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Gaku Shibasaki (柴崎 岳; Aomori, 28 de maio de 1992) é um futebolista que atua no Leganés e pela Seleção Japonesa de Futebol. Revelado pelo Kashima Antlers, ele participou da Copa da Ásia de 2015 e foi destaque da Copa do Mundo de Clubes da FIFA de 2016.

Carreira

Kashima Antlers
Gaku foi revelado pelo Kashima Antlers, no clube se profissionalizou, em 2011, e foi conquistando espaço sendo titular do meio-campo do Kashima.

Shibasaki foi sendo importante nas conquistas, sobretudo na temporada 2016, quando foi campeão japonês, e disputou o Mundial Inter-Clubes, marcando 2 gols importantes na final contra o Real Madrid. Esta visibilidade o levou a transferência ao futebol espanhol.

Tenerife
Shibasaki desembarcou nas Ilhas Canárias, em 2017, para atuar no segundo turno, da Liga Adelante no Tenerife. Fez ótima campanha, porém, o acesso bateu na trave na equipe azul das canárias.

Getafe
Suas boas atuações no Tenerife, fizeram o promovido Getafe, contrata-lo para a temporada 2017-2018.

Títulos
 Kashima Antlers
 Copa da Liga Japonesa 2011, 2012,2015
 Copa Suruga Bank: 2012, 2013
 Copa do imperador:2016
 Campeonato japonês:2016

Prêmios individuais
 99º melhor jogador do ano de 2016 (Marca)
 Bola de Bronze mundial de clubes FIFA 2016

Futebolistas do Japão
Futebolistas do Kashima Antlers
Futebolistas do Club Deportivo Tenerife
Futebolistas do Getafe Club de Fútbol
Futebolistas do Real Club Deportivo de La Coruña
Futebolistas do Club Deportivo Leganés
Jogadores da Seleção Japonesa de Futebol
Futebolistas da Copa da Ásia de 2015
Jogadores da Copa do Mundo FIFA de 2018
Futebolistas da Copa da Ásia de 2019
Jogadores da Copa América de 2019
Jogadores da Copa do Mundo FIFA de 2022


We are excited to announce that we will be playing the first of three Crybaby Comp release shows at the Comet Tavern on Saturday, June 16th. The comp features a ton of great local bands and a very new YMDITD track that will be on our up coming LP. Please come out and show some love to us and our extended family!
We are still mixing the LP and it is coming along nicely! We will be touring the west coast in late August in support of the new record. If you are interested in having us melt some faces in your town drop us a line and we'll do our best to make it there.


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Q: The correlation between the Residuals and the prediction $Cov(e,\hat{Y}) =0 $ assume a linear regression model: $y_i$ = $\beta_0$ + $\beta_1x_{i1}$..... + $\beta_px_{ip}$+ $\epsilon_i$
I'm asked to prove that:
$Cov(e,\hat{Y})$ = $0$
where: $e$ = the residuals vector
$\hat{Y}$ =  the predicted vector of Y
Hint: use the fact that $X^Te$ = $0$ (I already proved this fact)

A: You can write your estimator: $$\hat{Y} = X\hat{\beta}$$
Therefore, and by rules of Cov, you can take the constant matrix out (right side with transpose):
$$Cov(e, \hat{Y}) = Cov(e, X\hat{\beta}) = Cov(e, \hat{\beta})X^T$$
Now you can proove that:
$$Cov(e, \hat{\beta}) = 0$$
Since:
$$Cov(e, \hat{\beta}) = Cov(Y - \hat{Y}, \hat{\beta})= Cov(Y, \hat{\beta})-Cov(\hat{Y}, \hat{\beta})$$

*

*$$Cov(Y, \hat{\beta}) = Cov(Y, (X^TX)^{-1}X^TY) = Cov(Y,Y)\times((X^TX)^{-1}X^T)^T = \sigma^2IX(X^TX)^{-1} = \sigma^2X(X^TX)^{-1}$$

*$$Cov(\hat{Y}, \hat{\beta}) = Cov(X\hat{\beta}, \hat{\beta}) = X[Cov(\hat{\beta},\hat{\beta})] = X[\sigma^2(X^TX)^{-1}] = \sigma^2X(X^TX)^{-1}$$
Therefore:
$$Cov(Y, \hat{\beta})-Cov(\hat{Y}, \hat{\beta}) = \sigma^2X(X^TX)^{-1}-\sigma^2X(X^TX)^{-1}=0$$
Both equations rely on knowledge about the distribution of $\hat{\beta}\sim N\big(\beta, \sigma^2(X^TX)^{-1}\big)$ and that $\hat{Y} = X\hat{\beta} = X(X^TX)^{-1}X^TY$

redpajama_set_name: RedPajamaStackExchange


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Stephen Leonardi· 2 years ago
Over the years, the Yankees have had some of the best players in baseball. Very often, they are statistically near the top of the league on teams that finish near the very top of the standings. However, despite the amazing seasons, it seems that baseball's award voters have a bit of a bias against the Yankees.
With DJ LeMaheiu's past couple of seasons and the Judge/Altuve 2017 debate fresh on everyone's minds, lets take a look of a few other cases in recent memory.
2006 AL MVP
In 2006, it finally looked like Derek Jeter would win a regular season MVP. After years of star-caliber play, Jeter was in the midst of one of his best seasons slashing .343/.417/.483, 14 homers, 34 stolen bases and 5.6 bWar. Meanwhile, the Yankees finished with the best record in the American League. However, baseball's MVP voters decided that the Twins first baseman Justin Morneau was more deserving of the award. Morneau had a career year slashing .321/.375/.559, 34 home runs and a 4.3 bWar.
While Morneau had a nice year, he wasn't even the most valuable player on his team. Johan Santana led the AL in bWar and Joe Mauer also had a higher bWar. David Ortiz, Jermaine Dye and Travis Hafner had higher On-base and Slugging percentages. But what is most frustrating about the votes is that one writer placed Jeter 4th on the list and one placed him 6th.
In 2003, Hideki Matsui took MLB by storm. Godzilla played in every game for the Yankees who won 101 that year. Despite his strong rookie campaign, he would lose the Rookie of the Year vote by four points Angel Berroa. Now in hindsight, Berroa had a slightly higher bWar and was deserving of the award. However, it was the logic of the voters that clearly shows the anti-Yankees bias.
Two voters simply left Matsui off of the ballot. One writer, Bill Ballou of the Worcester Telegram, said that having Matsui on the ballot who played for 10 professional years in Japan was not in the spirit of the award. However, just two years earlier Ichiro won the award after playing nine seasons in Japan. And in 2000, Kazuhiro Sasaki won it after 10 years in Japan. Either all players who have played in foreign professional leagues should be removed from consideration or they should count. Not special rules that exclusively impact the Yankees.
In 2016, Gary Sanchez joined a Yankees team that was 53-53 and hit .299 with 20 home runs over the rest of the season. However, he lost the Rookie of the Year vote to Tigers pitcher Michael Fulmer who finished the year 11-7 with a 3.06 era and 132 ks in 159 innings. While Fulmer had a nice season, it wasn't anything special or historic. Meanwhile, Sanchez would have averaged over 60 home runs if he played a full MLB season.
It seemed that for a while Sanchez could do no wrong and would simply power a ball over the wall in every game, tying the MLB record for fastest to hit 20 homers. But some voters didn't really consider him for the award because he didn't play a full season. Three seasons later, Yordan Alvarez ran away with the award despite playing in only 83 games. Using bWar, Alvarez trailed Orioles starter John Means 5 to 3.7. Sanchez trailed Fulmer 5.4 to 3. Again it is a clear Yankees bias that led to the same voters not voting for Sanchez to reward Alvarez three seasons later.
This year, the Yankees have a few players that could walk away with some hardware. It could be DJ LeMahieu or Aaron Judge winning an elusive MVP award. And Kluber and Taillon are both candidates for comeback player of the year. However, if the vote looks like it will be close, it won't be surprising to see the anti-Yankees bias rear its ugly head once again.

redpajama_set_name: RedPajamaCommonCrawl


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Q: Html Parser margin is Negative I'm  using flutter_html 2.1.1 to parse the HTML page into my app,
my flutter version is 2.5.0-6.0.pre
here is where I call html praser
Container(
                          child: new Column(
                            children: <Widget>[
                              Html(
                                data: snapshot.data!.HTML_Data   ?? "",
                              ),
                            ],
                          )),

and the html content that I'm trying to parase is
<!DOCTYPE html PUBLIC "-//W3C//DTD XHTML 1.0 Transitional//EN" "http://www.w3.org/TR/xhtml1/DTD/xhtml1-transitional.dtd">

        <meta http-equiv="Content-Type" content="text/html; charset=utf-8" /><title>
        </title>

test

afeafef

af

eaf

ef

aef

a

efafew

but I'm getting this error
The following assertion was thrown building ContainerSpan(dirty):
'package:flutter/src/widgets/container.dart': Failed assertion: line 268 pos 15: 'margin == null || margin.isNonNegative': is not true.

A: I can see in your HTML code you have a style defined with negative margins. Since flutter_html is using those values in a Container widgets margin, and flutter widgets is not accepting negative values as margin, You're getting the error.
If you want you can override the margin using style provided by flutter_html but this will change the way your HTML will look on browser and in your app:
Html(
  data: snapshot.data!.HTML_Data ?? "",
  style: {
    'p': Style(margin: EdgeInsets.only(left: 0, top: 0, right: 0, bottom: 8)),
  },
),


I needed to bake something egg-free for a friend recently. All I could think of was shortbread. Boring. Shortbread sandwiched around tangy, creamy icing. Now you're talking. This whole batch of biscuits cost about the same as one melting moment from the sweaty jar at the local cafe.
These were perfect! Yummo and super easy and quick to make. I had to tweak the recipes I found to suit my ingredients. This is what I came up with.
Beat butter, vanilla and icing sugar until fluffy.
Sift together plain flour and cornflour and add to butter mixture in three batches, folding through.
Place small balls of batter about 2 cm's apart on a non-stick baking tray and flatten with a fork. Alternatively, you can pipe the mixture onto the tray, using a wide circular nozzle. I did the latter and got nice, evenly round biscuits.
Bake for 12-15 minutes at 170 degrees. Cool on cooling racks. Be careful moving the biscuits as they are quite soft and breakable while warm.
Cream all ingredients with a hand beater or free standing electric mixer until very pale, light and fluffy. Refrigerate until biscuits have completely cooled.
Pipe a dollop of icing onto one biscuit, then simply sandwich together with another.
The butter cream will still be soft. Refrigerate for ten minutes or until firm so they hold together when eaten. Store in an airtight container in the fridge.
Oh these look amazing. Could you make a batch for your dear, Melting Moment-deprived Mother?
These look and sound so good. I am addicted to limes! 🙂 You made such perfect little round shapes!


What Type of Anatomy Gives Rise To Earlier Varicose Vein Pain?
If you are asking the same types of questions, you are definitely not alone. Many people assume that only older people get varicose vein pain and that varicose vein treatment is only performed on older people. However, this is far from the truth!
It is fairly common for people to get varicose vein pain in their early twenties, especially when varicose veins run in their family. In fact, teenagers often get varicose veins too, although they don't always notice the symptoms until many years later. Although more rare, varicose veins with symptoms can even occur in children before puberty, less than ten years old. What this actual data shows is that many people are born with an anatomy and physiology that gives them a higher proclivity to develop varicose vein pain, regardless of their lifestyle or how they're raised as a child.
When younger people get varicose vein pain, their doctor will often advice them (or their parents) to get varicose vein treatment. The idea is to catch it early, ablate the impaired vein(s), and in doing so, prevent additional more extensive damage in connected veins or in different branches of the ablated vein(s). This includes deeper veins where varicosities cannot be seen through the skin but can be seen in the vein clinic with a duplex ultrasound.
First, you need to know that, barring an injury to a vein, there's always a strong genetic component to varicose veins when they occur in a young person. Basically, when symptomatic varicose veins develop in a young person, they were born with an anatomy that basically guaranteed they would develop varicose veins at a young age.
Over the years, researchers have debated whether it is an inherent weakness in the vein walls or a problem with the vein valves that contributes more to the early development of varicose veins. While both factors contribute, no doubt, most researchers now think that problems with vein valves play a more dominant role in the development of varicose vein pain in younger people, particularly in the saphenous vein system. The greater saphenous vein, sometimes referred to as the GSV, runs the entire length of the leg and is the largest vein in the body. The "small" saphenous vein is another large vein that joins to it.
Originally, researchers thought that people who developed varicose veins at a young age had weak vein valves which allowed reflux of blood, i.e. backflow of blood, which then caused blood to pool in the veins. Pooling of blood causes veins to enlarge and deform, in bad cases forming sinuous folds. While vein valves can be weak, or even deformed. It wasn't until the late 1990s that researchers began to figure out that the number of vein valves in the saphenous vein system varied A LOT and this variation occurred from birth.
A careful study in 1999 revealed a very wide variation in the number of vein valves people have. In the greater saphenous vein, researchers found that the number of valves ranged between 3 to l3, with an average of 8 valves! If you can imagine valves dispersed along the vein that runs the entire length of your leg, there's a big difference between 3 and 13! If you only had three valves, there would be a lot more pressure on each valve to prevent the backflow of blood than there would be if you had 8 or more valves. So, although your vein doctor may find venous reflux due to weaken saphenous vein valves when doing a duplex ultrasound, it may be due to the extra work each of your valves is having to do if you have a low number of vein valves.
In a 2008 study entitled, "An anatomical study of femoral vein valves near the saphenofemoral junction," researchers found that the terminal and the preterminal vein vales of the greater saphenous vein were MISSING in ten percent of the sixty-three veins they examined! The terminal vein is only 0.5 to 1.5 millimeters from where it connects to the femoral vein. The preterminal vein is 3 to 5 millimeters from this connection. These valves are particularly important because dozens of tributary veins join the saphenous vein in this small area. So, if you are in the ten percent that is missing one or both of these veins, you will be at an even greater risk for needing varicose vein treatment at a relatively young age. Further, you'll need to go to a top vein clinic that will take the time to do a complete duplex ultrasound scan of those tributary veins and the upper portion of the greater saphenous vein before they recommend a varicose vein treatment plan.
Not all trait variations matter to your overall health. For example, the total number of hairs on a human head, when a person is young, ranges from about 90,000 to 150,000. However, having 90,000 hairs versus 150,000 hairs probably isn't going to make a difference to your health. However, the number of vein valves you are born within your greater saphenous vein DOES matter and it matters a lot. If you have a low number, your probability of needing varicose vein treatment will be higher, regardless of your lifestyle.
Further, if you are a woman with a low number of vein valves, and you get pregnant, your chance of getting a more severe form of pregnancy-related varicose veins during pregnancy will be greater. The same will be true if you stand in one spot for your work.
So, the best action you can take if varicose veins run in your family is to be vigilant about catching it early. It is not always possible to do this just by examining your legs or waiting for symptoms like edema or pain to show up. It would be better for you to get a duplex ultrasound test at a vein clinic like Metro Vein Centers. The reason we mention this specific vein clinic is they have several vein centers around the country and are recognized as being one of the very best. Another benefit to Metro Vein Centers is you can get a free evaluation just by calling and making an appointment.


Most of the time, I'm all about providing encouragement and inspiration to entrepreneurs. They need it and they deserve it, because entrepreneurs are the lifeblood of our economy. But every so often, I try to give them a reality check, just to keep their feet on the ground and their nose to the grindstone.
Of course, there is much more, but I think you get the idea. I also hope these themes don't send a totally negative message, because the book is funny as well as thought provoking. I do believe we all need reality checks to face our challenges head-on, so that we can deal with them and survive, rather than just float along in the clouds until our dreams evaporate.
Protecting your company's assets should be your first priority. Assets include the obvious equipment, accounts receivable, and cash. Maybe more importantly, your long-term survivability is tied to intellectual property, like trade secrets and patents, as well as other less tangible items like your customer base, your experience, and your skills.
If you don't market your business, you won't have one. Marketing and advertising are business realties. Word-of-mouth and viral are not long-term solutions. It doesn't matter how good your product or service is if most of your potential customers don't know about it. With 150,000 new websites per day, customers won't find you by accident.
Before you start building a business, you really do need to know the basic concepts of leadership, management, and operations, and you need to know how these areas change as a business goes through its life cycle. These are the "street smarts" that many entrepreneurs try to acquire by fast talk and bravado. That's a painful and expensive way to learn any facts of life.


Maybe it's my age, but aren't the years rolling by quickly? Is it really 21 years since that crunch game at Edgar Street? A lot of proverbial water, sometimes choppy, has flowed under the bridge since then.
Was it really a year ago that we saw that outpouring of emotion when Wigan were the sacrificial lambs and the subsequent result saw us climb from, effectively, the workhouse into our own little place in Mayfair?
"Get off to bed" they said, "Big day tomorrow. Try to get some sleep".
Who are they kidding? Sleep? I've not slept for a week. Teeth done, in the bedroom sink with the Albion crest mirror, then stretched out on the bed, under the gaze of the 1982/83 squad, looking down from the wall opposite. Half asleep, half awake, replaying all that brought us to this – to the cusp of eternal glory – to the prospect of triangular corner flags at the Goldstone.


Last weekend, I went to a rather awkward book festival. On Tuesday, we discussed the Awkward Book Booth (check the comments for some brilliant reader suggestions). Today, some observations on the Awkward Book Panel.
There is nothing like an awkward panel to make book festival goers wish they had gone on a brewery tour instead. There you are, trapped in your rickety folding chair while three authors you've vaguely heard of say a whole lot of nothing for forty-five minutes, followed by a fifteen-minute question period in which even more nothing gets said. When the panel's over, you can't remember a single thing anyone said—you can't even remember what the panel was supposed to be about. Why are you even here? Why did you think you would find this stimulating? Can we go home now?
There is nothing more awkward than a panel where three authors who have obviously never heard of another spend forty-five minutes avoiding eye contact and otherwise pretending that the fact of one another's company onstage is nothing but a mildly embarrassing coincidence.
In contrast, there is nothing more fun for a book festival audience than a panel where three authors have obvious chemistry—teasing one another, responding to or expanding on one another's points, and generally promoting the illusion that authors all belong to one big club, complete with friendships and rivalries and much creative feuding.
If you are assigned to a panel with two authors you've never heard of, for heaven's sake reach out to them before the event. Look them up on the internet. Give them a call or e-mail and introduce yourself. Perhaps you can go out for a beer the night before the festival. Perhaps you can trade battle stories of panels past. Perhaps you can discover some interesting fodder for the panel.
A panel is not a one-woman (or one-man) show. No matter how engaging you and your panel-mates may be individually, things will be awkward if the three of you don't create something larger and more interesting together.
In this age of live-tweeted book festivals, it doesn't seem like the worst idea to spend some time before the panel jotting down thoughts and statements about your panel's topic, and asking yourself whether any of them could be re-worded to be more tweetable.
This idea will probably make some people shudder (part of me is shuddering as I write it) but if you want to get the most out of your time investment and reach a wider audience than the fifteen or twenty people sitting in those folding chairs, having some highly tweetable comments is a good way to do it.
And even if you're not lucky enough to have an iPhone-happy audience member live-tweeting your brilliant thoughts, chances are you will still be more succinct and memorable than you would have been otherwise. (this is not to say that you should prepare for your panel by coming up with sound bytes at the expense of deep thoughts on your subject. the tweetable stuff should emerge from the deep thoughts, not exist for its own sake).
In a perfect world, a panel moderator's questions would be scientifically calculated to draw out your most brilliant remarks and wittiest anecdotes.
In real life, your panel moderator will probably kick things off by reading factually incorrect bios of you and your fellow authors in a monotone, then asking questions of such galloping incoherence you will wonder if your festival-provided bottle of water has been dosed.
Classic job interview wisdom holds true for book panels: think about what you REALLY want to say, then find a way to say it, even if the actual questions are duds. Which facts, opinions, and anecdotes would be most interesting to your audience? Can you find a way to work them in? A panel with uninspired questions is just as disappointing to the audience as it is to the authors. We WANT to hear the juiciest things you have to say.
The people attending your panel are probably hot, cranky, hungry, and uncomfortable in those horrible folding chairs. If you can make our panel-going experience any less physically unpleasant, we may actually pay attention instead of day-dreaming, texting, or scouring the festival program for more stimulating events for which we could ditch your panel halfway through.
Can you get away with passing out cookies? You could lift us out of our existential misery with cookies. If cookies are too crumbly, what about a bag of Hershey's kisses? Licorice? Tic-Tac? ANYTHING?!?!?
Point is, if you hand out a treat, we will suddenly feel clever for attending your panel, and we will spend the whole panel thinking "I can't wait until this panel is over so I can tell my friends about the free cookies they missed" instead of just "I can't wait until this panel is over." And if you're really lucky, our moods will be so brightened by the unexpected treat, we will actually listen and ask questions and remember to buy your book.
In cases where handing out food items is inappropriate, you can still delight your audience with something unexpected—a prop? a great story? a handout? a surprise announcement? Whatever it is, make us feel lucky to be there, lucky not to have missed it, and eager to tell everyone about what happened.
Have you ever been to a book panel? What made it good? What made it awkward? Are author panels even worth it, or are they generally just exercises in awkardness? Who's the best author panelist you've ever seen, and why did they stand out?
One of the most cited reasons agents and editors give for declining manuscripts is "there wasn't enough conflict" or "the stakes weren't high enough." For this reason, writers have learned to pile on conflict—checking for internal and external tensions in every scene, giving each character a backstory wound, defining clear and compelling story goals, etc.
But while these strategies can and do lead to stronger story telling, they can also backfire in confusing ways. Over the past six months, the freelance editor version of myself has noticed a peculiar phenomenon: manuscripts with loads of conflict that are nevertheless deadly boring.
It turns out these writers had misplaced their conflict in various ways. It's like keeping gasoline in the trunk of your car instead of putting it in the tank. Sure, you have gas, but it's not doing you any good. Gas is only useful if it's in the tank—and conflict sort of works the same way.
Here are some of the weird places writers mistakenly stash their story's fuel.
Bonnie McPhee is a thirty-year old osteopath whose life has just hit a wall. Her boyfriend's sister is facing life in prison, her parents' house just got foreclosed on, and her neighbor's son got diagnosed with leukemia. Then she makes a startling discovery about her great-grandfather's past.
This story has so much drama—prison! deadly diseases! financial crises! dark family secrets!—but the protagonist's role in them is unclear. Where's Bonnie in all this? What does she stand to gain or lose? Why do we care that she resolves a dark secret from her great-grandfather's past? What about her?
Obviously, it is possible to craft a great novel in which the protagonist's friends and family are embroiled in crises—maybe the whole point is to show your MC's journey from being a doormat with no life of her own to refusing to let other people's drama dominate her existence. But if that's the case, you have to really show that journey and develop it just as much as you've developed the other crises; in other words, make it into a conflict.
Joe Kerp wants to be the first blind person in space, and is taking exhausting astronaut training sessions in his spare time. Along the way, his house gets broken into by a neighborhood thug, his mean coworker tries to get him fired, his girlfriend runs off with his best friend, and a freak snowstorm kills his prized plum trees.
Yes, our protagonist is subject to many trials, but they feel random and episodic—nothing connects to anything else. Because the conflicts don't connect to the larger story, the scope of their impact is very limited: you get a string of minor setbacks, none of which have any game-changing effect on Joe's goal of becoming an astronaut.
Now, if the neighborhood thug stole his top-secret astronaut files, and his girlfriend proceeds to run off with said neighborhood thug, and it turns out Joe is the center of an international space conspiracy, that's a different story. In general, conflict works better when it is tightly to connected to the internal and/or external story goals.
This one is pretty self-explanatory. If your novel contains a zillion flashbacks to the day your protagonist's little brother drowned in a swimming pool while your protagonist stood by, helpless, you'd better make sure that themes of guilt and helplessness come up in the present story's conflicts, whatever those conflicts may be. Otherwise, all those flashbacks are going to fall into the category of drama for the sake of drama—which does not make for compelling storytelling.
Ch. 1 There's a bomb on the cruise ship and we're all going to die!
Ch. 23 There's a bomb on the cruise ship and we're all going to die!
Ch. 49 There's a bomb on the cruise ship and we're all going to die!
Ch. 50 Bomb resolved! The End!
Keep things moving. No conflict is "too big" to stagnate.
Ch. 1: There's a bomb on the cruise ship and we're all going to die!
Ch. 2: Phone call from protagonist's mother. Bank is reposessing the house!
Ch. 3: Protagonist discovers dark secret from great-grandfather's past!
Ch. 4: Also, the ship's captain and crew are all strung out on heroin, and protagonist is a former addict!
Ch. 5: Also, dead whales are floating up beside the ship—why?!?
Readers get tired of investing emotionally in plotlines that repeatedly get yanked out from under their feet. If you choose to put a certain conflict in your novel, commit to it.
I feel the need to mention that any one of these so-called conflict "problems" could work fabulously as conscious, well-executed artistic decisions or constraints. I could imagine an incredible, Waiting for Godot-style bomb-on-cruiseship story in which the conflict literally never escalates. Or a novel in the vein of Slacker in which there is no single conflict running through the entire story. My intention here is not to list "rules", but rather observations on the most common failure modes in a certain type of manuscript.


Son of Long An airy Panda print Hawaiian shirt for the hot summer days.
This Milky white shirt is made from the soft silky fabric that makes it cool in summer with the excellent ventilation. Designed with loose fit Hawaiian style silhouette the shirt features convertible collar with full front button closure and short sleeve with roll-up cuffs.


text:
Stocks of MCMV, Smith strain and mutant MCMV lacking m157 (△m157)
Posted on February 28, 2019 by pdgf0890
Stocks of MCMV, Smith strain and mutant MCMV lacking m157 (△m157) 34 were produced in cell culture using B6 mouse embryo fibroblasts or by serial passage of salivary gland homogenates in BALB/c mice in vivo. Tissue culture-derived MCMV was used for inducing T-cell responses and salivary gland virus (SGV) for NK-cell studies. Mice were infected i.v. with 200 PFU LCMV-WE, 2×106 PFU VSVIND, 2×106 PFU VV, 2×106 PFU tissue culture-derived MCMV
(i.p.), 5×105 PFU tissue culture-derived Δm157 MCMV (i.v.) or 5×104 PFU SGV MCMV (i.p.). Cells (105–106 in 50–100 μL) were stained with appropriately diluted mAb (0.1–1 μg in 50–100 μL) in PBS containing 2% FBS and 0.1% NaN3 at 4°C for 30 min. The following fluorescence-labeled mAb were purchased from BD Pharmingen and eBioscience (NatuTec GmbH, Frankfurt, Germany): anti-CD3, -CD5, -CD8, -CD11b, -CD27, -CD62L, -CD127, buy Rapamycin -NK1.1. Anti-KLRG1 mAb (clone 2F1) 20 was produced in cell culture, purified using protein G and labeled with Alexa488 or Alexa647 (Molecular probes,
Invitrogen, Karlsruhe, Germany). LCMV- and VSV-specific CD8+ T cells were detected XAV-939 cost using PE-labeled H-2Db tetramers complexed with GP33 peptide (KAVYNFATM) and H-2Kb tetramers complexed with NP52 peptide (RGYVYQGL) generated in the laboratory as described 12. Samples were analyzed by a BD FACSCalibur flow cytometer (BD Biosciences) using CellQuest-Pro software (BD Biosciences). Spleen cells (105 in 200 μL) were stimulated for 5 h in 10 μg/mL brefeldin A with 10−6 M of the following peptides: LCMV GP33–41 (KAVYNFATM), MCMV M45985–993 (HGIRNASFI), MCMV M38316–323 (SSPPMFRV), MCMV m139419–426 (TVYGFCLL). Intracellular cytokine staining was performed with PE-labeled mAb specific for IFN-γ (XMG1.2, Ixazomib supplier eBioscience) and IL-2 (JES6-5H4, eBioscience)
using Cytofix/Cytoperm solution (BD PharMingen). Peptides were purchased from Neosystem (Straßburg, France). P14 chimeric mice were generated by adoptive transfer (i.v.) of 105 P14 T cells from P14 KLRG1 KO or P14 WT mice. Repetitive P14 T cell transfers to generate 1°, 2° and 3° memory P14 cells were performed as described 11. Memory P14 T cells used for repetitive adoptive transfers were purified using PE-labeled anti-Thy1.1 mAb and anti-PE MACS-MicroBeads (Milteny, Bergisch Gladbach). NK cells were activated in vivo by i.v. injection of VSVIND (2×106 PFU), VV (2×106 PFU), L. monocytogenes (106 CFU), LCMV (200 PFU) or 5×104 PFU MCMV (SVG) i.p. After 20 h, spleen cells were analyzed by staining with CD3-, CD11b-, CD27- and NK1.1-specific mAb. The activity of poly(I:C)-activated NK cells (200 μg i.p., 18 h) was determined by intracellular IFN-γ staining using plate-bound stimulation with anti-NK1.1 mAb (10 μg/mL) in the presence of 10 μg/mL brefeldin A or by classical 4 h 51Cr release assays using RMA-S target cells.
A large cause of the difference can be attributed to laboratory c
A large cause of the difference can be attributed to laboratory calibration bias, however, even when corrected, correlation between estimated and measured GFR remained weak.16 Modelled estimates by Douville et al.17 of decline in GFR by age, based on creatinine clearance measurements in 7551 outpatients (aged 18–90 years) with normal serum creatinine, suggest a decline in GFR from approximately 120 mL/min per 1.73 m2 in early
adulthood down to approximately 60 mL/min per 1.73 m2 when people are in their 80s. Selleck NVP-BGJ398 There was a continuous downward trend over 50 years of age and no significant differences between males and females. In contrast to the above, the study by Berg of 112 potential kidney donors (55% female) aged 21–67 years indicated a significant decline in GFR with age in males but not in females, over the age range of 20–50 years.18 The mean GFR (measured by inulin clearance) at 20–30 years was 119 (±12) mL/min per 1.73 m2 and 102 (±15) mL/min per 1.73 m2 in males and females, respectively, and were significantly different. The mean GFR at 40–50 years was 100 (±11) mL/min per 1.73 m2 and 105 (±11) mL/min per 1.73 m2 in males and females, respectively, and the differences were not significant.
The data suggested to the author that women seem to be protected in the pre-menopausal period. The apparent decline in males 20–50 years of age was consistent with the data reported by Rule et al.16 A critical analysis of studies on long-term medical outcomes (including renal see more function) in living kidney donors by Ommen and colleagues19 identified the following issues that Metalloexopeptidase limit
the ability to assess medical risks: virtually all studies are retrospective and commonly have large losses to follow up, As a consequence, assessment of the significance of findings of long-term renal function including the incidence of ESKD among donors is limited. Overall, in relation to renal outcomes, Ommen et al. consider that the available studies indicate no large decreases in GFR or increases in ESKD among donors. However, some studies suggest the potential for an increased risk of renal dysfunction in certain donors and given the limitations of the evidence, this suggests a cautionary approach should be taken in relation to 'marginal living donors'.19 The systematic review by Garg et al.20 considered the following two questions for kidney donors: What proportion of kidney donors develop proteinuria or a GFR < 60 mL/min? The systematic review considered any study where 10 or more healthy adults donated a kidney and where proteinuria or GFR was assessed at least 1 year later. Studies that did not separate healthy donors from those with overt proteinuria or GFR < 80 mL/min per 1.73 m2 were excluded. Forty-eight studies from 27 countries that followed a total of 5048 donors were identified.
In addition, basal secretion differed significantly between perip
In addition, basal secretion differed significantly between peripheral blood–derived and decidual macrophages for a broad spectrum of cytokines. Vemurafenib manufacturer When trophoblasts were pre-treated with an anti-Mamu-AG antibody, 25D3, there was no change in cytokine or chemokine secretion. Conclusion Macrophage cytokine expression can be modulated by trophoblast co-culture, but it remains unclear how Mamu-AG is involved. "
"Regulatory T cells (Tregs) migrate into
peripheral sites of inflammation such as allografts undergoing rejection, where they serve to suppress the immune response. In this study, we find that ∼30–40% of human CD25hi FOXP3+ CD4+ Tregs express the peripheral CXC chemokine receptor 3 (CXCR3) and that U0126 chemical structure this subset has potent immunoregulatory properties. Consistently, we observed that proliferative responses as well as IFN-γ production were significantly higher using CXCR3-depleted versus undepleted responders in the mixed lymphocyte reaction, as well as following mitogen-dependent activation of T cells. Using microfluidics, we also found that CXCR3 was functional on CXCR3pos Tregs, in as much as chemotaxis and directional persistence towards interferon-γ-inducible protein of 10 kDa (IP-10) was significantly greater for CXCR3pos than CXCR3neg Tregs. Following activation,
CXCR3-expressing CD4+ Tregs were maintained in vitro in cell culture in the presence of the mammalian target of rapamycin (mTOR) Florfenicol inhibitor rapamycin, and we detected higher numbers of circulating CXCR3+ FOXP3+ T cells in adult and pediatric recipients of renal transplants who were treated with mTOR-inhibitor immunosuppressive therapy. Collectively, these results demonstrate that
the peripheral homing receptor CXCR3 is expressed on subset(s) of circulating human Tregs and suggest a role for CXCR3 in their recruitment into peripheral sites of inflammation. Regulatory T cells (Tregs) are essential for the suppression of immune responses to foreign antigens, including alloantigens, and they are well established to function in the development and maintenance of self-tolerance 1, 2. Forkhead box P3 (FOXP3) has emerged as the master regulator of the development and function of Tregs in both mice and humans 3–5. Furthermore, expansion of CD4+FOXP3+ T-cell subsets is generally considered to be critical for tolerance induction and for the suppression of a wide range of immune-mediated diseases 6. Tregs utilize multiple mechanisms to suppress effector cell expansion and to mediate immunoregulation 1, 7. These include cell–cell contact-dependent suppression 8, secretion of immunosuppressive cytokines including IL-10 9, 10, TGF-β 11, 12 and IL-35 13, and the consumption of IL-2 produced by responder T cells 14.
Of the systemic autoimmune diseases, SLE is the most severe and a
Of the systemic autoimmune diseases, SLE is the most severe and affects about 1 in 1000 individuals. Circulating autoantibodies in SLE patients directly contribute to disease pathogenesis by forming immune complexes with ubiquitous antigens, for example DNA, and subsequently activating effector responses such as complement and production of pro-inflammatory cytokines. The resulting inflammation and organ damage further amplifies selleckchem autoreactive immune responses, forming a
self-sustaining and propagating vicious circle [1]. Systemic autoimmune diseases have traditionally been considered to be B-cell-dependent diseases due to the high levels of autoantibodies. In recent years it has, however, become clear that T cells have a major impact on the development and propagation of this group of diseases. A subset of T-helper cells that produce IL-17 (Th17) was initially implicated in the pathogenesis of autoimmune
disease in studies of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS) [2, 3]. Since then, Th17 cells AZD3965 research buy have been the subject of increasing attention in the context of systemic autoimmune diseases such as SLE, but also rheumatoid arthritis and psoriasis. In the latter two conditions, an increasing body of evidence implicates IL-17 and IL-17-producing cells in disease pathogenesis both in animal models and in humans, and points to NADPH-cytochrome-c2 reductase IL-17 as a promising therapeutic target, as reviewed in [4, 5]. In this review, we survey the information generated from human and animal studies pointing toward a role for IL-17 and Th17 cells in the
pathogenesis of systemic autoimmune diseases, especially SLE, and we explore the possible cellular and molecular mechanisms by which Th17 cells may contribute to disease. In addition, we discuss the relevance of this particular T-cell subset in the context of type I IFN-driven inflammation, the hallmark of systemic autoimmune diseases. T-helper-cell subsets are traditionally defined by their signature cytokine and lineage-specific transcription factors, for example IFN-γ and T-bet for Th1 cells, IL-4 and GATA-3 for Th2 cells. Th17 cells produce IL-17 and express the transcription factor RORγt [6]. They differentiate from naïve T cells following TCR activation and co-stimulation in the presence of the cytokines TGF-β and IL-6 [7, 8], and IL-23 has been shown to play a critical role in their expansion and terminal differentiation[9, 10].
34 4% TCRγδ+, respectively; Fig 3 lower left panel), and PEG-ADA
34.4% TCRγδ+, respectively; Fig. 3 lower left panel), and PEG-ADA led to a decrease in TCRαβ+ T cells, while
TCR γδ+ T cells expanded (approximately 30% and >70%, respectively), and these changes remained constant throughout the therapy. In addition, before the ERT, his T cell repertoire was comprised of low numbers of CD4+ CD45RA+ and high numbers of CD8+ CD45RO+ T-cells (5.6% vs. 71.3%, respectively; Fig. 3, lower right panel). However, these percentages started to change with ERT, and by 17 months, the percentages of naïve CD4+ and CD8+ T cells that were CD45RA+ had increased to 94.4% and 99.5%, respectively. We also evaluated T cell proliferation to PHA and found that before ERT, T-cells did not proliferate in response to PHA (PI = 0.99; SE = 1.14–1.15) when compared to healthy controls GSK-3 phosphorylation (PI = 6.40, see more SE = 16.03–22.03), and even after 3 months, there was no detectable lymphoproliferation (data not shown). However, after 6 months we observed proliferation of PBL to PHA (PI = 2.45; SE = 4.22–3.69), although low as compared to controls (PI = 3.53; SE = 6.45–7.97). The lymphoproliferation
to mitogen in the PB T cells from our patient at 50 months before ERT suggested that their functionality might be affected. In fact, SCID caused by mutations in the Rag1/Rag2 genes (the variant also known as classic Omenn syndrome) is characterized by marked lymphocytosis, even though these cells are non-functional and exhibit limited clonality [19]. T-cell spectratyping has been recently used as a tool to assess clonality in a revertant ADA-deficient patient treated with PEG-ADA [13]; therefore, we performed CD3 size spectratyping after 12 months of PEG-ADA therapy in our patient and found that he had a severely skewed distribution of
next peaks for all 24 Vβ families (Fig. 4). This was attributed to a markedly oligoclonal T cell repertoire in Vβ families 1, 4, 5, 8, 12, 13B, 18 and 24, while and clonal dominance the rest with a more restricted repertoire, in contrast to the polyclonal profile observed in T cells from a healthy age- and sex-matched control. In patients with somatic mosaicism due to reversion of mutations, the continued administration of PEG-ADA has shown to decrease the in vivo selective advantage of the revertant cells [12]. To evaluate this in our patient, we sequenced exon 4 again in the genomic DNA from PBL obtained before ERT, as well as 3- and 6-months post-therapy. These results showed that while the patient was heterozygous before PEG-ADA due to the revertant cells (Fig. 5, CTG-Leu, normal sequence along with CCG-Pro) after 3 months of therapy, the intensity of the reversion of the C > T peak decreased, and by 6 months, it disappeared (CCG, Pro, mutated sequence). Therefore, we conclude that the ERT eliminated the revertant cells in vivo in our patient.
In accordance with this, the helix-turn-helix structure character
In accordance with this, the helix-turn-helix structure characteristic of DNA-binding proteins was detected in the N-terminal region of MhuB (Fig. 3), suggesting that
this protein may act as a transcriptional regulator. To confirm iron-regulation of mhuA and mhuB transcription, total RNA isolated from V. mimicusΔiucD (for RT-qPCR) or 7PT (for primer extension) cells grown in +Fe and −Fe media were analyzed by RT-qPCR. The degree of mhuA transcription in the −Fe cells was dramatically increased (by 117.5-fold) compared with that in the +Fe cells (Fig. 5a). On the other hand, only drug discovery a slight increase (of 2.4-fold) was observed for the mhuB gene in the −Fe cells (Fig. 5a). These data suggest that expression of both mhuA and mhuB genes might be iron-regulated through putative Fur boxes located in the respective promoter regions. Furthermore, primer Selleck Sirolimus extension was performed to clarify the transcriptional start site of the mhuA gene. In the −Fe cells, the transcriptional start site could be mapped on the cytosine residue located 35 bases upstream
of the initiation codon (Fig. 5b). However, under the same analytical conditions, no extension band owing to mhuB transcript was detected even in the −Fe cells (data not shown). In order to characterize the function of the mhuB gene, the degree of expression of mhuA in the ΔiucD and ΔiucDΔmhuB strains was assessed by RT-qPCR. Deletion of the mhuB gene was confirmed by PCR analysis with the primer pair B5 and B6, and a PCR fragment (ca. 1.7-kb) containing the mhuB deletion was amplified using the ΔiucDΔmhuB chromosomal DNA as a template (Fig. 1a). Although mhuA expression of the Cepharanthine ΔiucDΔmhuB cells grown in the −Fe medium was increased by 80.3-fold compared with that
in the +Fe medium, this increase in mhuA transcription was 38.5% less than that found in the ΔiucD cells (Fig. 5a). To further examine the transcriptional regulation of mhuA, β-galactosidase reporter assay was performed for E. coli WAM131 carrying each of the following plasmids: pAA224, pVMB2 (encoding mhuA-lacZ fusion), and pVMB3 (encoding mhuB and mhuA-lacZ fusion) (Fig. 6a). The results are shown in Figure 6b. In WAM131/pAA224 cells, only basal levels of β-galactosidase activity were detected in both +Fe and −Fe media. However, WAM131/pVMB2 cells grown in −Fe medium showed a significant increase in β-galactosidase activity relative to the +Fe basal level. This increase in β-galactosidase activity might be explained by the presence of the putative Fur box in pVMB2. Moreover, WAM131/pVMB3 cells grown in the −Fe medium exhibited about 2.3-fold increases in the β-galactosidase activity compared to WAM131/pVMB2 cells grown in the same medium. These results indicate that transcription of the mhuA gene is controlled not only by the Fur box-containing promoter but also by MhuB, a LysR family of regulator. To confirm the role of mhuA in heme and hemoglobin utilization by V.
In cattle, L corymbifera can cause abortions and mastitis,[61] b
In cattle, L. corymbifera can cause abortions and mastitis,[61] but also gastrointestinal mycoses. Jensen et al. identified L. corymbifera as the cause of bovine gastrointestinal mycoses in more than 60% of the cases.[62] As Lichtheimia species are present in high amounts in cattle feed, oral inoculation of fungal spores and hyphae seems to be the most likely rout of infection.[16] Furthermore, mucoralean species including L. corymbifera and L. ramosa represent the majority of filamentous
fungi in rumen fluid of healthy cattle[63] and therefore endogenous infections might also occur. Limited spread from the intestinal tract is also the most Selleckchem MAPK inhibitor likely explanation for the cases of mesenteric lymphadenitis caused by L. corymbifera.
The affected animals appeared clinically healthy but displayed invasion of lymph nodes and subsequent necrosis and dystrophic calcification at slaughter.[64] Infections caused by Lichtheimia seem not to be restricted to bovines but might also affect other ruminants, as illustrated by a case of systemic infection in deer.[65] Equine hosts can also be infected by Lichtheimia species. Two cases of Lichtheimia infections in ponies were reported by Guillot et al. [66]. While one of the Cobimetinib animals suffered from localised cutaneous Lichtheimia infection and necrotic ulceration in the nostrils, the other died due to systemic mucormycosis. Postmortem examination revealed lesions in the lung, stomach, digestive tract and a large infarct in the brain. Pulmonary, gastrointestinal and disseminated Nabilone infections with Lichtheimia have also been described in birds.[67, 68] In a recent study on stork
chicks, L. corymbifera was identified as the second most common cause of fungal pneumonia, accountable for 18% of the cases.[69] In both mammalian and avian hosts, Lichtheimia can occur as coinfection with A. fumigatus.[62, 69, 70] Murine models are the most commonly used animal models for most fungal infections. Several different mouse models have been used to study Lichtheimia infections by various groups; however, a standardised and well-characterised model has not been established yet. In immunocompetent mice infected either intravenously or intracerebrally, both L. corymbifera and L. ramosa were shown to cause lethal disease with lesions predominantly affecting the central nervous system and the kidneys.[71, 72] In pregnant mice, the infection did also affect the placenta.[73] Immunosuppression by cortisone acetate increased the susceptibility to intravenous infection and led to more widespread organ pathology.[74] In contrast to systemic infection models, immunocompetent mice were resistant to oral and subcutaneous challenge with Lichtheimia.[74, 75] Similarly, development of clinical disease after pulmonary challenge via the intranasal or intratracheal route depended on immunosuppression.
Furthermore, the striking prognostic value of the analysis of imm
Furthermore, the striking prognostic value of the analysis of immune infiltrates in tumors has firmly established the capacity of adaptive immunity to control tumors [2, 4]. There are at least two major hurdles to
overcome in efforts to generate vaccines to cancer: the generation of sufficiently strong and long-lasting C59 wnt tumor-specific T-cell responses that do not destroy healthy self-tissues, and the recruitment of sufficient numbers of effector T cells into tumor sites and metastases. In order to address the first issue, one approach is to take advantage of the ability of CD4+ T helper cells to potently synergize with CD8+ T cells, promoting their activation and memory [5]. Although much of the effort in identifying T-cell epitopes for immunization in cancer has focused on self- or modified CT99021 self-antigens
[6], given the issue of self-tolerance which is further compounded by the ability of tumors to generate tolerance to themselves, it is difficult to generate sufficient T-cell help via the (modified) self-antigen route. A strategy that has long been considered to overcome this obstacle is the addition of foreign (e.g. xeno) antigens into cancer vaccines to boost immunity [7, 8], and more recent studies have provided direct evidence that the beneficial effects of this procedure are through the provision of T-cell
help [9-11]. A substantial advantage of employing foreign helper determinants physically linked to Phosphatidylinositol diacylglycerol-lyase determinants recognized by CD8+ T cells, rather than tumor-associated helper determinants, is that the tumor cannot use either downregulation of their own helper epitopes, or induction of tolerance against these foreign epitopes, as a means of escape. Interestingly, it has been theorized that MHC class II-restricted T cells are likely to be more self-tolerant than MHC class I-restricted T cells or B cells [12]. It would seem an insurmountable task for our immune system to become tolerant of all of the various self-antigens throughout our body. The task would be made much simpler if extensive tolerance were only needed for T cells recognizing antigens presented on the limited number of cells that express MHC class II; expression of MHC class II is restricted to several hematopoietic lineages and endothelial cells while the vast majority of cells in the body, the various parenchymal tissue cells, generally lack expression. This concept is consistent with observations of a state approaching ignorance to some self or neoself antigens by CD8+ T cells and B cells [13-15], while CD4+ T cells remain robustly tolerant [9, 13].
1), similar to other NOD mouse lines congenic for a resistant Idd
1), similar to other NOD mouse lines congenic for a resistant Idd3 locus 37–39. Consistent with previous findings 38 naïve CD4+ T cells
isolated from the spleen of NOD.B6Idd3 mice exhibited increased IL-2 secretion upon in vitro stimulation relative to NOD CD4+ T cells (Supporting Information Fig. 1). To determine the influence of Idd3 on FoxP3+Tregs, the frequency and number of gated CD4+CD3+ T cells expressing FoxP3 and CD25 (Fig. 2A) were assessed in the thymus, spleen, PaLN, and islets of age-matched NOD and NOD.B6Idd3 female mice via FACS. No difference in the frequency of FoxP3+Tregs was detected in the thymus of NOD and NOD.B6Idd3 mice suggesting that thymic development of FoxP3+Tregs is unaffected by IL-2 expression click here levels. On the other hand, an increased frequency and number of FoxP3+Tregs was detected in the PaLN and spleen of older NOD.B6Idd3 mice relative to age-matched NOD mice (Fig. 2A–C). In addition, the frequency of FoxP3+Tregs was significantly increased in the islets of selleck compound 10- and 16-wk-old NOD.B6Idd3 versus NOD female mice (Fig. 2B). Notably, however, a greater number of FoxP3+Tregs were detected in the islets of older NOD mice (Fig. 2C) reflecting increased T-cell infiltration of the islets relative to age-matched NOD.B6Idd3
mice. These data demonstrate that the frequency of FoxP3+Tregs is increased in the PaLN and islets of NOD.B6Idd3 mice compared with NOD mice. We and others have shown that Avelestat (AZD9668) CD62Lhi- versus CD62Llo-expressing FoxP3+Tregs exhibit increased suppressor activity 7, 19. Accordingly, CD62Lhi- and CD62Llo-expressing FoxP3+Tregs were examined
temporally in age-matched NOD.B6Idd3 and NOD female mice. Interestingly, age-dependent differences in the frequency and number of CD62Lhi- and CD62Llo-expressing FoxP3+Tregs were detected in the PaLN and islets of the respective groups of mice. NOD female mice exhibited a temporal decrease in the frequency of CD62LhiFoxP3+Tregs and a concomitant increase in CD62LloFoxP3+Tregs in PaLN (Fig. 3B). Although the number of CD62LhiFoxP3+Tregs progressively increased in the PaLN of NOD female mice (5.2×104 (4 wk) versus 9.0×104 (16 wk)), a greater increase in CD62LloFoxP3+Tregs numbers was detected (6.3×104 (4 wk) versus 14.9×104 (16 wk)) (Fig. 3C). In the PaLN of NOD.B6Idd3 mice, however, the frequency and number of CD62LhiFoxP3+Tregs showed no marked change with age, which were increased relative to age-matched NOD females (Fig. 3B and C). A similar scenario was observed in the islets of NOD and NOD.B6Idd3 female mice. A temporal increase in the frequency of CD62LloFoxP3+Tregs was detected in the islets of NOD female mice which was due to elevated numbers relative to CD62LhiFoxP3+Tregs (Fig. 3D and E). Despite a progressive decline, the frequency of CD62LhiFoxP3+Tregs in the islets of NOD.B6Idd3 female mice was elevated relative to age-matched NOD female mice (Fig. 3D and E).
Experimental evidence showed that antibodies targeting the high-a
Experimental evidence showed that antibodies targeting the high-affinity iron permease, an iron transporter cell membrane protein, protect DKA mice from infection with R.
oryzae infection.[37] FG-4592 datasheet Moreover, antibodies targeting the GRP78/CotH interactions (i.e. antiGrp78 antibodies[43] or antiCotH antibodies[47]) protected DKA mice from infection with R. oryzae. These findings lend support for the future development of novel passive immunisation strategies that target virulence traits of Mucorales. Mucormycosis is a lethal infection with very limited and mainly ineffective treatment options. Although considered rare, mucormycosis are on the rise and this increase is expected to continue due to the increased number of immunosuppressed patients and the severity in the immunosuppression regimens. Additionally, the increased cases of obesity and unhealthy life style will increase cases of diabetes, which are uniquely predisposed to mucormycosis. Clinical data point to the importance of iron acquisition in the pathogenesis of mucormycosis and subsequent research confirmed this observation. Although mucormycosis pathogenesis studies are at its infancy, recent major discoveries highlight the possibility of translating this knowledge into possible novel therapies urgently needed to improve the outcome of this disease.
This work was supported in part by Public Health Service grant R01 AI063503. The author received research grants or consultancy fees from the following companies to conduct Doxorubicin research on mucormycosis: Astellas, Enzon, Gilead, Merck and Pfizer. "
"Summary Aspergillus fumigatus is currently the major airborne fungal pathogen that menaces immunocompromised individuals. Germination ever of inhaled conidia is a hallmark of the early infection process, but little is known about the underlying mechanisms. The intention of our ongoing studies is the identification of A. fumigatus
proteins that are differentially expressed during germination and may provide insights in the germination process. Using a proteomic approach, we identified AFUA_5G09330 as a major hyphal-specific protein. This result was confirmed using monoclonal antibodies generated in this study. AFUA_5G09330 belongs to a fungal-specific protein family. The eponymous CipC protein of A. nidulans has been shown to be induced by concanamycin A, and transcriptional data from Cryptococcus neoformans demonstrate a strong up-regulation of the expression of a homologous gene during infection. Our data provide evidence that AFUA_5G09330 is a monomeric, cytoplasmic protein. We found no evidence for an overexpression of AFUA_5G09330 induced by concanamycin A or other stress conditions. AFUA_5G09330 is exclusively found in the hyphal morphotype that enables an invasive growth of A. fumigatus during infection.


Vivek Nayer, Chief Marketing Officer, Group Corporate Brand, Mahindra & Mahindra Ltd talks about the brand's new Rise Up Anthem, a rap mix that draws on the #LadkiHaathSeNikalJayegi campaign launched last year.
Six months ago, when we launched #LadkiHaathSeNikalJayegi, the core thought was to empower young women in the country through education. With the Rise Up anthem, the core thought is the same except that it is rendered in a more contemporary manner leveraging National Girl Child Day. I believe this anthem will appeal to millennials in a big way. Our message was not just about education for girls but also about enabling them to choose their own careers freely, however unconventional. In the previous film, there was a scene where the father tells his daughter to study hard and become an engineer, but she tells him that she would rather be a pilot. So the 'seed' for this film was already sowed in our previous one.
Like Mahindra, there are several brands that are doing good through their CSR initiatives. However, to drive change, we must enlist the support of the people and the community. We are fortunate that the Mahindra legacy gives us the credibility to enlist community support and drive societal change.


*Conditions Apply: All prices shown here are per person share twin (unless stated as single), in AUD, based on best available cruise fare at time of publication (16Apr19). All prices based on cash payment - credit card fees may apply. Ships gratuities are not included and paid onboard directly to cruise line. Cruise deposit, amendment and cancellation conditions apply. Travel agent service fees may apply. Special conditions apply - please ask for full details at time of enquiry. Prices calculated to include 20%/10% Ponant bonus discount which is already factored into listed prices and may vary at time of booking. All passports, vaccinations and visas are the responsibility of the travelling guest. **All airfares/taxes are based on 2019 rates/dates and are subject to change until bookable approx 10 months prior. Once issued all airfare taxes are due in full within 24 hours and subject to cancellation/change fees. Offer ends 30May19 or until sold out/withdrawn from sale and is subject to availability at time of booking. Travel insurance is mandatory but not included in package prices.
From Darwin to Broome, embark aboard Le lapérouse for an 11-day expedition cruise. At around two-thirds the size of France, Kimberley is one of the last unspoiled regions on the planet.


Check out Kid Glyde and Kelly Peters talking about the KBL program with Antwan Lewis.
Watch as two of the KBL teams go head to head in this Wonderama feature.
Check out the founder of the KBL in this Head and Shoulder commercial that features him and the Dynamic Rockers. This was aired during the VH1 Honors in 2017.
Other crew members in this video are Glyde (father of Kid Glyde), Spidey, Pete Nasty and Alexander the Great!


Is all the good news being saved up for a blockbuster press release?
Season ticket prices will be frozen at Division One levels until others in Division Two catch up or the U's get promoted.
Stadium sponsor will be a Cowling company and hopefully we can then play in blue & white home and away.
No news on transfers until the end of July when the desperate bargains and crocks are half price.
That all sounds very credible, do you have sources within the club?
No, but surely it is utterly predictable?
"Elementary Dr Watson" as the great detective might say.
Somewhat unsurprisingly the new stadium sponsor is Jobserve.
Absolutely nobody saw that coming.
Actually, it might be a smart bit of business. Not sure about all the ins and outs of it but my guess is this allows RC to introduce money into the club (should he so wish)without falling foul of FFP as its commercial income from a major sponsor rather than a sub from the owner.
The stadium rent is now linked to gate receipts and the sponsorship will match the rent paid. The more fans attend the higher the rent and the higher the sponsorship. The club will, in effect, have the stadium rent free.
Nobody has any idea what the attendance will be so how Cowling can say the new sponsorship will be double the previous deal I don't know. The sponsorship pays the rent, which is good, but if attendance falls(I'll be staggered if it doesn't) then I don't see any party being happy except Jobserve.
There is no indication whatsoever that any extra funds will be going to the club, despite the obvious opportunity to do this.


"This photo was sent to me by Eli da Conceição Santos. She tells me it was taken by a friend of hers in early October 2009 on the road to Bahía (Brazil). The witness stopped the car to take photos of the landscape, but the camera kept shutting off. Three attemtps were made, all of them unsuccessful. She resumed her journey.
"Upon returning home, she was amazed to see that a photo had in fact been taken of the landscape, displaying a yellow object in the sky.
"Everything points to the image being genuine, perhaps even a "chance" UFO, until its nature can be determined by an analysis of the original."
Many thanks to Ana Luisa for providing us with this photo!


Ajay Devgn, Emraan Hashmi, Ileana D Cruz, Esha Gupta have been cast in the upcoming Bollywood film Baadshaho.
Director Milan Luthria tweeted names of stars of his movie.
Director Milan Lutharia, who directed the super hit movie 'Once Upon A time in Mumbai', is now back with another film titled 'Baadshaho' which has actors Emraan Hashmi and Ajay Devgan in the lead roles. This is the second time after the film, 'Once Upon A Time in Mumbai', that both Ajay Devgan and Emraan Hashmi will be sharing screen space. Apart from these two actors, commando and force actor Vidyut Jammwal will also play a prominent role in the film.
Recreating the magic in Baadshaho…happy to be a part of this exciting project!
Ajay, Emraan in an emergency!
Baadshaho, a thriller set in the emergency era of the 70s is being produced by Bhushan Kumar and Milan Luthria. In an interview, Milan said that this is a historical fiction film which will have a lot of stuff that is exciting and unusual. He also added that a lot of research has been done on the subject and that the film will feature a lot of action and thrills with an emergency as a backdrop.
Ajay Devgan and Emraan Hashmi, who also starred in Milan's film Once Upon A time in Mumbai, will be sporting different looks in Baadshaho. 'The Dirty Picture' director will also be collaborating with a foreign action director. The film will feature music composed by Ankit Tiwari and will have Rajasthani folk songs with a funky twist.
There were enough speculations about who will play the female lead in the film. At first, Shruti Haasan was roped in on the project but she quit. Following her exit several top actresses including Aishwarya Rai was considered for the role. Now, however, it has been confirmed that actress Ileana D Cruz who is best known for her film Barfi, will be playing the female lead. Along with Ileana, actress Esha Gupta will also be seen in the film.
Emraan Hashmi, Our Next Superstar?
Emraan Hashmi who was going through a lean phase in his career is all set to prove his acting skills with Baadshaho. His previous seven films tanked without a trace at the box office. However with Azhar which released in May, the talented actor showed that he still has the power to attract audiences. With Baadshaho releasing this year and Raaz 4 releasing next year, the actor is ready for a huge comeback.
Ajay Devgan who was last seen in Drishyam, a box office success, will be seen next in Shivaay. Ajay, who is known for his action films, confirmed that Shivaay will have a lot of stunts and actions performed by him. He took to twitter to share the first look of his breathtaking film. Shivaay is expected to release on Diwali this year. His other upcoming movies that will be released next year include Satsang and Raajneeti 2.
The filming for Baadshaho will begin in the month of august this year. Although Ajay Devgan is busy shooting his much-hyped film Shivaay. He and the entire cast will come together in august to begin shooting. This multi starrer film will have a fifteen-month schedule in Mumbai as well as a two-month schedule in Rajasthan.
We can expect this movie to be as good as 'Once Upon A time in Mumbai'. So you guys stay tuned with us for latest updates about the movie.


Official government travel meant Tim could take a taxi, limo, or whatever else to the airport on the government's dime but, of course, Maria wanted to drive him.
"Just drop me off here," Tim said.
"No. I want to park and go in with you," Maria argued.
"Okay," she responded with tears in her eyes.
"No lloras, mi amor." Tim's Spanish was limited to very few words, but they were effective ones.
"I will," he assured her with an eye roll.
"I will, Babe. I promise." He gave her a kiss and then kissed her belly. He then opened the door, grabbed his pack, and left. Maria was two months pregnant.
They found out she was pregnant just a month before she was due to separate from the Air Force. This was a problem. The uneasiness of not having a job with full benefits weighed heavily on the expectant mother. That and the fact that Tim had recently found out that it was his turn to deploy.
They didn't tell anyone. They went up to Reno on a Saturday as Tim and Maria and came back on Sunday as Mr. and Mrs. Rogers. On Monday, they let the Air Force know, changing their statuses to "married" and naming each other as their spouse. A necessary step to ensure Maria would have medical coverage when she got out in a couple of weeks.
Of course, the families were disappointed when they were notified via speaker phone that Sunday on the drive back from Reno. They made the newlyweds promise a ceremony and party when Tim got back. It never happened.


text:
Q: Compose UI (recompose) with window Manager not working I'm working on floating window on android and i'm having a problem.
So I have my activity that calls my floating class that creates a the view and adds it to the windowmanager with a timer that is displayed and counting down. When trying the same code in a normal activity it works find :S?
Here is my viewmodel holding my mutableStateOf value
class WicViewModel : ViewModel() {

private val TAG = "WicViewModel"

private val a = 10000L
private val b = 1000L

private var _input: Long by mutableStateOf(a)

var input: Long
    get() = _input
    set(value) {
        if (value == _input) return
        _input = value

    }

fun start() {
    val timer = object : CountDownTimer(a, b) {
        override fun onTick(millisUntilFinished: Long) {
            Log.d("MYLOG", "text updated programmatically")
            input = millisUntilFinished

        }

        override fun onFinish() {
            input = 0
        }
    }
    timer.start()

}
}

Here is my class with the compose into windowmanager
class WicController constructor(val context: Context?, val viewModel: WicViewModel) {

private val TAG = "WicController"
private var windowManager: WindowManager? = null
private var wicView: View? = null
private lateinit var lifecycleOwner: CDOLifecycleOwner

fun show() {
    if (context == null) return
    val paramFloat = WindowManager.LayoutParams(
        WindowManager.LayoutParams.WRAP_CONTENT,
        WindowManager.LayoutParams.WRAP_CONTENT,
        getWindowType(),
        WindowManager.LayoutParams.FLAG_NOT_FOCUSABLE,
        PixelFormat.TRANSLUCENT
    )
    paramFloat.gravity = Gravity.CENTER or Gravity.END

    windowManager = context.getSystemService(Context.WINDOW_SERVICE) as WindowManager?

    val composeView = ComposeView(context.applicationContext)
    composeView.setContent {
        timerText(viewModel)
    }

    lifecycleOwner = CDOLifecycleOwner()
    lifecycleOwner.performRestore(null)
    lifecycleOwner.handleLifecycleEvent(Lifecycle.Event.ON_CREATE)
    ViewTreeLifecycleOwner.set(composeView, lifecycleOwner)
    ViewTreeSavedStateRegistryOwner.set(composeView, lifecycleOwner)
    windowManager?.addView(composeView, paramFloat)

}

fun hide() {
    windowManager?.removeView(wicView!!)
    context?.let { Demo.startCalldorado(it) }
}

private fun getWindowType(): Int {
    var windowType = WindowManager.LayoutParams.TYPE_SYSTEM_ERROR
    if (Build.VERSION.SDK_INT >= Build.VERSION_CODES.O) {
        windowType = WindowManager.LayoutParams.TYPE_APPLICATION_OVERLAY
    }
    return windowType
}

@Composable
fun timerText(viewModel: WicViewModel){
    Text(
        text = (viewModel.input / 1000).toString(),
        modifier = Modifier
            .padding(bottom = 8.dp)
            .fillMaxWidth(),
        fontSize = 13.sp,
        color = Color.White,

        )
}}

I know that the value is being changed but the compose is not recomposing itself
sometimes it may change but it very random.
I dont know if im doing it wrong or if compose is not made for windowmanager/floating window use, however I hope some of you guys on here can help me out since I cant find anything on the web about this.


text:
Team USA Basketball Vs. France: Game Time, TV Schedule And More
By T.J. Doyle Jul 29, 2012, 8:23am EDT
Share All sharing options for: Team USA Basketball Vs. France: Game Time, TV Schedule And More
Team USA Basketball begins their gold medal defense on Sunday morning, when they face Tony Parker and the French in an opening round Group A battle. The game can be seen live on NBC Sports Network or streamed on NBCOlympics.com.
LeBron James, Kevin Durant and their USA teammates will be heavy favorites against the French, despite the presence of several NBA players to go along with Parker on Team France. Boris Diaw, Ronny Turiaf, Nicolas Batum and Kevin Seraphin will certainly be familiar with their American counterparts, but the roster talent differential is simply too great for the French to overcome.
Here is what you need to know for Sunday's game:
Game Day/Time: Sunday, July 29, 9:30 a.m. EST
Location: Olympic Park Basketball Arena, London, England
Television Coverage: NBC Sports Network
For more on Team USA Basketball's run in the 2012 London Olympics, stay tuned to this StoryStream. For a complete schedule of events and dates medals will be awarded, visit NBC Sports' official Olympic website. For complete coverage from the 2012 London Olympics, keep checking this StoryStream and visit SB Nation's Olympics hub.
Team USA Wins Olympic Basketball Gold
London 2012 Olympics Medal Count: United States Captures Most Gold, Overall Medals
2012 Olympics Medal Count: United States Takes Home Five Medals On Opening Day


The Diver sisters live, work and tour together for most of the year in the US, but they still hang around together when they're at home. Happily they really like one another as people, and are so in tune, they finish each other's sentences.
While the two blonde sisters, Grainne and Joan, are chatty and outgoing, the dark-haired ones, Marie Therese and Angela, are quieter and happier to stay in the background. Although Marie Therese is the oldest, she's not the bossy one. She's too nice and serene, her sisters say, and she's a real dreamer and very easygoing. Grainne, who comes second, is the leader of the group and usually speaks on their behalf, and she's the dynamic one that the rest go to for advice. "Grainne is kind of the boss and she has great cop on," says youngest sister Joan.
The sisters bicker a bit when they're tired, but they don't tend to argue in general. If one of them gets down, the others rally around to cheer her up, and they know each other so well, they rub along together most harmoniously. "Angela is a worrier, but she's incredibly creative and loyal," says Grainne. "She gives us our sound. Joan is extremely considerate of other people and she looks after everyone else and is a very hard worker."
While they now live in a house they bought outside New York, the sisters grew up in the town of Bundoran in Donegal and attended Ard Lughaidh school. There are seven years between the oldest, Marie Therese, and youngest Joan. They inherited their musicality from their mum, Kathleen, who sang with her brothers Richard and Barney in the Richard Fitzgerald Ceili Band for many years. She had toured the world with the band before her daughters came along, as it happens. "She always sang in the house and our uncle would drop in and teach us to play music," Marie Therese recalls.
While they can all play several instruments, Marie Therese mainly plays piano and accordion, Grainne is on guitar, banjo, flute and viola, Angela mainly plays bass guitar, violin and banjo, and Joan is on drums and lead vocals. All of the sisters have great voices and harmonise naturally, which comes from years of being so much in tune at every level.
While their mum gave up touring when they came along, she was in demand locally to entertain the visitors who flocked to Bundoran during the summer. The girls learned their craft from her, as they used to play with her on stage and also at surfing events. They feel that they were "old souls" from an early age, as they got to have many experiences travelling to other counties and countries to play while still at school.
The sisters had a very happy childhood and can't say enough about how wonderful their parents are. Their mum is always very positive, and their dad, Sean, was very much outnumbered in the house, gender-wise. "He was the local driving test supervisor, and people still come up to us and say that our father either passed or failed them at driving," says Angela.
The sisters left Bundoran after school and travelled to Dublin to study. Marie Therese did a degree in performance at the College of Music, while Grainne went to Trinity to study maths and music. Angela studied violin and also did a course in retail management at the College of Marketing and Design, and Joan studied German and French at Trinity. Having originally performed as the Diver Sisters, a friend suggested the name, Screaming Orphans. Their big break came when Sinead O'Connor spotted them performing without music in a church in 1997 and invited them on her European and US Gospel Tour during the summer months. They were her support band and were also her backing singers during her set.
This led to them moving to the US in 2001 and begin touring around bars and clubs building up a fanbase, which went very well. They are in demand all the time now to perform at concerts and festivals, and their career highlights include appearing on David Letterman's TV show, topping the iTunes World Music charts, and recording with The Chieftains and Peter Gabriel. Singing in Central Park was another real highlight, they say.
Their new pop album, Life In A Carnival, is out this Friday, and they will tour it here and abroad.
While they're known for their Celtic music on one hand, the girls have a real pop/indie side and they fizz with energy and vitality on stage. The album, produced by John Reynolds, reflects the diversity of their sound and musicality as well as the myriad influences that inspire them.
The sisters don't date at present, partly because they're always on the road, and partly because it would mean the end for the band.
"At this stage, none of us can be replaced," says Grainne.
"Other bands can replace members but we can't as our sound comes from the four of us.
"If someone met Mr Perfect tomorrow, everyone else's career would be gone so you have to take that into consideration."
"But we're OK with that," her sister Joan points out, with a smile. "We're happy to keep doing this because we love it."


The CEO Student Ambassadors of the Business & Organization Leadership Development (BOLD) program are demonstrating their business savvy, leadership, and collaborative teamwork to deliver leadership development opportunities for all UWB undergraduates. On Tuesday, April 23rd, these students hosted a Leadership Lesson event headlined by entrepreneur and philanthropist, Naveen Jain.
Jain encouraged the nearly 150 undergraduate students in attendance to leverage their own potential to solve critical problems for humanity through the use of innovation and entrepreneurship.
How does one go about solving humanity's grandest challenges? To start, Jain's well-known mantra is, "If people don't think you are crazy, then you aren't thinking big". That's exactly how Jain obtained his extensive list of titles, which includes founder of INome, Infospace, Intellius, Moon Express, and the World Innovation Institute. His experience as a CEO includes both successes and failures.
Students actively participated throughout the event by asking tough questions of Jain who challenged them to think in a "different box", and "be bold", an apt challenge given the BOLD program's mission and vision.
Jain reminded students to always be mindful that, "Success is not about how much money you have in the bank", but rather that "Success is about how many lives you are able to positively change". He elaborated, "The day you become humble is the day you become successful." With that highlighted, it's no wonder the room was filled to capacity with students eager to hear a captivating lesson in leadership.
BOLD continues to exceed expectations in delivering motivation and direction to groom a new generation of leaders.


text:
#ifndef SUPERMARIO_SPRITE_H
#define SUPERMARIO_SPRITE_H

#include <stdio.h>
#include <stdlib.h>
#include <string.h>
#include <stdbool.h>
#include <SDL2/SDL.h>
#include "texture.h"
#include "../component/component.h"

// Constants
#define SPRITE_COUNT 50
#define SPRITE_EMPTY 0

// Object
typedef struct sprite_t {
    int cashId;
    const char *name;
    SDL_Texture *texture;
} Sprite;

// Methods
Sprite spriteCache[SPRITE_COUNT];
Sprite* sprite_create(SDL_Renderer *renderer, const char* name);
void sprite_delete(Sprite *sprite);
Sprite* sprite_get(SDL_Renderer *renderer, const char* name);
void sprite_render(SDL_Renderer *renderer, Sprite *sprite, int x, int y);

#endif

redpajama_set_name: RedPajamaGithub


Material: US made pure titanium post.
This earrings is made from brass that will naturally tarnish over time. If you want to keep it nice and shiny, you can take care of it by rubbing the lemon slice over your piece, rinse with water and dry with a soft cloth.


We know you know Company. But you should get to know us for great careers, too. And, right now, we're looking for an Insurance Claims Service Representative to start a Company career in Buffalo, NY. As an Insurance Claims Service Representative in a fast-paced call center environment where no two days are alike, you will be the first point of contact for customers involved in accidents.
At Company, it's not just a job, it's growth and opportunity.
There's one thing our associates all have in common: they found a career they never expected. With coaching and mentoring, you will find your position as an Insurance Claims Service Representative can become a career in the most unexpected and rewarding ways.
As a full-time Company associate, you'll be offered a comprehensive Total Rewards Program with a wide range of benefits. We said it's more than a job! Our benefits ensure a long-lasting career with us as your personal life and needs change.
This position is based in Getzville, NY (a suburb of Buffalo, NY). Get to know a little more about our location here and find out what makes working here pleasantly unexpected for our associates.
Company is an equal opportunity employer. Company conducts drug screens and background checks on applicants who accept employment offers.


text:
Work In Texas Veterans Jobs
Work In Texas
Justice, Bureau of Prisons/Federal Prison System Correctional Officer (Correctional Systems Officer) in Fort Worth, Texas
Why work for the Federal Bureau of Prisons? You can have a meaningful career with an agency that truly values a diverse workforce. You will find a diverse workforce employed from entry level jobs to senior management positions. We protect public safety by ensuring federal offenders serve their sentences of imprisonment in facilities that are safe, humane, and provide reentry programming. Employees at correctional facilities perform correctional work regardless of their specific occupation.
To be considered for the position, you must meet the following qualification requirements:Education: There is no substitution of education for specialized experience for this position at this grade level.Experience: You must have at least one year of specialized experience equivalent in difficulty and complexity to the next lower grade level in federal service. This experience must have equipped the applicant with the qualifications necessary to successfully perform the duties of the position.Some examples of qualifying experience are:Experience directly related to the various functions of the Mailroom and Receiving and Discharge areas; to include admission and release, physical processing, identification, coordination of prisoner transfers, security procedures, bus movement, final releases.Experience in supervising large groups of inmates in preparation for bus or airlift operations. This includes coordinating and carrying out various functions (i.e., visual searching, fingerprinting, photographing).Experience in carrying out the proper release of inmates who have completed their federal sentences; to include proper identification of inmates, review of clearances, fines, all forms of release paperwork, etc.Experience in coordinating exchanges of custody with federal and non-federal agencies.Medical Requirement: The Department of Justice, Bureau of Prisons has established the following medical requirements for Correctional Officer positions:The duties of these positions involve unusual mental and nervous pressure, and require arduous physical exertion involving prolonged walking and standing, restraining of prisoners in emergencies, and participating in escape hunts. Applicants must be physically capable of performing efficiently the duties of these positions, and be free from such defects or disease as may constitute employment hazards to themselves or others. The duties of a Correctional Officer are arduous; and sound health as well as physical fitness is required.If applicable, credit will be given for paid and unpaid experience. To receive proper credit, you must show the actual time (such as the number of hours worked per week) spent in activities.Your eligibility for consideration will be based on your responses to the questions in the application.
Justice, Bureau of Prisons/Feder...
Correctional Officer (Correction...
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Twisted Glass Blunt "Swished Edition" Cigarillo Mini Edition - THE G.B.S.
Introducing the New Twisted Glass Blunt Mini!
The Mini is designed for people who enjoy a smaller toke. Whether you only need the occasional hit, or you just enjoy long slow pulls that don't overwhelm you, the 50% smaller cherry on the Twisted Glass Blunt Mini is just what you've been waiting for!
The Swished Mini Edition is the newest spin on the most new and improved Twisted Glass Blunt! Works just like it's Big Brother but Easily packs up to 1.5 grams. Fits snug into your pocket for the moving and grooving of everyday life. Inhale the Difference today and never waste another dollar on wraps with this amazing addition!The Swished Edition has a New and Improved Swished-tip mouthpiece and filter system to improve airflow and pull. Take the #GlassBluntChallenge and become a believer today!
Rolling a blunt will never be the same again! The average consumer spends $15-25 per week on rolling papers and blunts alone. The Glass Blunt solves all your problems while still enjoying your favorite flavors with these simple steps: Easily pack up to 1.5 grams into the glass tube (with rubber cap on) and twist the screw counter-clockwise into the tube. After that, all the chambers will be loaded. After that all you need to do is light the end and puff, puff, pass.
To ash, simply twist the screw clockwise and the ash will get pushed out the glass leaving fresh trees for your next session.


Thanks to Kevin Hopper, the kids and I are finally moving past the nightmare and learning to laugh again.
They take the extra step and are personal and make sure I am satisfied with whatever decision they choose to take.
The staff at Hopper Law Firm PLLC will work tirelessly to help you out.
Friendly and professional staff provides a pleasant experience during a very stressful event.
I was glad that I had the experienced counsel of Hopper Law Firm PLLC to handle my case and guide me through the process.
I have my life back, my kids live with me, & a very nice settlement to top it off.
I was very impressed by the responsiveness and personal attention.
Through the years, I have always found the attorneys & staff to be both professional & personable.
Hopper Law Firm PLLC always goes above and beyond to help us out.
They were very easy to work with, answered all of my questions, and made me feel at ease during a stressful time.
Mr. Jones is great at answering your questions & will tell it to you straight.
Excellent staff. Professional and courteous.
No fun going to see a lawyer, but they all helped make the whole process easier.
I was pleasantly surprised to receive a settlement greater than I had expected. These guys worked hard for me. Thank you!
Thank goodness for Mr. Kevin Hopper!
They were able to help me receive the outcome I needed and I would recommend them to everyone.


MailChimp means creativity and serious business—thinking outside the box with purpose and heart. We wanted to produce a deck of cards that reflects this perspective in a simple, fun, elegant design.
A collaboration between MailChimp, Fuzzco, and Theory11. Sure to satisfy apes and humans alike.
MailChimp playing cards are a perfect blend of organic elements and iconic imagery - featuring custom court cards and ultra thin borders.
Fugees Family is a 501(c)(3) non-profit organization devoted to working with child survivors of war. The Fugees Family began ten years ago in Atlanta as a way to offer refugees free access to organized soccer. It's since grown into the only school in the United States dedicated to refugee education."
Once you buy one, you'll know what the hype is all about. theory11 creates the world's finest playing cards.
All theory11 decks are printed on sturdy Casino Q1 quality paper, with our signature premium 909 finish for perfect handling.
It's no secret that our decks are the best. Just check out one of the many articles featuring them around the web.
All theory11 decks are printed in the United States by the US Playing Card Company to ensure the highest level of quality.
Inspired by Chinese classical mythology of the miao nationality, a symbol of life. On behalf of good luck. These printed in USPCC, 3D display tech..
Featured #1 in the GQ Holiday Gift Guide. Playing cards fit for a king. The world's finest. The best.The World's FinestPLAYING CARDS FIT FOR A KIN..


Samoa is located in the Pacific Ocean east of Australia. The country consists of two larger islands, Upolu and Savai'l, and a few smaller ones. When visiting the islands you will find rugged cliffs, thick rainforests, crystal clear lagoons, sparkling waterfalls and extinct craters. The islands are also surrounded by amazing marine life which is easy to explore due to the shallow waters.
For information on Samoa's individual ports, please click on one of the choices below. If you would like information on cruises to Samoa, please call one of our Cruise Experts on 0800 008 6677.


text:
Dex Plans Radical Switch For 2014
By Simon Paice
Former Formula Renault BARC and Formula Ford GB racer Jack Dex has become the latest driver to target a switch from single-seater to sportscar racing for 2014, with the 21 year old hoping to join the Radical Clubmans Cup next season.
Dex, who has spent the majority of the last eighteen months on the sidelines, made a one-off appearance in this season's Dunlop MSA Formula Ford Championship of Great Britain in the SWB Motorsport-Sinter at Rockingham, though struggled against the faster Mygale cars.
After assessing his options in single-seaters, Dex has made the decision to target a future in sportscars, feeling it will provide a wider range of opportunities at more manageable budgets.
"Single seaters has just become far too expensive for such little track time," Dex told his official website. "It just wasn't worth it. I couldn't test as much as I needed to and was only competitive at circuits I managed to get some testing at. The Formula Ford car I had a brief go in this year just wasn't competitive, so was very frustrating for me.
"Next year I will drive for the first time in car racing, with a new team, driving a new car in a new championship. It's all very exciting and for my career. I need to redeem my reputation and start off competitively."
Alongside any race deal, Dex is also planning to continue running the successful SWB Motorsport kart team.
Formula FordHistoric Racing
How to not sit on the sidelines - Benn Tilley's story
By Senna Hamilton
Racing is alright when you have made it but how do you get there and what happens to all the other type of racing. This is Benn Tilley and this is his racing experience.
Josh Smith Wins Double Red Flagged Festival Final
By Connor Jackson
A dramatic Formula Ford Festival Final saw Josh Smith take the lead on the final lap to beat favourite Niall Murray over the line.
Murray and White Claim Semi Final Wins at Brands
Niall Murray and Oliver White took Semi-Final victories in the Festival, while Eastwell, Middlehurst became the first major casualties.


text:
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Sort By: Relevance Title Ascending Title Descending 1-10 of 19 (2 pages)
Michael Kors, Autumn/Winter 1997
...Michael Kors's Autumn/Winter 1997 show for his eponymous label was presented at New York fashion week. Masculine tailoring was a predominant theme within the collection, as sharp suits were paired with chunky turtleneck sweaters or left...
Céline, Spring/Summer 2000
...Michael Kors's Spring/Summer 2000 womenswear show for Celine was presented at Paris Fashion Week. The collection consisted of fluid lines with semi-circular, hourglass, kaftan, and halter neck dresses as well as sheath and wrap skirts...
...Michael Kors's Spring/Summer 2001 show for Celine was presented at Paris Fashion Week. The collection had a bohemian, casual feel and a touch of safari inspiration (as seen through the predominant use of khaki); popular pieces included...
Michael Kors, Spring/Summer 1995
...Michael Kors´s Spring/Summer 1995 show for his eponymous label took place at New York Fashion Week. The show displayed a collection of clean-cut strong pieces that gave a modern and sensual twist to the power dressing of the 1980s...
...Michael Kors's Spring/Summer 2000 show for his eponymous brand was presented at New York Fashion Week. Kors displayed a range of leisurewear and eveningwear. Women wore a close-fitting silhouette for daytime with bikinis, wrap skirts, mini...
...Michael Kors's Spring/Summer 1993 show for his eponymous label was presented at New York Fashion Week. As usual for Kors many supermodels walked the runway, including Christy Turlington, Naomi Campbell, Helena Christensen, and Cindy...
...Michael Kors's Spring/Summer 1990 womenswear collection was presented at New York Fashion Week. In the same year, Kors introduced a lower-priced 'Kors' line and a menswear collection, while also acting as the designer for Erreuno J...
...Michael Kors's 1991 Autumn/Winter collection was shown at New York Fashion Week. Models opened the show with complete beige ensembles of skirts, sweaters, pants and coats. Towards the middle of the show yellows and pinks were introduced...
...Michael Kors's 1993 Autumn/Winter womenswear show took place at New York Fashion Week. The collection featured a range of tailored suits and dresses in white, tonal grays, and black styled with leather gloves, leather baker boy and cloche...
...Michael Kors' Autumn/Winter 1994 show was presented at New York Fashion Week. Models such as Naomi Campbell, Helena Christensen and Shalom Harlow walked the runway wearing Kors' signature minimalist, tailored yet feminine clothing. The show...


This service allows to search similar images to the one provided as example.
random: retrieves a random set of images from the server. It does not need any other parameter.
image_file_name: name of the server file to be used as query.
file: image to be used as query.