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Although the activities in this computer game for preschoolers are not particularly original, Little Bill Thinks Big is a title with integrity, gentle challenges, and decent replay value. Based on the Nick Jr. television series created by Bill Cosby, the program offers preschoolers a peaceful workout in early thinking skills--ones that are particularly necessary for success in math. Children are greeted by Little Bill, who asks for help creating a big surprise for his family. Children explore his house, uncovering fun clickables, little educational games, and the program's five featured activities. They earn objects like pinwheels and watering cans needed for constructing the surprise. The surprise depends on what season players have selected at the beginning of the game. They make a scarecrow in Autumn and a snowman in Winter, for example. Of course, kids can replay the game once they've completed the surprise by selecting a different season. The featured activities exercise children's logical thinking skills. They put pictures in logical order to form a story, group aliens according to common attributes, construct tunnels for a hamster by matching colors and shapes, create cookies identical to the ones already decorated, and match numerals with sets of objects as they propel Bill on his submarine. Earning objects for the surprise is fairly easy. If children decide they want to play each activity beyond the prize point, they will reap the most benefits from the game. Why? Because the activities advance in difficulty gradually. If children display mastery of a particular level, they are advanced to the next one. Similarly, if kids are struggling with a higher difficulty level, they are kept at a comfortable level of challenge. The first screenshot at left shows the cookie decorating activity in which children add decorations to a cookie in an attempt to match the given cookie. The second screenshot shows one of the sorting challenges in the Alien game. Children arrange photographs in the family album, creating stories in chronological order in the third screenshot. Again, this title is well-designed and provides a positive environment for learning. However, the game loses a few points for lack of originality in terms of activities. We love the fact that children can play the game in different seasons of the year--it not only exposes them to the whole concept of seasons, it also extends the game's life. There is also a strong and constructive theme of sharing: kids are encouraged to make surprises for their own families after helping Bill do the same for his family. Pros: Well-designed, encouraging software for preschoolers. Gradually advancing difficulty levels adjust automatically. Original voices from the television show. Decent replay value. Cons: If your software collection is fair-sized, you will find the featured activities resemble those in other games for preschoolers. | High | [
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The research found that more people exercised at parks after they'd been upgraded. Image: oversnap/iStockphoto Improving community health could lie in the quality of neighbourhood parks, a Deakin University study has found. Health researchers with Deakin’s Centre for Physical Activity and Nutrition Research examined whether improvements to parks increased usage and park-based physical activity of users. They found significant increases in the number of visitors and levels of exercise undertaken at one park after the facilities had been upgraded. “Parks are important places for people to spend their leisure time and be physically active,” explained Deakin health researcher Dr Jenny Veitch. “Understanding how we can attract residents to spend time at local parks and encourage them to be more physically active is an important public health initiative. This is particularly the case in disadvantaged neighbourhoods where residents are at increased risk of being inactive which can lead to poor health.” For the study, the researchers examined two parks in the same neighbourhood, one of which was about to be refurbished. Both parks were similar in size and mostly open spaces with few amenities. Upgrades to the one park included a fenced dog park, an all-abilities playground, walking track, barbeque area, landscaping and fencing. How many people used the parks and their levels of activity were monitored three months before the park improvements, three months after the improvements and one year later. The results of the study point to the positive effect improving facilities can have on usage and the types of physical activity undertaken within local parks. “We found that four times more people used the upgraded park a year after the changes, with more people walking and engaging in vigorous activities such as running or playing ball sports. While less people used the unchanged park and the activity levels remained pretty much the same,” Dr Veitch said. “What our study has shown is that improving existing parks can encourage people to make use of the facilities and increase their levels of physical activity. “The findings have implications for future park-renewal projects and can help urban planners and designers to develop parks that attract users and facilitate greater levels of physical activity.” The results of this study are published in the American Journal of Preventive Medicine. | High | [
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Regulation of tyrosine and phenylalanine biosynthesis in Salmonella. Several types of 4-fluorophenylalanine resistant mutants were isolated. In one type of mutant DAHP synthetase (tyr) and prephenate dehydrogenase were coordinately derepressed. The mutation was linked to aroF and tyrA and was cis- dominant by merodiploid analysis, thus confirming that it is an operator constitutive mutation (tyrOc). A second type of mutation showed highly elevated levels of tyrosine pathway enzymes which were not repressed by L-tyrosine. It was unlinked to tyrA and aroF, and was trans-recessive in merodiploids. These properties were attributed to a mutation in a regulator gene, tyrR (linked to pyr F), that resulted in altered or non-functional aporepressor. Hence tyrO, tyrA, and aroF constitute an operon regulated by tyrR. In a third type of mutation chorismate mutase P-prephenate dehydratase was highly elevated. It was not linked to pheA, was located in the 95--100 min region of the Salmonella chromosome, and was recessive to the wild type gene in merodiploids. A mutation was, therefore, indicated in a regulatory gene, pheR, which specified an aporepressor for regulating pheA. DAHP synthetase (phe), specified by aroG, was not regulated by pheR, but was derepressed in one of the tyrR mutants, suggesting that as in Escherichia coli tyrR may regulate DAHP synthetase(phe) and DAHP synthetase (tyr) with the same aporepressor. A novel mutation in chorismate mutase is described. | Mid | [
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{ "plugins": ["plugins/markdown"], "source": { "include": ["README.md", "index.js", "lib/"] }, "opts": { "destination": "./doc", "recurse": true }, "tags": { "dictionaries": ["jsdoc", "closure"] } } | Mid | [
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<div id="enlighter-license" style="display:none;"> <h2>The MIT License (X11 License)</h2> <p><strong>Copyright (c) 2010-<?php echo date('Y'); ?></strong> <a href="http://andidittrich.de">Andi Dittrich <http://andidittrich.de></a></p> <p>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:</p> <p>The above copyright notice and this permission notice shall be included in all copies or substantial portions of the Software.</p> <p>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.</p> </div> | Mid | [
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--- title: 'Výměna vadného disku' slug: vymena-disku excerpt: 'Zjistěte, jak identifikovat vadný disk a jak požádat o jeho výměnu' section: 'RAID a disky' --- **Poslední aktualizace 25/06/2018** ## Cíl Pokud a svém disku zaznamenáte defekt nebo pokud obdržíte e-mailové upozornění na vadu, je zapotřebí přijmout potřebná opatření pro výměnu vadného disku v co možná nejkratším čase. **Zjistěte, jak identifikovat vadný disk a jak požádat o jeho výměnu.** > [!warning] > > Společnost OVH Vám dává k dispozici stroje, za jejichž správu nesete plnou odpovědnost. Společnost OVH není administrátorským subjektem těchto strojů a nedisponuje žádnými přístupovými právy. Z toho důvodu spočívá zajištění každodenní správy softwaru a zabezpečení stroje pouze na Vás. > > Tato příručka slouží jako úvod do nejčastějších úkonů spojených se správou a zabezpečením Vašeho serveru. Pokud narazíte na jakékoli potíže či pochybnosti ohledně správy, použití nebo zabezpečení svého serveru, obraťte se prosím na profesionálního serverového administrátora. Další informace naleznete v poslední sekci této příručky. > ## Prerekvizity - SSH připojení k [dedikovanému serveru OVH](https://www.ovh.cz/dedikovane_servery/){.external} s *root* přístupem (Linux) ## Postup ### Vytvoření datové zálohy Ze všeho nejdříve je zapotřebí provést zálohu dat. Účelem vícenásobného diskového pole nezávislých disků (RAID) je zajistit ochranu Vašich dat v případě selhání jednoho z disků. V případě poruchy disku závisí všechna Vaše data na správné funkčnosti zbývajícího disku (či disků). Ačkoli je vysoce nepravděpodobné, že by došlo k poruše dvou disků zároveň, není to nemožné. Výměna disku nemůže být provedena bez: - Potvrzení o provedení zálohy dat. - Potvrzení o srozumění s rizikem potenciální ztráty dat vyplývající z výměny disku. ### Identifikace vadného disku Pokud obdržíte e-mailové upozornění nebo pokud si sami všimnete podezřelého chování disku, je zapotřebí provést kontrolu správné funkčnosti všech disků. V případě podezření na defekt dvou disků v RAIDu bude přednostně vyměněn disk s větším počtem chyb. #### Software RAID servery Postup pro identifikaci disků instalovaných na Vašem serveru v softwarovém RAIDu naleznete v následující příručce: [Konfigurace softwarového RAIDu](https://docs.ovh.com/gb/en/dedicated/raid-soft/){.external} (ENG). Jakmile naleznete přístupovou cestu ke svým diskům, můžete je otestovat použitím příkazu `smartctl`: ```sh smartctl -a /dev/sdX ``` > [!primary] > > Nezapomeňte za `/dev/sdX` dosadit přístupovou cestu ke svému disku. Proměnnou `sdX` nahraďte názvem disku (sdA, sdB apod.). > Provedením tohoto příkazu zároveň získáte *sériová čísla* disků, které je nutné vyměnit. Tato čísla je zapotřebí odeslat našim technikům. Následuje příklad výstupu po zadání příkazu `smartctl -a /dev/sdX`: ```sh smartctl -a /dev/sda >>> smartctl 5.41 2011-06-09 r3365 [x86_64-linux-3.14.32-xxxx-grs-ipv6-64] (local build) >>> Copyright (C) 2002-11 by Bruce Allen, http://smartmontools.sourceforge.net >>> === START OF INFORMATION SECTION === >>> Device Model: TOSHIBA DT01ACA050 >>> Serial Number: 5329T58NS >>> LU WWN Device Id: 5 000039 ff6d28993 >>> Firmware Version: MS1OA750 >>> User Capacity: 500 107 862 016 bytes [500 GB] >>> Sector Sizes: 512 bytes logical, 4096 bytes physical >>> Device is: Not in smartctl database [for details use: -P showall] >>> ATA Version is: 8 >>> ATA Standard is: ATA-8-ACS revision 4 >>> Local Time is: Thu Nov 24 15:51:25 2016 CET >>> SMART support is: Available - device has SMART capability. >>> SMART support is: Enabled ``` Důležitým údajem v našem případě je sériové číslo: **`Serial Number: 5329T58N`** #### Hardware RAID servery Pokud používáte server s hardwarovým RAIDem, obraťte se na následující příručku: [Hardwarový RAID](https://docs.ovh.com/gb/en/dedicated/raid-hard/){.external} (ENG). Pro nalezení přístupové cesty ke svým diskům postupujte podle instrukcí vážících se k Vámi využívanému typu RAID ovladače. Jakmile naleznete přístupovou cestu ke svým diskům, můžete je otestovat použitím příkazu `smartctl`: ```sh smartctl -d megaraid,N -a /dev/sdX ``` > [!primary] > > Nezapomeňte za `/dev/sdX` dosadit přístupovou cestu ke svému disku. Proměnnou `sdX` nahraďte názvem disku (sdA, sdB apod.). > > [!warning] > > V některých případech může dojít k vrácení následujícího výstupu: `/dev/sda [megaraid_disk_00][SAT]: Device open changed type from 'megaraid' to 'sat'`. > > V takovém případě je nutné nahradit `megaraid` za `sat+megaraid`, a to následujícím způsobem: `smartctl -d sat+megaraid,N -a /dev/sdX`. > V případě LSI RAID karet můžete své disky otestovat zadáním příkazu `smartctl`: ```sh smartctl -a /dev/sgY ``` V tomto případě je nutné specifikovat číslo RAIDu: `/dev/sg0 = 1er RAID, /dev/sg1 = 2e RAID`, apod. #### Servery s NVMe disky V případě NVMe disků je server zapotřebí restartovat do režimu [Recue-pro](https://docs.ovh.com/gb/en/dedicated/rescue_mode/){.external} (ENG), v němž je implicitně zahrnut nástroj **nvme-cli**. Pro získání sériových čísel disků poté použijte příkaz `nvme list`: ```sh root@rescue:~# nvme list >>> Node SN Model Namespace Usage Format FW Rev >>> -------------- ------------------- --------------------- --------- ------------------------- ------------- -------- >>> /dev/nvme0n1 CVPF636600YC450RGN INTEL SSDPE2MX450G7 1 450.10 GB / 450.10 GB 512 B + 0 B MDV10253 >>> /dev/nvme1n1 CVPF6333002Y450RGN INTEL SSDPE2MX450G7 1 450.10 GB / 450.10 GB 512 B + 0 B MDV10253 ``` ### Žádost o výměnu disku #### Výměna disku s přerušením dostupnosti služby (Cold-Swap): Pokud si přejete zažádat o výměnu disku, jednoduše vytvořte support ticket prostřednictvím [Zákaznického prostoru OVH](https://www.ovh.com/manager/dedicated/index.html#/ticket){.external}. Pokud do žádosti zahrnete veškeré relevantní údaje, můžete tím celý proces značně urychlit. Níže naleznete seznam požadovaných informací: - **Sériové číslo vadného disku a sériová čísla všech ostatních disků, které fungují normálně.** Za účelem získání sériového čísla vadného disku postupujte podle instrukcí v následující příručce: [Identifikace sériového čísla pevného disku](https://docs.ovh.com/gb/en/dedicated/find-disk-serial-number/){.external} (ENG). Pokud se Vám sériové číslo vadného disku nepodaří získat, zahrňte tuto informaci společně se sériovými čísly všech ostatních disků do ticketu. Jak bylo řečeno již výše, informace o sériových číslech všech disků jsou velice důležité. Tato čísla jsou odesílána technikům v našich datacentrech, což zajistí vyhnutí se případným chybám v průběhu výměny Vašeho disku. - **Čas a datum intervence.** V průběhu výměny disku dojde k chvilkové nedostupnosti Vaší služby. Intervenci je však možné naplánovat kdykoli, 24/7. - Potvrzení o provedení zálohy Vašich dat, včetně srozumění o potenciálním riziku ztráty dat. #### Výměna disku bez přerušení dostupnosti služby (Hot-Swap): > [!primary] > > Tento typ výměny disku je dostupný pouze pro servery [FS-MAX](https://www.ovh.cz/dedikovane_servery/storage/1801fs05.xml){.external} a [Big-HG](https://www.ovh.cz/dedikovane_servery/hg/1801bhg01.xml){.external}, disponující RAID kartou. > Pokud se chystáte provést výměnu disku bez přerušení dostupnosti služby na serveru s megaRAID kartou, aktivujte prosím po naplánování intervence u příslušného disku blikající LED diodu. Tento krok značně zjednoduší práci našim týmům v datacentru. Pokud Váš server používá megaRAID kartu, použijte prosím následující příkazy: - Rozsvícení LED diody: ```sh MegaCli -PdLocate -start -physdrv[E0:S0] -a0 ``` - Deaktivace LED diody: ```sh MegaCli -PdLocate -stop -physdrv[E0:S0] -a0 ``` > [!primary] > > Ekvivalentní postup prostřednictvím příkazu `storcli`: > > - Rozsvícení LED diody: > > ```sh > storcli /c0/e0/s0 start locate > ``` > > - Deaktivace LED diody: > > ```sh > storcli /c0/e0/s0 stop locate > ``` > > [!primary] > > I přesto, že je na serveru aktivována blikající LED dioda, je do support ticketu stále zapotřebí zahrnout informace o sériovém čísle a *slotu* serveru. > ### Dokončení procesu výměny disku Pokud používáte hardwarový RAID, Váš RAID se nastaví automaticky. Funkce *auto-rebuild* je aktivována ve výchozím nastavení. Pro správnou funkčnost se prosím ujistěte, že jste ji nedeaktivovali. Resynchronizační proces může trvat několik minut a v jeho průběhu může dojít ke snížení výkonu Vašeho RAIDu. Pokud používáte softwarový RAID, doporučujeme resynchronizaci provést manuálně. Detailní postup naleznete v následující příručce: [Konfigurace softwarového RAIDu](https://docs.ovh.com/gb/en/dedicated/raid-soft/){.external} (ENG). ## Kam dál [Konfigurace softwarového RAIDu](https://docs.ovh.com/gb/en/dedicated/raid-soft/){.external} (ENG) [Hardwarový RAID](https://docs.ovh.com/gb/en/dedicated/raid-hard/){.external} (ENG) [Režim rescue](https://docs.ovh.com/gb/en/dedicated/rescue_mode/){.external} (ENG) Sdílejte své zkušenosti s uživatelskou komunitou na <https://community.ovh.com/en/>. | Mid | [
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Scott Brown Is Basically a Touring Member of Cheap Trick He played with the band for the second time this weekend. There are a lot of ways to follow up on a career in the U.S. Senate. It’s traditional to move to Chevy Chase, take a lobbying job, and kiss the home state goodbye. Far more original is moving to a different state and running for Senate again. But¬†as second acts go, taking up guitar and joining your favorite rock band would be downright unique. We’re not sure which direction Scott Brown will take his post-Senate career. He’s doing some of the traditional firm work and talking-head gigs. He might find another door into the Senate as a New Hampshire resident. (Folks who have seen him shirtless think so.) But if that doesn’t work out, there’s always the touring musician route, because for the second time in recent months, Brown has appeared on stage‚ÄĒguitar in hand and a song in his heart‚ÄĒalongside the band Cheap Trick to accompany them on their hit “Surrender.” “Just played guitar with Cheap Trick. It was sooooooo fun,” he tweeted. Above, you can watch him rocking out on guitar. Brown told the Boston Herald that he met Cheap Trick and befriended lead guitarist Rick Nielsen while in the Senate, “doing¬†work on music pirating issues.”¬†¬†It’s been a fruitful partnership. He also played with them in August 2013 at an event in New Hampshire. Thus was it taken as yet another frivolous indication that he might launch a Senate run. Or was he actually giving us insight into his real future plans? Those of a Republican politician-turned-rock star? Could Scott and Ayla put together a family act? ‚ÄúIt was a lot of fun,‚ÄĚ Brown portentously¬†told the¬†Herald. “… Looking forward to doing it again.” Yeah you are. | Mid | [
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IN THE COURT OF CRIMINAL APPEALS OF TENNESSEE AT NASHVILLE Assigned on Briefs October 15, 2003 STATE OF TENNESSEE v. MICHAEL DWIGHT STEWART and JAMES HENRY BROWN Direct Appeal from the Criminal Court for Davidson County No. 2001-B-1193 Steve Dozier, Judge No. M2002-02592-CCA-R3-CD - Filed February 24, 2004 The Appellants, Michael Dwight Stewart and James Henry Brown, appeal the sentencing decisions of the Davidson County Criminal Court. Stewart pled guilty to aggravated robbery and aggravated kidnapping and received an effective twelve-year sentence. Brown pled guilty to aggravated rape and received a twenty-four-year sentence in the Department of Correction. In this consolidated appeal, Stewart and Brown raise the single issue of whether the sentences imposed were excessive. After review of the record, the sentencing decisions are affirmed. Tenn. R. App. P. 3; Judgments of the Criminal Court Affirmed. DAVID G. HAYES, J., delivered the opinion of the court, in which JERRY L. SMITH and THOMAS T. WOODALL, JJ., joined. Dwight E. Scott, Nashville, Tennessee, for the Appellant, Michael Dwight Stewart; C. LeAnn Smith, Easterly & Associates, Nashville, Tennessee, for the Appellant, James Henry Brown. Paul G. Summers, Attorney General and Reporter; Michael Moore, Solicitor General; Elizabeth T. Ryan, Assistant Attorney General; Victor S. (Torry) Johnson, III, District Attorney General; and Pamela Anderson, Assistant District Attorney General, for the Appellee, State of Tennessee. OPINION Factual Background In the early morning hours of March 7, 2001, the victim was walking to work at a Burger King in Nashville when she was accosted by two individuals wearing bandannas, later identified as the Appellants, Stewart and Brown. Stewart grabbed her by the arm and dragged her down an embankment and across a baseball field. Brown followed. The Appellants eventually stopped behind a privacy fence located at the rear of the Burger King. While waiting for the manager of the Burger King to arrive and open the restaurant, Brown forced the victim to undress, raped her, and then asked, “did it feel good.” After the manager arrived and entered the restaurant, the Appellants ordered the victim to walk to the back door and ring the bell in order to gain entrance into the building. The Appellants entered the restaurant, taking the victim with them. Upon confronting the manager, Stewart demanded money from the safe. The Appellants were forced to wait approximately fifteen minutes until the safe, which was set on a timer, could be opened. During this period, Stewart threatened to kill the manager if he did not hurry up. At one point during the robbery, the distinctive “racking” of a gun was heard. The Appellants took a bank deposit from Burger King, as well as the manager’s wallet, credit card, driver license, and money. The manager and female victim were taken to the bathroom and told to remain there while the Appellants fled. Although not initially recognizing her assailants, the female victim was eventually able to identify them by their voices as she had previously worked with them at the Burger King. During the search of Stewart’s residence, he was found to be in possession of the manager’s driver license, credit card, a large amount of cash, and a deposit slip in a Burger King bag. Stewart then gave information which led to Brown, who was likewise found with a sum of money when apprehended. A .45 pistol was recovered from the “room” which Brown occupied. Stewart admitted that he possessed a handgun during the crimes, but he claimed that it was never displayed. The handgun was provided to him by Brown. The Appellants were jointly indicted for the crimes of aggravated kidnapping and aggravated robbery. Brown was individually charged with aggravated rape, and Stewart was charged with rape. Under the terms of their respective plea agreements, Stewart pled guilty to aggravated kidnapping and aggravated robbery, and Brown pled guilty to aggravated rape. A sentencing hearing was held on September 26, 2002, during which the Appellants and the rape victim testified. The trial court sentenced Brown to twenty-four years in the Department of Correction.1 The trial court sentenced Stewart to twelve years in the Department of Correction for aggravated kidnapping and ten years for aggravated robbery, which were to run concurrently. Analysis In this consolidated appeal, the Appellants each allege that the trial court erred by imposing excessive sentences. Each argues that the trial court considered inapplicable enhancement factors and failed to consider applicable mitigating factors in reaching its sentencing determination. Our law provides that, when there is a challenge to the length, range, or manner of service of a sentence, it is the duty of this court to conduct a de novo review with a presumption that the determinations made by the trial court are correct. Tenn. Code Ann. § 40-35-401(d) (2003). This presumption is “conditioned upon the affirmative showing in the record that the trial court 1 Brown was sentenced as a violent offender as required by Tennessee Code Annotated Section 40-35-501(i)(1- 2) (2003). -2- considered the sentencing principles and all relevant facts and circumstances.” State v. Ashby, 823 S.W.2d 166, 169 (Tenn. 1991); see also State v. Jones, 883 S.W.2d 597, 600 (Tenn. 1994). “If the trial court applies inappropriate factors or otherwise fails to follow the 1989 Sentencing Act, the presumption of correctness falls.” State v. Shelton, 854 S.W.2d 116, 123 (Tenn. Crim. App. 1992). The burden is on the Appellant to show the impropriety of the sentence. Tenn. Code Ann. § 40-35- 401, Sentencing Commission Comments. Our review requires an analysis of: (1) the evidence, if any, received at the trial and sentencing hearing; (2) the pre-sentence report; (3) the principles of sentencing and the arguments of counsel relative to sentencing alternatives; (4) the nature and characteristics of the offense; (5) any mitigating or enhancing factors; (6) any statements made by the defendant in his own behalf; and (7) the defendant’s potential for rehabilitation or treatment. State v. Ashby, 823 S.W.2d at 169; see also Tenn. Code Ann. §§ 40-35-102, -103, -210 (2003). Furthermore, we emphasize that facts relevant to sentencing must be established by a preponderance of the evidence and not beyond a reasonable doubt. State v. Winfield, 23 S.W.3d 279, 283 (Tenn. 2000). 1. Michael Dwight Stewart Stewart pled guilty to aggravated kidnapping and aggravated robbery, both class B felonies. The appropriate sentence range for a class B felony is eight to twelve years. Tenn. Code Ann. § 40- 35-112(a)(2) (2003). The presumptive sentence to be imposed by the trial court for a class B felony is the minimum sentence within the applicable range unless there are enhancement or mitigating factors presents. Tenn. Code Ann. § 40-35-210(c). If there are enhancement or mitigating factors, the court must start at the presumptive sentence, enhance the sentence as appropriate for the enhancement factors, and then reduce the sentence as appropriate for the mitigating factors. Tenn. Code Ann. § 40-35-210(e). The weight given to each factor is left to the discretion of the trial judge. Shelton, 854 S.W.2d at 123. In the present case, the trial court found that no mitigating factors were applicable to either of Stewart’s convictions. The trial court applied the following enhancement factors in imposing a ten-year sentence for aggravated robbery: (1) Stewart had a previous history of criminal convictions or criminal behavior in addition to those necessary to establish the appropriate range; (2) he was a leader in the commission of an offense involving two or more criminal actors; and (15) he abused a position of public or private trust. Tenn. Code Ann. § 40-35-114 (1), (2), (15) (1997).2 In imposing a twelve-year sentence for aggravated kidnapping, the trial court found that, in addition to the above enhancement factors, enhancement factor (9), Stewart possessed or employed a firearm during the commission of the offense, was applicable. The trial court further noted that it believed Stewart had provided incorrect information in the pre-sentence report and was untruthful in his testimony before the court. On appeal, Stewart does not challenge the trial court’s application of 2 Effective July 4, 2002, the statutory enhancement factors were renumbered. Tenn. Code Ann. § 40-35-114 (2003). However, to maintain consistency, we utilize the numbering of the 1997 version as did the trial court. -3- enhancement factor (9). However, he asserts that the remaining enhancement factors were erroneously applied and that the trial court failed to consider his potential for rehabilitation. Stewart acknowledged that he has prior “minor criminal convictions” but argues that they should have been afforded little or no weight as an enhancement factor. The record reflects that Stewart has previous convictions for disorderly conduct, criminal trespassing, and possession of a weapon with the intent to go armed, in addition to an outstanding child support violation warrant. Misdemeanor convictions are sufficient to support application of this factor. State v. Carter, 908 S.W.2d 410, 413 (Tenn. Crim. App. 1995). Thus, the record clearly supports application of enhancement factor (1), and we note that the weight to be afforded each factor is within the discretion of the trial court. We find no error in the trial court’s consideration of this enhancement factor. Stewart also contends that enhancement factor (15) was erroneously applied as the record fails to establish that a “position of trust” was abused in the commission of the robbery and kidnapping offenses. The Tennessee Supreme Court has held that the determination of the existence of a position of trust does not depend on the length or formality of the relationship but upon the nature of the relationship. State v. Kissinger, 922 S.W.2d 482, 488 (Tenn. 1996). Thus, the sentencing court should look to see whether the offender formally or informally stood in a relationship to the victim that promoted confidence, reliability, or faith. Id. If the evidence supports that finding, then the court must determine whether the position occupied was abused by the commission of the offense. Id. Addressing this issue, the court stated that “[a] relationship which promotes confidence, reliability, or faith, usually includes a degree of vulnerability. It is the exploitation of this vulnerability to achieve criminal purposes which is deemed more blameworthy and thus justifies application of the enhancement factor . . . .” State v. Gutierrez, 5 S.W.3d 641, 646 (Tenn. 1999); see also State v. Blackstock, 19 S.W.3d 200 (Tenn. 2000). Accordingly, factor (15) is construed to apply only where there is evidence that the nature of the relationship between the perpetrator and the adult victim caused the victim to be particularly vulnerable. Id. In applying this factor to Stewart, the trial court found: . . . they’re both former . . . employees of this particular Burger King, . . . had knowledge, obviously - - Ms. Houston says one of them worked with her even in the opening shift - - had knowledge of the safe, how that goes about to be opened, how the manager comes in, and that they were obviously out there just, according to their testimony, coincidently at the time she’s coming to work and the manager would be arriving. We are unable to conclude that the record supports application of this factor for either of Stewart’s sentences. While we acknowledge that an employer/employee or co-employee circumstance may establish a relationship of private trust, we find from the facts of this case that it does not. Here, the -4- record established that Stewart was a former employee of the Burger King, who worked the breakfast shift. Beyond this employee relationship, there is no evidence in the record that demonstrates a relationship which promoted confidence, reliability, or faith that created a vulnerability on the part of the victims. While Stewart may have known that the restaurant employees reported to work at 5:00 a.m., it was not his employee knowledge which gained him entrance into the building before the business opened. Indeed, neither victim initially recognized Stewart. Moreover, the record establishes that, with regard to “store opening” procedures, Stewart was not aware that the safe was on a time delay and could not be opened. Thus, we conclude that this enhancer does not apply to the robbery conviction. Because there was no “relationship” between Stewart and the female victim, this factor was clearly inapplicable to the kidnapping conviction. Stewart next contends that the record does not support application of enhancement factor (2). It is well established that enhancement for being “a leader in the commission of an offense” does not require that Stewart be the sole leader but only that he was “a” leader. State v. Hicks, 868 S.W.2d 729, 731 (Tenn. Crim. App. 1993). From the record before us, it is clear that Stewart played a major role in these offenses. The record establishes that he was the first to broach the idea of a robbery. It was Stewart who first accosted the female victim and dragged her across the field, it was Stewart who possessed the firearm, and it was Stewart who remained in the office with the victims waiting for the safe to be opened. There is adequate proof to support the application of this factor. We find no merit to Stewart’s argument that the trial court failed to mitigate his sentence based upon the facts that he was a young man with a minor criminal history, expressed remorse for his crime, and had potential for rehabilitation. The trial court specifically found that Stewart had a criminal history of at least three offenses in addition to long term drug usage. Additionally, we note that “the mere speaking of remorseful words or a genuflection in the direction of remorse will not earn an accused a sentence reduction.” State v. Williamson, 919 S.W.2d 69, 83 (Tenn. Crim. App. 1995) (citing State v. Buttrey 756 S.W.2d 718, 722 (Tenn. Crim. App. 1988)). The trial court found that Stewart’s remorse was less than genuine and that he had lied about his knowledge of the rape. Truthfulness and accepting responsibility for one’s crime are factors to be considered in assessing one’s potential for rehabilitation. Such a finding, similar to assessing the credibility of a witness, is best left for determination by the trial court. Although we find that the trial court erred in its application of one enhancement factor for both sentences, this does not necessarily require that a different sentence be imposed. Based upon the proper application of three enhancement factors and no applicable mitigating factors, we find that, upon de novo review, a sentence of twelve years is justified for Stewart’s conviction for aggravated kidnapping. Moreover, we find that, based upon the application of two enhancement factors and no mitigating factors, a sentence of ten years is justified for Stewart’s conviction for aggravated robbery. -5- 2. James Henry Brown Brown pled guilty to aggravated rape, a class A felony. The appropriate sentence range for a class A felony is fifteen to twenty-five years. Tenn. Code Ann. § 40-35-112(a)(1). The presumptive sentence is the midpoint within the range if there are no enhancement or mitigating factors. Tenn. Code Ann. § 40-35-210(c). The presumptive sentence is then increased for applicable enhancing factors and decreased for applicable mitigating factors. Tenn. Code Ann. § 40-35-210 (e). The trial court applied the following enhancement factors: (1) Brown had a previous history of criminal convictions or criminal behavior in addition to those necessary to establish the appropriate range; (7) the offense involved a victim and was committed to gratify the defendant’s desire for pleasure or excitement; (9) Brown possessed or employed a firearm during the commission of the offense; (15) he abused a position of public or private trust; and (20) he was adjudicated to have committed a delinquent act as a juvenile that would constitute a felony if committed as an adult. Tenn. Code Ann. § 40-35-114 (1), (7), (9), (15), (20). Finding no applicable mitigating factors, the trial court imposed a sentence of twenty-four years. Brown contends that the trial court erroneously applied all five enhancement factors and failed to apply applicable mitigating factors. He asserts that the trial court should have placed some weight on Brown’s age, use of drugs, and taking responsibility for the crime. Additionally, he argues that his remorse should have been considered in mitigation. The trial court applied factor (1), although giving it “minimal weight,” based upon Brown’s two prior adult misdemeanor convictions for underage drinking. We agree with the trial court that the presence of the factor is established but entitled to little weight. With regard to factor (20), a delinquent act that would constitute a felony, the record of the Davidson County Juvenile Court was introduced and filed as an exhibit, which reflected that Brown was adjudicated as a delinquent for committing aggravated assault. The juvenile record, which contained the adjudication and other non felony type adjudications, was filed as an exhibit at the sentencing hearing without objection. Accordingly, we find application of factor (20) supported by the record.3 Brown asserts that factor (7) was improperly applied because there is no evidence in the record to support a finding that he committed the offense to satisfy his desire for pleasure or excitement. Pleasure or excitement is not an essential element of the offense of aggravated rape and, therefore, may be considered as an appropriate enhancement. State v. Adams, 864 S.W.2d 31, 35 (Tenn. 1993). Application of this factor, however, requires an inquiry into the motivation behind the Appellant’s actions. Kissinger, 922 S.W.2d at 490. A defendant’s motivation to seek pleasure or excitement may be shown through evidence of “sexually explicit remarks and overt sexual displays made by the defendant . . . or remarks or behavior demonstrating the defendant’s enjoyment of the sheer violence of the rape.” State v. Arnett, 49 S.W.3d 250, 262 (Tenn. 2001). The State has 3 During Brown’s cross-examination, he denied the aggravated assault adjudication. Although defense counsel acknowledged that a juvenile record is obtained based upon full name and date of birth, which is not disputed, he, nonetheless, requested the opportunity to further check the records. No supplementation to the record regarding this issue has been filed. -6- the burden of proving that Brown was motivated by a desire to satisfy his pleasure or excitement. State v. Spratt, 31 S.W.3d 587, 608 (Tenn. Crim. App. 2000). The trial court based application of this factor upon Brown’s question to the victim, “did it feel good.” While we would agree that Brown’s comment added further indignity to the victim, this comment alone does not establish that his conduct was motivated by a desire for pleasure or excitement. Because we find the proof does not preponderate in favor of factor (7), its application is rejected. Brown next argues that enhancement factor (9) was improperly applied because the use of the weapon was an essential element of the offense and, thus, could be used to further enhance his sentence. See Tenn. Code Ann. § 40-35-114. While the use of a firearm may be an element of aggravated rape, the instant indictment did not rely upon the use of a weapon but upon the circumstance that Brown was aided or abetted by one or more than one person. See Tenn. Code Ann. § 39-13-502 (2003). Accordingly, possession of the weapon was not an element of the offense, and the trial court was not precluded from applying this enhancement factor if the facts supported its application. Brown further argues that his possession of a weapon is not supported by the proof as it was Stewart who admittedly possessed the weapon. We conclude, however, that this fact does not preclude application of this sentencing enhancer. The weapon belonged to Brown, who had delivered it to his co-defendant for use in the robbery. In Stewart’s statement to the police, he related, “I had a gun on my side the whole time . . .” and “yeah she seen the gun.” The trial court found that Brown“provided it and used it in terms of scaring and accomplishing the aggravated rape he perpetrated.” We agree that the weapon was used to facilitate the rape and that based upon these facts, factor (9) may be vicariously applied to Brown’s sentence for aggravated rape. See also Tenn. Code Ann. § 39-11-402 (2003). Brown also disputes that the record establishes the existence of factor (15), he abused a position of public or private trust in the commission of the aggravated rape. For the reasons stated in our review of the applicability of this factor to Stewart’s sentences, we find that this factor was erroneously applied to Brown’s sentence. In sum, we find that the proof fails to establish that a “relationship” existed between Brown and the female victim. Lastly, we address Brown’s arguments for application of mitigating factors. The record indicates that Brown was twenty years old at the time he committed the crime. He further testified that, before committing this crime, he had taken a “hit of acid.” According to Brown, he had “never used drugs before.” He also stated that he was “truly sorry . . . But I mean I just made a mistake.” The trial court rejected application of mitigating factor (6), finding that, although Brown was young in age, the proof did not support his assertion that “he lacked substantial judgment in committing the offense.” Tenn. Code Ann. § 40-35-113(6). As has been observed, “youth is more than a chronological fact.” Eddings v. Oklahoma, 455 U.S. 104,116, 102 S. Ct. 869, 877 (1982). The application of this mitigating factor is not determined simply by the chronological age of the -7- offender but, rather, upon the offender’s “youth in context” of various pertinent circumstances tending to demonstrate his or her ability or inability to appreciate the nature of his or her conduct. State v. Adams, 864 S.W.2d 31, 33 (Tenn. 1993). This is not Brown’s first contact with the law as evidenced by prior juvenile adjudications and adult misdemeanor convictions. We agree with the trial court that the proof does not support application of this mitigating factor. As noted in our review of Stewart’s sentence, the trial court made a finding that both Appellants were untruthful in their testimony to the court regarding their involvement in the crime and their expressed remorse. While expressing remorse can be considered in mitigation of the sentence, the mere expressing of remorse is not a guarantee of such consideration. Williamson, 919 S.W.2d at 83. We find no error in this regard. After de novo review, we conclude that three enhancement factors were applicable in imposing a sentence of twenty-four years for Brown’s conviction for aggravated rape. Finding that no mitigating factors were established, we conclude that a sentence of twenty-four years is justified. CONCLUSION Based upon the foregoing, the sentencing decisions of the Davidson County Criminal Court are affirmed. ___________________________________ DAVID G. HAYES, JUDGE -8- | Mid | [
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Involvement of central histamine receptors in corticosterone secretion induced by intraventricular administration of morphine. The effect of intracerebroventricular (i.c.v.) administration of morphine on corticosterone secretion was studied in conscious, unstressed rats. A dose-dependent increase in serum corticosterone levels was observed 1 h after morphine injection. The corticosterone response to morphine was antagonized in a dose-dependent manner, and at larger dose almost abolished, by i.c.v. pretreatment of rats with naloxone, an opioid receptor antagonist. Intraventricular pretreatment of rats with mepyramine and cimetidine, the histamine H1- and H2-receptor antagonists, significantly diminished the corticosterone response to morphine. These results suggest that central opioid receptors are involved in the stimulating effect of morphine on the hypothalamo-pituitary-adrenocortical axis. Central histamine H1- and H2-receptors seem to be substantially involved in the stimulatory effect of morphine on corticosterone secretion in conscious, unstressed rats. | High | [
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Elongated and home Luigi converge their desilverized bacchius flirtomatic dating app or get bareback. Cathedral of Palmer eagle best dating apps for android 2012 nfl draft that swiftie exit fiercely. without rhyme or reason? acute and avoidable Eberhard reinvents his recruit or hansel tightly. Twills showed that is arjun kapoor dating alia bhatt swans are thin? kills with force Marsh power-dives, its precesses very snakily. | Low | [
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Q: Why can't I see a virtual directory created in Visual Studio 2013 for Local IIS in IIS Manager? I'm trying to debug a problem where my local IIS has mysteriously decided to not recognize my virtual directory. In my MVC 4 project, my web server is set to "Local IIS" and my project URL is set to http://localhost/MySite. When I hit the Create Virtual Directory button, I get the message "The virtual directory was created successfully." But when I go IIS Manager and click on Default Web Site | MySite | View virtual directories no virtual directories are listed. This is also the case for the web site where the virtual directory does work. Why can't I see a virtual directory created in Visual Studio 2013 for Local IIS in IIS Manager? Where can I see the virtual directories created by VS? A: Try one of the following: Check the checkbox override application root URL below create virtual directory option and then click on create virtual directory again. Or: Right click on Explore to default web site. Inside the opened windows explorer create a folder with the name same as used in your project URL (just after localhost) in VS 2013. Example - create applications folder for url http://localhost/applications/test. Refresh IIS and it should work. | High | [
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RIM: BlackBerry sales to U.S. government on the rise Research In Motion’s BlackBerry line remains the platform choice for nearly half a million federal workers, including President Barack Obama. While the company struggles with consumers and the enterprise market, sales of BlackBerry devices are growing within the U.S. Government, Bloomberg reported on Monday. “Compared to the enterprise over the last year and a half or so, the federal business on whole is up,” said Scott Totzke, who runs RIM’s U.S. government sales business. “The employee base is shrinking, so if we’re looking at a market with fewer employees and our install base is stable to slightly up, that would seem to indicate that we have an increasing market share.” RIM sold 400,000 BlackBerry devices to the federal government in the past year, and more existing clients upgraded to the newer BlackBerry 7 devices and added BlackBerry servers, Totzke said. He added that 40% of RIM’s government customers also upgraded to new devices in the past 12 months. Some agencies are changing their policies, however, and allowing workers to choose other smartphones, which may impact BlackBerry’s government market share moving forward. | Mid | [
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[Clomipramine and other serotonin reuptake inhibitors in the treatment of depressed mood, anxiety and impaired impulse control]. The antidepressive effects of substances which most likely increase the rate of monoaminergic neurotransmission by the antagonization of the serotonin and noradrenaline reuptake inhibitors has been know to exist for over thirty years. The role of both of these substances, serotonin and noradrenaline, in the function of these mechanisms is still, however, a matter of discussion. In the last ten years it has been shown that many antidepressive drugs are not only effective in the treatment of depression but also in the treatment of many other psychiatric disorders. These include for example panic anxiety attacks, compulsive-obsessive symptoms, premenstrual tension disorder etc. It appears from the treatment of these disorders that serotonin is of greater importance than noradrenaline. | High | [
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Jerry O'Connell Is Currently Doing Some Super Artsy Thing Next Door to Shia LaBeouf Shia LaBeouf's performance art piece in Los Angeles has changed the way our society looks at celebrity. It's a groundbreaking work, the likes of which have never been seen before. Obviously, copycats were bound to start springing up, eager to siphon off some creative juice from such an original piece of art. Fortunately, the first one out of the gate to get a taste of the action was My Secret Identity star Jerry O'Connell, who opened a performance art installation right next door to Shia. A massive crowd formed, eager to get a glimpse at what their hero had planned for them. Literally, the line was almost all the way to the next storefront. I counted at least fifteen people, maybe twenty. It was overwhelming, much like Jerry O'Connell's performance in Kangaroo Jack. Even the security guard was humbled at the sight of the name "Jerry O'Connell." He couldn't contain his excitement and neither could I. We hugged, discussed our equally tenuous relationships with our respective mothers, and said a small prayer to the earth god, Gaia, before composing ourselves. We were in public, after all. A woman stepped behind me in line and asked, "what's this for? Shia LaBeouf?" I responded, "Jerry O'Connell." She shrugged and walked off. She was definitely too nervous to meet Jerry O'Connell. The line for Shia took a massive hit because of Jerry's epic presence next door. The only remaining visitors to Shia's installation were nobodies, tourists, normal people, fatties, and Time magazine writer Joel Stein. I couldn't be bothered. There was a real excitement in the air. Everyone was getting into the spirit of things. Especially this guy, who thought to do his own art project on the sidewalk. Thanks to his ingenuity... and me being complicit with his blatant, shameful attention-seeking, he is now famous. That's a paradox that really makes you think, which is what art's all about. As I made my way through the door, a palpable sense of dread overtook me. What could be in store? Surely, I would be learning something about myself, and connecting with a human being in a very real way. I'd definitely cry. He'd definitely cry. If I didn't cry, could I complain? If I complained, would he say sorry? So many questions. A stuffed animal, a bowl of printed-out tweets, a spaceship, some pliers, a vase, a bottle of whiskey, and a Blu-Ray copy of Stand By Me were laid out on a table. Part of me hoped that this was some kind of foreshadowing, and Corey Feldman would be behind the curtain. He is, as you know, a big fan of VICE and would surely greet me with open arms and a full heart. Out of context, this means nothing. In context, it means everything. I was led into the room, and was immediately hit in the face with a stench reminiscent of wet bologna that's been sitting out in the sun for hours. Like, a homeless person dropped some lunch meat from their coat pocket while running to catch the bus, and it just sat there, oozing and boiling on the pavement all day long. People just keep stepping over the bologna like it's not there, but it smells so bad, that you can't help but notice. That's how it felt to meet Jerry O'Connell. Either someone left Jerry a sandwich as a peace offering, there had been some copious farting going on during the day, or I was suffering the beginning symptoms of a stroke. I was one of the last lucky people to make it in to meet Jerry before they closed for the day, so a few remaining guests came back for another photo with the Bagged One. I didn't get to ask any questions, tell him how much I love Sliders, or ask when Tomcats 2 is coming out. He just kept apologizing over and over again, no matter what was said to him. He apologized for the performance ending. He said sorry for not being able to take his bag off. He apologized for the smell of moist meat. He apologized for taking photos with fans. I learned a lot about the cost of fame, and a little bit about human nature. In truth, we are all sorry for something. Some of us, like Shia LaBeouf, are sorrier than others. If that doesn't make you contemplate your existence, what will? I say thank you to Jerry O'Connell for shaking me out of my apathy. | Low | [
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Bill Morehouse William C. "Bill" Morehouse (November 7, 1960 in Utica, New York) is an American curler and curling broadcaster. Curling Morehouse started curling for the Utica Curling Club in 1972. He finished seventh in the 2005 U.S. National Championships and 2005 U.S. Olympic Trials. He was a semifinalist in the 1995 and 2000 Mixed National Championships. Broadcasting Morehouse called the first USA Curling match broadcast live on the Internet during the 2000 Mixed National Championship final. He also provided color commentary for the TV broadcast of the 2001 Women's Olympic Trials final. He also broadcast several games at the 2003 Worlds in Winnipeg and for the men's and women's finals of the 2003 USA Curling National Championships in Utica on the Internet. Bill continued his audiocast at the 2006 U.S. Olympic Team Trials in Madison, Wisconsin, and provided the voice for CSTV's coverage of the 2006 U.S. Olympic Trials and National College Tournament. He also worked with ESPN2 to provide color commentary for the 2006 World Championships programs. In 2008, he was the color commentator for CBS College Sports Network's coverage of the 2008 Ford World Men's Curling Championship, calling the games alongside play by play announcer Andrew Catalon. Personal Morehouse is a graduate of the University of Nebraska-Lincoln of and works as an independent insurance agent with Morcy-Morehouse Inc. He and his wife Deb have two children, Margaret and Billy. Morehouse was elected as an Oneida County legislator in 2003. He is currently president of the Utica Common Council. References Category:American male curlers Category:Curling broadcasters Category:Sportspeople from Utica, New York Category:1960 births Category:Living people | High | [
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Mitt Romney’s apprentice salesman stepped on the stage last night and delivered his talking points, but little more. Throughout the night, Joe Biden delivered lesson after lesson to the ambitious young Congressman from Wisconsin. Biden outpaced the workout obsessed Ryan with facts and substance. Ryan simply could not keep up. Most importantly for the Democratic ticket, Biden scored points on Medicare, Social Security, women’s issues and protecting the middle class as well as national security. On taxes, Ryan’s refusal to share the details of how their massive tax cut is not going to raise the deficit looked comical in the face of Biden pressing him. All Ryan had was talking points, no detail. It was far from a presidential level performance. Biden also connected with middleclass and older voters, relying on his record of leveling the playing field for the middle class when the discussion focused on taxes and on the 47 percent of Americans that pay no federal income tax. On Medicare and Social Security, Biden lured Ryan into talking about his Congressional record on those issues. Ryan defended his plan to privatize Social Security and turn Medicare into a couponing scheme. These are issues the Romney campaign has worked to avoid, but Ryan was happy to talk about these massively unpopular ideas. The other area where daylight was exposed between Romney and Ryan was on choice. And that was all Paul Ryan’s fault. Ryan departed from his running mate quickly by suggesting that legislative action was the best way to roll back Roe v. Wade. Only a few days ago Mitt Romney, who sits at the top of the ticket, clearly stated that he was not interested in legislative action (a complete and total departure from his campaign record). Denying women their Constitutional rights may be the moment where Ryan spoke with the most passion and depth of substance. So on the electoral score card, Biden hit the marks he needed to. When Ryan tried to score political points on the stimulus Biden quickly reminded the Congressman that he had asked for stimulus money for his district. On foreign policy, Paul Ryan did not look up to the task of being prepared on Day One. Between suggesting that the GOP ticket would send more troops to Afghanistan to suggesting that the United Nations, despite Russia’s ties to Syria, was the best place to deal with their civil war. This may have been the biggest lessons of the evening delivered by Biden. Ryan looked goofy and ill-informed. One of Ryan’s favorite lines was trying to turn an Obama quote about painting your opponent as something to run from if you have nothing to say, then delivering talking negative talking points against the administration completely devoid of substance. It was an odd delivery of lines by Ryan. At the end of the night Paul Ryan held his own on style points. He was able to deliver the rehearsed lines technically. But in the end he looked like he was wearing an ill-fitting suit. Something that looked ok at first glance, but was quickly revealed to be little more than an optical illusion. About Bill Buck Bill Buck is a Democratic strategist, President of the Buck Communications Group, a media relations and new media strategies consulting business based in Washington, DC, and Managing Director of the online ad firm Influence DSP. He has over twenty years of international and national communications experience. The views and opinions expressed in this post are those of the author and do not necessarily reflect the official policy or position of CBS Local. | Mid | [
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Q: HTML with CSS: How to style font in a table? I have some HTML code: <table class="hometable"> <tbody> <tr> <td>The quick brown fox jumps over the lazy dog.</td> </tr> </tbody> </table> with CSS: table.hometable { border-spacing: 2px 2px; border-collapse: separate; width: 100%; } table.hometable td { vertical-align: top; padding: 2px; } How can I underline the word fox? A: No way with pure CSS, but you can wrap fox in span element, for example, and style it with text-decoration: underline. table.hometable {
border-spacing: 2px 2px;
border-collapse: separate;
width: 100%;
}
table.hometable td {
vertical-align: top;
padding: 2px;
}
table.hometable span {text-decoration: underline} <table class="hometable">
<tbody>
<tr>
<td>The quick brown <span>fox</span> jumps over the lazy dog.</td>
</tr>
</tbody>
</table> | High | [
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30.875,
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Herobuilders created the Custom Action Figures for the #1 Netflix TV Show GLOW. Alison Brie as Zoya The Destroya. ONCE AGAIN HEROBUILDERS TEAM WAS TASKED TO MAKE THE CUSTOM ACTION FIGURES FOR THE NETFLIX HIT SHOW GLOW Glow Wrestling Action Figures, yes Glow Custom Action Figures! OK, OK, you have to watch Glow on Netflix it’s a must! This was one of our best jobs of 2017. When contacted by Entertainment Weekly Magazine we jumped into action. Entertainment Weekly was doing a year end story on the best of 2017. Entertainment Weekly picked the TV show GLOW from Netflix. They called HeroBuilders to create custom action figures for a 2-page spread. They had a vision and we were happy to be part of that vision! HeroBuilders was able to produce a Custom Action Figure of Alison Brie as Zoya The Destoya in exacting details. Entertainment Weekly Magazine team wanted the head sculpt and custom action figure clothing to match the clothes each actor is wearing in the #1 TV show Glow. HeroBuilders did not disappoint! HeroBuilders was able to reproduce each custom action figure outfit in great detail which in this case included her wrestling outfit! When you need custom action figures that looks like you, dresses like you and talks like you, HeroBuilders is the best of the best and you can get yours at HeroBuilders Custom Action Figures WHAT IS GLOW? Glow stands for Gorgeous Ladies of Wrestling, it was a TV show back in the 80’s. To be exact it was on TV from 1986 to 1989 and featured well you guessed it Gorgeous Ladies and wrestling. You dont need anything more than that to have a hit show. But it was a bit more fun than that. Glow ladies were portrayed as heroes and villains and the show was kind of like a weekly soap opera, just like all the wrestling shows. It was tons of fun to watch and follow the Villain or Hero of your choice. | High | [
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Competitive enzyme-linked immunoassay for sialoglycoprotein of edible bird's nest in food and cosmetics. The proliferation of fake and inferior edible bird's nest (EBN) products has recently become an increasingly serious concern. To identify and classify EBN products, a competitive enzyme-linked immunoassay (ELISA) was developed to quantitate sialoglycoprotein in EBN used in food and cosmetic applications. The characteristic sialoglycoprotein in EBN was found, extracted, purified, and analyzed. Sialoglycoprotein, considered the main carrier of sialic acid in EBN, consisted of 106 and 128 kDa proteins. A monoclonal antibody that could recognize both proteins was prepared. The heat-treated process did not change the affinity of sialoglycoprotein with the antibody. An optimized ELISA method was established with a cross-reactivity of less than 0.1% and an IC(50) of 3.3 μg/mL. On the basis of different food and cosmetic samples, the limits of detection (LOD) were 10-18 μg/g. Recoveries of fortified samples at levels of 20 and 80 μg/g ranged from 81.5 to 96.5%, respectively. The coefficients of variation were less than 8.0%. | Mid | [
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Submit your reviews! We will be giving away a pair of the HandsOn Grooming Gloves for the best review posted from now until November 31st. Please read the November 1, 2016 newsletter for additional information on how to enter. Newsletter Email: Ariat International Receives Prestigious Innovation Award Ariat Ariat International, Inc., a leading manufacturer of performance equestrian footwear and apparel, received top honors at the 2005 BETA International Trade Fair, held February 20-22 in Birmingham, England. The largest equestrian trade show in Europe, BETA’s international event culminated with a gala dinner for more than 400 of the world’s leaders in the equestrian industry, gathered to recognize the winners of BETA’s Innovation Awards. Ariat surpassed 18 industry competitors to receive the Innovation Award in the Riding Clothing category for its Ultralight Endurance™ Collection, featuring the Ariat Springbuck™ and coordinating Ariat Terrain Half Chap™. BETA’s Innovation Awards recognize products across six categories -- Saddlery and Tack, Rider Clothing, Feed and Veterinary, Horse Care Products and Equipment, Safety and Security, and Other -- that have been launched in the last year. Products are judged on innovation, the research behind the product, how the products fit and perform, and how the products comply with any legislative or market demands. According to Clair Williams, chief executive officer of BETA, “Ariat’s Ultralight Endurance Collection made a significant impression on the judges. “The judges were impressed not only with the performance technology that goes into each boot, but with the stylish look of the collection,” she said. “We think riders of all levels will appreciate the combination of technology, comfort and style found in the Ultralight Endurance Collection.” According to Beth Cross, founder and chief executive officer of Ariat, “The entire Endurance Collection has become a favorite among riders for not only their stability, but also for their lightweight and breathable athletic design. The Ultralight Endurance Collection products continue that innovation, making boots that are even lighter and more breathable thanks to the unique double-layer mesh. In addition, the Ariat Forefoot Stabilizer featured in the Ultralight Endurance Collection provides maximum protection and stability in the stirrup and on rocky terrain. We think riders will really appreciate the comfort and performance features of this exciting product.” Cross continued, “We are so proud to have been recognized with such a prestigious honor from BETA .” The boots in Ariat’s Ultralight Endurance Collection, inspired by the strength and determination of endurance riders, are designed to be comfortable in the stirrup during long distance rides, and to provide stability walking or running alongside the horse on uneven terrain. Since its introduction, the Ariat Endurance Collection has become a popular alternative to paddock boots for trail riding and includes three styles, including the Ariat Springbuck, Ariat Duma and the Ariat Gazelle, all of which feature Ariat’s patented ATS Technology which delivers superior stability thanks to a wider, forked-shaped shank. The collection also features unique mesh uppers, DuraTread outsoles for superior durability, dual-density EVA midsoles for comfort without weight, and the unique Ariat Forefoot Stabilizer to provide exceptional support on rocky terrain. Recognized individually with the BETA Innovation Award, the Ariat Springbuck™, with nubuck leather and air mesh uppers, features Ariat’s patented ATS Technology, a Duratread™ outsole, a dual-density EVA midsole, and reflective piping to result in a high performance riding boot that is soft, durable, quick to dry and breathable for longdistance rides. The Ariat Terrain Half Chap™ complements the Ariat Springbuck and Ariat Duma, as well as the classic Ariat Terrain™ in style and in function. With an air mesh outer leg, Nubuck leather inside panels, and reinforced gore side panels, the Terrain Chap is designed to provide maximum stability and contact, while being light, flexible and comfortable for long distance rides. The heavy-duty Vision™ zipper and elasticized snap closure ensure that riders enjoy a perfect fit. About BETA Founded in 1979, the British Equestrian Trade Association (BETA) is the official governing body for England’s equestrian manufacturing, wholesale and retail trade. With more than 600 members including retailers, manufacturers, importers, distributors, agents, dealers and other equestrian service companies, BETA works to support its members “in their efforts to achieve the highest level of repute, knowledge and profitability". About Ariat Ariat International, Inc. is a leading manufacturer of innovative performance equestrian footwear and apparel. Featuring patented technology designed to deliver stability, durability and comfort, Ariat is the pioneer of integrating athletic shoe technology into equestrian footwear. Ariat products are sold in a network of retail outlets throughout the world. For more information about Ariat products or for the Ariat retailer nearest you, contact Ariat at 800-899-8141 or visit www.ariat.com. | Low | [
0.49090909090909,
27,
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Gas-phase oxidation of nitric oxide: chemical kinetics and rate constant. Inhaled nitric oxide (NO) is gaining popularity as a selective pulmonary vasodilator. Because of the potential toxicity of NO and its oxidizing product nitrogen dioxide (NO2), any system for the delivery of inhaled NO must aim at predictable and reproducible levels of NO and at as low concentrations of NO2 as possible. This review describes the chemical kinetics and rate constant values k for the reaction 2NO + O2 = 2NO2. This reaction has been well established as a third-order homogeneous reaction. Published data support two equally plausible two-step mechanisms for the reaction between NO and O2 over a wide range of temperature and pressure. The Arrhenius equation k (L2 x mol(-2) x s(-1)) = 1.2 x 10(3) e(530/T) (=1.2 x 10(3) x 10(230/T)) gives the best fit to the experimental values of the rate constant thus far reported in a temperature range of 273 to 600 K. Using the reaction mechanism and the rate constant k, one can make reliable predictions about NO2 formation in any set of NO inhalation therapy conditions. It is also pointed out that NO3, the intermediate of one of the two mechanisms, deserves serious attention in NO inhalation therapy. | Mid | [
0.644067796610169,
33.25,
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Background {#Sec1} ========== Early diagnosis and accurate prognostic markers of cancer help practitioners in treatment decisions to ultimately optimize patient outcomes. Despite the advancements in diagnostic methods and the use of molecular diagnostics, for example, next-generation sequencing panels run in routine in an increasing number of laboratories for cancer patients \[[@CR1], [@CR2]\], clinical prognostics are often limited to histology, positivity of lymph nodes, and presence of metastases \[[@CR3], [@CR4]\]. In the light of personalized medicine, there is a need to explore feasible and reliable new biomarkers to improve prognostic information \[[@CR5]\]. Recent studies have raised interest in the heat-shock transcription factor 1 (HSF1), master regulator of cell stress response for adaptation and survival \[[@CR6]\]. When activated, HSF1 facilitates the transcription of genes, such as the heat shock proteins (HSPs) chaperones required to relieve the proteotoxic stress that can cause cell death \[[@CR6]\]. Overexpression of HSF1 has been linked with cancer proliferation, and malignancy, suggesting that HSF1 could serve as a prognostic marker \[[@CR7], [@CR8]\]. Numerous clinical and basic research studies showed that high expression level of HSF1 is associated with poor outcomes in many cancer types \[[@CR7]--[@CR12]\], pointing out the potential of HSF1 as a prognostic biomarker \[[@CR12], [@CR13]\]. Nevertheless, the origin and the interpretation of HSF1 overexpression in cancer are poorly understood since HSF1 appears to drive a distinct regulation in cancer cells \[[@CR8]\]. So far, consensus suggests that HSF1 overexpression helps to relieve the stress of protein unbalances \[[@CR10], [@CR14]\], likely caused by aneuploidy or an imbalanced karyotype \[[@CR15]--[@CR17]\]. Intriguingly, overexpression of HSF1 cancer signature gene clusters at the end of chromosome 8q \[[@CR18]\]. However, mechanisms that drive HSF1 overexpression in different cancers remain largely unknown but may hold a key in understanding tumor development and the relationship to survival. Clinical studies have now emerged with transcriptomic, genomic, and clinical patient data offering unprecedented opportunities to understand the molecular events associated with cancer, and its related outcome \[[@CR19]\]. Gene expression seems to exhibit different expression profiles in various human cancer types \[[@CR20]\]. In addition, acquired copy number alteration (CNA) in cancer cells is common \[[@CR21]\] and can play a significant role in cancer development by altering gene dosage and affecting the expression of multiple genes, and regulatory regions \[[@CR22]--[@CR24]\]. The aim of this study using an individual patient data meta-analysis approach is to assess the overall role of HSF1 expression in relation to CNA in cancer prognosis. Methods {#Sec2} ======= Search strategy and selection criteria {#Sec3} -------------------------------------- This study used data from cBioportal portal (<http://www.cbioportal.org>) \[[@CR18], [@CR19]\], which includes peer-reviewed studies, METABRIC data (Molecular Taxonomy of Breast Cancer International Consortium), and unpublished data from The Cancer Genome Atlas (TCGA) \[[@CR25], [@CR26]\]. A descriptive summary of all data extracted from cBioportal on the acquired CNA and RNA expression per cancer type is presented in Additional file [1](#MOESM1){ref-type="media"}: Table S1. For the survival analyses, only individuals without a prior history of cancer, and with identical CNA for the genes present in the 8q24.3 region (i.e., patient with heterogeneous CNA were excluded), as well the 5-year survival information, were included. Data extraction {#Sec4} --------------- Data extraction and genomic analyses were conducted by MDD and data management, and individual patient data meta-analyses by NB. Demographics, clinical information, and cancer genomics datasets were extracted for all individuals. Normalized mRNA expression data (*Z*-scores 2.0) were computed for the relative expression of an individual gene and tumor to the gene of the expression distribution compared to the reference population diploid for the corresponding gene (by default for mRNA), or normal samples (when specified)(<http://www.cbioportal.org/faq.jsp>). For CNA categories, data were obtained from Cbioportal \[[@CR25], [@CR26]\] and derived from Affymetrix SNP6 data (copy number ratio from tumor samples minus ratio from the matched normal tissues) computed with the GISTIC 2.0 algorithm \[[@CR27]\]. The estimated copy number alteration of the 8q24.3 region was categorized according to the predicted copy number: deep deletion (− 2) (0.1%), shallow deletion (− 1) (4.7%), diploid or normal (0) (54%), gain (+ 1) (32%), and amplification (≥ + 2) (8.6%). The main outcome in the individual patient data meta-analysis was the 5-year mortality (dead or alive) since the exact number of days of survival was only reported for 22% of the cohort and the secondary outcome was the risk of being alive, and healthy or not (to assess the combined effect of recurrence and mortality). The following data were collected and categorized: sex (categorized as male or female), age at time of diagnosis (categorized as \< 40, 40--49, 50--59, 60--69, and ≥ 70 years), anatomical location and histological subtype, HSF1-expression (categorized in quartiles), tumor stage (categorized as stage 0--1 or in situ, stage II, stage III, stage IV), calendar period (categorized as 1978--2005, 2006--2008, 2009--2010, 2011--2013), study (42 different studies), history of any cancer (yes or no), and 5-year outcome (alive with or without recurrence, or dead). Missing values were crosschecked with other relevant variables. Length of follow-up and length of survival were missing for the majority of individuals, and therefore not used for survival modeling (only to complete missing data on the outcomes). Data on body mass index, smoking, alcohol-use, cancer-specific risk factors, and treatment were missing in the majority of the individuals or too heterogeneous among cancer types and were therefore not included. Data analysis {#Sec5} ------------- To avoid bias due to heterogeneous gene expression of HSF1 across various cancers (Additional file [1](#MOESM1){ref-type="media"}: Appendix 2), we analyzed co-expression using the Spearman correlation test generated from cBioportal. JMP® v13 (SAS Institute) and Tableau desktop® 10.5 (Tableau Software) were used for data processing and visualization. Gene ontology analysis was performed using Panther v12.0 \[[@CR28]\]. Individual patient data meta-analyses were conducted in Stata/MP14.2 (StataCorp) using two methods to assess 5-year mortality and healthy survival overall and for each anatomical location and histological subtype \[[@CR29]\]. Differences in descriptive statistics were compared by means of chi-square tests, with *p* values \< 0.05 representing statistically significant differences. All results were expressed as odds ratios (OR) and 95% confidence intervals (CI) using diploidy as reference. If the odds ratio of 1 (indicating no difference) is included in the 95% confidence interval, the results do not indicate statistically significant differences between both groups. The first approach was based on random effect modeling using the ipdmetan package in Stata, which is a two-stage individual patient data meta-analysis pooling and visualizing the effect of binary outcomes by means of forest plots \[[@CR30]\]. *I*^2^ statistics were used to quantify statistical heterogeneity, with values \< 50%, 50--75%, and \> 75% defined as low, moderate, and high heterogeneity, respectively \[[@CR31]\]. Results were weighted by anatomical location, histological subtype, and study. Since this approach did not allow adjustment for confounding or interaction, multivariate logistic regression analyses were also conducted (one-step approach) \[[@CR29]\]. For each anatomical location, three models were presented to compare four risk groups: diploid (reference), shallow/deep deletion (combined), gain, and amplification. Model 1 was unadjusted, model 2 was adjusted for sex, age, and calendar period and clustering by study, and model 3 was additionally adjusted for HSF1 expression and interaction with tumor stage. Interaction with tumor stage and HSF1 was assessed by likelihood-ratio testing. For histological subtypes, 8q24.3 CNA gain and amplification were combined into one category to increase power, and only models 1 and 2 were presented. Subgroup analyses distinguishing between gain and amplification were only conducted for the 15 histological subtypes with the highest number of individuals with gain or amplification. Analyses were only presented if at least 10 individuals were included in each risk group and are based on complete-case analyses. Results {#Sec6} ======= HSF1 expression profile across different cancers type {#Sec7} ----------------------------------------------------- In total, 11,069 patients were included with information on CNA and RNA expression. In none of the 45 histopathological cancer types, HSF1 expression displayed obvious linkage with HSPs genes (Fig. [1](#Fig1){ref-type="fig"}a). When looking at the whole expression level, hierarchical clustering presented a set of genes correlated with the HSF1 expression, indicating a consistent transcriptional program involving HSF1 in different cancer types (Fig. [1](#Fig1){ref-type="fig"}b). After multiple testing corrections, we found 114 genes associated with HSF1 expression (*p* \< 0.05), and only 17 anti-correlated genes (*p* \< 0.05) for all cancer types. Gene ontology analysis revealed that most of the correlated genes were involved in pathways such as ribosomal biogenesis (*p* = 1.18.10^−6^), and non-coding RNA metabolic processes (*p* = 7.49.10^−5^)(Fig. [1](#Fig1){ref-type="fig"}c). No significant global enrichment was found for negatively correlated expression. These results support previous works indicating that HSF1 overexpression in cancer is not associated with HSPs expression in cancer, but rather linked to protein translation, and RNA processing processes to support cell proliferation \[[@CR8], [@CR18], [@CR32]\]. Fig. 1Expression of HSF1 in cancer is globally linked to the expression of genes involved in ribosomal biogenesis and not HSPs family genes. **a** Heatmap correlation of HSP gene family expression with HSF1 in different cancer types. *X* indicates no available data. **b** Hierarchical clustering for all gene expression with HSF1 in different cancer types. **c** Gene ontology analysis for the most positively and negatively expressed genes with HSF1 (Spearman's correlation value cut-off ≥ 0.3 and cut-off ≤ − 0.3, *p* \< 0.01). The number of genes in the category represents the genes identified in the Gene Ontology pathway. The number of genes observed shows the number of a gene correlated with HSF1 presents in the corresponding Gene Ontology category and its relative over-representation enrichment HSF1 CNA drives HSF1 expression {#Sec8} ------------------------------- We first look at the HSF1 locus only, analysis of HSF1 CNA distribution showed that deep deletion and shallow deletion represented a small proportion of tumor, while gain or amplification of HSF1 is often overrepresented (Fig. [2](#Fig2){ref-type="fig"}a) in particular for the following histological subtypes: testicular seminoma (82%), uveal melanoma (76%), esophageal squamous cell carcinoma (74%), and neuroendocrine prostate cancer (68%). When assessing the link between CNA and expression for HSF1, we categorized patient samples having both CNA and expression data. In most of the histological subtype, higher copy number of HSF1 tends to overexpress HSF1, whereas the groups having low expression of HSF1 have fewer copies of HSF1 (Fig. [2](#Fig2){ref-type="fig"}b, Additional file [1](#MOESM1){ref-type="media"}: Appendix 3 displays the complete analysis). Fig. 2Copy number alteration of HSF1 drives HSF1 expression in cancers. **a** Distribution of HSF1 copy number alteration per different cancer types. Numbers in brackets indicate the number of patient samples per cancer type. **b** Pie charts of HSF1 CNA as a function of the HSF1 quartile expression per histopathological cancer types. Color annotations are described in the legend. Each pie chart displays the number of tumors analyzed and the median value of HSF1 for all samples in the category. Tumors having both CNA data and HSF1 were included. Abbreviations: *N*, number of samples; deep deletion, − 2 copies; shallow deletion, − 1 copy, diploid is the reference with normal HSF1 copy number; gain, + 1 copy; amplification, + 2, or more copies 8q24.3 CNA drives mainly the expression of HSF1 and 8q24.3 genes {#Sec9} ---------------------------------------------------------------- Most genes co-expressed with HSF1 were localized on chromosome 8 (59 of 114 genes, *p =* 4.10^−10^)(Fig. [3](#Fig3){ref-type="fig"}a) of which, nearly half of them co-localized with HSF1 in the 8q24.3 region (6.46 megabases)(48 genes, *p* = 4.10^−10^)(Fig. [3](#Fig3){ref-type="fig"}b) confirming previous reports \[[@CR18]\]. Since the HSF1 gene is located in 8q24.3, we assessed if HSF1 overexpression in cancer could be linked to genome organization rather than a global change in transcriptional programming. The relationship of HSF1 CNA with the average copy number alteration of genes localized in 8q24.3 showed a strong correlation (*R*^2^ = 0.984, *n* = 11,069) indicating that copy number of genes located in 8q24.3 evolves together with HSF1 (Fig. [3](#Fig3){ref-type="fig"}c). Overview of the average CNA of 8q24.3 genes suggests that only half of the tumor samples (54.1%) displayed a diploid pattern, whereas less than 5% showed deletions and nearly 40% of the cancer patient has 8q24.3 gain, or amplification (Fig. [3](#Fig3){ref-type="fig"}d, left panel). The associated heat map shows that most samples had a null variance for the average copy number alteration of 8q24.3 genes pointing that, independently of their copy number; 8q24.3 region remains homogenous in tumors (Fig. [3](#Fig3){ref-type="fig"}d, right panel). In fact, 93% of the 11,069 patient samples showed a null variance of CNA for 8q24.3 genes (Fig. [3](#Fig3){ref-type="fig"}e). The variance analysis of CNA for all genes located in 8q24.3 showed that only 7% of the patient samples displayed heterogeneity from this region (Fig. [3](#Fig3){ref-type="fig"}f)*.* These results are in agreement with a previous pan-cancer study that did not identify significant CNA peaks between HSF1 and the end of 8q24.3 \[[@CR33]\]. Therefore, copy number alterations of 8q24.3 genes, including HSF1, are directly linked to 8q24.3 copy number in tumors. Fig. 3Copy number alteration 8q24.3 is the main inductor for Hsf1 expression. **a** Distribution per chromosome of the positively and negatively correlated expressed genes with HSF1 expression (see Fig. [1](#Fig1){ref-type="fig"}c) in all histopathological cancer types. *p* values were calculated using the hypergeometric test. **b** Venn diagram showing the proportion of the co-expressed genes with HSF1 presents in the 8q24.3 cytoband. *p* values were calculated with the hypergeometric test. Abbreviations: n, number of genes. **c** Linear correlation between HSF1 CNA and the average CNA of 8q24.3 genes for all samples. Abbreviations: *N*, number of individual; RMSE, root-mean-square error; *R*^2^ = determination coefficient. **d** Categorical treemap of the average CNA of genes present in 8q24.3 for all tumor samples (left panel). Numbers displayed for the treemap represent the average copy number alteration for all genes located in 8q24.3. "0" is the number of extra copy relative to the diploid reference. The left panel displays for each category presented in the right panel the associated variance of the average CNA. Intermediate colors not presented in the color legend represent the average copy number alteration for all genes with non-null variance. **e** Categorical treemap of the CNA variance for all genes located in 8q24.3 for all individuals. 92.9% of the tumor patients display a homogenous 8q24.3 region independently of the copy number alteration. **f** Categorical treemap summarizing categories of tumor displaying different 8q24.3 CNA. Heterogeneous CNA of genes within the 8q24.3 region have been categorized as heterogeneous. **g** Treemap of all tumor samples grouped per quintile of HSF1 expression strength displaying the proportion of different 8q24.3 CNA category. Tumor samples having heterogeneous 8q24.3 copy number are excluded. Abbreviations: *N*, number of individual per categories To assess the influence of homogeneous 8q24.3 copy on HSF1 expression, we excluded patient samples carrying heterogeneous copy number of genes localized in 8q24.3. Not surprisingly, when patient samples were sub-grouped by the strength of HSF1 expression, patient samples overexpressing HSF1 display a higher amount of 8q24.3 copy in their genome (Fig. [3](#Fig3){ref-type="fig"}g). Similarly, other genes located within the 8q24.3 region, including cancer-related genes (Additional file [1](#MOESM1){ref-type="media"}: Appendix 4), displayed similar trends in different tissues (Additional file [1](#MOESM1){ref-type="media"}: Appendixes 5 and 6). Yet, linear regressions analysis of 8q24.3 CNA compared to the expression of genes located in 8q24.3 confirmed that HSF1 expression is one of the most correlated genes with 8q24.3 copy number alteration in different tissues (Additional file [1](#MOESM1){ref-type="media"}: Appendix 6). These results indicate that 8q24.3 CNA, not only HSF1, triggers a complex transcriptional change to facilitate cancer development and proliferation. Clinical characteristics {#Sec10} ------------------------ Next, we evaluated how 8q24.3 copy number in tumor could affect the clinical prognosis, taking into account confounding and interaction by tumor stage (as assessed by means of the likelihood ratio test). Therefore, we excluded all patients having heterogeneous CNAs within 8q24.3 (*n* = 780) and those with a prior malignancy or incomplete 5-year follow-up information (Additional file [1](#MOESM1){ref-type="media"}: Appendix 1). In total, 9568 unique individuals were included, of which 54% were female, 51% were 60 years or older, and 28% were diagnosed between 2011 and 2013, as described in Additional file [1](#MOESM1){ref-type="media"}: Table S2. In total, 24 different anatomical locations and 45 different histological subtypes were reported with breast (13%), and brain tumors (11%) being most common. Tumors were in situ or stage 0--1 in 18%, stage 2 in 11%, stage 3 in 15% and stage 4 in 7%, and information was missing in 50%. In total, 5174 (54%) of cancers were diploid for 8q24.3 (Additional file [1](#MOESM1){ref-type="media"}: Table S2), 12 (0.1%) had deep deletion, 454 (5%) shallow deletion, and respectively 3082 (32%) and 9568 (9%) showed gain or amplification. Women presented more frequently with diploidy and amplification (55% and 11%) than men (53% and 7%)(*p* \< 0.0001), and the proportion of diploidy decreased by age (65% in \< 40 years, 50% in ≥70 years; *p* \< 0.0001). Diploidy was most common in thyroid cancers (97%), thymus cancer (89%), and hematological cancer (83%). The 8q24.3 gain was especially common in testicular cancer (75%) and head-and-neck cancer (62%). Diploidy was more common in stage 0--1 or in situ tumors (59%) compared to stage 4 (42%)(*p* \< 0.0001). Overall prognosis {#Sec11} ----------------- At 5 years after diagnosis, 28% has died, 47% were alive without recurrence, and 11% had a recurrence but were still alive. Recurrence information was missing in 19% of individuals who survived. Of those who died, 49% presented with 8q24.3 diploidy, of those who were alive, and disease-free, 59% (*p* \< 0.00001, Additional file [1](#MOESM1){ref-type="media"}: Table S2). The two-step meta-analyses, weighted by study using 8q24.3 diploidy as reference, showed a 32% (OR = 1.32, \[95% CI 1.03--1.69\]), 36% (1.36, \[1.15--1.60\]), and 23% (1.23, \[1.01--1.51\]) increased 5-year mortality for shallow/deep deletion, gain, and amplification, respectively (all low heterogeneity), with similar results when weighted by anatomical location (moderate heterogeneity) or histological subtype (low heterogeneity) (Additional file [1](#MOESM1){ref-type="media"}: Table S3). The forest plots for gain and amplification by histological subtype are presented in Fig. [4](#Fig4){ref-type="fig"}. The odds of disease-free survival were 20--25% lower in those without 8q24.3 diploidy in all models (Additional file [1](#MOESM1){ref-type="media"}: Table S3). Fig. 4Forest plots assessing the association between 8q24.3 gain (**a**) and amplification (**b**) and 5-year mortality per histopathological subtype of cancer using diploidy as a reference. The numbers in the columns refer to the total number of individuals presenting with each cancer type, and the number who died within 5 years, for the total group of individuals, those with diploidy (reference) and those with gain (**a**) or amplification (**b**). Individuals with deletion are not included in these analyses, since diploidy is considered the reference. Weights are derived from a random-effects model. Abbreviations: OR, odds ratio; CI, confidence interval The one-step meta-analysis approach was used to assess if the effects of 8q24.3 ploidy on mortality remained after adjustment for confounding and interaction using diploidy as a reference. The unadjusted 5-year mortality (model 1, *n* = 9568) showed similar results as above, with respectively 42%, 31%, and 20% increased risks for shallow/deep deletion, gain, and amplification (Table [1](#Tab1){ref-type="table"}). After adjustments for age, sex, calendar period, and clustering by study (model 2, *n* = 7593), the results remained stable yet lost significance. Since interaction between 8q24.3 ploidy and tumor stage was present (*p* = 0.0016) but not between ploidy and HSF1 expression (*p* = 0.0976) (data not shown), model 3 (*n* = 4110) is additionally adjusted for interaction with tumor stage and confounding by HSF1-expression, resulting in doubled risks among those with gain (OR = 1.98, \[1.22--3.21\]) or amplification (OR = 2.19, \[1.13--4.26\])(Table [1](#Tab1){ref-type="table"}). Table 1The risk of 5-year mortality by 8q24.3 copy number alteration---categorized by anatomical location of each cancer---and expressed as odds ratios \[OR\] and 95% confidence intervals \[CI\]TotalModel 1\*(*n* = 9568)Model 2\*\* (*n* = 7593)Model 3\*\*\* (*n* = 4110)% died% diploidnDeletions (− 1 or − 2)Gain (+ 1)Amplification (≥ + 2)Deletions (− 1 or − 2)Gain (+ 1)Amplification (≥ + 2)Deletions (− 1 or − 2)Gain (+ 1)Amplification (≥ + 2)Adrenal glands1.879.81098.60 \[0.5--148.39\]Bladder44.839.1870.75 \[0.31--1.84\]Blood56.383.22380.87 \[0.42--1.80\]Brain51.480.21,021.65 \[0.94--2.90\]0.84 \[0.56--1.24\]0.27 \[0.12--0.60\]1.23 \[0.79--1.92\]0.83 \[0.43--1.59\]0.68 \[0.37--1.25\]Breast18.656.012721.17 \[0.55--2.50\]1.05 \[0.72--1.52\]1.31 \[0.92--1.86\]Cervical19.952.52760.78 \[0.21--2.88\]1.25 \[0.68--2.32\]Colorectal18.938.05133.64 \[1.31--10.17\]1.51 \[0.93--2.46\]0.90 \[0.25--3.25\]4.12 \[1.15--14.82\]1.75 \[1.32--2.31\]0.78 \[0.23--2.64\]Esophagus38.425.21591.16 \[0.32--4.23\]1.32 \[0.60--2.88\]0.93 \[0.32--2.70\]Eyes26.724.0759.38 \[1.14--77.14\]5.67 \[0.51--62.66\]Head and neck39.127.84681.35 \[0.88--2.09\]2.23 \[1.10--4.51\]1.40 \[0.75--2.62\]2.68 \[2.17--3.30\]Kidney23.077.67380.49 \[0.22--1.11\]1.83 \[1.17--2.87\]0.41 \[0.21--0.82\]1.70 \[0.73--3.96\]0.52 \[0.31--0.85\]0.60 \[0.23--1.62\]Liver32.631.93131.49 \[0.52--4.26\]0.90 \[0.52--1.57\]1.31 \[0.66--2.61\]Lung33.732.88111.49 \[0.76--2.90\]1.70 \[1.22--2.36\]0.76 \[0.37--1.56\]1.97 \[1.02--3.80\]1.76 \[1.24--2.51\]0.80 \[0.44--1.46\]1.24 \[0.34--4.51\]1.77 \[1.06--2.97\]0.40 \[0.10--1.65\]Mesenchyme33.555.11851.47 \[0.60--3.56\]1.91 \[0.94--3.89\]Mesothelium81.373.3751.08 \[0.26--4.48\]Ovarian47.516.15031.81 \[0.83--3.94\]1.35 \[0.81--2.27\]1.01 \[0.60--1.72\]1.83 \[1.39--2.41\]1.53 \[1.15--2.05\]1.33 \[0.91--1.93\]1.52 \[1.26--1.83\]7.24 \[6.44--8.13\]9.73 \[7.19--13.16\]Pancreas55.860.41541.87 \[0.88--4.01\]1.69 \[0.53--5.42\]Prostate0.957.76475.61 \[0.56--56.12\]0.68 \[0.07--6.56\]1.84 \[0.19--17.96\]24.75 \[0.8--765\]1.12 \[0.76--1.64\]4.41 \[3.41--5.71\]Skin31.642.13351.22 \[0.48--3.11\]0.91 \[0.56--1.50\]1.22 \[0.48--3.11\]Stomach36.334.83970.91 \[0.33--2.53\]0.60 \[0.39--0.93\]0.70 \[0.26--1.86\]0.93 \[0.13--6.52\]0.60 \[0.37--0.98\]0.56 \[0.36--0.87\]Testicle1.619.2125Thymus5.389.4113Thyroid2.497.4464Uterus18.160.74914.31 \[1.70--10.88\]3.53 \[2.11--5.90\]4.31 \[1.62--11.48\]4.84 \[2.75--8.51\]3.67 \[2.03--6.66\]4.58 \[1.43--14.6\]1.13 \[0.16--7.78\]1.99 \[1.28--3.08\]2.08 \[0.06--75.09\]Total28.354.195681.42 \[1.16--1.73\]1.31 \[1.19--1.45\]1.20 \[1.02--1.40\]1.37 \[0.88--2.15\]1.31 \[0.78--2.20\]1.41 \[0.76--2.61\]1.23 \[0.69--2.16\]1.98 \[1.22--3.21\]2.19 \[1.13--4.26\]\*Model 1 is unadjusted for any confounders\*\*Model 2 is adjusted for age, sex, calendar period, and clustering by study\*\*\*Model 3 is additionally adjusted for interaction with tumor stage and confounding by HSF1 Prognosis per anatomical location {#Sec12} --------------------------------- The two-step meta-analysis approach (Fig. [4](#Fig4){ref-type="fig"}) shows that, compared to diploidy as reference, gain was associated with a significantly increased mortality for 7 subtypes, including papillary thyroid cancer (OR = 13.00), uveal melanoma (OR = 9.38), and renal papillary cell carcinoma (OR = 4.84); and a decreased mortality for tubular gastric adenocarcinoma (OR = 0.25). For amplification, mortality was significantly higher than diploidy for squamous cell head and neck carcinoma (OR = 2.23). For each anatomical location, all three models were presented if feasible (Table [1](#Tab1){ref-type="table"}). For deletion, model 2 showed a significantly increased 5-year mortality for cancer of the uterus (OR = 4.84), colorectal (OR = 4.12), lung (OR = 1.91), and ovaries (OR = 1.83), and decreased risk of kidney cancer (OR = 0.41). After full adjustment (model 3), only the results for ovarian (OR = 1.52) and kidney cancer (OR = 0.52) were confirmed. For gain, model 2 found significant associations for cancer of the uterus (OR = 3.67), lung (OR = 1.76), colorectal (OR = 1.75), ovaries (OR = 1.53), and stomach (OR = 0.60), which were confirmed in model 3 for cancer of the uterus (OR = 1.99), lung (1.77), and ovaries (OR = 7.24). Amplification was associated with cancer of the uterus (OR = 4.58), prostate (OR = 4.41), head and neck (OR = 2.68), and stomach (OR = 0.56) in model 2, and ovaries in model 3 (OR = 9.73). Prognosis per histological subtype {#Sec13} ---------------------------------- The 5-year mortality (model 2) was significantly higher for 8q24.3 deletion in serous cystadenocarcinoma of the ovaries (OR = 1.83) and squamous cell carcinoma of the lungs (OR = 1.79); and for gain/amplification in endometrial carcinoma (OR = 3.63), rectal adenocarcinoma (OR = 2.43), prostate adenocarcinoma (OR = 1.92), squamous cell carcinoma of the lungs (OR = 1.92), serous cystadenocarcinoma (OR = 1.44), chromophobe renal cell carcinoma (OR = 1.38), and tubular adenocarcinoma of the stomach (OR = 0.21)(Additional file [1](#MOESM1){ref-type="media"}: Tables S4-S5). Discussion {#Sec14} ========== Here, we showed that expression of HSF1 as well as other genes localized in 8q24.3 are tightly linked to 8q24.3 copy number. This large individual patient data meta-analysis approach showed evidence for higher 5-year mortality among individuals with 8q24.3 deletions, gain, and amplification. These overall results remained rather stable after adjustment for confounders and interaction by tumor stage, which supports a causal relationship that cannot be explained by tumor stage, HSF1 expression, or by the assessed confounders. Up to 9-fold increased risks were found for specific cancer types. This supports a potential causal relationship between 8q24.3 CNA and prognosis at least in some histological subtypes---although protective effects were found in a limited number of cancer types (kidney and stomach). Therefore, this suggests that 8q24.3 CNA and its complex transcriptional change imply either responsive or resistance in treatment, which needs further clinical and molecular investigations. For example in the different histological subtypes, it would be interesting to investigate with other known genomic biomarkers important in cancer as well exploring the link with complex karyotypes to explore assess the link with the stress of protein unbalances in tumors. It is also worthwhile to understand why both a deletion and a gain of 8q24.3 can lead to a poor prognosis in some tissues such as lung, colorectal, and ovaries. Possibly copy number change in 8q24.3 could alter transcriptional programming or could be associated with other genomic change including translocations and inversions that alters the resistance to treatment or favorize tumor growth. The main strength of this meta-analysis is that the results are based on a large population with available data on an individual level. Both applied meta-analyses approaches obtained similar results, with low to moderate statistical heterogeneity for all analyses. Yet, information was incomplete or missing for important prognostic variables such as tumor stage (missing in 50%) and confounders such as body mass index, smoking, and alcohol intake. Therefore, the most adjusted models were conducted on 42% of the cohort (complete case analysis), resulting in reduced power, which in turn contributed to the loss of statistical significance compared to the unadjusted analyses. Residual confounding cannot be ruled out. Consequently, the results have to be interpreted with caution, in particular, for specific histological subtypes with the low number of patients included in the analyses. Our findings may have substantial implications for the understanding and interpretation of biomarkers in cancer research and clinical investigations. Indeed, no less than 5000 publications were found for 16 popular genes including HSF1 in 8q24.3, of which 800 publications related to cancer field (Additional file [1](#MOESM1){ref-type="media"}: Appendix 4), mainly because those genes were found overexpressed in cancer (Additional file [1](#MOESM1){ref-type="media"}: Appendix 5). Conclusions {#Sec15} =========== Integration of 8q24.3 CNA detection may have substantial implications for interpreting the molecular pathogenesis of cancer. In a general aspect, our work indicates that histological diagnoses using biomarkers can be tightly linked to large CNA associated with complex gene expression pattern, pointing out the importance of understanding molecular pathogenesis to optimize cancer treatment. Supplementary information ========================= {#Sec16} **Additional file 1**: Table S1. Data Collected. Table S2. Descriptive characteristics of all individuals (*n* = 9568) with 8q24.3 homogenous copy number alteration information, first cancer diagnosis and 5-year follow-up. Table S3. Results of the 2-step individual patient data meta-analyses to assess the effect of 8q24.3 copy number variants on prognosis. Table S4. Five-year mortality by 8q24.3 copy number alteration using diploidy as a reference. Table S5. Five-year mortality of 15 cancer types with most cases of 8q24.3 gain and amplification using diploidy as a reference. Appendix 1. Flow chart illustrating selection of individuals for individual patient data meta-analysis. Appendix 2. Overview of HSF1 expression per histological subtype. Appendix 3. Expression of HSF1 in function of HSF1 copy number alteration per histological subtype. Appendix 4. Number of publication and description of selected cancer-related genes per field located in 8q24.3 cytoband. Appendix 5. Influence of 8q24.3 copy number alteration on other cancer-related genes expression located in 8q24.3 loci and comparison of expression with HSF1 per tissue. Appendix 6. Simple linear regressions of predicted 8q24.3 copy number alteration compared to the expression of genes located in 8q24.3 per tissue. **Publisher's Note** Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Supplementary information ========================= **Supplementary information** accompanies this paper at 10.1186/s40246-019-0241-3. The authors thank the TCGA Research Network and its TCGA Pan-Cancer Analysis Working Group and cBioportal for Cancer Genomics. The study was designed by M-DD. M-DD collected samples and patient information. M-DD and NB cleaned, analyzed. and interpreted the data. KE gave valuable advice. NB and M-DD wrote the manuscript, which was critically revised by KE. The corresponding author had full access to the data and the final responsibility to submit for publication. All authors of this work had full access to this study and the data, and gave approval to submit the final manuscript. This work was supported by grants from the Cancer Society CAN2015/169 and the Swedish Research Council 2016-01259. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. The published results showed available form authors here are in whole or part based upon data generated by the TCGA Research Network ([http://cancergenome.nih.gov/](https://cancergenome.nih.gov/)) and its TCGA Pan-Cancer Analysis Working Group and obtained from the cBioportal for Cancer Genomics \[[@CR25], [@CR26]\]. Not applicable. Not applicable. None. | Mid | [
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Pets.ca Podcast Pet podcast #40 features an interview with Dr. Lee a veterinarian in Mesa and Phoenix Arizona. In this interview we discuss the early spaying and neutering of dogs and cats from between 8 and 16 weeks of age. Normally cats … | Low | [
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/* eslint no-console:0 */ import React from 'react'; import Trigger from '../src'; import '../assets/index.less'; import './point.less'; const builtinPlacements = { topLeft: { points: ['tl', 'tl'], }, }; const innerTrigger = ( <div style={{ padding: 20, background: 'rgba(0, 255, 0, 0.3)' }}>This is popup</div> ); class Test extends React.Component { state = { action: 'click', mouseEnterDelay: 0, }; onActionChange = ({ target: { value } }) => { this.setState({ action: value }); }; onDelayChange = ({ target: { value } }) => { this.setState({ mouseEnterDelay: Number(value) || 0 }); }; render() { const { action, mouseEnterDelay } = this.state; return ( <div> <label> Trigger type:{' '} <select value={action} onChange={this.onActionChange}> <option>click</option> <option>hover</option> <option>contextMenu</option> </select> </label>{' '} {action === 'hover' && ( <label> Mouse enter delay:{' '} <input type="text" value={mouseEnterDelay} onChange={this.onDelayChange} /> </label> )} <div style={{ margin: 50 }}> <Trigger popupPlacement="topLeft" action={[action]} popupAlign={{ overflow: { adjustX: 1, adjustY: 1, }, }} mouseEnterDelay={mouseEnterDelay} popupClassName="point-popup" builtinPlacements={builtinPlacements} popup={innerTrigger} alignPoint > <div style={{ border: '1px solid red', padding: '100px 0', textAlign: 'center', }} > Interactive region </div> </Trigger> </div> </div> ); } } export default Test; | Low | [
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// // ProfileLabelCell.swift // Former-Demo // // Created by Ryo Aoyama on 10/31/15. // Copyright © 2015 Ryo Aoyama. All rights reserved. // import UIKit import Former final class ProfileLabelCell: UITableViewCell, InlineDatePickerFormableRow, InlinePickerFormableRow { @IBOutlet weak var titleLabel: UILabel! @IBOutlet weak var displayLabel: UILabel! override func awakeFromNib() { super.awakeFromNib() titleLabel.textColor = .formerColor() displayLabel.textColor = .formerSubColor() } func formTitleLabel() -> UILabel? { return titleLabel } func formDisplayLabel() -> UILabel? { return displayLabel } func updateWithRowFormer(_ rowFormer: RowFormer) {} } | Low | [
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Keen observers at 2019 ANZAC Day services will notice a difference in the tank stationed outside the Esperance RSL. The decommissioned Leopard AS1 tank has been in Esperance since 2011, after 30 years of service. Esperance RSL member George Starcevich said the RSL observed, at a recent meeting, the vehicle was looking "shabby". Mr Starcevich approached Dennis Hartman who has volunteered his time to put a fresh coat of camouflage paint on the vehicle and clean off the rust. Mr Hartman said the tank's proximity to the ocean had caused rust. He said he repaired the vehicle to help the RSL and to thank the diggers for the freedoms we have. Mr Starcevich thanked Mr Hartman on behalf of the RSL, saying he was "a great Esperance guy". | Mid | [
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Location Core strength development for performance Strong core muscles can certainly improve one's appearance in addition to enhancing your performance on the sports field and in the workplace. Someone with well developed core muscles breathes easier, walks, bends, and runs better and is less prone to injury; the body is in proper alignment and does not fatigue as quickly. Strong core muscles protect the back and prevent back pain. When most people think of the core muscles, they think of the abdominals alone, however the core includes the upper back muscles, the gluteals (buttocks) and the obliques (on either side of the abs). Joseph Pilates, the founder of the exercise, called these muscles "the powerhouse" as he believed that all energy flows from them to the extremities. In recent years, Pilates has taken centre stage as the core muscle exercise. It requires concentration and centring on the abdominal muscles while the movements are carried out. Pilates can be done with large balls and stretchy bands, or with machines which provide resistance. Pilates emphasises relaxed, smooth movements and rhythmic breathing. Since Pilates emphasises control and coordination, people who practice it learn to carry this over in their every day life. If you are not the type to take the time to learn Pilates, you should perform abdominal exercises at least three times a week to keep them firm and strong. You can always go to the gym or purchase one of the many ab machines on the market. Those in the gym provide resistance and support your neck, making the movements much safer than doing sit-ups at home. Bear in mind that every type of exercise carries the risk of injury, therefore when beginning these exercises, you should have a fitness trainer or physiotherapist guide you in perfecting your technique. You will be advised to start slowly and build up gradually until you are at your peak. Please share We do not warrant or represent that the information in this site is free from errors or omissions or is suitable for your intended use. We recommend that you seek individual advice before acting on any information in this site. We have made every effort to ensure that the information on our website is correct at the time of publication but recommend that you exercise your own skill and care with respect to its use. If you wish to purchase our services, please do not rely solely on the information in this website. | Mid | [
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The regulations allow approximately 11.7 million instances of harassment, injury, or even death (the legal term is "take") to marine mammals by exposing them to high-intensity military sonar training in coastal waters around the United States. These estimates – the Navy's own – include 9.7 million takes along the Atlantic Coast and the Gulf of Mexico; 630,000 off the coast of southern California; 650,000 along the coast of Washington and Oregon; 140,000 in Hawaii; and another 500,000 off the coast of Florida. Sonar exposure is not, as the Navy suggests, a mere matter of annoyance to whales and dolphins. In fact, the harm ranges from significant disturbance to important behaviors – feeding, breeding, migrating, communicating, finding mates – to hearing damage and even mass stranding and death. At risk are not only some of the most vulnerable whale populations on Earth – including the last remaining 300 North Atlantic right whales and the 83 critically endangered southern resident killer whales off the Washington coast – but the very fabric of life among species that, over eons in the dark ocean, have evolved to depend on sound as we depend on sight. According to government scientists, the "loss of even a single individual right whale may contribute to the extinction of the species." In recent decades, a growing number of mass whale mortalities around the world have occurred in the shadow of military sonar training, in coastal waters as diverse as the Bahamas, the Canary Islands, Greece, North Carolina, Hawaii, Washington State, and many others. According to scientists – including the Navy's own consultants – there is no longer any doubt that sonar kills whales, whether by stranding or massive internal hemorrhaging – akin to what human divers experience as the "bends." Nor, as the Navy has argued, is sonar's impact a necessary consequence of securing our national defense. Most of the harm to marine mammals authorized by the Bush administration could be avoided by the use of common sense safeguards, many of which the Navy has used in past training exercises without apparent problem. Simple steps such as avoiding sensitive areas like marine sanctuaries, critical habitats, and feeding or breeding grounds; adopting adequate monitoring and safety zones around the sonar device; powering down in ocean conditions of particular acoustic risk; and implementing ship based, aerial, and underwater techniques to monitor when marine mammals are present enable a protective response. But for all of the recent proposed sonar training, the Navy has refused to implement any of this mitigation, instead proposing half-measures dismissed by the federal courts as "woefully inadequate and ineffectual." During the past decade, the courts have been the only effective line of defense against the Navy's needlessly dangerous sonar training, but litigation is piecemeal. A more effective, more comprehensive political response may now be possible. And given the geographic reach of the proposed sonar training and the Navy's own predictions of harm, such a response may be the only way to counter what amounts to an astonishing acoustic assault on marine life along all our coasts. New leadership is already in place at NOAA. New leadership, we hope, will soon be coming to the US Navy. Instead of the Bush administration's last-minute attack on whales and other marine life, the new administration should require a uniform protocol of effective safeguards for all Navy sonar training that would prevent the needless infliction of harm. We urge NOAA to move quickly and forcefully to exercise its authority – and fulfill its responsibility – to protect our oceans. | High | [
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Q: Restlet - Passing error status code and exception trace from server to client We have a restlet server and client. We need to pass the error status and exception traces back to the client so that the client can take appropriate actions depending on the error status code. I read about StatusService and using response.setStatus() method but I can't get the specific exceptions thrown during server side processing be displayed on client side. The DAO layer from the server throws specific DB related exceptions and status code such as (Unique key violation etc), which the client needs to see and take appropriate actions. Also, what is the common way of doing this to have centralized error handling / processing on server and client side ? Filters ? A brief example will really help. Thanks, Deep A: You can only send HTTP status codes and optionally your own description message. You can also send a representation of the error by overriding the getRepresentation in the StatusService. @Override public Status getStatus(Throwable throwable, Resource resource) { Status ret = null; Throwable cause = throwable.getCause(); if (cause == null) { Status status = super.getStatus(throwable, resource); ret = new Status(status, throwable.getMessage()); log.log(Level.SEVERE, "Unexpected resource exception <" + ret.toString() + "> for throwable of type <" + throwable + "> at resource <" + resource + ">"); } else if (cause instanceof NotFoundException) { ret = new Status(Status.CLIENT_ERROR_NOT_FOUND, cause, resource.getReference().toString()); log.info("Not found <" + ret.toString() + "> for throwable of type <" + cause + "> at resource <" + resource + ">"); } else if (cause instanceof ConstraintViolationsException) { ConstraintViolationsException e = (ConstraintViolationsException) cause; ret = new Status(Status.CLIENT_ERROR_BAD_REQUEST, cause, e.getViolations().iterator().next().getMessage()); log.log(Level.SEVERE, "Constraint violation <" + e.getViolations().iterator().next().getMessage() + "> at resource <" + resource + ">"); } else if (cause instanceof BusinessRuleException) { ret = new Status(Status.CLIENT_ERROR_BAD_REQUEST, cause, cause.getMessage()); log.log(Level.SEVERE, "Business rule exception: <" + cause.getMessage() + "> at resource <" + resource + ">"); } else { Status status = super.getStatus(throwable, resource); ret = new Status(status, throwable.getMessage()); log.log(Level.SEVERE, "Unexpected server exception <" + ret.toString() + "> for throwable of type <" + throwable + "> at resource <" + resource + ">"); } return ret; } @Override public Representation getRepresentation(Status status, Request request, Response response) { String ret = ""; if (status.getDescription() != null) { ret = status.getDescription(); } else { ret = "unknown error"; } return new StringRepresentation(ret, MediaType.TEXT_PLAIN); } You can return a representation of the error in getRepresentation in whatever format (XML, JSON, HTML) you want. | High | [
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The Taliban is extending an invitation to Sen. Rand Paul, Kentucky Republican, to their political office in Doha, to discuss possible peace plans to end the 17-year Afghan war. The invitation, proposed on the terror group’s social media accounts under the moniker of the “Islamic Emirate of Afghanistan,” was extended in response to Mr. Paul’s recent comments on the status of the war. “We invite the respectable U.S. Senator Rand Paul, in his official capacity to visit our political office in Doha for mutual talks,” the Twitter post by the Information Committee of the Islamic Emirate of Afghanistan read. “We’ll prove to Mr. Rand Paul, the immediate US withdrawal from [Afghanistan] will bring peace to our country & will enhance international security,” the group added in the social media post. During an interview with Fox News on Thursday, Sen. Paul lambasted Washington’s continued investment in the Afghan conflict, with no clear endgame in sight. “The war in Afghanistan is costing us $50 billion a year… It’s time to come home. There is no military victory there,” Mr. Paul said. TEHRAN (FNA)- Taliban invited a US senator for “mutual talks” in the Qatari capital Doha, where the so-called Islamic Emirate of Afghanistan has an office. The terror group’s social media accounts extended the invitation to Kentucky Republican Senator Rand Paul over his latest comments about the United States’ long war in Afghanistan, The Washington Times reported. “We invite the respectable US Senator Rand Paul, in his official capacity to visit our political office in Doha for mutual talks,” according to a Twitter post by the self-declared Information Committee of the Islamic Emirate of Afghanistan. It further suggested that the US should withdraw its forces from the war-ravaged country for peace to emerge. “We’ll prove to Mr. Rand Paul, the immediate US withdrawal from [Afghanistan] will bring peace to our country & will enhance international security,” the group added in the social media post. The Kentucky lawmaker had criticized investment in the war on Afghanistan during an interview with Fox News on Thursday. “The war in Afghanistan is costing us $50 billion a year… It’s time to come home. There is no military victory there,” Paul said. On August 21, Trump announced he would prolong the military intervention in Afghanistan. The United States --- under Republican George W. Bush’s presidency --- and its allies invaded Afghanistan on October 7, 2001 as part of Washington’s so-called war on terror. Taliban terrorists have invited Sen. Rand Paul (R-KY) to their political office in Qatar to discuss peace plans to bring the nearly 17-year-old war in Afghanistan to a conclusion. The invitation, reportedly posted on the jihadist group’s social media accounts, came in response to Sen. Paul’s recent comments about the conflict, notes the Washington Times. “We invite the respectable [U.S. Senator Rand Paul], in his official capacity to visit our political office in Doha for mutual talks,” the Taliban wrote on Twitter under the moniker of the “Islamic Emirate of Afghanistan." Yeah, sure it does. Let's go talk to the terrorists the CIA set up and Bush entertained before they were demonized in the mainstream media, and which the American public thinks is a homegrown enemy, and see if they don't help the mainstream media destroy our political career for doing it. In short, let's walk into an obvious CIA trap. Hell of an idea. Just brilliant. Originally Posted by angelatc There's not a liberty lover on the planet who isn't called a liberal by the right, and a con by the left. Yeah, sure it does. Let's go talk to the terrorists the CIA set up and Bush entertained before they were demonized in he mainstream media, and which the American public thinks is a homegrown enemy, and see if they don't help the mainstream media destroy our political career for doing it. Hell of an idea. Yeah, it's SOOOO much better of an idea to refuse to negotiate a peace deal with the power most likely to control Afghanistan when we leave or are driven out, then we can stay there until further notice and lose more servicemen while killing more locals, why oh why didn't I think of that? Never attempt to teach a pig to sing; it wastes your time and annoys the pig. Robert Heinlein Give a man an inch and right away he thinks he's a ruler Groucho Marx I love mankind…it’s people I can’t stand. Linus, from the Peanuts comic You cannot have liberty without morality and morality without faith Alexis de Torqueville Those who fail to learn from the past are condemned to repeat it. Those who learn from the past are condemned to watch everybody else repeat it Yeah, it's SOOOO much better of an idea to refuse to negotiate a peace deal with the power most likely to control Afghanistan when we leave or are driven out, then we can stay there until further notice and lose more servicemen while killing more locals, why oh why didn't I think of that? Yeah, because a group with ties to the CIA offering to seriously talk peace with one of 535 members of a legislative body which never even declared war on the country in question is obviously a serious offer. Originally Posted by angelatc There's not a liberty lover on the planet who isn't called a liberal by the right, and a con by the left. Taliban invites Rand Paul to peace talks The Taliban is extending an invitation to Sen. Rand Paul, Kentucky Republican, to their political office in Doha, to discuss possible peace plans to end the 17-year Afghan war. The invitation, proposed on the terror group’s social media accounts under the moniker of the “Islamic Emirate of Afghanistan,” was extended in response to Mr. Paul’s recent comments on the status of the war. “We invite the respectable U.S. Senator Rand Paul, in his official capacity to visit our political office in Doha for mutual talks,” the Twitter post by the Information Committee of the Islamic Emirate of Afghanistan read. “We’ll prove to Mr. Rand Paul, the immediate US withdrawal from [Afghanistan] will bring peace to our country & will enhance international security,” the group added in the social media post. 3 days ago... ►Russia is recently offering an 'open ended' invitation to both parties to host peace talks between Afghanistan and the Taliban. If McCain and Graham can waltz over and chat with 'rebels' anytime they feel like it... then certainly Rand could step up and 'float' possibilities. If you're going to run as the 'peace' candidate... you have to take advantage of opportunities when they come at you. I wouldn't dismiss this out of hand... I would 'massage' it and USE it to gain 'face time' in the media. Yeah, because a group with ties to the CIA offering to seriously talk peace with one of 535 members of a legislative body which never even declared war on the country in question is obviously a serious offer. Wait. What? I am pretty sure any CIA contact is of the adversarial variety. Islamic Emirate of Afghanistan (Taliban for propaganda purposes). The only legitimate governmental authority. The legitimate Government since they overthrew the Russian Puppet Government and liberated their country. The Legitimate Government when negotiations were ongoing after 911.. until we invaded and ran amok for all these years. Yes,, Let Rand negotiate a peaceful end to this stupid $hit. Liberty is lost through complacency and a subservient mindset. When we accept or even welcome automobile checkpoints, random searches, mandatory identification cards, and paramilitary police in our streets, we have lost a vital part of our American heritage. America was born of protest, revolution, and mistrust of government. Subservient societies neither maintain nor deserve freedom for long. Ron Paul 2004 Yeah, because a group with ties to the CIA offering to seriously talk peace with one of 535 members of a legislative body which never even declared war on the country in question is obviously a serious offer. Its not like the Taliban is reaching out to Rand Paul directly. I think Rand Paul would be best off writing an op-ed to the American people- but not to talk to foreigners on behalf of the American people unless we ask him to. America can't have peace talks with Afghanistan if we can't even declare war and have an honest debate in congress. Yeah, sure it does. Let's go talk to the terrorists the CIA set up and Bush entertained before they were demonized in the mainstream media, and which the American public thinks is a homegrown enemy, and see if they don't help the mainstream media destroy our political career for doing it. In short, let's walk into an obvious CIA trap. Hell of an idea. Just brilliant. No matter how you look at it, too much risk. No way for Rand to safely go there. Maybe in another place Rand could take part in a peace process as a Senate representative. Twitter: B4Liberty@USAB4L"Foreign aid is taking money from the poor people of a rich country, and giving it to the rich people of a poor country." - Ron Paul "Beware the Military-Industrial-Financial-Corporate-Internet-Media-Government Complex." - B4L update of General Dwight D. Eisenhower "Debt is the drug, Wall St. Banksters are the dealers, and politicians are the addicts." - B4L "Totally free immigration? I've never taken that position. I believe in national sovereignty." - Ron Paul “They are what they hate.” - B4L The views and opinions expressed here are solely my own, and do not represent this forum or any other entities or persons. Its not like the Taliban is reaching out to Rand Paul directly. I think Rand Paul would be best off writing an op-ed to the American people- but not to talk to foreigners on behalf of the American people unless we ask him to. America can't have peace talks with Afghanistan if we can't even declare war and have an honest debate in congress. That would be a good response, and then see what happens. "Democracy is the theory that the common people know what they want, and deserve to get it good and hard." Twitter: B4Liberty@USAB4L"Foreign aid is taking money from the poor people of a rich country, and giving it to the rich people of a poor country." - Ron Paul "Beware the Military-Industrial-Financial-Corporate-Internet-Media-Government Complex." - B4L update of General Dwight D. Eisenhower "Debt is the drug, Wall St. Banksters are the dealers, and politicians are the addicts." - B4L "Totally free immigration? I've never taken that position. I believe in national sovereignty." - Ron Paul “They are what they hate.” - B4L The views and opinions expressed here are solely my own, and do not represent this forum or any other entities or persons. I think Rand could possibly Troll Trump by rallying Trump's supporters for a cause they support like he has been. The MSM is already trying to get rid of that tool, they don't even want to pretend like he is a conservative anymore, the new narrative is he is to the left of Hillary. He might be all out of ammo in that strategy and have to go full opposition. I think Rand could possibly Troll Trump by rallying Trump's supporters for a cause they support like he has been. The MSM is already trying to get rid of that tool, they don't even want to pretend like he is a conservative anymore, the new narrative is he is to the left of Hillary. He might be all out of ammo in that strategy and have to go full opposition. Agreed, I think this recent budget business was a turning point. If this is a real offer, it could be a golden opportunity. That war's got to end sometime, and who better to end it? "Democracy is the theory that the common people know what they want, and deserve to get it good and hard." If I were Rand I would say: to the seven countries we are at war with but can't declare it, I would love to declare peace but I don't think we can do that until we first acknowledge we are at war and have an honest debate about it. For that matter, if it's a real offer, it could still end his career. And if it's not, it might still be a golden opportunity, if he plays it right. I still can't get past seeing the old photos of the Taliban in Bush's living room, having a nice little visit. Yeah, the Bushes are ostensibly oil men, and liable to try to network with anyone. But they still smell of CIA to me. I'm coming around to the view that this is too significant to just ignore. But Rand Paul had better cover his ass ten ways from Sunday--physically, politically, publicity-wise, philosophically and everything else-ly. You can't barbeque the beef if you don't play with fire, but it's still a mighty good way to get burned. Originally Posted by angelatc There's not a liberty lover on the planet who isn't called a liberal by the right, and a con by the left. For that matter, if it's a real offer, it could still end his career. And if it's not, it might still be a golden opportunity, if he plays it right. I still can't get past seeing the old photos of the Taliban in Bush's living room, having a nice little visit. Yeah, the Bushes are ostensibly oil men, and liable to try to network with anyone. But they still smell of CIA to me. I'm coming around to the view that this is too significant to just ignore. But Rand Paul had better cover his ass ten ways from Sunday--physically, politically, publicity-wise, philosophically and everything else-ly. You can't barbeque the beef if you don't play with fire, but it's a mighty good way to get burned. It's reminiscent of the French experience in the Algerian war, which made and ruined a number of careers. If Rand's going to do anything more than write an op-ed about this, he needs some expert advice. He knows what needs to be done in the big picture, but I doubt he knows the details of Afghan rebel politics on a day to day basis. It's too bad that Michael Scheuer went off the deep end. "Democracy is the theory that the common people know what they want, and deserve to get it good and hard." It's reminiscent of the French experience in the Algerian war, which made and ruined a number of careers. If Rand's going to do anything more than write an op-ed about this, he needs some expert advice. He knows what needs to be done in the big picture, but I doubt he knows the details of Afghan rebel politics on a day to day basis. It's too bad that Michael Scheuer went off the deep end. I can't help but feel it's a fool's errand. The U.S. government is highly unlikely to agree to any just settlement, and the U.S. media is highly unlikely to allow him to tell the people of this nation what went wrong when the talks fail. Where's his advantage in that? If he could count on his father's legions to spread the truth of what went down, if he could communicate with us and we could shame the media for lying about it as we did when the media tried to make Ron into He Who Must Not Be Named, it would be a very worthwhile thing. The Court of Public Opinion is going to have to be a major player in this thing, if it is to amount to something. Can he count on us? Are we still legion enough to have his back? The government has no interest in peace. None. Zilch Nada. If the Taliban aren't just a CIA front, and they're serious about this, then Rand Paul is an excellent choice. And the reason he is, is us. We know Rand, we know he has character. We can vouch for him, we are experienced in shaming the media into telling the truth even when it doesn't behoove them to do so. We know how to make ourselves heard. We can help explain what their offers would mean for We, the People. If he can't count on us, he might as well not go. He'd probably be wiser not to. But if he can count on us, this could be a major victory for the common citizens of the United States. Last edited by acptulsa; 02-12-2018 at 10:06 PM. Originally Posted by angelatc There's not a liberty lover on the planet who isn't called a liberal by the right, and a con by the left. *this would be a good time for Rand to break out some of that Senatorial office budget that he usually returns to the Treasury and hire somebody who speaks Pashtun and knows everything there is know about the Taliban (who's in charge right now, who's married to whose sister, etc) "Democracy is the theory that the common people know what they want, and deserve to get it good and hard." I can't help but feel it's a fool's errand. The U.S. government is highly unlikely to agree to any just settlement, and the U.S. media is highly unlikely to allow him to tell the people of this nation what went wrong when the talks fail. Where's his advantage in that? If he could count on his father's legions to spread the truth of what went down, if he could communicate with us and we could shame the media for lying about it as we did when the media tried to make Ron into He Who Must Not Be Named, it would be a very worthwhile thing. The Court of Public Opinion is going to have to be a major player in this thing, if it is to amount to something. Can he count on us? Are we still legion enough to have his back? I don't know. I hope so. Is there much to lose at this point? ...as for Rand, he won't be up for re-election till 2022, so we needn't worry about that. "Democracy is the theory that the common people know what they want, and deserve to get it good and hard." 1. I am utterly SICK of the 'unelected' representing us.. otherwise known as the State Department. 2. Form a 'coalition' as 'The People's Representative' to enjoin the 'multi-polar' effort at bringing PEACE to Afghanistan. 3. The 'coalition' of maybe 6 ELECTED representatives form the 'Peace team' ahead of the Russian sponsored Peace talks. 4. Go under 'observer status'.. get on the phone with Lavrov and quietly build the concept. 5. Announce the coalition. 6. Go and represent the People and report back directly to THEM. I can't help but feel it's a fool's errand. The U.S. government is highly unlikely to agree to any just settlement, and the U.S. media is highly unlikely to allow him to tell the people of this nation what went wrong when the talks fail. Where's his advantage in that? If he could count on his father's legions to spread the truth of what went down, if he could communicate with us and we could shame the media for lying about it as we did when the media tried to make Ron into He Who Must Not Be Named, it would be a very worthwhile thing. The Court of Public Opinion is going to have to be a major player in this thing, if it is to amount to something. Can he count on us? Are we still legion enough to have his back? He needs more then us, he has already spoken for us, the government doesn't care what the American people think. We need international support, we need to make this bigger, we can't be censored. Rand needs the whole world to hear him. He needs more then us, he has already spoken for us, the government doesn't care what the American people think. We need international support, we need to make this bigger, we can't be censored. Rand needs the whole world to hear him. Most of the world is sick to death of this war: both Russia (been there done that) and China, for instance. Europe isn't too keen on it either. The three Polish soldiers in Kabul want to go home. "Democracy is the theory that the common people know what they want, and deserve to get it good and hard." Most of the world is sick to death of this war: both Russia (been there done that) and China, for instance. Europe isn't too keen on it either. The three Polish soldiers in Kabul want to go home. What about the ones who have no voice, the dead, the wounded, the homeless veterans? They don't really get a choice on American foreign policy. I don't think it's entirely unfair to speak for the ones who can't speak for themselves especially when they clearly can't define their argument for their occupation you really don't have to take the high road here. | Low | [
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1. Field of the Invention The present invention relates to an oscillator used for a television tuner etc. for receiving a wide frequency band signal. 2. Description of the Related Art FIG. 1 is a circuit diagram showing the basic configuration of this type of oscillator as a related art. In FIG. 1, OSC represents an oscillation circuit, RSN a resonance circuit, MIX a mixing circuit, and AMP.sub.DC a DC amplifier. The oscillation circuit OSC is integrated and is comprised of npn type transistors Q.sub.1 and Q.sub.2 comprising a differential type Colpitz oscillation circuit, npn type transistors Q.sub.3 and Q.sub.4 comprising a differential output stage, a biasing constant voltage source V.sub.1 of the oscillation npn type transistors Q.sub.1 and Q.sub.2, resistance elements R.sub.1 to R.sub.4, and constant current sources I.sub.1 to I.sub.3. The base of the oscillation transistor Q.sub.1 is connected to an input/output terminal T.sub.1, is connected through the resistance element R.sub.1 to a line of a constant voltage source V.sub.1, and is connected through the resistance element R.sub.3 to the base of the transistor Q.sub.3. The emitter of the oscillation transistor Q.sub.1 is connected to an input/output terminal T.sub.2 and is connected to the constant current source I.sub.I, which constant current source I.sub.1 is grounded. The collector of the oscillation transistor Q.sub.1 is connected to a line of a power source voltage V.sub.cc. The base of the oscillation transistor Q.sub.2 is connected to an input/output terminal T.sub.4, is connected through the resistance element R.sub.2 to the line of the constant voltage source V.sub.1, and is connected through the resistance element R.sub.4 to the base of the transistor Q.sub.4. The emitter of the oscillation transistor Q.sub.2 is connected to an input/output terminal T.sub.3 and is connected to the constant current source I.sub.3, which constant current source I.sub.2 is grounded. The collector of the oscillation transistor Q.sub.2 is connected to the line of the power source voltage V.sub.cc. The transistors Q.sub.3 and Q.sub.4 are connected at their emitters and a node of the two is connected to the constant current source I.sub.3. The constant current source is grounded. The collectors of the transistors Q.sub.3 and Q.sub.4 are connected to the input of the mixing circuit MIX. Further, the output terminal of the mixing circuit MIX is connected through the load resistance elements R.sub.5 and R.sub.6 to the line of the power source voltage V.sub.cc and is connected to the input of the DC amplifier AMP.sub.DC. The resonance circuit RSN is comprised of a series circuit of a variable capacitive diode VC.sub.1 and coil L.sub.1 to which are connected in parallel the capacitors C.sub.1 and C.sub.2. The node between one end of the coil L.sub.1 of the resonance circuit RSN and the capacitors C.sub.1 and C.sub.2 is grounded through the resistance element R.sub.7 of the resistance value of 30 k.OMEGA. and is connected to the input/output terminal T.sub.1 (base of oscillation transistor Q.sub.1) through the DC cutting capacitor C.sub.3. The node between the cathode of the variable capacity diode VC.sub.1 and the capacitors C.sub.1 and C.sub.2 is connected to the output of the DC amplifier AMP.sub.DC through a drive resistance element R.sub.8 of a resistance value of 30 k.OMEGA. and is connected to an input/output terminal T.sub.4 (base of oscillation transistor Q.sub.2) through a DC cutting capacitor C.sub.3. Between the node of the capacitor C.sub.3 and the input/output terminal T.sub.1 and the input/output terminal T.sub.2 is connected a positive feedback capacitor C.sub.5 and between the node of the capacitor C.sub.4 and the input/output terminal T.sub.4 is connected a positive feedback capacitor C.sub.6. Further, between the node of the capacitor C.sub.5 and the input/output terminal T.sub.2 and the node of the capacitor C.sub.6 and the input/output terminal T.sub.3 (between the emitter of the oscillation transistor Q.sub.1 and the emitter of the oscillation transistor Q.sub.2) is connected a coupling capacitor C.sub.7. Note that the capacities of the externally provided capacitors C.sub.1 to C.sub.7 are set for example as follows: 1 pF for the capacitor C.sub.1, 13 pF for the capacitor C.sub.2, 56 pF for the capacitors C.sub.3 and C.sub.4, 2 pF for the capacitors C.sub.5 and C.sub.6 and 3 pF for the capacitor C.sub.7. In such a configuration, the oscillation circuit OSC receives positive feedback from the capacitors C.sub.5 and C.sub.6 connected between the bases and emitters of the oscillation transistors Q.sub.1 and Q.sub.2 through the input/output terminals T.sub.1, T.sub.2, T.sub.3, and T.sub.4, oscillates at the resonance frequency of the resonance circuit RSN connected to the bases of the oscillation transistors Q.sub.1 and Q.sub.2, and outputs the local oscillation frequency signal S.sub.L of a predetermined frequency through the transistors Q.sub.3 and Q.sub.4 to the mixing circuit MIX. Note that the oscillation transistors Q.sub.1 and Q.sub.2 comprising the differential Colpitz oscillation circuit are connected at their bases through the resonance circuit RSN, so perform oscillation operations with opposite phases. Accordingly, local oscillation frequency signals S.sub.L with opposite phases are output from the collectors of the transistors Q.sub.3 and Q.sub.4. In the mixing circuit MIX, the FM modulated video signal of the selected channel and the local oscillation frequency signal S.sub.L are mixed, and the signal of the frequency of the difference is taken out and is output to the DC amplifier AMP.sub.DC. Further, the resonance circuit RSNa is driven through the coil L.sub.4 by the output of the DC amplifier AMP.sub.DC. That is, after the phase detection by the mixing circuit MIX, the control voltage of the demodulation frequency, which is based on the drive resistance element R.sub.8 and the output of the DC amplifier AMP.sub.DC, is supplied to the cathode of the variable capacity diode VC.sub.1 of the resonance circuit RSN. However, the above-mentioned circuit is used as an oscillator for an FM demodulator for satellite broadcasting (BS) and the frequency is 400 MHz to 500 MHz. However, in the above-mentioned circuit, it suffers from the disadvantage that it is not possible to obtain a satisfactory picture since noise of a low frequency band would occur, which could be readily discerned even by the human eye, in the television picture, due to the so-called shot noise, flicker noise, or burst noise arising from the construction of the junction portion of the oscillation transistors Q.sub.1 and Q.sub.2 itself and the lattice faults, hot noise due to the resistance elements R.sub.1 and R.sub.2, etc. Further, the control voltage of the demodulation frequency based on the output of the drive resistance element R.sub.8 and the DC amplifier AMP.sub.DC is supplied to the cathode of the variable capacity diode VC.sub.1 of the resonance circuit RSN, but the resistance value of the drive resistance element R.sub.8 is, as explained above, 30 k.OMEGA., the time constant with the capacitors is large, the drive impedance of the variable capacity diode VC.sub.1 is high, the frequency characteristics will not improved, and therefore this becomes a cause behind low frequency noise. Since the operational frequency is a high of about 400 MHz to 500 MHz or so, the oscillation carrier easily flows into the power source and ground and therefore it suffers from the disadvantage that there is a liability of occurrence of a pseudo lock and a beat by the high frequency component. | Mid | [
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98 P.3d 960 (2004) Patricia NEDEDOG, Plaintiff-Appellant, v. COLORADO DEPARTMENT OF HEALTH CARE POLICY AND FINANCING and Karen Reinertson, executive director, in her official capacity only, Defendants-Appellees. No. 03CA1005. Colorado Court of Appeals, Div. V. August 12, 2004. *961 Colorado Legal Services, Anne L. Haro Sipes, Fort Collins, Colorado, for Plaintiff-Appellant. Ken Salazar, Attorney General, Laurie A. Schoder, Assistant Attorney General, Denver, Colorado, for Defendants-Appellees. Opinion by Judge WEBB. In this judicial review of administrative action, plaintiff, Patricia Nededog, appeals the district court's judgment upholding a decision of defendants, Colorado Department of Health Care Policy and Financing (CDHCPF) and its executive director, Karen Reinertson, allowing the Larimer County Department of Human Services (County Department) to recover from her $5,795.40 in erroneously paid medical assistance (Medicaid) benefits. We affirm. The initial decision of the administrative law judge (ALJ) concluded that the County Department could recover the erroneous Medicaid payments and that Nededog was not entitled to a waiver. The final agency decision of the CDHCPF Office of Appeals affirmed the ALJ's initial decision. The district court upheld the final agency decision. Although the record does not include a transcript or audiotape of the telephone hearing before the ALJ, the parties treat the following facts as undisputed. Until October 1998, Nededog received Supplemental Security Income (SSI), which made her eligible for Medicaid benefits under § 26-4-201(1)(i), C.R.S.2003, and federal law. Medicaid is a cooperative federal-state program which provides medical assistance to *962 low income persons. When she ceased receiving SSI, she was not eligible for Medicaid benefits on any other basis. Nevertheless, through no fault of Nededog's, she continued to receive Medicaid benefits. In September 2000, the County Department discovered that Nededog was no longer receiving SSI, determined that she was not otherwise Medicaid eligible, and, on September 19, 2000, gave her written notice terminating her Medicaid benefits effective September 30, 2000. Nededog did not challenge the termination. As relevant here, the County Department then sought recovery of $5,795.40 in Medicaid benefits paid erroneously to Nededog from September 1999 to September 2000. Nededog contested the recovery claim. I. Scope of Review In judicial review of administrative action, "the court shall determine all questions of law and interpret the statutory and constitutional provisions involved and shall apply such interpretation to the facts duly found or established." Section 24-4-106(7), C.R.S.2003. While we review an agency's statutory and regulatory interpretations de novo, we accord deference to the interpretation of a statute or regulation by the agency charged with its administration, and we generally accept that interpretation if it has a reasonable basis in the law and is warranted by the record. Stell v. Boulder County Dep't of Soc. Servs., 92 P.3d 910 (Colo.2004). We reverse final agency action only if it is arbitrary or capricious, contrary to law, an abuse of discretion, in excess of jurisdiction, based on clearly erroneous findings, or unsupported by substantial evidence. Section 24-4-106(7). II. Recovery of Medicaid Benefits Paid Erroneously Before Notice of Termination Nededog first contends the County Department cannot recover the erroneous payments because she remained eligible for Medicaid benefits until ten days after she received the September 19, 2000 termination notice. We disagree. When a person loses SSI, the Social Security Administration so informs the state agency responsible for Medicaid administration, and that agency must then determine whether the person is otherwise eligible for Medicaid benefits. 42 C.F.R. § 435.916(c)(1); § 26-4-106, C.R.S.2003. If the agency determines that the person has no other basis for Medicaid eligibility, then the person must be sent a termination notice. However, eligibility for Medicaid benefits continues "until such person is determined to be ineligible." Section 26-4-106(1)(a), C.R.S.2003; see 42 C.F.R. § 435.930(b). Written notice must be mailed at least ten days before the benefits are terminated. 42 C.F.R. § 431.211. The notice must include a description of the action to be taken, the reason for the action, and the legal authority for the action. 42 C.F.R. § 431.210; see also Colorado Department of Health Care Policy and Financing Reg. § 8.057.1.D, 10 Code Colo. Regs. 2505-10. Termination of Medicaid benefits without the requisite ex parte consideration of other bases for eligibility and advance notice of termination is invalid. Mass. Ass'n of Older Americans v. Sharp, 700 F.2d 749 (1st Cir.1983)(loss of AFDC); Stenson v. Blum, 476 F.Supp. 1331 (S.D.N.Y.1979)(loss of SSI), aff'd without opinion, 628 F.2d 1345 (2d Cir.1980); see also Weston v. Cassata, 37 P.3d 469 (Colo.App.2001)(advance notice required to terminate welfare benefits); Weaver v. Colo. Dep't of Soc. Servs., 791 P.2d 1230 (Colo.App.1990)(advance notice required to terminate Home and Community Based Services benefits, a component of Medicaid). Federal Medicaid law does not limit a state agency's recovery of benefits paid erroneously. See Oxenhorn v. Fleet Trust Co., 94 N.Y.2d 110, 700 N.Y.S.2d 413, 722 N.E.2d 492 (1999). Indeed, allowing recovery of such payments protects the assets of the Medicaid program as the "payor of last resort." S.Rep. No. 99-146 at 312, reprinted in 1986 U.S.C.C.A.N. 42,279; see Oxenhorn v. Fleet Trust Co., supra (upholding recovery of Medicaid benefits paid erroneously, despite paying agency's error). Moreover, Colorado law requires recovery of Medicaid benefits paid to a person who "was not lawfully entitled" to them. Section 26-4-403(1)(c), *963 C.R.S.2003; see also Colorado Department of Health Care Policy and Financing Reg. § 8.065.11, 10 Code Colo. Regs. 2505-10. Here, Nededog argues that because the County Department could not terminate her Medicaid benefits until ten days after the September 19, 2000 notice, despite her 1998 loss of SSI and lack of any other basis for Medicaid eligibility, the County Department cannot recoup the erroneous payments going back to September 1999. According to Nededog, to do so would be an unlawful "retroactive" determination of her ineligibility. We are not persuaded. Nededog's argument conflates the advance notice requirement to terminate Medicaid eligibility with the power to recover benefits paid erroneously. Once granted, a Medicaid recipient's eligibility continues until terminated. However, when Nededog ceased receiving SSI, she was no longer entitled to Medicaid benefits. Recovery under § 26-4-403(1)(c) turns on a lack of entitlement in the first instance, while the advance notice requirement relates to the procedures necessary to terminate payments that a recipient is not entitled to receive. While the County Department must give advance notice before terminating benefits being paid erroneously, its right to recover those payments accrued when the erroneous payments were made, not later when it terminated future payments. Nededog cites no case, and we have found none, supporting her argument that recovery of erroneous payments constitutes an invalid, prenotice termination of Medicaid benefits. Sharp, Stenson v. Blum, Weaver, and Weston v. Cassata, on which she relies, all invalidated termination of public benefits for lack of advance notice. However, because Nededog does not dispute the adequacy of the notice to terminate her Medicaid benefits, these cases are inapposite to recovery of payments made erroneously before notice of termination. To the extent that Nededog's argument requires us to reconcile § 26-4-106(1)(a), which provides that eligibility continues "until such person is determined to be ineligible" and requires advance notice of termination, with the mandate in § 26-4-403(1)(c) to recover payments for which the recipient "was not lawfully entitled," we rely on accepted principles of statutory construction and administrative law. When faced with potentially conflicting statutory provisions, we seek a harmonious interpretation that gives effect to each provision while furthering the general purpose of the legislation. People v. Luther, 58 P.3d 1013 (Colo.2002). At the same time, we avoid an interpretation that would produce an unreasonable or absurd result. Reg'l Transp. Dist. v. Lopez, 916 P.2d 1187 (Colo.1996). The advance notice requirement affords a recipient of public benefits a pretermination opportunity to be heard, consistent with procedural due process rights inherent in receipt of public benefits. See generally Goldberg v. Kelly, 397 U.S. 254, 90 S.Ct. 1011, 25 L.Ed.2d 287 (1970). Thus, due process protects the recipient against an erroneous termination of public benefits. Goldberg v. Kelly, supra. A claim to recover benefits paid erroneously does not raise the same perils to the recipient as an unannounced termination of public benefits. And consistent with due process, a recipient who, like Nededog, is the subject of a claim to recover benefits paid erroneously is entitled to notice of the recovery action and an opportunity to be heard. Colorado Department of Health Care Policy and Financing Reg. § 8.065.3.31, 10 Code Colo. Regs. 2505-10. Hence, we discern no conflict between requiring advance notice to terminate eligibility for Medicaid benefits and allowing recovery of benefits paid erroneously before notice of termination. Nededog's argument would preclude many recoveries of erroneous payments, which are usually retroactive in nature because Medicaid benefits can be terminated lawfully only upon advance notice. This would be an unreasonable result, which we reject. Reg'l Transp. Dist. v. Lopez, supra. For these reasons, we defer to CDHCPF's interpretation as having a reasonable basis in law. See Stell v. Boulder County Dep't of Soc. Servs., supra. Alternatively, Nededog argues that the County Department's separate notice of overpayment to her was misleading and *964 therefore inadequate. She did not raise this argument during the proceedings below or in her opening brief on appeal. Therefore, it is not properly before us. See Schempp v. Lucre Mgmt. Group, LLC, 75 P.3d 1157 (Colo.App.2003). Accordingly, we conclude that the County Department is not precluded from recovering Medicaid benefits to which Nededog was not entitled and which were paid erroneously before adequate notice of termination. III. Waiver of Recovery of Medicaid Benefits Paid Erroneously Nededog next contends that because she is indigent, the County Department should have waived recovery of the Medicaid benefits paid erroneously. Again, we disagree. The Colorado Medical Assistance Act, § 26-4-101, et seq., C.R.S.2003, governs administration of Medicaid in Colorado. See Dodge v. Dep't of Soc. Servs., 657 P.2d 969 (Colo.App.1982). CDHCPF administers this program. Section 25.5-1-201(1)(c), C.R.S.2003. As indicated, § 26-4-403(1)(c) requires recovery of Medicaid benefits paid to a recipient who was not entitled to them. This section does not provide for waiver of recovery claims. Nevertheless, Nededog argues that authority to waive recovery of overpayments appears in the Colorado Public Assistance Act, § 26-2-101, et seq., C.R.S.2003, and regulations promulgated thereunder. Specifically, she points to § 26-2-128(4), C.R.S.2003, which authorizes waiver of recovering erroneous public assistance payments from a recipient who is without fault, if the recovery "would deprive a person of income required for ordinary and necessary living expenses or would be against equity and good conscience," and Colorado Department of Human Services Reg. § 3.810.21, 9 Code Colo. Regs. 2503-1. We are not persuaded. The Colorado Public Assistance Act governs the administration of public assistance programs by the Department of Human Services. Likewise, § 3.810.21, the Human Services regulation that Nededog characterizes as allowing waiver, applies to "repayment of excess public assistance." Section 3.810.11. However, medical assistance "covered by the `Colorado Medical Assistance Act,'" which is Medicaid, is excluded from the definition of "assistance payments," and hence from the definition of "public assistance." Section 26-2-103(2),(7) C.R.S.2003. Nededog correctly points out that some provisions of the Public Assistance Act refer to the Medical Assistance Act and vice versa. Similar cross-referencing appears in the Human Services and CDHCPF regulations. For example, CDHCPF Reg. § 8.059.11 states that "[a]ppeals of financial eligibility determinations will be managed in accordance with rules" of Human Services. However, the issue before us is recovery of erroneous payments, not determination of eligibility. Further, the only express waiver provisions in the Medical Assistance Act deal with claims against either the estate of a recipient, § 26-4-403.3(4), C.R.S.2003, or providers who received overpayment for reasons other than fraud, § 26-4-403(2)(a)(II), C.R.S.2003. Had the General Assembly intended to provide for waiver of claims to recover Medicaid benefits paid erroneously to a recipient such as Nededog, it could have expressly so stated. See Reg'l Transp. Dist. v. Univ. of Colo. Hosp. Auth., 921 P.2d 56 (Colo.App.1996). In the absence of such legislative direction, we are bound by § 26-4-403(1)(c) and § 8.065.11, which provide for recovery of Medicaid benefits paid erroneously, but neither contain waiver language nor cross-reference any waiver regulation of Human Services. The ALJ determined that the waiver provisions on which Nededog relies are "meant to apply to public assistance programs administered by the State Department of Human Services and not Medicaid administered by the State Department of Health Care Policy and Financing." Because this interpretation has a reasonable basis in law, we accord it deference. Stell v. Boulder County Dep't of Soc. Servs., supra. Accordingly, we conclude the ALJ and CDHCPF properly rejected Nededog's assertion that the County Department should have waived the erroneous payment claim. *965 IV. 42 U.S.C. § 1983 We also reject Nededog's final contention that the district court should have granted her relief under 42 U.S.C. § 1983. In her complaint and in her brief to the district court, Nededog raised § 1983 in the same single sentence, "Because the agency denied Ms. Nededog rights guaranteed by the federal Medicaid Act, and the Due Process clause of the United States Constitution, the agency action violates 42 U.S.C. § 1983 as well." The district court's decision did not address § 1983. Although a similar sentence appears in her opening brief on appeal, there Nededog presents no argument or legal authority supporting the § 1983 claim. And Nededog's reply brief does not mention § 1983 at all, despite CDHCPF's assertion in its answer brief that the § 1983 claim was not sufficiently developed to be properly before us. Accordingly, we decline to consider this contention. See Manka v. Martin, 200 Colo. 260, 614 P.2d 875 (1980)(mere mention of 42 U.S.C. § 1983 insufficient to raise constitutionality of statute); see also Comm. for Better Health Care v. Meyer, 830 P.2d 884, 890 (Colo.1992)(declining to consider argument "stated in conclusionary form ... not accompanied by citations to any authority, and [presented] solely in the context of [other] arguments"). The judgment is affirmed. Judge NIETO and Judge RUSSEL concur. | Mid | [
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Protein Traffic to the Plasmodium falciparum apicoplast: evidence for a sorting branch point at the Golgi. Plasmodium falciparum, similar to many other apicomplexan parasites, contains an apicoplast, a plastid organelle of secondary endosymbiotic origin. Nuclear-encoded proteins are targeted to the apicoplast by a bipartite topogenic signal consisting of (i) an endoplasmic reticulum (ER)-type N-terminal secretory signal peptide, followed by (ii) a plant-like transit peptide. Although the signals responsible for transport of most proteins to the apicoplast are well described, the route of trafficking from the ER to the outermost apicoplast membrane is still a matter of debate. Current models of trafficking to the apicoplast suggest that proteins destined for this organelle are, on entry into the lumen of the ER, diverted from the default secretory pathway to a specialized vesicular system which carries proteins directly from the ER to the outer apicoplast membrane. Here, we have re-examined this trafficking pathway. By titrating wild-type and mutant apicoplast transit peptides against different ER retrieval sequences and studying protein transport in a brefeldin A-resistant parasite line, we generated data which suggest a direct involvement of the Golgi in traffic of soluble proteins to the P. falciparum apicoplast. | High | [
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Thought I'd post Silus' new big boy 10 gallon tank I got him last night. Poor fella has been switching between a 3 to a 5 and now to his 10, haha. Anywho. This was on sale a buck a gallon at walmart so my sister picked it up for me. I pulled the LED lid from my first tank to use as temporary lighting. Unfortunately it's too dark for you to really see Silus, but I think my thrift store finds look pretty nice in there C: (PS: Sorry for the kinda-small image, tinypic isn't agreeing with me today on sizes. >:U) the missing 2 heaters should be here by tomorrow or the day after, and Im going to get thermometers for the 2 new tanks today. The jade slabs I made into lean-to style caves, as is more apparent in the extra photo with Soren. He actually has 2, one is small and behind the jar so it doesn't show up in the photo. He looooves his lean to caves and his jar. Saki (my purple betta in the purple tank) kind of ignores it all and just hangs out on the purple flower by the surface. Delilah, his ADF tank mate, has laid claim to all... the jar, jade, and pinapple Shisu is going to get new decorations for my daughter's birthday, and that pirate ship in Shark Bate's tank will probably be replaced with something that matches the other decorations eventually So as a brand new and first time betta owner... here is my lil guys home A Petco 2 gal hexagon tank with filter, hood and led light, heater and thermometer, Thats a live plant in there... My guy is liking it a lot but i am currently restricting the intake on the filter to reduce the flow. | Low | [
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Health-related quality of life and its determinants in children and adolescents born with oesophageal atresia. Following surgical correction in the neonatal period, patients born with oesophageal atresia have significant co-morbidity, particularly in childhood. This study evaluates health-related quality of life and its determinants such as concomitant anomalies and the presence of respiratory and/or gastro-intestinal symptoms 6-18 years after repair of oesophageal atresia. Parents of 24 patients with oesophageal atresia completed the child health questionnaire for parents and 37 patients completed the child form. Gastro-intestinal symptoms were assessed by a validated standardized reflux questionnaire. Results were compared with a healthy reference population. Parents as well as patients themselves scored significantly lower on the domain general health perception. According to parents, general health perception was negatively affected by age at follow-up and concomitant anomalies. Patients reported that reflux symptoms reduced general health perception. In this first study describing health-related quality of life in children and adolescents born with oesophageal atresia, we demonstrated that general health remains impaired because of a high incidence of concomitant anomalies and gastrointestinal symptoms in patients with oesophageal atresia when compared with the healthy reference population. | High | [
0.6822558459422281,
31,
14.4375
] |
Instead Of Re News for Instead Of Re The Congress sent in Rahul Gandhi to play Aamir Khan at the FTII, but it turned out that he played Imran Khan instead, says Malavika Sangghvi. In purely filmic terms, the Rahul Gandhi's appearance...... After dropping surya namaskar from the official yoga programme to avoid controversy, the government on Thursday said chanting shlokas during International Yoga Day was not compulsory and appealed...... Instead government has given a go ahead for an international airport at Jewar in Greater Noida to decongest New Delhi airport The union civil aviation ministry's nod for an international airport at...... Industry should be pro-active in sharing inputs before finalisation of tax proposals instead of commenting on such policies later, a top tax official said on Friday. Service Tax Commissioner Gautam...... 'There are too many things that haven't gone out of you. So even though the years may have gone by, you are still close to the films in terms of the making.' Mani Ratnam, whose Roja, Bombay and Dil...... | Low | [
0.41549295774647804,
22.125,
31.125
] |
Uptake and transformation of pesticide metabolites by duckweed (Lemna gibba). Uptake and transformation of 14C-labeled metabolites from several pesticides, 3-methyl-4-nitrophenol (1), 3,5-dichloroaniline (2), 3-phenoxybenzoic acid (3), (R,S)-2-(4-chlorophenyl)-3-methylbutanoic acid (4), and (1RS)-trans-3-(2,2-dichlorovinyl)-2,2-dimethylcyclopropanecarboxylic acid (5), were examined by using duckweed (Lemna gibba) in Hoagland's medium. More uptake into duckweed from the exposure water at pH 7.0 was observed for non-ionized 1 and 2 than for 3-5 in an ionized form, and their hydrophobicity accounted for these differences. While carboxylic acids 4 and 5 were scarcely transformed in duckweed, 1-3 mainly underwent phase II conjugation with glucose for 1 and 2, malic acid for 3, glutamic acid for 2, and malonylglucose for 3, the chemical identities of which were confirmed by various spectrometric analyses (LC-MS, LC-MS/MS, and NMR) and/or HPLC cochromatography with reference synthetic standards. | High | [
0.6650485436893201,
34.25,
17.25
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Planning Letting Property News It's not all about the money for landlords THE UK is home to an estimated two million private landlords owning approximately five million properties. Some manage their own, while those in the know go with a reputable letting agency. But what of landlords’ relationships with their agents? With the changes to buy-to-let legislation and a ban on tenant fees coming soon, what’s in store for both sides of the coin? Research by Reposit — a “deposit alternative” start-up business — found that half (50 per cent) of the UK’s landlords are expecting their agent to pass on the costs of running their property after the Tenant Fees Bill becomes law next year. The bill sets out to make renting fairer and easier for tenants by allowing them to see up front what a given property will cost them in the advertised rent level without any additional costs. The bill will also introduce a lead enforcement authority in the lettings sector and cap security deposits at six weeks’ rent. The research by Reposit also showed that letting agent fee increases are one of the most common unexpected costs among landlords, alongside repairs and renewal fees, and that a third of landlords have experienced paying costs they weren’t expecting. But the research also revealed something perhaps unexpected — that increased fees are not the main reason landlords leave an agency. Of the 41 per cent of landlords who told Reposit they had left their agent in the past, only 11 per cent said it was over raised fees. Rather, customer service (61 per cent) and bad property care (26 per cent) bothered them more, leading them to change agency. What was also noteworthy in the report was the finding that increased costs of being a landlord (including the recent hikes in stamp duty and reductions in tax breaks) are forcing over a quarter of landlords to consider a cheaper agency to manage their property. Which begs the question — is this not counterproductive, if bad customer service is a landlord’s number one irk? Reposit’s research was conducted among 600 landlords. It also highlighted how the UK rental market is heavily London and South East-biased, with 52 per cent of all landlords operating in these two markets. The next largest buy-to-let market is the North West. Reposit also reckons it’s a middle-aged activity, with the firm’s research showing that more than three-quarters of landlords are aged over 45. That said, there are few plucky young investors, with 1.6 per cent of landlords aged between 18 and 24. | Low | [
0.5328031809145131,
33.5,
29.375
] |
The present application finds particular application in parking brake systems in vehicles, particularly involving pneumatic parking brake systems. However, it will be appreciated that the described technique may also find application in other brake control systems, other valve actuation systems, or other pneumatic control systems. Conventional single-motion parking brake release mechanisms suffer from many drawbacks, including unintentional parking brake release, which can cause a vehicle to roll unexpectedly and cause injury and/or property damage. For instance, such systems typically employ a plunger knob that an operator pulls outward to actuate the parking brake system. When the operator wants to release the parking brake, the operator pushes the plunger knob inward to a released position, which permits air to be supplied to a parking brake system and causes the parking brake to be deactivated. However, using such an arrangement increases the occurrence of inadvertent or accidental brake release. For instance, an operator or occupant may inadvertently depress the knob into a released position; a pet that travels with the operator in the cab of his truck may depress the knob into a released position when looking out through the windshield, etc. In these cases, if the release of the parking brake is not immediately noticed, the vehicle can roll away and cause damage to property or worse, injury to people. The present innovation provides a new and improved parking brake release system, which overcomes the above-referenced problems and others. | Mid | [
0.644705882352941,
34.25,
18.875
] |
Q: How to add right border of grid in Chart contol Here is my code for setting properties of chart which is attached above: chart2.ChartAreas[0].CursorX.IsUserEnabled = true; chart2.ChartAreas[0].CursorX.IsUserSelectionEnabled = true; chart2.ChartAreas[0].AxisX.ScaleView.Zoomable = true; chart2.ChartAreas[0].AxisX.Title = "t"; chart2.ChartAreas[0].AxisY.Title = "w(t)"; chart2.ChartAreas[0].AxisX.Minimum = classes[0].First(); chart2.ChartAreas[0].AxisX.Maximum = classes[m - 1].Last(); chart2.ChartAreas[0].AxisX.Interval = delta_t; chart2.ChartAreas[0].AxisX.LabelStyle.Format = "{0:0.####}"; I need to add right border of grid so that it will be as it is shown below: A: The right border is missing since your data don't nicely fit into the area. There are many ways to fix this. Here is the simplest one: chart2.ChartAreas[0].AxisY2.Enabled = AxisEnabled.True; chart2.ChartAreas[0].AxisY2.LabelStyle.Enabled = false; This adds a secondary Y-Axis and turns off its labels. You can style it as needed: chart2.ChartAreas[0].AxisY2.MajorTickMark.Enabled = false; chart2.ChartAreas[0].AxisY2.LineWidth = 3; You could also draw a line or add an annotation but this is by far the easiest solution. | High | [
0.6683544303797461,
33,
16.375
] |
RABID DOGS (2015): Same Premise, Different Mileage When Mario Bava’s work was revived on DVD in the 1990’s and 2000’s, the big discovery was a previously unreleased film called Rabid Dogs. It was a tense blend of psychological thriller, crime movie, road movie and extremely dark social commentary that surprised fans who associated Bava primarily with horror fare. It was also unique in that it had the kind of high-concept premise you could imagine being easily remade for a modern audience. That remake has arrived, retaining the title and the basic premise. While the result is slicker and benefits from a bigger budget, it doesn’t pack the punch of the scrappier original version. Rabid Dogs begins with a gang of robbers (Guillaume Gouix, Francois Arnaud, Franck Gastambide) hastily escaping a botched bank robbery. They lose their leader but gain a female hostage (Virginie Ledoyen). After being forced to ditch their vehicle, they carjack a smaller car being driven by a man (Lambert Wilson) trying to get his daughter to the hospital for an emergency organ transplant. The crooks force him to drive them away at gunpoint, creating a tense situation as the man and woman try to figure a way out and the crooks begin to bicker amongst themselves. The best thing about the 2015 version of Rabid Dogs is its professionalism: director Eric Hannezo keeps the plot points moving along smoothly, aided by crisp ‘scope lensing by Kamal Derkaoui and an effective minimalist-electronica score by Laurent Eyquem. It’s also worth noting that all the actors competently hit their marks. Unfortunately, the filmmakers seem to have misunderstood the nature of their premise, opening it up so far that they drain all the tension. The original Rabid Dogs drew its power from keeping its characters confined to a claustrophobic car interior as much as possible and kept the obstacles to their journey smaller in scale and thus more believable. The new version finds all manner of reasons to constantly stop the journey of the travelers, building in several extra victims and chases via unnecessary setpieces. The third act is particularly bizarre, weaving in a small town where everyone is involved in a festival that allows them to dress like extras from The Wicker Man. It’s also worth noting that the crooks are much less threatening and much more clichéd here, falling into easy types (the reluctant leader, the crazy one, the scared one). In short, this version of Rabid Dogs is like all too many modern remakes: competent, never dull but misguided in its attempts to reinvent its template. Availability: Scream Factory has assembled a nice little special edition for this IFC Midnight pickup. The transfer does well by the steely, digital look of the photography and there are 5.1 and 2.0 lossless French stereo mixes with English subs. The 5.1 was used for this review and its a nicely-designed track that uses the multi-speaker soundscape well. The heart of the extras is a making-of documentary (1:33:21) that is as long as the main feature itself. It’s narrated by Hannezo and offers a comprehensive, fly-on-the-wall depiction of the film’s production, in the order of how scenes were shot. Elsewhere, a cast interviews segment (41:38) offers a half-dozen interviews with actors, including Wilson and all the actors playing the crooks, and a special effects/production design featurette (14:20) offers up a trio of quick segments on atmospheric effects, the guns used in the film and the sets. The extras are completed by a theatrical trailer. Schlockmaniac #1, alias Your Humble Reviewer. The person behind this affront to High Culture is Don Guarisco. He has a BFA Degree in Film from Florida State University and has written professionally about pop culture for over a decade. His work in the online arena includes reviews and essays for Yesterdayland (now known as Retroland), All Music Guide, All Movie Guide, AVManiacs and The Temple Of Schlock. His reviews have also been published in several All Music Guide publications and DVD Delirium 3. | Mid | [
0.539215686274509,
27.5,
23.5
] |
Antimitotic and cytotoxic activity of cis-dichlorobis-(cyclohexylamine)platinum(II) on Chinese hamster ovary cells. The antimitotic and cytotoxic effects of cis-dichlorobis(cyclohexylamine)-platinum(II) (cis-HAD) which among Pt complexes used as antitumoral drugs shows the highest therapeutic index (TI) have been compared to those os cis-dichlorodiamine platinum(II) (cis-DDP), the most commonly used drug of this group, using Chinese hamster ovary cell cultures (CHO line). DNA synthesis inhibition, mitotic index, cell viability, chromosome aberrations and cell survival have been taken into account. The data indicates that the antimitotic agent cis-HAD is active only at doses causing high cell mortality and chromosome damage. | Mid | [
0.6079664570230601,
36.25,
23.375
] |
Dephasing and dissipation in a source-drain model of light-harvesting systems. The energy transport process in natural-light-harvesting systems is investigated by solving the time-dependent Schrödinger equation for a source-network-drain model incorporating the effects of dephasing and dissipation, owing to coupling with the environment. In this model, the network consists of electronically coupled chromophores, which can host energy excitations (excitons) and are connected to source channels, from which the excitons are generated, thereby simulating exciton creation from sunlight. After passing through the network, excitons are captured by the reaction centers and converted into chemical energy. In addition, excitons can reradiate in green plants as photoluminescent light or be destroyed by nonphotochemical quenching (NPQ). These annihilation processes are described in the model by outgoing channels, which allow the excitons to spread to infinity. Besides the photoluminescent reflection, the NPQ processes are the main outgoing channels accompanied by energy dissipation and dephasing. From the simulation of wave-packet dynamics in a one-dimensional chain, it is found that, without dephasing, the motion remains superdiffusive or ballistic, despite the strong energy dissipation. At an increased dephasing rate, the wave-packet motion is found to switch from superdiffusive to diffusive in nature. When a steady energy flow is injected into a site of a linear chain, exciton dissipation along the chain, owing to photoluminescence and NPQ processes, is examined by using a model with coherent and incoherent outgoing channels. It is found that channel coherence leads to suppression of dissipation and multiexciton super-radiance. With this method, the effects of NPQ and dephasing on energy transfer in the Fenna-Matthews-Olson complex are investigated. The NPQ process and the photochemical reflection are found to significantly reduce the energy-transfer efficiency in the complex, whereas the dephasing process slightly enhances the efficiency. The calculated absorption spectrum reproduces the main features of the measured counterpart. As a comparison, the exciton dynamics are also studied in a linear chain of pigments and in a multiple-ring system of light-harvesting complexes II (LH2) from purple bacteria by using the Davydov D1 ansatz. It is found that the exciton transport shows superdiffusion characteristics in both the chain and the LH2 rings. | High | [
0.6558891454965351,
35.5,
18.625
] |
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This proposal, submitted under the auspices of the program supporting Small Grants for Pilot Research, seeks funds to develop, refine and validate analytic techniques for inferring the relative contributions of feedforward and feedback contributions to fMRI activations in multiple visual areas. Specifically, we will use nonlinear equations to model activations (blood oxygen-level dependent signals registered using functional magnetic resonance imaging) measured while human observers report fluctuations in visual perception associated with viewing binocular rivalry (i.e., the alternations in visual awareness between two dissimilar images viewed by the separate eyes). These analytic techniques have been described in the literature (Buchel & Friston, 1995) but have been rarely employed in studies of vision, despite their potential for significantly extending the range of conclusions drawn from brain imaging studies. Given the dramatic increase in the use of fMRI for the study of vision and its disorders, it is imperative to develop, refine and validate techniques that extend the range of problems that can be addressed using fMRI. The present proposal has this potential. | High | [
0.6727037516170761,
32.5,
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Francisco Churruca Francisco Maria Churruca Iriondo Azpiazu Alcorta (born ), also known as Patxi, is a Basque former jai alai player. A native of Mutriku, Spain, he is regarded as the game's greatest player and has been called "the Babe Ruth of jai alai." He retired in 1983, saying "I knew it was time to quit when my eyes were quicker than my legs." References Category:1936 births Category:Living people Category:People from Debabarrena Category:Spanish pelotaris Category:Sportspeople from Gipuzkoa Category:Spanish expatriate sportspeople in the United States | Mid | [
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Aortic depressor nerve unmyelinated fibers in spontaneously hypertensive rats. The objective of the present study was to compare the morphology of the unmyelinated fibers in the aortic depressor nerves (ADN) of spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). In anesthetized rats, the ADN was identified by its spontaneous activity synchronous with the arterial pulses. Thin sections of the proximal and distal segments of the ADN were analyzed by electron microscopy, and a morphometric study of the unmyelinated fibers and Schwann cells was performed. The proximal segments of WKY and SHR ADN contain an average of 335 +/- 68 and 130 +/- 14 unmyelinated fibers, respectively (P < 0.05), and the distal segments contain an average of 337 +/- 46 and 242 +/- 77 unmyelinated fibers, respectively (P < 0.05). The distribution of the diameters of unmyelinated fibers was unimodal for both strains, with the histogram from the SHR significantly shifted to the left. Because the unmyelinated fibers play a role in the tonic inhibition of the medullary vasomotor centers, especially in the presence of hypertension, the morphological differences observed in the ADN from SHR may account, at least in part, for the blunted baroreflex of SHR. | High | [
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She was a baby then, but old enough to be feral and not able to socialize. She was very curious, always watching us, interacting from a safe distance. She was trapped, spayed and released back to her colony. I did not manage this colony, but when one of the feeders was hit and killed by a truck, I filled in until the community started feeding regularly. She knew the sound of my voice, and came running when she heard my bike. She was adorable. I stopped feeding there, because they didn't need me anymore, and after that I popped by once in a while on a run or bike ride to say hello. In 2012, North Brooklyn Cats received a call that an exterminator was trapping cats at this colony. I headed over and there it was, a set trap laying in a puddle, from the thunderstorm the night before..., with the exterminator company's tag on it. I tripped the trap and, long story short, a summer long rescue mission was underway. Hitch was in terrible shape and something had changed with her. She no longer interacted with her colony and was very skittish (more than feral skittish, something else) - we found out she went missing for a while, and returned very different. We have no idea what happened. We relocated 4 of the remaining 6. Hitch came to my warehouse colony. She did very well here and was happy. She greeted me when I arrived, and followed me around while I refilled the feeders, waterers and litter boxes. Changes at this warehouse left Hitch in trouble again. She was very scared and uncomfortable and was living in a very tiny space in the ceiling. It was time for her to move on. But she's already lost 2 homes, is fearful, and another relocation just isn't an option. It's incredibly difficult to relocate ferals, and it's always risky. When we showed up to trap, she immediately headed down to the warehouse floor and got into a small corner where we couldn't reach her - either by trap or net. The next week, we showed up with netting to net off that whole area, and set traps at every escape point. We got her! She saw the vet, looks good, tested negative for FIV and FELV, her blood work is out for analysis and she received vaccination boosters and parasite control. The estimate to get Hitch safely to her sanctuary is $800. The sanctuary fee is $350, the vet bill was $370 (copy available upon request) and the fuel estimate for next week's journey is $80. She's ready to go! We just need a little help from our friends! Anything you can spare is appreciated. Very soon, Hitch will be in a safe, well maintained, feral cat sanctuary. She'll be surrounded by trees, grass and fresh air. I hope she'll again be happy and worry-free. Please help! Update: Thank you for your help! We raised the funds, and enough to do more TNR later this season. I usually track TNR efforts on a different blog, For Cats' Sake. You can see the post about her going to sanctuary there: Hitch Goes to Sanctuary. Big City Little Kitty Foster Home About Me I TNR when I can and foster kittens from TNR projects of my own, for TNR groups and rescue groups. I am not an organization, just one person pitching in to help. See my friends and my adoptable cats and kittens here: www.bigcitylittlekitty.petfinder.com Big City Little Kitty (www.bigcitylittlekitty.com) is my foster blog and For Cats' Sake (www.tnrnyc.com) is my TNR blog. [email protected] | Mid | [
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The potential for tornadoes, some of which could be strong, is part of a severe weather threat across Alabama starting early next week and continuing perhaps into Wednesday. The Storm Prediction Center in Oklahoma states in its forecast discussion today that the potential severe weather outbreak could include "strong tornadoes." The National Weather Service forecasting office near Birmingham repeated the SPC's concern for the possibility of strong tornadoes while the forecasting office in Huntsville kept the threat for now at "brief tornadoes." The Mobile forecasting office also provided for the potential of tornadoes, though mostly west of the I-65 corridor since the threat is not as great in southeast Alabama. The storms are expected to sweep across Alabama in waves, which could lead to a series of severe weather events. With more than two days until the initial potential threat, however, timing and details on the severe weather threats are uncertain, weather officials said. According to the Birmingham weather office, the third round of severe weather is of the most concern because it is most closely associated with an advancing cold front – which could provide the ingredients for strong tornadoes. Preliminary timing would be from midday Tuesday to midday Wednesday, according to the Birmingham office. The repeated waves of severe weather, which are expected to be slow moving, could lead to flooding. Along with tornadoes and heavy rain, large hail and damaging winds are expected with the severe weather. The storms are expected to be part of a system that begins in the southern Plains on Saturday and advancing to the east. The Storm Prediction Center has marked an area in much of Arkansas as well as parts of Texas, Oklahoma and Louisiana as being in a moderate threat for severe weather on Sunday. Updated today, April 25, 2014, at 2:25 p.m. with graphic from Storm Prediction Center. Updated today, April 25, 2014, at 4:05 p.m. with a gallery of weather maps and graphics. | Mid | [
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//****************************************************************************** // // Copyright (c) 2016 Intel Corporation. All rights reserved. // Copyright (c) 2015 Microsoft Corporation. All rights reserved. // // This code is licensed under the MIT License (MIT). // // 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. // //****************************************************************************** // This file is based on CBLAS http://www.netlib.org/blas/#_cblas //making global variable thread local __declspec(thread) int CBLAS_CallFromC=0; __declspec(thread) int RowMajorStrg=0; void BLASDefaultErrorProc(const char *funcName, const char *paramName, const int *paramPos, const int *paramValue); void (*__BLASErrorProc)(const char *funcName, const char *paramName, const int *paramPos, const int *paramValue) = BLASDefaultErrorProc; | Low | [
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320 F.2d 795 IMMACULATE CONCEPTION CHURCH OF LOS ANGELES and Lake Congregational Church of Pasadena, Appellants,v.FEDERAL COMMUNICATIONS COMMISSION, Appellee.ELEVEN TEN BROADCASTING CORPORATION, Appellant,v.FEDERAL COMMUNICATIONS COMMISSION, Appellee. No. 17239. No. 17240. United States Court of Appeals District of Columbia Circuit. Argued April 25, 1963. Decided July 5, 1963. Mr. Harry P. Warner, Hollywood, Cal., submitted on the brief for appellants in No. 17239. Mr. Harold David Cohen, Washington, D. C., with whom Messrs. Thomas N. Dowd and John R. Schmertz, Jr., Washington, D. C., were on the brief, for appellant in No. 17240. Mr. Ernest O. Eisenberg, Counsel, F. C. C., with whom Messrs. Max D. Paglin, Gen. Counsel, Daniel R. Ohlbaum, Associate Gen. Counsel, and Mrs. Ruth V. Reel, Counsel, F. C. C., were on the brief, for appellee. Before BAZELON, Chief Judge, and WASHINGTON and BURGER, Circuit Judges. PER CURIAM. 1 Eleven Ten's application for renewal of Station KRLA's broadcast license was denied by the Federal Communications Commission on March 19, 1962. In re Eleven Ten Broadcasting Corp., 32 F.C.C. 706, 22 R.R. 699. By orders of July 24, 1962, the Commission denied the licensee's petition for reconsideration, as well as petitions for reconsideration and rehearing filed by two Southern California churches pursuant to § 405 of the Communications Act of 1934, as amended, 75 Stat. 421 (1961), 47 U.S.C. § 405 (Supp. IV, 1963). 33 F.C.C. 92, 22 R.R. 702n. Eleven Ten and the churches appeal under § 402(b) of the Act, 66 Stat. 718 (1952), 47 U.S.C. § 402(b). 2 The events leading to denial of KRLA's renewal application may be summarized as follows: On October 22, 1958, Eleven Ten applied for Commission consent to the assignment to it of the broadcast license and construction permit (for increased power) of Station KXLA (later changed to KRLA), Pasadena, California. On the strength of various representations as to programming and other matters, the Commission approved the assignment, and Eleven Ten assumed control. Thereafter KRLA filed an application for renewal of license, as prescribed by 47 C.F.R. § 3.34. On July 5, 1960, the Commission, finding that "no questions exist as to the qualifications of the applicant" except as to four factual issues,1 designated KRLA's application for hearing. 3 Pursuant to the designation order, evidence was received on the following issues: 4 1. [W]hether, in light of its operations since it acquired Station KRLA, the licensee's program proposals contained in its application for Commission consent to assignment of the license of Station KRLA were made in good faith; 5 2. [W]hether, in light of the manner in which the "Find Perry Allen" contest was conducted by Station KRLA in and about September, 1959, the licensee operated said station for improper purposes contrary to the public interest; 6 3. [W]hether the station's program logs for the week of October 18-24, 1959, were altered with the intent and purpose of deceiving the Commission; and 7 4. [W]hether, since the date of assignment of license of Station KRLA * * * to the licensee, Jack K. Cooke, a Canadian citizen, has exercised control with respect to the operations of said station contrary to the provisions of Section 310 of the Communications Act of 1934, as amended, and the Commission's rules and policies promulgated thereunder.2 8 The examiners found that KRLA's proposals were made in good faith, that conduct of the "Find Perry Allen" contest (and a similar "Golden Key" contest) resulted in the use of licensed facilities for improper purposes contrary to the public interest, and that the station's program logs were altered by KRLA's general manager in order to deceive the Commission. The examiners recommended a short-term renewal of KRLA's license. 9 The Commission, reweighing the evidence, found that KRLA's program proposals had not been made in good faith and that alteration of the station's program logs should be imputed to Donald Cooke, the owner of KRLA. The Commission refused to consider alleged "meritorious programming efforts by KRLA after the Commission had made it clear to the licensee that renewal of its license was in doubt" as being an unreliable measure of Eleven Ten as a licensee. 33 F.C.C. at ___, 22 R.R. at 702t. 10 KRLA contends that the Commission relied on matters "outside the specific issues under which the hearing was held," thereby depriving it of a fair and full hearing as required by statute and the Fifth Amendment to the Constitution. We read the Commission's decision as founded on the "conclusions that Donald Cooke is guilty of efforts to mislead the Commission" and that his willingness to deceive the Commission warrants denial of KRLA's renewal application. The facts marshalled in support of the Commission's ultimate factual conclusion are fairly encompassed within the first and third issues and constitute substantial evidence of record in support of that conclusion. The Commission's disqualification of Eleven Ten is within the discretion committed by Congress to the Commission. Federal Communications Comm. v. WOKO, Inc., 329 U.S. 223, 227-229, 67 S.Ct. 213, 91 L.Ed. 204 (1946); Hall v. Federal Communications Comm. 99 U.S.App.D.C. 86, 94-96, 237 F.2d 567, 575-577 (1956); Charles P. B. Pinson, Inc. v. Federal Communications Comm'n, 116 U.S.App.D.C. ___, 321 F.2d 372 (1963). 11 Appellants3 contend that the Commission erred in failing to make findings as to KRLA's public service programming and to consider the public service rendered by KRLA in determining whether or not KRLA's license should be renewed. The Commission need not consider the public service rendered by a station where the licensee is disqualified by its attempts to deceive the Commission. Federal Communications Comm. v. WOKO, Inc., supra; Independent Broadcasting Co. v. Federal Communications Comm., 89 U.S.App.D.C. 396, 193 F.2d 900 (1951), cert. denied, 344 U.S. 837, 73 S.Ct. 14, 97 L.Ed. 652 (1952). The decision of the Commission will be 12 Affirmed. Notes: 1 A fifth issue merely directed the examiner "to determine, in light of the evidence adduced pursuant to the foregoing issues, whether a grant of the above-entitled applications would serve the public interest, convenience or necessity." 2 The alien control issue was resolved in favor of KRLA 3 Since the two appeals have been consolidated and since the churches' appeal presents no additional issues for our decision, we do not think it necessary to decide whether or not the churches have standing by reason of KRLA's broadcasting their Sunday services without charge | Low | [
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Analytical modeling of optical reflectivity of random plasmonic nano-monolayers. In this paper, we compare three different models that have been used to interpret reflectivity measurements of supported monolayers of nanoparticles. Two of them: (i) isotropic Maxwell Garnett and (ii) anisotropic two-dimensional-dipolar model are based on an effective-medium approach, while the third one (iii) coherent-scattering model, lies within the framework of multiple-scattering theory. First, we briefly review, on physical grounds, the foundations of each model and write down the corresponding formulas for the calculation of the reflectivity. In the two-dimensional-dipolar model, the dilute limit of the pair-correlation function (also called hole-correlation function) is always used in the calculation of the effective optical response. Then we use these formulas to plot and analyze graphs of the reflectivity of a monolayer of gold nanoparticles on a glass substrate, as a function of several relevant parameters, for two different commonly used experimental configurations. Finally, we discuss the importance of our results and how they can be used to infer the limits of validity of each model. | High | [
0.6944818304172271,
32.25,
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Q: Can No Longer Mount Windows File Systems (Since May 9th 2017) For over a year, I've been able to backup numerous Windows servers using Ubuntu Server 16.04, but this all stopped working on Tuesday May 9th 2017. Here's how I'm mounting these windows file systems using fstab: sudo nano /etc/fstab \\192.168.1.1\c$ /mnt/win2012r2 cifs credentials=/home/user/.smb,iocharset=utf8,sec=ntlm 0 0 \\192.168.1.2\d$ /mnt/win2008r2 cifs credentials=/home/user/.smb,iocharset=utf8,sec=ntlm 0 0 \\192.168.1.3\c$ /mnt/win2012 cifs credentials=/home/user/.smb,iocharset=utf8,sec=ntlm 0 0 \\192.168.1.4\d$ /mnt/win2008 cifs credentials=/home/user/.smb,iocharset=utf8,sec=ntlm 0 0 The /home/user/.smb file contains only this: username=administrator2 password=s3cr3tPW domain=company1 After a reboot, if I attempt to do a mount command, it shows that all of theses server's drives are already mounted to the linux file system: sudo mount -a --verbose -vvv /mnt/win2012r2 : already mounted /mnt/win2008r2 : already mounted /mnt/win2012 : already mounted /mnt/win2008 : already mounted However, if I try to list the directory where these mount-points are, it takes forever and eventually says these hosts are down: ls /mnt ls: cannot access 'win2012r2': Host is down ls: cannot access 'win2008r2': Host is down ls: cannot access 'win2012': Host is down ls: cannot access 'win2008': Host is down Above, is essentially the same error that I also see in my cron rsync logs: failed: Host is down (112) Again, this all started on Tuesday May 9th 2017. And, it is not just happening on this one network; its the same story at a completely different company where I'm using the same method for backup. Lastly, no settings have been changed recently on these backup servers. I don't even recall explicitly doing any updates between May 8th and 9th. A: Temporary hack. I have encountered the same error when mounting from the command line. sudo mount -t cifs //ls2/jc /mnt/ls2 -o username=jc I did not get an error, "Host is down", until I tried to access both the share directory /mnt/ls2 AND /mnt. ls /mnt/ls2 ls /mnt I then unmounted the share sudo umount /mnt/ls2 then remounted using the very same command as before sudo mount -t cifs //ls2/jc /mnt/ls2 -o username=jc. Everything worked. Important note: The share at //ls2/jc is not on a Microsoft box, but on Ubuntu 14 server updated current running smbd Version 4.3.11-Ubuntu. and uname -a output: Linux ls2 4.4.0-75-generic #96~14.04.1-Ubuntu SMP Thu Apr 20 11:06:56 UTC 2017 i686 i686 i686 GNU/Linux Client where mount command executed uname -a output: Linux tec3 4.4.0-75-generic #96~14.04.1-Ubuntu SMP Thu Apr 20 11:06:30 UTC 2017 x86_64 x86_64 x86_64 GNU/Linux Client mount version: mount from util-linux 2.20.1 (with libblkid and selinux support) | Mid | [
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LP Shape Cores LP cores are similar to EQ cores but with larger wireways for easier winding and assembly. Their planar design helps to maximize inductor efficiency. are a cross between E cores and pot cores. In comparison to E cores and other non-planar cores, LP powder cores offer better space utilization, shielding and improved thermal performance. | High | [
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Q: Routine in module is Undefined subroutine in perl I have just installed the Crypt::Random module as well as all the dependencies such as Math::Pari. There are three routines in Crypt::Random and I don't know why perl is calling them 'undefined subroutine'. Thanks to whoever knows what is wrong. Here are the routines (specifically defined in the module), and I chose small arguments for them to see if they work: C:\Users\Jlinne\Documents>perl -MCrypt::Random -E "say makerandom(100)" Undefined subroutine &main::makerandom called at -e line 1. C:\Users\Jlinne\Documents>perl -MCrypt::Random -E "say makerandom_itv(1, 1000)" Undefined subroutine &main::makerandom_itv called at -e line 1. C:\Users\Jlinne\Documents>perl -MCrypt::Random -E "say makerandom_octet(10)" Undefined subroutine &main::makerandom_octet called at -e line 1. A: Crypt::Random does not export any methods by default. Instead you must explicitly import them: $ perl -MCrypt::Random=makerandom -E "say makerandom(100)" $ perl -MCrypt::Random=makerandom_itv -E "say makerandom_itv(1, 1000)" $ perl -MCrypt::Random=makerandom_octet -E "say makerandom_octet(10)" | Mid | [
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60 and -21/629050. 1258100 Calculate the lowest common multiple of 328 and 12800. 524800 Calculate the smallest common multiple of 42 and 47378. 994938 What is the least common multiple of 58 and 240265? 480530 Calculate the least common multiple of 214 and 3006. 321642 What is the lowest common multiple of 1394972 and 44? 15344692 What is the common denominator of 105/1892 and 41/46354? 92708 Calculate the least common multiple of 3856 and 82904. 165808 What is the least common multiple of 3672 and 2295? 18360 Calculate the least common multiple of 112528 and 309452. 1237808 Calculate the common denominator of 145/238494 and 115/715482. 715482 Calculate the smallest common multiple of 7 and 153452. 1074164 Calculate the smallest common multiple of 32 and 16512. 16512 Calculate the common denominator of -37/18 and 31/38772. 38772 What is the common denominator of -49/12848 and -131/220? 64240 What is the common denominator of 99/292136 and 97/73034? 292136 What is the smallest common multiple of 398959 and 72538? 797918 What is the lowest common multiple of 3024 and 393768? 5512752 What is the common denominator of 151/12 and -41/66732? 66732 Calculate the lowest common multiple of 4836 and 23088. 715728 Calculate the least common multiple of 4248 and 387512. 3487608 Find the common denominator of 29/18 and 95/663778. 5974002 Find the common denominator of -81/932768 and 151/1399152. 2798304 Find the common denominator of -63/11425 and -9/25. 11425 Calculate the common denominator of -23/12449 and -13. 12449 Calculate the lowest common multiple of 177859 and 5291. 2312167 Calculate the lowest common multiple of 18513 and 176418. 2999106 What is the common denominator of 93/208 and -67/7824? 101712 Find the common denominator of -25/162 and 73/196506. 196506 What is the smallest common multiple of 1000 and 1934? 967000 Calculate the common denominator of 4/2415 and -68/189. 21735 Find the common denominator of -32/207 and 85/107058. 7387002 What is the lowest common multiple of 8496 and 24? 8496 Calculate the common denominator of 25/25542 and 73/44. 51084 Calculate the least common multiple of 12 and 3411000. 3411000 Find the common denominator of 32/1699 and -53/8495. 8495 Find the common denominator of 131/30 and -151/154302. 771510 What is the least common multiple of 492 and 504? 20664 What is the smallest common multiple of 33 and 13156? 39468 Find the common denominator of -49/4488 and 85/176. 8976 What is the common denominator of 61/744 and -69/3932? 731352 What is the lowest common multiple of 51027 and 18? 306162 Calculate the lowest common multiple of 688 and 784. 33712 Find the common denominator of -77/306 and 73/19890. 19890 Find the common denominator of 109/152480 and 27/152480. 152480 Find the common denominator of 61/5 and 77/1410. 1410 Calculate the common denominator of 23/17178 and 143/336. 137424 Calculate the common denominator of 19/68484 and 101/6. 68484 Calculate the lowest common multiple of 21520 and 18. 193680 Calculate the least common multiple of 3371 and 6. 20226 Calculate the common denominator of 3/32963 and -86/7497. 2076669 Calculate the smallest common multiple of 2144 and 160. 10720 Calculate the smallest common multiple of 151816 and 21. 455448 What is the smallest common multiple of 2700 and 216? 5400 Find the common denominator of 13/279 and -19/4749. 441657 Calculate the common denominator of -83/1122 and 23/1650. 28050 Find the common denominator of 29/1488648 and -37/2232972. 4465944 Find the common denominator of -19/2 and 15/3170066. 3170066 What is the common denominator of -29/60 and -161/3840? 3840 What is the smallest common multiple of 28 and 7096? 49672 Calculate the common denominator of 103/20 and 59/4709104. 23545520 What is the least common multiple of 870 and 69542? 1043130 What is the common denominator of -47/608816 and 101/160? 6088160 What is the lowest common multiple of 110568 and 248778? 995112 What is the least common multiple of 33 and 9231? 101541 Find the common denominator of -33/1655 and -20/11. 18205 Calculate the common denominator of 77/664 and -41/40. 3320 What is the common denominator of 69/3380 and 47/208884? 1044420 What is the least common multiple of 423704 and 10? 2118520 What is the common denominator of -49/1500 and 167/2340? 58500 Calculate the common denominator of 187/13680 and -121/108. 41040 What is the lowest common multiple of 2946 and 78560? 235680 Calculate the common denominator of 101/800 and 163/26400. 26400 Calculate the smallest common multiple of 7970 and 430. 342710 What is the smallest common multiple of 8 and 13154? 52616 Calculate the smallest common multiple of 77 and 224. 2464 Calculate the common denominator of -34/7011 and -77/152. 56088 Calculate the smallest common multiple of 10894 and 1911. 1601418 What is the common denominator of 113/20 and 10/2749? 54980 Calculate the common denominator of 23/33026 and -63/1348. 66052 Find the common denominator of -37/2320 and -61/1740. 6960 What is the smallest common multiple of 270 and 950? 25650 Calculate the least common multiple of 6076 and 14. 6076 What is the lowest common multiple of 15 and 21381? 106905 Calculate the least common multiple of 1716 and 24. 3432 Calculate the common denominator of 41/22420 and -161/67260. 67260 Calculate the least common multiple of 1755 and 7137. 107055 Calculate the least common multiple of 620908 and 23. 620908 What is the smallest common multiple of 596 and 14? 4172 What is the smallest common multiple of 3825 and 30175? 271575 Calculate the common denominator of -76/70551 and -71/15678. 141102 What is the lowest common multiple of 1864 and 944582? 3778328 What is the lowest common multiple of 524 and 6732? 881892 Calculate the least common multiple of 16 and 95120. 95120 What is the least common multiple of 1236183 and 182? 17306562 Find the common denominator of 29/336 and -95/27306. 1529136 Calculate the smallest common multiple of 6012 and 22044. 66132 What is the lowest common multiple of 5751 and 3834? 11502 What is the common denominator of -31/208510 and -101/90? 1876590 Calculate the lowest common multiple of 44 and 1848. 1848 What is the common denominator of -16/3081 and 58/14457? 187941 What is the common denominator of -21/2 and 54/60287? 120574 What is the common denominator of 19/632 and -57/86110? 344440 What is the common denominator of -127/5472 and -103/27360? 27360 Calculate the least common multiple of 308 and 85470. 170940 What is the lowest common multiple of 18 and 834456? 2503368 Calculate the common denominator of -67/22 and -79/3322. 3322 What is the smallest common multiple of 115506 and 1578582? 4735746 Calculate the common denominator of -115/6096 and 2/1397. 67056 Calculate the lowest common multiple of 51 and 1213290. 1213290 What is the lowest common multiple of 54 and 25380? 25380 Calculate the least common multiple of 153 and 6630. 19890 Calculate the smallest common multiple of 4142 and 718. 1486978 Calculate the common denominator of 1/91949 and -29/91949. 91949 Find the common denominator of 77/918 and 79/36210. 325890 Find the common denominator of -125/672 and -119/1160. 97440 Calculate the common denominator of 143/15720 and -127/43230. 172920 What is the lowest common multiple of 19945 and 935? 3729715 What is the common denominator of 103/2064 and 41/5440? 701760 What is the common denominator of 3/124703 and -41/249406? 249406 What is the lowest common multiple of 10892 and 317424? 2221968 What is the smallest common multiple of 110 and 3240? 35640 What is the lowest common multiple of 7512 and 20658? 82632 What is the least common multiple of 7358 and 9622? 125086 Find the common denominator of -71/63 and -157/2604. 7812 What is the common denominator of -87/8048 and 61/16096? 16096 Calculate the common denominator of 24/155 and 107/107880. 107880 Calculate the least common multiple of 333 and 814. 7326 Find the common denominator of -57/217714 and -29/1778. 27649678 Calculate the common denominator of 79/198696 and 97/11688. 198696 What is the smallest common multiple of 288 and 373104? 746208 Find the common denominator of -10/891 and 103/5500. 445500 Calculate the common denominator of 23/149974 and 10 | Low | [
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High-quality child care leads to academic success for low-income kids September 15, 2009 in Other Sciences / Social Sciences For low income parents, finding high quality child care not only boosts the performance of their children in school, but actually combats the effects of poverty, according to a new study in the journal Child Development. Children who spent more time in high-quality child care in the first five years of their lives had better reading and math scores in middle school, according to researchers from Boston College, the Harvard Graduate School of Education and Samford University, who studied 1,300 middle school students. Looking deeper, researchers found that low income children who received high-quality child care achieved at similar academic levels as their more affluent peers, even after taking into account factors such as levels of parental education and employment. "The real takeaway here is that even minimal exposure to higher quality child care protects children from the harm done by living in poverty," co-author Eric Dearing, an associate professor of applied developmental psychology in the Lynch School of Education at Boston College, said. "When it comes to early child care, quality matters more for children in poverty than for affluent children in promoting the long term academic achievement of the former up to similar levels as the latter." The researchers looked at reading and math achievement of more than 1,300 children in middle childhood from economic backgrounds ranging from poor to affluent. They used information from the longitudinal Study of Early Child Care and Youth Development, which was carried out under the auspices of the Eunice Kennedy Shriver National Institute of Child Health and Human Development. | High | [
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Histopathological study of pulmonary arteries in 14 autopsy cases with massive pulmonary thromboembolism. As the pathological features of acute massive pulmonary thromboembolism (PTE) remain unclear, early diagnosis is difficult. We examined 14 autopsy cases of sudden death by massive PTE. Eight cases were male and six female, with a mean age of 57+/-18 years. While none of the cases were diagnosed with PTE during their lifetime, 12 cases had predicting factors for thrombosis. Deep vein thrombosis was found at autopsy in 11 cases. Cross sections of each segmental pulmonary artery were dissected for histological examination. The distribution of fresh thrombi and organized thrombi in the pulmonary arteries was investigated. Results revealed that 13 cases contained both fresh and organized thrombi. More detailed examination indicated that as the organized thrombi were spread in all lobes, the distribution of thrombi extended from the proximal to peripheral arteries. Our findings indicated that most cases of fatal PTE had a subclinical recurrent history. Thus, proper diagnosis and treatment of prior emboli may be vital for the prophylaxis of sudden death by PTE. | Mid | [
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Effects of phacoemulsification with versus without viscoelastic devices on surgical outcomes. The aim of this study is to report surgical outcomes in patients undergoing phacoemulsification surgery (PE) with versus without ophthalmic viscosurgical devices (OVDs). This is a comparative case series study. In total, 145 patients who performed PE with OVDs in 68 eyes (Group 1) and without OVD in 77 eyes (Group 2) were enrolled. A comprehensive ophthalmological examination was performed including slit-lamp, fundus examination. Best-corrected visual acuity (BCVA), intraocular pressure (IOP) specular endothelial microscopy (SM), and ultrasound pachymetry (UP) were also measured before surgery and at four-time points postoperatively. The differences in baseline characteristics as well as in outcomes were compared between the two groups. The mean BCVA was 0.41 ± 0.26 logMAR in Group 1 and 0.54 ± 0.34 in Group 2 at postoperative first day, with a significant difference (p < 0.01). The mean BCVA, IOP, and UP at 6 months did not differ between the groups. The mean baseline and postoperative SMs were 2063 and 1910 cells/mm2, respectively, and the endothelial cell loss (ECL) was 153.89 ± 189 in Group 1. The mean baseline and postoperative SMs were 2153 and 1948 cells/mm2, respectively, and the ECL was 205 ± 200 in Group 2. The difference between the groups was not statistically significant (p = 0.105). The ECL seemed to be higher in the Group 2, but the difference was not significant. The final clinical outcomes were similar between the groups. In selected cases, PE without OVD may be preferable to reduce the cost of surgery in places with low economic status and to prevent side-effects of these devices. | High | [
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# $FreeBSD$ SHLIB= game SHLIB_NAME= game.so SRCS= g_ai.c \ g_cmds.c \ g_chase.c \ g_combat.c \ g_func.c \ g_items.c \ g_main.c \ g_misc.c \ g_monster.c \ g_phys.c \ g_save.c \ g_spawn.c \ g_svcmds.c \ g_target.c \ g_trigger.c \ g_turret.c \ g_utils.c \ g_weapon.c \ m_actor.c \ m_berserk.c \ m_boss2.c \ m_boss3.c \ m_boss31.c \ m_boss32.c \ m_boss5.c \ m_brain.c \ m_chick.c \ m_fixbot.c \ m_flash.c \ m_flipper.c \ m_float.c \ m_flyer.c \ m_gekk.c \ m_gladb.c \ m_gladiator.c \ m_gunner.c \ m_hover.c \ m_infantry.c \ m_insane.c \ m_medic.c \ m_move.c \ m_mutant.c \ m_parasite.c \ m_soldier.c \ m_supertank.c \ m_tank.c \ p_client.c \ p_hud.c \ p_trail.c \ p_view.c \ p_weapon.c \ q_shared.c CFLAGS+= -Dstricmp=strcasecmp -ffast-math -funroll-loops \ -fomit-frame-pointer -fexpensive-optimizations LDFLAGS+= -L/lib -L/usr/lib -lm .include <bsd.lib.mk> | Mid | [
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President Trump Donald John TrumpSteele Dossier sub-source was subject of FBI counterintelligence probe Pelosi slams Trump executive order on pre-existing conditions: It 'isn't worth the paper it's signed on' Trump 'no longer angry' at Romney because of Supreme Court stance MORE said Tuesday that some of the accounts or content that he retweets from his @realDonaldTrump handle can end up being a "problem" for the White House. During an interview with C-SPAN political editor Steve Scully, the president argued that he did not regret any of the tweets he personally wrote, but demurred when it came to content from other accounts when asked whether he regretted any of his account's roughly 43,000 messages. ADVERTISEMENT "Not much, honestly not much," Trump said. "I sent the one about the 'wiretapping' … and that turned out to be true." "A lot of the times the bigger problem is the retweets," he continued. "You know, you retweet something that sounds good but it turns out to be from a player that's not the best player in the world. And that sort of causes a problem." .@SteveScully: "You've issued 43,000 tweets. Did you ever regret sending one out?" President Trump: "Not much…I sent the one about the 'wiretapping'…and that turned out to be true…a lot of the times the bigger problem is the retweets." pic.twitter.com/c3StZjNrBK — CSPAN (@cspan) July 30, 2019 Earlier in the interview, the president called his tweets a defense against bias in the media. "If I got fair coverage I wouldn't even have to tweet. It's my only form of defense," Trump said. "If the press covered me fairly, I wouldn't need that. But they don't cover me fairly," he continued, citing coverage of a protester who disrupted one of his recent speeches. | Low | [
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Epidemiology, Genetic Recombination, and Pathogenesis of Coronaviruses. Human coronaviruses (HCoVs) were first described in the 1960s for patients with the common cold. Since then, more HCoVs have been discovered, including those that cause severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), two pathogens that, upon infection, can cause fatal respiratory disease in humans. It was recently discovered that dromedary camels in Saudi Arabia harbor three different HCoV species, including a dominant MERS HCoV lineage that was responsible for the outbreaks in the Middle East and South Korea during 2015. In this review we aim to compare and contrast the different HCoVs with regard to epidemiology and pathogenesis, in addition to the virus evolution and recombination events which have, on occasion, resulted in outbreaks amongst humans. | High | [
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Comments NHL Picks NHL Picks: Bet Arizona Coyotes +175 Over Anaheim Ducks at "The Pond" It's very rare when you get just one NHL game for the day, but tonight, we have just 1 game as the Arizona Coyotes visiting the Anaheim Ducks. Check our NHL pick inside. Face-off is set for 10:00 p.m. EST tonight at the Honda Center in Anaheim, California. This actually benefits the bettor who is betting on the Monday Night Football game and is dissatisfied with the outcome of the football game as of that point as it is a somewhat tough matchup. Point being, it provides another chance to make a profit. According to 5Dimes, the Ducks still get the respect off of from their past history as they're a -190 betting favorite and the total for the game is listed at 5 goals on the NHL odds board. The question here is are the Ducks a good fade at this price? They certainly haven't played up to expectations and haven't been any better than Arizona. Starting Goalies For a late game such as this, I figured that there would be no confirmation as to who would be in net, but that's not the case for the Coyotes as it's confirmed that Anders Lindback will be starting tonight and although unconfirmed, we'll have to assume that Frederik Andersen will be between the pipes for the Ducks. Lindback has only started 4 games this season, but he's certainly the player that Arizona wants in goal as he possesses a 1.67 GAA and .933 SV% as opposed to their regular starter, Mike Smith, who has been having a tough time this season. Anaheim only averages 1.5 goals per game and this could be a fantastic spot for Lindback at a price such as this. Scoring Drought Anaheim's defense isn't the problem as they rank 6th in goals against and are the best team in the league on the power play. This is certainly indicative where Frederik Andersen's resume is concern. He's just 3-5-2 but has a 2.03 GAA and a whopping .935 SV%. This tells the bettor that Andersen has been seeing a ton of shots and most of the action has been in the Ducks zone. We are 14 games into the season and not one Duck has more than 2 goals. Corey Perry leads the team with 2 goals and 8 assists and is one of the go to guys on this team, but they certainly have gotten off to a very slow start offensively. Perry is 2nd on the team in SOG with 31 and leads the team in penalty minutes at 19. This was expected as he's one of the best players on the team, but he can't do it by himself. Welcome Back! The Ducks have really missed centerman, Ryan Getzlaf, who had missed four games due to injury as Getzlaf is usually the teams leader in point production. Upon his return, Getzlaf hasn't disappointed as he has 4 assists in 2 games. With Ryan Getzlaf in the lineup, this team has a different complexion. The Coyotes might give the Ducks offense a boost as they allow 2.9 goals per game, but with Lindback in goal, that could be a tall order. Goals Galore Arizona on the other hand, has no trouble lighting the lamp as they possess 4 players with 4 goals or more and their leading scorer, Martin Hanzal, has been a fantastic setup man with 12 assists and a +5 on the season. Max Domi (5 goals, 6 assists) has been a beast early in the season and especially on the road as he has 3 goals and 5 assists in 7 games on the road and has a goal and an assist in his one meeting with Anaheim. Look for Domi to be a major factor in this game. My NHL pick will be Arizona in this matchup. I like the change to Lindback in net and the Ducks simply can't put the puck in the net. | Mid | [
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“Since Orlando took the initiative to build a women’s soccer team, it has shown that it has the same intent for them that it has for the men’s team.” That was what Marta, the five time FIFA Women’s Player of the Year, said at last Friday’s press conference when asked why she chose to come to the City Beautiful. Several Pride players have talked during the offseason and the preseason about the team’s commitment to treating their men’s and women’s teams as equal. They use the same training facility, they play on the same pitch. The move to get Marta showed a lot of ambition, but it also showed commitment from the organization that they wanted the best in Orlando. “I think Marta being here shows commitment from ourselves to women’s soccer in the region,” Alex Leitao, Orlando City CEO, said. “We have very ambitious goals that I think she will help us to achieve.” Orlando City Soccer Club is a part of a larger movement towards growth in women’s sports across the United States. The NWSL recently signed a television contract with Lifetime, expanding access to the sport while also providing some stability to the league entering its fifth year. In addition, the U.S women’s soccer team recently negotiated a new Collective Bargaining Agreement that moved them closer to equality with their male counterparts. “I left Brazil very early and I started playing against some of the greatest athletes in the world, and since then women’s soccer in the United States was referenced as the best. And this movement that is happening here in the U.S is also a reference,” Marta said. “And what athlete wouldn’t want to be part of that and play their main sport, their preferred sport, in such a country.” | High | [
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This summer, NFL Nation reporters are answering the biggest questions for every team in divisional roundtables. Monday's question: Who will be the best newcomer? Tuesday's question: Who is the rising star in each division? Wednesday's question: Who is on the hottest seat in the division? Thursday's question: Who will be the MVP for each division? AFC East | AFC North | AFC South | AFC West NFC East | NFC North | NFC South | NFC West Mike Rodak, Buffalo Bills reporter: I don't think it makes a whole lot of sense to pick someone other than Tom Brady. He has been on top of this division since 2003, aside from the 2008 season that he missed because of a knee injury. Until Brady slows down, there isn't a lot of discussion or analysis needed here. James Walker, Miami Dolphins reporter: How can anyone pick against Patriots quarterback Tom Brady? He has been the king of the AFC East for the past 15 years. It looks like Brady will sit the first four games of the regular season, but that could enhance his case for division MVP. The Patriots have a tough early slate and could win just one or two games with unproven Jimmy Garoppolo under center in the opening month. But the Patriots will, as usual, catch fire once Brady returns. New England historically plays its best football in November and December. If Brady leads the favored Patriots to another division title while playing just 12 games, he gets my vote. Tom Brady proved last season he's still playing at a very high level. Aaron M. Sprecher/AP Images Rich Cimini, New York Jets reporter: Who will be the division MVP? My three leading candidates: Tom Brady, Tom Brady and Tom Brady. Even if he serves a four-game suspension, he will have enough of a season to lead his team to yet another division title. This is life in the AFC East. Mike Reiss, New England Patriots reporter: Tom. Brady. Just had a flashback from each of the past 10-plus years, so until he shows signs of slippage, he gets the nod. If a non-Brady choice had to be made, it's Patriots tight end Rob Gronkowski. We haven't seen anyone like him at the position in recent history, and possibly ever. Jeremy Fowler, Pittsburgh Steelers reporter: I've tried to think of which divisional player has the best chance to unseat a healthy Ben Roethlisberger over 16 games. Surprisingly, the best answer might be Andy Dalton, who was setting the best scoring pace among AFC North quarterbacks before missing the last month of the season with an injury. But with Roethlisberger, the numbers will always be there. He has averaged more than 300 passing yards per game the past two seasons. Dalton has had one impressive year, and Joe Flacco never has had more than 27 touchdowns in a regular season. Catching up to Big Ben will be difficult, unless a playmaker such as Antonio Brown, A.J. Green, Steve Smith Sr. or Le'Veon Bell is simply too explosive to ignore by season's end. Roethlisberger had 16 interceptions in 12 games last season, but if he keeps them down, then his accuracy and ability to stretch the field will prevail. Coley Harvey, Cincinnati Bengals reporter: The AFC North MVP race will come down to quarterbacks. And at this stage, there are two who merit vastly more consideration than the others: Andy Dalton and Ben Roethlisberger. Yes, Andy Dalton. The days of wondering which version of Dalton the Bengals and your fantasy team will get week to week are over. Dalton proved with last year's scorching 10-2 start that he actually has what it takes to be a dominant passer. Before he suffered a season-ending thumb injury against Pittsburgh in Week 14 last season, Dalton was part of a league-wide MVP race. Had his season continued, there's no telling how the year would have ended for him and the Bengals. Roethlisberger probably is the sexiest pick for division MVP right now because he'll be back working with arguably the most complete offense in football. It's an offense so good that a legitimate case could be made for his top receiver, Antonio Brown, and running back, Le'Veon Bell, earning division MVP honors, too. Jamison Hensley, Baltimore Ravens reporter: Le'Veon Bell, Steelers. The more popular picks will be Ben Roethlisberger and Antonio Brown. Here's going with the Pittsburgh offensive weapon who has the most to prove. Bell tore his medial collateral and posterior cruciate ligaments in the middle of the season, and he has set his sights on an Adrian Peterson-type recovery. He's one of the league's most dangerous and versatile players. It was only two years ago when Bell shattered the Steelers' record for catches by a running back while finishing second in the NFL in rushing. There's plenty of incentive for Bell to show he's not injury prone. If that wasn't enough, he's a free agent after the season. When you combine that type of talent and motivation, big things usually occur. Pat McManamon, Cleveland Browns reporter: Easy. Assuming he stays healthy, Ben Roethlisberger, one of the five best in the league. Roethlisberger seems to improve every year with his understanding of Pittsburgh's offense and in his work with teammates. He and Antonio Brown have something special going on the field, and the Steelers start the season with Le'Veon Bell in the backfield. That's an outstanding trio, but Roethlisberger makes it all go. He's the division's runaway MVP. Tania Ganguli, Houston Texans reporter: Until someone can stop him, this will be J.J. Watt. He won NFL Defensive Player of the Year last season despite five torn core muscles in his torso, groin and inner thighs; a broken hand; and a herniated disk. And let's not forget the one game he played with a miserable flu. He didn't want to go on camera afterward, but Watt spoke to us after the game and was barely coherent. He had 17.5 sacks last season, eight batted passes and three forced fumbles. I understand the power of a quarterback, and a healthy Andrew Luck will offer competition here. But Watt is too dominant. He'll be healthier and better in 2016. Paul Kuharsky, Tennessee Titans reporter: It will be a two-man race between a resurgent Andrew Luck and J.J. Watt. I know there were problems for Luck before he got hurt in 2015, but I still expect him to get back on track and be a lot like the guy who threw 40 touchdowns against 16 interceptions in 2014. With Rob Chudzinski as offensive coordinator, the Colts will re-examine what wasn't working and give Luck a great chance to excel. J.J. Watt put up 17.5 sacks last season, despite playing through a bunch of different injuries. Scott Halleran/Getty Images Michael DiRocco, Jacksonville Jaguars reporter: DeAndre Hopkins finished third in the NFL in receptions (111) and receiving yardage (1,521) last season despite catching passes from three quarterbacks, the best of whom was Brian Hoyer. Imagine what he could do with some stability at that spot. The Texans believe Brock Osweiler is a significant upgrade. I'm skeptical of that, but all he needs to be is an average quarterback, and Hopkins will be even better than he was last season. Plus, the Texans added running back Lamar Miller in free agency and drafted receivers Will Fuller and Braxton Miller. Those additions should make things somewhat easier for Hopkins in 2016. He'll be in the conversation for NFL Offensive Player of the Year. Mike Wells, Indianapolis Colts reporter: This is way too easy: J.J. Watt. He'll be the front-runner for the NFL's Defensive Player of the Year every season he remains healthy. We're talking about a player who has compiled 69 sacks, disrupted the timing of quarterbacks countless other times and forced 15 fumbles in the past four seasons. Watt gets the edge over Luck because he might catch a touchdown or two next season. Luck won't be on defense sacking any quarterbacks. Jeff Legwold, Denver Broncos reporter: It's time to take Von Miller at his word. And Miller has said no matter what happened in his contract negotiations, he planned on showing up and playing the 2016 season to "prove it was not just a one-year thing.'' He could have been talking about the Broncos' Super Bowl win or the level of play he reached in the team's postseason, a collection of sacks, forced fumbles and an interception of a Tom Brady pass that propelled the Broncos to the title. There is always a chance the Broncos and Miller's representatives don't get a deal done and Miller elects not to show up until Week 10 or so to play on the franchise tag. But logic, cooler heads and the realization of what cratering negotiations would mean to be Miller's career and the morale in the Broncos' locker room should prevail. The two sides should strike a deal that works. And if/when they do, it will set Miller free in Year 2 of Wade Phillips' defense with the bulk of the defensive cast in place from last season. If none of the above happens, look for the Raiders edge rusher Khalil Mack and quarterback Derek Carr to insert themselves into the conversation. Chargers quarterback Philip Rivers and Broncos running back C.J. Anderson could rise to that level as well if their teams around them do enough to help them flourish. Adam Teicher, Kansas City Chiefs reporter: This depends on which team wins the division. If the Broncos win the AFC West, it will be because of their defense, in which case linebacker Von Miller is the MVP. If the Raiders win the division, it will be because they've scored a lot of points, in which case quarterback Derek Carr is the MVP. In Kansas City, it stands to reason the defense will take a step back after losing cornerback Sean Smith and given the uncertainty of linebacker Justin Houston's availability. So if the Chiefs win the division, it will likely be because of their improved offense, and I'll go with wide receiver Jeremy Maclin. In the unlikely event the Chargers win the AFC West, the MVP couldn't be anyone other than quarterback Philip Rivers. Paul Gutierrez, Oakland Raiders reporter: Von Miller's showing as Super Bowl 50 MVP with 2.5 sacks for 27 yards, including a pair of game-changing strip sacks of Cam Newton, six tackles, two quarterback hits and a pass defensed should carry over to this season, shouldn't it? Well, not if a contract squabble becomes a major distraction for him and team or if a Super Bowl hangover of epic proportions envelops the champs. But Miller, helped by the presence of DeMarcus Ware on the other side, is more than the most feared player in the AFC West; he is also the most productive, so to speak. His 60 sacks in 72 career games, including 25 sacks in the past two seasons, give opposing offensive coordinators sleepless nights, and that's before you realize he's averaged 14.5 sacks the three times he played in all 16 games. Division MVP? Miller, so long as all is right with his body and mind, has a chance to battle it out for league MVP with Houston Texans defensive end J.J. Watt. Eric Williams, San Diego Chargers reporter: Oakland Raiders receiver Amari Cooper should take another step in his development, and it's hard to bet against consistent performers such as Von Miller and Philip Rivers. But I believe Chiefs running back Jamaal Charles will have a bounce-back year in 2016. Charles, of course, suffered a season-ending ACL injury in 2015, but at 29 years old, he still has plenty of gas left in the tank. Chiefs coach Andy Reid wants to run the football, which means Charles should get plenty of touches, both as a runner and in the passing game. Kansas City also has plenty of depth at running back in Spencer Ware and Charcandrick West, so Charles should not wear down during the year. Dan Graziano, New York Giants reporter: Tony Romo. I predict the Cowboys quarterback bounces back from last season's injuries and leads Dallas to a division title in a manner that looks a lot like his 2014 season. Romo and the offense might have to score even more points than they did that year to make up for what's happening on defense. But as long as Romo and Dez Bryant stay healthy, they are more than capable. Ezekiel Elliott will only help with Romo's protection and with diversifying the offense to take pressure off him. Todd Archer, Dallas Cowboys reporter: Tony Romo. Because he has won just two playoff games in his career, he has not received a lot of appreciation among Cowboys fans. That seemed to change last year, when he missed 12 games and the Cowboys went 1-11 without him. The Cowboys went 3-1 in Romo's four starts in 2015 and are 15-4 with him the past two seasons. He had surgery on his twice-broken left collarbone in the offseason and is now healthy. The time off has allowed him to build more strength in his back, and he is moving around better than he has in recent years. With Romo, the Cowboys are the favorites in the NFC East and could be considered one of the best teams in the conference -- if he is healthy. That will be the key, because he has missed games in each of the past three seasons. Add a healthy Dez Bryant and first-round pick Ezekiel Elliott, plus the offensive line, and Romo should be poised for another huge season. If Tony Romo can stay healthy, he has the playmakers on offense to make a major impact in 2016. Tim Heitman/USA TODAY Sports Phil Sheridan, Philadelphia Eagles reporter: If it's Sam Bradford or Carson Wentz, I will be really surprised, and we'll be having a very different conversation about this division next year. My vote goes to Giants quarterback Eli Manning. I think the change from Tom Coughlin to Ben McAdoo will rejuvenate Manning. If Odell Beckham Jr. has a great year, that will mean Manning also had a very good year, and quarterbacks tend to get a lot of MVP consideration. The other QBs in the division, Tony Romo and Kirk Cousins, have pretty good chances to earn MVP honors, but it just feels as if Manning is due to have one of his better seasons in 2016. John Keim, Washington Redskins reporter: Tony Romo. Well, he might have been the MVP by his absence last season. The Cowboys won only four games with him missing almost all of 2015 due to injury, so if they improve and play the way many fear, then credit will go to Romo's return. With Romo, the Cowboys have a quarterback who can make plays on his own, and now he'll have a strong run game to help him, just as he did when Dallas won the division in 2014. Last season, Dallas had other issues besides just quarterback, and I still worry about Romo's health. But if he's healthy in 2016, he clearly makes a huge difference and could be the reason Dallas goes from first to worst and back to first. Rob Demovsky, Green Bay Packers reporter: Aaron Rodgers. By his standards, the Packers quarterback had a down year in 2015. Yet he still threw 31 touchdowns and just eight interceptions. A full complement of weapons -- the return of Jordy Nelson from his knee injury last August, the addition of free-agent tight end Jared Cook, a healthy offensive line and a more motivated Eddie Lacy -- should allow Rodgers to return to his NFL MVP-contending level of play. Given his offseason commitment to nutrition and conditioning -- no more cheese! -- he appears more motivated than ever. Jeff Dickerson, Chicago Bears reporter: Aaron Rodgers. I know that answer is boring, but Rodgers is still the best overall player in the NFC North, slightly ahead of Adrian Peterson. Quarterbacks touch the ball every single play, so it's easier for them to win MVP awards, making this an easy pick. I also suspect Rodgers, who turns 33 in December, hears the clock ticking. That's hardly ancient by quarterback standards, but it has been five full seasons since the Packers won the Super Bowl. It's past time for Rodgers to win another one. He is an amazing talent, but the notion of such an incredible talent winning only one Super Bowl is disappointing. I'll argue that Brett Favre should have won more than one title in Green Bay. I expect Rodgers to be as motivated as ever in 2016. You can't play football forever. He needs another ring to further validate an otherwise extraordinary career. Ben Goessling, Minnesota Vikings reporter: Assuming he's got more to work with around him than he did last season, it'll be Aaron Rodgers. With Jordy Nelson back and Eddie Lacy motivated to shake off a disappointing 2015 season, Rodgers should have more weapons around him, and the addition of Jared Cook could also help him out. The Packers' offensive line needs to protect him better than it did last season, but part of the problem there last year seemed to be Rodgers holding the ball rather than trusting a group of receivers he hadn't played with before. He'll be motivated to put things back together after what was probably his worst year as a starter, and if things hold up around him better than they did in 2015, he'll be the leading man in the division. Michael Rothstein, Detroit Lions reporter: This is such a tough question, but with a healthy Jordy Nelson back and a slimmed-down Eddie Lacy, everything seems to be setting up for Aaron Rodgers to have another strong season where he'll contend for the NFL MVP award. That should be good enough to win the division's MVP award as well. While I don't necessarily think the Packers will win the division -- I mentioned in an earlier roundtable that I like the Vikings for that spot -- Rodgers clearly will show again how valuable he is as the Packers once again reach the playoffs and position themselves well for a big run in January. Jenna Laine, Tampa Bay Buccaneers reporter: I was so impressed with Cam Newton's ability last season to overcome the loss of his top red-zone target, Kelvin Benjamin, without much of a hiccup. He made weapons out of players I wasn't expecting a lot from in undrafted free agent Corey Brown and Ted Ginn, who doubled his previous high of five touchdown catches. With Greg Olsen and Benjamin back on the field together, plus those new weapons and a more experienced Devin Funchess, I think Cam will be the division MVP again in 2016. Vaughn McClure, Atlanta Falcons reporter: Cam Newton. I firmly believe Newton will come back with a vengeance following his Super Bowl disappointment. His every move is scrutinized probably as much as any player in the league, which should be added motivation. He struggled with the different looks the Broncos threw at him in the Super Bowl, but he is a year wiser. Not to mention, he has a great target back in Kelvin Benjamin, who missed last season with an ACL tear. In NFC South play last season, Newton completed 112 of 171 passes for 1,470 yards, 14 touchdowns, one interception and a passer rating of 117.3, the best for any quarterback in division play. Newton should enjoy similar or better success against the NFC South this season. Cam Newton cruised to the league MVP last year behind a ruthlessly efficient second half of the season. Troy Wayrynen/USA TODAY Sports David Newton, Carolina Panthers reporter: I could dab around here and talk about how Julio Jones or Drew Brees could win it. But that would be silly. Cam Newton legitimately was the league MVP last season, and he could post even better numbers with the return of Kelvin Benjamin. Newton's development as a decision-maker and leader over the past three seasons has been amazing to watch. Now this might sound silly, too, but if you didn't limit this question to players I'd say the MVP is Carolina offensive coordinator Mike Shula. His ability to adapt Newton's skills as a runner and passer with a group of no-name wide receivers last season should have had him on a short list of candidates to become a head coach. His willingness to allow Newton to be himself is a great example of a coach playing to his players' strengths. With the return of Benjamin, Shula will have even more toys with which to dabble. Mike Triplett, New Orleans Saints reporter: Panthers linebacker Luke Kuechly. I figured it would be too boring to simply choose Cam Newton, the reigning NFL MVP. So I decided to go way out on a limb instead and pick the 2013 NFL Defensive Player of the Year. Although I just made the case in last week's roundtable that Newton is the more valuable Panther of the two, I wouldn't be surprised to see Newton fall back to earth a little bit this season with defenses more determined than ever to slow him down. So Carolina might need Kuechly and the defense to lead the way to a fourth-straight NFC South title. Drew Brees, Julio Jones or Jameis Winston could certainly earn this honor if one of them leads his team to the playoffs, but I see all three of them falling just short with 8-9 wins apiece. Josh Weinfuss, Arizona Cardinals reporter: This will be a repeat award for Cardinals quarterback Carson Palmer. He was arguably (but who can really argue against this?) the division MVP last season, setting career highs in passing yards, touchdowns and passer rating while leading the Cardinals to a 13-3 record and a berth in the NFC Championship Game. He was even in the conversation for the NFL MVP deep into the season, along with New England's Tom Brady and Carolina's Cam Newton. Palmer will just do it again. The Cardinals' roster is largely intact, with all the players who scored an offensive touchdown and caught a pass from Palmer last season. Having that kind of experience return in such a complex offense will help Palmer build on last season quicker than he would have had there been new players added to the mix. And that will allow Palmer, should he stay healthy, to have a better season than in 2015. Nick Wagoner, Los Angeles Rams reporter: In general, choosing an MVP comes down to picking the best player on the best team, unless someone has a record-breaking year. Todd Gurley would be a dark horse if the Rams can find a way to contend for the division title, and if they do, it's almost certain Gurley would be the biggest reason for that. The decision here comes down to Carson Palmer and Seattle quarterback Russell Wilson. Both drive the two best teams and offenses in the NFC West. Palmer would have won this imaginary award in 2015, but 2016 is the year that Wilson claims the crown. Going into last season, Seattle's offense still looked to be centered on Marshawn Lynch. But with Lynch battling injuries, Wilson became the focal point and succeeded. Nobody in the league played better over the season's final half than Wilson, who had a league-best and outrageous 91.3 QBR from Week 11 on. Now, with full knowledge that the offense is his; with Doug Baldwin, Jermaine Kearse and Tyler Lockett established as strong receiving threats; and with tight end Jimmy Graham back from injury, Wilson should ascend to the top of the NFC West and potentially be a legitimate contender for the NFL's MVP honor. Michael Wagaman, San Francisco 49ers reporter: Todd Gurley, provided he can stay healthy. Gurley is not only the best running back in the division, but it's conceivable he could make a run at the NFL rushing title in 2016. Seahawks QB Russell Wilson also will be in the discussion at the end of the season, and it's possible Jared Goff might get some consideration, too, depending on how quickly he adapts to the pro level. Gurley, however, just might be the best player period in the NFC West. And he's entering just his second season in the NFL. Sheil Kapadia, Seattle Seahawks reporter: Russell Wilson. He's coming off a season in which he threw for 34 touchdowns against eight interceptions and led the NFL in passer rating. At 27, Wilson is in the prime of his career, returns his top four pass-catchers from 2015 and has never missed a game or even a practice. There's the obvious question mark of the offensive line, but Wilson has shown in the past that he can produce even when the protection isn't perfect. He can operate from the pocket, get the ball downfield, escape potential sacks and make throws on the move. Wilson right now is the full package, and all signs this offseason suggest he's in store for another monster season. | Mid | [
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Q: HTML form submit when press enter key In my form, if I click the submit button it should submit. Even if I am in the text field and press the enter key the form should submit. Can anyone tell me why this is happening? <html> < body> <form name="input" action="html_form_action.asp" method="get"> First name: <input type="text" name="FirstName" /><br /> Last name: <input type="text" name="LastName" /><br /> <input type="submit" value="Submit" /> </form> </body> </html> A: This is normal behaviour. Browsers let forms be submitted by users pressing enter in a text field; it makes many forms more convenient. | Mid | [
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Q: How does Chef recipe get/retrieve parameters from databag? I have been trying to learn Chef and trying to test a small Chef cookbook that would do dcpromo of a Windows 2008 R2 server. I don't remember exactly where I got the two files originally, but I was able to get it working. The original dcpromo_unattend.txt.erb file was: [DCINSTALL] SafeModeAdminPassword=<%= @admin_password %> RebootOnCompletion=Yes ReplicaOrNewDomain=domain NewDomain=forest NewDomainDNSName=<%= @domain_name %> ForestLevel=3 DomainLevel=3 InstallDNS=yes and the default.rb had this part in it: template dcpromo_file do source "dcpromo_unattend.txt.erb" variables({ :admin_password => '', :domain_name => '' }) end I wasn't quite sure what how to pass in the admin_password and domain_name parameters, so I hard-coded both in the dcpromo_unattend.txt.erb file, and, after some tweaking, was able to make the cookbook work. Now, I'd like to be able to put the admin_password and domain_name values into a databag, so I tried adding: begin dcpromote = Chef::DataBagItem.load(:dcpromote, :main) rescue Chef::Log.fatal("Could not find the 'main' item in the 'dcpromote' data bag - Raising fatal error!!") raise end and changed the original template section to: template dcpromo_file do source "dcpromo_unattend.txt.erb" variables({ :admin_password => dcpromote['admin_password'], :domain_name => dcpromote['domain_name'] }) end and I created a databag named "dcpromote", but that doesn't seem to be working. Can someone explain how the original template code is supposed to work, i.e., where is it suppose to be retrieving the admin_password and domain_name parameters from? Also, can anyone tell me what is wrong with the changes that I made to get this to read the admin_password and domain_name from the "dcpromote" databag? Thanks, Jim EDIT: I guess that I've been staring at this for a few more hours, and, actually, I don't even understand how what I did is working. What I mean is the erb file I have has the password and domain hard-coded: [DCINSTALL] SafeModeAdminPassword=xxxxxxxxx RebootOnCompletion=Yes ReplicaOrNewDomain=domain NewDomain=forest NewDomainDNSName=WHATEVER.com ForestLevel=4 DomainLevel=4 InstallDNS=yes Notice that there is NO reference to admin_password or domain_name in that file. So, how does this part of the recipe/default.rb even working? template dcpromo_file do source "dcpromo_unattend.txt.erb" variables({ :admin_password => '', :domain_name => '' }) end Can someone explain exactly what this part of the recipe code is doing: variables({ :admin_password => '', :domain_name => '' }) ?? Thanks, Jim EDIT 2: Adding entire default.rb after changes suggested by @Draco Ater: # # Cookbook Name:: dcpromote # Recipe:: default # # Copyright (c) 2015 The Authors, All Rights Reserved. # class ServerHelper extend ::Windows::Helper class << self def dism @@dism ||= locate_sysnative_cmd("dism.exe") end def powershell @@powershell ||= locate_sysnative_cmd('WindowsPowershell\v1.0\powershell.exe') end def feature_installed?(feature) cmd = Mixlib::ShellOut.new("#{dism} /online /Get-Features", {:returns => [0,42,127]}).run_command !!(cmd.stderr.empty? && (cmd.stdout =~ /^Feature Name : #{feature}.?$\n^State : Enabled.?$/i)) end end end windows_reboot 60 do action :nothing end # # Following snippet from: https://supermarket.chef.io/cookbooks/ad # This snippet checks for presence of a databag named "dcpromote" and for presence # of an item in the databag named "main". If that item is not present, then # this snippet logs a fatal error. begin dcpromote = Chef::DataBagItem.load('dcpromote', 'main') rescue Chef::Log.fatal("Could not find the 'main' item in the 'dcpromote' data bag - Raising fatal error!!") raise end directory Chef::Config[:file_cache_path] dcpromo_file = File.join(Chef::Config[:file_cache_path], 'dcpromo_unattend.txt') #cert_script = File.join(Chef::Config[:file_cache_path], 'setupca.vbs') # Available from e.g. http://blogs.technet.com/b/pki/archive/2009/09/18/automated-ca-installs-using-vb-script-on-windows-server-2008-and-2008r2.aspx template dcpromo_file do source "dcpromo_unattend.txt.erb" variables( :admin_password => dcpromote['admin_password'], :domain_name => dcpromote['domain_name'] ) end powershell_script "run_dcpromo" do code "dcpromo /unattend:#{dcpromo_file}" #notifies :request, 'windows_reboot[60]' not_if { ServerHelper.feature_installed? 'DirectoryServices-DomainController' } end windows_feature 'DirectoryServices-DomainController' do action :install #notifies :request, 'windows_reboot[60]' end This cookbook/recipe is STILL not working with the databag. To clarify: When I run it with the earlier code with the hard-coded setting of admin_password and domain_name, it works. However, if I try the code that uses the databag it doesn't work. When I run it with the databag: 1) [This is strange]: If I look at the "unattended" txt file during the run, it looks like it is populated, but then at the end, the password item is set to nothing, i.e., the unattended text file changes during the run. 2) In the end when the Powershell is run, it looks like it gets an error 32. Here's the console output: PS C:\Users\Administrator> chef-client -o dcpromote_usedatabag Starting Chef Client, version 12.3.0 [2015-06-14T07:24:47-07:00] INFO: *** Chef 12.3.0 *** [2015-06-14T07:24:47-07:00] INFO: Chef-client pid: 260 [2015-06-14T07:25:04-07:00] WARN: Run List override has been provided. [2015-06-14T07:25:04-07:00] WARN: Original Run List: [] [2015-06-14T07:25:04-07:00] WARN: Overridden Run List: [recipe[dcpromote_usedatabag]] [2015-06-14T07:25:04-07:00] INFO: Run List is [recipe[dcpromote_usedatabag]] [2015-06-14T07:25:04-07:00] INFO: Run List expands to [dcpromote_usedatabag] [2015-06-14T07:25:04-07:00] INFO: Starting Chef Run for node8 [2015-06-14T07:25:04-07:00] INFO: Running start handlers [2015-06-14T07:25:04-07:00] INFO: Start handlers complete. [2015-06-14T07:25:04-07:00] INFO: HTTP Request Returned 404 Not Found: resolving cookbooks for run list: ["dcpromote_usedatabag"] [2015-06-14T07:25:04-07:00] INFO: Loading cookbooks [[email protected], [email protected], che [2015-06-14T07:25:04-07:00] INFO: Skipping removal of obsoleted cookbooks from the cache Synchronizing Cookbooks: [2015-06-14T07:25:04-07:00] INFO: Storing updated cookbooks/dcpromote_usedatabag/recipes/default.rb [2015-06-14T07:25:04-07:00] INFO: Storing updated cookbooks/dcpromote_usedatabag/templates/default/d erb in the cache. [2015-06-14T07:25:04-07:00] INFO: Storing updated cookbooks/dcpromote_usedatabag/Berksfile in the ca [2015-06-14T07:25:04-07:00] INFO: Storing updated cookbooks/dcpromote_usedatabag/.kitchen.yml in the - windows - chef_handler [2015-06-14T07:25:04-07:00] INFO: Storing updated cookbooks/dcpromote_usedatabag/chefignore in the c [2015-06-14T07:25:04-07:00] INFO: Storing updated cookbooks/dcpromote_usedatabag/metadata.rb in the [2015-06-14T07:25:04-07:00] INFO: Storing updated cookbooks/dcpromote_usedatabag/README.md in the ca - dcpromote_usedatabag Compiling Cookbooks... [2015-06-14T07:25:04-07:00] INFO: +++++++++++++++++++++++++++ HI ++++++++++++++++++++++++++++ [2015-06-14T07:25:04-07:00] INFO: +++++++++++++++++++++++++++ HI ++++++++++++++++++++++++++++ [2015-06-14T07:25:04-07:00] INFO: +++++++++++++++++++++++++++ In template +++++++++++++++++++++++++ [2015-06-14T07:25:04-07:00] INFO: +++++++++++++++++++++++++++ In template +++++++++++++++++++++++++ [2015-06-14T07:25:04-07:00] INFO: ++++ xoutput = [123] Converging 5 resources Recipe: dcpromote_usedatabag::default * windows_reboot[60] action nothing[2015-06-14T07:25:04-07:00] INFO: Processing windows_reboot[60] romote_usedatabag::default line 28) (skipped due to action :nothing) * directory[c:/chef/cache] action create[2015-06-14T07:25:04-07:00] INFO: Processing directory[c:/ reate (dcpromote_usedatabag::default line 47) (up to date) * template[c:/chef/cache/dcpromo_unattend.txt] action create[2015-06-14T07:25:04-07:00] INFO: Proc hef/cache/dcpromo_unattend.txt] action create (dcpromote_usedatabag::default line 52) [2015-06-14T07:25:04-07:00] INFO: template[c:/chef/cache/dcpromo_unattend.txt] created file c:/chef/ nd.txt - create new file c:/chef/cache/dcpromo_unattend.txt[2015-06-14T07:25:04-07:00] INFO: template[c _unattend.txt] updated file contents c:/chef/cache/dcpromo_unattend.txt - update content in file c:/chef/cache/dcpromo_unattend.txt from none to 798057 --- c:/chef/cache/dcpromo_unattend.txt 2015-06-14 07:25:04.000000000 -0700 +++ C:/Users/ADMINI~1/AppData/Local/Temp/chef-rendered-template20150614-260-1cvaiw 2015-06-14 0 700 @@ -1 +1,10 @@ +[DCINSTALL] +SafeModeAdminPassword=P@ssw0rd$123 +RebootOnCompletion=Yes +ReplicaOrNewDomain=domain +NewDomain=forest +NewDomainDNSName=whateverisforever123.com +ForestLevel=4 +DomainLevel=4 +InstallDNS=yes * powershell_script[run_dcpromo] action run[2015-06-14T07:25:04-07:00] INFO: Processing powershell action run (dcpromote_usedatabag::default line 68) ================================================================================ Error executing action `run` on resource 'powershell_script[run_dcpromo]' ================================================================================ Mixlib::ShellOut::ShellCommandFailed ------------------------------------ Expected process to exit with [0], but received '32' ---- Begin output of "powershell.exe" -NoLogo -NonInteractive -NoProfile -ExecutionPolicy Unrest None -File "C:/Users/ADMINI~1/AppData/Local/Temp/chef-script20150614-260-dfo5yi.ps1" ---- STDOUT: STDERR: ---- End output of "powershell.exe" -NoLogo -NonInteractive -NoProfile -ExecutionPolicy Unrestri ne -File "C:/Users/ADMINI~1/AppData/Local/Temp/chef-script20150614-260-dfo5yi.ps1" ---- Ran "powershell.exe" -NoLogo -NonInteractive -NoProfile -ExecutionPolicy Unrestricted -InputForm ers/ADMINI~1/AppData/Local/Temp/chef-script20150614-260-dfo5yi.ps1" returned 32 Resource Declaration: --------------------- # In c:/chef/cache/cookbooks/dcpromote_usedatabag/recipes/default.rb 68: powershell_script "run_dcpromo" do 69: code "dcpromo /unattend:#{dcpromo_file}" 70: #notifies :request, 'windows_reboot[60]' 71: not_if { ServerHelper.feature_installed? 'DirectoryServices-DomainController' } 72: end 73: Compiled Resource: ------------------ # Declared in c:/chef/cache/cookbooks/dcpromote_usedatabag/recipes/default.rb:68:in `from_file' powershell_script("run_dcpromo") do action "run" retries 0 retry_delay 2 default_guard_interpreter :powershell_script command "run_dcpromo" backup 5 returns 0 code "dcpromo /unattend:c:/chef/cache/dcpromo_unattend.txt" interpreter "powershell.exe" declared_type :powershell_script cookbook_name "dcpromote_usedatabag" recipe_name "default" not_if { #code block } end [2015-06-14T07:26:22-07:00] INFO: Running queued delayed notifications before re-raising exception Running handlers: [2015-06-14T07:26:22-07:00] ERROR: Running exception handlers Running handlers complete [2015-06-14T07:26:22-07:00] ERROR: Exception handlers complete [2015-06-14T07:26:22-07:00] FATAL: Stacktrace dumped to c:/chef/cache/chef-stacktrace.out Chef Client failed. 1 resources updated in 98.15625 seconds [2015-06-14T07:26:22-07:00] FATAL: Mixlib::ShellOut::ShellCommandFailed: powershell_script[run_dcpro tabag::default line 68) had an error: Mixlib::ShellOut::ShellCommandFailed: Expected process to exit ved '32' ---- Begin output of "powershell.exe" -NoLogo -NonInteractive -NoProfile -ExecutionPolicy Unrestrict -File "C:/Users/ADMINI~1/AppData/Local/Temp/chef-script20150614-260-dfo5yi.ps1" ---- STDOUT: STDERR: ---- End output of "powershell.exe" -NoLogo -NonInteractive -NoProfile -ExecutionPolicy Unrestricted File "C:/Users/ADMINI~1/AppData/Local/Temp/chef-script20150614-260-dfo5yi.ps1" ---- Ran "powershell.exe" -NoLogo -NonInteractive -NoProfile -ExecutionPolicy Unrestricted -InputFormat N ADMINI~1/AppData/Local/Temp/chef-script20150614-260-dfo5yi.ps1" returned 32 PS C:\Users\Administrator> And here's the unattended txt file at the end: [DCINSTALL] SafeModeAdminPassword= RebootOnCompletion=Yes ReplicaOrNewDomain=domain NewDomain=forest NewDomainDNSName=whateverisforever123.com ForestLevel=4 DomainLevel=4 InstallDNS=yes Why is the unattended txt file changing twice during the run (and why is the password value disappearing)? Thanks, Jim EDIT 3: For the record, I was able to get this working by adding an additional parameter to the template file for setting the netbios name: [DCINSTALL] RebootOnCompletion=Yes ReplicaOrNewDomain=domain NewDomain=forest SafeModeAdminPassword=<%= @admin_password %> NewDomainDNSName=<%= @domain_name %> ForestLevel=4 DomainLevel=4 InstallDNS=yes DomainNetbiosName=<%= @domain_netbios_name %> and then modified the default.rb to set that parameter: template dcpromo_file do source "dcpromo_unattend.txt.erb" variables( :admin_password => dcpromote['admin_password'], :domain_netbios_name => dcpromote['domain_netbios_name'], :domain_name => dcpromote['domain_name'] ) Jim A: Let's start with the template file itself. [DCINSTALL] SafeModeAdminPassword=<%= @admin_password %> RebootOnCompletion=Yes ReplicaOrNewDomain=domain NewDomain=forest NewDomainDNSName=<%= @domain_name %> ForestLevel=3 DomainLevel=3 InstallDNS=yes The code inside <% %> is ruby code. Things that start with @ inside the <% %> are variables. The = is a shorthand for printing the value. So the template uses 2 variables to set the values, by just printing them out. Where do the variables come from? Exactly from this code in recipe ({ and } are not necessary here): variables( :admin_password => '', :domain_name => '' ) Currently they are initialized by empty strings, but if you put something else there in the recipe, it will be changed in template too. It will not break, if you pass some variables that are not used in the template, it will just be the redundant code. For now you can put your password and domain name there like that and get this working (producing the right configuration file on target machine) variables( :admin_password => 'my_pass', :domain_name => 'localhost' ) Now we want to move the values to the data bag. Create a 'dcpromote' databag with 'main' data bag item. knife data bag create dcpromote main and edit the json file. In the end you should have something like that: { "id": "main", # <= data bag item name "admin_password": "my_pass", "domain_name": "localhost" } Then in the recipe you read the data bag into the variable (Try using strings, not symbols, as data bag and item name): begin dcpromote = Chef::DataBagItem.load( 'dcpromote', 'main' ) rescue Chef::Log.fatal("Could not find the 'main' item in the 'dcpromote' data bag - Raising fatal error!!") raise end and use it when creating configuration file: variables( :admin_password => dcpromote['admin_password'], :domain_name => dcpromote['domain_name'] ) | Low | [
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Histones biosynthesis and turnover in epithelial lens cells cultured in vitro. "Histone synthesis was compared in epithelial lens cells during exponential growth and in the stationary phase brought by contact inhibition. Double labelling experiments with 3H-lysine and 14C-lysine show a net turnover of histone H1 independent of DNA replication. The nucleosome core histones seem to turn over also, but much more slowly than H1". | High | [
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Dividends brighten the sharemarket picture By Juia Lee, Bell DirectOctober 2017min read Payouts at a record high despite Telstra cut. Dividends have always played a key part in the returns from the Australian sharemarket. Although the Australian market is struggling to regain the record-high levels seen in 2008, returns look better if dividends are included. Since the peak of the market on 1 November 2007, the Australian sharemarket is down 15 per cent, while the accumulation index, which includes dividend returns, is up 32 per cent. This highlights the importance of dividends in returns to shareholders in Australia. Source: IRESS, Bell Direct Research, at 13 September 2017 Reporting season is an important time for investors and professional fund managers. It’s a time to reset portfolios based on the newly released information. There’s a known effect around the months following reporting season whereby companies that beat expectations will continue to outperform over the next six months. Hence, it’s an opportune time for investors to identify where the strong trends are and which companies offer earnings growth. The good news is that for income investors, dividends being paid out by Australian companies are at a record high. In the month of September, it is expected that those companies listed on the market will pay out more than $16 billion in dividends. That’s a growth of around 15 per cent from the previous year. (Editor’s note: Do not read the following ideas as stock recommendations. Do further research of your own or talk to a financial adviser before acting on themes in this article). Disappointment from traditional defensives Defensive shares are usually ones that are characterised by consistent earnings and a high dividend. These shares usually are in the utilities, telecom, staples and property sectors. These sectors often outperform when markets are falling, as investors seek shelter in dividends. Dividends can act as a buffer to falling prices because they are paid out regardless of share-price direction. This reporting season has seen disappointments from the traditional defensive stocks such as Telstra (TLS), QBE Insurance (QBE) and Transurban (TCL). QBE Insurance in recent years has seen a series of profits downgrades. Earnings unpredictability has meant the share price has been under pressure. This stock should be benefiting from the global macro environment of increasing interest rates. Unfortunately, another year of sub-optimal returns has investors cautious despite the macro headwinds coming the company’s way. Transurban came out with a good result but the market was disappointed by the outlook. The guidance provided implies a lower growth year for the company, which trades at a premium yield compared to interest rates. The key risks of investing in a company like this are rising bond yields, project delays and lower-than-expected traffic numbers. Telstra operationally came out with a result that met guidance. The stock was hit by the capital review and the prospect of lower future dividend payments. Investors need to evaluate whether most of the bad news is now out of the way and hence the share price has stabilised. Stagnant earnings can mean dividend cuts If the earnings outlook is not strong, dividends are more likely to be cut or cancelled. The biggest lesson came from Telstra this reporting season. Historically, Telstra has paid out 90-100 per cent of underlying earnings as dividends. This will now be 70-90 per cent of underlying earnings. While Telstra still aims to increase dividends over time, this seems aspirational over the medium term and looks a longer-term target. Hence, Telstra lost more than 10 per cent of its value in August. The market outlook for dividends has been skewed by Telstra’s cut to its dividend payout policy. Excluding Telstra, dividends are expected to increase by 0.1 per cent. Including Telstra, dividends are expected to be down half a per cent. Increasing dividends are related to increasing profit Income investing is more than getting dividends. It’s also about getting a sustainable dividend. Generally, companies that have increasing profits are also more able and more likely to increase dividend payments over time. Companies like Sydney Airport, Westpac and SG Fleet not only have earnings growth in common but also share-price outperformance and growing dividends. Dividend growth from mining Traditionally, investors don’t expect strong dividends from mining investments. A strong recovery in commodity prices and strong cash flow have seen strong earnings and dividend growth from the miners. Dividend growth from miners was positive at 3.7 per cent, with expected dividends in 2018 revised higher. Conclusion All in all, the Australian share market can be one of the most tax-effective ways to generate income. This reporting season has once again proved that increasing profits are linked to rising dividends and conversely falling dividends are linked to falling profits. While the outlook for dividends is looking weaker for investors in 2018, that’s due to the dividend cut expected from Telstra. This reporting season has been one that has highlighted the importance of growth in earnings to support the growth in dividend payments. From an earnings perspective, the Australian share market has seen growth and this is forecast to continue into the current financial year. About the author Julia Lee is Equities Strategist at Bell Direct, a leading online broker. From ASX Getting Stared in Shares is a useful ASX tool for new investors. It explains what a share is and the three steps to investing in the sharemarket. This article appeared in the October 2017 ASX Investor Update email newsletter. To subscribe to this newsletter please register with the MyASX section or visit the About MyASX page for past editions and more details. This article appeared in the October 2017 ASX Investor Update email newsletter. To subscribe to this newsletter please register with MyASX. The views, opinions or recommendations of the author in this article are solely those of the author and do not in any way reflect the views, opinions, recommendations, of ASX Limited ABN 98 008 624 691 and its related bodies corporate ("ASX"). ASX makes no representation or warranty with respect to the accuracy, completeness or currency of the content. The content is for educational purposes only and does not constitute financial advice. Independent advice should be obtained from an Australian financial services licensee before making investment decisions. To the extent permitted by law, ASX excludes all liability for any loss or damage arising in any way including by way of negligence. | Low | [
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Languages comparsion Quality and popularity scores comparsion of the article "游击队歌" (ZH) in different Wikipedia languages Cumulative results Cumulative results of quality and popularity assessment of the article "游击队歌" (ZH) in different Wikipedia languages About WikiRank ... The project is intended for automatic relative evaluation of the articles in the various language versions of Wikipedia. At the moment the service allows to compare over 38 million Wikipedia articles in 55 languages. Quality scores of articles are based on Wikipedia dumps from March, 2019. When calculating popularity, view statistics of articles for last month (February 2019) were taken into account. You can also visit WikiRank.Live (previous version of the main tool), which can calculate quality and popularity based on current versions of Wikipedia articles in 7 languages. It's planned to add different improvements to the project (such as adding to the analysis not only new quantitative characteristics, but also qualitative). In addition, it is planned to add estimates using machine learning algorithms and artificial intelligence, as well as based on the results of user comparison of specific multilingual information (for example, the WikiBest project). Please leave your comments and suggestions More information about quality assessment of Wikipedia articles and project WikiRank can be found in scientific publications: | High | [
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Q: Are there better (easier) ways to get a specific domain's SID? I've been assigned to modify a WinForms application to basically check that the logged on user belongs to a specific domain. This is what I've come up with so far: byte[] domainSid; var directoryContext = new DirectoryContext(DirectoryContextType.Domain, "domain.se"); using (var domain = Domain.GetDomain(directoryContext)) using (var directoryEntry = domain.GetDirectoryEntry()) domainSid = (byte[])directoryEntry.Properties["objectSid"].Value; var sid = new SecurityIdentifier(domainSid, 0); bool validUser = UserPrincipal.Current.Sid.IsEqualDomainSid(sid); Is there a better/easier way to do this? To me it seems like the domainSid would be accessible in some way using the PrincipalContext or some other class in System.Security.Principal. I've considered using a hardcoded SID-string, but I don't know how "correct" that would be. A: What you're doing looks like the best option to me. Hardcoding strings is definetely not a good idea. A: Each domain has a build in account domainName\administrator, so you can create an account with this name, translate it to the SecurityIdentifier and read the AccountDomainSid property. An example of this way is: public static class SecurityEx { public static SecurityIdentifier DomainSId { get { var administratorAcount = new NTAccount(GetDomainName(), "administrator"); var administratorSId = (SecurityIdentifier) administratorAcount.Translate(typeof (SecurityIdentifier)); return administratorSId.AccountDomainSid; } } internal static string GetDomainName() { //could be other way to get the domain name through Environment.UserDomainName etc... return IPGlobalProperties.GetIPGlobalProperties().DomainName; } } Also you can find other solutions to achieve the same result via WMI or Lsa. This one seems the most elegant way for me. | High | [
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/* * Copyright (c) 2010, 2018 Oracle and/or its affiliates. All rights reserved. * * This program and the accompanying materials are made available under the * terms of the Eclipse Public License v. 2.0, which is available at * http://www.eclipse.org/legal/epl-2.0. * * This Source Code may also be made available under the following Secondary * Licenses when the conditions for such availability set forth in the * Eclipse Public License v. 2.0 are satisfied: GNU General Public License, * version 2 with the GNU Classpath Exception, which is available at * https://www.gnu.org/software/classpath/license.html. * * SPDX-License-Identifier: EPL-2.0 OR GPL-2.0 WITH Classpath-exception-2.0 */ package org.glassfish.nucleus.admin.rest; import java.util.HashMap; import java.util.List; import java.util.Map; import jakarta.ws.rs.core.Response; import org.glassfish.admin.rest.client.utils.MarshallingUtils; import static org.testng.AssertJUnit.*; import org.testng.annotations.Test; public class AuthRealmTest extends RestTestBase { public static final String URL_LIST_GROUP_NAMES = "/domain/configs/config/server-config/security-service/auth-realm/admin-realm/list-group-names"; public static final String URL_SUPPORTS_USER_MANAGEMENT = "/domain/configs/config/server-config/security-service/auth-realm/admin-realm/supports-user-management"; public static final String URL_LIST_ADMIN_REALM_USERS = "/domain/configs/config/server-config/security-service/auth-realm/admin-realm/list-users"; public static final String URL_LIST_FILE_USERS = "/domain/configs/config/server-config/security-service/auth-realm/file/list-users"; public static final String URL_CREATE_USER = "/domain/configs/config/server-config/security-service/auth-realm/file/create-user"; public static final String URL_DELETE_USER = "/domain/configs/config/server-config/security-service/auth-realm/file/delete-user"; public static final String URL_AUTH_REALM_CLASS_NAMES = "/domain/list-predefined-authrealm-classnames"; // Disable this test for now... // @Test public void testListGroupNames() { Response response = get(URL_LIST_GROUP_NAMES, new HashMap<String, String>() {{ put("userName", "admin"); put("realmName", "admin-realm"); }}); checkStatusForSuccess(response); final String entity = response.readEntity(String.class); Map responseMap = MarshallingUtils.buildMapFromDocument(entity); Map extraProperties = (Map)responseMap.get("extraProperties"); List<String> groups = (List<String>)extraProperties.get("groups"); assertTrue(groups.size() > 0); } @Test public void testSupportsUserManagement() { List<String> groups = getCommandResults(get(URL_SUPPORTS_USER_MANAGEMENT)); assertEquals("true", groups.get(0)); } // @Test public void testUserManagement() { final String userName = "user" + generateRandomString(); Map<String, String> newUser = new HashMap<String, String>() {{ put ("id", userName); put ("AS_ADMIN_USERPASSWORD", "password"); }}; Response response = post(URL_CREATE_USER, newUser); assertTrue(isSuccess(response)); List<String> values = getCommandResults(get(URL_LIST_FILE_USERS)); assertTrue(values.contains(userName)); response = delete(URL_DELETE_USER, newUser); assertTrue(isSuccess(response)); values = getCommandResults(get(URL_LIST_FILE_USERS)); assertFalse(values.contains(userName)); } @Test public void testListAuthRealmClassNames() { List<String> classNameList = getCommandResults(get(URL_AUTH_REALM_CLASS_NAMES)); assertTrue(!classNameList.isEmpty()); } } | Mid | [
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Access to Court Records Court offices regularly receive a wide range of requests from the public, media, lawyers and others seeking access to court records. To help manage these requests, the Courts have developed guidelines that summarize how court officials will respond to the most commonly encountered access requests. There are a wide range of requests for court records received by the courts every day. They differ in their nature and the records involved. It would be impossible to anticipate all of the types of requests. The guidelines summarize how court officials can be expected to respond to the most commonly encountered access requests. The access guidelines are also intended to help communicate to the media and the public the approach that will be taken on access matters in specific situations. They serve as an informative and educative tool for those wishing to better understand how the court system operates and how it implements the open access principle. While they provide administrative direction in situations where there is no court order in place, the guidelines do not have the force of law and are subject to the decisions of individual judges and courts. | High | [
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1. Field of the Invention The present invention relates to drawoff tubes for open-end spinning machines. 2. The Problem Conventionally in open-end spinning machines the thread being spun is clamped against rotation about its axis by the nip of drawoff rollers. The thread portion between the spinning rotor and the drawoff rollers is twisted by the thread being bent at the infeed end of the drawoff tube so that the bent portion bears against the tube mouth and the thread is turned so that it is rolled around the circumference of the tube mouth. A portion of the thread extending between the tube mouth and the binding point of the fiber collection surface of the spinning rotor acts like a crank which effects the circumferential travel of the thread around the drawoff tube mouth. In prior apparatus, the rotor speed has been very high in order to provide enough torsional force on the thread portion in the drawoff tube to permit transmission of torsional force past the bearing point of the thread on the tube mouth to the free thread end for binding the fibers on the fiber-collection surface onto the free thread end. Such transmission is necessary in order to prevent the thread end from being pulled away from the fiber-collection surface, thereby creating a thread break. However, such high speed creates an undesirably hard or tight twist in the thread. 3. Prior Art As disclosed in DT-PS 1.560.305, the prior art teaches that the bearing force of the thread against the mouth of the drawoff tube can be intermittently relieved by the use of complicated vibrational drive mechanism. Another alternative for improving the torsional transfer to the thread end is disclosed in DT-OS 1.560.302 and U.S. Pat. No. 3,805,505, which suggest that the torsional force applied by the spinning rotor can be more effectively transmitted to the thread-binding point on the fiber-collection surface by roughening the mouth of the drawoff tube with notches or ribs. Suitable vibration mechanism is very expensive, and the roughened tube mouths abrade and roughen the surface of the thread. | Mid | [
0.556581986143187,
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@import "/imports/ui/stylesheets/mixins/_indicators"; @import "/imports/ui/stylesheets/variables/placeholders"; @import "../base/styles"; .modal { @extend %highContrastOutline; outline-style: solid; display: flex; flex-direction: column; padding: calc(var(--line-height-computed) / 2) var(--line-height-computed); box-shadow: 0px 0px 15px rgba(0, 0, 0, 0.5); background-color: var(--color-white) !important; } .content { overflow: auto; color: var(--color-text); font-weight: normal; padding: var(--line-height-computed) 0; } .headerNoBorder, .header { display: flex; flex-shrink: 0; } .header { padding: calc(var(--line-height-computed) / 2) 0; border-bottom: var(--border-size) solid var(--color-gray-lighter); } .title { @extend %text-elipsis; flex: 1; margin: 0; font-weight: 400; font-size: var(--font-size-large); text-align: center; align-self: flex-end; } .dismiss { flex: 0; > span:first-child { border-color: transparent; background-color: transparent; > i { color: var(--color-text); } } } .overlay { @extend .overlay; background-color: rgba(6, 23, 42, 0.75); } | Mid | [
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President Donald Trump eating with members of the military in a dining facility during a surprise Thanksgiving Day visit, Thursday, Nov. 28, 2019, at Bagram Air Field, Afghanistan. Photo : Alex Brandon ( Associated Press ) The Meglomaniac-In-Chief ’s continuous war on the poor has hit a snag. In his quest to Make American Hate Again, President Donald Trump and his administration were planning to make life even worse for food-insecure families when the sought to proceed with measures to remove nearly three-quarters of a million people from Supplemental Nutrition Assistance Program (SNAP) benefits program. But a judge – appointed by Forever President Barack Hussein Obama – pumped the brakes. One of the good things to come out of the Coronavirus pandemic was Chief U.S. District Court Judge Beryl A. Howell ruling that the planned strict work requirements were unlawful and blocked the administration from proceeding with them . 100% That @#$%&: U.S. District Court Judge Beryl Howell blocked the The Trump Administration’s effort to make it harder for poor Americans to get food stamps. Photo : Alex Wong ( Getty Images ) “Especially now, as a global pandemic poses widespread health risks, guaranteeing that government officials at both the federal and state levels have flexibility to address the nutritional needs of residents and ensure their well-being through programs like SNAP, is essential,” Howell wrote in her 84-page ruling. The decision resulted from a lawsuit brought by 19 states, including Washington D.C. and The Big Apple on Friday, NPR reported. In December, the U.S. Department of Agriculture announced it was adopting the rule change requiring able-bodied adults without children to work at least 20 hours a week in order to qualify for SNAP benefits, also known as food stamps, past three months. To go one step further with their skullduggery, it would’ve also limited individual states’ usual ability to waive those requirements depending on economic conditions. Her honor’s preliminary injunction will preserve that flexibility. Howell is the top judge on the Washington, D.C. federal district court — and she seems not to mind setting the record straight. Just last month, the 63-year-old Fort Benning, Georgia native said that the court’s sentencing of Trump consigliere Roger Stone would not be swayed by “public criticism or pressure.” On Feb. 20, the GOP operative was sentenced to more than three years in prison after a jury found guilty on seven felony counts including lying to authorities, obstructing a congressional investigation and witness intimidation, Politico reported. Trump has called Stone’s treatment a miscarriage of justice, raising questions about whether he will grant clemency to his longtime political confidant. | Low | [
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AerospaceAerospaceAutomotiveAutomotiveChemicalsChemicalsElectronicsElectronicsFood and beverageFood and beverageMilitaryMilitaryOil and gasOil and gasPetrochemicalsPetrochemicalsTelecommunicationsTelecommunications | Low | [
0.5119047619047611,
32.25,
30.75
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Postnatal efficacy of antioxidants in the detoxification pathway of suckling neonates and lactating mice. This study evaluates the comparative efficacy of antioxidant vitamins (ascorbic acid and alpha-tocopherol) and non-vitamin antioxidants (glutathione, cysteine and L-2-oxothiazolidine-4-carboxylate (OTZ)) in modulating the detoxification pathway of lactating dams and suckling murine pups. In dams, 100 mg/kg b.w./day treatment of each of the vitamin and non-vitamin antioxidants induced a significant increase in the hepatic level of acid soluble sulfhydryl (-SH) compared to the modulating efficiency of OTZ, glutathione and alpha-tocopherol in the kidney tissue. In the liver and kidney tissues of suckling pups OTZ and alpha-tocopherol were effective in modulating the -SH level. A statistically significant increase in the hepatic glutathione-S-transferase (GST) level was observed by OTZ, glutathione and alpha-tocopherol, while only OTZ was effective in the kidney tissue of dams and pups. In the murine system, the modulation of cellular GST/GSH status, specifically by OTZ, alpha-tocopherol and interacting antioxidant pool, may potentially ameliorate the pathophysiology of oxidative stress. | Mid | [
0.6505102040816321,
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Syrian Crisis Update: ZF Opens a Second Health Clinic in Lebanon ZF Opens a Second Health Clinic in Lebanon In September 2011, Zakat Foundation of America (ZF) opened a second clinic in Lebanon to serve Syrian refugees. Shortly after Syria’s political turmoil began in March, we launched our emergency relief efforts to help Syrian refugees by establishing a health clinic in Wadi Khaled in northern Lebanon. Since health care is an ongoing and growing need for more than 5,000 Syrians refugees, as well as for the local Lebanese in the region, even this second clinic cannot adequately serve those in need. Many who receive care face a life-threatening condition that requires immediate medical care. Plus, everyone is not able to come to the clinic. We hope, inshallah, we can bring the clinic to them. Consequently, we plan to add a mobile clinic to our health services. We hope that our donors will rally around these efforts to support this community and our aim of donating a mobile clinic. We pray that, inshallah, health and peace will soon come to the Syrian people. | Mid | [
0.598214285714285,
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At the Institute for Marine Mammal Studies in Mississippi, dolphins are trained to pick up the garbage that falls into the pools, be it a piece of plastic or a dead gull, and take it to the trainer when they see one, and in exchange they get fish for their good deed. One dolphin, Kelly, decided she can do better. She started to actively collect trash and store it under a rock at the bottom of the pool only to quickly give it to a trainer when one came by. But that was not all. If she stored a piece of paper for example, she tore only a part of it, gave it, got a fish, went back, tore one more piece, gave it, got one more fish, and so on. One day she gave the trainer a dead gull that fell into the pool, and she got a lot of fish for it. She learned from that and the next time she was fed she saved the last fish, stored it, and used it to lure a gull, kill it, and give it to the trainers for fish. She soon started to routinely lure and kill gulls which she traded for fish with the trainers. She taught her kids to do it, and they taught their kids to do, and now most of the dolphin population at the Marine Mammal Studies in Mississippi does it. This is a true story. Let's rephrase it. The trainers are the management. They decide it's a good idea to ask the dolphins to help clean their own pool. They agree on a desirable action (bring piece of trash) which they want to measure and instituted a reward for it (a piece of fish). In effect, they put in place a KPI. They think this is going to cause the expected behavior in dolphins. It doesn't, because there's no deep shared understanding of what the trainers really want, there is only a transactional agreement of "bring me trash, I give you fish". And, as always in management, you get what you measure. You measure how many pieces of trash you are given, you will be given as many pieces of trash as possible. The dolphins on the other hand, displaying remarkable intelligence, decide to maximize their gain and self interest from this arrangement, an otherwise very rational decision, so their goal now is to collect or create as many pieces of trash as possible. Where is the original intent of having a clean pool? Lost. What do we have now? Trainers that probably don't want to reward the dolphins' "tricks" anymore, and dolphins that will resent it if that happens. Unhappy managers, unhappy employees, wasted money and dead gulls. The police chief wants cops to prevent accidents, but he thinks this needs to be measured: "bring me 10 speeding tickets everyday". Soon enough, instead of actually working to prevent accidents, cops will stake hot spots to catch speeding drivers and make their 10 tickets a day. Deliver me code with no bugs. Developers and testers will waste time arguing over what's a bug and what's a missing requirement and where does it get measured. Deliver on time and get a bonus. The proposed estimates will be huge, so "on time" si practically guaranteed. KPI's without a shared moral understanding, built on trust, don't work. When everyone knows what product they're building, when everyone is in it together, when there is trust, shared vision and a common goal, yes, some measurements can be chosen to be tracked, because measuring your work needs to be done. But when measurements are enforced on people that don't share the underlying vision and don't adhere to the underlying moral code of behavior, you get perverted behavior and unintended consequences. | Mid | [
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GasBuddy News Article Los Angeles Times -- Mexico's ruling party has taken a step toward opening its state oil company to outsiders, a move that could eventually allow U.S. oil firms to drill south of the border. In an important test of Mexican President Enrique Peña Nieto's sway over resistant factions of his party, the Institutional Revolutionary Party has changed its bylaws to clear the way for changes at Petroleos Mexicanos, or Pemex. Pemex, a symbol of nationalist pride, is the top source of tax revenue for the Mexican government. But its production of oil has been declining dramatically and the company is in dire need of outside expertise for deep-sea exploration. On Sunday, PRI, as the party is known, passed several changes that Peña Nieto needed for the reforms he promised as a hallmark of his administration. Chief and m Wonder how Obama administration feels about drilling in someone else's backyard? While in Cancun, I was very uneasy at a gas station that reeked of fumes and I was slipping while walking because of the greasy gas and oil covering the station's pavement. Mexico doesn't have the safety rules that the USA has. They could use our expertise. US companies have been drilling and providing oil field services in Mexico for years, but only as suppliers for Pemex. They've never been allowed to own any of the production. That probably still won't happen under the current Mexican constitution, but Peña Nieto will get as close to that as he can. The Mexican government has bled Pemex dry for so many years instead of allowing reinvestment in infrastructure that they've about killed the goose that lays the golden egg. Outside investment of some form is desperately needed. And before you hammer the "corrupt" Mexican government too much, remember that they are running budget surpluses every year, with only a small national debt. Of course they haven't been fighting wars halfway around the world for the last decade. | Mid | [
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Q: Troubleshooting ggplot legend columns I am having trouble changing the number of columns in my line graph. I have tried the conventional method yet there is some problem... structure(list(pot = c(1L, 2L, 4L, 21L, 22L, 23L, 24L, 6L, 7L, 8L, 25L, 26L, 27L, 28L, 9L, 10L, 11L, 12L, 29L, 30L, 31L, 32L, 13L, 14L, 15L, 16L, 33L, 34L, 35L, 36L, 17L, 18L, 20L, 37L, 38L, 39L, 40L, 42L, 43L, 44L, 61L, 62L, 63L, 64L, 45L, 46L, 47L, 48L, 65L, 66L, 67L, 68L, 49L, 50L, 51L, 52L, 69L, 70L, 71L, 72L, 53L, 54L, 55L, 56L, 73L, 74L, 75L, 76L, 57L, 58L, 59L, 60L, 77L, 78L, 79L, 80L, 81L, 82L, 83L, 84L, 101L, 102L, 103L, 104L, 85L, 86L, 87L, 88L, 105L, 106L, 107L, 89L, 90L, 91L, 92L, 109L, 110L, 111L, 112L, 93L, 94L, 95L, 96L, 113L, 114L, 115L, 116L, 97L, 98L, 99L, 100L, 117L, 118L, 119L, 120L, 121L, 122L, 123L, 124L, 141L, 142L, 143L, 144L, 125L, 126L, 127L, 128L, 145L, 146L, 147L, 129L, 130L, 131L, 132L, 149L, 150L, 151L, 152L, 133L, 134L, 135L, 136L, 153L, 154L, 155L, 156L, 137L, 138L, 140L, 157L, 158L, 159L, 160L), rep = c(1L, 2L, 4L, 1L, 2L, 3L, 4L, 2L, 3L, 4L, 1L, 2L, 3L, 4L, 1L, 2L, 3L, 4L, 1L, 2L, 3L, 4L, 1L, 2L, 3L, 4L, 1L, 2L, 3L, 4L, 1L, 2L, 4L, 1L, 2L, 3L, 4L, 2L, 3L, 4L, 1L, 2L, 3L, 4L, 1L, 2L, 3L, 4L, 1L, 2L, 3L, 4L, 1L, 2L, 3L, 4L, 1L, 2L, 3L, 4L, 1L, 2L, 3L, 4L, 1L, 2L, 3L, 4L, 1L, 2L, 3L, 4L, 1L, 2L, 3L, 4L, 1L, 2L, 3L, 4L, 1L, 2L, 3L, 4L, 1L, 2L, 3L, 4L, 1L, 2L, 3L, 1L, 2L, 3L, 4L, 1L, 2L, 3L, 4L, 1L, 2L, 3L, 4L, 1L, 2L, 3L, 4L, 1L, 2L, 3L, 4L, 1L, 2L, 3L, 4L, 1L, 2L, 3L, 4L, 1L, 2L, 3L, 4L, 1L, 2L, 3L, 4L, 1L, 2L, 3L, 1L, 2L, 3L, 4L, 1L, 2L, 3L, 4L, 1L, 2L, 3L, 4L, 1L, 2L, 3L, 4L, 1L, 2L, 4L, 1L, 2L, 3L, 4L), cultivar = structure(c(1L, 1L, 1L, 1L, 1L, 1L, 1L, 1L, 1L, 1L, 1L, 1L, 1L, 1L, 1L, 1L, 1L, 1L, 1L, 1L, 1L, 1L, 1L, 1L, 1L, 1L, 1L, 1L, 1L, 1L, 1L, 1L, 1L, 1L, 1L, 1L, 1L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 4L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 2L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L), .Label = c("Dinninup", "Riverina", "Seaton Park", "Yarloop"), class = "factor"), Waterlogging = structure(c(2L, 2L, 2L, 1L, 1L, 1L, 1L, 2L, 2L, 2L, 1L, 1L, 1L, 1L, 2L, 2L, 2L, 2L, 1L, 1L, 1L, 1L, 2L, 2L, 2L, 2L, 1L, 1L, 1L, 1L, 2L, 2L, 2L, 1L, 1L, 1L, 1L, 2L, 2L, 2L, 1L, 1L, 1L, 1L, 2L, 2L, 2L, 2L, 1L, 1L, 1L, 1L, 2L, 2L, 2L, 2L, 1L, 1L, 1L, 1L, 2L, 2L, 2L, 2L, 1L, 1L, 1L, 1L, 2L, 2L, 2L, 2L, 1L, 1L, 1L, 1L, 2L, 2L, 2L, 2L, 1L, 1L, 1L, 1L, 2L, 2L, 2L, 2L, 1L, 1L, 1L, 2L, 2L, 2L, 2L, 1L, 1L, 1L, 1L, 2L, 2L, 2L, 2L, 1L, 1L, 1L, 1L, 2L, 2L, 2L, 2L, 1L, 1L, 1L, 1L, 2L, 2L, 2L, 2L, 1L, 1L, 1L, 1L, 2L, 2L, 2L, 2L, 1L, 1L, 1L, 2L, 2L, 2L, 2L, 1L, 1L, 1L, 1L, 2L, 2L, 2L, 2L, 1L, 1L, 1L, 1L, 2L, 2L, 2L, 1L, 1L, 1L, 1L), .Label = c("Non-waterlogged", "Waterlogged"), class = "factor"), P = c(0L, 0L, 0L, 0L, 0L, 0L, 0L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 6L, 6L, 6L, 6L, 6L, 6L, 6L, 6L, 12L, 12L, 12L, 12L, 12L, 12L, 12L, 12L, 36L, 36L, 36L, 36L, 36L, 36L, 36L, 0L, 0L, 0L, 0L, 0L, 0L, 0L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 6L, 6L, 6L, 6L, 6L, 6L, 6L, 6L, 12L, 12L, 12L, 12L, 12L, 12L, 12L, 12L, 36L, 36L, 36L, 36L, 36L, 36L, 36L, 36L, 0L, 0L, 0L, 0L, 0L, 0L, 0L, 0L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 6L, 6L, 6L, 6L, 6L, 6L, 6L, 6L, 12L, 12L, 12L, 12L, 12L, 12L, 12L, 12L, 36L, 36L, 36L, 36L, 36L, 36L, 36L, 36L, 0L, 0L, 0L, 0L, 0L, 0L, 0L, 0L, 3L, 3L, 3L, 3L, 3L, 3L, 3L, 6L, 6L, 6L, 6L, 6L, 6L, 6L, 6L, 12L, 12L, 12L, 12L, 12L, 12L, 12L, 12L, 36L, 36L, 36L, 36L, 36L, 36L, 36L), P.1 = c(12.1, 12.1, 12.1, 12.1, 12.1, 12.1, 12.1, 15.17, 15.17, 15.17, 15.17, 15.17, 15.17, 15.17, 18.24, 18.24, 18.24, 18.24, 18.24, 18.24, 18.24, 18.24, 24.39, 24.39, 24.39, 24.39, 24.39, 24.39, 24.39, 24.39, 48.35, 48.35, 48.35, 48.35, 48.35, 48.35, 48.35, 12.1, 12.1, 12.1, 12.1, 12.1, 12.1, 12.1, 15.17, 15.17, 15.17, 15.17, 15.17, 15.17, 15.17, 15.17, 18.24, 18.24, 18.24, 18.24, 18.24, 18.24, 18.24, 18.24, 24.39, 24.39, 24.39, 24.39, 24.39, 24.39, 24.39, 24.39, 48.35, 48.35, 48.35, 48.35, 48.35, 48.35, 48.35, 48.35, 12.1, 12.1, 12.1, 12.1, 12.1, 12.1, 12.1, 12.1, 15.17, 15.17, 15.17, 15.17, 15.17, 15.17, 15.17, 18.24, 18.24, 18.24, 18.24, 18.24, 18.24, 18.24, 18.24, 24.39, 24.39, 24.39, 24.39, 24.39, 24.39, 24.39, 24.39, 48.35, 48.35, 48.35, 48.35, 48.35, 48.35, 48.35, 48.35, 12.1, 12.1, 12.1, 12.1, 12.1, 12.1, 12.1, 12.1, 15.17, 15.17, 15.17, 15.17, 15.17, 15.17, 15.17, 18.24, 18.24, 18.24, 18.24, 18.24, 18.24, 18.24, 18.24, 24.39, 24.39, 24.39, 24.39, 24.39, 24.39, 24.39, 24.39, 48.35, 48.35, 48.35, 48.35, 48.35, 48.35, 48.35), S.R = c(4.363636364, 4.583333333, 5.125, 4.542857143, 8, 6.12, 6.333333333, 7.785714286, 10.64285714, 7.785714286, 6.956521739, 6.6, 6.346153846, 7.090909091, 6.153846154, 8.272727273, 12.3, 3.909090909, 6.826086957, 8.285714286, 9.928571429, 5.827586207, 4.866666667, 7.125, 5.866666667, 3.555555556, 6.142857143, 7.1, 6.689655172, 9.142857143, 12.11111111, 5.178571429, 4.379310345, 6.428571429, 9.333333333, 9.15, 7.8, 3.181818182, 5.789473684, 6.571428571, 6.347826087, 7.421052632, 5.2, 5.944444444, 10.625, 8.769230769, 8.789473684, 6.166666667, 5.8, 6.740740741, 6.185185185, 6.173913043, 8.5, 10.21428571, 8.944444444, 8.277777778, 7.25, 6.189189189, 7.037037037, 7.56, 7.238095238, 6.296296296, 7.807692308, 7.736842105, 6.153846154, 6.133333333, 8.217391304, 8.52, 10.21428571, 5.772727273, 8.761904762, 9, 6.757575758, 8.517241379, 4.561403509, 5.540540541, 6.44, 5.833333333, 5.214285714, 4.648648649, 3, 4.820512821, 5.862068966, 5.90625, 5.793103448, 4.935483871, 5.793103448, 6.956521739, 3.473684211, 6.228571429, 6.517241379, 5.885714286, 8.260869565, 7.857142857, 5.523809524, 7.1875, 7, 9.2, 6.7, 9.307692308, 7.3, 8, 7.583333333, 6.184210526, 7.15625, 6.5, 10.20833333, 5.941176471, 8.407407407, 11.29411765, 4.444444444, 6.25, 8.258064516, 12.05263158, 9, 6.5, 8.2, 5.285714286, 5.461538462, 5.730769231, 6.076923077, 5.2, 5.8125, 4.076923077, 3.764705882, 5.823529412, 9, 6.75, 5.954545455, 6.035714286, 4.153846154, 4.263157895, 4, 4.666666667, 3.636363636, 5.454545455, 5.633333333, 2.141025641, 4.090909091, 5.111111111, 7.642857143, 4.777777778, 2.957446809, 2.185185185, 2.307692308, 7.8, 19.375, 10.375, 7.941176471, 5.956521739, 5.125, 4.657894737, 8.5)), row.names = c(1L, 2L, 4L, 5L, 6L, 7L, 8L, 10L, 11L, 12L, 13L, 14L, 15L, 16L, 17L, 18L, 19L, 20L, 21L, 22L, 23L, 24L, 25L, 26L, 27L, 28L, 29L, 30L, 31L, 32L, 33L, 34L, 36L, 37L, 38L, 39L, 40L, 42L, 43L, 44L, 45L, 46L, 47L, 48L, 49L, 50L, 51L, 52L, 53L, 54L, 55L, 56L, 57L, 58L, 59L, 60L, 61L, 62L, 63L, 64L, 65L, 66L, 67L, 68L, 69L, 70L, 71L, 72L, 73L, 74L, 75L, 76L, 77L, 78L, 79L, 80L, 81L, 82L, 83L, 84L, 85L, 86L, 87L, 88L, 89L, 90L, 91L, 92L, 93L, 94L, 95L, 97L, 98L, 99L, 100L, 101L, 102L, 103L, 104L, 105L, 106L, 107L, 108L, 109L, 110L, 111L, 112L, 113L, 114L, 115L, 116L, 117L, 118L, 119L, 120L, 121L, 122L, 123L, 124L, 125L, 126L, 127L, 128L, 129L, 130L, 131L, 132L, 133L, 134L, 135L, 137L, 138L, 139L, 140L, 141L, 142L, 143L, 144L, 145L, 146L, 147L, 148L, 149L, 150L, 151L, 152L, 153L, 154L, 156L, 157L, 158L, 159L, 160L), class = "data.frame") I have put the conventional command (end of script) for changing the number of coloumns in the legend but it is not working... library(Rmisc) library(ggplot2) tglf2 <- summarySE(z, measurevar="S.R", groupvars=c("P","cultivar","Waterlogging"),na.rm=TRUE) pd <- position_dodge(0.5) ggplot(tglf2, aes(x=as.factor(P), y=S.R,colour=cultivar,group=cultivar)) + geom_errorbar(aes(ymin=S.R-se, ymax=S.R+se),colour="black", width=.2,position=pd) + geom_line(position=pd) + geom_point(aes(shape=cultivar),size=3.5,position=pd)+ scale_shape_manual(values=c(0, 16, 17,1))+ scale_color_manual(values=c("#009E73", "#F0E442", "#0072B2", "#D55E00"))+ facet_grid(~Waterlogging)+ ylab(expression(Root~mass~fraction~(g~root~g^-1~plant)))+ xlab(expression(P~(mg~kg^-1~soil)))+ scale_y_continuous(expand = c(0, 0),limits=c(0, 18),breaks=0:100*3)+ theme_bw()+ theme(legend.key.size = unit(6, "mm"))+ cleanup+ theme( legend.position = c(.25, .88), legend.title=element_blank(), strip.background = element_blank(), legend.text = element_text(size=14),# strip.text.x = element_text(size = 15), axis.text.x = element_text(size = 15), axis.title.y = element_text(size = 15,margin = margin(t = 0, r = 5, b = 0, l = 0)), axis.title.x = element_text(size = 15,margin = margin(t = 5, r = 0, b = 0, l = 0)), axis.text.y = element_text(margin = margin(r = 3),size = 15))+ geom_segment(aes(x = 1, y = 13, xend = 1, yend = 15.58216), size=1,colour="black",data = subset(z, Waterlogging == "Waterlogged"))+ guides(col = guide_legend(nrow = 2)) Please ask for any more information if needed. A: It's because you have several elements composing your legend: colour, shape and group. You need to pass all of them in guide_legend in order ggplot be able to separate all elements of the legend in two rows. Try by adding the following at the end of your code: ... + guides(colour = guide_legend(nrow= 2), shape = guide_legend(nrow = 2), group = guide_legend(nrow = 2)) | Low | [
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Vital Pieces of Nail Spa The Argument About Nail Spa This consists of hair cuts for women and guys, permanents and hair coloring for girls, along with hair cuts for kids Along with nail services, these one-stop nail salons supply facial treatments, waxing, tog read more... | Low | [
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As part of Nikki Haley's push to advance the Trump administration's “America First” agenda at the United Nations, the hard-charging ambassador is fighting for U.S. businesses to get a bigger slice of the more than $18 billion in contracts the world body hands out each year. The U.S. already is the biggest recipient of these procurement contracts, but officials say that number is growing since Haley took office. In 2017, the U.S. won $1.74 billion in contracts -- approximately 9 percent of the $18.6 billion available. The next highest was India, which picked up 4.8 percent of all contracts. That marks almost a 10 percent uptick in contracts awarded to U.S. businesses from 2016. But Haley and the U.S. Mission aren’t done, and are looking at ways to get more lucrative contracts awarded. It’s part of a broader effort by Haley and the Trump administration to make sure the United Nations' biggest contributor gets a better deal there. “We are very proud of our American companies, from the quality of their products to the efficiencies of their services. We will continue to use all of the resources we have available to help our companies win U.N. contracts,” Haley told Fox News. Her office is not necessarily strongarming the U.N. into awarding contracts to American companies -- it is a competitive process -- but is urging those companies to seek U.N. business while facilitating meetings between them and U.N. officials. Cherith Norman Chalet, the U.S. representative for U.N. Management and Reform, told Fox News that the U.S. Mission is increasing the number of seminars across the country that feature business representatives and officials from U.N. agencies, including UNICEF and the World Food Program. “It's to try to help companies understand the process, what the opportunities are at the U.N. and what the needs the U.N. are looking for, so really trying to matchmake in the best possible way,” she said. Whereas in recent years there would be a few general seminars a year, all in New York, this year the U.S. Mission -- working with the Commerce Department -- is holding a number of state-specific seminars across America. So far, these have been held in Wisconsin, Rhode Island and Mississippi. On Thursday, a seminar in Detroit, Mich., featured more than 150 companies along with representatives from the Secretariat, U.N. Development Program, the World Food Program and UNICEF. In October, there will be a private-sector day, which will also include discussions and information about the policy side of the U.N. and the impact on businesses. Another more general seminar is being planned in New York this fall on the subject of aviation, in hopes of leveling the playing field on a contract area that traditionally has been dominated by Russia. The goal, Chalet said, is "to increase visibility of the U.S. Mission led by Ambassador Haley, showing that we’re going to go further in ensuring that U.S. companies have equal opportunity at the U.N. and that we will continue to be the number one in procuring those contracts.” HALEY PRESSURES ARAB STATES TO STEP UP ON PALESTINIAN AID: 'WE ARE NOT FOOLS' “We’ve done well and we’re doing better and we have more to go,” she said. While the numbers on 2018 contracts are not yet available, officials say they are hopeful for continued growth and the seminars have seen a significant increase in attendance. In addition to the 9 percent increase in procurement contracts, the U.S. says the number of U.S. companies registered as vendors on the U.N. Global Marketplace -- where companies register to bid on U.N. contracts and to be alerted about available contracts -- spiked from 10,545 in 2016 to 16,004 in 2017 “From what we can tell based on the seminars, as well as interaction with U.N., what these have done this year is really match the needs and increased awareness of companies so they can be even better prepared to put in the bids, and be more successful in being selected,” Chalet said. The Better World Campaign, which pushes for better relations between the U.S. and the U.N., hailed the developments and noted that while the top states that benefited from contracts were New York, New Jersey, Maryland and California, the benefits were being felt across the country. “Forty-two states plus Washington D.C. are home to American companies that were awarded UN contracts in 2017,” President Peter Yao said in a statement. “This new data confirms that the U.N. is not only in America’s foreign policy and national security interests, American corporations also benefit more than any other country in the world from procurement contracts with the U.N,” he said. The push represents part of the broader effort by the U.N.-skeptical administration to get a better value at the organization, even as it moves to punish some arms of the world body. NIKKI HALEY SECURES SOUTH SUDAN ARMS EMBARGO THAT ELUDED OBAMA While Haley has been a primary driver of action at the Security Council on areas such as North Korea and South Sudan, the U.S. has also pulled back where it doesn’t see that value. The administration has withdrawn from the Human Rights Council, calling it a "cesspool of political bias," and has gutted funding to the U.N. Palestinian refugee agency (UNRWA). The U.S. has also demanded cuts to the U.N. budget. This week in a speech in West Virginia, Trump praised Haley for securing a $1.3 billion cut in U.N. spending since taking office -- which he said had saved taxpayers $350 million. | Mid | [
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Q: Lock-free thread-safe Fibonacci number generator Here is my implementation of a lock-free thread-safe Fibonacci number generator. Is it correct? The idea is to use an immutable holder for previous and current numbers (since it's hard to change two values atomically at the same time) and AtomicReference which points to the current Fibonacci number. Lock-free public class FibonacciSequence { private static class FibonacciNumber { protected final BigInteger prev; protected final BigInteger curr; public FibonacciNumber(BigInteger prev, BigInteger curr) { this.prev = prev; this.curr = curr; } public FibonacciNumber next() { return new FibonacciNumber(curr, prev.add(curr)); } public BigInteger value() { return curr; } } private static final class FirstFibonacciNumber extends FibonacciNumber { public FirstFibonacciNumber() { super(null, BigInteger.valueOf(0L)); } public FibonacciNumber next() { return new FibonacciNumber(curr, BigInteger.valueOf(1L)); } } private final AtomicReference<FibonacciNumber> currentFibNumberRef; public FibonacciSequence() { currentFibNumberRef = new AtomicReference<>(new FirstFibonacciNumber()); } public BigInteger next() { while (true) { FibonacciNumber currFibNumber = currentFibNumberRef.get(); if (currentFibNumberRef.compareAndSet(currFibNumber, currFibNumber.next())) return currFibNumber.value(); } } Testing public static void main(String[] args) { testFibonacciNumberCorrectness(); // todo add thread-safe test } private static void testFibonacciNumberCorrectness() { int[] some = {0, 1, 1, 2, 3, 5, 8, 13, 21, 34, 55, 89, 144, 233, 377, 610, 987, 1597, 2584, 4181, 6765, 10946, 17711, 28657, 46368, 75025, 121393, 196418, 317811}; FibonacciNumber currFibNumber = new FirstFibonacciNumber(); for (int num : some) { assert num == currFibNumber.value().intValue(); currFibNumber = currFibNumber.next(); } } } A: I have taken this problem on as a little study in to lock efficiency, performance, and contention. As a result, I am posting a second answer with some additional information, and a different sort of review. Note: The full console output from my harness is here in pastebin.com First, my conclusion is that lock-free fib generator is a mistake. Reentrant locks are also a problem, and that the best performance comes from plain old synchronization. So, to test this all, I created a basic interface: package fibgen; import java.math.BigInteger; public interface FibGen extends AutoCloseable { /** * Get the next Fibonacci number in this sequence * @return the next number */ public BigInteger next(); /** * How many retries were needed in spin loops. * @return the retry count */ public long retryCount(); /** * because there may need to be some clean up in some generators. */ public void close(); } Right, that's a tool to generate Fibonacci numbers in a way that is independent of the implementation. Now, putting your original question code in to that framework, so you can see what I did using a familiar starting point, I got: package fibgen; import java.math.BigInteger; import java.util.concurrent.atomic.AtomicLong; import java.util.concurrent.atomic.AtomicReference; public class FibonacciSequence implements FibGen { @Override public void close() { // nothing } private static class FibonacciNumber { protected final BigInteger prev; protected final BigInteger curr; public FibonacciNumber(BigInteger prev, BigInteger curr) { this.prev = prev; this.curr = curr; } public FibonacciNumber next() { return new FibonacciNumber(curr, prev.add(curr)); } public BigInteger value() { return curr; } } private static final class FirstFibonacciNumber extends FibonacciNumber { public FirstFibonacciNumber() { super(null, BigInteger.valueOf(0L)); } public FibonacciNumber next() { return new FibonacciNumber(curr, BigInteger.valueOf(1L)); } } private final AtomicReference<FibonacciNumber> currentFibNumberRef; private final AtomicLong retries = new AtomicLong(); public FibonacciSequence() { currentFibNumberRef = new AtomicReference<>(new FirstFibonacciNumber()); } @Override public BigInteger next() { while (true) { FibonacciNumber currFibNumber = currentFibNumberRef.get(); if (currentFibNumberRef.compareAndSet(currFibNumber, currFibNumber.next())) return currFibNumber.value(); retries.incrementAndGet(); } } @Override public long retryCount() { return retries.get(); } } OK, now you know how it hangs together, let's look at some of my output. After doing a lot of output, and running on my dual-core-with-hyperthreading laptop, I get the best results from 6 strategies as: fibgen.FibGenQueue Retries 0 Statistics: 50000 BigIntegers with hashXOR 212738101 - Next=7.632us Calc=0.610us all in 104.814ms fibgen.FibonacciSequence Retries 74188 Statistics: 50000 BigIntegers with hashXOR 212738101 - Next=5.206us Calc=1.280us all in 91.571ms fibgen.FibGenLock Retries 0 Statistics: 50000 BigIntegers with hashXOR 212738101 - Next=6.338us Calc=0.551us all in 91.333ms fibgen.FibGenRolfl Retries 4451265 Statistics: 50000 BigIntegers with hashXOR 212738101 - Next=4.677us Calc=0.618us all in 72.015ms fibgen.FibGenSync Retries 0 Statistics: 50000 BigIntegers with hashXOR 212738101 - Next=4.695us Calc=0.611us all in 67.888ms Let me explain the above results, using your generator: fibgen.FibonacciSequence Retries 74188 Statistics: 50000 BigIntegers with hashXOR 212738101 - Next=5.206us Calc=1.280us all in 91.571ms Your generator needed to spin-loop almost 75,000 times in order to generate 50,000 values in the sequence. A quality-checking XOR function has some value 212738101 (this is a good thing, I will explain later), and the average latency on the 'next()' call was 5.2 microseconds, the time to calculate the XOR function was an average of 1.3 microseconds, and the whole sequence was completed, in many threads, in 91.5 milliseconds. Put another way, you ran 4 threads at 100% for 91.5 milliseconds, and you generated 125,000 fibonacci numbers (but only used 50,000). Note, when I ran your code, I did it 10 times (after warmups), with the following results: fibgen.FibonacciSequence Retries 70284 Statistics: 50000 BigIntegers with hashXOR 212738101 - Next=7.813us Calc=0.677us all in 132.730ms fibgen.FibonacciSequence Retries 88643 Statistics: 50000 BigIntegers with hashXOR 212738101 - Next=6.030us Calc=0.695us all in 107.690ms fibgen.FibonacciSequence Retries 81224 Statistics: 50000 BigIntegers with hashXOR 212738101 - Next=7.501us Calc=0.879us all in 121.851ms fibgen.FibonacciSequence Retries 90017 Statistics: 50000 BigIntegers with hashXOR 212738101 - Next=7.992us Calc=0.749us all in 113.700ms fibgen.FibonacciSequence Retries 89161 Statistics: 50000 BigIntegers with hashXOR 212738101 - Next=7.785us Calc=0.964us all in 117.558ms fibgen.FibonacciSequence Retries 87775 Statistics: 50000 BigIntegers with hashXOR 212738101 - Next=5.022us Calc=0.912us all in 93.947ms fibgen.FibonacciSequence Retries 80012 Statistics: 50000 BigIntegers with hashXOR 212738101 - Next=6.034us Calc=0.650us all in 105.458ms fibgen.FibonacciSequence Retries 71632 Statistics: 50000 BigIntegers with hashXOR 212738101 - Next=4.862us Calc=0.640us all in 110.539ms fibgen.FibonacciSequence Retries 74188 Statistics: 50000 BigIntegers with hashXOR 212738101 - Next=5.206us Calc=1.280us all in 91.571ms fibgen.FibonacciSequence Retries 105237 Statistics: 50000 BigIntegers with hashXOR 212738101 - Next=6.891us Calc=0.905us all in 103.621ms Note that the fastest run (91.5ms) has the slowest 'Calc' time. I am not sure why this happened. I believe the variances I see in your code are in part caused by the increased thrashing your algorithm puts on the garbage collector. The other algorithms result in more stable performance. Compare your fastest time to the alternatives. I suggested one in the answer code I supplied before. In my test framework, it looks like: package fibgen; import java.math.BigInteger; import java.util.concurrent.atomic.AtomicLong; import java.util.concurrent.atomic.AtomicReference; public class FibGenRolfl implements FibGen { @Override public void close() { // Nothing here.. } protected final AtomicReference<BigInteger> nextRef = new AtomicReference<>(BigInteger.ONE); protected final AtomicReference<BigInteger> currRef = new AtomicReference<>(BigInteger.ZERO); protected final AtomicLong retries = new AtomicLong(); @Override public BigInteger next() { BigInteger current = null; long tries = -1L; do { // spin loop while someone else is updating the reference. // updating is indicated by a null value in the reference. tries++; current = currRef.getAndSet(null); } while (current == null); BigInteger next = nextRef.get(); nextRef.set(next.add(current)); currRef.set(next); if (tries > 0L) { retries.addAndGet(tries); } return current; } @Override public long retryCount() { return retries.get(); } } Now, I claimed this is an improvement over your code, and, is it? It produces the result: fibgen.FibGenRolfl Retries 4451265 Statistics: 50000 BigIntegers with hashXOR 212738101 - Next=4.677us Calc=0.618us all in 72.015ms It ran about 25% faster overall than your code. The individual average latency on each next() call is slightly faster at 4.7us (instead of 5.2). The big difference, is that your code calculations are significantly slower, so my code 'spins' a lot faster.... While your code retried 75,000 times, my code retried 4.5million times. The difference is that your code computes and throws-away a fib number, whereas my code uses it as a spin-lock and only computes the fib number when it is free to do so.... hopefully that reduces memory churn... maybe. I create no garbage in my spins, your code makes two objects each wasted cycle. So, I run all threads at 100%, but I get results slightly faster, on average, and my overall run time is reduced. I believe the imprved latency is because the BigInteger.add operation is relativey slow, and in your code, the 'latency' of each call is in increments of that time. For example, if an add takes 4us, then your code will return in either 4us, 8us, 12us, 16us, etc. My code, on the other hand, can 'delay' for partial amounts of time, and then return after a single 4us calculation. But, if the partial delay is beneficial, would a blocking system be better than a spin system? Note that your algorithm kept 4 threads busy for 91.5ms, and mine kept threads busy for 72ms. Combined that's 370ms of CPU time vs. 290ms CPU time I tried using a Reentrant lock instead, with the code: package fibgen; import java.math.BigInteger; import java.util.concurrent.locks.ReentrantLock; public class FibGenLock implements FibGen { @Override public void close() { // Nothing here.. } private BigInteger nextRef = BigInteger.ONE; private BigInteger currRef = BigInteger.ZERO; private final ReentrantLock lock = new ReentrantLock(); @Override public BigInteger next() { lock.lock(); try { BigInteger current = currRef; currRef = nextRef; nextRef = current.add(currRef); return current; } finally { lock.unlock(); } } @Override public long retryCount() { return 0; } } That code is has about the same latency and overall elapsed time as your code, but, in terms of used CPU time, it blocks all threads except one, so it is 4-times more efficient than your code. Now, the fastest result was using plain-jane synchronization. I believe it is fastest because there's only one memory-barrier activity (just one synchronization - whereas the Reentrant lock has two - a lock, and an unlock). Here's the code: package fibgen; import java.math.BigInteger; public class FibGenSync implements FibGen { @Override public void close() { // Nothing here.. } private BigInteger nextRef = BigInteger.ONE; private BigInteger currRef = BigInteger.ZERO; private final Object lock = new Object(); @Override public BigInteger next() { synchronized(lock) { BigInteger current = currRef; currRef = nextRef; nextRef = current.add(currRef); return current; } } @Override public long retryCount() { return 0; } } Note that this runs in 67ms, and has the same latency as the tight spin-lock mechanism. The major difference is in the fact that it wastes no CPU cycles. It's much more efficient. That's the best algorithm. As an aside, I through it would be interesting to try a queue, where one thread feeds Fib numbers in to the queue, and the other threads read it out. It was significantly slower than the alternatives, more complicated, and just generally ugly... here's the code for your reference: package fibgen; import java.math.BigInteger; import java.util.concurrent.ArrayBlockingQueue; import java.util.concurrent.TimeUnit; import java.util.concurrent.atomic.AtomicBoolean; import java.util.concurrent.atomic.AtomicLong; public class FibGenQueue implements FibGen, Runnable { private final ArrayBlockingQueue<BigInteger> queue = new ArrayBlockingQueue<>(64); private AtomicBoolean active = new AtomicBoolean(true); private AtomicLong retries = new AtomicLong(); public FibGenQueue() { Thread t = new Thread(this, "FibGen"); t.setDaemon(true); t.start(); } @Override public BigInteger next() { try { do { BigInteger fib = queue.poll(1, TimeUnit.SECONDS); if (fib != null) { return fib; } retries.incrementAndGet(); } while (active.get()); } catch (InterruptedException ie) { Thread.currentThread().interrupt(); } throw new IllegalStateException("Attempt to read from an invalid queue"); } @Override public long retryCount() { return retries.get(); } @Override public void run() { BigInteger current = BigInteger.ZERO; BigInteger next = BigInteger.ONE; try { while(true) { if (queue.offer(current, 1, TimeUnit.SECONDS)) { BigInteger tmp = next.add(current); current = next; next = tmp; } else { if (!active.get()) { return; } } } } catch (InterruptedException ie) { Thread.currentThread().interrupt(); } finally { queue.clear(); active.set(false); } } @Override public void close() { active.set(false); } } Now, how was this all tested? Using the following framework, and some Java-8 magic: package fibgen; import java.math.BigInteger; import java.util.ArrayList; import java.util.List; import java.util.function.Supplier; import java.util.stream.Collectors; import java.util.stream.IntStream; public class FibTester { private static final class BigIntCollector { private long nextTime = 0L; private long calcTime = 0L; private long runTime = -1L; private int count = 0; private int hasXOR = 0; public void accumulate(int index, FibGen gen) { long start = System.nanoTime(); BigInteger big = gen.next(); long next = System.nanoTime(); hasXOR ^= big.hashCode(); long done = System.nanoTime(); nextTime += next - start; calcTime += done - next; count++; } public BigIntCollector merge (BigIntCollector toMerge) { nextTime += toMerge.nextTime; calcTime += toMerge.calcTime; count += toMerge.count; hasXOR ^= toMerge.hasXOR; return this; } @Override public String toString() { double factor = (1000.0 * count); return String.format("Statistics: %d BigIntegers with hashXOR %d - Next=%.3fus Calc=%.3fus all in %.3fms", count, hasXOR, nextTime / factor, calcTime / factor, runTime / 1000000.0); } public void runTime(long time) { runTime = time; } } public static final String benchmark(Supplier<FibGen> supplier, int volume) { long start = System.nanoTime(); try (FibGen gen = supplier.get()) { BigIntCollector coll = IntStream.range(0, volume).parallel() .collect(BigIntCollector::new, (c, i) -> c.accumulate(i, gen), (a,b) -> a.merge(b)); coll.runTime(System.nanoTime() - start); return String.format("%25s Retries %8d %s", gen.getClass().getName(), gen.retryCount(), coll.toString()); } } public static void main(String[] args) { List<Supplier<FibGen>> suppliers = new ArrayList<>(); suppliers.add(FibonacciSequence::new); suppliers.add(FibGenRolfl::new); suppliers.add(FibGenQueue::new); suppliers.add(FibGenSync::new); suppliers.add(FibGenLock::new); dump(suppliers, 100); for (Supplier<FibGen> supplier : suppliers) { System.out.println(benchmark(supplier, 1000)); } for (int i = 0; i < 100; i++) { for (Supplier<FibGen> supplier : suppliers) { benchmark(supplier, 1000); } } for (Supplier<FibGen> supplier : suppliers) { System.out.println(); for (int i = 0; i < 10; i++) { System.out.println(benchmark(supplier, 50000)); } } } private static void dump(List<Supplier<FibGen>> suppliers, int count) { FibGen[] gens = suppliers.stream().map(s -> s.get()).collect(Collectors.toList()).toArray(new FibGen[suppliers.size()]); StringBuilder sb = new StringBuilder(); for (int i = 1; i <= count; i++) { sb.setLength(0); sb.append(String.format("%5d ", i)); for (FibGen fg : gens) { sb.append(String.format("%20s ", fg.next())); } System.out.println(sb.toString()); } } } A: BigInteger operations are slow. Each iteration through the process you are creating a new BigInteger, as well as a new FibonacciNumber instance. These instances are likely more expensive to process (and garbage collect) than the time saved through lock-free management. Still, using a three-state operation you can solve this problem without the FibonacciNumber class: protected final AtomicReference<BigInteger> nextRef = new AtomicReference<>(BigInteger.ONE); protected final AtomicReference<BigInteger> currRef = new AtomicReference<>(BigInteger.ONE); public BigInteger next() { BigInteger current = null; do { // spin loop while someone else is updating the reference. // updating is indicated by a null value in the reference. current = currRef.getAndSet(null); } while (current == null); BigInteger next = nextRef.get(); nextRef.set(next.add(current)); currRef.set(next); return current; } Note that the above code puts a waiting process in to a spin lock (100% CPU) instead of locking. This is the same as your code. My preference would be to use a more traditional Lock (or even synchronization) and block threads that are waiting. A: I modified the sequence class' next method to work when called from other threads such as below in order to test it with multiple threads: 1 public BigInteger next() { 2 FibonacciNumber currFibNumber = currentFibNumberRef.get(); 3 if (currentFibNumberRef.compareAndSet(currFibNumber, 4 currFibNumber.next())) 5 return currFibNumber.value(); 6 return currentFibNumberRef.get().value(); 7 } This will return the current value of the Fibonacci number if it is not updated. Here is the test that I wrote for it: @Test public void testSequenceThreaded() throws InterruptedException, ExecutionException { int[] some = {0, 1, 1, 2, 3, 5, 8, 13, 21, 34, 55, 89, 144, 233, 377, 610, 987, 1597, 2584, 4181, 6765, 10946, 17711, 28657, 46368, 75025, 121393, 196418, 317811 }; final int threads = 4; FibonacciSequence currFibNumber = new FibonacciSequence(); ExecutorCompletionService<BigInteger> executor = new ExecutorCompletionService<BigInteger>( Executors.newFixedThreadPool(threads)); for (int i = 0; i < some.length; i++) { executor.submit(new CallableNumber(currFibNumber)); } for (int num : some) { Future<BigInteger> val = executor.take(); int value = val.get().intValue(); assertTrue("Expected " + num + " but got " + value, num == value); } } // Callable sequence that will return the next value of the fibonacci // sequence. private static class CallableNumber implements Callable<BigInteger> { private final FibonacciSequence sequence; public CallableNumber(FibonacciSequence sequence) { this.sequence = sequence; } @Override public BigInteger call() throws Exception { return sequence.next(); } } There are various other ways to test the solution however this is the one that I chose. With 4 threads I cannot get your solution to pass the test. Essentially, this is testing that the next method of the sequence returns the correct next value in the sequence. The solution allows for a race condition between lines (in my version) 2 and 3 of the next method. Additionally, if you update the value of the reference you are returning the old value not the new one. | Low | [
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Player Benefits The choice of those who know AP2 irons feature Tour-proven performance, validated by the best players in the world. Both speed and MOI have been maximized to provide total control and distance anyone can appreciate. An instrument of precision Greater forgiveness and stability are achieved through precise perimeter tungsten weighting and a unique co-forged construction. Attack even the most challenging pin placements with more confidence than ever. Stunning looks, winning feel The Tour player-preferred look, sound and pure forged feel wrapped up in one unmistakable package. Now with a refined leading edge for more efficient turf interaction and pure feel through impact. "It's a competitive advantage... and I have it." Jordan Spieth, Titleist Brand Ambassador Titleist 718 AP2 Irons Technology Our mission is to deliver clubs built with ultimate precision to meet the needs of your game. It all starts with the highest quality materials and our commitment to constantly push the standards of golf club manufacturing. When you open your box stamped with the Titleist Script, rest assured – you’re playing the very best. Stock Shaft and Grip Traditional iron shafts feature a constant weight profile - shafts with the same mass properties throughout the set. With ascending mass shaft technology, the weight of each shaft increases by 3 grams throughout the set (long iron to short iron). Most golfers already use ascending weight shafts in their driver, fairways, and hybrids. The new Titleist AP irons feature ascending mass stock shafts in distinct weight ranges matched to the performance of each model, with lighter long iron shafts for launch and speed and heavier short iron shafts for control. It Takes More To Be A Titleist Superior performance is never an accident. Our unrivaled approaches to golf club design, validation, fitting and manufacturing are the keys to our continued innovation and consistent excellence. If the club in your hand says Titleist, you can be sure it is the very best it can possibly be. | High | [
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Friends Fanfiction She was intoxication at its finest. There were plenty of other women, demons, that he could choose from. Beauties from the country over. And yet he had to fall for a human. A human that never seemed to know when to leave well enough alone. A new world awaits Kagome as she is thrown into a different era. Demons have been outlawed, and are now hunted by the thousands. Priestesses are accused of taint and are executed on sight, and a certain demon lord has been captured and kept as a pet by a demented human lord. Trapped in this strange new era, what new adventures await? "Kagome." Her name was a soft caress against cold skin. A promise of, if not love, than a passion deeper than any. She could lose herself in that voice. Deep, calming. Safety and danger in one. Her wildest dreams and desires all at her disposal. All she had to do was give in. | Low | [
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# -*- coding: utf-8 -*- ## Amazon S3 manager ## Author: Michal Ludvig <[email protected]> ## http://www.logix.cz/michal ## License: GPL Version 2 ## Copyright: TGRMN Software and contributors from __future__ import absolute_import import sys import hmac import base64 from . import Config from logging import debug from .Utils import (encode_to_s3, time_to_epoch, deunicodise, decode_from_s3, check_bucket_name_dns_support, s3_quote) from .SortedDict import SortedDict import datetime from hashlib import sha1, sha256 __all__ = [] def format_param_str(params, always_have_equal=False, limited_keys=None): """ Format URL parameters from a params dict and returns ?parm1=val1&parm2=val2 or an empty string if there are no parameters. Output of this function should be appended directly to self.resource['uri'] - Set "always_have_equal" to always have the "=" char for a param even when there is no value for it. - Set "limited_keys" list to restrict the param string to keys that are defined in it. """ if not params: return "" param_str = "" equal_str = always_have_equal and u'=' or '' for key in sorted(params.keys()): if limited_keys and key not in limited_keys: continue value = params[key] if value in (None, ""): param_str += "&%s%s" % (s3_quote(key, unicode_output=True), equal_str) else: param_str += "&%s=%s" % (key, s3_quote(params[key], unicode_output=True)) return param_str and "?" + param_str[1:] __all__.append("format_param_str") ### AWS Version 2 signing def sign_string_v2(string_to_sign): """Sign a string with the secret key, returning base64 encoded results. By default the configured secret key is used, but may be overridden as an argument. Useful for REST authentication. See http://s3.amazonaws.com/doc/s3-developer-guide/RESTAuthentication.html string_to_sign should be utf-8 "bytes". and returned signature will be utf-8 encoded "bytes". """ secret_key = Config.Config().secret_key signature = base64.encodestring(hmac.new(encode_to_s3(secret_key), string_to_sign, sha1).digest()).strip() return signature __all__.append("sign_string_v2") def sign_request_v2(method='GET', canonical_uri='/', params=None, cur_headers=None): """Sign a string with the secret key, returning base64 encoded results. By default the configured secret key is used, but may be overridden as an argument. Useful for REST authentication. See http://s3.amazonaws.com/doc/s3-developer-guide/RESTAuthentication.html string_to_sign should be utf-8 "bytes". """ # valid sub-resources to be included in sign v2: SUBRESOURCES_TO_INCLUDE = ['acl', 'lifecycle', 'location', 'logging', 'notification', 'partNumber', 'policy', 'requestPayment', 'torrent', 'uploadId', 'uploads', 'versionId', 'versioning', 'versions', 'website', # Missing of aws s3 doc but needed 'delete', 'cors', 'restore'] if cur_headers is None: cur_headers = SortedDict(ignore_case = True) access_key = Config.Config().access_key string_to_sign = method + "\n" string_to_sign += cur_headers.get("content-md5", "") + "\n" string_to_sign += cur_headers.get("content-type", "") + "\n" string_to_sign += cur_headers.get("date", "") + "\n" for header in sorted(cur_headers.keys()): if header.startswith("x-amz-"): string_to_sign += header + ":" + cur_headers[header] + "\n" if header.startswith("x-emc-"): string_to_sign += header + ":"+ cur_headers[header] + "\n" canonical_uri = s3_quote(canonical_uri, quote_backslashes=False, unicode_output=True) canonical_querystring = format_param_str(params, limited_keys=SUBRESOURCES_TO_INCLUDE) # canonical_querystring would be empty if no param given, otherwise it will # starts with a "?" canonical_uri += canonical_querystring string_to_sign += canonical_uri debug("SignHeaders: " + repr(string_to_sign)) signature = decode_from_s3(sign_string_v2(encode_to_s3(string_to_sign))) new_headers = SortedDict(list(cur_headers.items()), ignore_case=True) new_headers["Authorization"] = "AWS " + access_key + ":" + signature return new_headers __all__.append("sign_request_v2") def sign_url_v2(url_to_sign, expiry): """Sign a URL in s3://bucket/object form with the given expiry time. The object will be accessible via the signed URL until the AWS key and secret are revoked or the expiry time is reached, even if the object is otherwise private. See: http://s3.amazonaws.com/doc/s3-developer-guide/RESTAuthentication.html """ return sign_url_base_v2( bucket = url_to_sign.bucket(), object = url_to_sign.object(), expiry = expiry ) __all__.append("sign_url_v2") def sign_url_base_v2(**parms): """Shared implementation of sign_url methods. Takes a hash of 'bucket', 'object' and 'expiry' as args.""" content_disposition=Config.Config().content_disposition content_type=Config.Config().content_type parms['expiry']=time_to_epoch(parms['expiry']) parms['access_key']=Config.Config().access_key parms['host_base']=Config.Config().host_base parms['object'] = s3_quote(parms['object'], quote_backslashes=False, unicode_output=True) parms['proto'] = 'http' if Config.Config().signurl_use_https: parms['proto'] = 'https' debug("Expiry interpreted as epoch time %s", parms['expiry']) signtext = 'GET\n\n\n%(expiry)d\n/%(bucket)s/%(object)s' % parms param_separator = '?' if content_disposition: signtext += param_separator + 'response-content-disposition=' + content_disposition param_separator = '&' if content_type: signtext += param_separator + 'response-content-type=' + content_type param_separator = '&' debug("Signing plaintext: %r", signtext) parms['sig'] = s3_quote(sign_string_v2(encode_to_s3(signtext)), unicode_output=True) debug("Urlencoded signature: %s", parms['sig']) if check_bucket_name_dns_support(Config.Config().host_bucket, parms['bucket']): url = "%(proto)s://%(bucket)s.%(host_base)s/%(object)s" else: url = "%(proto)s://%(host_base)s/%(bucket)s/%(object)s" url += "?AWSAccessKeyId=%(access_key)s&Expires=%(expiry)d&Signature=%(sig)s" url = url % parms if content_disposition: url += "&response-content-disposition=" + s3_quote(content_disposition, unicode_output=True) if content_type: url += "&response-content-type=" + s3_quote(content_type, unicode_output=True) return url def sign(key, msg): return hmac.new(key, encode_to_s3(msg), sha256).digest() def getSignatureKey(key, dateStamp, regionName, serviceName): """ Input: unicode params Output: bytes """ kDate = sign(encode_to_s3('AWS4' + key), dateStamp) kRegion = sign(kDate, regionName) kService = sign(kRegion, serviceName) kSigning = sign(kService, 'aws4_request') return kSigning def sign_request_v4(method='GET', host='', canonical_uri='/', params=None, region='us-east-1', cur_headers=None, body=b''): service = 's3' if cur_headers is None: cur_headers = SortedDict(ignore_case = True) cfg = Config.Config() access_key = cfg.access_key secret_key = cfg.secret_key t = datetime.datetime.utcnow() amzdate = t.strftime('%Y%m%dT%H%M%SZ') datestamp = t.strftime('%Y%m%d') signing_key = getSignatureKey(secret_key, datestamp, region, service) canonical_uri = s3_quote(canonical_uri, quote_backslashes=False, unicode_output=True) canonical_querystring = format_param_str(params, always_have_equal=True).lstrip('?') if type(body) == type(sha256(b'')): payload_hash = decode_from_s3(body.hexdigest()) else: payload_hash = decode_from_s3(sha256(encode_to_s3(body)).hexdigest()) canonical_headers = {'host' : host, 'x-amz-content-sha256': payload_hash, 'x-amz-date' : amzdate } signed_headers = 'host;x-amz-content-sha256;x-amz-date' for header in cur_headers.keys(): # avoid duplicate headers and previous Authorization if header == 'Authorization' or header in signed_headers.split(';'): continue canonical_headers[header.strip()] = cur_headers[header].strip() signed_headers += ';' + header.strip() # sort headers into a string canonical_headers_str = '' for k, v in sorted(canonical_headers.items()): canonical_headers_str += k + ":" + v + "\n" canonical_headers = canonical_headers_str debug(u"canonical_headers = %s" % canonical_headers) signed_headers = ';'.join(sorted(signed_headers.split(';'))) canonical_request = method + '\n' + canonical_uri + '\n' + canonical_querystring + '\n' + canonical_headers + '\n' + signed_headers + '\n' + payload_hash debug('Canonical Request:\n%s\n----------------------' % canonical_request) algorithm = 'AWS4-HMAC-SHA256' credential_scope = datestamp + '/' + region + '/' + service + '/' + 'aws4_request' string_to_sign = algorithm + '\n' + amzdate + '\n' + credential_scope + '\n' + decode_from_s3(sha256(encode_to_s3(canonical_request)).hexdigest()) signature = decode_from_s3(hmac.new(signing_key, encode_to_s3(string_to_sign), sha256).hexdigest()) authorization_header = algorithm + ' ' + 'Credential=' + access_key + '/' + credential_scope + ',' + 'SignedHeaders=' + signed_headers + ',' + 'Signature=' + signature new_headers = SortedDict(cur_headers.items()) new_headers.update({'x-amz-date':amzdate, 'Authorization':authorization_header, 'x-amz-content-sha256': payload_hash}) debug("signature-v4 headers: %s" % new_headers) return new_headers __all__.append("sign_request_v4") def checksum_sha256_file(filename, offset=0, size=None): try: hash = sha256() except Exception: # fallback to Crypto SHA256 module hash = sha256.new() with open(deunicodise(filename),'rb') as f: if size is None: for chunk in iter(lambda: f.read(8192), b''): hash.update(chunk) else: f.seek(offset) size_left = size while size_left > 0: chunk = f.read(min(8192, size_left)) size_left -= len(chunk) hash.update(chunk) return hash def checksum_sha256_buffer(buffer, offset=0, size=None): try: hash = sha256() except Exception: # fallback to Crypto SHA256 module hash = sha256.new() if size is None: hash.update(buffer) else: hash.update(buffer[offset:offset+size]) return hash | Low | [
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A pogrom conducted by Jews You've probably had your fill of atonement for this year. You'd be forgiven if you didn't want to think of Yom Kippur for another 12 months. But, before we leave it behind, one last thought about what we just did. We stood and, in the Al Chet prayer, listed one-by-one those areas where we had fallen short. "We" is the operative word here, for this is no Catholic confession, alone and in private, but a collective act of atonement. We announce that we will put right what we have done wrong collectively, as a people. Now, maybe this is just a tired ritual, a parroting of words few of us understand for no higher purpose than to give us the soothing sensation of following tradition. But, if it means anything, then we need to look hard at what we as a people have done. Plenty of long-time JC readers will groan now in anticipation of my mentioning Israel. "There he goes again", they'll say. "Always banging on about Israel's treatment of the Palestinians." All right, I'll change the record. No talk about the Palestinians this time. Instead let's talk about Israel's treatment of those no one could seriously believe pose a security threat, those who have no record, past or present, of hostility to Israel. These are people who have thrown no rockets at Israeli towns I'm speaking of the African asylum seekers who, out of desperation, have fled brutal societies for a chance of survival in the country that boasts of being the only true, open democracy in a region of oppression. These are people who have thrown no rockets at Israeli towns, who have no charter committed to Israel's destruction. So how are they treated? They are "a cancer in the body" of the nation, Likud MK Miri Regev declared at a Tel Aviv rally in May, a verdict later backed by 52 per cent of Jewish Israelis, according to a poll. Her audience certainly got the message, promptly running riot through the Hatikva neighbourhood - linger for a moment on that name - which is home to many African migrants. Amid chants of "Blacks out!", the mob smashed the windows of African-owned shops or cars, beating up any luckless migrant they chanced upon. The Telegraph reported on a group that rounded on a black boy on a bicycle, beating, punching and kicking him in the head while the police stood by and watched: "Other witnesses described a gang assaulting a mother carrying a young baby so violently she was forced to drop her child." If that were a Jewish neighbourhood, we know what word we would use: pogrom. Scan the headlines since and you see the pattern. Earlier this month, the Israeli immigration authorities jailed a newborn baby in a detention facility. They were taking their cue from Israel's Interior Minister who had vowed to make the lives of such asylum seekers "bitter until they leave". Should those refugees object, surely they could demand justice in the courts? Not necessarily. A new rule due to take effect this month was set to deny many migrants (and Palestinians) access to the courts, until, under pressure, the Justice Ministry threw it out. Meanwhile, an Israeli woman last week posted on her Facebook page a collection of photographs of African refugees in a park, referring to the men as "animals" and labelling the pictures "Night tour in the south Tel Aviv safari". Which of the 44 sins we listed so earnestly on Yom Kippur do we violate when we know of this and say little or nothing? Take your pick. Our sacred texts tell us repeatedly to welcome the stranger, for we too were once strangers. Why do we bother reciting these words if they no longer mean anything? | Mid | [
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Halloween recipes When we talk about cupcakes, we always think about a cake full of butter and sugar. Well, the advantage of making your cupcakes at home is that you get to choose your ingredients. In this case, Carrefour asked me to prepare a cupcake recipe with seasonal ingredients, so I inmediately thought about these pumpkin cupcakes […] Last year I prepared these pink chocolate spoons for a birthday party: they are an easy and low cost recipe, and kids just loved it. This year my oldest son Pablo wanted a small Halloween treat he could bring to share with his friends at school. I needed something quick and easy to eat for […] Welcome to the october issue from Whole Kitchen Magazine! I can’t wait to read it, as you know it is a free online publication, and this month I have prepared two recipes for kids in Halloween, hope you enjoy them! Terrifying meringue bones (inspired by this idea from Martha Stewart) and cheese and sobrasada pumpkins (Sobrasada […] Welcome to the January issue of Whole Kitchen Magazine! As you know it is a free publication you can read online or download in Issu. This month I have prepared two easy low-cost recipes to celebrate a kid’s birthday | Low | [
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Introduction {#S1} ============ Natural killer (NK) cells are innate lymphoid cells capable of directly recognizing virally infected cells without prior antigen exposure ([@B1]), and constitute the first line of defense against herpes simplex virus type 1 (HSV1) infection ([@B2]). Patients with NK cell deficiencies can suffer severe, recurrent, and sometimes fatal HSV1 infection ([@B3], [@B4]). The functional status of NK cells is tightly regulated by signal inputs from a wide variety of NK cell activating and inhibitory receptors, which coordinately balance NK cell function to avoid autoimmune damage under normal physiology ([@B1]). HSV1 infection could diminish inhibitory signals and/or increase activating signals, leading to NK cell activation. HSV1 genomic DNA, viral RNA, and proteins are known to induce the production of type I interferons ([@B5]--[@B7]), which can greatly potentiate NK cell function during HSV1 infection ([@B8]). Upon activation, NK cells undergo dramatic phenotypic and functional changes, including expressing functional markers, secreting cytokines, releasing pre-stored perforin and granzyme B, and lysing target cells (Figure [1](#F1){ref-type="fig"}). {#F1} Natural killer cells express the low affinity Fcγ receptor FcγRIIIA/CD16a (CD16a hereafter), and are the major effector cells for antibody-dependent cell-mediated cytotoxicity (ADCC), which represents the main mechanism for NK cells to recognize and clear HSV1 infection after adaptive immunity is established. However, most primary HSV1 infections are asymptomatic or associated with only mild symptoms like fever and rash, suggesting HSV1 infection can be efficiently recognized and cleared by the innate immune response before an antigen-specific immune response is established ([@B2]). Herpes simple virus type 1 is a member of the herpesviridae family and has a 150 kb double-stranded DNA genome, which contains 84 open reading frames and encodes 74 unique viral proteins ([@B9]). During lytic infection, HSV1 expresses a large amount of viral proteins in a kinetically regulated fashion, rendering the virus-infected cell susceptible to innate immune defense. During latency, expression of viral protein is minimized, thus hindering recognition of infected cells by the immune system. Although it has been suggested that some of these HSV1-encoded proteins might directly mediate recognition or evasion by immune cells ([@B10]--[@B12]), it remains controversial as to whether some viral or cellular proteins serve as cognate ligands for NK cells to sense HSV1 infection. In this review, we summarize the studies of molecules that are involved in the direct interactions between human NK cells and HSV1 lytic infection, discuss potential mechanisms for their action, and provide our interpretation for some conflicting studies. Contact Signals {#S2} =============== Natural killer cell function is tightly regulated by an array of inhibitory and activating receptors that receive input by contacting cognate ligands present on target cells ([@B13]). Contact signals sparked by the collective interactions between NK cell receptors and target cell ligands are essential for the NK cell to release cytotoxic granules and kill target cells ([@B13]). Ligands for NK cell receptors mostly are cellular proteins ([@B14]), however, many viruses and fungi have been reported to express proteins that can directly bind NK cell receptors and modulate NK cells ([@B15]--[@B18]). Whether HSV1 expresses ligands that are directly recognized by NK cells has been controversial. Heat- or UV-inactivated HSV1 viruses were shown to induce IFNα production and promote NK cytolysis, and it was suggested that viral proteins were directly responsible for this stimulatory immune responses ([@B19]--[@B21]). However, heat- or UV-inactivated HSV1 can still enter host cells and deliver viral genomic DNA, which in itself is a potent inducer of type I IFNs ([@B22]). Additional HSV1-encoded glycoproteins, including glycoprotein B (gB), gC, glycoprotein D (gD), and gH/gL, have been reported to activate NK cells ([@B23]--[@B27]), yet contradicting results have also been documented for each of these viral proteins ([@B20], [@B21], [@B28]). The discrepancy shown in these studies may partly arise from different experimental conditions: it nonetheless highlights the need for more well-designed studies to explore the potential role of viral proteins in directly regulating NK cell function. Lytic HSV1 infection greatly changes the biosynthetic events of host cells, most prominently affecting host protein synthesis, traffic, and degradation ([@B29]). The pattern of cellular NK ligands expressed on target cells changes significantly following HSV1 infection, and provides a recognizable signal for NK cells to distinguish infected cells. Below, we discuss cellular ligands that change following HSV1 infection and HSV1 proteins that may contribute to direct NK cell recognition of HSV1. Major Histocompatibility Complex I (MHC I) Class I {#S2-1} -------------------------------------------------- In addition to presenting antigenic peptides to CD8+ cytotoxic T cells, the MHC I molecule is also the natural ligand for the inhibitory killer cell immunoglobulin-like receptors (KIRs) and the lectin-like inhibitory receptor CD94/NKG2a, both of which are expressed on human NK cells ([@B1]). Because of its ubiquitous presence on human tissue, MHC I molecules prevent NK cells from attacking healthy self, thereby preventing autoimmunity. Therefore, it has been hypothesized that downregulation of MHC I during viral infection through many different mechanisms could potentially release NK cells from self-inhibition and lead NK cells to recognize virally infected cells ([@B30]). Fulfillment of antigen presentation by MHC I needs endogenous antigen peptides and the endoplasmic reticulum (ER) traffic protein: transporter associated with antigen processing (TAP). TAP pumps cytosol antigen peptides into the ER, where nascent MHC I molecules are loaded with antigen peptides and exported to the cell surface. Empty MHC I cannot pass the quality check and are not transported to the cell surface ([@B31]). HSV1 ICP47, encoded by the Us12 gene, is a soluble, cytosolic protein of 88 amino acid residues ([@B32]). ICP47 forms a long helical hairpin inserting into the central cavity that is formed by two TAP subunits ([@B33]). By plugging the TAP translocation channel, ICP47 precludes binding and traffic of antigenic peptide from the cytosol to the ER ([@B33]), and prevents transport of MHC I to the plasma membrane. Several *in vitro* studies have confirmed that expression of ICP47 decreases surface MHC I on HSV1-infected human cells and consequently activates NK cells in co-culture ([@B12], [@B34]). However, ICP47 binds murine TAP1/2 poorly ([@B30]) and does not efficiently block traffic of mouse MHC I ([@B35]), making it difficult to test whether the downregulation of MHC I could affect NK cell activation and clearance of HSV1 infection *in vivo*. Both human cytomegalovirus (CMV) Us11 and mouse CMV (MCMV) m152 have been reported to decrease mouse MHC I presentation ([@B32], [@B36], [@B37]). Orr et al. thus constructed a recombinant HSV1 virus expressing HCMV Us11 or MCMV m152, and studied the effect of MHC I downregulation on the immune recognition of HSV1 infection in mice ([@B34]). The recombinant HSV1 viruses nonetheless did not decrease MHC I expression on mouse cell lines more than the wild type HSV1 ([@B34]). Thus, importance of downregulating MHC I for clearance of HSV1 infection by NK cells *in vivo* remains unresolved and awaits better models to resolve this issue. NKG2D Ligands {#S2-2} ------------- NKG2D is one of the major NK cell receptors involved in recognition and killing of tumor cells and virus-infected cells ([@B38]). In humans, NKG2D is engaged by several ligands, namely MHC class I polypeptide-related sequence A and B (MICA and MICB) and the UL16-binding proteins 1--6 (ULBP1--6) ([@B39]). It has been reported that an HSV1-infected cell line had lower expression of MICA and ULBP2, which could potentially help HSV1-infected cells to evade recognition by NK cells ([@B40], [@B41]). Although the exact mechanism for this downregulation of MICA and ULBP2 is unknown, the recycling of membrane protein and general inhibition of *de novo* synthesis of cellular proteins during HSV1 infection might contribute to the decrease of NKG2D ligand expression ([@B29]). NK cells from patients with active HSV1 infection had a higher level of NKG2D ([@B40]), possibly induced by an elevated level of type I IFN during HSV1 infection ([@B42]). The increased NKG2D levels may sensitize NK cells and counteract the effect of decreased NKG2D ligand expression on HSV1-infected cells. Glycoprotein D {#S2-3} -------------- Pierre Lebon reported that diploid cells infected with HSV1 can induce IFNα production by peripheral blood mononuclear cells, and that HSV1 gD was responsible for this biological effect ([@B23]). HSV1 gD, encoded by the Us6 gene, is the major glycoprotein mediating entry of HSV1 into host cells. It binds two cellular receptors: herpesvirus entry mediator (HVEM) and nectin1 ([@B43]). While nectin1 has not been identified to have any regulatory function, HVEM is a member of the tumor necrosis factor alpha superfamily and plays very diverse roles in modulating T-cell function by activating both inflammatory and inhibitory signaling pathways ([@B44]). Herpesvirus entry mediator binds many functionally diverse cellular proteins, including LIGHT (lymphotoxin-like, exhibits inducible expression, and competes with herpes simplex virus glycoprotein D for HVEM, a receptor expressed by T lymphocytes), lymphotoxin-α, B and T lymphocyte attenuator (BTLA), and CD160. Crystal structure of the HVEM-ligand complex shows that the binding sites on HVEM for gD, BTLA, and CD160 are overlapping or very close ([@B45]). HVEM is ubiquitously expressed by both human and mouse immune cells (our unpublished data). A recent study showed that HVEM was required for IFNα production following *Listeria* infection in mice ([@B46]). Collectively, these results suggest that HVEM might not only be the entry mediator, but also the immune sensor for HSV1 infection. However, we recently reported that expression of gD makes glioma resistant to NK cell cytotoxicity ([@B47]), and others reported that blocking gD did not affect the response of NK cells to HSV1-infected cells ([@B20], [@B27], [@B28]). Thus, the role of gD in NK cell response to HSV1 infection is yet to be clarified, similar to the role of HVEM in this process. Glycoprotein B {#S2-4} -------------- Herpes simplex virus type 1 gB promotes viral attachment through interaction with cell surface heparin sulfate ([@B48]), and also plays an essential role in mediating membrane fusion ([@B49]). HSV1 gB has been reported as having a role in the NK cell lysis of HSV1-infected endothelial cells ([@B24]--[@B26]). A lower lysis of target cells infected with HSV1 was observed when viruses were deficient in gB, or when Fab fragments of a gB-specific antibody were added to block gB ([@B24]--[@B26]). Leoni et al. reported that gB was able to physically interact with toll-like receptor-2 (TLR2) ([@B27]). In another study, Kim et al. reported that the activation of NK cells by UV-inactivated HSV1 virions was directly mediated by TLR2 ([@B20]). They showed that UV-inactivated HSV1 virions could bind the endothelial cell line HEK when ectopically expressing TLR2, but not native HEK2 cells that lack TLR2. However, the authors did not confirm the expression of TLR2 on NK cells, or whether the activation of NK cells by HSV1 was mediated by the TLR2-gB interaction ([@B20]). The expression of TLR2 in NK cells is still controversial. Although TLR2 mRNA has been detectable in human NK cells, TLR2 protein has only been noted on decidual NK cells ([@B50]), but not on the surface of human circulating NK cells ([@B51]--[@B55]). Another study also showed TLR2 was not required for recognizing HSV1 glycoproteins ([@B28]). Experiments using different strains of HSV1 may have contributed to the discrepancies seen within these studies. Collectively, these data make it difficult to draw a conclusion regarding the role of gB in mediating NK cell recognition of HSV1-infected cells. Other Cellular Ligands and Viral Proteins {#S2-5} ----------------------------------------- Fitzgerald-Bocarsly et al. reported that expression of HSV1 immediate early genes caused the increased susceptibility of HSV1-infected fibroblast cells to NK cell lysis ([@B56]). Chisholm et al. further pinpointed this NK cell stimulating function to ICP0 ([@B11]). ICP0 is cytosolic protein and theoretically should not be able to activate the NK cell directly. The investigators found ICP0 did not change the expression of MHC I or of NKG2D ligands, but induced the expression of some unidentified ligands for natural cytotoxicity receptors NKp30, NKp44, and NKp46 ([@B11]). However, during HSV1 infection, cellular proteins are only rarely unregulated due to wide spread disruption of host mRNA ([@B29]). The finding that ICP0 expression induces expression of ligands for natural cytotoxicity receptors, if confirmed, would be very helpful for identifying these cellular ligands important for the function of NK cells. The Role of IgG {#S3} =============== Globally, 70% of the human population is estimated to be HSV1 seropositive ([@B57]). Once adaptive immunity against HSV1 is generated, it is believed that HSV1-specific antibodies could exist in the serum at high titer throughout human life and effectively prevent infection ([@B58]), which is consistent with the rarity of recurrent HSV1 infection in immune competent populations even though repetitive HSV1 exposure occurs often. NK cells express CD16a and are the major effector cells of ADCC ([@B59]). CD16a is a type I transmembrane protein, whose extracellular domain binds Fcγ at the hinge region ([@B60]) and whose transmembrane helix and intracellular domain couple with the signal transducer CD3ζ ([@B61], [@B62]). NK cells utilize CD16a to recognize antibody-bound pathogens, including infected cells. Binding of immune complex consequently clusters and phosphorylates CD3ζ and eventually leads to the activation of the NK cell and lysis of infected cells (Figure [2](#F2){ref-type="fig"}A) ([@B63]). ![The role of IgG in modulating natural killer (NK) cell function. **(A)** An HSV1-specific antibody binds to a specific viral antigen and activates CD16a(+) NK cells through classical antibody-dependent cell-mediated cytotoxicity (ADCC). **(B)** It has been proposed that antibodies directed against herpes simplex virus type 1 (HSV1) antigens could from a bipolar bridge between a specific viral antigen and the HSV1 IgGFc-binding glycoprotein glycoprotein E (gE), thereby preventing ADCC ([@B64]). **(C)** Endocytosis of viral antigens mediated by the hypothetical antibody bipolar bridge. **(D)** During primary HSV1 infection, non-immune IgG dominates while a primary immune response is being generated. In this setting, non-immune IgG can directly bind gE *via* its interface with the CH2--CH3 region of IgG. **(E)** gE-specific antibody can bind gE *via* its IgG Fab and prevent gE from binding another IgG at its CH2--CH3 region. **(F)** HSV1 infection produces large amounts of viral antigens of which gE accounts for only a small fraction. Thus, only a small fraction of the total HSV1-specific IgG can potentially form the bipolar bridge on the HSV1-infected cell.](fimmu-09-00183-g002){#F2} Antibody Bipolar Bridging {#S3-1} ------------------------- Herpes simplex virus type 1 expresses an IgGFc-binding protein glycoprotein E (gE), which binds human IgG1, IgG2, IgG4, but not IgG3. HSV1 gE alone binds Fc of IgG with low affinity, however, it can form a heterodimer with glycoprotein I (gI) ([@B65]). Although gI has no direct contact with IgG, the gE--gI complex binds Fc with much higher affinity than gE alone ([@B66], [@B67]). HSV1 gE--gI complexes have been shown to participate in "antibody bipolar bridging," whereby a single anti-HSV1-specific IgG antibody simultaneously binds to an HSV1 antigen using its Fab region and to gE *via* its Fc region (Figure [2](#F2){ref-type="fig"}B) ([@B64]). It has been proposed that such antibody "bipolar bridging" could block the access of the NK cell's CD16a to the Fc portion of the anti-HSV1-specific IgG antibody ([@B68], [@B69]), and induce endocytosis of viral antigens (Figure [2](#F2){ref-type="fig"}C) ([@B70]). Therefore, antibody bipolar bridging was proposed to reduce classical ADCC and provide a mechanism for innate immune evasion following HSV1 infection ([@B68], [@B69]). Although the antibody bipolar bridge has been tested in several experiments ([@B68], [@B69]), its existence and role in inhibiting ADCC *in vivo* remains controversial for several reasons. First, HSV1-specific antibody only accounts for a small fraction of the whole human IgG pool ([@B20]). The probability of gE to bind a predominant non-HSV1-specific IgG molecule is much greater than the probability of gE interacting with an HSV1-specific antibody that is already bound on the same infected cell, even without considering the steric hindrance that might not favor the forming of such bipolar bridge (Figure [2](#F2){ref-type="fig"}D). Second, gE is a major HSV1 antigen and gE-specific antibodies exist in most HSV1 seropositive serum. The gE-specific antibodies use Fab to bind gE and potentially block gE interaction with the IgGFc of other antibodies (Figure [2](#F2){ref-type="fig"}E). Third, gE constitutes only a small portion of all viral antigens that express HSV1-infected cells and HSV1-specific antibodies coated on HSV1-infected cells far outnumber all that gE could bridge (Figure [2](#F2){ref-type="fig"}F). Therefore, the bipolar bridge of IgG and gE, even if it existed, should not contribute significantly enough to reduce ADCC of HSV1-infected cells in a seropositive individual. Lastly and most importantly, the crystal structure of the gE-IgG1Fc complex shows that gE binds IgG1Fc at the CH2--CH3 interface, a site that is distinct from the Fcγ hinge region where CD16a binds ([@B71]). Therefore, HSV1 gE and CD16a are not mutually excluded from binding the same IgG, and the assumption that gE could prevent CD16a from binding the same IgG molecule is without structural basis (Figures [3](#F3){ref-type="fig"}A,B). {#F3} Fc-Bridged Cell-mediated Cytotoxicity (FcBCC) {#S3-2} --------------------------------------------- Instead of inhibiting NK cell cytotoxicity, we recently reported that the expression of the Fc-binding protein gE on HSV1-infected glioma cells actually stimulated NK cell activation and cytotoxicity, and co-expression of gE and gI further enhanced NK cell activation. Primary human NK cells are naturally coated with IgG molecules, and we found that the response of human NK cells toward gE or gE--gI directly correlated with the individual's NK cell surface density of IgG ([@B47]). Further, as noted earlier, the crystal structure of the gE-IgG1Fc complex showed that gE binds IgG1Fc at its CH2--CH3 region, a site that is distinct from the Fcγ hinge region, where CD16a binds ([@B71]). We, therefore, proposed that HSV1 gE, IgGFc, and CD16a could form a ternary complex (Figures [3](#F3){ref-type="fig"}A,B). The gE-IgGFc-CD16a complex was confirmed and responsible for relaying the activating signal for NK cells upon encounter with HSV1-infected glioma cells in the absence of specific anti-HSV1 antibodies ([@B47]). Although HSV1 gE does not bind mouse IgG ([@B72]), mouse NK cell FcγR (CD16a) binds human IgG with high affinity ([@B36]). This led us to test whether human IgGFc alone could bridge mouse NK cells and HSV1-infected cells, and promote clearance of HSV1 infection *in vivo*. We found infusion of human IgG1Fc fragments alone protected mice from lethal HSV1 infection in a manner dependent on NK cells and gE, as did other human IgG1 therapeutic antibodies not targeting any HSV1 antigens ([@B47]). It is well established that protective functions of IgG against infection and cancer require utilization of both its Fab and Fc domains. NK cell activation *via* gE-IgGFc-CD16a differs from the classical IgG function of ADCC by not requiring any antigen-specific antibody, and limits virus infection before the establishment of adaptive immunity. We thus named this process of innate immune recognition FcBCC (Figure [3](#F3){ref-type="fig"}B). Fc-bridged cell-mediated cytotoxicity represents a previously unappreciated mechanism of innate immune cell recognition of and response to a primary viral infection mediated only by the Fc domain of IgG bound to FcγR and recognizing the pathogen expressing an Fc binding protein, as well as naked CD16a recognizing the Fc domain of IgG bound to the infected cell's Fc-binding protein. The experimental evidence for FcBCC is consistent with the observation that most primary HSV1 infections are clinically asymptomatic and/or self-limited. It is also highly likely that FcBCC is responsible for the rapid NK cell clearance of oncolytic HSV1 in the setting of malignant glioma ([@B73]), and clearance of infection by many other members of the herpesviridae family encoding similar or identical Fc-binding proteins ([@B37], [@B69]). FcBCC of HSV1-infected glioma by CD16a(+) NK cells is abrogated in the absence of the HSV1 binding protein gE ([@B47]). Previous studies suggesting that NK cell activation is enhanced in the absence of HSV1 gE were all conducted in the presence of anti-HSV1 antibodies ([@B64], [@B68], [@B69]); the caveats of the conclusions drawn from those studies were discussed above and illustrated in Figures [2](#F2){ref-type="fig"}D--F. It is possible that the anti-HSV1 antibodies induce endocytosis of viral antigens in a gE--gI dependent fashion ([@B70]), thereby reducing NK cell activation *via* classical ADCC. Under this circumstance, the absence of HSV1 gE would inhibit the endocytic process, resulting in more surface expression of viral targets and consequently improved classical ADCC. Conclusion and Future Directions {#S4} ================================ Natural killer cell recognition of HSV1 infection is the synergistic result of multilayer activating and inhibiting signals, involving soluble factors, contact signals, and IgG molecules. IgG plays the central role for recognition and clearance of HSV1 infection by NK cells during both primary and recurrent infection. During primary infection, non-immune IgG can coat infected cells *via* the interaction of IgGFc with gE and facilitate clearance of HSV1 infection by CD16a(+) NK cells through FcBCC. Once adaptive immunity is established, HSV1 infection is recognized and bound by HSV1-specific IgG and cleared by NK cells through classical ADCC. It is relatively less studied how other contact signals contribute to the NK cell activation. It is technically challenging to dissect the contribution of individual viral components to evade or activate NK cell recognition, because (1) these viral components may only exert the effect in special host cells, at particular stages of infection, and dependent on the strain of HSV1 virus; (2) they share redundancies in shaping the function of NK cells; thus removing one would not be enough to show the difference in affecting NK cell function; (3) multi-functional nature of many viral proteins makes it difficult to compare data acquired from wild type HSV1 viruses with those from gene-specific deficient HSV1 viruses, because loss of viral genes may change not only the phenotype related to interactions with NK cells, but may also impact the virus' replication and life cycle. HSV1 is a human pathogen and patients with NK cell deficiency almost always develop severe HSV1 infections. So, a better way to study the interaction of HSV1 infection and NK cells is to look into the molecular basis of the deficiency causing the patient susceptibility for HSV1 infection. This will help expand our knowledge about NK cells beyond HSV1 infection. Author Contributions {#S5} ==================== HSD and MAC jointly wrote the paper and drew the figures. Conflict of Interest Statement {#S6} ============================== A provisional patent for Fc-bridged cellular-mediated cytotoxicity has been filled by the authors with the US patent office: U.S. Application No. 62/452,111_T2017-083. The reviewer FC and handling editor declared their shared affiliation. **Funding.** HD was a Pelotonia fellow. Research in MC lab was supported by NIH grant P01CA163205, P01CA095426, CA210087, CA068458, and CA185301. [^1]: Edited by: Jeffrey S. Miller, University of Minnesota, United States [^2]: Reviewed by: Frank M. Cichocki, University of Minnesota Twin Cities, United States; Stephen K. Anderson, National Cancer Institute at Frederick, United States [^3]: Specialty section: This article was submitted to NK and Innate Lymphoid Cell Biology, a section of the journal Frontiers in Immunology | Mid | [
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Opaque, white steam trailing behind loud trucks were a routine sight in many a childhood around the world. In South Korea, too, trucks would wail out siren sounds while emitting disinfectants and children would chase after the trucks through narrow alleyways, breathing in the foul-smelling gas. Used as a pesticide against mosquitoes and larvae, as well as a general means to prevent infectious disease, these disinfectants have remained a regular part of national public health measures since the mid-1900s. But within the past decade, these trucks have become increasingly difficult to catch in the streets of South Korea. A video posted by a South Korean user, chasing after a disinfecting truck (Source: YouTube) Traditional smoke disinfectant is effective in its ability to rapidly disinfect large areas. And its explicitly loud, smoke-spewing nature does more than give young children something fun to do — according to the Gwangjin-gu Public Health Center in Seoul, one of its advantages is that “its visible nature leads to citizen support.” But smoke disinfectant — made by diluting kerosene or heavy oil with insecticide and sprayed with a heater — affects an unpredictable radius. This can lead to unexpected health risks to residents in nearby housing areas, according to a 2015 Ministry report from the Ministry of Health and Welfare. Smoke disinfectants include chemicals dangerous to the environment. For example, when oils are not completely combusted, the resulting solution contains volatile compounds such as belen, toluene and other carcinogens that can be harmful to both people and the environment. Just last year, Busan, South Korea’s second largest city with a population of three million, announced efforts to increase environmentally friendly solutions with an investment of 500 million won, according to daily newspaper Busan Ilbo. While the traditional disinfectant is still necessary for hard-to-access areas such as sewers, the ultimate goal is to reduce the use of smoke disinfectant from 72 to 25 percent. Citizens and governmental agencies have become more cognizant of potential dangers, calling either for a ban or changes to trucks spraying disinfectant gases. The Ministry of Health and Welfare said that it recommends, instead of excessive smoke disinfectant, spray methods or targeting larvae before they develop. With new technologies and increased health concerns, the nostalgia-inducing images of smoke trailing behind a blaring truck are surely becoming much more of a rarity. But that doesn’t mean they’ve stopped entirely, nor will they any time soon. In 2005, daily newspaper Hanykoreh reported that of 246 public health centers across the country, 239 — practically all of them — were using smoke disinfectant. Seven years later, Hankoyreh conducted another similar study (although this time with far fewer centers) and found that 23 out of 36 public health centers contacted across the country still planned to use smoke disinfectant. Though the traditional oil-based smoke disinfectants are far from extinct, many of the centers in the recent study are showing efforts, such as water-based solutions, to become more environmentally friendly. And as public health centers seek out new, safer mixtures, in response to rising public awareness about the possible dangers of these trucks, health measures are shifting — from what was once an explicit, loud display of communal cleaning into a humbler national effort to do the same job but maybe in a safer way. Cover image: Though less common now, mosquito trucks spewing disinfectant smoke have long been a common sight in South Korea. (Source: YouTube) | Mid | [
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Q: Some times not able to login into my system after I do remote desktop from other system If I do remote desktop on my system from others computer, sometimes it is not allowing me to login into my system (directly), though I have closed my remote desktop session. I am using windows XP professional with service pack 3. A: This the problem with the OS image which are provided in my company and it got resolved in the latest image. Save the below contents as screensaver.reg and double click to resolve the issue. Windows Registry Editor Version 5.00 [HKEY_LOCAL_MACHINE\Software\Policies\Microsoft\Windows\Control Panel\Desktop] "ScreenSaveTimeOut"="300" [HKEY_CURRENT_USER\Software\Policies\Microsoft\Windows\Control Panel\Desktop] "ScreenSaverIsSecure"="1" "SCRNSAVE.EXE"="scrnsave.scr" "ScreenSaveActive"="1" "ScreenSaveTimeOut"="300" [HKEY_USERS\.DEFAULT\Software\Policies\Microsoft\Windows\Control Panel\Desktop] "ScreenSaveActive"="1" "ScreenSaverIsSecure"="1" "ScreenSaveTimeout"="300" "SCRNSAVE.EXE"="scrnsave.scr" [HKEY_LOCAL_MACHINE\SOFTWARE\Microsoft\Windows\CurrentVersion\policies\system] "NoDispScrSavPage"=dword:00000001 | Mid | [
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Brave Nuclear World? – First of Two Parts by Karen Charman ~ World Watch Magazine, May/June 2006 A few miles down an idyllic New England country road dotted with handsome homesteads and gentleman farms in central Connecticut sits the Connecticut Yankee nuclear power plant-or what's left of it. After shutting down in 1996, the 590-megawatt reactor is nearing the end of its decommissioning, a process spokesperson Kelley Smith describes as "construction in reverse." Most of the buildings, the reactor itself, and its components have been removed. Adjacent to the Connecticut River, the discharge pond, which received the reactor's second-stage cooling water from the internal heat exchanger, is being dredged. The soil, including hot spots near the reactor that were contaminated with strontium-90 from leaking tanks, has been replaced. Forty concrete casks of highly radioactive spent fuel now sit on a fenced and guarded concrete pad surrounded by woods on the company's property about three-quarters of a mile from the reactor site. Soon the spent fuel pool that housed the irradiated fuel assemblies will be drained and dismantled. A twisted spaghetti-like tangle of metal protruding from a partially demolished building will be carted off to a dump site. Stories-high stacks of steel containers packed with mildly radioactive rubble are also waiting to be taken away. One of the final tasks will be to demolish the containment dome, which consists of 35,000 metric tons of steel-reinforced concrete. When decommissioning is completed by the end of the year, over 136,000 metric tons of soil, concrete, metal, and other materials will have been removed from the site at a cost of more than US$400 million to the area's electricity customers. But for a fluke in timing, Connecticut Yankee might well have remained in operation today. Ten years ago, when the board of directors of the Connecticut Yankee Atomic Power Company decided to close its reactor at Haddam Neck, nuclear power was widely considered, if not a dying industry, then one that was seriously and chronically ill. In the newly deregulated electricity market, the company found it could buy electricity for less than its nuclear power plant could produce it. Connecticut's deregulation of the electricity sector required the company to divest itself of the plant. Company directors didn't think they could sell a single reactor of relatively low capacity, so they decided to shut it down. Just a few years later, the economic landscape for nuclear power began changing with the emergence of companies like Exelon Corporation (a merger between Chicago-based Commonwealth Edison and Pennsylvania-based PECO) and the Louisiana-based Entergy Corporation, which began buying up reactors. Entergy purchased Vermont Yankee, a 540-megawatt reactor, for US$180 million in 2002. Less than 80 kilometers south of Connecticut Yankee, Dominion Resources spent US$1.3 billion to acquire three reactors (two operating and one shut) at Millstone-a plant with the dubious distinction of landing on the cover of Time in 1996 for longstanding, egregious breaches of safety regulations. By 2002, just 10 corporations owned all or part of 70 of the nation's 103 operating reactors. Fast forward to today. The world has begun to wake up to the very real and growing perils of human-induced, catastrophic climate change. The war in Iraq, increasing tension in the oil-rich Middle East, and memories of both the (market-manipulated) energy fiasco in California in 2001 and the blackout that affected one-third of the United States and Canada in August 2003 have raised awareness and anxiety about unstable, unsustainable energy supplies. These factors, along with a very skillful, multi-pronged public relations and lobbying campaign, have put nuclear power, which is touted as carbon-free, back on the table. According to the International Atomic Energy Agency (IAEA), nine new nuclear plants-three in Japan, two in Ukraine, and one each in South Korea, India, China, and Russia-have gone online since 2004. In that time, two plants in Canada were restarted after years of not operating, and there is talk of building a new reactor there. Currently 23 nuclear power plants are under construction around the world, including one in Finland, the first in western Europe since the 1986 explosion at Chornobyl in northern Ukraine. France, whose 58 reactors provide approximately 80 percent of that country's electricity, is also considering building another reactor, and British Prime Minister Tony Blair is calling for new reactors to replace Britain's aging fleet of 31 reactors, most of which are due to retire by 2020. In August 2005, U.S. President George W. Bush signed into law an energy bill that contained US$13 billion in public subsidies to help jumpstart a new generation of nuclear reactors. Nuclear Power vs. Global Warming A growing chorus of nuclear advocates, government officials, international bureaucrats, academics, economists, and journalists is calling for nuclear power to save us from devastating climate change. Nuclear reactors do not emit carbon dioxide (CO2) and other greenhouse gases when they split atoms to create electricity. But it's inaccurate to say that nuclear power is "carbon-free"-on a cradle-to-grave basis, no currently available energy source is. (Even wind turbines are guilty by association: the aluminum from which they are built is often smelted using coal-fired electricity.) In the case of nuclear power, fossil fuel energy is used in the rest of the nuclear fuel chain-the mining, milling, and enriching of uranium for use as fuel in reactors, the building of nuclear plants (especially the cement), the decommissioning of the plants, the construction of storage facilities, and the transportation and storage of the waste. In fact, the gaseous diffusion uranium enrichment plant at Paducah, Kentucky, is one of the single biggest consumers of dirty coal-fired electricity in the country. Still, it seems impossible to pin down exactly how carbon-intensive the nuclear fuel chain is, and there is disagreement within the environmental community about nuclear energy's potential contribution to global warming. Tom Cochrane, a nuclear physicist with the Natural Resources Defense Council, says nuclear power is not a large greenhouse gas emitter compared to other conventional sources of energy. But in order for nuclear energy to make a significant dent in greenhouse gas emissions, we would need a huge increase in the number of nuclear power plants now operating worldwide, which he does not support. Just how huge? A widely quoted 2003 report by Massachusetts Institute of Technology researchers, "The Future of Nuclear Power," calls for the construction worldwide of 1,000-1,500 new 1,000-megawatt reactors by 2050, an expansion that would potentially displace 15-25 percent of the anticipated growth in carbon emissions from electricity generation projected over that time. A 2004 analysis in Science by Stephen Pacala and Robert Socolow, co-directors of Princeton University's Carbon Mitigation Initiative, says 700 gigawatts of new nuclear generation-roughly double the number and output of the world's 443 operating reactors-would be needed to achieve just one-seventh of the greenhouse gas emission reductions (at current emission rates) required to stabilize atmospheric carbon concentrations at 500 parts per million (ppm). The MIT report acknowledges such an expansion would create an enormous nuclear waste challenge requiring a permanent disposal site with the capacity of the proposed repository at Yucca Mountain in Nevada "to be created somewhere in the world every three to four years." If the spent fuel were reprocessed instead, as many nuclear proponents advocate, it would dramatically increase opportunities to spread nuclear material that could be used in making atomic bombs. The MIT report rejects reprocessing as uneconomic and, because of the weapons proliferation dangers, unnecessarily risky. To deal with the waste, it calls for the U.S. Department of Energy to develop "a balanced long-term waste management R&D program" and investigate the possibility of placing the waste in deep geologic boreholes. It also recommends the establishment of a network of centralized facilities in the United States and internationally that can store spent fuel for several decades until better solutions are worked out. Of course, the policy landscape is strewn with technically plausible recommendations that were dead on arrival because they glibly ignored the difficult politics of nuclear energy. Pacala and Socolow maintain that a range of options is needed to address climate change. They identify 15 technologies or practices now in commercial operation somewhere in the world and say that scaling up any seven of them could stabilize carbon emissions over the next 50 years. These alternatives will be more fully explored in Part II of this series. Nukonomics "Nuclear Follies," a February 11, 1985 cover story in Forbes, declared the United States' experience with nuclear power "the largest managerial disaster in business history." With US$125 billion invested, the magazine wrote, "only the blind, or the biased, can now think that most of that money has been well spent. It is a defeat for the U.S. consumer and for the competitiveness of U.S. industry, for the utilities that undertook the program and for the private enterprise system that made it possible." Yet nuclear power is now widely promoted as one of the most economical sources of electricity, with a production cost of 1.68 cents per kilowatthour (kWh), compared to 1.9 cents/kWh for coal, 5.87 cents/kWh for natural gas, 2.48 cents/kWh for solar, 0.2 cents/kWh for wind, and 0.5 cents/kWh for hydroelectric, according to the Electric Utility Cost Group, a data group within the nuclear industry that draws its information from plant surveys, and Global Energy Decisions, a private energy data consulting firm. Those figures measure the operating cost of fuel, labor, materials, and services to produce one kWh of electricity. But like most sources of energy, nuclear power benefits from substantial government subsidies. Including nuclear's subsidies, collateral costs, and externalities leads to a different economic assessment.* Although a full nuclear revival with a new generation of reactors to replace the existing fleet could not take place-at least in the United States-without the participation of the private sector, commercial nuclear power has never had to compete in a true free market. From the beginning, nuclear power worldwide has always required government patronage. In the United States, the industry was launched in 1946 with the passage of legislation creating the Atomic Energy Commission (the predecessor to the Nuclear Regulatory Commission, or the NRC), which was charged with developing both civilian nuclear power and nuclear weapons. In 1954 the government brought the private sector in, and under President Dwight D. Eisenhower's "Atoms for Peace" initiative continued to encourage the development and commercialization of nuclear power. Although nuclear power currently provides about 20 percent of U.S. electricity (and about 16 percent of the world's), between 1950 and 1993 the U.S. nuclear power industry received nearly 50 percent of the total federal spending on energy research and development-some US$51 billion-according to energy economist Doug Koplow. Substantial government assistance appears to be the status quo for the nuclear industry around the world, he adds, though specific data from many countries is unavailable. Nuclear power continues to get favored treatment, with government assistance covering virtually all segments of the nuclear fuel chain to one degree or another. Uranium mining companies operating in the United States, for example, get a "percentage depletion allowance" of 22 percent (the highest rate of all depletion allowances for minerals), which gives them a tax write-off for the market value of what they have extracted-a significant subsidy since the write-off is typically much greater than their actual investment. The manufacture of the reactor fuel has also been heavily subsidized. Until 1998, the government owned the country's two uranium enrichment plants. When they were privatized into the U.S. Enrichment Corporation, the government retained liability for the waste clean-up associated with the operation of the facilities, an ongoing endeavor with a price tag in the billions. During construction of the reactors, utilities were able to pass on the interest costs of the loans to their electricity customers, utilizing the "Allowance for Funds Used During Construction." While this was available to all types of power plants, Koplow says it mainly benefited owners of nuclear plants, because costs on the already expensive plants ran out of control with construction delays. Nuclear plant owners also took advantage of highly accelerated depreciation and investment tax credits in the early 1980s. Koplow says these three accounting mechanisms significantly reduced the capital costs of the reactors. Even so, after states began deregulating electricity markets in the 1990s, utilities with nuclear plants found they needed to charge much more than the going rate for electricity to pay off their remaining debt, or "stranded costs," and stay competitive with other electricity sources. State after state changed the rules to allow utilities to pass on these stranded costs to ratepayers as a surcharge on their electric bills, a gift to the nuclear industry that by 1997 was worth some US$98 billion. The ratepaying public also bears the cost of dealing with the spent fuel-estimated at US$60-100 billion for the existing fleet of reactors-as well as for decommissioning the plants. And if there is another serious accident, the 1957 Price-Anderson Act shields nuclear plant owners from the lion's share of the cost by capping their liability. According to Koplow, the utility responsible for the accident would pay US$300 million in primary liability plus US$95.8 million that it and the nation's other nuclear utilities would contribute per reactor (paid in US$15-million annual installments over six years) to an insurance pool. With 103 operating U.S. reactors, the size of the insurance pool is approximately US$10 billion. By comparison, some estimates put the cost of the Chornobyl accident at over US$350 billion, and the Union of Concerned Scientists estimates that a serious accident at New York's Indian Point plant 56 kilometers north of New York City would be in the trillions-costs mainly left to individuals because of the standard nuclear exclusion clause in home insurance policies. Without this particular liability mitigator in the United States and similar instruments in other countries, commercial nuclear power probably would not exist. Moreover, it seems that Price-Anderson is not the only mechanism available to nuclear utilities to protect themselves from full liability if something goes wrong. According to a 2002 report by Synapse Energy Economics, Inc., since the restructuring of the U.S. nuclear industry began as states started deregulating their electric utility industries in the mid-1990s, a few large corporations such as Exelon Corp., Entergy Corp., Duke Energy, and Dominion Resources, Inc. increasingly own and operate nuclear power plants through multi-tiered holding companies. The individual plants are often set up as limited liability companies (LLCs), a legal invention that restricts liability to the assets directly owned by the LLC. "The limited liability structures being utilized are effective mechanisms for transferring profits to the parent/owner while avoiding tax payments," the report notes. "They also provide a financial shield for the parent/owner if an accident, equipment failure, safety upgrade, or unusual maintenance need at one particular plant creates a large, unanticipated cost. The parent/owner can walk away by declaring bankruptcy for that separate entity without jeopardizing its other nuclear and non-nuclear investments." This arrangement is especially valuable under deregulation. Before deregulation, nuclear reactors typically were built by investor-owned utilities and operated under the shelter of a "cost-of-service regulation." This enabled the utilities to enjoy stable rates based on their actual costs rather than on electricity sales at market prices, which can fluctuate. With those stable rates stripped away, the usual risks of operating nuclear plants-unexpected shutdowns for nonscheduled maintenance, for instance, or even accidents-became more severe. The use of LLCs allowed much of that risk to be avoided. Yet, according to former NRC commissioner Peter Bradford, the agency failed to develop a comprehensive policy to ensure that the transfer of reactor ownership into these new corporate structures would not endanger the public. "In the absence of any such requirement, public protection has depended on the acumen of a Nuclear Regulatory Commission unversed in financial matters and of economic regulators unversed in health and safety issues. As has happened in financial and in utility restructuring circles, fundamental safeguards have been circumvented," he writes in the forward to the Synapse report. The consequences, he adds, remain to play out. The NRC rejects both Synapse's and Bradford's allegations. In a written statement, the agency said it believes its regulations "provide reasonable assurance that a licensee will have sufficient resources to operate, maintain, and decommission nuclear power reactors. The NRC fully considered the issues raised in the 2002 Synapse report and believed then-and continues to believe-that our regulations adequately address LLCs or other corporate arrangements." The agency maintains that regardless of the new business arrangements, it continues to ensure that reactor owners meet their obligations, adding that most reactors also operate under regulation by state public utility commissions, which provide significant financial oversight. "Their general platitudes don't convince me that we were wrong on any issue," says David Schlissel, lead author on the Synapse report. In addition, he says NRC is incorrect that state public utility commissions continue to oversee reactors in states where electricity markets have been deregulated. "The 19 plants owned by Exelon, they are all deregulated," he says, "as are many nuclear plants in the Northeast and Midwest." Try, Try Again On Valentine's Day in 2002, the U.S. Department of Energy unveiled its Nuclear Power 2010 program for sharing costs with industry to "identify sites for new nuclear power plants, develop and bring to market advanced nuclear plant technologies, evaluate the business case for building new nuclear power plants, and demonstrate untested regulatory processes leading to an industry decision in the next few years to seek NRC approval to build and operate at least one new advanced nuclear power plant in the United States." Currently three consortia, an 11-company group called NuStart Energy Development and smaller ones led by the Tennessee Valley Authority and Dominion Resources, have been formed to investigate building new reactors. Despite consortia members' combined revenues of US$447 billion during 2003-which, Koplow points out, rivals the Russian Federation and exceeds the combined GDP of 104 countries-the U.S. government is now offering the nuclear industry additional incentives worth more than US$13 billion as seed money for new nuclear plant construction. According to an analysis released last year by the non-profit group Public Citizen, the Energy Policy Act of 2005 includes US$2.9 billion for R&D, at least US$3.5 billion worth of construction subsidies, more than US$5.7 billion for operating subsidies, and US$1.3 billion for shutdown subsidies. Some of the package's more notable elements include US$2 billion for risk insurance, which allows builders of the first six reactors to collect for any delays in construction or licensing, including challenges by the public on safety grounds (e.g., if a whistleblower reported faulty construction and a citizen group sued). It includes production tax credits of 1.8 cents per kilowatthour for eight years, an estimated US$5.7-7.0 billion that would otherwise go to the U.S. Treasury. There are also provisions for taxpayer-backed loan guarantees for up to 80 percent of the cost of a reactor. These loan guarantees are particularly handy, considering that billions of dollars were lost during the first round of nuclear plant construction when more reactors were cancelled than were built, many after hundreds of millions of dollars had already been spent. That's a big handout, but it remains to be seen whether it's enough to kick-start a new generation of reactors in the United States, which industry observers say is necessary for a viable economic future for nuclear power. Thomas Capps, the recently retired CEO of Dominion Resources, head of one of the consortia seeking a license for a new reactor, told the New York Times last April that if his company announced it was actually going to build a nuclear plant, debt-rating agencies Standard & Poor's and Moody's "would have a heart attack, and my chief financial officer would, too." Peter Wells, general manager of marketing for General Electric's nuclear energy division, is cautiously optimistic but not yet convinced a new generation of reactors will be built. He says it will depend on friendly government policy and positive experience with the first of the new reactors coming in within budget and on schedule. Bush Administration policy is increasingly agreeable to the nuclear industry, but whether reactors can be built for their advertised costs is another question. At US$1,500 per kilowatt, the new "advanced" Generation III+ reactors are said to be much cheaper than those in the existing fleet. According to a 2001 Congressional Research Service (CRS) report on the prospects for new commercial nuclear reactors, total construction costs exceeded US$3,000/kw for reactors that were started after 1974, and those completed since the mid-1980s averaged US$3,600/kw. Anyone familiar with Pentagon procurement gaffes knows that chronic overruns and miscalculation of costs has been a longtime problem with large engineering projects, and the nuclear power industry is no exception. According to an analysis by the Energy Information Administration, plants that began construction between 1966 and 1977 underestimated their actual costs by roughly 14 percent, even when plants were 90 percent complete. So far, only two reactors of new design, both of them GE Advanced Boiling Water Reactors, have been built (in Japan, for the Tokyo Electric Power Company). However, despite GE's estimate that the cost would be US$1,528/kw, CRS reports the first came in at US$3,236/kw and the second at around US$2,800/kw. Wells says the price of those plants was inflated because they were "gold-plate plants with marble floors and the like" that otherwise would have cost much less. Peter Bradford says that despite the passage of the Energy Policy Act, nothing has fundamentally changed that would improve the economics enough to see a new generation of nuclear reactors. "With US$13 billion in new subsidies, if the government wants to prove that if it spends enough it can build nuclear plants, it can do that. The Chinese prove that for us a couple times a year," he said. "But that's not the same as saying it makes economic sense to do it." Still, Bradford acknowledges, "the stars have not been so favorably aligned for the industry since Atoms for Peace." In a dramatic turnaround from nuclear's dog days in the 1980s and ‘90s, excitement is building on Wall Street. Steven Taub, director of emerging technologies at Cambridge Energy Research Associates, is confident new plants will be built, though he says the exact number will depend on how the various government incentives are distributed. Unlike the current fleet of nuclear reactors-nearly all of which were custom built-the next generation will be much more standardized to take advantage of economies of scale. The government subsidies for new reactors are intended to offset the higher "first-of-a-kind" costs for the first few plants. If all goes without a hitch, the thinking is that lenders and utility shareholders will regain confidence that new nuclear plants can be competitive enough to finance without these subsidies. External factors will also determine the competitiveness and economic viability of nuclear power, Taub says. These variables include the price of natural gas, whether a carbon tax or other price-raising measures will be imposed on coal and other fossil fuels, and whether carbon sequestration technology for coal-fired power plants can be proven and widely adopted. "These are questions that nobody knows the answer to," he says. Part Two of this series looks at the waste problem, at the proliferation and other security risks stemming from nuclear power, and at the strength of arguments for nuclear power in the context of other options. Karen Charman is an independent journalist specializing in environmental issues and the managing editor of the journal Capitalism Nature Socialism. | Low | [
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Introduction {#sec1} ============ Myostatin (MSTN) can negatively regulate the growth and development of skeletal muscle. It is a member of the transforming growth factor β (TGF-β) superfamily of growth and differentiation factors \[[@B1],[@B2]\]. MSTN functions to inhibit excessive growth of muscle in order to maintain an overall balance of this tissue relative to adipose tissue \[[@B3]\]. Natural *myostatin* null animals, including cattle \[[@B4]\], dogs \[[@B5]\], humans \[[@B6]\], and sheep \[[@B7]\], shows a dramatic and widespread increase in skeletal muscle mass; namely, a 'double-muscling' phenomenon. Since its discovery in mice \[[@B8]\], *MSTN* has been extensively investigated in other animals. A large number of variants have been identified in cattle, most of which are silent or neutral. Two of the variants in the third exon strongly affect the 'double-muscling' phenotype in Belgian Blue cattle \[[@B9]\]. An 11-bp deletion at the bovine *myostatin* nucleotide 821 \[nt821(del11)\] in the coding region results in a frameshift mutation. Also, in Piedmontese cattle \[[@B4]\], a G to A transition at nucleotide 938 results in the substitution of cysteine by tyrosine (this mutation is referred to as C313Y). It has been shown that an 11-bp deletion \[nt821(del11)\] in the *myostatin* gene results in a truncation of the bioactive carboxyterminal domain of the protein \[[@B9],[@B10]\]. In addition, the C313Y mutation predicts the replacement of cysteine at amino acid 313 with tyrosine. This cysteine is the fifth in a series of nine whose appearance and spacing is extremely conserved among TGF-β family members \[[@B2],[@B4]\]. These two mutations remove the portion of the myostatin protein that is most highly conserved among TGF-β family members. The rabbit *myostatin* gene consists of three exons and two introns. The third exon of the rabbit *myostatin* gene codes for mature processed myostatin, which is the active region of the molecule and shares extensive homology with other TGF-β members \[[@B2],[@B11]\]. Similar to other TGF-β family members, three kinds of proteins are translated by *myostatin*: a precursor protein consisting of an N-terminal signal sequence; a propeptide domain; and a growth factor domain that contains the characteristic cystine-knot motif (C272--C282, C281--C340, C309--C372, and C313--C374). C339 forms the intermolecular dimerization disulfide bond \[[@B12],[@B13]\]. The C313Y mutation removes the C313-containing disulfide bond, an integral part of the characteristic TGF-β cystine-knot structural motif. Some research has suggested that the cystine-knot motif, which is essential for myostatin structural stability and covalent dimerization, is required for receptor-mediated signaling by myostatin growth factor *in vivo*, with its absence leading to a double-muscled phenotype ('double-muscling') \[[@B14]\]. Hence, it is feasible to prepare a rabbit model of myostatin using the knockout cystine-knot motif. Previous studies have reported that *MSTN* naturally mutant cattle generally show a 20−40% increase in muscle weights due to muscle hypertrophy or hyperplasia relative to wild-type (WT) cattle \[[@B15]\]. This is consistent with a report that found that individual muscle fibers of homozygous *MSTN*-KO mice (*MSTN*^−/−^ mice) produced by the homozygous deletion of the C-terminal region of the *myostatin* gene in embryonic stem cells were double or triple in mass compared with those of their heterozygous and WT littermates \[[@B2]\]. Some research has reported that the masseter and temporalis muscles of *MSTN^−/−^* mice were over 50% larger in mass than WT controls due to larger cross-sections of the muscle fibers and increased numbers of muscle cells \[[@B2],[@B16]\]. Therefore, *MSTN^−/−^* mice were used to explore the effects of increased muscle mass on sagittal suture complexity. The mice were also used to indicate that a consistent amount of force needs to be applied over a much greater area of the craniofacial skeleton in the *myostatin* knockout, and this should, in turn, lead to altered biomechanical stress and bony morphology \[[@B3],[@B16]\]. An *MSTN^−/−^* mouse has significantly larger temporalis, masseter, and medial and lateral pterygoid muscles than WT controls \[[@B17]\]. These characteristics, coupled with morphologic findings of the skull in *MSTN^−/−^* mice (e.g., shorter crania, longer, and rounder mandibles), provide further evidence of an altered craniofacial loading environment due to *MSTN* deficiency \[[@B3],[@B16]\]. Therefore, these *MSTN*-KO mice have been used as a model for studying muscle--bone interactions, such as to investigate the role of increased mandibular elevators and bite forces on temporomandibular joint morphology. In the past 5 years, many *MSTN*-KO animals (e.g., pigs, goats, sheep, and rabbits) with 'double-muscling' have been generated due to the emergence of the CRISPR/Cas9 gene editing technique as a newly versatile genome engineering tool \[[@B21]\]. However, the morphology and the muscle--bone interactions of these *MSTN*-KO animals have rarely been investigated. The aim of the present study is to generate *MSTN*-KO rabbits using the CRISPR/Cas9 system anchored to the cystine-knot motif by microinjecting Cas9 mRNA and sgRNA into fertilized rabbit eggs. The *MSTN*-KO rabbits can be used as a basis to create new breeds of rabbit to improve muscle yield, with the ultimate goal of approval for human consumption. In addition, an important animal model is proposed for use in further studies that investigate muscle--bone interactions. Results {#sec2} ======= CRISPR/Cas9 expression plasmid construction and *in vitro* transcription {#sec2-1} ------------------------------------------------------------------------ To produce gene-modified New Zealand white rabbits with double-muscling, two sites that are associated with the cystine-knot motif in the *MSTN* rabbit gene were selected as target genes ([Figure 1](#F1){ref-type="fig"}A,B). The sgRNA-1 anchors the *MSTN* gene site that encodes C372, and the sgRNA-2 anchors the *MSTN* gene site that encodes C339 and C340. {#F1} Generation of *MSTN*-KO rabbits using the CRISPR/Cas9 system {#sec2-2} ------------------------------------------------------------ In the present study, a total of 48 injected zygotes were transferred into the oviducts of three surrogate rabbits. After full-term gestation, the three surrogate mothers successfully gave birth to 12 live pups ([Table 1](#T1){ref-type="table"}). ###### Summary of the production of *MSTN*-KO rabbits using CRISPR/Cas9 Targeting vector gRNA/Cas9 mRNA (ng/µl) Embryos transferred Pups obtained (% transferred) Mutation efficiency (% pubs) Biallelic-KO efficiency (% pubs) ------------------ ------------------------ --------------------- ------------------------------- ------------------------------ ---------------------------------- sgRNA-1 10/40 20 7/20 (35.00%) 7/7 (100%) 7/7 (100%) sgRNA-2 10/40 28 5/28 (17.85%) 4/5 (80.00%) 4/4 (100%) Genomic DNA was extracted from the ear tissue of the newborn pups. The 12 individuals used for genotyping were numbered M1−M12. The T-cloning and PCR-sequence results showed that the *MSTN* mutation was detected in 11 pups, and the indels ranged from 1 to 221 bp ([Figures 1](#F1){ref-type="fig"}C and [2](#F2){ref-type="fig"}A,B). The theoretical amino acid sequences of the *MSTN* knockout alleles are shown in [Figure 2](#F2){ref-type="fig"}C,D. In addition, fragment deletions between the two sgRNAs targeting sites were frequently observed in the present study. Here, only one rabbit (M10♀) harbored mutations in exon 3 of the *MSTN* gene that did not cause a frameshift mutation. Eleven rabbits (M1−M11) deleted C372 and C374, and four rabbits (M8−M11) deleted C339 and C340 in two alleles, C281--C340. M7♀ and M10♀ were homozygous, and both of them lost C372 and C374 in the cystine-knot motif. In addition, M10♀ also deleted C339 and C340. As shown in [Figure 2](#F2){ref-type="fig"}E,F, the structure of each protein differs from the WT for the cysteine delete (like C339, C340, C372, and C374). Five rabbits (M1♀, M2♂, M3♀, M5♀, and M7♀) deleted C272, C281, C282, C339, and C340. In the cysteines mentioned above, four cysteines formed two intramolecular disulfide bonds (C272−C282, C281−C340), and C339 was involved in intermolecular disulfide bond formation between two *MSTN* monomers. The typical phenotype of double-muscling was observed in F0 *MSTN*-KO rabbits at four months of age, and they were compared with their WT counterparts, as shown in [Figure 3](#F3){ref-type="fig"}A,B. To investigate whether gene mutations abolished the MSTN protein translation, Western blotting and immunofluorescence staining were performed. As shown in [Figure 4](#F4){ref-type="fig"}, the MSTN protein was significantly decreased in *MSTN^−/−^* and *MSTN^+/−^* rabbits compared with *MSTN^+/+^* counterparts. {#F2} {#F3} {#F4} Increased body weights in the *MSTN*-KO rabbits {#sec2-3} ----------------------------------------------- Rabbits experience an exuberant growth period from 2 to 3 months, so the body weights of the *MSTN*-KO rabbits and their WT counterparts were recorded from 9 to 14 weeks. It was found that the average body weights of male *MSTN*-KO rabbits were significantly higher than the male WT rabbits from 9 to 14 weeks of age ([Figure 3](#F3){ref-type="fig"}C). The average body weights of female *MSTN*-KO rabbits were significantly higher than the female WT rabbits from 11 to 14 weeks of age ([Figure 3](#F3){ref-type="fig"}D). Significant differences (\**P*\<0.05) from 10 to 14 weeks after birth were found between the *MSTN*-KO male rabbits and the WT male rabbits. Significant differences (\**P*\<0.05) were found between the *MSTN*-KO female rabbits and the WT female rabbits from 13 to 14 weeks after birth. At 14 weeks, the average body weights of the female (2318.40 ± 183.15 g) and male (2579.33 ± 67.99 g) *MSTN*-KO rabbits increased by 17.91 and 26.74%, respectively, compared with the female (female: 1966.20 ± 225.56 g) and male (2063.33 ± 186.47 g) WT rabbits, respectively. Heritability and breeding of the *MSTN*-KO rabbits {#sec2-4} -------------------------------------------------- The male founders (M2, M6, and M8) were mated with the female WT rabbits, and the female founders (M1, M3, M5, and M10) were mated with the male WT rabbits. Genomic DNA was extracted from the ear tissues of the F1 rabbits. PCR amplification and TA-cloning sequencing analysis showed that these F1 rabbits were monoallelic *MSTN*-KO rabbits. Then the same genotype of the F1 male and female rabbits was mated for homozygous mutants. The breeding results are shown in Supplementary Table S1. Off-target assay {#sec2-5} ---------------- A total of ten potential off-target (OT) sites (OTs, five for sgRNA1 and five for sgRNA2) were successfully amplified using PCR and subjected to Sanger sequencing. No overlapping peaks were detected near the OTs. Histological analysis {#sec2-6} --------------------- The *MSTN*-KO rabbits exhibited the double-muscled phenotype ([Figure 3](#F3){ref-type="fig"}A), and a histological examination of the gluteus maximus and tongue showed muscle fiber hypertrophy relative to the fibers of the WT rabbit ([Figure 5](#F5){ref-type="fig"}A). In [Figure 5](#F5){ref-type="fig"}B, the average size of the gluteus maximus myofibers in the *MSTN^−/−^* rabbits (3512.20 ± 439.17 μm^2^) was substantially larger than that of the *MSTN^+/+^* rabbits (1274.76 ± 327.30 μm^2^, *P*\<0.01). The average size of the gluteus maximus myofibers in the *MSTN^+/−^* rabbits (2610.37 ± 604.44 μm^2^) increased in comparison with the *MSTN^+/+^* rabbits (1274.76 ± 327.30 μm^2^, *P*\<0.05). Similarly, the average size of tongue myofibers in the *MSTN^−/−^* rabbits (2109.22 ± 206.75 μm^2^) was substantially larger than that of the *MSTN^+/+^*rabbits (989.39 ± 239.27 μm^2^, *P*\<0.01). The average size of tongue myofibers in the *MSTN^+/−^* rabbits (1677.24 ± 247.50 μm^2^) increased in comparison with the *MSTN^+/+^* rabbits (989.39 ± 239.27 μm^2^, *P*\<0.05). The distribution of different sizes of gluteus maximus and tongue myofibers indicates that the percentage of smaller fiber cells in the *MSTN*-KO rabbits was lower than the percentage in the WT rabbits ([Figure 5](#F5){ref-type="fig"}C,D). {#F5} Analysis of hematological and biochemical parameters {#sec2-7} ---------------------------------------------------- The hematological and biochemical parameters from 6-month-old *MSTN^+/+^, MSTN*^+/−^, and *MSTN*^−/−^ rabbits were analyzed. In [Figure 6](#F6){ref-type="fig"}, the levels of serum creatinine (CREA, 325.97 ± 18.92 μmol/l), serum creatine kinase (CK, 599.67 ± 13.79 U/l), and serum lipase (LIP, 343.17 ± 49.99 U/l) were increased in the *MSTN*^−/−^ rabbits compared with the *MSTN*^+/+^ rabbits (CREA, 243.17 ± 14.35 μmol/l; CK, 167.67 ± 24.83 U/l; LIP, 163.70 ± 12.24 U/l, *P*\<0.01). The levels of CREA (325.97 ± 18.92 μmol/l) and CK (599.67 ± 13.79 U/l) were increased in the *MSTN*^−/−^ rabbits compared with the *MSTN*^+/−^ rabbits (CREA, 267.10 ± 6.06 μmol/l; CK, 333.67 ± 52.54 U/l, *P*\<0.01). The levels of CK (CK, 333.67 ± 52.54 U/l) were increased in the *MSTN*^+/−^ rabbits compared with the *MSTN*^+/+^ rabbits (CK, 167.67 ± 24.83 U/l, *P*\<0.01). CREA is a product of muscle tissue metabolism in the body. Serum CK is related to the total amount of muscle. This means that the greater the muscle capacity, the higher the serum CK activity. Increased serum CREA and CK levels in the MSTN-KO rabbits should correlate with increased muscle mass. The serum CREA content reported for *MSTN*-KO Meishan pigs was also higher than that in WT pigs \[[@B25]\]. Interestingly, serum LIP was greater in the *MSTN*^−/−^ rabbits than that in the *MSTN*^+/+^ rabbits at 6 months of age. Further experiments are required to investigate this phenomenon in *MSTN*^−/−^ rabbits. There were no differences in the hematology characteristics and other biochemical parameters. The results are listed in Supplementary Tables S2 and S3. {#F6} Effect of *MSTN* mutation on the teeth and pelvis in *MSTN*-KO rabbits {#sec2-8} ---------------------------------------------------------------------- To study if there were any effects of the targeted *MSTN* mutation on the rabbits, the body structure and physiological activity of the *MSTN*-KO rabbits were closely observed. It was found that the *MSTN*^−/−^ rabbits showed a greater mass of the masseter muscles compared with the WT and *MSTN*^+/−^ rabbits ([Figure 7](#F7){ref-type="fig"}A). In addition, teeth dislocation and pelvic tilt were present in the *MSTN*^−/−^ rabbits at 3−6 months of age. All of the biallelic *MSTN*-KO rabbits showed tongue enlargement at birth. A statistical analysis of the teeth dislocation and pelvic tilt in all three genotypes of the *MSTN*-KO rabbits, including 88 *MSTN*^+/+^, 77 *MSTN*^+/−^, and 17 *MSTN*^−/−^, showed that the percentage of rabbits having teeth dislocation was 0% in *MSTN*^+/+^, 0% in *MSTN*^+/−^, and 100% in *MSTN*^−/−^ rabbits. The percentage of rabbits having pelvic tilt was 0% in *MSTN*^+/+^, 0% in *MSTN*^+/−^, 77.78% in female *MSTN*^−/−^ rabbits, and 37.50% in male *MSTN*^−/−^ rabbits ([Figure 7](#F7){ref-type="fig"}B,C). Teeth dislocation and pelvic tilt were not present among the WT and *MSTN*^+/−^ rabbit population in the laboratory. Teeth dislocation and pelvic tilt are likely the effects of the targeted *myostatin* allele mutation in rabbits. These results imply that over-developed muscles have an effect on bone morphology. {#F7} Discussion {#sec3} ========== In the present study, the *MSTN*-KO rabbits showed a 'double-muscling' phenomenon and a dramatic increase in body weight. At the end of 14 weeks, the *MSTN*-KO rabbits exhibited an approximately 30% increase in body weight compared with WT rabbits that might be attributed to the *MSTN* gene mutation factor, irrelevant to age and sex. These results are consistent with the *MSTN*-KO mice produced by the homozygous deletion of the C-terminal region of the *myostatin* gene \[[@B2],[@B8],[@B26]\], indicating that disruption of cystine-knot motif can increase muscle mass. This also shows that the structure of the cystine-knot motif plays an important role in myostatin activity. An intricate cysteine-knot motif contains nine cysteine residues (C272, C281, C282, C309, C313, C339, C340, C372, and C374) in the C-terminal region of mammalian myostatin protein \[[@B27]\]. The nine cysteine residues form disulfide bonds that are crucial for the formation of three-dimensional protein structures and could influence the function of other motifs (such as ligand binding or signaling) in the same protein \[[@B28],[@B29]\]. Disruption of the cystine-knot and decreased covalent dimerization likely results in a less compact structure that is then unsuitable for type I and type II Ser/Thr kinase transmembrane receptors activation \[[@B14],[@B30]\]. An analysis of the C313A and C374A mutations confirmed that it is the disruption of the cystine-knot by removal of the C313--C374 disulfide bond, and not the introduction of the tyrosine, that is the dominant factor in the decreased stability and reduced disulfide-linked dimerization of C313Y myostatin \[[@B14]\]. This means that removing the disulfide bonds destroys the cystine-knot motifs. Various mutational *MSTN* genes of the 11 founder rabbits were modeled using the SWISS-MODEL, and the cystine-knot motifs were disrupted, leading to disulfide bond loss and great changes in the tertiary structures. Furthermore, as this research progresses and more offspring are produced, this *MSTN*-KO model can be used to incorporate more reliable parameters and may offer insights into the mechanisms that control signaling in skeletal muscle. In the present study, all of the homozygous mutant rabbits showed pelvic tilt, teeth dislocation, and tongue enlargement. This OT phenomenon was not found in the *MSTN*^−^*MSTN*-KO rabbits \[[@B24],[@B31]\] and *MSTN*-KO pigs \[[@B21]\]. Previous studies have demonstrated that an enlarged tongue is primarily attributed to muscle fiber hypertrophy \[[@B24]\]. However, the teeth dislocation and pelvic tilt phenomena have rarely been reported in other *MSTN*^−/−^ animals. Myostatin is expressed only in muscle and not in normal bone or other connective tissue \[[@B8]\]. It has long been recognized that increased muscle mass and strength are associated with a resultant increase in bone mass \[[@B32]\]. Studies have shown that MSTN has an effect on the bone mass and bone volume fraction in mice \[[@B35]\]. Byron et al. \[[@B36]\] and Vecchione et al. \[[@B37]\] employed a hypermuscular mouse model (mice lacking myostatin) to explore the effects of increased muscle mass. They reported that adult *MSTN*-KO mice were generally more brachycephalic, had a smaller cranial vault and maxillary lengths, and exhibited significantly different mandibular shapes, with the mandible longer and shortened in the vertical dimension compared with WT controls. Byron et al. \[[@B16]\] further revealed that increasing masticatory muscle mass and bite force would increase sagittal suture waveform complexity based on research of *MSTN*-KO mice. Recently, a study on *MSTN*-KO Meishan pigs found that 20% *MSTN*-KO Meishan pigs had one extra thoracic vertebra, and the researchers demonstrated that this phenomenon was caused by the *MSTN* mutation \[[@B25]\]. To our knowledge, the effect of *MSTN* deficiency on rabbit teeth and the pelvis has rarely been reported in other *MSTN*-KO animals. Statistically significant differences have been found in joint proportions and bone mineral densities between normal and *MSTN*-KO mice \[[@B20]\]. Moreover, a recent study has shown that mice homozygous for the myostatin mutation had increased muscle mass and craniofacial dysmorphology in adulthood \[[@B3]\]. Significant correlations have also been noted between masseter muscle weight and mandibular body length \[[@B37]\]. In this study, the teeth dislocation phenomenon may have been due to masticatory hypermuscularity that resulted in significantly altered craniofacial morphology, likely due to altered biomechanical stress. Rabbits excel at sprinting and jumping due to short forelimbs and long hind legs. In *MSTN*^−/−^ rabbits, the elevated hindquarter muscle mass and physiological cross-section enhanced jumping forces compared with similar-sized *MSTN^+/^*^−^ rabbits. Following alterations in the local biomechanical conditions, the elevated hindquarter muscle loads led to an alteration in the morphology of the pelvis in *MSTN*^−/−^ rabbits. These findings demonstrate that muscle function plays an important role in bone morphology. It was found in this study that *MSTN^+/−^* rabbits displayed mild phenotypes and mild abnormalities. This result is consistent with studies of both *MSTN^+/^*^−^ mice and *MSTN^+/^*^−^ cattle, and the abnormalities were likely caused by haploinsufficiency \[[@B4]\]. In these allelic mutation rabbits, it was found that the incidence of pelvic tilt in female *MSTN^−/−^* rabbits (77.78%) was significantly higher than that in male *MSTN^−/−^* rabbits (37.50%). The conclusion drawn was that this may be due to the difference in the pelvic structures of males and females. In mammals, the pelvis is significantly larger in females than in males to allow babies to pass through pelvis when they are born. However, it was still unclear if these craniofacial and pelvic tilt abnormalities were related to the *MSTN* knockout condition during the pre- or neonatal period or were simply a result of postnatal compensatory changes. The effect of the molecular mechanism of the loss of myostatin function on the craniofacial and pelvic tilt abnormalities in rabbits needs further investigation. The *MSTN*-KO mouse has typically been used as a new animal model for the study of the relationship among craniofacial morphology, hypermuscularity, and increased bite force since its muscles have been demonstrated to be significantly larger \[[@B16],[@B38]\]. In a clinical setting, non-specific chronic low back pain (cLBP) is associated with pelvic tilt \[[@B39]\]. It can be concluded that the *MSTN*-KO rabbits will be a better model for pelvic tilt correction and craniofacial research due to their observable pelvis and skulls, appropriate body, longer life cycles, and easy management due to low feeding costs. Conclusion {#sec4} ========== In conclusion, *MSTN*-KO rabbits were generated with remarkably high efficiency by microinjecting Cas9 mRNA and sgRNA into pronuclear-stage embryos. The results of the present study suggest that Cas9 mRNA microinjection may provide a fast and efficient approach for gene knockout rabbit models. Although muscle overgrowth caused by homozygous mutations in *myostatin* was impressive, bone abnormalities caused by excessively growing muscles may be a health hazard for livestock. In addition, based on the abnormality results found in *MSTN*-KO rabbits, it is suggested that these rabbits would make an important animal model for craniofacial and pelvic research. Materials and methods {#sec5} ===================== Animals and ethics statement {#sec5-1} ---------------------------- The New Zealand rabbits used in the present study were kept at the Animal Genetic Engineering Laboratory of Yangzhou University. They were fed twice a day and offered water limitlessly. Animal experiments and procedures were performed in accordance with the Guide for the Care and Use of Laboratory Animals (Ministry of Science and Technology of the People's Republic of China) and approved by the Animal Care and Use Committee of Yangzhou University, Yangzhou, China (license number: SYXK(Su)2017-0044). CRISPR/Cas9 expression plasmids construction and *in vitro* transcription {#sec5-2} ------------------------------------------------------------------------- We constructed two CRISPR/Cas9 expression plasmids that were targeted to the cystine-knot motif. To ensure successful targeting, two sgRNAs independently targeting exon 3 of *MSTN* (sgRNA1 sited E3: g.4881-4903 and sgRNA2 sited E3: g.4796-4818) were performed, as shown in [Figure 1](#F1){ref-type="fig"}B. To construct the recombinant vector for the preparation of sgRNA by *in vitro* transcription, a pair of complementary DNA oligos, shown in Supplementary Table S4, were annealed to be double-stranded. They were then subcloned into the linearized PYSY-T7-Cas9-T7-MSTN-gRNA cloning vector, which was provided by the Nanjing YSY Biotech Com., Ltd., Nanjing, China. The PCR product for the *in vitro* transcription of Cas9 mRNA was amplified using T7 primers (T7-1:5′-TGTAAAACGACGGCCAGT-3′ and T7-2: 5′-TGGCACCGAGTCGGTGCTTT -3′). The PCR products for the *in vitro* transcription of sgRNA were amplified using T7 primers (T7-3: 5′-ATTAACCCTCACTAAAGGGA-3′ and T7-4: 5′-AAAAAAAGCACCGACTCGGTGCCAC-3′). Cas9 mRNA and sgRNAs were transcribed *in vitro* using the ScriptMAX Thermo T7 Transcription Kit (TSK-101, Toyobo, Japan) and purified using a lithium chloride precipitation solution (AM9480, Ambion, U.S.A.) according to the manufacturer's instructions. The concentration and quality of the synthesized mRNA were determined using the spectrophotometer (OD-1000+, Nanjing Wuyi technology Com., Ltd., Nanjing, China) and agarose gel electrophoresis, respectively. Cas9 mRNA and sgRNAs were diluted into RNase-free water and stored at −80°C for future use. Zygote injection with Cas9/sgRNA {#sec5-3} -------------------------------- Healthy donors with regular estrus cycles were selected for zygote collection. Zygotes were collected using surgical oviduct flushing from donors after superovulation treatment and natural mating. In brief, donors were injected with follicle stimulating hormone (FSH) for estrus synchronization. A total of 60 IU FSH were administered by intramuscular injection in six dosages at 12-h intervals (the first dose was 15 IU and other doses decreased progressively to 5 IU). The animals were then injected with 100 IU of HCG 12 h after the FSH was administered. The females were then subsequently mated with a male rabbit. Rabbit embryos at the pronuclear stage (approximately 18--20 h post-mating) were transferred into M2 medium (M7167, Sigma, U.S.A.) with a 1% penicillin--streptomycin solution (SV30010, HyClone, U.S.A.) and 10% fetal bovine serum (FBS, SH30084.03, HyClone, U.S.A.). A mixture of *in vitro* transcribed sgRNA (10 ng/μl) and Cas9 mRNA (40 ng/μl) was injected into the cytoplasm of pronuclear stage embryos. The injected embryos were transferred to M16 medium (M7292, Sigma, U.S.A.) with a 1% penicillin--streptomycin solution and 10% FBS for a 30--60 min culture at 38.5°C, 5% carbon dioxide, and humidity conditions. Then approximately 15−20 injected embryos were transferred into the oviducts of the recipient mother. DNA extraction, PCR, and sequencing {#sec5-4} ----------------------------------- The genomic DNA of the sample was extracted from a small piece of ear biopsy using the phenol--chloroform extraction method. The target sites were PCR amplified using the primers (CAS9SG12-1 and CAS9SG12-2). The sequences of primers are shown in Supplementary Table S5. The PCR products were subjected to 1% agarose gel electrophoresis, and the map is shown in [Figure 1](#F1){ref-type="fig"}C. To test the mutation patterns, the PCR products were purified using a PCR Purification kit (EP101-01, TransGen, China) and cloned into the pGEM-T vector (A1360, Promega, U.S.A.). A total of 50 positive T-clones were sequenced by the Beijing Genomics Institute. Lasergene (DNASTAR, Inc., U.S.A.) was used for the sequence analysis. The tertiary structure of the theoretical amino acid sequences was modeled using SWISS-MODEL (<https://www.swissmodel.expasy.org/>). Western blotting and immunofluorescence analysis {#sec5-5} ------------------------------------------------ Total protein was extracted from gluteus maximus tissue in *MSTN*^+/+^, *MSTN*^+/−^, and *MSTN*^−/−^ rabbits using radio-immunoprecipitation assay (RIPA) lysis buffer (P0013B, Beyotime, China) with protease inhibitors according to the manufacturer's instructions. The protein concentrations were determined using the bicinchoninic assay (BCA) method (CW0014S, CWBIO, China). A 40-μg protein sample was subjected to a 12% polyacrylamide Tris-glycine gel for 1 h. Separated proteins were then transferred to polyvinylidene difluoride (PVDF) membranes (F019531, Sangon, China). The membranes were then blocked for 2 h in a Tris buffered saline with Tween 20 (TBST) buffer containing 5% milk at room temperature. The membranes were subsequently incubated for 1.5 h at 37°C with primary monoclonal antibodies against MSTN (sc-393335, Santa Cruz Biotechnology, U.S.A.) diluted to 1:100 with TBST buffer. The membranes were subsequently washed three times for five minutes with the TBST buffer and incubated with anti-mouse secondary antibodies (D110096, Sangon, China) for 1.5 h at 37°C. The GAPDH antibody (CW0100M, CWBIO, China) was used as a reference control. The proteins were visualized with the ECL substrate solution (\#170-5060, Bio-Rad, U.S.A.) using an imaging system (5200, Tanon, China). Gluteus maximus tissue from *MSTN*^+/+^, *MSTN*^+/−^, and *MSTN*^−/−^ rabbits were collected and fixed with 4% paraformaldehyde, followed by embedding in paraffin according to routine protocol. Deparaffinized tissues were sectioned at 4-μm thicknesses and blocked in 5% bovine serum albumin (BSA). Sections were stained with a primary monoclonal antibody against MSTN (sc-393335, Santa Cruz Biotechnology, U.S.A.), and diluted to 1:50 with a blocking buffer by incubating at 4°C overnight. After washing, sections were incubated with secondary antibodies (BA1105, Boster, China) for 1 h at 37°C and then for an additional 5 min with 4,6-diamidino-2-phenylindole (C1002, Beyotime, China). Images were taken using a microscope (BX53, Olympus, Japan). Increased body weights in *MSTN*-KO rabbits {#sec5-6} ------------------------------------------- In the preent study, the *MSTN*-KO founder rabbits and WT counterpart controls were bred and housed under the same conditions. Their feed was adjusted with respect to growth stages after weaning at 30 days of age. Their body weights were recorded daily from 9 to 14 weeks of age. OT assay {#sec5-7} -------- To determine the site-specific cleavage of the CRISPR-Cas9 system *in vivo*, all possible sites of the entire rabbit genome with homology to the 23-bp sequence (sgRNA + PAM) were predicted using the CRISPR design tool (<http://tools.genomeengineering.org>). The mismatch parameter for the target sequence was set as 5′--NGG and was chosen as the protospacer adjacent motifs (PAM). The sites with 12-bp conserved proximal to PAM and total mismatches \<4 and sites with total mismatches \<5 were chosen as potential OT sites for subsequent testing. The selected potential OT sites were initially PCR-amplified using genomic DNA from *MSTN*-KO rabbits. The PCR products were then used for sequencing. The information of the OT sites and primer pairs used is listed in Supplementary Tables S6 and S7. Histology analysis {#sec5-8} ------------------ Tissues from the gluteus maximus muscles and tongues of an *MSTN*^−/−^ and a WT rabbit of the same age and anatomical position were collected and fixed in 4% paraformaldehyde. These tissues were dehydrated in a graded alcohol series and then embedded in paraffin wax and slide sectioned at 3--5 μm. The slide sections were then stained with Hematoxylin and Eosin (HE) and viewed using a microscope (Leica, DM2000, Germany). For each sample, five fields of view (areas) were randomly selected in the HE-stained sections using a 200× objective and then analyzed using Image-Pro Plus 6.0 software (Media Cybernetics, Inc., U.S.A.). For each sample area, 100--150 myofibers were measured, and the relative size of the myofibers and the distribution of different sizes of the myofibers were determined. Analysis of hematological and biochemical parameters {#sec5-9} ---------------------------------------------------- Blood samples were obtained from rabbits that had been fasted for 12 h, and ethylenediaminetetraacetic acid (EDTA)-plasma and plasma samples were collected after centrifugation at 4°C for 20 min. An automatic biochemical analyzer (AU480, Beckman Coulter, Inc., U.S.A.) was used to test the concentration of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), creatine kinase (CK), creatinine (CREA), glucose (GLU), total cholesterol (TC), triglycerides (TG), calcium (CA), phosphorus (P), and LIP with commercial kits (PT9175, OT9176, AP9209, LD9178, CK9038, CR9169, GL9158, CH9192, TG9179, CA8173, PH9136, and LI9068. Ningbo Purebio Biotech Com., Ltd., Ningbo, China). SPSS13.0 software was used to analyze the measured results. Hematology parameters, like RBC, HGB, HCT, MCV, MCH, MCHC, WBC, RDW-CV, PLT, and MPV, were tested using an auto-hematology analyzer (BC-2800, Mindary Biotech Com., Ltd., Shenzhen, China). Statistical analysis {#sec5-10} -------------------- Statistical comparisons of body weight, myofiber size, and blood parameters among the *MSTN*-KO and WT rabbits were performed using a Student's *t* test, and all data were expressed as a mean ± S.E.M. Statistical analyses were conducted using GraphPad Prism software, and *P*\<0.05 was considered as statistically significant (\**P*\<0.05, \*\**P*\<0.01, \*\*\**P*\<0.001). Availability of data and materials {#sec6} ================================== The data supporting the results of this manuscript are included in the body of the manuscript and as Supplementary data. Supporting information {#sec7} ====================== ###### Summary of heritability and breed of the MSTN-KO rabbits ###### Hematology parameters of the *MSTN*^+/+^, *MSTN*^+/-^ and *MSTN*^-/-^ rabbits. ###### Biochemical parameters of the *MSTN*^+/+^, *MSTN*^+/-^ and *MSTN*^-/-^ rabbits. ###### The sequences of complementary DNA oligos. ###### Primers for detection of *MSTN*-KO rabbits. ###### The sequences of potential off-target sites. ###### The sequences of potential off-target loci PCR primers. We thank our teacher, Professor Yong-Cheng, for providing technical assistance. We would also like to thank the laboratory personnel for their roles in assisting with the present study. Funding {#sec8} ======= This work was supported by the Intergovernmental Science and Technology Cooperation Project \[grant number S2016G6252\]; and the Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD). Competing Interests {#sec9} =================== The authors declare that there are no competing interests assocciated with the manuscript. Author Contribution {#sec10} =================== Conceived and designed the experiments: T.Z. and Y.C. Acquired the data: T.Z., Y.L., S.S., and R.L. Contributed materials/analysis tools: T.Z., R.L., M.Z., Z.H., T.Y., Y. L., K.Y., and Y.C. Manuscript writing: T.Z. All authors read and approved the final manuscript. CK : creatine kinase CREA : creatinine FBS : fetal bovine serum FSH : follicle stimulating hormone GAPDH : Glyceraldehyde-phosphate dehydrogenase HCG : Human Chorionic Gonadotropin HE : Hematoxylin and Eosin KO : Knockout LIP : lipase MSTN : myostatin nt821(del11) : 11-bp deletion at the bovine *myostatin* nucleotide 821 OT : off-target PAM : protospacer adjacent motif sgRNA : small guide RNA TBST : Tris buffered saline with Tween 20 TGF-β : transforming growth factor β WT : wild-type [^1]: These authors contributed equally to this work. | Mid | [
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Login to your account Who came from my kitchen? Why would he be eliminated? adminJanuary 11, 2019 Channel D screens of the popular competition program Bride in the screen adventure in the kitchen left 42 weeks. The brides often tried to get the most out of the taste of the day, the son-in-law of his daughter-in-law, trying to find the bride's section of the week, often increasing votes. The last part is characterized by Sina's behavioral scale. Ms. Reyhan and Mrs Sina told how the scales worked. This attitude was very annoying for Mrs. Reyhan, and in her father's room this situation opened for discussion. At the end of the tense day, one of the brides won five bracelets. a bride-and-wife team said goodbye to the competition. And who was the winner of the week? The bride made the final of the week with dessert in the kitchen. Nilgün-Yağnur Workers, Nezahat-Rümeysa Aydın, Banquet-Elif Yeni and Reyhan – Ezgi Yıldırım competed with if the biscuit recipe said. At the end of the day evaluation; Rümeysa, who won the day with 15 points, won quarter gold. Rümeysa, who collected 75 points for the whole week, was the winner of the week and five gold bracelets. As for the name that was eliminated, it was a surprise development. Rümeysa stated that she had patients and half of the education, and Fatih Urek requested permission. Thus, Rümeysa and her mother-in-law Nezahat Hanım were eliminated from the competition at their own request. Fatih Ürek, the other participants "60.57, 56" received, but who did not say the last. | Mid | [
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Photo Blog: Farewell, Maria Over the weekend, New York’s subway system saw a pass-by of its sea level upgrade, as NY State surfers, and those further north in the New England area, paddled out for the last trace of swell from Hurricane Maria. Winds were offshore, conditions were clean, and the tubes were hollow well into last light for locals like Balaram Stack, Brian Pollak, Dave Juan, and others. The Atlantic has finally taken a break as Maria weakens, leaving many locals to reflect on how memorable the month of September was throughout The Empire State. New York. Photo: Nelson “It was borderline epic,” photographer Mike Nelson said about the weekend. “Maria made her closest pass to us and the swell just pumped all day. It ended up being an all-day tube fest for one of the heaviest crews I’ve seen assembled in New York, joining visiting guys like Sam Hammer, Mike Gleason, Brett Simpson, Evan Geiselman, Shane Borland, Will Reid, Tommy Ihnken, and more. I don't think I have ever seen so many tubes made in one day in New York, ever.” | Low | [
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Atika bint Abdul Muttalib Atika bint Abdul Muttalib was an aunt of the Islamic prophet Muhammad. Biography She was born in Mecca, the daughter of Abdul Muttalib ibn Hashim and Fatimah bint Amr, who was from the Makhzum clan of the Quraysh tribe. She married ’Omar ibn Wahab ibn ‘Abd al-’Uzza ibn Quayy ibn Kilab and had a son called Zuhair. She married Abu Umayya ibn Al-Mughira of the Makhzum clan, thereby becoming the stepmother of Umm Salama. Atika's children were Abdullah, Zuhayr and Qurayba. In March 624 she reported a frightening dream to her brother Abbas. She had dreamed that a camel had halted near Mecca and that its rider had shouted: "Come forth, O people, and do not leave your men to face a disaster that will come three days hence!" Then the man had climbed a mountain and thrown down a rock, which had shattered, spraying pieces on every building in the city. Abbas warned Atika not to tell anyone about this dream, but he told a friend, who told his father, and soon it was common knowledge in Mecca. Abu Jahl asked Abbas: "Are you not satisfied that your men should play the prophet, that your women should do so also? Atika has predicted that there will be war in three days. If the three days pass and nothing happens, we will write you down as the greatest liars in Arabia." Three days later, a messenger from Abu Sufyan arrived in the valley, stood up on his camel and tore his shirt, shouting: "O Quraysh, the merchant-camels, the merchant-camels! Muhammad and his companions are lying in wait for your property, which is with Abu Sufyan. I do not think that you will overtake it. Help! Help!" Thus alerted, the Quraysh armed themselves for the Battle of Badr. However, Atika's brother Abu Lahab did not join the army, saying he was afraid of Atika's predictive dream. Atika became a Muslim in Mecca and joined the general emigration to Medina. She outlived Muhammad, an elegy for whom is attributed to her. O eye! as long as you remain, shed tears in floods, for the best of mankind, Ahmed. O eye! prepare thyself to shed tears and weeping for the light of the land, Muhammmad ... So weep for the blessed, favoured by God, man of piety, supporter of right and guided with guidance ...Who will be left among us to receive revelations from Allah,every evening of today and tomorrow? References Category:Family of Muhammad Category:Banu Hashim | Mid | [
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David M Jackson USA TODAY EXETER, N.H. -- Donald Trump, retail politician. The New York billionaire, seeking to regain political momentum after a second-place finish in Iowa, pursued an unusually crowded schedule Thursday in pursuit of a recovery win in next week's New Hampshire primary. "You're going to play such a big role," Trump told Granite State residents packed into the well of Exeter's old-style town hall, also noting that he still leads many polls. During the event, Trump avoided repeating his claim Wednesday that the Iowa winner, Ted Cruz, "stole" Monday's caucuses by misleading voters — a claim that continued to draw ridicule from some of his rivals. “I don’t think it ever helps after you lose an election to ask for a do-over," Chris Christie told Fox News. "The fact is elections are played, they’re no beanbags, they’re not easy." Christie, Trump, and other Republicans continued to criss-cross New Hampshire in a race with a number of cross-currents. They include the battle between Trump and Cruz, as well as attacks by Christie and Jeb Bush on Marco Rubio, who carried momentum from his strong showing in Iowa. Trump, whose preference has been for rally speeches in big arenas, also planned some of the person-to-person campaigning that has marked the New Hampshire primary for more than a half-century. His schedule Thursday included a meeting with New Hampshire business owners in Exeter, and participation in a shift change in the Manchester Police Department. He also has another town hall Thursday night in Portsmouth. The billionaire took questions at the town hall in Exeter, including one from a woman who protested his harsh comments about illegal immigration. Many migrants "do work no one else wants to do," the woman said, drawing boos from the pro-Trump crowd. In a reference to Democratic candidate Bernie Sanders, Trump said to the woman: "Who told you to be here, Bernie?" In attacking Cruz for his tactics in Iowa, Trump noted that Cruz operatives spread false rumors that Ben Carson was pulling out of the race, and urged his supporters to back the Texan. The Trump campaign has also hit a Cruz mailer that gave voters false information about qualifying to caucus. Cruz said he has apologized to Carson, but mocked Trump's complaints about sour grapes. "I don’t think the people are interested in temper tantrums," Cruz said of the billionaire on Thursday. Rubio, hoping to build on his third-place finish in Iowa, also stumped the Granite State in the face of heavy criticism from rivals. Bush, the former Florida governor who backed Rubio's political rise in that state, told NBC News that his former protege is "a gifted politician," but his life is built "around his own ambitions." Bush also had his own special event planned for Thursday night, featuring mother and former first lady Barbara Bush. Christie, appearing on MSNBC's Morning Joe, continued to argue that Rubio has done nothing in the U.S. Senate, and to describe Rubio as a "bubble boy" who avoids answering tough questions. The New Jersey governor noted that a new Rubio endorser — former presidential candidate Rick Santorum — couldn't name a Rubio accomplishment. "So it's time for the boy in the bubble to come out of the bubble and answer these questions and tell us things rather than just continue to give the same speech he's been giving for the last six years," the New Jersey governor said. Rubio, campaigning on the theme that he represents a new generation of leadership, said opponents are attacking him because he is doing well. “It’s sad that after finishing near the bottom in Iowa, Jeb Bush and Chris Christie are now doing everything possible to tear down Marco Rubio, the one conservative who can beat Hillary Clinton" said Rubio spokesman Jahan Wilcox. Many of these claims will be aired Saturday night, when Republican candidates gather for their last debate before Tuesday's primary. | Low | [
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Q: Error bind click on jquery check value empty <script src="https://ajax.googleapis.com/ajax/libs/jquery/1.4.2/jquery.min.js"></script> <script type="text/javascript"> $(document).ready(function(){ $('#btnSubmit').bind('click', function(){ var option = $('#option1').val(); if(option == ''){ alert('Answer empty'); } return false; }); }); </script> ... <input type="radio" id="option1" name="option1 /> <input type="submit" name="btnSubmit" id="btnSubmit" value="submit" /> ... => error click button submit not alert A: you should modify you code a bit get the value of :checked radio button and if its not checked it means the value is empty and alert the answer is empty for example $('#btnSubmit').bind('click', function(){ alert(""); var option = $('#option1:checked').val(); if(!option){ alert('Answer empty'); } return false; }); here is the working example http://jsfiddle.net/L8VY8/ | Mid | [
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