{\mathrm{HO}}}_{\lambda}(\underbrace{1, \dots, 1}_m;k_1,k_2,k_3) =& 2^{2|\lambda|} \prod_{1 \le i <j \le m} \frac{(\rho_i+ \rho_j+k_3)_{\lambda_i+\lambda_j} (\rho_i- \rho_j+k_3)_{\lambda_i-\lambda_j}} {(\rho_i+ \rho_j)_{\lambda_i+\lambda_j} (\rho_i- \rho_j)_{\lambda_i-\lambda_j}} \\ & \quad \times \prod_{j=1}^m \frac{(\frac{k_1}{2} +k_2 + \rho_j)_{\lambda_j} (\frac{k_1+1}{2} + \rho_j)_{\lambda_j}} {(2 \rho_j)_{2 \lambda_j}} \end{aligned}$$ with $\rho_j= (m-j)k_3 + \frac{k_1}{2}+k_2$. Here $(a)_n = \Gamma(a+n) / \Gamma(a)$ is the Pochhammer symbol. Substituting $(n^m)$ for $\lambda$, we have $$\begin{aligned} & P^{{\mathrm{HO}}}_{(n^m)} (1^m; k_1,k_2,k_3) \notag \\ =& \prod_{1 \le i <j \le m} \frac{(k_1+2 k_2+(2m-i-j+1)k_3)_{2n}} {(k_1+2 k_2+(2m-i-j)k_3)_{2n}} \cdot \prod_{j=0}^{m-1} \frac{2^{2n} (k_1+2 k_2+j k_3)_n (k_1+k_2+\frac{1}{2}+j k_3)_n} {(k_1 +2 k_2+2 j k_3)_{2n}}. \label{eq:moment_product1}\end{aligned}$$ A simple algebraic manipulation of the first product on the right-hand side of yields $$\prod_{1 \le i <j \le m} \frac{(k_1+2 k_2+(2m-i-j+1)k_3)_{2n}} {(k_1+2 k_2+(2m-i-j)k_3)_{2n}} = \prod_{j=0}^{m-1} \frac{(k_1+2k_2+ 2jk_3)_{2n}}{(k_1+2k_2+j k_3)_{2n}}$$ and therefore we obtain $$P_{(n^m)}^{{\mathrm{HO}}} (1^m; k_1,k_2,k_3) = \prod_{j=0}^{m-1} \frac{2^{2n} (k_1+k_2+\frac{1}{2}+j k_3)_n}{(n+k_1+2k_2+jk_3)_{n}}.$$ Combining the above result with equation , we have $$\label{eq:Main2} \left\langle \Psi^{{\mathrm{BC}}}(\bz;1)^m \right\rangle_{n}^{k_1,k_2,k_3} = \prod_{j=0}^{m-1} \frac{2^{2n} \Gamma(n+ \tilde{k}_1+2\tilde{k}_2+j \tilde{k}_3 ) \Gamma(n+ \tilde{k}_1+\tilde{k}_2+\frac{1}{2}+j \tilde{k}_3 )} {\Gamma( \tilde{k}_1+\tilde{k}_2+\frac{1}{2} +j \tilde{k}_3) \Gamma(2n+ \tilde{k}_1+2\tilde{k}_2+j \tilde{k}_3 )}.$$ Finally, we apply the formula $$\Gamma(2a) = \frac{2^{2a-1}}{\sqrt{\pi}} \Gamma(a) \Gamma(a+\frac{1}{2})$$ to $\Gamma(2n+\tilde{k}_1+2\tilde{k}_2+j \tilde{k}_3)$ in equation and we then have the theorem. \[cor:Main\] It holds that $$\left\langle \Psi^{{\mathrm{BC}}}(\bz;1)^m \right\rangle_{n}^{k_1,k_2,k_3} \sim {\mathcal{F}}(m;\tilde{k}_1,\tilde{k}_2,\tilde{k}_3) \cdot n^{m(\tilde{k}_1+\tilde{k}_2)+\frac{1}{2}m(m-1)\tilde{k}_3},$$ as $n \to \infty$. The claim follows from the previous theorem and the asymptotics of the gamma function (cf ): $\Gamma(n+a) \sim \Gamma(n) n^a$ for a constant $a$. Random matrix ensembles associated with compact symmetric spaces ================================================================ Finally, we apply the theorems obtained above to compact symmetric spaces as classified by Cartan. These symmetric spaces are labeled A I, BD I, C II, and so on, see e.g. Table 1 in [@CM]. Let $G/K$ be such a compact symmetric space. Here $G$ is a compact subgroup of $GL(N,{\mathbb{C}})$ for some positive integer $N$, and $K$ is a closed subgroup of $G$. Then the space $G/K$ is realized as the subset $S$ of $G$: $S \simeq G/K$ and the probability measure $\dd M$ on $S$ is induced from the quotient space $G/K$. We consider $S$ as a probability space with the measure $\dd M$ and call the random matrix ensemble associated with $G/K$. See [@Duenez] for details. The random matrix ensembles considered in §\[subsectionA\], §\[subsectionAI\], and §\[subsectionAII\] are called Dyson’s circular $\beta$-ensembles, see [@Dyson; @Mehta]. The identities in these subsections follow immediately from expressions and (see also Example \[ExFq\]) . Similarly, identities after §\[subsectionB\] follows from Theorem \[Thm:MainTheorem\], Theorem \[Thm:Main2\], and Corollary \[cor:Main\]. Note that the results in §\[subsectionA\], §\[subsectionB\], §\[subsectionC\], and §\[subsectionD\] are results for compact Lie groups (which are not proper symmetric spaces) previously presented in [@BG]. $U(n)$ – type A {#subsectionA} --------------- Consider the unitary group $U(n)$ with the normalized Haar measure. This space has a simple root system of type A. The corresponding p.d.f. for eigenvalues $z_1,\dots,z_n$ of $M \in U(n)$ is proportional to $\Delta^{{\mathrm{Jack}}}(\bz;1)$. This random matrix ensemble is called the circular unitary ensemble (CUE). For complex numbers $\eta_1,\dots,\eta_L, \eta_{L+1},\dots, \eta_{L+K}$, it follows from equation that $$\begin{aligned} & \left\langle \prod_{i=1}^L \det(I+\eta_i^{-1} M^{-1}) \cdot \prod_{i=1}^K \det(I+\eta_{L+i} M) \right\rangle_{U(n)} \\ =& \left\langle \prod_{i=1}^L \Psi^{{\mathrm{A}}}(\bz^{-1};\eta_i^{-1}) \cdot \prod_{i=1}^K \Psi^{{\mathrm{A}}}(\bz;\eta_{L+i}) \right\rangle_{n,2} = \prod_{i=1}^L \eta_i^{-n} \cdot s_{(n^L)} (\eta_1,\dots,\eta_{L+K}).\end{aligned}$$ In addition, from equation we obtain $$\left\langle |\det(I+ \xi M)|^{2m} \right\rangle_{U(n)} = \prod_{j=0}^{m-1}\frac{j! (n+j+m)!}{(j+m)! (n+j)!} \sim \prod_{j=0}^{m-1}\frac{j!}{(j+m)!} \cdot n^{m^2}$$ for any $\xi \in {\mathbb{T}}$. $U(n)/O(n)$ – type A I {#subsectionAI} ---------------------- Consider the ensemble $S(n)$ associated with the symmetric space $U(n)/O(n)$. The space $S(n)$ is the set of all symmetric matrices in $U(n)$. The corresponding p.d.f. for eigenvalues $z_1,\dots,z_n$ is proportional to $\Delta^{{\mathrm{Jack}}}(\bz;2) = \prod_{1 \le i<j \le n} |z_i-z_j|$. This random matrix ensemble is called the circular orthogonal ensemble (COE). We have $$\begin{aligned} &\left\langle \prod_{i=1}^L \det(I+\eta_i^{-1} M^{-1}) \cdot \prod_{i=1}^K \det(I+\eta_{L+i} M) \right\rangle_{S(n)} \\ =& \left\langle \prod_{i=1}^L \Psi^{{\mathrm{A}}}(\bz^{-1};\eta_i^{-1}) \cdot \prod_{i=1}^K \Psi^{{\mathrm{A}}}(\bz;\eta_{L+i}) \right\rangle_{n,1} = \prod_{i=1}^L \eta_i^{-n} \cdot P_{(n^L)}^{{\mathrm{Jack}}} (\eta_1,\dots,\eta_{L+K};1/2).\end{aligned}$$ For $\xi \in {\mathbb{T}}$, we obtain $$\left\langle |\det(I+ \xi M)|^{2m} \right\rangle_{S(n)} = \prod_{j=0}^{m-1} \frac{(2j+1)! (n+2m+2j+1)!}{(2m+2j+1)! (n+2j+1)!} \sim \prod_{j=0}^{m-1}\frac{(2j+1)!}{(2m+2j+1)!} \cdot n^{2m^2}.$$ $U(2n)/Sp(2n)$ – type A II {#subsectionAII} -------------------------- Consider the ensemble $S(n)$ associated with the symmetric space $U(2n)/Sp(2n)$. The space $S(n)$ is the set of all self-dual matrices in $U(2n)$, i.e., $M \in S(n)$ is a unitary matrix satisfying $M=J \trans{M} \trans{J}$ with $J=\(\begin{smallmatrix} 0 & I_n \\ -I_n & 0 \end{smallmatrix} \)$. This random matrix ensemble is called the circular symplectic ensemble (CSE). The eigenvalues of $M \in S(n)$ are of the form $z_1,z_1,z_2,z_2,\dots,z_n,z_n$ and so the characteristic polynomial is given as $\det(I+xM)= \prod_{j=1}^n (1+x z_j)^2$. The corresponding p.d.f. for $z_1,\dots,z_n$ is proportional to $\Delta^{{\mathrm{Jack}}}(\bz;1/2)=\prod_{1 \le i<j \le n} |z_i-z_j|^4$. We have $$\begin{aligned} &\left\langle \prod_{i=1}^L \det(I+\eta_i^{-1} M^{-1})^{1/2} \cdot \prod_{i=1}^K \det(I+\eta_{L+i} M)^{1/2} \right\rangle_{S(n)} \\ =& \left\langle \prod_{i=1}^L \Psi^{{\mathrm{A}}}(\bz^{-1};\eta_i^{-1}) \cdot \prod_{i=1}^K \Psi^{{\mathrm{A}}}(\bz;\eta_{L+i}) \right\rangle_{n,4} = \prod_{i=1}^L x_i^{-n} \cdot P_{(n^L)}^{{\mathrm{Jack}}} (\eta_1,\dots,\eta_{L+K};2).\end{aligned}$$ For $\xi \in {\mathbb{T}}$, we obtain $$\left\langle |\det(I+ \xi M)|^{2m} \right\rangle_{S(n)} = \prod_{j=0}^{2m-1} \frac{\Gamma(\frac{j+1}{2}) \Gamma(n+m+\frac{j+1}{2})} {\Gamma(m+\frac{j+1}{2}) \Gamma(n+\frac{j+1}{2})} \sim \frac{2^m}{(2m-1)!! \ \prod_{j=1}^{2m-1}(2j-1)!!} \cdot n^{2m^2}.$$ $SO(2n+1)$ – type B {#subsectionB} ------------------- Consider the special orthogonal group $SO(2n+1)$. An element $M$ in $SO(2n+1)$ is an orthogonal matrix in $SL(2n+1,{\mathbb{R}})$, with eigenvalues given by $z_1,z_1^{-1},\cdots, z_n,z_n^{-1},1$. From Weyl’s integral formula, the corresponding p.d.f. of $z_1,z_2,\dots,z_n$ is proportional to $\Delta^{{\mathrm{HO}}}(\bz;1,0,1)$, and therefore it follows from Theorem \[Thm:MainTheorem\] that $$\left\langle \prod_{i=1}^m \det(I+x_i M) \right\rangle_{SO(2n+1)} = \prod_{i=1}^m (1+x_i) \cdot \left\langle \prod_{i=1}^m \Psi^{{\mathrm{BC}}}(\bz;x_i) \right\rangle_{n}^{1,0,1} = \prod_{i=1}^m x_i^n (1+x_i) \cdot P_{(n^m)}^{{\mathrm{HO}}}(x_1,\dots,x_m;1,0,1).$$ Here $P_\lambda^{{\mathrm{HO}}}(x_1,\dots,x_m;1,0,1)$ is just the irreducible character of $SO(2m+1)$ associated with the partition $\lambda$. Theorem \[Thm:Main2\], Corollary \[cor:Main\], and a simple calculation lead to $$\left\langle \det(I+ M)^m \right\rangle_{SO(2n+1)} = 2^{m} \prod_{j=0}^{m-1} \frac{ \Gamma(2n+ 2j+2 ) } {2^{j} (2j+1)!! \ \Gamma(2n+ j+1)} \sim \frac{2^{2m}}{\prod_{j=1}^{m} (2j-1)!!} n^{m^2/2+m/2}$$ in the limit as $n \to \infty$. $Sp(2n)$ – type C {#subsectionC} ----------------- Consider the symplectic group $Sp(2n)$, i.e., a matrix $M \in Sp(2n)$ belongs to $U(2n)$ and satisfies $M J \trans{M}=J$, where $J=\(\begin{smallmatrix} O_n & I_n \\ -I_n & O_n \end{smallmatrix} \)$. The eigenvalues are given by $z_1,z_1^{-1},\cdots, z_n,z_n^{-1}$. The corresponding p.d.f. of $z_1,z_2,\dots,z_n$ is proportional to $\Delta^{{\mathrm{HO}}}(\bz;0,1,1)$ and therefore we have $$\left\langle \prod_{i=1}^m \det(I+x_i M) \right\rangle_{Sp(2n)} = \left\langle \prod_{i=1}^m \Psi^{{\mathrm{BC}}}(\bz;x_i) \right\rangle_{n}^{0,1,1} = \prod_{i=1}^m x_i^n \cdot P_{(n^m)}^{{\mathrm{HO}}}(x_1,\dots,x_m;0,1,1).$$ Here $P_\lambda^{{\mathrm{HO}}}(x_1,\dots,x_m;0,1,1)$ is just the irreducible character of $Sp(2m)$ associated with the partition $\lambda$. We obtain $$\left\langle \det(I+ M)^m \right\rangle_{Sp(2n)} = \prod_{j=0}^{m-1} \frac{\Gamma(2n+2j+3) }{2^{j+1} \cdot (2j+1)!! \ \Gamma(2n+j+2)} \sim \frac{1}{ \prod_{j=1}^{m} (2j-1)!!} \cdot n^{m^2/2+m/2}.$$ $SO(2n)$ – type D {#subsectionD} ----------------- Consider the special orthogonal group $SO(2n)$. The eigenvalues of a matrix $M \in SO(2n)$ are of the form $z_1,z_1^{-1},\cdots, z_n,z_n^{-1}$. The corresponding p.d.f. of $z_1,z_2,\dots,z_n$ is proportional to $\Delta^{{\mathrm{HO}}}(\bz;0,0,1)$, and therefore we have $$\left\langle \prod_{i=1}^m \det(I+x_i M) \right\rangle_{SO(2n)} = \left\langle \prod_{i=1}^m \Psi^{{\mathrm{BC}}}(\bz;x_i) \right\rangle_{n}^{0,0,1} = \prod_{i=1}^m x_i^n \cdot P_{(n^m)}^{{\mathrm{HO}}}(x_1,\dots,x_m;0,0,1).$$ Here $P_\lambda^{{\mathrm{HO}}}(x_1,\dots,x_m;0,0,1)$ is just the irreducible character of $O(2m)$ (not $SO(2m)$) associated with the partition $\lambda$. We have $$\left\langle \det(I+ M)^m \right\rangle_{SO(2n)} = \prod_{j=0}^{m-1} \frac{\Gamma(2n+2j)}{2^{j-1} \, (2j-1)!! \ \Gamma(2n+j)} \sim \frac{2^m}{\prod_{j=1}^{m-1} (2j-1)!!} \cdot n^{m^2/2-m/2}.$$ $U(2n+r)/(U(n+r)\times U(n))$ – type A III ------------------------------------------ Let $r$ be a non-negative integer. Consider the random matrix ensemble $G(n,r)$ associated with $U(2n+r)/(U(n+r)\times U(n))$. The explicit expression of a matrix in $G(n,r)$ is omitted here, but may be found in [@Duenez]. The eigenvalues of a matrix $M \in G(n,r) \subset U(2n+r)$ are of the form $$\label{eq:Eigenvalues} z_1,z_1^{-1},\cdots, z_n,z_n^{-1},\underbrace{1,1,\dots, 1}_r.$$ The corresponding p.d.f. of $z_1,z_2,\dots,z_n$ is proportional to $\Delta^{{\mathrm{HO}}}(\bz;r,\frac{1}{2},1)$, and therefore we have $$\left\langle \prod_{i=1}^m \det(I+x_i M) \right\rangle_{G(n,r)} = \prod_{i=1}^m (1+x_i)^r \cdot \left\langle \prod_{i=1}^m \Psi^{{\mathrm{BC}}}(\bz;x_i) \right\rangle_{n}^{r,\frac{1}{2},1} = \prod_{i=1}^m (1+x_i)^r x_i^n \cdot P^{{\mathrm{HO}}}_{(n^m)}(x_1,\dots,x_m;r,\frac{1}{2},1).$$ We obtain $$\begin{aligned} & \left\langle \det(I+ M)^m \right\rangle_{G(n,r)} = 2^{mr} \left\langle \Psi^{{\mathrm{BC}}}(\bz;1) \right\rangle_{n}^{r,\frac{1}{2},1} \\ =& \frac{\pi^{m/2}}{\prod_{j=0}^{m-1} 2^{j} (r+j)! } \prod_{j=0}^{m-1} \frac{\Gamma(n+r+j+1)^2} {\Gamma(n+\frac{r+j+1}{2}) \Gamma(n+\frac{r+j}{2}+1)} \sim \frac{\pi^{m/2}}{2^{m(m-1)/2} \prod_{j=0}^{m-1} (r+j)! } \cdot n^{m^2/2 + rm}.\end{aligned}$$ $O(2n+r)/(O(n+r) \times O(n))$ – type BD I ------------------------------------------ Let $r$ be a non-negative integer. Consider the random matrix ensemble $G(n,r)$ associated with the compact symmetric space $O(2n+r)/(O(n+r) \times O(n))$. The eigenvalues of a matrix $M \in G(n,r) \subset O(2n+r)$ are of the form . The corresponding p.d.f. of $z_1,z_2,\dots,z_n$ is proportional to $\Delta^{{\mathrm{HO}}}(\bz;\frac{r}{2},0,\frac{1}{2})$, and therefore we have $$\left\langle \prod_{i=1}^m \det(I+x_i M) \right\rangle_{G(n,r)} = \prod_{i=1}^m (1+x_i)^r \cdot \left\langle \prod_{i=1}^m \Psi^{{\mathrm{BC}}}(\bz;x_i) \right\rangle_{n}^{\frac{r}{2},0,\frac{1}{2}} = \prod_{i=1}^m (1+x_i)^r x_i^n \cdot P_{(n^m)}^{{\mathrm{HO}}}(x_1,\dots,x_m;r,1,2).$$ We obtain $$\left\langle \det(I+ M)^m \right\rangle_{G(n,r)} = 2^{mr} \prod_{j=0}^{m-1} \frac{\Gamma(2n+4j+2r+3)}{2^{2j+r+1}(4j+2r+1)!! \ \Gamma(2n+2j+r+2)} \sim \frac{2^{mr}}{\prod_{j=0}^{m-1}(4j+2r+1)!!} \cdot n^{m^2+rm}.$$ $Sp(2n)/U(n)$ – type C I ------------------------ Consider the random matrix ensemble $S(n)$ associated with the compact symmetric space $Sp(2n) /(Sp(2n)\cap SO(2n)) \simeq Sp(2n)/U(n)$. The eigenvalues of a matrix $M \in S(n) \subset Sp(2n)$ are of the form $z_1,z_1^{-1},\cdots, z_n,z_n^{-1}$. The corresponding p.d.f. of $z_1,z_2,\dots,z_n$ is proportional to $\Delta^{{\mathrm{HO}}}(\bz;0,\frac{1}{2},\frac{1}{2})$, and therefore we have $$\left\langle \prod_{i=1}^m \det(I+x_i M) \right\rangle_{S(n)} = \left\langle \prod_{i=1}^m \Psi^{{\mathrm{BC}}}(\bz;x_i) \right\rangle_{n}^{0,\frac{1}{2},\frac{1}{2}} = \prod_{i=1}^m x_i^n \cdot P_{(n^m)}^{{\mathrm{HO}}}(x_1,\dots,x_m;0,2,2).$$ We obtain $$\left\langle \det(I+ M)^m \right\rangle_{S(n)} = \prod_{j=0}^{m-1} \frac{(n+2j+3) \Gamma(2n+4j+5)}{2^{2j+2}(4j+3)!! \ \Gamma(2n+2j+4)} \sim \frac{1}{2^m \prod_{j=1}^m (4j-1)!!} \cdot n^{m^2+m}.$$ $Sp(4n+2r)/(Sp(2n+2r) \times Sp(2n))$ – type C II ------------------------------------------------- Let $r$ be a non-negative integer. Consider the random matrix ensemble $G(n,r)$ associated with the compact symmetric space $Sp(4n+2r)/(Sp(2n+2r) \times Sp(2n))$. The eigenvalues of a matrix $M \in G(n,r) \subset Sp(4n+2r)$ are of the form $$z_1,z_1,z_1^{-1},z_1^{-1},\cdots, z_n,z_n, z_n^{-1},z_n^{-1}, \underbrace{1,\dots,1}_{2r}.$$ The corresponding p.d.f. of $z_1,z_2,\dots,z_n$ is proportional to $\Delta^{{\mathrm{HO}}}(\bz;2r,\frac{3}{2},2)$, and therefore we have $$\begin{aligned} \left\langle \prod_{i=1}^m \det(I+x_i M)^{1/2} \right\rangle_{G(n,r)} =&\prod_{i=1}^m (1+x_i)^r \left\langle \prod_{i=1}^m \Psi^{{\mathrm{BC}}}(\bz;x_i) \right\rangle_{n}^{2r,\frac{3}{2},2} \\ =& \prod_{i=1}^m (1+x_i)^rx_i^n \cdot P^{{\mathrm{HO}}}_{(n^m)}(x_1,\dots,x_m;r,\frac{1}{4},\frac{1}{2}).\end{aligned}$$ We obtain $$\begin{aligned} \left\langle \det(I+ M)^m \right\rangle_{G(n,r)} =& \frac{2^{4mr+m^2+m}}{\prod_{j=0}^{m-1} (4j+4r+1)!!} \cdot \frac{\prod_{p=1}^{4m} \Gamma(n+r+\frac{p+1}{4})}{\prod_{j=1}^{2m} \Gamma(n+\frac{r}{2}+\frac{j}{4}) \Gamma(n+\frac{r+1}{2}+\frac{j}{4})} \\ \sim & \frac{2^{4mr+m^2+m}}{\prod_{j=0}^{m-1} (4j+4r+1)!!} n^{m^2+2mr}.\end{aligned}$$ $SO(4n+2)/U(2n+1)$ – type D III-odd ----------------------------------- Consider the random matrix ensemble $S(n)$ associated with the compact symmetric space $SO(4n+2)/(SO(4n+2) \cap Sp(4n+2)) \simeq SO(4n+2)/U(2n+1)$. The eigenvalues of a matrix $M \in S(n) \subset SO(4n+2)$ are of the form $z_1,z_1,z_1^{-1},z_1^{-1},\cdots, z_n,z_n, z_n^{-1},z_n^{-1}, 1,1$. The corresponding p.d.f. of $z_1,z_2,\dots,z_n$ is proportional to $\Delta^{{\mathrm{HO}}}(\bz;2,\frac{1}{2},2)$ and therefore we have $$\begin{aligned} \left\langle \prod_{i=1}^m \det(I+x_i M)^{1/2} \right\rangle_{S(n)} =&\prod_{i=1}^m (1+x_i) \left\langle \prod_{i=1}^m \Psi^{{\mathrm{BC}}}(\bz;x_i) \right\rangle_{n}^{2,\frac{1}{2},2} \\ =& \prod_{i=1}^m (1+x_i) x_i^n \cdot P^{{\mathrm{HO}}}_{(n^m)}(x_1,\dots,x_m;1,-\frac{1}{4},\frac{1}{2}).\end{aligned}$$ We obtain $$\left\langle \det(I+ M)^m \right\rangle_{S(n)} = \frac{2^{m^2+5m}}{\prod_{j=1}^{m} (4j-1)!!} \cdot \prod_{j=1}^{2m} \frac{\Gamma(n+\frac{j}{2}+\frac{3}{4}) \Gamma(n+\frac{j}{2})} {\Gamma(n+\frac{j}{4}) \Gamma(n+\frac{j}{4} +\frac{1}{2})} \sim \frac{2^{m^2+5m}}{\prod_{j=1}^{m} (4j-1)!!} \cdot n^{m^2+m}.$$ $SO(4n)/U(2n)$ – type D III-even -------------------------------- Consider the random matrix ensembles $S(n)$ associated with the compact symmetric space $SO(4n)/(SO(4n) \cap Sp(4n)) \simeq SO(4n)/U(2n)$. The eigenvalues of the matrix $M \in S(n) \subset SO(4n)$ are of the form $$z_1,z_1,z_1^{-1},z_1^{-1},\cdots, z_n,z_n, z_n^{-1},z_n^{-1}.$$ The corresponding p.d.f. of $z_1,z_2,\dots,z_n$ is proportional to $\Delta^{{\mathrm{HO}}}(\bz;0,\frac{1}{2},2)$ and therefore we have $$\left\langle \prod_{i=1}^m \det(I+x_i M)^{1/2} \right\rangle_{S(n)} = \left\langle \prod_{i=1}^m \Psi^{{\mathrm{BC}}}(\bz;x_i) \right\rangle_{n}^{0,\frac{1}{2},2} = P_{(n^m)}^{{\mathrm{HO}}}(x_1,\dots,x_m;0,-\frac{1}{4},\frac{1}{2}).$$ Hence we obtain $$\left\langle \det(I+ M)^m \right\rangle_{S(n)} = \frac{2^{m^2+m}}{\prod_{j=1}^{m-1} (4j-1)!!} \cdot \prod_{j=0}^{2m-1} \frac{\Gamma(n+\frac{j}{2}+\frac{1}{4}) \Gamma(n+\frac{j-1}{2})} {\Gamma(n+\frac{j-1}{4}) \Gamma(n+\frac{j+1}{4})} \sim \frac{2^{m^2+m}}{\prod_{j=1}^{m-1} (4j-1)!!} \cdot n^{m^2-m}.$$ Final comments ============== We have calculated the average of products of the characteristic moments $\langle \prod_{j=1}^m \det(I+x_j M) \rangle$. We would also like to calculate the average of the quotient $$\left\langle \frac{\prod_{j=1}^m \det(I+x_j M)}{\prod_{i=1}^l \det(I+y_i M)} \right\rangle_n^{k_1,k_2,k_3}.$$ Expressions for these quotients have been obtained for the classical groups (i.e., $(k_1,k_2,k_3)=(1,0,1), (0,1,1), (0,0,1)$ in our notation) in [@BG], but the derivation of expressions for other cases remains an open problem. <span style="font-variant:small-caps;">Acknowledgements.</span> The author would like to thank Professor Masato Wakayama for bringing to the author’s attention the paper [@Mimachi]. [GaWa]{} G. E. Andrews, R. Askey, and R. Roy, “Special Functions”, Encyclopedia Math. Appl. 71, Cambridge Univ. Press, Cambridge, 1999. D. Bump and P. Diaconis, Toeplitz minors, J. Combin. Theory Ser. A [**97**]{} (2002), 252–271. D. Bump and A. Gamburd, On the averages of characteristic polynomials from classical groups, Comm. Math. Phys. [**265**]{} (2006), 227–274. M. Caselle and U. Magnea, Random matrix theory and symmetric spaces, Physics Reports [**394**]{} (2004), 41–156. J. F. van Diejen, Properties of some families of hypergeometric orthogonal polynomials in several variables, Trans. Amer. Math. Soc. [**351**]{} (1999), 233–270. E. Dueñez, Random matrix ensembles associated to compact symmetric spaces, Comm. Math. Phys. [**244**]{} (2004), 29–61. F. J. Dyson, Statistical theory of the energy levels of complex systems. I, J. Mathematical Phys. [**3**]{} (1962), 140–156. P. J. Forrester and J. P. Keating, Singularity dominated strong fluctuations for some random matrix averages, Comm. Math. Phys. [**250**]{} (2004), 119–131. G. Heckman and H. Schlichtkrull, “Harmonic Analysis and Special Functions on Symmetric spaces”, Perspect. Math. [**16**]{}, Academic Press, San Diego, 1994. K. Johansson, On Szegö’s asymptotic formula for Toeplitz determinants and generalizations, Bull. Sci. Math. (2) [**112**]{} (1988), 257–304. —–, On fluctuations of eigenvalues of random Hermitian matrices, Duke Math. J. [**91**]{} (1998), 151–204. J. Kaneko, Selberg integrals and hypergeometric functions associated with Jack polynomials, SIAM J. Math. Anal. [**24**]{} (1993), 1086–1110. —–, $q$-Selberg integrals and Macdonald polynomials, Ann. scient. Éc. Norm. Sup. $4^{\text{e}}$ série [**29**]{} (1996), 583–637. J. P. Keating and N. C. Snaith, Random matrix theory and $\zeta(1/2+it)$, Comm. Math. Phys. [**214**]{} (2000), 57–89. —–, Random matrix theory and $L$-functions at $s=1/2$, Comm. Math. Phys. [**214**]{} (2000), 91–110. I. G. Macdonald, “Symmetric Functions and Hall Polynomials”, 2nd ed., Oxford University Press, Oxford, 1995. S. Matsumoto, Hyperdeterminant expressions for Jack functions of rectangular shapes, arXiv:math/0603033. M. L. Mehta, “Random Matrices”, 3rd ed., Pure and Applied Mathematics (Amsterdam) 142, Elsevier/Academic Press, Amsterdam, 2004. K. Mimachi, A duality of Macdonald-Koornwinder polynomials and its application to integral representations, Duke Math. J. [**107**]{} (2001), 265–281. <span style="font-variant:small-caps;">Sho MATSUMOTO</span>\ Faculty of Mathematics, Kyushu University.\ Hakozaki Higashi-ku, Fukuoka, 812-8581 JAPAN.\ `[email protected]`\ [^1]: Research Fellow of the Japan Society for the Promotion of Science, partially supported by Grant-in-Aid for Scientific Research (C) No. 17006193. [^2]: The connection between ours notation and van Diejen’s [@Diejen] is given by $\nu_0 = k_1+k_2, \ \nu_1=k_2, \ \nu=k_3$.

Q: Rails 4 .where nested model search Hi, I have a Model of Users and a Model of Products. My Model Products belongs_to my Model User and a User has_many Products. My question is how can i search 1 or multiple products matching a user attribute? exemple: Product.where(price: 10) for user.where(id: 2) What is the solution for nested model search, i'm a bit lost. Many Thanks A: Since products belongs to user (and user has_many products), you can query off of the relation: user = User.find(2) products = user.products.where(price: 10)

Q: Python not finding file in the same directory I am writing a simple script that attaches file to a mail, but it is not finding the file. This is my one block: # KML attachment filename='20140210204804.kml' fp = open(filename, "rb") att = email.mime.application.MIMEApplication(fp.read(),_subtype="kml") fp.close() att.add_header('Content-Disposition','attachment',filename=filename) msg.attach(att) The file 20140210204804.kml is present in the same folder as the script. I am getting below error: IOError: [Errno 2] No such file or directory: '20140210204804.kml' Any help is appreciated. A: The working directory is not set to the directory of the script, but to the current directory where you started the script. Use __file__ to determine the file location and use that as a starting point to make filename an absolute path: import os here = os.path.dirname(os.path.abspath(__file__)) filename = os.path.join(here, '20140210204804.kml')

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Evaluating Current Scar Assessment Methods. Current scar surveys have included many questions to evaluate the physical characteristics of scars, with some expanding to include physical implications and patient opinions. This review provides an analysis of frequently used scar assessment methods to date and highlights potential areas for improvement. We build the case that a new assessment tool is necessary, specifically one that centers on psychosocial consequences of scars that influence patient decision making for treatment, allowing physicians to individualize treatment conversations with patients. We postulate that survey techniques used in consumer product marketing, such as choice-based conjoint analysis, may be effective in determining the factors strongly influencing patient decision making and spending in scar treatment; therefore, more research in this area is warranted. By incorporating these psychosocial and economic considerations driving scar treatment decisions, future scar assessment tools may accomplish much more than characterizing/documenting the clinical aspects of scars. Rather, these patient-centered, holistic tools may be implemented by plastic surgeons and other clinicians specifically to provide patients with personalized treatment options that maximize long-term patient satisfaction.

Bill Potter wasn’t eager to abandon his high-end house last month during evacuations forced by a massive Idaho wildfire, but he felt reassured when his insurance company sent a team to protect his home near the world-class ski resort of Sun Valley. “I was more than impressed,” he said of the water tanker truck and crew privately contracted by his insurer to patrol his road and keep watch over his family’s home, custom-crafted from parts of antique barns. Potter is a member of the AIG Private Client Group, which is geared toward wealthy policyholders and offers a personal wildfire-protection program for customers in select areas in the western United States. The program, still considered a novel service in a niche market, operates under the premise that it is cheaper to defend multimillion-dollar homes against fire than to replace them. Companies such as AIG, Chubb and Fireman’s Fund are competing to offer extra layers of protection to “gold-plate” properties owned by the well-heeled, said Jim Whittle, assistant general counsel with the American Insurance Association. Services range from clearing trees and brush from around a home before a fire can start to applying flame-retardant chemicals to the perimeter of a property in the midst of a blaze, according to industry literature. Jack Dies, head of Sun Valley Insurance and an AIG broker, said premiums for such policies average up to $7,000 a year but those costs are dwarfed by the value of properties at stake. Whittle could not quantify how widespread privately funded wildfire protection has become since first emerging less than a decade ago. But insurance plans offering such services have grown more popular as homes increasingly encroach on the “wildland-urban interface,” where the fringes of communities meet undeveloped, often rugged terrain. Between 2000 and 2010, 10 million U.S. homes were built in or bordering fire-prone wild lands, representing two-thirds of all houses built during that period, according to research conducted by the U.S. Forest Service and others. “It’s entirely likely it will be a continued pattern and approach,” Whittle said of private fire protection. The presence of private firefighters gained greater attention this summer as dozens of large blazes raging across the drought-parched West strained traditional government firefighting resources at the local, state and federal levels. Property losses are estimated to have run into the hundreds of millions of dollars. AFFLUENT MOUNTAIN COMMUNITIES Potter was one of thousands of residents forced in August to flee a wildfire in Idaho’s Sawtooth Mountains that threatened a scenic river valley whose homeowners included celebrities such as actor Tom Hanks. Land and properties in the area are collectively valued at up to $8 billion. Hundreds of federal firefighters fought the blaze, battling flames door to door with support from water-dropping helicopters and airplane tankers. By the time it was over, the so-called Beaver Creek blaze had blackened 112,000 acres (45,300 hectares) of tinder-dry pine forests and sagebrush flats. Just one home was lost in the blaze. None of several insurers – including AIG – that underwrite multimillion-dollar homes in fire-prone regions agreed to interviews about wildfire protection services. On its website, AIG Private Client Group pledges to use a proprietary wildfire mapping system to determine which of its insured homes are most vulnerable and to automatically send crews to take measures such as blanketing a house with fire-resistant foam. Homeowners are not required to alert the company or even be on the premises for the emergency fire protection clause to kick in. Potter said he was unaware that his policy provided for such services until the AIG private fire crew arrived on his street. “It must have been in the fine print of the contract. But I was duly impressed with their presence,” Potter said. COSTLY POLICIES Dies said crews hired by the company consist mostly of trained firemen with extensive fire-protection backgrounds. “The theory is, if they can save one house, their bottom line is a whole lot better,” he said. Firefighting experts still are evaluating how to best integrate insurance-hired resources. Private crews out to protect specific individual properties in the midst of mass evacuations can pose a challenge to federal fire managers trying to marshal manpower and resources over a wide area, said Steve Gage, assistant operations director for fire and aviation management for the U.S. Forest Service. He said the agency has sought to accommodate insurance company contract crews and engines in recognition of the valuable services they provide for certain homeowners. But tactics and objectives sometimes differ between traditional wildland firefighters and private asset-protection operations. In some cases, the industry can end up competing with the government for a limited supply of contract fire engines and residents become concerned about what seems to be government crews working their neighbor’s home but not theirs, Gage said. “The industry is about profit and loss and they’re in business to make money,” he said.

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The examples shown don’t really have to be used inside but most of these were meant for indoor, porch, deck or patio installation.Most fit into a copper rectangular pan but could fit in any large rectangular or square water container. Palm tree copper fountain with HeronClick to Enlarge You can Hop around the main pages on my site by clicking pictures below.

AUSTIN, Texas—As South by Southwest approached, tech and cultural leaders from more than a hundred countries were preparing to flock to the festival this weekend to network, build buzz and down a few drinks. Walt Disney Co. rented out a sausages-and-beer restaurant to create an immersive experience promoting its X-Men spinoff movie, “The New Mutants.” DTSQ, a South Korean rock band, was ready to fly halfway around the world to play for 40 minutes on a rooftop bar. Austin food truck owner Kati Luedecke was preparing to order 1,200 turkey legs from a nearby town. Then last week, city officials abruptly canceled South by Southwest. The same global crowd that made the festival a major moneymaker now made it a potential public safety threat in a time of coronavirus. The rapidly spreading virus is now expected to cut into global economic growth this year. It has already been brutal for the fast-growing global events industry. Organizers of Coachella, the annual music and arts festival that draws 200,000 people to the Southern California desert, postponed the event for six months. The BNP Paribas Open, a high-profile international tennis tournament in Indian Wells, Calif., called off this year’s event. That doesn’t count dozens of smaller professional conferences and sporting events canceled across the globe that reliably pump cash into regional economies. Even the Tokyo Summer Olympics might yet be curtailed.

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Human neonates use vision to guide behavior, form caregiver attachments, and build more complex visual and cognitive abilities. Defining the mechanisms by which vision comes 'online' in time for birth is thus essential to understand the development of normal and pathological visual processing. Visual perception requires the development of organized receptive fields as well as the development of cortical states that generate visual alertness and attention. Animal models have provided a mechanistic understanding of the former, but insight into the mechanisms by which alert visual response dynamics develop has been limited by a paucity of unanesthetized animal models with demonstrated homology to fetal and perinatal human cortical activity. To overcome this limitation, my collaborators and I have made a significant investment in the characterization of a behaving infant rat model that recapitulates early human cortical activity development. We propose to use this model to identify the network mechanisms that drive the development of cortical alertness, and characterize their role in the perinatal functional maturation of the visua response. In prior studies we identified a rapid maturation of visual cortical activity occurring 23 weeks before term (birth) in humans and 1-2 days before eye opening in rats. Before this switch cortical activity is dominated by network silence, interrupted by infrequent, large amplitude oscillatory bursts that occur both spontaneously and in response to light. The electrographic signature of alertness typical of the adult waking state, namely the activated or desynchronized state in the EEG, is not observed at these ages even when the infant is clearly awake. This period ends suddenly when oscillatory bursts are replaced by fast visual responses superimposed on an activated cortical state during wakefulness, which we call visual alertness. We will test the hypothesis the emergence of visual alertness is the result of rapid development of feed-forward cortical inhibition and a surge in norephinephrine (NE) release occurring just before eye opening. Our results will provide a novel understanding of how changing cortical network properties influence development of vision, and how ontogenetic control of the timing of these properties is achieved. We expect this information will inform the diagnosis and treatment of central visual and attention deficits prevalent in pre-term and other at risk infants.

Property Lines is a column by Curbed senior reporter Patrick Sisson that spotlights real estate trends and hot housing markets across the country. Comments, tips, and suggestions on where Property Lines should head next are welcome at [email protected] . If you’ve ever wondered how different cities’ signature parks, like New York’s Central Park or Chicago’s Lincoln Park, would look if they were designed in the 21st century, keep your eyes on Raleigh, North Carolina. Dorothea Dix Park, currently taking shape on a former mental hospital campus adjacent to the southern city’s growing downtown, may be the nation’s most exciting park project right now. It’s being described as the Central Park of North Carolina—and it’s not hard to see why. How many cities get to build a new, 308-acre downtown park on protected land that’s mostly been spared the last century of urban development and redevelopment? How many get to do so after projects like the High Line, Beltline, and others have showcased the promise and peril of contemporary parks as engines for both redevelopment and displacement? In February, the city council approved a new master plan for the Raleigh park from Michael Van Valkenburgh Associates, the landscape design firm behind Brooklyn Bridge Park and Maggie Daley Park in Chicago. It features a multifaceted design incorporating community spaces, botanic gardens, water features, and secluded woods. “Operating a park while planning a park, this isn’t how things normally happen,” says Kate Pearce, planning supervisor for Dorothea Dix Park in Raleigh. “This will continually challenge us to be bold, but it’ll also be a testing ground for new ideas.” While a spokesperson for the firm wouldn’t comment on the plan—“the project is just emerging from the planning stage and not yet a landscape design”—others have described it as balancing between two visions, acting as both a bridge to a more bustling 21st-century civic center and an escape into nature in the middle of the city. The city’s parks department and the public-private conservancy that will manage Dix will begin updating park infrastructure this year, in anticipation of breaking ground on phase one next year. There’s no final price tag on the project, but Pearce has previously said similar projects cost about a million dollars per acre. Modern parks create place, and define a lifestyle City leaders hope the park will be not only a major amenity for current city residents, but also a magnet for talent and development. Mayor Nancy McFarlane, who helped spearhead the push to purchase the land and develop the park, says part of the drive to develop Dix is rooted in economic shifts. “Twenty years ago, you recruited the business, and then everybody moved,” McFarlane tells Curbed. “Now, it’s the reverse: In a global economy, we’re finding that people pick where they want to live first. Economic development is about providing the quality of life to attract the best talent.” In Raleigh, McFarlane says, “we’re surrounded by top-tier universities graduating great talent. My job is to get them to stay, and Dix Park is a huge piece of offering them the quality of life they seek.” But in the push to build the city’s next great public space, will Dix Park disrupt communities adjacent to the park, especially in lower-income areas? New green developments, especially signature parks, have been seen as both a benefit and an accelerant for gentrification in other cities. Neighborhoods near the park, especially Fuller Heights, Caraleigh, and Carolina Pines, offer affordable living options that don’t have many protections from speculation or rising property values fueled by the new park. “This kind of green space is a great way to create value in urban space without having to make as significant an investment,” Winifred Curran, a DePaul professor who teaches sustainable urban development, told Curbed. “It’s easier to build a park than a housing complex.” Like many other U.S. cities, Raleigh, one of the fastest-growing cities in North Carolina, is in the midst of a prolonged development boom raising serious concerns about affordability. Roughly $2 billion in downtown commercial development has been delivered, planned, or announced since 2015, and a leading developer just pitched a $2 billion multi-use soccer stadium complex that aims to reshape Raleigh’s downtown. Pearce says the entire team working on Dix has been mindful that a successful park needs to be successful for those who live here, and must care about the sustainability of place as much as it does ecological sustainability. In addition to the lengthy community outreach that helped shape Dix Park’s master plan, a two-year process that engaged more than 65,000 residents, the city is currently working on what it is calling an “edge study” to determine how park development, and adjacent real estate development, can be harnessed and steered to create a more equitable future. “I think in Raleigh—especially with the development trends and the fear of displacement and the actual displacement that’s happening—housing is a big issue,” Jacquie Ayala, a member of a park advisory committee made up of local residents, told Next City. “What we want to do is make sure that folks who have historically not had opportunities, that we can use the park as a place to really foster that true community development.” Dix can be more than a park, says Pearce. It can be a platform to address issues of housing and social justice. Park and city staff are already looking at creating programs such as workforce training or teen volunteer corps that could lead to permanent jobs. “We could have just designed the park and the 300 acres and that would be it,” says Pearce. “But because it’s so important to the city, and it has a rich history and legacy, we’ve been intentional thinking about how it’ll impact the city.” Turning a space on seclusion into one of inclusion Creating a new signature space for Raleigh and its residents requires connecting with the surrounding community. The land’s history makes that a unique challenge. Named after Dorothea Dix, a pioneering advocate for better prisons and treatment for Americans with mental illness, the hospital site has always stood apart from the city. Original developers chose Dix Hill because it was seen as a “place of perfect health with a commanding view of Raleigh.” Purchased by the city for $52 million in 2015, the campus has long been self-contained and shut off from the surrounding urban landscape, ringed by roadways. “Dix Park was so cut off from the community, many people who have been in Raleigh their entire life never entered it,” says Pearce. “Because it was a closed mental health hospital campus, due to stigma, it wasn’t on the radar, it wasn’t a place you should or would go.” But that seclusion has proven to be a benefit. “We want to continue its role as a therapeutic center,” says Pearce. “That’s the legacy we’ve tried to address in the master plan, and something we’ve tried to use to transform the place. The goal is to change the narrative and bring the community inside.” Mayor McFarlane wants the city to improve transit access and offer more car-free options to get to Dix. That means more bike and pedestrian connections, as well as adding a stop to the in-development bus rapid-transit system and a link to a nearby rail line. A great park for the future of the entire community As workers begin upgrading the park and look ahead to the first phase of the park’s design, there’s also the question of what happens to existing buildings on campus. While the mental hospital has shut down, roughly 200 state workers, employed by the Department of Health and Human Services, still show up to the campus each day. By 2025, all state work will have stopped, and the park conservancy will have a total of 85 buildings and roughly one million square feet of indoor space to redesign, reimagine, and program. The beginnings of the new section of Dix Park may be found in a project to convert a campus chapel into a community space. Right now, a big part of building the new park is making locals aware of the possibilities. Last year, organizers planted a massive field of sunflowers, which became a social media sensation and drew many to Dix for the first time (the plantings will be repeated this year). Dix Park will grow, and redefine, the city’s park system, says Pearce. The sheer scale and possibilities of Dix—tested with a recent hip-hop music festival, Dreamville, organized by J. Cole—will help the department evolve. Pearce believes that as the contours of the city’s great new public space take shape, it’s these kinds of events that encourage the community to take ownership of the city’s new communal backyard. “How will Dix park change surrounding space and be this democratic space for everyone?” says Pearce. “The park will be of the city, and push the city forward. But, as we’re creating a great park for the future of the community, if we don’t look at how it impacts the community as a whole, we’re going to have unintended consequences.”

Peter Mettler film on tar sands to make North American premiere at TIFF On this page Feature story - August 3, 2009 Greenpeace Canada is pleased to announce that Petropolis: Aerial Perspectives on the Alberta Tar Sands will make its North American debut at the prestigious Toronto International Film Festival this September. Shot primarily from a helicopter in cinematic high-definition, Petropolis offers an unparalleled view of the largest industrial project on earth. The film, directed by award-winning filmmaker Peter Mettler, is a visual exploration of the tar sands that brings viewers directly into the oily belly of the beast. "There has been a lot of debate about the tar sands, but the opportunities to actually see and somehow experience them have been rare," said Mettler. "The beauty of cinema is that it can deliver an experience at least somewhat close to the real thing - in this case though, seriously lacking the smell." The 43-minute film is part of TIFF's Real to Reel programme and will compete in the short documentary category. It's the first film ever produced by Greenpeace Canada and has only been screened on one other occasion, at the Visions du Réel film festival in Nyon, Switzerland, where it won the "Prix du jury du jeune public" (Public youth prize) in April. For more than 20 years, Peter Mettler's films and collaborations have taken a unique and influential position within cinema. His visionary meditation Gambling, Gods and LSD (2002) won the director a Genie Award for Best Documentary, and his collaborations such as a cinematographer on the early films of Atom Egoyan and Jennifer Baichwal's Manufactured Landscapes have been acclaimed for their visual acuity. "Petropolis is a beautiful film on a very ugly subject," said Spencer Tripp, communications director at Greenpeace Canada and the executive producer of the film. "By showcasing the extreme destruction of the tar sands, this film will help raise awareness of the consequences of our reliance on dirty oil." Canada's tar sands are an oil reserve the size of England. Extracting the crude oil called bitumen from underneath unspoiled wilderness requires a massive industrialized effort with far-reaching impacts on the land, air, water, and climate, as well as First Nations communities downstream. In addition to Mettler's film, Greenpeace conducted interviews for presentation solely as short "webisodes" online at the film's website (http://www.petropolis-film.com/). These further illuminate the wide-reaching development with first-hand accounts from residents of Fort Chipewyan, Fort McMurray, Fort Saskatchewan and leading climate and water experts.

Despite its iconic status as the king of dinosaurs, Tyrannosaurus rex biology is incompletely understood. Here, we examine femur and tibia bone microstructure from two half-grown T. rex specimens, permitting the assessments of age, growth rate, and maturity necessary for investigating the early life history of this giant theropod. Osteohistology reveals these were immature individuals 13 to 15 years of age, exhibiting growth rates similar to extant birds and mammals, and that annual growth was dependent on resource abundance. Together, our results support the synonomization of “Nanotyrannus” into Tyrannosaurus and fail to support the hypothesized presence of a sympatric tyrannosaurid species of markedly smaller adult body size. Our independent data contribute to mounting evidence for a rapid shift in body size associated with ontogenetic niche partitioning late in T. rex ontogeny and suggest that this species singularly exploited mid- to large-sized theropod niches at the end of the Cretaceous. Moreover, by histologically quantifying the ontogenetic age of BMRP 2002.4.1 and BMRP 2006.4.4 and inferring skeletal maturity, we present new data that can be used to evaluate competing taxonomic hypotheses regarding these and other mid-sized tyrannosaur specimens discovered in the HCF, specifically whether BMRP 2002.4.1 (and by proxy other specimens) represents an adult “pygmy” genus of tyrannosaurid, “Nanotyrannus.” Here, we examine the femur and tibia bone microstructure of two tyrannosaur skeletons of controversial taxonomic status recovered from the HCF: BMRP (Burpee Museum of Natural History) 2002.4.1, a largely complete specimen composed of nearly the entire skull and substantial postcranial material, and BMRP 2006.4.4, a more fragmentary specimen. Respectively, we estimate these specimens to be 54 and 59% the body length of FMNH (Field Museum of Natural History) PR 2081 (“Sue”) ( 6 , 7 ), one of the largest known T. rex. The ontogenetic age of BMRP 2002.4.1 was previously reported by Erickson ( 8 ) as 11 years based on fibula osteohistology. However, because the fibula grows more slowly than the weight-bearing femur and tibia, it does not reflect annual increases in body size or relative skeletal maturity as accurately [e.g., ( 9 )]. We use femur and tibia data to (i) provide detailed comparative intra- and interskeletal histological descriptions, (ii) quantify the ontogenetic age and relative skeletal maturity of these specimens, and (iii) allow empirical observation of annual growth rate, with emphasis on variability during the life history of tyrannosaurs ( 10 ). After the publication of its discovery from the famous Hell Creek Formation (HCF) in 1905, the carnivorous dinosaur Tyrannosaurus rex ( 1 ) was met with intense scientific interest and public popularity, which persists to the present day ( 2 ). Numerous hypotheses concerning T. rex biology and behavior result from decades of research primarily focused on skeletal morphology and biomechanics [e.g., ( 3 ) and references therein]. Only within the past 15 years has bone histology been applied to investigate the aspects of T. rex life history inaccessible from gross examinations, addressing questions concerning ontogenetic age, growth rate, skeletal maturity, and sexual maturity. In 2004, two teams independently assessed the growth dynamics of T. rex using osteohistology. Their results suggest that T. rex had an accelerated growth rate compared with other tyrannosaurids and achieved adult size in approximately two decades ( 4 , 5 ). The teams focused on growth curves, rather than on detailed analyses or interpretations of bone tissue microstructures. However, osteohistology is critical for establishing a baseline against which skeletal maturity and growth changes in cortical morphology related to life events in this taxon can be tested. Identifying the timing of growth acceleration and empirically quantifying juvenile T. rex growth rates are of special importance because the juvenile growth record is lost in older individuals because of bone remodeling and resorption ( 4 , 5 ). Prondvai et al. ( 13 ) demonstrated that inaccurate bone microstructure interpretations are possible if the mineralized tissue is observed in only a single plane; specifically, the more slowly formed parallel-fibered mineral arrangement could be mistaken for the rapidly deposited woven-fibered mineral arrangement, which has direct bearing on growth rate interpretations. Therefore, the femur of BMRP 2006.4.4 was longitudinally sectioned in an anterolateral-posteromedial plane, and the tibia of BMRP 2002.4.1 was sectioned in a medial-lateral plane to accurately assess tissue organization and associated relative growth rates ( Figs. 1C and 2B , and figs. S2, B and C, S5, and S7). In the femur of BMRP 2006.4.4, vascular canals are arranged parallel to the plane of section and to the shaft of the long bone. Adjacent to the vascular canals, bone fibers are highly anisotropic in CPL and contain osteocyte lacunae with long axes arranged parallel to the vascular canals and plane of section. Tissue of the laminae between primary osteons varies locally in degree of isotropy, with corresponding variable shape in osteocyte lacunae. On the medial side of the longitudinal section through the tibia of BMRP 2002.4.1, vascular canals are arranged obliquely with numerous communications (fig. S5B). From the mid- to the outer cortex, vascular canals are more uniformly parallel to the bone shaft, with fewer transverse Volkmann’s canals (fig. S5C). Adjacent to vascular canals, fibers of the primary osteons are anisotropic in CPL with longitudinally flattened osteocyte lacunae. Fibers within the primary laminae vary locally in isotropy and osteocyte lacuna orientation ( Fig. 2B ). The lateral cortex is thinner than the medial cortex, and vascular canals are more closely spaced with fewer communicating canals (fig. S5D). In the femur of BMRP 2006.4.4, there is an annulus at the periosteal surface on the medial side ( Fig. 1D ), but when followed posteriorly, the annulus is within the outer cortex, while fibrolamellar tissue makes up the cortex of the periosteal surface ( Fig. 1E ). Within the innermost cortex on the anterolateral side, six LAGs are closely spaced ( Fig. 2D ). Because of resorption from the medullary drift, these LAGs are absent within the innermost cortex of the posterior and lateral sides. Cyclical growth marks (CGMs), resembling tree rings in transverse thin section, were observed in the femora and tibiae of both BMRP specimens. Studies on extant vertebrates demonstrate that CGMs result from brief interruptions in osteogenesis, occurring with annual periodicity and typically coinciding with the nadir ( 12 ). The annual pauses in bone apposition are recorded as CGMs in cortical microstructure as either pronounced lines of arrested growth (LAGs) or diffuse annulus rings. On the basis of counting CGMs, BMRP 2002.4.1 was at least 13 years old at death (13 CGMs in the femur and 10 CGMs in the tibia), and BMRP 2006.4.4 was at least 15 years old at death (15 CGMs in the femur and 13 to 18 CGMs in the tibia). Typically, vertebrate long bone cortices will exhibit widely spaced CGMs within the cortex when young, corresponding to high annual osteogenesis. In subadults, CGMs become more closely spaced as osteogenesis decreases approaching adult size [e.g., ( 10 )]. In contrast to these frequently observed patterns, the spacing of CGMs was unexpectedly variable throughout the femur and tibia cortices of both BMRP specimens. Of special note, within the medullary cavity of the femur and tibia of BMRP 2006.4.4, isotropic, vascularized, primary tissue is separated from the cortex by a lamellar endosteal layer. These features are morphologically consistent with medullary bone ( 11 ); however, additional studies on the systemic nature of this tissue throughout BMRP 2006.4.4 and biochemical tests on this tissue are necessary to test this hypothesis. In the tibia transverse section of BMRP 2002.4.1 ( Fig. 2A and fig. S4), longitudinal primary osteons are isotropic in circularly polarized light (CPL), but fibers of primary osteons encircling laminar, circular, and plexiform vascular canals are anisotropic. In contrast, primary osteons in the tibia of BMRP 2006.4.4 are frequently isotropic regardless of vascular canal orientation. Because of its proximal sampling location, the cortical shape of the tibia from BMRP 2006.4.4 in transverse section differs from that of BMRP 2002.4.1 and incorporates the fibular crest on the lateral side (figs. S2D and S8, A and F). Highly vascularized reticular woven tissue is present on the anterior and anterolateral periosteal surfaces ( Fig. 2C ). In both individuals, the thickest tibial cortex is located anteriorly. ( A ) Transverse mid-cortex thin section of BMRP 2002.4.1. Longitudinal POs are evident, and PPL emphasizes osteocyte lacuna density and variability in shape within laminae. CPL reveals varying birefringence associated with bone fiber orientation, but with a weak arrangement of fibers parallel to the transverse plane of section. Many POs are composed of highly isotropic fibers with rounded osteocyte lacunae. ( B ) Longitudinal thin section of the mid-cortex of BMRP 2002.4.1. Vascular canals appear as near-vertical, dark columns. Adjacent to the vascular canals, the POs contain laterally compressed osteocyte lacunae. CPL demonstrates that the laterally compressed osteocyte lacunae of POs are embedded within a uniformly birefringent matrix (anisotropic), indicating that the lamellae of POs are LP. Osteocyte lacunae orientation varies in the thin laminae between POs. In CPL, the laminae are weakly isotropic, corresponding to the weak arrangement of parallel fibers in transverse section. ( C ) In transverse thin section, the periosteal surface of BMRP 2006.4.4 on the anterior side consists of reticular POs within laminae of highly isotropic, woven tissue. ( D ) Within the anterior and anteromedial innermost cortex of BMRP 2006.4.4, in transverse thin section, six closely spaced LAGs are visible interstitially. Blue lines highlight the LAG trajectories. ( A ) Mid-cortex of the transverse thin section of BMRP 2002.4.1. Plane-polarized light (PPL) emphasizes osteocyte lacuna density and variability in shape within the laminae, as well as longitudinal primary osteons. In CPL, there is a weak preferred fiber arrangement parallel to the transverse plane of section reflected by regional birefringence. Many primary osteons (POs) have uniformly isotropic fibers with rounded osteocyte lacunae. ( B ) Mid-cortex of the transverse thin section of BMRP 2006.4.4. Osteocyte lacuna density and variability in shape within the laminae are evident in PPL. CPL reveals varying birefringence associated with bone fiber orientation, but there is a weak preferred fiber arrangement parallel to the transverse plane of section reflected by regional birefringence. Many POs are composed of uniformly isotropic fibers with rounded osteocyte lacunae. ( C ) Longitudinal section of the mid-cortex of BMRP 2006.4.4. Vascular canals appear as near-vertical, thin, dark columns. As in the transverse section, the primary laminae between POs contain variably arranged osteocyte lacunae. In CPL, the laminae are weakly isotropic (I), corresponding to the poorly organized parallel orientation of fibers in the transverse plane. The laterally compressed osteocyte lacunae in POs are embedded within a uniformly birefringent [anisotropic (AN)] matrix in CPL, indicating that the PO lamellae are longitudinally oriented parallel-fibered bone (LP). ( D ) On the posteromedial side of the transverse section of BMRP 2006.4.4, there is a parallel-fibered annulus located at the periosteal surface (thickness indicated with blue line). Photographed in CPL. ( E ) In the transverse section on the posterolateral side, the annulus shown in (D) (blue lines) is overlain by highly isotropic woven-fibered laminae. For detailed, orientation-specific histology descriptions, refer to the Supplementary Materials. In general, the femur and tibia cortical bones of BMRP 2002.4.1 and BMRP 2006.4.4 can be classified as a woven-parallel complex. Vascularity and osteocyte lacuna density are uniformly high throughout ( Figs. 1 and 2 ). In the femora, the primary and secondary osteons surrounding vascular canals are frequently isotropic in the transverse section ( Fig. 1, A and B ) and anisotropic in the longitudinal section ( Fig. 1C ). Also in the transverse section, femur primary tissue exhibits moderate anisotropy regionally and weak anisotropy locally, corresponding to a loose arrangement of mineralized fibers in parallel (e.g., Fig. 1, A and B , and fig. S3B). DISCUSSION Limb bones exhibit moderate growth rates and tension loading Comparison of BMRP 2002.4.1 and BMRP 2006.4.4 bone fiber organization in the transverse and longitudinal sections using CPL confirms that primary tissue is generally poorly organized parallel fibered to weakly woven. Dense osteocyte lacunae and poor bone fiber organization, in combination with a rich vascular network of reticular, laminar, and plexiform primary osteons, are characteristics that empirically correspond to elevated osteogenesis ranging from 5 to 90 μm/day (10). Nonetheless, the frequency of longitudinal vascularity, as well as regionally prevalent poorly organized parallel fiber bundles within the transverse sections, suggests that annual growth rates were nearer the lower bound (10). The BMRP individuals did, however, experience occasional periods of faster growth indicated by bands of regionally isotropic woven laminae with reticular vascularity (e.g., Figs. 1E and 2C, and figs. S6D and S8, C and D) (10). In both BMRP specimens, the majority of primary osteons as well as some secondary osteons were isotropic in the transverse section. Corresponding anisotropy in longitudinal examination confirms that the fiber bundles within osteons are longitudinally arranged (Figs. 1C and 2B, and fig. S5, B to D). Studies on long bone response to loading show that longitudinal collagen fiber orientation within secondary osteons is commonly found in habitually tension-loaded regions (14), which may also apply to primary osteon collagen fiber orientation. As such, future studies on tyrannosaurid locomotion biomechanics may benefit from incorporation of osteohistology. Relative skeletal maturity Rather than exhibiting an external fundamental system (EFS) (Fig. 3), a woven-parallel complex extends to the periosteal surface in both tyrannosaurid specimens. Thus, histology supports morphological observations that BMRP 2002.4.1 and BMRP 2006.4.4 were skeletally immature individuals at death (10). In lieu of epiphyseal fusion, which most reptile taxa lack, an EFS is the only way to conclusively confirm attainment of asymptotic adult body length from the long bones of a vertebrate. When present, the EFS occupies the periosteal surface as either closely spaced LAGs (separated by micrometers) (Fig. 3A) or as a thick, primarily avascular annulus (Fig. 3B) (10). CGMs close to the periosteal surface can sometimes be mistaken for an EFS. In the case of BMRP 2006.4.4, an annulus is present at the periosteal surface of both the femur (Fig. 1D) and tibia (fig. S8E), but when the annulus is followed around the cortex, in both cases it becomes embedded within the outer cortex and superseded by woven primary tissue (Figs. 1E and 2C). The proximity of the annulus to the periosteal surface instead suggests that BMRP 2006.4.4 died soon after growth resumed following the annual hiatus and that cortical osteogenesis was directional. Fig. 3 The presence of an EFS at the periosteal surface of a long bone indicates skeletal maturity, while the absence of an EFS indicates that the bone is still growing at the time of death. (A) An EFS composed of tightly stacked birefringent LAGs (between blue arrowheads) at the periosteal surface of an Alligator mississippiensis. (B) The EFS (between blue arrowheads) in an ostrich (Struthio camelus) is made of nearly avascular, birefringent parallel-fibered to lamellar primary tissue. (C) No EFS is present at the periosteal surface of the femur of BMRP 2002.4.1, (D) the tibia of BMRP 2002.4.1, (E) the femur of BMRP 2006.4.4, or (F) the tibia of BMRP 2006.4.4. All panels are shown in transverse thin section, with CPL. Ontogenetic age On the basis of femur CGM count, BMRP 2002.4.1 was >13 years old at death, which is 2 years older than the original estimate by Erickson (8) based on fibula CGM count. The slightly larger BMRP 2006.4.4 was >15 years old. The number of CGMs missing due to medullary expansion is unknown, precluding an exact age at death for BMRP 2002.4.1 and BMRP 2006.4.4. Although the number of missing CGMs could be predicted on the basis of innermost zonal thicknesses and a process of retrocalculation [e.g., (5, 10)], the variable spacing between CGMs observed in BMRP 2002.4.1 and BMRP 2006.4.4 and other tyrannosaurs (15) renders the technique unreliable in this case, and it was not attempted. Within the innermost cortex of BMRP 2006.4.4, there is a tight stacking of six CGMs (Fig. 2D). Because the CGMs remain parallel about the cortex and do not merge, they either represent a single hiatus in which growth repeatedly ceased and resumed (totaling 13 years of growth) or up to 6 years where relatively little growth occurred annually (totaling up to 18 years of growth) (9, 16). This tight stacking of six CGMs is not observed in the femur of BMRP 2006.4.4, which preserves 15 CGMs. The CGM count from the partial tibia of BMRP 2006.4.4 is questionable because the proximal sampling location away from midshaft incorporates the fibular crest, introducing associated regions of remodeling and directional growth affecting apposition interpretations. Because of this and their absence in the femur, the observed grouping of six CGMs is conservatively interpreted as a single hiatus event. Similar instances of a single hiatus represented by narrowly spaced LAGs are reported in other tyrannosauroids (15). If this grouping of CGMs instead represents 6 years of protracted growth, then BMRP 2006.4.4 demonstrates the extent to which these individuals could adjust growth rate based on resource availability, in this case prolonging the ontogenetic duration of BMRP 2006.4.4 as a mid-sized carnivore. Bone tissue organization was similar across femora and tibiae, suggesting that both bones record annual increases in body size equally well. If the stacked CGMs of BMRP 2006.4.4 reflect a single hiatus, then each femur preserved more CGMs than the associated tibia. Previous studies demonstrated that intraskeletal inconsistencies in CGM counts are due to variable rates of medullary cavity expansion or cortical drift across elements (9, 17, 18) when sampled at midshaft. Therefore, our preliminary assessment of T. rex intraskeletal histology suggests that the femur is more informative than the tibia, despite regions of cortical remodeling from tendinous entheses about the cortex. Additional intraskeletal histoanalyses of tyrannosaurid specimens are necessary to test whether the femur is the preferred weight-bearing bone for simultaneous assessments of annual growth rates and skeletochronology. In addition to ontogenetic zonal thickness variability within the cortex, zonal thickness also changed with respect to cortical orientation. That is, zones were often much thinner relative to one another on one side of the transverse section and much thicker on another side (e.g., fig. S4, G and H). This pattern is particularly noticeable in the tibia of BMRP 2002.4.1 (medial cortical zones are thickest) and the femur of BMRP 2006.4.4 (posteromedial cortical zones are thickest). This observation implies that directional cortical growth occurred over ontogeny and stresses the necessity of complete transverse sections for histological analysis: Obtaining a fragment or core for study from one orientation may result in erroneous interpretations of growth rate and skeletal maturity. Variability in annual growth as a response to resource abundance Interpretations of relative maturity in nonavian dinosaurs often rely on reported trends in the thickness of cortical zones between CGMs from the inner to the outer cortex (10). Zone thickness is typically greatest within the innermost cortex, corresponding to rapid annual growth early in life. Zones become progressively thinner in the mid- to the outer cortex of older individuals, as annual growth rate decreases approaching asymptotic body length. These general trends provide the interpretive foundation for the two previous histology-based ontogenetic studies on Tyrannosaurus growth (4, 5). The spacing of CGMs within the outer cortices of BMRP 2002.4.1 and BMRP 2006.4.4 (Fig. 4) is narrower than between some CGMs deeper within the cortices, which suggests that, although not adults, the specimens were approaching a body length asymptote at about one-half the body length of FMNH PR 2081. However, annual zonal thicknesses between CGMs deeper within the cortices of BMRP 2002.4.1 (Fig. 4A) and BMRP 2006.4.4 (Fig. 4B) are variable, and zones do not consistently progress from widely spaced within the inner cortex to more closely spaced in the outer cortex. Because of unpredictable spacing within the cortex, reduced zonal thickness near the periosteal surface is likely an unreliable indicator of skeletal maturity in BMRP 2002.4.1 and BMRP 2006.4.4. Variable zonal thicknesses are, thus, likely to be observed in ontogenetically older T. rex individuals. To test this hypothesis, we examined femur and tibia thin sections from T. rex specimens USNM PAL (National Museum of Natural History) 555000, MOR (Museum of the Rockies) 1125, MOR 1128, MOR 1198, and CCM (Carter County Museum) V33.1.15. In all individuals, variability in annual zonal thicknesses was observed. In particular, compared to zone spacing within the mid-cortex, noticeably thinner zones are present within the innermost cortex of USNM PAL 555000 (Fig. 4C) and MOR 1128 (Fig. 4D). These results contradict the mathematically predictable zonal spacing in T. rex long bones reported by Horner and Padian (5), which used some of the same specimens reassessed in the present study. Results further suggest not only that BMRP 2002.4.1 and BMRP 2006.4.4 had not yet entered the accelerated growth period proposed for this taxon (4, 5) but also that the accuracy of the generalized T. rex body mass curve from Erickson et al. (4) would be affected by undetected individual variation in annual growth. Fig. 4 Examples of variable CGM (blue lines) spacing in tyrannosaurids examined for this study. (A) The variability of CGM spacing in the femur of BMRP 2002.4.1 and (B) the tibia of BMRP 2006.4.4 may imply that these individuals were approaching asymptotic body length. However, CGMs within the innermost cortices of much larger T. rex specimens (C) USNM PAL 555000 and (D) MOR 1128 demonstrate that the CGM spacing is not a reliable indicator of relative maturity status. All panels are shown in transverse thin section. Variable LAG spacing is reported in ornithomimids, ornithopods [(19) and references therein], and other tyrannosauroids (15) and may correlate with annual resource abundance (12, 19). Our data suggest that this trait also characterizes T. rex: Because the level of bone tissue organization within zones remained the same from the innermost cortex to the periosteal surface in the BMRP specimens, growth rates were within a similar range from year to year. To produce these extremes in annual bone apposition, the duration of the growth hiatus must have varied annually. On the basis of the larger T. rex specimens examined here for comparison, the adjustment of annual growth hiatus duration in response to resource abundance is a physiological characteristic observed throughout T. rex ontogeny. Regardless of cause, unpredictable CGM spacing observed here and in previous studies stresses caution when inferring relative maturity based on cortical LAG spacing (19). The observation of closely spaced CGMs within the innermost cortices of larger T. rex validates our interpretation that the thin zonal spacing observed in the outermost cortices of BMRP 2002.4.1 and BMRP 2006.4.4 are not reliable indicators of relative maturity when an EFS is absent. Implications for the Nanotyrannus hypothesis The bone microstructural interpretations discussed here not only provide insight into T. rex ontogeny but also have bearing on discussions concerning CMNH (Cleveland Museum of Natural History) 7541 and Nanotyrannus. CMNH 7541 consists of a small isolated skull 572 mm in length (20). Inferred to be sympatric with T. rex, it was originally named Gorgosaurus lancensis (21). In 1988, Bakker et al. (22) redescribed CMNH 7541 as an adult specimen of a new genus, Nanotyrannus. Using an extensive empirical dataset, Carr and Williamson (23) formally synonymized Nanotyrannus into Tyrannosaurus in 2004, supporting the interpretation of CMNH 7541 as a juvenile T. rex proposed by Rozhdestvensky in 1965 (24). Presently, most tyrannosaurid specialists consider CMNH 7541 and possible referred specimens to be juvenile T. rex based on morphological skull features shared with those found in undisputed juvenile individuals of other tyrannosaurid taxa [e.g., (2, 20, 23, 25–28)]. Nonetheless, several publications have since argued for the validity of Nanotyrannus based not only on morphological characters of the CMNH 7541 type skull but also on characters from the somewhat larger skull of BMRP 2002.4.1 (720 mm in length) [e.g., (29–33)], which some researchers have assigned to Nanotyrannus based on shared morphological characters they consider adult autapomorphies of the taxon [e.g., (29–33)]. Currently, BMRP 2002.4.1 is the only accessioned specimen with postcranial skeletal elements preserved that is specifically argued by proponents of Nanotyrannus as belonging to that genus [e.g., (29–32)]. Because CMNH 7541 lacks the postcranial skeleton and proponents of Nanotyrannus refer BMRP 2002.4.1 to that taxon, the limb bone histology of BMRP 2002.4.1 (and additionally BMRP 2006.4.4; see the Supplementary Materials for taxonomic discussion) reveals the life history of CMNH 7541 by proxy. Here, we provide histological data that can be used to reject the hypothesis that Nanotyrannus was erected on the basis of a skeletally mature “pygmy” individual, resulting in two remaining alternative hypotheses: (i) Nanotyrannus is a valid taxon, but the holotype and all currently referred specimens including BMRP 2002.4.1 and BMRP 2006.4.4 are immature, with no skeletally mature individuals yet known; and (ii) CMNH 7541, BMRP 2002.4.1, BMRP 2006.4.4, and other mid-sized tyrannosaurid specimens collected from the HCF represent juvenile ontogenetic stages of T. rex. Thus far, the femur and tibia of BMRP 2002.4.1 and BMRP 2006.4.4 are the only weight-bearing bones of Upper Cretaceous HCF tyrannosaurids described histologically from complete transverse sections, and these universally demonstrate features characteristic of actively growing juvenile dinosaurs that had not yet entered an exponential phase of growth (as demonstrated by our new data identifying noticeably thinner zones within the innermost cortex of large-bodied T. rex specimens such as USNM PAL 55500). On the basis of these data, the latter hypothesis is most parsimonious and is congruent with the morphology-based conclusions of Carr (20) and Carr and Williamson (23). Incorporating additional mid-sized HCF tyrannosaurid specimens into this histology-based relative maturity assessment is necessary to further support or refute the parsimonious hypothesis.

Corning’s future vision of glass Videos My Comments I had heard about Corning’s new series of videos about glass being more than just windows, mirrors and drinks containers. Their vision in these videos was to have windows, mirrors and similar objects as display surfaces for computer-hosted data; as well as for other applications like photovoltaic (solar) cells or electrochromic uses like tinting or frosting on demand. Some of these visions include windows that are clear but become frosted “on demand” for privacy or show images or text such as a themed photo cluster or a diagram, with some being touchscreens for interacting with the display or being a control surface for lighting for example. The applications were being extended to automotive use like the glass displays being part of a dashboard for example. This has been made feasible through efforts like the “Gorilla Glass” technology that is now being implemented in smartphones, tablets and large displays like TVs. Here, this glass is about an increasingly-tough surface or about a thinner glass surface for an LCD or OLED display application (including a touchscreen) being as tough as a glass surface of regular thickness. It is even worth noting that Philips was also involved in “taking glass further” with mirrors that are displays and lately with an OLED light / solar-cell combination which is transparent one moment and a light-source another moment while supplying extra power during the day. This latter application was pitched again at cars with a way of bringing more light in to the car but also working as an interior light when it is darker. At least this shows that there will be many different game-changers when it comes to the design of display and similar technologies.

VICTORIA, B.C. - Andrew Weaver, leader of the B.C. Green Party, responded to the government’s announcement that it anticipates it will bring legislative changes to enable ridesharing in Fall 2018. “I am very disappointed that the government will not keep its promise to bring ridesharing to British Columbians by the end of this year,” said Weaver. “It has been five years since ridesharing was first introduced into B.C. There have since been reports that ridesharing companies are operating without proper oversight, regulation and insurance. Further, all three parties agreed to bring in ridesharing in the last election and have now had significant time to consult stakeholders and assess the various ramifications of regulating this industry in British Columbia. “The creative economy and innovation are the future of our province. We cannot be tech innovators if we’re not willing to embrace innovation. As new technologies emerge, government should proactively examine the evidence and openly debate the issue in a timely manner so that we do not fall behind the curve. “On Thursday, for the third time, I will introduce legislation that will enable ridesharing to finally operate in a regulated fashion in B.C. I hope both parties will take this opportunity to engage in a substantive debate on the details of this issue so that we can move past rhetoric and vague statements and finally get to work delivering for British Columbians." -30- Media contact Jillian Oliver, Press Secretary +1 778-650-0597 | [email protected]

A woman named ‘Aaishah, from Pakistan, relates the following experience: I was once busy reciting the Quraan Majeed, as was my habit, when my eldest son, Shafee’, who was approximately six years old at the time, emerged from the house to play outside. We are still unsure as to exactly how it happened, but he somehow closed the door of the car on his finger! His hand was injured so badly that his third finger was almost totally separated from his right hand. The finger just managed to remain attached to his hand by a thin strip of skin. I was seated in our home, reciting Surah Ar-Rahmaan, and remained oblivious to what had transpired. My husband, on seeing our son injured, did not wait to inform me of what had happened but instead instantly bundled him into the car and raced off to the nearest doctor. On arriving at the doctor’s surgery, the doctor urged him to rush Shafee’ to the Civil Hospital. I was just about completing Surah Ar-Rahmaan when the guard started urgently shouting for me. I did not turn my attention to him and indicated that he should wait as I wished to complete the surah before hearing his message. When I had completed reciting the surah, I turned to him and he informed me of the tragedy that had befallen my son. On receiving the news, I also set out for the Civil Hospital. The doctors had used stitches to reattach his finger but felt that the finger would not successfully connect and join with the hand and it would thus be better to remove it altogether. I, however, could not tolerate the thought of my son living with only four fingers on his hand and begged them to give the finger a chance. In this way, two days passed with the finger attached, until the signs of infection and decay became apparent. The hand began to emit the odor of disease and we now feared that the infection had spread to the rest of his hand. In desperation, one of the most prominent surgeons of Karachi, Dr. Pinthu, was summoned. When Dr. Pinthu examined my son’s hand, he supported the opinion of the other surgeons, claiming that my son’s finger was beyond saving, and also declared that the right hand would have to be amputated until the wrist on account of the infection. Overcome by a mother’s love for her child, I pleaded with Dr Pinthu to prescribe more medication which would hopefully remove the infection and save my son’s hand. Dr. Pinthu became angry and admonished me saying, “If you refuse to allow us to amputate until his wrist, the infection will spread! Within 24 hours, we will be forced to amputate until his elbow!” Hearing this, I stood up and exited the hospital. I had turned to the best surgeons in the city and they had failed to save my son’s hand. I should rather turn to Allah Ta‘ala and place my reliance and faith in Him. Still standing outside the hospital, I began to make du‘aa to Allah Ta‘ala saying, “O Allah! This tragedy struck while I was reciting your Quraan Majeed! O Allah! You have complete control over the entire world and You are all powerful! Do not let me become despondent of Your mercy! O Allah, have mercy on my son! O Allah! I will recite one entire Quraan in the next day, You save my son!” In order to console me, the Doctor gave me two capsules to give my son and a bottle of Dettol to disinfect his wound. The amputation, however, was scheduled to take place in 24 hours. I turned my complete attention to Allah Ta‘ala and placed my complete confidence in Him alone for that 24 hours. I remained in the Hospital and began to recite the Quraan Majeed with my husband until we had together completed a khatam of the Quraan Majeed in 17 hours. In these 17 hours, the wounds on the hand of Shafee’ miraculously dried and all the signs of infection miraculously disappeared. What all the doctors and surgeons combined were unable to accomplish, Allah Ta‘ala had done for us in just a few moments. The surgeons were speechless and realized that all their degrees were worthless before the Quraan Majeed of Allah Ta‘ala. This incident transpired 14 years ago and the hand of Shafee’ healed so completely that not even a scar can be seen today. (Quraan ke Hayrat Angez Waaqi‘aat pg. 151)

Introduction ============ Rationale --------- Early life experience is a determinant of social inequalities in physical, mental, and social well-being \[[@ref1]-[@ref6]\]. Children living in poverty are more likely to suffer from developmental and health problems, and childhood interventions can decrease incidence and prevalence of these problems \[[@ref7]-[@ref12]\]. The proposed project is aimed to assess and improve a childhood intervention: the *Naître et grandir* (N&G) website and newsletter on child development, education, health, and well-being, which includes the Information Assessment Method (IAM) that allows N&G readers to continuously assess, and subsequently the N&G editors to improve, the content shared on the N&G website and newsletter. Parents with low education and low income, hereafter referred to as parents with low socioeconomic status (SES), typically have a low literacy level (limited ability to acquire, understand, evaluate, and use written information). Low parental literacy level is particularly detrimental to child health: a low literacy level is associated with worse health status, difficulties accessing health care, and poorer preventive health behavior and self-management of health problems \[[@ref13]-[@ref23]\]. Education and income are the most important SES indicators, and together, they are strongly associated with child health status \[[@ref24],[@ref25]\]. According to research on information-seeking behavior, parents with low SES have greater information needs than parents with high SES \[[@ref26]\]. The use of high-quality online information can improve quality of life and have positive family, economic, and social impacts on low-SES parents, including refugee and homeless parents \[[@ref27]-[@ref31]\]. High-quality information and literacy-related interventions can reduce unnecessary calls and visits to health professionals, increase knowledge and self-efficacy, and improve health \[[@ref16]-[@ref19],[@ref32]-[@ref47]\]. N&G \[[@ref48]\] is a website independent from industry funding that provides high-quality information (based on research syntheses and validated by experts) on child development, education, health, and well-being. N&G users can access hundreds of information pages (1 page per topic) that are organized in age group categories, ranging from pregnancy to the age of 8 years. N&G also produces a weekly newsletter to support parents, including those with a low literacy level, having children under the age of 8 years. N&G partnered with investigators from McGill University to validate and implement the IAM to continuously assess and improve content shared on the N&G website and newsletter \[[@ref49]-[@ref53]\]. In line with the Canadian Institutes of Health Research (CIHR)'s definitions \[[@ref54]\], the IAM is a knowledge translation tool for monitoring N&G information use, and its impact on parents is measured by expected health/well-being benefits. It is also fostering parent engagement by enabling parents to interact with N&G editors by providing feedback on the information content. The IAM questionnaire includes 7 questions (with clickable answers and 2 comment boxes), allowing users to rate on the situational relevance, cognitive/affective impact, intention to use and expected benefits of specific information content (N&G information page), and write comments. During our pilot phase (September 1, 2014, to August 31, 2016), we collected 34,021 IAM ratings (completed IAM questionnaires) from parents, relatives, and professionals (education, health, and social services) who read N&G content. In line with studies on social inequalities in Web information use \[[@ref55]-[@ref61]\], the statistical analysis of these ratings revealed a social gradient: low-SES parents underuse N&G and the IAM ([Figure 1](#figure1){ref-type="fig"}). Results also indicated that low-SES parents are more likely to report decreased worries and increased confidence as a result of using N&G information \[[@ref50]\]. There is a need to understand this gradient to improve N&G content and reach low-SES parents and a need to explore how the use of knowledge translates into health and well-being outcomes for low-SES parents and children. {#figure1} Goal and Objectives ------------------- This study (research protocol) has been recently funded by CIHR. As per CIHR's definition of knowledge translation ("making people aware of knowledge and facilitating knowledge use to improve health") \[[@ref62]\], our goal is to improve how low-SES parents engage with and use online information about child development, education, health, and well-being; learn how this format for knowledge sharing translates to improved health and well-being outcomes for low-SES parents and their children; and explore their interaction with Web editors to influence content (responsible for websites' content). On the basis of the N&G team\'s (the director and 2 coordinators) questions and using the Knowledge-to-Action framework \[[@ref63]\], we determined 4 research objectives: - Objective 1: Identify low-SES parents' views on barriers and facilitators to accessing, understanding, and using N&G information content and to interacting with N&G editors via the IAM. - Objective 2: Adapt N&G content/functions and the IAM tool (user-centered design) to reduce barriers and optimize facilitators identified in phase 1 and implement new versions labeled N&G+ and IAM+. - Objective 3: Evaluate whether N&G+ and IAM+ result in a higher proportion of low-SES parents engaging with the N&G site and the content provided and interacting with editors via the IAM. - Objective 4: Describe how expected health and well-being benefits of N&G+ information use (reported via IAM+) are experienced by parents with low SES and their children. Systematic Literature Review and Theoretical Model -------------------------------------------------- The nominated principal investigator (NPI) led a CIHR-funded systematic review and proposed a comprehensive harmonized typology of (1) outcomes associated with the use of online consumer health information and (2) conditions (network and resources) leading to these outcomes \[[@ref64]-[@ref67]\]. A total of 68 studies were analyzed using framework synthesis \[[@ref68],[@ref69]\]. This synthesis was based on an initial framework derived from information studies \[[@ref49],[@ref70]-[@ref78]\] and led to propose an innovative theoretical model ([Figure 2](#figure2){ref-type="fig"}) \[[@ref66],[@ref67]\]. This model includes positive and negative health outcomes of online consumer health information in a primary care context and is (information) consumer oriented. The model comprises 13 main concepts (42 factors and outcomes) and will be used in this study to inform data collection and analysis, for example, the phase 1 qualitative interview guide and interpretive thematic analysis. The model will contribute to establish a chain of evidence linking ultimate outcomes of information (such as health outcomes), intermediary outcomes (such as cognitive impact of information), and conditions associated with outcomes (information needs and seeking behaviors and contextual factors). {#figure2} ### Outcomes The model includes an organizational level of information outcome (eg, increased or decreased use of health services) and 4 individual levels of outcomes of information. The latter outcomes reflect how information is valuable from the consumer's perspective: situational relevance, cognitive impact, use of information (conceptual, legitimating, instrumental, and symbolic use), and subsequent health and well-being outcomes. ### Conditions The model includes conditions associated with outcomes of information in relation to a specific situation: a particular information object is acquired or delivered (eg, a Web page or a newsletter) in a particular situation (eg, before or during or after an encounter with someone) directly or with help from a relative or a professional. The main conditions are information needs and seeking behaviors; individual characteristics (such as electronic health literacy); social and technical factors (such as social networks); relationships with professionals (such as teachers, clinicians, and social workers); and access to education, health, and social services. The first phase of this study will specifically look into conditions experienced by low-SES parents, such as media competence. Direct acquisition of online information depends on an impetus to search (motivation), momentary internet connection, internet search skills, and one's ability to understand the content that may or may not be adapted to their individual literacy level \[[@ref79]-[@ref81]\]. Approximately 95% of parents of preschool children have direct individual access to the internet in Quebec \[[@ref61]\], and parents can also access it at office workplaces and public libraries \[[@ref79]-[@ref81]\]. Literacy level is generally defined as the degree to which a person has the ability to "acquire, understand, evaluate, and use information" needed to obtain services and make appropriate decisions \[[@ref23]\]. Computer literacy, information literacy, and health literacy are interdependent (eg, a person with a low literacy level has a low level of health literacy). Culture is central in literacy, and one's literacy level depends on one's ability to understand systems of symbols from one's own culture or a dominant culture and language, for example, immigrants and refugees may have a higher literacy level in their country of origin compared with their adoptive country \[[@ref23]\]. As mentioned in our model, the literacy level is *situational* and *contextual*, given that a social network can compensate for an individual's low literacy level. Mediated (by someone else) acquisition of information is very common. The absence of an individual connection 24/7 is no longer the primary barrier to seeking health information \[[@ref80]\]; for example, our pilot data show that 18.1% of IAM ratings concerned N&G information seeking for someone else's child (eg, relative's, friend's, neighbor's, or client's child). Even homeless parents or recent immigrants and refugees can acquire online consumer health information directly or mediated by their social network, including community organizations; public libraries; and education, health, and social services \[[@ref23],[@ref27]-[@ref31]\]. Indeed, information studies show that consumers combine mediated information with direct acquisition of online health information, the latter allowing them to probe information provided by professionals \[[@ref64]-[@ref67]\]. For analytical purpose, we conceive these combinations as the interpenetration of social systems centered on communicative action, for example, the health system (mediated access) and a consumer parent system (direct access and mediated access via their social network) \[[@ref82]-[@ref85]\]. Significance ------------ Our project focuses on all Canadian parents with low SES who acquire (direct or mediated) online information about child development, education, health, and well-being. In Canada, 42% of nonelderly adults \[[@ref16],[@ref17]\] and 15% of children live in low-income households \[[@ref86]\]. In Quebec, 36% of parents report living in poverty \[[@ref87]\]. The demand for information is very high, resulting in frequent internet searches; for example, parents search the internet for child-related information on average 1.3 times per week in Quebec, and 73% of parents report that the internet constitutes their first-line source of parenting information \[[@ref88]\]. ###### Main features of *Naître et grandir* and *AboutKidsHealth*. Main features *Naître et grandir* \[[@ref48]\] *AboutKidsHealth* \[[@ref94]\] ------------------------ -------------------------------------------------------------------------------------------------- ------------------------------------------------------------- Website annual traffic 24 million worldwide visits 16.8 million worldwide visits Information Developmental, educational, health, and well-being information about children aged under 8 years Health information about children aged under 19 years Language French English, French, and 10 other languages Targeted audience Parents, relatives, and caregivers Parents, relatives, and caregivers and health professionals Specifically, our project is important for about half the population of parents of children under 19 years, namely, parents with a low literacy level. Low literacy is a major concern in Canada \[[@ref16],[@ref17],[@ref19],[@ref20],[@ref23]\]. Results of the 2011 to 2012 survey of a representative sample of 25,267 Canadian parents aged 16 to 65 years showed that 49% of parents have a low literacy level: \[[@ref89],[@ref90]\] they have difficulty finding, understanding, and using information presented in a dense or lengthy text; navigating complex digital texts; interpreting and evaluating information (constructing meaning); and disregarding irrelevant or inappropriate content when there is competing information (including when correct content is more prominent). Furthermore, our results may help any parent who faces a transitory low literacy level because of a stressful situation. This interdependence between information and emotion is well established in the information literature \[[@ref91],[@ref92]\]. Our project nevertheless does not focus on the few *information-poor* parents without access (direct or mediated) to online information. In the United States, only 1% of 18- to 29-year olds did not use the internet in 2015 \[[@ref93]\]. The Quebec 2015 survey of a representative sample of 23,693 parents of preschool children showed that only 1.5% of parents never know where to find child information \[[@ref61]\]. According to information studies, the *information-poor* parents (1) perceive themselves as persons who cannot be helped, (2) adopt self- or group-protective behaviors, (3) are secretive and mistrust others, and (4) consider exposure to information as a risk (harm outweighing benefits) \[[@ref30]\]. Our project engages a partnership between N&G and *AboutKidsHealth* (AKH) \[[@ref94]\], both popular comprehensive Web-based resources ([Table 1](#table1){ref-type="table"}). Both resources contain text with a readability level below high school (this level may be higher for disease-related information), visual illustrations, and complementary simple illustrative videos. For each Web page, an audio help system highlights words as they are spoken. In 2016, our librarian did an environmental scan of Canadian parental websites and found multiple specialized resources but only 12 comprehensive resources (including N&G and AKH). Although this study is a priority in a Canadian context, our results can be important to and applied by all Web editors who provide health information, thereby benefitting all adults with a low literacy level (not only parents). For example, Health Canada policies recommend funding projects that aim to improve access to, and conduct research on, information for Canadians with a low literacy level \[[@ref23]\]. Information systems are key components of health systems and crucial to meet human rights and the democratic right to know and communicate \[[@ref31],[@ref95]-[@ref100]\]. Among adults, the most frequent searches for information are about health \[[@ref101]\]. The demand for high-quality low-literacy health information is, hence, very high. Methods ======= Organizational Participatory Research Approach ---------------------------------------------- Our project uses an organizational participatory research (OPR) approach. OPR is a form of integrated knowledge translation that blends action research and organizational learning to undertake research with organizations and improve practice \[[@ref102]-[@ref107]\]. N&G (organization) proposed the research questions and will participate in all research steps. The NPI has OPR experience and expertise. The NPI led a CIHR-funded systematic review on OPR key processes and outcomes \[[@ref107]\]. A steering committee composed of the NPI, the coprincipal investigator, the partner (principal knowledge user), another knowledge user (AKH), and 2 low-SES parents will meet before and after each phase for planning and interpreting results, respectively. All team members will be consulted and have the opportunity to influence the steering committee's decision making. Methodology and Methods ----------------------- A mixed-methods multiphase design will be used \[[@ref108],[@ref109]\]. Ethical approval has been recently obtained from the institutional review board (IRB) of the Faculty of Medicine at McGill University (IRB\#A10-E69-17B). Phases 1, 3, and 4 will be informed by our theoretical model ([Figure 2](#figure2){ref-type="fig"}). ### Phase 1 (Objective 1): Identify Barriers and Facilitators to Use Naître et Grandir and Interact With Editors Via Information Assessment Method #### Design We will conduct an exploratory qualitative interpretive study to have a better understanding of barriers and facilitators in using N&G and interacting with editors via IAM \[[@ref110]\]. Qualitative research is appropriate as it provides in-depth descriptions from the stakeholders' viewpoint and helps researchers to understand their constitutive elements and variants \[[@ref111]\]. #### Setting and Participants Participants will be 20 users and 20 nonusers of IAM and N&G (additional participants will be recruited to achieve data saturation). First, users will be recruited among low-SES parents who indicate that they agree to be contacted when they complete an IAM questionnaire on N&G and who have used N&G and IAM at least once. N&G will send the group an invitation to participate in a research project via an email containing the research team's full identification and contact information. The research team will only communicate with N&G users who responded with an interest to participate in the research project via email or phone. Eligible parents will have no high school diploma and have an annual family income lower than Can \$40,000 (Quebec poverty line). Second, nonusers (10 who never used the IAM and 10 who never used N&G) will be recruited by a principal investigator (CL) and a collaborator (GD, N&G Director) who work with community organizations for parents with low SES. #### Data Collection A research assistant having experience in qualitative interviews with low-SES persons will conduct individual 60-min semistructured face-to-face interviews at the location of each participant's choice. In line with sociological and information studies \[[@ref112],[@ref113]\], interviews will explore how participants experience, conceptualize, perceive, and understand aspects of N&G information and the IAM. The interview guide will consist of open-ended questions addressing the participants' routines in terms of internet use (both for their personal and children's development information needs), their experience in the use of IAM and N&G's information, the facilitating aspects of N&G and IAM, perceived barriers in their experience, and suggestions to improve the N&G website and IAM. On the basis of the theoretical model, the interview guide will be developed in a simplified language with input from team members and the steering committee. We will conduct 2 pilot interviews to ensure the questions are comprehensible for the participants. The recruited respondents will receive Can \$20 as compensation for their time. In addition to the research assistant's observation notes, interviews will be audio recorded and transcribed verbatim. #### Data Analysis Two principal investigators (PP and CL) have experience in qualitative research and 1 (CL) has experience in qualitative research with populations in situations of vulnerability. With the research assistant and a research trainee, they will read notes and interviews and meet regularly to build memos (meeting minutes with arguments for and against each analytical decision, as rigor is mainly based on researchers' reflexivity in this design \[[@ref110]\]), case summaries, and themes (definitions and key examples) using hybrid deductive-inductive thematic analysis \[[@ref114],[@ref115]\]. The research assistant will manage the analysis using specialized software (NVivo11). Themes will be derived from our theoretical model ([Figure 2](#figure2){ref-type="fig"}; deductive coding) and emerge from the data (inductive coding). Major themes will be barriers and facilitators. For each type of participant (user/nonuser), additional parents will be recruited up to saturation (no new parents' views of barrier or facilitator). Then, we will harmonize themes \[[@ref116]\]. For each theme and definition, we will identify terms, confirm the usage of these terms in reference documents, distinguish correct from incorrect usage, and retain terms that facilitate unambiguous communication. This will lead us to classify, group, and clarify barriers and facilitators in a coherent taxonomy, which will be reviewed by team members and the steering committee. Findings will provide recommendations for improving IAM and N&G. ### Phase 2 (Objective 2): Improve Naître et Grandir and Information Assessment Method Two team members (FL and GD) are head directors of the N&G website and will lead this phase. Phase 1 findings will inform the production and implementation of IAM+N&G+ (user-centered design). This version will integrate the perspectives of low-SES parents, the steering committee, research team members, and N&G staff on how to overcome barriers and optimize facilitators. Production of this version will be planned with 2 Web editors and 2 Web engineers from the N&G team. According to Web engineers, 6 months is an ample time frame for production and beta testing. All necessary resources at N&G will be made available to implement IAM+N&G+. Two half-day meetings with principal investigators and N&G staff have been deemed sufficient to plan changes with editors and engineers. The N&G Director stated that she will implement what will be requested by the phase 1 participants, as her mandate (N&G mission) is to specifically address information needs of parents with low SES. For their part, AKH will redesign their website, integrate phase 1 results in this study, and implement IAM+. ### Phase 3 (Objective 3): Evaluate Use of Information Assessment Method+ Naître et Grandir+, Information Use, and Benefits #### Design We will conduct a quantitative prospective longitudinal study to evaluate the impact of the intervention (IAM+N&G+). #### Setting Weekly numbers of N&G sessions and IAM ratings will be monitored over 2 years. A session starts when someone opens a Web page and ends when the person (or a relative with the same IP address) does not use the website for more than 30 min. For each quintile of SES, data will be collected for 9 months preimplementation (IAM/N&G) and 9 months postimplementation (IAM+N&G+). To avoid bias related to the *novelty effect*, data collected in the 3 months immediately following the implementation will be excluded from the analysis. The chosen periods also ensure seasonal comparability of the collected outcome data (before and after intervention). #### Participants All N&G readers and IAM raters across Canada will participate. #### Measurement N&G and McGill already use Google Analytics, an objective and reliable automatic data collection of N&G readers' demographic characteristics and website use behavior (based on javascript codes in each Web page) \[[@ref117]-[@ref120]\]. IAM raters' demographic data are collected with a questionnaire (linked to an anonymized identifier). The validated IAM questionnaire \[[@ref53]\] collects self-reported information use and subsequent expected health/well-being benefits for parents and their child. ###### Types of outcomes monitored weekly. Type Outcome Description and data source ------ ------------------- ----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------- A1 N&G^a^ sessions Weekly number of unique sessions (Google Analytics) A2 N&G read Weekly proportion of sessions with at least 1 page entirely read (Google Analytics) A3 IAM^b^ ratings Weekly number of IAM questionnaires submitted B1 N&G mediated Weekly proportion of IAM ratings information used for the child of someone else B2 N&G used Weekly proportion of IAM ratings information used for oneself and one's child C Expected benefits Weekly proportion of IAM ratings expected health or well-being benefit for a parent and child, including at least 1 of the following self-perceived benefits (IAM choices of response): improvement of the health or well-being of a child, being less worried, prevention of a problem or the worsening of a problem, handling a problem, and being more confident to decide something with someone else ^a^N&G: *Naître et grandir*. ^b^IAM: Information Assessment Method. #### Outcomes In line with CIHR knowledge translation guidance \[[@ref54]\], 3 types of outcomes will be considered weekly ([Table 2](#table2){ref-type="table"}): (A) N&G and IAM use, (B) self-reported N&G information use, and (C) subsequent expected benefits. #### Covariates The main predictor will be participants' SES as determined by the Quebec Index of Material and Social Deprivation, a validated ecological measure of the (education, income, and employment) disadvantage of a given geographic area (postal code) \[[@ref121],[@ref122]\]. For each session, an index will be automatically assigned using (1) the reported postal code and the Canadian Deprivation Index Assignment Program (CDIAP) of the Public Health Agency of Canada when the data source is IAM and (2) the postal code matched to the session geotag via the "Dissemination Area Boundary File" of Statistics Canada and the CDIAP when the data source is Google Analytics. This will allow for the identification of low-SES participants (highest quintile of material and social deprivation). Using Google Analytics, participants' demographic variables that will be considered in all analyses are age, gender, rural/urban location, and province. In addition, Web page--specific variables will be included to assess potential confounding and effect modifications. For each session, the type of device (Google Analytics: phone, tablet or laptop, and desktop), the audio-guide use (Google Analytics: yes or no), and the readability score of pages entirely read (automatic extraction and measurement using a text classifier validated for French) \[[@ref123]\] will be collected. #### Study Size On the basis of our 2-year pilot data (2014/09-2016/08), we anticipate about 5 million N&G sessions and 15,000 IAM ratings from Canadian participants during each period (pre- and postimplementation). #### Anticipated Results The IAM+N&G+ will result in an increase of all outcomes (N&G and IAM use, self-reported N&G information use, and subsequent expected health and well-being benefits for parents and children such as *decreased worries* and *health improvement*, respectively). #### Statistical Analysis Linear mixed modeling will integrate spatial analytics (geomatics) and account for the clustered nature of the data. The pre/post status, the SES quintile of deprivation, and potentially confounding variables will be included as fixed-effects covariates. The inference model will incorporate random effect terms for individual variables and Web page--specific variables. For each outcome, an interaction term of the SES quintile of deprivation and the pre/post status will be included to assess the pre/post change for each quintile. Estimated regression coefficients and variance parameters will be reported along with appropriate confidence intervals. ### Phase 4 (Objective 4): Describe Parent and Child Outcomes of Naître et Grandir+ Information Use #### Design We will conduct a qualitative interpretive study to generate an in-depth description of parent and child outcomes from the parents' perspective \[[@ref124]\]. On the basis of our systematic review \[[@ref66],[@ref67]\], we anticipate 3 types of parent outcomes (decreased worries, increased confidence, and self-management) and 2 types of child outcomes (prevented problem and improved development, health, and well-being). Our pilot data (34,021 IAM ratings) also suggest parents rarely report potential negative consequences of using information, for example, vaccine adverse effect (n=183; 0.5%). In outcomes research, qualitative methods are appropriate for exploring complex outcomes from the stakeholders' perspective, such as life experiences \[[@ref111],[@ref125]-[@ref131]\]. In our study, information can influence parent decision making, but the relationship between information and decision is not simple. Our qualitative study will (1) identify causal events, (2) map them in a complex causal network, and (3) build a chronological chain of qualitative evidence between N&G information and a parents' decision that affects knowledge, attitude, or behavior \[[@ref131],[@ref132]\]. #### Participants Participants who received the N&G+ newsletter, used IAM+ at least once, have agreed to be contacted for research, and live in a high deprivation area will be approached for recruitment. The recruitment procedure will be the same as for phase 1. In 2015, more than 24,000 families received, upon request, the weekly newsletter. We will begin by recruiting 30 parents (and continue recruitment, as needed, to achieve data saturation) who report, via IAM+, positive health and well-being outcomes and/or potential negative consequences of information (prioritizing those who live in the areas of highest deprivation). As we are looking for individual stories for about 6 types of outcomes (some less frequently reported than others), data saturation may not be reached with fewer than 50 participants \[[@ref111],[@ref133]-[@ref135]\]. #### Data Collection The research assistant having experience in qualitative interviews with low-SES persons will conduct 60-min face-to-face interviews to elicit participants' IAM+ ratings. The interview guide will be based on our theoretical model ([Figure 2](#figure2){ref-type="fig"}) and input from team members and the steering committee. To stimulate recall (memory), the interviewee will be given the list of recent texts they rated and their ratings. For each newsletter, the research assistant will ask open questions regarding what happened to them and/or their children that led them to report an expected outcome (positive or negative). Participants will be interviewed twice 3 months apart to increase the number of described outcomes and avoid fatigue of long interviews. Participants will receive Can \$20 per interview as compensation for their time. In addition to the research assistant's observation notes, interviews will be audio recorded and transcribed verbatim. #### Data Analysis Two principal investigators (PP and CL) have experience in qualitative research. With the research assistant, a collaborator anthropologist having expertise in life histories (MB) and a research trainee will read notes and interviews and meet regularly. For each case (information used with at least 1 outcome experienced by a parent and a child), they will interpret the data in the form of a *small story* \[[@ref112],[@ref136]-[@ref138]\]. This method allows researchers to describe a person's individual experience (including all perceived influences) and helps the researcher understand the individual's attitude and behavior \[[@ref33]\]. In research meetings, 2 questions will be answered through recorded discussion of arguments for and against each analytical decision (rigor based on sharing reflexivity): is the case story clear? and are the causal network and chain of evidence trustworthy? Disagreements about clarity and trustworthiness of case stories will be resolved with 3 other team members having experience in qualitative research (Bouthillier, Thoër, and Smythe). Case stories will be reviewed by all team members and the steering committee. This may detect issues and result in the principal investigators and research assistant revising parts of their analysis. #### Anticipated Results This will generate up to 10 case stories per outcome type, being the first in-depth qualitative description of low-SES parents' perspective on outcomes of online child information use. Results ======= The project was funded in 2017 by the CIHR and received an ethics approval by the McGill University's IRB. Data collection for phase 1 was completed in 2018. Phases 2 to 4 will be completed by 2020. Findings from this study will be used to develop a free toolkit, useful to all Web editors, with recommendations for improving health information for low-SES persons and interactions with them using IAM. Results will be published in peer-reviewed journals and presented at national and international scientific conferences. Discussion ========== Direct Impact on *Naître et grandir* and *AboutKidsHealth* ---------------------------------------------------------- Any improvement of knowledge translation tools and websites such as IAM, N&G, and AKH can have an important impact as it affects a large population of individuals with a low literacy level. In fact, the effectiveness of childhood education interventions has been demonstrated repeatedly \[[@ref16]-[@ref19],[@ref23],[@ref27]-[@ref47]\]. In our 2-year pilot data, parents expected health and well-being benefits (for themselves or their child) from using N&G information in 65.4% of all IAM ratings (n=34,021) \[[@ref50]\]. In accordance with knowledge translation and implementation research \[[@ref62]\], we will not replicate effectiveness studies and rather focus on improving interventions that work. Our project can improve engagement (number of visits) with websites providing high-quality low literacy information; in turn, online parenting information improves parents' knowledge, attitudes, and behaviors \[[@ref139]-[@ref145]\]. Given our integrated knowledge translation (participatory research) approach, N&G and AKH will adapt their content for low-SES users as we generate results. In addition, IAM+ will better support low-SES parents' interactions with Web editors and empowerment. Thus, our results can immediately benefit millions of information users with a low literacy level (children's parents and relatives), for example, in Canada ([Table 3](#table3){ref-type="table"}). IAM+N&G+ can be seen as an innovative intervention that complements traditional literacy programs (eg, family literacy classes). Indeed, interventions that somewhat compensate for a low literacy level can greatly improve parents' and children's health and well-being \[[@ref23]\]. Thus, our results can have a positive impact on 55% of the Canadian working age, those who have a low level of *health literacy* and need compensatory help to manage their health \[[@ref23],[@ref89],[@ref90]\]. Specifically, IAM+N&G+ can help Canadians in francophone minority communities, as 500,000 annual N&G website visits originate from them. Research with these communities is very underfunded, thus a CIHR priority \[[@ref146]\]. As stated in the October 2016 report of the Commissioner of Official Languages \[[@ref147]\], early childhood development in these communities *is hindered by a lack of resources*, and *the absence of specific funding* has left them *vulnerable and often incapable of meeting their needs*. ###### Targeted population in Canada. Across Canada IAM^a^ *Naître et grandir* (new version) IAM *AboutKidsHealth* (new version) ------------------------------------- ---------------------------------------------------------------------------------------------------------------------------- --------------------------------------------------------------------------------------------------------------- Families^b^ 1.3 million families have French as mother tongue (couples with children and single-parent families with at least 1 child) 5.8 million families (couples with children and single-parent families with at least 1 child)---all languages Children's parents and relatives^b^ 2.8 million adults aged 20 to 69 years have a low literacy level (and French as mother tongue) 12 million adults aged 20 to 69 years have a low literacy level Website visits from Canada 8.3 million^c^ visits in 2015 mainly from Quebec (7.8 million), Ontario (304,000), and New Brunswick (70,000) 1.5 million visits in 2015 mainly on Web pages in English (58%), French (16%), Spanish (14%), and Arabic (5%) ^a^IAM: Information Assessment Method. ^b^Statistics Canada 2015. ^c^76% of parents of children aged under 8 years consult *Naître et grandir* in Quebec (on average 1.3 times per week). Potential Impact Beyond *Naître et grandir* and *AboutKidsHealth* ----------------------------------------------------------------- Results will inform the development of an open access online tool kit on how to adapt websites and IAM+ for a low literacy audience (a growing consideration of many Web editors). The tool kit will be designed to be generalizable to all types of online consumer health information in Canada. It will include guidance with 3 main messages: (1) how to produce simple information in lay language with audio and visual content, (2) how to better interact with low-SES persons using IAM+, and (3) how to use consumers' IAM+ ratings and feedback to continuously optimize information content. The tool kit will be freely available to any Web editor via the Quebec SPOR-SUPPORT Unit and IAM websites. The NPI has experience in developing tools and leads the method development platform of the Quebec SPOR- SUPPORT Unit. Our primary knowledge translation goal for knowledge user audiences will be to raise awareness about our main messages and drive attention to the tool kit. A secondary knowledge translation goal will be to support the implementation of the toolkit by Web editors. Knowledge users will disseminate our work in multiple Canadian organizations. As per reviews on scaling up \[[@ref148]-[@ref150]\], we will update our 2016 environmental scan and contact all Canadian websites targeting parents. A specialized librarian (collaborator) will reach additional health websites through librarian listservs and peer networks. Team members will raise general awareness for the tool kit and deliver our main messages to a variety of academic and nonacademic knowledge user audiences via a range of knowledge translation strategies (conference presentations, open access peer-reviewed publications, plain language summaries and grey literature, social media, and networks). Multiple knowledge translation channels will be used including Twitter (\@UniteSoutien) and websites such as the Quebec SPOR-SUPPORT Unit and the IAM websites \[[@ref151],[@ref152]\]. Contribution to Scientific Knowledge ------------------------------------ Our project will advance knowledge on the value of online information for, and interaction with, low-SES persons to strengthen health systems. On the one hand, this project is the first to systematically explore health and well-being outcomes for low-SES parents and children associated with parenting information websites. Most studies focus on discussion forums that can be intimidating to low-SES parents \[[@ref140],[@ref142],[@ref143],[@ref153],[@ref154]\]. On the other hand, many studies concern relational marketing and website feedback buttons \[[@ref52],[@ref155]-[@ref158]\], but we know of none that addresses interactions between low-SES persons and Web editors (such as interaction through IAM+). Timeline and Potential Challenges --------------------------------- Overall, 3 years will be needed to complete this project ([Figure 3](#figure3){ref-type="fig"}). Our phases are simple and well defined, and our planning is realistic. In phases 1 and 4, we anticipate no recruitment difficulties. Many parents have already agreed to be contacted for research, and N&G will facilitate the recruitment. Phase 2 is feasible, and the deliverables are realistic given that N&G has already implemented IAM, McGill and N&G have a strong OPR partnership, and N&G is committed to implementing IAM+N&G+. In phase 3, the large number of N&G readers guarantee a large sample. To control for potential seasonal variation in the number of sessions pre- and postimplementation, monitoring will be conducted during the same seasons. To control for contextual changes, variables such as type of device, age, gender, and location are covariates. We have opted for a prospective longitudinal study as monitoring is embedded in N&G routines. In addition, although randomization would provide a higher level of evidence, it was considered unethical to randomly assign low-SES parents to N&G+ or N&G information and impractical for such a popular website (contamination bias) \[[@ref159]\]. Moreover, 3 typical potential sources of biases in longitudinal designs may not affect our study: the use of proportions will control for historical events, there will be no *respondent fatigue* as our 2-year pilot data showed that the monthly number of IAM raters is stable, and the social desirability bias will affect pre- and postimplementation periods in a similar manner. {#figure3} Considering the commitment, expertise, and networks of our team, we expect no major challenges. This project is highly facilitated by the participatory research approach (a form of integrated knowledge translation). In addition, it is sustainable as our results will be applied and sustained by 2 longstanding organizations. N&G is fully funded since 1998 by the Lucie et André Chagnon Foundation (one of the largest philanthropic agencies in Canada) and is a priority of this foundation. AKH is owned by the Hospital for Sick Children (Toronto) and is fully funded since 2004 by multiple maternal and child health agencies. Conclusions ----------- The results of this study will provide a deep understanding of how low-SES parents use online child information and interact with Web editors. Following the implementation of IAM+N&G+, results will also elucidate subsequent health outcomes for low-SES parents and children after interaction with Web editors have been optimized. Thus, our results can immediately benefit millions of information users, children's parents and relatives in particular, with a low literacy level. The authors wish to thank Dr Suzanne Smythe (Simon Fraser University, Canada), Mr Sean Schurr (AboutKidsHealth, Canada), Maria de Carmen Reyes (Centro de Investigación en Geografía y Geomática, Mexico), and Ms Catherine Chouinard (Avenir d'enfants, Canada) for their collaboration in developing this proposal. N&G is funded by the philanthropic organization "Fondation Lucie et André Chagnon." PP holds an investigator salary award from the Fonds de recherche en santé du Québec. This study has been funded by the CIHR (\#PJT153200). Conflicts of Interest: None declared. AKH : AboutKidsHealth CDIAP : Canadian Deprivation Index Assignment Program CIHR : Canadian Institutes of Health Research IAM : Information Assessment Method IRB : institutional review board N&G : Naître et grandir NPI : nominated principal investigator OPR : organizational participatory research SES : socioeconomic status

This invention relates to a demodulator for a code-division multiple-access (CDMA) communication system of the block-spreading type. CDMA is a spread-spectrum system employed in personal communication systems and other mobile communication systems, in which multiple stations transmit simultaneously over the same frequency band. In a block-spreading CDMA system, data to be transmitted are divided for modulation into P-bit blocks. Each block is converted to a Q-chip codeword, which is then further modulated by a spreading code to generate a baseband transmit signal. (P and Q are positive integers.) The Q-chip codewords are mutually orthogonal and are the same at all transmitting stations, but each station uses a different spreading code. A receiver demodulates the data transmitted from a particular station by, for example, multiplying the incoming baseband signal by that station's spreading code, correlating each resulting block with all possible codewords, and selecting the codeword that gives the highest correlation. It is known that the channel capacity of such a system can be improved if the receiver takes steps to cancel interference between different transmitting stations. One interference-canceling system relies on the fact that signals from different transmitting stations usually arrive with different strengths. The receiver first demodulates the strongest signal, then cancels it out as interference and demodulates the strongest remaining signal, continuing in this way until all signals have been demodulated. Unfortunately, this system does not work well when several signals arrive with substantially the same strength. Another possible system demodulates the signals from all transmitting stations in parallel, subtracting the estimated interference generated by each station from the signals of all the other stations. The process can be iterated to obtain increasingly accurate estimates of the transmitted signals and their interference. This system appears to work well in theory, but when its actual behavior is simulated it performs poorly, because it fails to take maximum advantage of the available interference information. The initial estimates of interference from a given station, for example, are always derived from a signal from which interference has not yet been removed.

Richard Hart Brown Richard Hart Brown (June 15, 1941 – June 23, 2005) was a founder of Interoperative Neurophysiological Monitoring and a leading expert on Amusement Ride and Roller Coaster safety. He was a founder of ASNM | American Soc of Neurophysiologic Monitoring and a charter member of the ABNM | ABNM American Board of Neurophysiologic Monitoring he was a member of many ANSI boards relating to materials and Amusement Ride Safety. References External links Los Angeles Times Obituary Find A Grave Category:1941 births Category:2005 deaths Category:American neuroscientists

Do you avoid adopting from an animal shelter because you worry about behavior issues or because you want a specific breed? Or maybe you'd like something other than a cat or dog? We have some great news for you. READ MORE Advertisement The Human Equivalent of Feeding Your Pet Snacks By Amanda Baltazar You hear a whine from under the dinner table and there sits your poor dog waiting for you to toss him a metaphorical bone — or maybe even a real one. But what you have is a cookie, so you toss him that instead. No harm done, right, it’s only a cookie? In fact, given the size difference of humans and animals, a small portion of something for us can almost constitute a meal for your dog or cat. Our pets need remarkably few calories compared to our own caloric needs. Read on to see what different snacks mean in human terms when you feed them to your pet. WARNING: Consult your vet before providing any "human food" as some may be dangerous for pets. 1. Oatmeal Cookie One small oatmeal cookie for a 20 pound dog is the caloric equivalent of an entire hamburger for a person. For a human, that’s around 300 calories, or almost a sixth of the average woman’s recommended daily calories and an eighth of man’s daily calorie intake. It could be worse, though: An oatmeal cookie at least provides some fiber — chocolate chip cookies, meanwhile, are a definite no-no since chocolate is harmful, and even toxic, to dogs. 2. Hot Dog One hot dog for a 20 pound puppy is the caloric equivalent of three hamburgers for a person. That single hot dog may not look like much but it has around 175 calories, which is a third of what a 20 pound dog should be consuming. “I think people get gratification out of their pet eating and being happy about it, but they don’t think about the long-term consequences,” says Dr. James Darden, DVM, chief of staff at Banfield Pet Hospital in East Houston, Texas. 3. Cheese One ounce of cheese for a 20 pound dog is the caloric equivalent of 1 ½ chocolate bars for a person. Cheese is loaded with fat — a single 1 oz. slice of American cheese packs 105 calories and 5.5 grams of saturated fat, while Cheddar is even worse: 114 calories and 6 grams of fat. That ounce of cheese constitutes about a third of a small dog’s daily required calories, says Dr. Darden. “And for a cat it’s worse — it’s about half his daily caloric intake, so two slices of cheese for a cat is all it needs in a day.” 4. Potato Chip One potato chip for a 10 pound cat is the caloric equivalent of half a hamburger for a person. You may think that a thin potato chip is lighter than air, but don’t forget that it’s been fried in saturated fat and coated in sodium. For your small cat, you’re almost providing lunch with a potato chip. A superior option, says Dr. Darden, is a small handful of kibble. He suggests you subtract whatever you feed your cat as a snack from her evening meal so she doesn’t overeat. 5. Cup of Milk One cup of milk for a 10 pound cat is the caloric equivalent of five chocolate bars for a person. Besides the fact that whole milk provides 122 calories per cup — and even skim clocks in at 86 calories — neither dogs nor cats should drink it because it can upset their stomach, says Dr. Darden. A good alternative is fruits or vegetables, especially frozen, such as green beans, peas, and apples. (Ed. Note: Consult your vet before providing any "human food," as some fruits and vegetables are dangerous for pets.) 6. Peanut Butter A single ounce of peanut butter (about a tablespoon) is close to cheese in calories, packing around 94 calories. It also contains around 8 grams of saturated fat, which is 12% of what a human needs, and of course far higher for a dog or cat. Just 8 to 10 tablespoons of seemingly innocuous peanut butter may be delicious, but it would provide all the calories a 30 pound dog should eat in a single day. And for a 10 pound dog, just three tablespoons would fulfill his daily caloric requirements. 7. Jerky Strips Jerky strips are beloved by dog owners because they’re easy and make no mess, but a single jerky strip provides around 88 calories. “So three of them for a small dog provides most of his caloric needs without any [significant nutritional value],” says Dr. Darden. “Every time you give one of these treats you’re filling him up with extra calories and making our obesity numbers increase.” Jerky strips are also very high in sodium (providing around 12% of a human’s daily sodium needs), which can lead to high blood pressure in both dogs and cats. 8. Tuna Almost every cat loves tuna, but at 36 calories per ounce she shouldn’t be eating much of it, if at all. Despite the fact that tuna is a good lean protein source, it’s not providing a balanced diet, says Darden. An ounce of tuna provides about 16% of the daily calories required for a 10 pound cat, he adds. “I’d stick with premium [pet food] brands rather than getting tuna off the shelf and preparing it myself.” What About Pet Treats? Commercial pet treats are okay in moderation and if they are of high quality. Ask your veterinarian for some recommendations and don't forget to subtract the treat's calories from your pet's overall daily calorie consumption so he or she doesn't inadvertently become overweight. Comments 3 Hi, I have to admit that i feed my dog too much. I don't really know how many calories she should eat per day; she's overweight and 9 yrs. old. The vet has told us to cut back, but she has built up a ferocious appetite! We give her half a can of "Mighty Dog" in the morning and the other half at night and some treats in-between and when she "makes" outside, (she doesn't make in the house lol). i love her and really want to help her lose weight :( She's half miniature doberman pinscher and half dachshund and she's adorable, it's just that her head is so much smaller than her body :( Switch Mighty Dog to a high quality diet food and make sure those treats are TINY. The dog is happy because you are giving her a treat, not because it is big. Consider slicing some carrots or apples into small pieces and having them handy. Frozen peas can also be a great treat. And do not give up if your dog immediately turns up her nose at the diet food. You are weaning her from the equivalent of McD's to a healthy weight-control diet and it may take some time. A dog will not starve itself to death. Continue to offer NOTHING but the new food and she will cave and eat it within 2-3 days. A little tough-love is important sometimes. Dividing the same amount of food into 3 daily feedings instead of 2 can also help. Few things will help your pet live longer, healthier, happier lives than being at a lean body weight. It will also save you vet bills down the road. Google "Purina Life Span Study" to learn more. Good luck!

Familial hypercholesterolemia among unselected contemporary patients presenting with first myocardial infarction: Prevalence, risk factor burden, and impact on age at presentation. Familial hypercholesterolemia (FH) is a hereditary disease carrying a substantial lifetime risk of coronary heart disease. To assess the prevalence of FH and its impact on age at presentation among unselected patients with first myocardial infarction (MI). In a multi-center cross sectional study, we identified 1381 unselected patients presenting with a first MI between 2010 and 2012. Clinical FH was assessed using both the Dutch Lipid Clinic Network (DLCN) criteria and the Simon Broome criteria. Based on the DLCN criteria, 2.0% of patients with first MI had "probable/definite" FH, whereas 4.7% had "possible" FH according to the Simon Broome criteria. In the 291 (21%) patients with premature MI, 6.9% had "probable/definite" FH (DLCN criteria), and 11.0% had "possible" FH (Simon Broome criteria). Nearly all premature "probable/definite" and "possible" FH patients had at least one additional marker of high cardiovascular risk including current smoking (72%-80%) and hypertension (40%-44%). In multivariable-adjusted linear regression modeling, patients with "probable/definite" FH using DLCN criteria had their first MI 14.6 years (95% confidence interval [CI], 9.6-19.6 years) earlier than non-FH patients. Likewise, "possible" FH patients using Simon Broome criteria were associated with having an MI 9.1 years (95% CI = 6.3-12.4) earlier than non-FH patients. Clinical FH is common and associated with markedly earlier age of first MI, especially when combined with additional markers of high risk, indicating an unmet need for earlier identification of FH to ensure global risk factor control. First MI constitutes a unique opportunity to detect families with unknown FH.

Lewis Hamilton (footballer) Lewis Emmanuel Hamilton (born 21 November 1984) is an English footballer who plays for Horsham. Playing career Hamilton made his Football League debut for Queens Park Rangers in the Championship after coming on as a substitute against Burnley at Turf Moor on 19 April 2005. He then moved to Aldershot Town, and then Lewes, where he was part of the 2007–08 Conference South winning side. Hamilton signed for Tonbridge Angels in July 2008 after a successful trial. Hamilton left Tonbridge in December 2009 and subsequently rejoined Lewes. Hamilton signed for Isthmian League side Horsham at the start of the 2013–14 campaign. Honours Lewes Conference South Champion: 2007–08 References External links Lewis Hamilton profile from tonbridgeangels.co.uk Lewis Hamilton profile from qpr.co.uk Lewis Hamilton plays in the FA Cup, TheMirror.co.uk Category:1984 births Category:Living people Category:Sportspeople from Derby Category:English footballers Category:Association football defenders Category:Derby County F.C. players Category:Queens Park Rangers F.C. players Category:Aldershot Town F.C. players Category:Lewes F.C. players Category:Tonbridge Angels F.C. players Category:English Football League players Category:National League (English football) players Category:Horsham F.C. players

The cheering echoes still throughout librarianship. Recent court decisions—such as the HathiTrust’s win over the Authors Guild—strengthen the use of the concept of “fair use” to exempt from copyright the reproduction of material, liberate the free digitization of so-called “orphan works,” and allow free public access to the results. Yet even those cheering the loudest caution that there are still no definitive rules to apply to these victories. The victories are yet evidence of the value of well-organized efforts to prevent copyright from locking up our intellectual and cultural resources. The leaders of the Library Copyright Alliance (LCA), comprised of the Association of Research Libraries, the American Library Association (ALA), and the Association of College and Research Libraries (an ALA division), deserve the cheers and the continuing support of librarians. A huge, much more important question lurks over the entire struggle. We have to participate in the ongoing effort to decide whether the digital brave new world into which we are moving will offer people more freedom of access to information and entertainment, or confine our intellectual resources in a maze of impenetrable legal walls that could ultimately end much of the intellectual freedom we have enjoyed through the print era. Is technology liberating information, or will it allow special interests to use the law to deny access to it? Currently there are many attempts to create models for a digital information future. In most of them, the concept of a book collection is replaced by a universal online catalog of digitized works that everyone can simply tap for downloading onto their own devices. The problem is that many will not be able to afford the fees for such access. Proposed models that require us to pay for each use of our intellectual resources are far more plentiful than those that let us pay once for all of our uses of them. In the print era, individual purchase and ownership of a work allowed the owner and borrowers to use that work in any way they wished. It could be sold, given away, lent, or locked away by the “owner.” The inexorable march to digitization has already challenged those rights of ownership and in some proposed models it eliminates them altogether. Right now it looks like the intermediaries—vendors, publishers, wholesalers, et al.—have taken control through contracts and laws, giving them temporary power to dictate pay-per-view rules for the dissemination of digital material. I say “temporary,” because it is now clear that courts, legislatures, organizations of stakeholders and interested parties, and creators can bring pressures to bear to change the operating model. It would be foolish to predict the result of these struggles so early in the game. It took centuries for us to develop the fragile system of copyright and custom that gave us the existing scheme for information and entertainment in physical formats. When all that information and entertainment float in a digital cloud of bits and bytes, it will be more difficult to create a set of rules for their use. Many take comfort in the thought that the familiar physical formats, especially printed books, will continue to be around for a long time. They say the “book” will never disappear. The arrival now of technological change with accelerating speed means it is time to safeguard our values in the new ­paradigm. We can predict that while it may be a long struggle, change will come faster than we expect. For those of us who believe in free, open access to the information and entertainment that make up our culture, we must work with strong groups like LCA to guarantee that the coming upheaval liberates access to our intellectual assets. Along with allies and constant vigilance, we can fight off any effort to control our intellectual legacy by those who seek to use it for monetary gain. It is our duty to ensure that as technology marches on, we use it to allow our cultural resources to be accessed more freely, not locked up in an economic prison. John N. Berry III Editor-at-Large This article was published in Library Journal. Subscribe today and save up to 35% off the regular subscription rate. About John N. Berry III John N. Berry III ([email protected]) is Editor-at-Large, LJ. Berry joined the magazine in 1964 as Assistant Editor, becoming editor-in-Chief in 1969 and serving in that role until 2006. Comments From the above: In the print era, individual purchase and ownership of a work allowed the owner and borrowers to use that work in any way they wished. It could be sold, given away, lent, or locked away by the “owner.” … but Mr. Berry does not include in his list the right to reproduce & distribute. The following is from the 26MAR2012 version of the Copyright Limitations & Exceptions Treaty as proposed by the IFLA at WIPO — now since modified — while the IFLA WIPO delegation was headed by the past president of the ARL: Article 7 — Right to Reproduction and Supply of Copies by Libraries and Archives 1) It shall be permitted for a library or archive to reproduce and to supply a copy of a copyright work, or of material protected by related rights, to a library or archive user, or to another library or archive in connection with a request by a user at that library or archive, for the purpose of education, research, or private use, provided that such reproduction and supply is in accordance with fair practice. In this essay, Berry is addressing half of the issue. Even as content owners seek to restrict users’ rights via restrictive licensing agreements on the one hand, socially produced content (open access, creative commons, etc.) is freeing up content on the other hand. As Stewart Brand famously stated in The Media Lab, “Information wants to be free. Information also wants to be expensive.” The point is, we do have options to expand and improve socially-constructed, freely accessible content, even as we work to preserve user rights under commercial licenses.

require "backup/config/dsl" require "backup/config/helpers" module Backup module Config class Error < Backup::Error; end DEFAULTS = { config_file: "config.rb", data_path: ".data", tmp_path: ".tmp" } class << self include Utilities::Helpers attr_reader :user, :root_path, :config_file, :data_path, :tmp_path # Loads the user's +config.rb+ and all model files. def load(options = {}) update(options) # from the command line unless File.exist?(config_file) raise Error, "Could not find configuration file: '#{config_file}'." end config = File.read(config_file) version = Backup::VERSION.split(".").first unless config =~ /^# Backup v#{ version }\.x Configuration$/ raise Error, <<-EOS Invalid Configuration File The configuration file at '#{config_file}' does not appear to be a Backup v#{version}.x configuration file. If you have upgraded to v#{version}.x from a previous version, you need to upgrade your configuration file. Please see the instructions for upgrading in the Backup documentation. EOS end dsl = DSL.new dsl.instance_eval(config, config_file) update(dsl._config_options) # from config.rb update(options) # command line takes precedence Dir[File.join(File.dirname(config_file), "models", "*.rb")].each do |model| dsl.instance_eval(File.read(model), model) end end def hostname @hostname ||= run(utility(:hostname)) end private # If :root_path is set in the options, all paths will be updated. # Otherwise, only the paths given will be updated. def update(options = {}) root_path = options[:root_path].to_s.strip new_root = root_path.empty? ? false : set_root_path(root_path) DEFAULTS.each do |name, ending| set_path_variable(name, options[name], ending, new_root) end end # Sets the @root_path to the given +path+ and returns it. # Raises an error if the given +path+ does not exist. def set_root_path(path) # allows #reset! to set the default @root_path, # then use #update to set all other paths, # without requiring that @root_path exist. return @root_path if path == @root_path path = File.expand_path(path) unless File.directory?(path) raise Error, <<-EOS Root Path Not Found When specifying a --root-path, the path must exist. Path was: #{path} EOS end @root_path = path end def set_path_variable(name, path, ending, root_path) # strip any trailing '/' in case the user supplied this as part of # an absolute path, so we can match it against File.expand_path() path = path.to_s.sub(/\/\s*$/, "").lstrip new_path = false # If no path is given, the variable will not be set/updated # unless a root_path was given. In which case the value will # be updated with our default ending. if path.empty? new_path = File.join(root_path, ending) if root_path else # When a path is given, the variable will be set/updated. # If the path is relative, it will be joined with root_path (if given), # or expanded relative to PWD. new_path = File.expand_path(path) unless path == new_path new_path = File.join(root_path, path) if root_path end end instance_variable_set(:"@#{name}", new_path) if new_path end def reset! @user = ENV["USER"] || Etc.getpwuid.name @root_path = File.join(File.expand_path(ENV["HOME"] || ""), "Backup") update(root_path: @root_path) end end reset! # set defaults on load end end

Posts tagged with: retribution If God wants to make my happiness complete, he will grant me the joy of seeing some six or seven of my enemies hanging from those trees. Before their death I shall, moved in my heart, forgive them all the wrong they did me in their lifetime. One must, it is true, forgive one’s enemies – but not before they have been hanged. Richard John Neuhaus, over at the First Things blog On The Square, posts an excerpt from the upcoming print edition that excoriates the NAB translation (also noted at Mere Comments). Neuhaus writes of Jesus’ answer in Matt. 18:22 to Peter’s question, “Lord, how many times shall I forgive my brother when he sins against me? Up to seven times?” that “Jesus obviously intended hyperbole, indicating that forgiveness is open-ended. Keep on forgiving as you are forgiven by God, for God’s forgiving is beyond measure or counting.” It’s not so much that I think that Neuhaus’ comment is wrong as I think it misses perhaps the primary allusion in Jesus’ statement: a reversal of the commitment to escalating retribution that marks Lamech’s legacy. Thus we read in Genesis 4:23-24 of Lamech, “I have killed a man for wounding me, a young man for injuring me. If Cain is avenged seven times, then Lamech seventy-seven times.”

Q: Replacing text globally with line break in React Native/Javascript I want to replace an xml tag <Add with \n<Add so that it open a new line for every <Add. However I tried .replace(/\<Add/g, '\n') It shows a blank screen. I also tried replace it once .replace('\<Add', '\n') It works with the first <Add replaced by line break. But I need to reaplce all <Add with a line break... Why I can't replace text with "\n" globally? How can I do it in react native? A: Considering: .replace('\<Add', '\n') Works for the first, but not others, do the replacement using the global flag: .replace(/(<Add)/g, '\n$1')

// CodeContracts // // Copyright (c) Microsoft Corporation // // All rights reserved. // // MIT License // // Permission is hereby granted, free of charge, to any person obtaining a copy of this software and associated documentation files (the "Software"), to deal in the Software without restriction, including without limitation the rights to use, copy, modify, merge, publish, distribute, sublicense, and/or sell copies of the Software, and to permit persons to whom the Software is furnished to do so, subject to the following conditions: // // The above copyright notice and this permission notice shall be included in all copies or substantial portions of the Software. // // THE SOFTWARE IS PROVIDED *AS IS*, WITHOUT WARRANTY OF ANY KIND, EXPRESS OR IMPLIED, INCLUDING BUT NOT LIMITED TO THE WARRANTIES OF MERCHANTABILITY, FITNESS FOR A PARTICULAR PURPOSE AND NONINFRINGEMENT. IN NO EVENT SHALL THE AUTHORS OR COPYRIGHT HOLDERS BE LIABLE FOR ANY CLAIM, DAMAGES OR OTHER LIABILITY, WHETHER IN AN ACTION OF CONTRACT, TORT OR OTHERWISE, ARISING FROM, OUT OF OR IN CONNECTION WITH THE SOFTWARE OR THE USE OR OTHER DEALINGS IN THE SOFTWARE. using System; using System.Collections.Generic; using System.Text; using System.Diagnostics.Contracts; namespace Tests.Sources { [ContractClass(typeof(GenericAbstractClassContracts<,>))] public abstract class GenericAbstractClass<A,B> where A: class,B { public abstract bool IsMatch(B b, A a); public abstract B ReturnFirst(B[] args, A match, bool behave); public abstract A[][] Collection(int x, int y); public abstract A FirstNonNullMatch(bool behave, A[] elems); public abstract C[] GenericMethod<C>(A[] elems); } [ContractClassFor(typeof(GenericAbstractClass<,>))] internal abstract class GenericAbstractClassContracts<A,B> : GenericAbstractClass<A,B> where A : class, B { public override bool IsMatch(B b, A a) { throw new NotImplementedException(); } public override B ReturnFirst(B[] args, A match, bool behave) { Contract.Requires(args != null); Contract.Requires(args.Length > 0); Contract.Ensures(Contract.Exists(0, args.Length, i => args[i].Equals(Contract.Result<B>()) && IsMatch(args[i], match))); return default(B); } public override A[][] Collection(int x, int y) { Contract.Ensures(Contract.ForAll(Contract.Result<A[][]>(), nested => nested != null && nested.Length == y && Contract.ForAll(nested, elem => elem != null))); Contract.Ensures(Contract.ForAll(0, x, index => Contract.Result<A[][]>()[index] != null)); throw new NotImplementedException(); } public override A FirstNonNullMatch(bool behave, A[] elems) { // meaningless, but testing our closures, in particular inner one with a static closure referring to result. Contract.Ensures(Contract.Exists(0, elems.Length, index => elems[index] != null && elems[index] == Contract.Result<A>() && Contract.ForAll(0, index, prior => Contract.Result<A>() != null))); // See if we are properly sharing fields. Contract.Ensures(Contract.Exists(0, elems.Length, index => elems[index] != null && elems[index] == Contract.Result<A>() && Contract.ForAll(0, index, prior => Contract.Result<A>() != null))); // See if we are properly sharing fields. Contract.Ensures(Contract.Exists(0, elems.Length, index => elems[index] != null && Contract.ForAll(0, index, prior => Contract.Result<A>() != null))); throw new NotImplementedException(); } public override C[] GenericMethod<C>(A[] elems) { Contract.Requires(elems != null); Contract.Ensures(Contract.Result<C[]>() != null); Contract.Ensures(Contract.ForAll(Contract.Result<C[]>(), resultElem => Contract.Exists(elems, orig => resultElem.Equals(orig)))); throw new NotImplementedException(); } } public class ImplForGenericAbstractClass : GenericAbstractClass<string, string> { public override bool IsMatch(string b, string a) { return b == a; } public override string ReturnFirst(string[] args, string match, bool behave) { for (int i = 0; i < args.Length; i++) { if (IsMatch(args[i], match)) return args[i]; } return default(string); } public override string[][] Collection(int x, int y) { var result = new string[x][]; for (int i=0; i<result.Length; i++) { result[i] = new string[y]; for (int j = 0; j < y; j++) { if (x == 5 && y == 5 && i == 4 && j == 4) { // behave badly continue; } result[i][j] = "Foo"; } } return result; } public override string FirstNonNullMatch(bool behave, string[] elems) { if (!behave) return "foobar"; for (int i = 0; i < elems.Length; i++) { if (elems[i] != null) return elems[i]; } return null; } public override C[] GenericMethod<C>(string[] elems) { List<C> result = new List<C>(); foreach (var elem in elems) { if (elem is C) { result.Add((C)(object)elem); } } if (typeof(C) == typeof(int)) { // behave badly result.Add((C)(object)55); } return result.ToArray(); } } partial class TestMain { partial void Run() { var i = new ImplForGenericAbstractClass(); i.FirstNonNullMatch(behave, new string[]{null, "a",null,"b"}); } public ContractFailureKind NegativeExpectedKind = ContractFailureKind.Postcondition; public string NegativeExpectedCondition = "Contract.Exists(0, elems.Length, index => elems[index] != null && elems[index] == Contract.Result<A>() && Contract.ForAll(0, index, prior => Contract.Result<A>() != null))"; } }

Q: How to get konsole work on gns3 i am interested in making my devices display in tabs when working on GN3. i made some research and found out that konsole can do that. i installed it. i have gone to preferences => edit => set KDE konsole amazingly when i open the console of a device it i need it to display the router or device i intend working with normally. how do i fix this A: it is simple, just to preferences => edit => general, on the tab for console change the command there to console application commands: konsole --new-tab -p tabtitle=%d -e telnet %h %p then {the second console application commands: Local serial connections (remember to install socat) konsole --new-tab -p tabtitle=%d -e socat UNIX-CONNECT:"%s" stdio,raw,echo=0

Q: strace: order of and <... resumed> I'm writing a script that analyzes file access traced with strace. The trace contains some calls which have been interrupted by another process. strace shows them with <unfinished ...> and <... close resumed> (in case of an interrupted close call) markers. [pid 26817] 12:48:22.972737 close(449 <unfinished ...> [pid 28708] 12:48:22.972797 fcntl(451, F_SETFD, FD_CLOEXEC <unfinished ...> [pid 26817] 12:48:22.972808 <... close resumed> ) = 0 The process and all its threads have been traced with strace -f -tt -p <pid> The man page is uncertain about when the call has been finished. If a system call is being executed and meanwhile another one is being called from a different thread/process then strace will try to preserve the order of those events and mark the ongoing call as being unfinished. When the call returns it will be marked as resumed. While I'd assume that, natually the resumed marker will indicate that the call is now finished. I'd like to ask if it is so. Can the above trace excerpt be reconstructed to A [pid 28708] 12:48:22.972797 fcntl(451, F_SETFD, FD_CLOEXEC <unfinished ...> [pid 26817] 12:48:22.972808 close(449) = 0 or should it be reconstructed to B [pid 26817] 12:48:22.972737 close(449) = 0 [pid 28708] 12:48:22.972797 fcntl(451, F_SETFD, FD_CLOEXEC <unfinished ...> The order is crucial here since there may be multiple calls between the unfinished and resumed and one of them might do something with the file that is about to be closed at the moment. A: The system call begins when strace writes the line close(449 <unfinished ...>, and ends when it outputs <... close resumed>. The close is not interrupted by any other call or signal: the other call is executed by another process, while the kernel is closing your file descriptor. There is no way to know which is the exact point when the file descriptor is closed; the only thing you know is that it is not closed until the syscall is executed, and that it is closed when the syscall finishes.

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We all know that there have been some very nasty attacks on Palin from some feminists, as well as a lot of condescension from the Maureen Dowd types who look down their noses at a small-town, gun-owning, Walmart-going, Bible-believing mom with five kids. But it takes two to do the culture-war tango. For instance, in The American Spectator, one Jeffrey Lord rightly deplores the feminist attacks on Palin. Then he goes on to say: This election is now being fought openly between, as Whittaker Chambers once described the same fight in a different era, “those who reject and those who worship God.” Between those who believe “if man’s mind is the decisive force in the world, what need is there for God?” — and America’s own Joan of Arc, Sarah Palin. If Barack Obama is an atheist, that’s news to me. And I certainly hope that Palin doesn’t actually see herself as Joan of Arc on a God-given crusade. (It’s interesting how the left-wing caricature of Palin is barely distinguishable from the right-wing icon.) Praising Palin’s decision to keep her baby with Down’s Syndrome and to encourage her pregnant 17-year-old daughter Bristol to bear her child, Lord writes: Twice over in two now ongoing and very public situations, Sarah Palin has focused on the love of God rather than herself. To those who have vested their life and career comfortably believing there is little need for God because what of what rolls around aimlessly in their heads and those of their like-minded friends at any given moment, to those who view government and the power of the state as an object of worship, this is taken as a serious, gut-level threat. A threat to the existence of their own very carefully structured non-religious secular value system. Glossing over Lord’s apparent assumption that Palin expects to have no personal joy or satisfaction from her special-needs child or her grandchild, and that her decision was solely a sacrifice to God, this is a pretty nasty portrayal of secularists. Further down, it is compounded by nasty swipes at insufficiently masculine liberal men (“Glutted with Hollywood pâté, Al Gore would have a coronary trying to keep up with Palin, who probably wouldn’t be bringing along any seriously good wine as he races through the backwoods. Once off the basketball court, Obama would be clueless on snowshoes with a gun and a charging moose”). On a less hysterical note, Jonah Goldberg in National Review defends Palin against the “she’s not a real woman” attacks … and then sneers that the same people would consider “a childless feminist who looks like a Bulgarian weightlifter in drag” a real woman. On Townhall.com, Kevin McCullough speculates that “modern feminists” hate Palin because she’s a real woman: She has a manly, and (according to several women I’ve overheard) handsome husband. She is content in their life together as a couple where each goes out and works hard. As a mom she is parenting her kids giving them what mothers give best, and her husband, gives what only a father can. She’s not afraid to don some lipstick and use her comely attraction to romance “her guy” one night, and turn around and beat back corruption as a fierce defender of what is right the next day. As opposed to, say, the notoriously unwomanly Geraldine Ferraro (married mother of three) and Nancy Pelosi (a married mother of five whom a poster on Michelle Malkin’s blog charmingly described the other day as “the result of mixing June Cleaver with Code Pink, Steroids and a strap on”)? A pro-life activist suggests one of the reasons liberals despise Republican vice-presidential nominee Sarah Palin so passionately may be because she gave birth to her son despite a diagnosis of Down syndrome. … Mark Crutcher, the president of Life Dynamics Incorporated (LDI), notes that in America today, 90 percent of all Down syndrome children are killed in the womb. “I wonder what the people who are doing that — the parents who are ‘choosing’ to have their child executed — what they think when they look at Sarah Palin and her family, when they see the example of that family welcoming a Down syndrome child in and loving that child. I wonder what those people think,” Crutcher contends. “I also wonder whether this is where you’re seeing some of this hatred and venom that’s coming from the godless Left directed at [Palin]. I’m beginning to wonder if Sarah Palin isn’t rubbing their noses in their own shame.” What hateful tripe. If 90 percent of people who find out they are carrying a fetus with Down’s Syndrome terminate their pregnancies, there must be quite a few non-liberals among them (and even, I daresay, quite a few conservatives). And frankly, if Sarah Palin’s example is going to be used as a moral club to beat those who make the choice to terminate a pregnancy under those circumstances, an angry response will be justified. 7 responses to “More Palin: The other side of the culture war” I appreciate your taking on both sides of the culture war over Palin. I’ve been rather disgusted with the whole story-with the bullsh*t whining of feminists and lefties about “hypocracy” and “see what abstinance only got her daughter” bla bla, as well as the absolute contempt, and dare I say projection, on the right of anyone who criticizes a “real American” like Palin. Spare me. What bothers me so much about all of this, though, is that it distracts from the real issue, which is governing. In my opinion, and I know many will disagree with me, the addition of Palin to the ticket was about politics, not governing. She energizes the base, but brings no expertise, and inspires no confidence in the ability of the McCain administration to govern effectively. I’ll admit I don’t like McCain very much. Even though his voting record suggest thoughtful moderation, his public persona is anything but thoughtful or moderate. Palin seems to have added an energized resentment to the ticket, and little more. I would like to argue with you about her candidacy being a step forward for women. I see it as cynical tokenism. I certainly appreciate that women politicians need not march in lockstep with feminists, that women politicians and voters care about some things more than “reproductive rights” and “choice”, and I admire the way Palin’s personal choices line up with her politics. But she’s pretty much a big liar with no demonstrated grasp of foreign policy, and her/McCain’s attempts to gloss over that with some such crap about Alaska being near Russia is infuriating. There are other women out there, conservatives and moderates and liberals, who are more accomplished, more articulate, not currently evading abuse of power investigations, who could have been elevated to the second highest office on merit alone. I’ve always had a grudging respect for Liddy Dole and Kay Bailey Hutchison, and Christie Whitman even though I don’t agree with all of their politics. I just don’t see what Palin has to offer, other than a gigantic distraction from any serious issues. But you often manage to get me to think about things differently, so I await your response. Oh-LOVED the line about the confluence of the left wing caricature and the right wing icon. Brilliant. ada47 is right on. The issue with Sarah Palin is primarily whether she’s fit to hold the office she’s running for, and all of these questions about the reactions of various cadres to her are tertiary. Palin was clearly chosen for her ability to pump-up the religious right, who were in a Schiavo-like coma where McCain is concerned before her selection. McCain also fantasized that she would appeal to centrists as another maverick, and to disaffected female-identity-driven Hillary supporters. The secondary issues – policy positions – aren’t pressing because she doesn’t have positions on much of anything beyond birthing babies and attracting big-box retail to small towns. If a complete and sober assessment shows that Palin is not fit to hold office, by reason of preparation, intellect, and temperament, than the most virulent reactions to her from any cadre are in fact reasonable. And from what I’ve seen, that’s what’s going on: a laughably inappropriate candidate has been chosen to grace the Republican ticket, and all of the people who’ve been paying attention are pissed. Not just whackos, but serious conservatives like Wick Allison, George Will, David Brooks, David Drezner, Charles Krauthammer, Peggy Noonan, Mike Murphy, David Frum, Richard Brookhiser and Ross Douthat. You add Glenn Greenwald and Kay Parker to the list of the early Palin supporters who’ve thought better of their first reaction. The novelty of a woman on the Republican ticket has given way to a sober assessment of Palin’s severe lack of ability and preparation for a job that could very likely land her in the Oval Office. Serious conservatives are saying “thanks but no thanks” to this Nowhere Woman. Cathy Young, a writer and journalist, was born in Moscow, Russia in 1963, and came to the United States in 1980. She is a graduate of Rutgers University. From 1993 to 2000, Young wrote a weekly column for The Detroit News. From 2000 to 2007, she was a weekly columnist for The Boston Globe (where she is still a frequent op-ed contributor) as well as a monthly columnist for Reason magazine. At present, she is a weekly columnist for Newsday, a contributing editor/feature writer for Reason and a regular columnist for RealClearPolitics.com. She has written for numerous other publications, from The New York Times, The Washington Post and The Wall Street Journal to Salon.com and The Weekly Standard. Young is the author of two books: Growing Up in Moscow: Memories of a Soviet Girlhood (1989) and Ceasefire: Why Women and Men Must Join Forces to Achieve True Equality (1999). Young has appeared on numerous radio and television shows including To the Contrary (PBS), Talk of the Nation and Fresh Air (NPR) and The O'Reilly Factor (Fox News). She is also a frequent speaker on college campuses and has participated in conferences including the 2012 Battle of Ideas in London.

2-styrylchromones as novel inhibitors of xanthine oxidase. A structure-activity study. The purpose of this study was the evaluation of the xanthine oxidase (XO) inhibition produced by some synthetic 2-styrylchromones. Ten polyhydroxylated derivatives with several substitution patterns were synthesised, and these and a positive control, allopurinol, were tested for their effects on XO activity by measuring the formation of uric acid from xanthine. The synthesised 2-styrylchromones inhibited xanthine oxidase in a concentration-dependent and non-competitive manner. Some IC50 values found were as low as 0.55 microM, which, by comparison with the IC50 found for allopurinol (5.43 microM), indicates promising new inhibitors. Those 2-styrylchromones found to be potent XO inhibitors should be further evaluated as potential agents for the treatment of pathologies related to the enzyme's activity, as is the case of gout, ischaemia/reperfusion damage, hypertension, hepatitis and cancer.

Florida Sen. Marco Rubio on Tuesday defended controversial efforts by Florida Gov. Rick Scott to purge the Sunshine State's voter rolls, denying it has targeted Hispanics. "I wouldn't characterize it as an effort to purge Latinos from the voting rolls," Rubio told reporters at a breakfast hosted by Bloomberg News. "I think there's the goal of ensuring that everyone who votes in Florida is qualified to vote. If you're not a citizen of the United States, you shouldn't be voting. That's the law." Rubio, the highest-ranking Hispanic official in Florida, is seen as a potential pick by likely GOP presidential nominee Mitt Romney as a running mate. Scott is also a Republican. The Justice Department on Tuesday filed suit against the state to stop the voter purge, arguing in part that it violates a federal law that bans such steps within 90 days of a federal election. (Florida's primary is Aug. 14.) The ACLU of Florida also has filed a lawsuit, saying the effort violates the 1965 Voting Rights Act, which protects minority groups. The civil liberties organization says Hispanics make up 14% of the Florida electorate but are 61% of several thousand registered voters who have been told to provide proof of citizenship or lose their right to vote. Meanwhile, Florida is suing the federal Department of Homeland Security to get access to a database the state says could help identify non-citizens on the voter rolls. So far, state officials say 96 ineligible voters have been identified. Rubio said there could be "a legitimate debate" about how to carry out the purge, but he called it a worthwhile effort. "We know that there are at least 80 to 90 names on the list that don't belong," he said. "We should be concerned about that. We should be concerned about people that are registered in multiple states. And we should be concerned about our list that includes the names of people who have passed away, because I think that could lend itself to mayhem and madness."

1. Field Apparatuses and methods consistent with exemplary embodiments relate to a controlling a peripheral device connected to a display apparatus and, more particularly, to controlling the peripheral device based on the booting time of the peripheral device. 2. Description of the Related Art With development of technology, an electronic apparatus may provide various services and functions including phone call, data transmission, and multitasking functions. The display apparatus may be connected to various peripheral devices such as a set-top box, a DVD player, and a home theater, and may receive and output contents provided by the respective peripheral devices. In order to receive contents from various peripheral devices, a user may control the operation of each peripheral device by using a remote controller for controlling each peripheral device. Recently, an integrated remote controller capable of controlling a display apparatus and a peripheral device in an integrated manner has been developed. Therefore, a user may control operations of a display apparatus and a peripheral device which is connected to the display apparatus through the integrated remote controller. Particularly, it is possible to control power of a display apparatus and a peripheral device connected to the display apparatus through the integrated remote controller. That is, the display apparatus may boot the operating system of the display apparatus according to a turn-on command received from the integrated remote controller, and may transmit a turn-on signal for turning on the peripheral device to the integrated remote controller when the booting is completed. Accordingly, the integrated remote controller transmits, to the peripheral device, an infrared (IR) signal with respect to a control command included in the turn-on signal received from the display apparatus, and the peripheral device can perform the process of booting the operating system of the peripheral device according to the IR signal received from the integrated remote controller However, when the display apparatus and the peripheral device are controlled by the related-art integrated remote controller, the display apparatus may not recognize that the peripheral device is being booted according to the IR signal received from the integrated remote controller. Instead, the display apparatus may determine that the power of the peripheral device is turned off and may provide a user interface (UI) for controlling power of the peripheral device. Since the boot time of all the peripheral devices is not the same, if the peripheral device requires a long boot time, the display apparatus may determine that the power of the peripheral device is turned off even though the peripheral device is booting its operating system, thereby providing a power-related UI of the corresponding peripheral device. Accordingly, upon receiving a user request, the integrated remote controller may retransmit a related IR signal to the peripheral device while the peripheral device is booting its operating system, and therefore the peripheral device may reboot the operating system according to the IR signal retransmitted from the integrated remote controller. Therefore, there may be a problem that, it takes a long time for contents provided by the peripheral device to be output through the display apparatus, and the user may erroneously perceive that the peripheral device is malfunctioning even though the peripheral device is operating normally.

Recently, reduction of a vehicle noise (for example, an airflow noise or machine sound) in a vehicle such as a passenger car has been further developed. However, according to continually increasing of needs for a comfortable riding environment, a necessity for a reduction of tire noise has increased more than before. In order to reduce a noise of tread with respect to a road, various shapes of tread have been developed. A purpose of such a noise reduction technique is for dispersing noise frequencies generated by the tread to wideband frequencies, so as to reduce the noise near to a level of so-called white noise. Further, relatively high temperature heat is generated from the tire mounted on the vehicle due to a high-speed rotation thereof or friction with the road surface. However, rubber which is a major component of the tire has a low heat dissipation performance due to the material characteristics thereof. For this reason, heat generated from the tire is not properly transmitted to an outside, therefore the lifespan of each component may be shortened, and the tire may be separated or ruptured due to a serious deterioration in tire durability. In particular, radial tires for trucks or buses which are used in harsh conditions, or run-flat tires for the purpose of traveling in an emergency situation are greatly influenced by durability due to a temperature. When the run-flat tire travels in an emergency situation (in the case that pressure inside the tire is 0 psi), a periodically fluctuating load is applied to the tire, which causes a bending and stretching motion of the sidewall. When the inside of the tire is filled with air, a degree of bending and stretching motion in the sidewall is relatively small, but when the run-flat tire travels in an emergency situation of 0 psi, the degree thereof becomes large. In this case, heat is generated from the side wall by the continuously repeated large bending and stretching motion and thermal stress is continuously applied to sidewall reinforcing rubber for supporting the tire against load, causing a rupture in the tire. In order to solve the problems, techniques for forming protruded cooling fins on the sidewall have been developed. For example, Korean Patent Laid-Open Publication No. 10-2010-0070796 discloses a pneumatic tire including blade-shaped structures and cooling fins formed on a sidewall for improving heat dissipation performance. However, these techniques have a problem that a resonance phenomenon occurs by an airflow noise generated during high speed air collapsing due to the cooling fins, and thereby the noise is significantly increased. Accordingly, a technique capable of reducing an amount of heat convection in the sidewall from which a lot of heat is generated, as well as decreasing the airflow noise is required for a pneumatic tire. In addition, for a conventional tire, since cooling fins are formed at fixed intervals for reducing heat generation and turbulence regularly generated by the collision of high speed air is insufficient for effectively radiating heat. That is, if sufficient turbulence is not generated, the air resistance does not easily decrease. Accordingly, there is still a need for the pneumatic tire to reduce the amount of heat convection in the sidewall from which a lot of heat is generated, as well as efficiently decrease the air resistance.

Montana Highway 15 from Shelby to Great Falls is a step back to the old west. You drive by miles of the high plan farms that helped to win the west. The drive is a mix of farms and rolling hills. If you stop and let your imagination run you can still see the giant herds of Bison roaming the open plans.

Job gap study finds hardship in Virginia According to an annual job gap study, Virginia and other states are struggling to offer enough jobs that pay a living wage of at least $15 an hour. Virginia Organizing, a nonpartisan statewide organization, released the results of the 15th annual study by The Alliance for a Just Society on Wednesday via a tele-media conference. The report finds a shrinking proportion of jobs that pay enough for families to make ends meet, with the number of job seekers exceeding the number of jobs that pay a living wage. In Virginia, there are about seven job seekers for every job that pays a living wage in a single adult household. That number increases to 16 job seekers for every living wage job available in a two-child, single parent household. Nationally, the report found an increasing share of low-wage jobs since the end of the Great Recession. It said the share of jobs that pay below the $15-an-hour, low-wage threshold increased from 36.5 percent in 2009 to 39.4 percent in 2012. There were 51.4 million low-wage jobs in 2012. During the press conference in Virginia, speakers expressed concern that the state has not agreed to expand Medicaid. “This report shows what Virginians already know — we need better wages and better social safety net programs in Virginia,” Virginia Organizing chairperson Sandra A. Cook, said in a statement. “Medicaid expansion and an increase in the minimum wage can clearly help those working low-wage jobs have more financial security and add more to the economy through being able to afford to spend money in local communities. These things are good for all of us.”

When the Lovelight Starts Shining Through His Eyes "When the Lovelight Starts Shining Through His Eyes" is a song written by Holland–Dozier–Holland and recorded in 1963 by Motown singing group The Supremes. It is notable as the Supremes' first Billboard Hot 100 Top 40 recording, following seven previous singles between January 1961 and September 1963 which failed to enter the Top 40. The single is also notable as the first Supremes single written and produced by Holland–Dozier–Holland, who had previously created hits for Martha and the Vandellas and Mary Wells. Overview Recording By 1963, the Supremes were struggling to find a pop hit. Until then, the Supremes was a regional R&B favorite, with their most successful single being "A Breathtaking Guy", which peaked at number 75 on the Hot 100. The group's competitors inside Motown included The Marvelettes, Motown's first successful female group, but also with Martha and the Vandellas, whose early hits included "(Love Is Like A) Heat Wave" and "Quicksand". Struggling to find producers who could give the Supremes a successful hit after both he and Smokey Robinson had failed, Motown CEO Berry Gordy decided to have the team of Holland–Dozier–Holland, who would end up being the dominant songwriting and producing team of Motown, produce a song for the Supremes. "Lovelight" would eventually be released after Gordy's Quality Control Department approved of the song. Reception Released on October 31, 1963, "When the Lovelight Starts Shining Through His Eyes" was the Supremes' first Top 40 pop hit since signing with Motown in 1961. Eventually reaching number 23 on the Billboard Hot 100 and number 2 on the Cash Box R&B chart, Gordy decided to have Holland-Dozier-Holland on board as the group's sole producers from then on. It also nearly made the Top 10 in Australia. After the unsuccessful rush-release of the Phil Spector-inspired "Run, Run, Run", the Supremes would eventually eclipse their female peers after releasing "Where Did Our Love Go" in the summer of 1964. Personnel Lead vocals by Diana Ross Background vocals by Florence Ballard and Mary Wilson Additional vocals (growling before instrumental) by: The Four Tops (Levi Stubbs, Abdul "Duke" Fakir, Lawrence Payton and Renaldo "Obie" Benson) and Holland–Dozier–Holland (Edward "Eddie" Holland, Jr., Lamont Dozier and Brian Holland) Instrumentation by The Funk Brothers Written by Holland–Dozier–Holland Produced by Lamont Dozier and Brian Holland Chart history Later Versions Dusty Springfield included the song on her 1964 debut album A Girl Called Dusty. The Zombies did a version in 1965 (available on Live At The BBC, released 2003) In 1975, Motown Records released a new version of the song (catalog number 1334) by The Boones, a vocal quartet featuring four daughters of Pat Boone (including Debby of "You Light Up My Life" fame). This version reached No. 25 on Billboard magazine's Adult Contemporary chart. The Seattle-based electro-pop band Brite Futures included this song on their 2012 posthumous album "When The Lights Go Out". References External links Category:1963 singles Category:The Supremes songs Category:Songs written by Holland–Dozier–Holland Category:1963 songs Category:Song recordings produced by Brian Holland Category:Song recordings produced by Lamont Dozier

Q: вопрос о списке в Android Studio Хочу осуществить переход на новую Activity после нажатия на первый элемент списка, но выдает ошибку в последней строке с getApplicationContex, с чем это может быть связано? final String[] Spisok = new String[]{ "Что", "Как", "Для кого"}; private ArrayAdapter<String> mAdapter; @Override protected void onCreate(Bundle savedInstanceState) { super.onCreate(savedInstanceState); mAdapter = new ArrayAdapter<String>(this, android.R.layout.simple_list_item_1, Spisok); setListAdapter(mAdapter);; } @Override protected void onListItemClick(ListView l, View v, int position, long id) { super.onListItemClick(l, v, position, id); if(position==0) { Intent intent = new Intent(getApplicationContext(), MainActivity.class); getApplicationContex.startActivity(intent); } A: Потому что это метод. Вы не поставили скобки. Исправьте на: getApplicationContext().startActivity(intent);

1. The U.S. transportation secretary called for an inquiry into the F.A.A.’s certification of the Boeing 737 Max 8. Elaine Chao asked her agency’s internal watchdog to audit the approval process, which has been under scrutiny since the crash last week of an Ethiopian Airlines jet — the second deadly crash involving the aircraft in less than five months. One concern is the role that Boeing employees played. Since 2005, the agency has allowed manufacturers to choose their own employees to act on behalf of the F.A.A. to help certify new aircraft.

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Intramuscular electrical stimulation for hemiplegic shoulder pain: a 12-month follow-up of a multiple-center, randomized clinical trial. Assess the effectiveness of intramuscular electrical stimulation in reducing hemiplegic shoulder pain at 12 mos posttreatment. A total of 61 chronic stroke survivors with shoulder pain and subluxation participated in this multiple-center, single-blinded, randomized clinical trial. Treatment subjects received intramuscular electrical stimulation to the supraspinatus, posterior deltoid, middle deltoid, and upper trapezius for 6 hrs/day for 6 wks. Control subjects were treated with a cuff-type sling for 6 wks. Brief Pain Inventory question 12, an 11-point numeric rating scale was administered in a blinded manner at baseline, end of treatment, and at 3, 6, and 12 mos posttreatment. Treatment success was defined as a minimum 2-point reduction in Brief Pain Inventory question 12 at all posttreatment assessments. Secondary measures included pain-related quality of life (Brief Pain Inventory question 23), subluxation, motor impairment, range of motion, spasticity, and activity limitation. The electrical stimulation group exhibited a significantly higher success rate than controls (63% vs. 21%, P = 0.001). Repeated-measure analysis of variance revealed significant treatment effects on posttreatment Brief Pain Inventory question 12 (F = 21.2, P < 0.001) and Brief Pain Inventory question 23 (F = 8.3, P < 0.001). Treatment effects on other secondary measures were not significant. Intramuscular electrical stimulation reduces hemiplegic shoulder pain, and the effect is maintained for > or =12 mos posttreatment.

Pro - Support of the hobby and flying field. Con - You have to pretend the to understand your friends desire to fly electric, that's just wrong. Pro - You get to meet funny people like me. Con - You may have to wait your turn to fly. Pro - You get to fly with other people. Used to fly by myself and there were moments where you would look around and wonder... did anybody see that?!?! LOL PRO: A true club works together to maintain a place to fly, enjoys each others involvement as a hobbyist, and continues promote model aviation by supporting those involved (training, parts, gain knowledge or insight about the hobby, and to challenge each others abilities in the name of good fun in the form of heckling). This is a place of fun and happiness with other rc pilots to learn from. CON: There really isn't a CON if you keep this saying in mind: "At the end of the day, all we ever want to do is go have some fun and fly our airplanes" Keep it FUN! And for crying out loud be nice! You learn so much from other people, and it's an absolute joy to be a part of a like minded group of hobbyists. Used to fly by myself and there were moments where you would look around and wonder... did anybody see that?!?! LOL PRO: A true club works together to maintain a place to fly, enjoys each others involvement as a hobbyist, and continues promote model aviation by supporting those involved (training, parts, gain knowledge or insight about the hobby, and to challenge each others abilities in the name of good fun in the form of heckling). This is a place of fun and happiness with other rc pilots to learn from. CON: There really isn't a CON if you keep this saying in mind: "At the end of the day, all we ever want to do is go have some fun and fly our airplanes" Keep it FUN! And for crying out loud be nice! You learn so much from other people, and it's an absolute joy to be a part of a like minded group of hobbyists. Iím fortunate that we have many excellent pilots that have taught me much. The 2 gents Iím thinking of are IMAC World Champs and will almost give you the shirts off their backs to help. Also the best flying facilities require that you be a member of the AMA and the club. Iím fortunate that we have many excellent pilots that have taught me much. The 2 gents Iím thinking of are IMAC World Champs and will almost give you the shirts off their backs to help. Also the best flying facilities require that you be a member of the AMA and the club. i am very fortunate enough to have become with both that you speak of and i totally agree! meeting them through imac... that is one thing about a club you meet people like that!

Charles Mann (American football) Charles Andre Mann (born April 12, 1961) is a businessman and former American football player. He played as a defensive end in the National Football League (NFL) for the Washington Redskins and San Francisco 49ers. Mann was a four-time Pro Bowler in 1987, 1988, 1989, 1991. Early life Mann was born in Sacramento, California and attended Valley High School. College career Mann attended and played college football at the University of Nevada, where he played defensive end from 1979 to 1982. During his senior season, he led the Big Sky Conference with 14 sacks and was named the conference's Most Valuable Defensive Lineman. In 2015, he earned his bachelor's degree in business administration from Strayer University. Two years later, June 24, 2017, he received an MBA from Strayer University. Professional career Mann was drafted in the third round of the 1983 NFL Draft by the Washington Redskins and by his second season, he was the starting left defensive end, opposite to Dexter Manley. During this time, Mann had double-digit sack seasons four times, including a career-high 14.5 in 1985, which was just his third season in the NFL. Mann finished his career with the Redskins with 82 sacks, second-most in franchise history, and 17 forced fumbles, the most in franchise history, and also won Super Bowl XXII and Super Bowl XXVI. He was released by the Redskins and signed as a free agent with the San Francisco 49ers in 1994, where he won another Super Bowl (Super Bowl XXIX) before retiring. After football Mann helped found the Good Samaritan Foundation with his Washington teammates Art Monk, Tim Johnson and Earnest Byner. The foundation provides youth with the environment needed to equip them with the skills, training and resources necessary to compete successfully in society through the Student Training Opportunity Program (STOP). The program serves more than 50 high school students, four days a week during the school year and five days a week during the summer providing after-school programs, tutoring and mentoring. In 1993, Mann was voted the "Washingtonian of the Year." Among his many accomplishments, Mann serves as a member of the board of Inova Health Systems and as Chairman of the Inova Alexandria Hospital Quality Committee, the board of the McLean School and a Deacon with Grace Covenant Church in Chantilly, Virginia. He also serves on the Honorary Board of Directors for Easter Seals Serving DC|MD|VA, located in Silver Spring, MD. Prior to starting his own company, Mann was aligned with some of the best known brands locally and nationally: ESPN, BET, WUSA (TV) and WJFK-FM as Color Analyst & Reporter. McDonald's, Diet Coke and Swanson as Spokesman. Mann has been involved with National Kidney Foundation, United Way and the Ronald McDonald House Charities, The Border Babies Foundation, the "Read And Achieve Program," "Why School is Cool" Program, The Metropolitan Boys and Girls Clubs, Children’s Hospital, The Children’s Cancer Foundation and President Clinton’s National Service Initiative Committee. He is also an advocate of player safety while upholding the intensity of sports, focusing his efforts with an impact sensor device company, Brain Sentry. Mann, his wife of more than 30 years, Tyrena, and their three children, daughter Camille, son Cameron Wesley and daughter Casey live in the Washington area. References External links Category:1961 births Category:Living people Category:American football defensive ends Category:National Conference Pro Bowl players Category:Nevada Wolf Pack football players Category:San Francisco 49ers players Category:Washington Redskins players Category:Super Bowl champions

Dopamine-dependent responses to cocaine depend on corticotropin-releasing factor receptor subtypes. The effects on locomotor response to cocaine challenge, acquisition of cocaine conditioned place preference and cocaine-induced dopamine (DA) release in nucleus accumbens and ventral tegmental area by the non-specific corticotropin-releasing factor (CRF) receptors antagonist alpha-helical CRF, the selective CRF receptor subtype 1 antagonist CP-154,526 and the selective CRF receptor subtype 2 antagonist anti-sauvagine-30 (AS-30) were investigated in rats. Both alpha-helical CRF (10 microg, i.c.v.) and CP-154,526 (3 microg, i.c.v.) decreased the cocaine-induced distance travelled, whereas AS-30 (3 microg, i.c.v.) did not show such an effect. The CRF receptor antagonists also have significant effects on stereotype counts induced by cocaine injection, in which the alpha-helical CRF or CP-154,526 but not AS-30 did significantly reduce the stereotype counts. alpha-Helical CRF (10 microg) prior to each injection of cocaine blocked cocaine conditioned place preference with no significant difference observed in the time spent in the drug-paired side between post- and pre-training and both 1 and 3 microg CP-154,526 also had significant inhibitory effects on cocaine-induced place preference. However, pre-treatment with an i.c.v. infusion of AS-30 (1 or 3 microg) prior to each injection of cocaine did not affect the acquisition of conditioned place preference. The alpha-helical CRF and CP-154,526 reduced extracellular DA levels of nucleus accumbens and ventral tegmental area in response to the injection of cocaine. However, both alpha-helical CRF and CP-154,526 did not modify extracellular DA levels under basal conditions. In contrast, the i.c.v. infusion of AS-30 had no effects on either the basal DA or the cocaine-induced increase in DA release in nucleus accumbens and ventral tegmental area. These findings demonstrate that activation of the CRF receptor is involved in behavioral and neurochemical effects of cocaine challenge and cocaine reward and that the role of CRF receptor subtypes 1 and 2 in cocaine-induced locomotion, reward and DA release is not identical. The CRF receptor subtype 1 is largely responsible for the action of the CRF system on cocaine locomotion and reward. These results suggest that the CRF receptor antagonist, particularly the CRF receptor subtype 1 antagonist, might be of some value in the treatment of cocaine addiction and cocaine-related behavioral disorders.