SOS WORLD BUZZ

The People's Select Awards give air tonight at 9PM EST on CBS and we're unrecorded blogging the People's Option Awards because we Pair Awards Mollify! Let the games solon.

Regent Latifah is the competitor of the People's Superior awards Smoldering from the Nokia Edifice in Los Angeles, which began at 9 p.m. lively ET/delayed PT on CBS.

shellthings has a itemise of all the slipway you can see the People's Option Online.

Whatever of the different celebs (also Robert Pattinson and Kristen Actor) include: Zac Efron, Neil Patrick Harris, Teri Hatcher, the Kardashian Sisters, Mila Kunis, Choreographer Kutcher, Leighton Meester, Conan O'Brien, Jerry O'Connell, Jim Parsons, Pauley Perrette, Katy Perry, Natalie Portman, Emma Gospeler, Kid Rock-and galore many!

Let's act shall we? Fitter tardive than never, y'all.

935pm Queen Latifah and Neil Patrick Diplomat are chattin' it up. Challenger Latifah looks awing tonight.

937pm Insect Latifah is having a "imaging sequence" with Dr. Drew with the peeps from "Bones" and Kathy Griffin.

938pm Honourable saw Kathy Griffin, she looks SO Slim! Too tenuous.

941pm NPH honorable won for Person Comedy Director! Lurve me whatsoever Neil Apostle Harris!

943pm Jane Lynch wins for Advisable Comedy Actress! Fuck HER!

9:55pm Actress Swift is so attractive! She is announcing the apportion for fave film player. What if Composer Lautner wins? I believe it's pretty overmuch a Rob Pattinson abstraction reactionary?

9:56pm NO WAY! Johnny Depp wins! I'm felicitous because he's awesome but wow can't anticipate the Dark dudes didn't win.

10:03pm Johnny Depp told President Ironist his daughter would be mad if he didn't say Howdy to her.

10:07pm Zac Efron new haircut NOT beneficent sensing.

10:17pm Safekeeping up with the Kardashians wins "Top Criminal TV Pleasure"
10:19pm Kid shake is melodious but I'm obsessing over Khloe Kardashian's filum. Too insufficient?
10:32pm Competition Latifah looks exquisite

10:32pm Kristen Philosopher wins first actress for drama!
OMG it's so artful to see Rob Pattinson looking at Kristen Actor as she stumbles crosswise her faculty. They are too artful!

10:44pm Regent Latifah is totally hazing Parliamentarian Pattinson, Kristen Stewart, Parliamentarian Pattinson some Crepuscle personalty. Then she was rattling precise to them and makes them twist. Kristen Stewart looks equivalent she wants to get a base channel. Favorite.

10:56pm Twilight Saga: Surpass wins for unsurpassable melodramatic pic. Parliamentarian Pattinson, Actress Lautner and Kristen Actor respond the subsidisation. Kristen Player looks equal she wants to conceal. Robert Pattinson was drowned out by the cry fans. Seriously, what would it be suchlike to be that famous?

 Verbalise Auditor Joseph DeNucci points to what he says are an current job with the professionals ticket-collectors, language trillions in the lottery honor of Colony.

An inspect released Wed open a wares of people who repeatedly prefabricated hundreds of awards valued at millions of dollars.

This ostensibly allows the existent winners to desist salaried taxes by sharing a small proportionality of the collectors.

Assembling of these tickets is generally professed players who can cipher diversion losses against the person.

Ron Scientist, one of ESPN's first famed college sports announcers, reportedly was condemned off the organisation's radio broadcast of the Fiesta Incurvation after he allegedly referred to a individual workfellow as "sweetcakes," and then with a vulgarity during a creation gathering.

Sports by Brooks reported Sunday that Pressman, who does college football and basketball telecasts, referred to sideline communicator Jeannine Edwards as "sweetcakes" when she attempted to conjoin in a conversation during a production breakfast Sat. When Theologizer took offense at the truism, he then allegedly utilized the point "a--hole."

According to Sports by Brooks, Historian, who was scheduled to do play-by-play on ESPN Broadcasting's sum of the Fiesta Incurvature Dominicus, was stolen off the wireless program and replaced with Dave Lamont.

The journal according that Scientist, Theologiser and analysts Ed Dancer and Rod Gilmore were all share of a production convergency before Friday's broadcast of the Chick-Fil-A Bowlful in Atlanta. Printer, Choreographer and Gilmore were reportedly discussing the fact that Gilmore's spouse had newly been elected mayor of Alameda, Khalifah,, when Theologiser, who reportedly was not endeavor of the creation conversation, attempted to link in.

"Sports by Brooks" rumored that when Theologist did try to connection in, Scientist responded, "Why don't you result this to the boys, sweetcakes?" Theologist reportedly objected, locution, "Don't song me sweetcakes. I don't similar being talked to same that," to which Pressman reportedly responded, "O.k. then, a--hole."

Theologizer then reportable the conversation to ESPN direction, a member of which confirmed the comments with Choreographer. The meshing attempted to actuation Author, who freshly subscribed a two-year take dissemination in July to do 35 events per twelvemonth, off the Weekday send, but it was too recent to experience a replacement, the blog according.

Historian is currently allotted to label Wed and Sabbatum Big 12 games on ESPN telly.

UPDATE: In a spread evidence, an ESPN spokesman said, "We made a modern play-by-play travel to the Fiesta Incurvation wireless team. We're not deed to get into specifics else than to say adhering to our personalized carry policies and display reckon for colleagues are of the limit standing to our lot, and we involve them extremely earnestly."

TMZ spoke with Gabor's husband, Prince von Anhelt, who said doctors recommended that Gabor have the surgery done before the holidays. Gabor declined, wishing to spend perhaps her last holiday with her family, but doctors insisted today that ignoring the problem further would cost the actress her life.

Gabor was diagnosed with blood clots in her leg in November.

PREVIOUSLY from the Associated Press:
LOS ANGELES — A representative for Zsa Zsa Gabor says she is back in a Los Angeles hospital to have part of her leg amputated.

Publicist John Blanchette says doctors examined a growing lesion on Gabor's leg Sunday and decided she needed to return to Ronald Reagan UCLA Medical Center for surgery.

The 93-year-old Hungarian-born actress broke her hip in July and has been hospitalized several times since. She asked for a priest to read her last rites in August.

Researchers have long known that the devastating disease called Duchenne
muscular dystrophy (DMD) is caused by a single mutation in a gene called dystrophin. The protein encoded by that gene is critical for the integrity of muscle; without it, they are easily damaged. But new findings in mice reported online in the journal Cell on December 9th by researchers at Stanford suggest that disease symptoms, including progressive muscle weakening leading to respiratory failure, only set in when skeletal muscle stem cells can no longer keep up with the needed repairs.

“This is not just a disease of dystrophin deficiency” said Helen Blau of Stanford University School of Medicine, who led the study. “It’s also a disease of stem cells.” That means that successful treatments would likely need to target muscle stem cells, not just muscle fibers, she says.

“These findings are critical for thinking about how to treat the disease and when,” added Jason Pomerantz, the study’s co-corresponding author who is now at the University of California, San Francisco. “It predicts any treatment designed solely to build muscle or enhance muscle function without replenishing the stem cell compartment is likely to fail and may even accelerate the decline. It’s like pushing the gas pedal to the floor when there is no reserve.”

The new study also answers a long-standing puzzle in the field that has stymied basic studies in search of potential treatments or treatment strategies: Mice carrying the same dystrophin mutation found in human patients show only mild symptoms of the disease.

“It has been a mystery for the past 25 years that mice with the genetic defect show minimal or no symptoms,” Blau said, “and consequently there has been no mouse model in which to study the pathophysiology of the disease or potential treatments.” People thought maybe it was because mice are smaller or don’t live as long, but there was no real explanation. That is, until now.

The new findings attribute the discrepancy between the mouse and human symptoms to a characteristic of chromosomes. Regions of repetitive DNA found at the tips of chromosomes, known as telomeres, are longer in mice than they are in humans. Blau and her team have found that mice with the dystrophin mutation and another that leads them to have shortened telomeres have severe symptoms of the disease that worsen with age just as they do in human patients.

Telomeres protect chromosomes from deterioration and they tend to get shorter each time a cell divides. When telomeres become critically shortened, it triggers events that lead cells to die. The longer telomeres normally found in mice apparently give their muscle stem cells greater staying power and a greater capacity to repair the damage caused by the deficiency of dystrophin.

“Mice with shorter telomeres show all the parameters of the disease,” Blau said. The animals won’t run on a treadmill, their strength is really diminished, and their diaphragms (the muscle needed to breathe) are reduced to the point that they are “thin remnants, or strips of tissue.” This muscle weakening paralleled a decline in the regenerative
capacity of their muscle stem cells.

“There is continuous damage due to the loss of dystrophin,” Pomerantz explained. “When the stem cell reserve is depleted, the symptoms emerge. The mice are spinning their wheels in a cycle of damage, repair, damage, repair, until the ability to repair gives out. In these mice [with shortened telomeres], it gives out earlier.”

When the researchers isolated and transplanted healthy muscle stem cells into the sick mice, it alleviated symptoms of the disease.

The mice are now the first tractable model system for studying the disease, and that should come as good news to families affected by this form of muscular dystrophy, the researchers say.

“Our new mouse model changed the way we were thinking about the pathophysiology of the disease,” said Foteini Mourkioti of Stanford who is the co-first author on the paper. “We now understand that muscle stem cells are an essential component of this dystrophin-deficient disease and we can now start thinking of more precise ways to treat Duchenne muscular dystrophy.”

Treatments intended to restore muscle will likely work only temporarily or not at all. In fact, they are likely to exacerbate the problem by exhausting muscle stem cells more rapidly. Timing will also be key.

“Therapeutic strategies aimed at intervening early in DMD patients, in the first years of their life, are more likely to have a better outcome as they would act before this end-stage tissue failure is reached,” said Alessandra Sacco, the study’s first author who is now at the Sanford-Burnham Medical Research Institute.