Source: http://www.thehollywoodgossip.com/2013/04/kyle-richards-i-want-more-children/
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Monday, April 29, 2013
PST: Late own-goal torpedoes Wigan vs. Spurs
Under Roberto Mart?nez, Wigan Athletic have accrued a reputation for late season sprints that ensure Premier League survival. This year, however, you have to wonder if their luck has run out, with a late own goal costing them full points today against Tottenham.
The Latics got off to a bad start, with goalkeeper Joel?s attempted clearance in the ninth minute careening off Gareth Bale for the game?s opening goal. But they responded. Two minutes later, Emmerson Boyce?s header had them even, and shortly after halftime, Callum McManaman?s shot from well beyond the edge of the box gave Wigan a 2-1 lead.
But just before full time, Boyce gave his goal back. Amid a late push from Spurs, a ball sent across the six by Aaron Lennon went past Bale, off Boyce?s shins, and into the Wigan net, costing the Latics two points.
Had they held on, Wigan would have been out of the drop. They?d have equaled Aston Villa?s 34 points with a better goal difference (what would have been -22 versus -27). Instead, they stay 18th, albeit two points back instead of three.
Hosting Sunderland on Monday, Villa have a chance to gain ground on Wigan, though the Latics will have their match-in-hand back by the time the round?s over. However, if Villa?s suddenly five up instead of three, Wigan not only need full points in their makeup game, they also likely need to beat Villa on the season?s last day to win survival.
That May 19 match in Wigan?s shaping up to be one of the more dramatic in Premier League history, but had the Latic?s form been rewarded in recent weeks, they may have been able to avoid this fate. They played poorly last weekend at West Ham, but in the previous round they outplayed Manchester City at Eastlands only to leave Manchester with a 1-0 loss. Today they played the key part in both Spurs goals, costing them two crucial points.
It?s a woulda-coulda game that every 18th place team can play. Wigan had 34 rounds to avoid this situation, one in which they find themselves every year. Yet here we are, again, with the Latics pushing their luck once more. At some point, they?re going to hit a wammie.
Wigan is in the middle of their typical push, but the breaks aren?t going their way. As a result, that push isn?t being reflected in the table, forcing us to ask whether if it can be considered a push at all.
Maybe this is the year the Latics? unlikely run finally ends.
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Paul McCartney and Wings: Hi Hi Hi
This is a good song. No one is saying that you should listen to it while in any type of altered mental state whatsoever. It's just a good song. The Wings recorded it in 1972 and it got pretty popular, though the BBC was turned off by some of its lyrics. Paul apparently had this to say about their concerns:
     |
Source: http://feeds.gawker.com/~r/gizmodo/full/~3/zs9mFpyYGBA/paul-mccartney-and-wings-hi-hi-hi
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Sunday, April 28, 2013
Jessica Simpson's Parents Are Splitting Up Her Life Insurance ...
Remember that sneaky, sneaky, MAJOR life insurance policy Joe Simpson took out on his daughter?
Well, turns out he WON'T get to keep it to himself!
In his divorce with Tina Simpson, Joe will have to split Jessica Simpson?s life insurance policy in half.
Guess keeping it secret didn't work!
The exes have finalized their divorce, and it seems they?re keeping things pretty equal in the end.
Not only will the $4.5 million life insurance policy be divided equally, but the parents will also split interest on Jessica and Ashlee Simpson?s management fees!
They?ve also figured out a satisfactory way to split up other money and properties as Joe will keep half of their Sherman Oaks house, all his personal effects and bank accounts, the 2012 Mercedes SLS and 2011 Mercedes S63, and a many stocks.
Meanwhile, Tina gets the house in Waco, over ten bank accounts, a 2010 Range Rover Sport, 2011 Porsche 997 coupe, and much more!
Considering how nasty this split appeared to be at first, we?re happy to hear it?s all settled and finalized.
We just wonder what Jessica thinks about the life insurance policy!
[Image via Nikki Nelson/WENN.]
Tags: ashlee simpson, break up, divorce, jessica simpson, joe simpson, life insurance, life insurance policy, settlement, split, tina simpson
Source: http://perezhilton.com/2013-04-26-jessica-simpsons-parents-divorce-splitting-life-insurance-policy
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Friday, April 26, 2013
Sandra Beltran, Mexican cartel 'queen,' pleads guilty in US
Sandra?Beltran?pleaded guilty Tuesday to being an accessory after the fact to an operation linking?Mexico's Sinaloa cartel and Colombia's Norte Valle cartel.
A Mexican woman known as a drug cartel queen has pleaded guilty in Miami to charges arising from a major cocaine trafficking case.
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Court records show?Sandra?Avila?Beltran?pleaded guilty Tuesday to being an accessory after the fact in an organization that included Juan Diego Espinosa Ramirez. He was her boyfriend at the time.
Espinosa was a former liaison between Mexico's Sinaloa cartel and Colombia's Norte Valle cartel. He pleaded guilty in 2009 to cocaine trafficking charges.
A statement signed by Avila, who was known as the "Queen of the Pacific," says she provided money to Espinosa for travel and lodging so he could evade arrest by authorities between 2002 and 2004.
The 52-year-old Avila faces a maximum of 15 years in prison at a July 25 sentencing hearing.
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Thursday, April 25, 2013
Researchers Find Hormone That Grows Insulin-Producing Cells
A microscopy image of a rat pancreas shows the insulin-making cells in green.
Masur/Wikimedia.orgA microscopy image of a rat pancreas shows the insulin-making cells in green.
Masur/Wikimedia.orgThe work is only in mice so far, but it sure is intriguing.
A newly found hormone revs up production of cells that make insulin ? the very kind that people with advanced diabetes lack.
Harvard scientists, reporting the discovery Thursday in Cell, call the hormone betatrophin because it stimulates the production of beta cells in the pancreas. These cells make insulin, which the body needs to control blood sugar. ("Trophin" comes from "nourishing" in Greek.)
When researchers turned on the betatrophin gene in the livers of diabetic lab mice, the number of beta cells in their pancreas glands tripled within 10 days and their blood sugar went down.
Humans have betatrophin genes too, as do all mammals. So Harvard's Doug Melton thinks he's got his hands on something that just might get at a root cause of diabetes.
"I'm very excited about it," Melton tells Shots. "It isn't every day one discovers a new hormone ? especially one that affects the cell I'm obsessed with, the beta cell."
He's not alone. Mary-Elizabeth Patti of the Joslin Diabetes Center in Boston, who wasn't involved in the work but is familiar with the findings, also calls the discovery exciting.
"I'm sure this will stimulate a lot of work to look at effects of this protein and rapidly investigate whether this could be a new approach to treating diabetes," Patti tells Shots.
Human experiments with betatrophin are several years off ? perhaps five years, Melton guesses.
First, researchers need to make the hormone in large amounts, then show it works consistently and safely in animals. But at this early stage, hopes are running high.
"If I'm right," Melton says, "you would inject this hormone once a month or once a year, give yourself new beta cells, and they would then very accurately control blood sugars by instantaneously producing just the right amount of insulin. They should reduce the complications of your disease because you're back to the normal control of your blood sugar."
Patti cautions that "it's rare there's a single unique hormone that does everything." And she wonders whether people with Type 2 diabetes, who are resistant to insulin, make betatrophin in normal amounts.
"If someone is insulin-resistant, why wouldn't he make more of this protein and respond to it?" Patti asks. "The question is: Do diabetics make sufficient amounts of this hormone or not? And if they do, do they respond to it or are they resistant to it?"
Melton acknowledges that his scenario of curing diabetes with periodic doses of betatrophin "is the dream of what would happen."
"Let's also remember that at the beginning of new discovery, people like me are always very optimistic," Melton says. "I'm also cognizant of the fact that it could get complicated." He notes that leptin, another hormone, was supposedly going to cure obesity when it was discovered in 1994. But it hasn't worked out that way.
For the past decade, Melton and his colleagues at the Harvard Stem Cell Institute have been pursuing a very different diabetes-cure strategy: tricking stem cells to morph into pancreatic beta cells. That work continues, and he hopes in the next year or so to report "that we're making bucket loads" of beta cells derived from stem cells.
But meanwhile, the group decided to explore what happens when mice are given a synthetic peptide, developed some years back by the firm Novo Nordisk, that blocks insulin receptors. Would mice given this peptide, called S961, compensate by making more insulin?
"We thought the mouse's beta cells would either work harder to produce more insulin or really boost beta cell replication," Melton says.
Luckily for them, mice given S961 promptly started making more beta cells. So then the researchers looked in various tissues ? fat, liver, muscle, brain ? to see what genes were turned on.
"What popped out near the top of the list of the most abundantly activated genes was this gene that no one had really studied, that we called betatrophin," Melton says.
Within a day or so after its release, the hormone boosts beta cell replication up to thirtyfold. And it doesn't seem to do anything else. That's important because it lowers the risk that betatrophin would cause unwanted side effects or even, in the worst case, promote cancer.
One intriguing discovery so far is that the betatrophin gene gets turned on in pregnant mice. That makes sense, since pregnancy requires a boost in insulin to enable the mother to keep blood sugar levels normal in the face of an increased carbohydrate load.
The Harvard researchers don't know yet if pregnant humans produce more betatrophin, but they plan to find out.
They're also planning an ambitious agenda of follow-on experiments. First, they want to figure out how betatrophin works and look for the receptor on pancreas and possibly other cells that the hormone activates. "We don't need the receptor" to pursue treatment possibilities, Melton says, "but we would like to have it."
Second, they want to make betatrophin in large amounts for further mouse and eventually human experiments.
Third, they want to give betatrophin to rodents with diabetes ? not just genetically induced disease, but diabetes caused by overfeeding animals to make them obese, the way that Type 2 diabetes is caused in humans.
They hope that giving such animals betatrophin will not only normalize their blood sugars, but also prevent the heart, blood vessel, nerve and immune system complications that shorten the lives of people with diabetes. Only that would be a true cure.
By the way, Melton thinks that betatrophin might prevent Type 1 diabetes, too, the type that generally arises earlier in life after an overactive immune system destroys beta cells.
To do that, you'd have to identify people at risk of developing Type 1 diabetes ? for instance, because a sibling already had it ? and monitor them for signs they were getting it too, then giving betatrophin along with immune-suppressing drugs to halt the disease in its tracks.
Melton ticks off the pluses and minuses at this early stage. "On the positive side, betatrophin is very robust in its activity, it's very specific to beta cells, it improves animals' handling of blood sugar, and the human gene for it is virtually identical to the mouse gene," Melton says.
"On the negative side, we don't know its mechanism of action and we haven't yet demonstrated its safety and efficacy in humans," he says.
There are enough positives at this point that betatrophin has already been licensed by Janssen Pharmaceuticals, a division of Johnson & Johnson, and a German biotech firm called Evotec, which already has 15 scientists working on betatrophin.
If Melton's wishes pan out, a percentage of the huge potential profits would go not to him, he says, but to Harvard and his lab.
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Workplace Collaboration Service Convo Releases Updated iOS App With Redesigned News Feed And Comment System
There are very few platforms that have something that you use on a daily basis, let alone on a minute-by-minute basis. Team communication platform service, Convo, is one of those for us at TechCrunch. Today, the company has released an update for its essential iOS app, which is something that we use here quite often to communicate about everything you can think of. Since using the service, our team has generated more than 100,000 interactions, averaging 1,200 of them a day, with 95 percent of our team present on the platform on those days. Its desktop version is in real time, acting like a threaded IRC chat. The service overall isn’t without its faults, but it’s difficult to build team and enterprise software that can make everyone happy. One of the top complaints that we had was about its iOS app, which was lacking proper iPhone 5 and retina support, along with some general usability issues. Today’s app udpate is all about speed, commenting and a slicker design that will help you get through all of the threaded discussions your team is having since you checked in last. The feed This is the most important part of Convo, especially when you’re on the go. In today’s update, you’re able to scan and refresh the main feed quickly, and when you tap on the comments for any given thread, they slide over from the right. This is a huge improvement from the previous version, which loaded the thread into a new page: That update alone will save time, as you can jump back and forth between threads that you’re participating in and make decisions on whether to get involved in one quicker. Additionally, you’ll be able to “Like” things, which is a passive way of saying that you’ve seen something or agree with something, depending on how your team uses it. Images are also clearer thanks to the retina support and complete overhaul of how they’re displayed. Depending on how you use the service, images could play a huge role in the conversation that you’re having. If it’s about a piece of artwork for your app, seeing images at the highest resolution possible is the only way that you’ll be able to make a decision on whether to use them or feedback that you might have for your designer. Cleanup and sharing In addition to the feed overhaul, Convo has beenSource: http://feedproxy.google.com/~r/Techcrunch/~3/4w3xNYT6Lxk/
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