Mitt Romney's money advantage could tip the scales. By Gil Kaufman
Mitt Romney Photo: Getty Images
Tuesday's Florida primary could be make-or-break for the two men battling to secure the Republican presidential nomination. After seemingly taking the first two contests (the Iowa caucus was belatedly handed to former Pennsylvania Senator Rick Santorum) and then losing by double digits in South Carolina last week, former Massachusetts Governor Mitt Romney appears to have gotten his groove back.
The on-and-off leading contender in the hotly contested GOP presidential scrum still has a solid New Hampshire win in his pocket, but his team is looking for a convincing win in the first big state on the primary map, Florida, to help solidify his lead and possibly push him out of reach of his rivals.
Newt Gingrich has a W in his column from South Carolina, but the conservative firebrand has seen his poll position slip over the past week. That drop is mostly due to Romney putting up two solid debate performances last week and splashing out millions from his massive campaign war chest on ads attacking the former House Speaker.
So what should voters be on the lookout for on Tuesday?
Money: Gingrich's win in South Carolina helped him raise $1 million to spend on ads in Florida — combined with $2.5 million from the outside group Winning Our Future. But those figures paled next to the estimated $15 million that Romney (and his affiliates) spent to saturate the airwaves in a state where media ubiquity helps seal the deal. Tough ads linking Gingrich to Freddie Mac and the housing crisis and reminding Hispanic voters that he once called Spanish the language of the "ghetto" showed a tougher side of the Romney team.
Too-close-to-call: If Romney can't deliver a decisive win in Florida over Gingrich, the former House leader may be able to make good on his promise this week to hang around until this summer's RNC convention. A solid victory, though, could cause Gingrich's donations to shrink and push him back out of contention.
Hispanic vote: Both Romney and Gingrich — Santorum is polling well behind both men and Rep. Ron Paul has decided to skip campaigning in Florida to focus elsewhere — heavily courted the state's 1.5 million Hispanic voters. Gingrich called Romney the GOP field's most anti-immigration candidate at Thursday's debate and the men have very different views on how to deal with illegal immigrants who are already in the country.
The debate factor: After Gingrich zoomed back into contention thanks to some strong debate performances before the South Carolina contest, Romney's team put their candidate on the attack in the two pre-Florida showdowns. The tactic worked, as Romney put the usually unflappable Gingrich on his heels. Exit polls could show how big an impact those debate performances had on voters' decisions.
Herman Helper?: Momentary field leader Herman Cain dropped out of the race due to a series of sexual harassment and infidelity allegations in December, but he got his name back on voter's lips this week when he "enthusiastically" endorsed Gingrich. But given the tawdry allegations that undid Cain and Gingrich's own battle to turn talk away from his three marriages, it will be interesting to see if Cain's endorsement gave Gingrich a bump or peeled voters away.
Check back for up-to-the-minute coverage on the primary races and stick with PowerOf12.org throughout the 2012 presidential election season.
Liam Neeson is not stuck in the wilderness with the wolves. The poor wolves in the wilderness are stuck with Liam Neeson.
The actor's latest vehicle, The Grey, finished in first place at the box office this weekend, banking a strong $20 million in its first week of release nationwide.
Last week’s #1, Underworld Awakening, slipped to second, although the return of Kate Beckinsale as Selene added $12.5 million to a nice total of $45.1 million.
The second of three new arrivals at the movies this past weekend, One for the Money, settled for third place. The Katherine Heigl-led film made $11.8 million.
Rounding out the top five were Red Tails ($10.4M) and Man on a Ledge, which disappointed somewhat in its first week of release, earning only $8.3 million.
Meanwhile, a couple of potential Oscar favorites rallied a bit in the second half of our weekend top 10, which you can see in its entirety below:
AMSTERDAM (Reuters) ? Dutch Electronics giant Philips will book further, unspecified, restructuring charges in the first half of 2012, Chief Executive Officer Frans van Houten said on Monday.
"The first half of 2012 will see the impact of these charges and overall we are cautious about the development of the first half of the year. It is not going to be an easy first half," said Van Houten.
Earlier on Monday, Philips reported a 45 percent fall in fourth-quarter core profit due to losses at both its health and lighting divisions, and said it was cautious about 2012 given uncertainty in the global economy, particularly in Europe.
Van Houten also said the firm is committed to achieving its 2013 financial targets.
(Reporting By Roberta B. Cowan, Editing by Mark Potter)
DAKAR (Reuters) ? Senegal's opposition called on Saturday for more "resistance" against President Abdoulaye Wade, after a night of riots over his plans to run for a third term in elections next month.
Local media reported that one policeman was killed during the riots, in which protesters threw rocks, overturned cars and burned tyres and security forces fired tear gas, raising worries of growing instability in West Africa's most peaceful nation.
Calm had returned to the capital Dakar by morning and security boosted around the presidential palace. Truckloads of police in full riot gear patrolled the city, armed with tear gas grenade launchers, according to a Reuters witness.
"We are asking the people to remain alert and to resist Abdoulaye Wade," Abdoul Aziz Diop, the spokesman for opposition activist movement M23 told Reuters by telephone Saturday. "If Wade tries to impose himself on us ... we will resist."
He said that opposition figures and activist leaders were meeting Saturday to discuss their next steps.
The clashes came after Senegal's top legal body late on Friday night validated the candidacy of 85-year-old Wade and 13 rivals for the February 26 vote, but turned down the presidential bid of world music star Youssou N'Dour, saying he did not have the required 10,000 signatures of support.
Wade's rivals say the constitution sets an upper limit of two terms on the president. But Wade, who came to power in 2000 and was re-elected in 2007, has argued his first term pre-dated the 2001 amendment establishing the limit.
Wade appeared on state television late Friday and made an appeal for calm, promising elections would be free and fair.
"Stop these displays of petulance which will lead to nothing," he said. "The electoral campaign will be open. There will be no restrictions on freedom."
Senegal is the only country in mainland West Africa to have not had a coup since the end of the colonial era. February's poll, and a possible run-off a few weeks later, are seen as a test of social cohesion in the predominantly Muslim country.
Critics say that Wade, who spent 26 years in opposition to Socialist rule, has done nothing during his 12 years in power to alleviate poverty in a country where formal employment is scarce, and has dragged his heels on tackling official graft.
Wade points to spending on education and infrastructure projects such as roadbuilding as proof of progress toward turning Senegal into an emerging market country and a trade hub.
His candidacy has raised eyebrows abroad. The senior U.S. State Department official for Africa, William Fitzgerald, told French RFI radio that Wade's candidacy was "a bit regrettable."
Rival presidential hopeful Amsatou Sow Sidibe called on Wade to withdraw his candidacy voluntarily. "Peace and tranquility in Senegal depends on it," she told Reuters by telephone.
Local television said one policeman died from head injuries after clashes in the capital Dakar late Friday, but this could not be independently confirmed. Reuters reporters saw youths set fire to tyres and overturn cars.
One witness said a police station in the central town of Kaolack had been ransacked, while state radio said the local headquarters of Wade's liberal PDS had been burned down. Street protests were also reported in the towns of Thies and Mbour.
(Writing by Richard Valdmanis; Editing by Rosalind Russell)
The nation?s gross domestic product went up 2.8 percent in the final three months of 2011, falling slightly short of the 3 percent increase expected by many analysts. NBC?s Brian Williams reports.
>>>we learned today the
u.s. economy
continuing to grow now, though it's a slower pace than expected.
gross domestic product
bumped up 2.8% in the final three months of
2011
. that's disappointing some economis economists who have been looking for 3% growth. when companies have large inventories, they produce less in the feature, which could mean slower growth and fewer
american jobs
.
LOS ANGELES ? Directors Guild of America Awards regular Martin Scorsese and first-timer Michel Hazanavicius are the favorites as Hollywood's top filmmaker group prepares to hand out prizes.
Past winner Scorsese is nominated again for the guild's feature-film honor for his Paris adventure "Hugo," while Hazanavicius scored his first nomination for his silent-movie "The Artist."
Also in the running are Woody Allen for his romantic fantasy "Midnight in Paris"; David Fincher for his thriller "The Girl with the Dragon Tattoo"; and Alexander Payne for his family drama "The Descendants."
The Directors Guild Awards are one of Hollywood's most accurate forecasts for who will win at the industry's top honors, the Academy Awards, which will be handed out Feb. 26. Only six times in the 63-year history of the guild awards has the winner failed to take home the Oscar for best director, and more often than not, the film winning the best director Oscar is voted best picture.
Fincher had been the favorite going into the Directors Guild ceremony last year for "The Social Network," but Tom Hooper came away the winner for "The King's Speech." Hooper went on to win the Oscar, too, and his film also earned best picture.
This time, Fincher's the odd man out at the Directors Guild show. The other four guild nominees made the best-director cut at Tuesday's Oscar nominations, but Fincher missed out. The fifth Oscar slot went to Terrence Malick for the family chronicle "The Tree of Life."
French filmmaker Hazanavicius, whose credits include the spy spoofs "OSS 117: Cairo, Nest of Spies" and "OSS 117: Lost in Rio," had been a virtual unknown in Hollywood until "The Artist," his black-and-white throwback to early cinema that has been a favorite at earlier film honors.
"The Artist" won the Golden Globe for best musical or comedy and is considered a best-picture front-runner for the Oscars.
But Scorsese won the Globes' singular directing prize over Hazanavicius.
Unlike Hazanavicius, the other nominees all have competed for Directors Guild honors before. Scorsese earned his ninth and 10th guild nominations this season; besides feature-film, he's nominated for documentary directing for "George Harrison: Living in the Material World."
Scorsese is a past feature-film winner for 2006's "The Departed," as well as a TV drama winner a year ago for an episode of "Boardwalk Empire." The family film "Hugo" was a departure for Scorsese, known for dark crime tales, and the movie also was his first shot in 3-D.
Allen has been nominated five times and won for 1977's "Annie Hall." He had not been nominated since his 1989 "Crimes and Misdemeanors" but has been on a critical and commercial resurgence for "Midnight in Paris," his biggest hit in decades.
This was the third nomination for Fincher. Payne was nominated one time previously, for 2004's "Sideways."
Kelsey Grammer is the host for the guild ceremony, which is not televised. Awards presenters include Oscar nominees George Clooney ("The Descendants"), Michelle Williams ("My Week with Marilyn"), Gary Oldman ("Tinker Tailor Soldier Spy"), Jean Dujardin and Berenice Bejo ("The Artist"), and Octavia Spencer and Jessica Chastain ("The Help").
If you're a PC or Mac gamer, chances are you've used Steam, Valve Software's leading digital distribution platform for games. Today sees the launch of the official Steam app for Android, a new application that gives you access to the Steam store and community features like Steam chat on-the-go. If you're big on Steam and the Steam community, this could definitely be worth a look.
It's worth clarifying that this isn't a fully-fledged Steam client for Android, so you won't be playing Portal 2 on your Galaxy Tab any time soon, unfortunately. All it lets you do is buy PC and Mac games and chat to your Steam friends.
While the app itself is freely available on the Android Market (see the link after the jump), you'll need to be part of the Steam Mobile beta group in order to use it, or you'll be rejected at the login screen. This is a little strange given that the app is openly advertised on SteamPowered.com with no mention that a beta invite is required. So keep an eye on this one, folks. All signs point to a possible public launch in the near future. If you are in the beta group, however, you'll find a handy Market link after the break.
RIO DE JANEIRO ? Three bodies were pulled from the rubble of three collapsed buildings on Thursday, an official with the Rio de Janeiro Fire Department said. Another 21 people were still missing after the buildings went down in the city's historic center.
Mayor Eduardo Paes said a structural problem may have caused a building of about 20 stories to collapse at about 8:30 p.m., and that apparently caused the collapse of two smaller buildings nearby. Officials were still investigating the causes, however.
In addition to the dead and missing, at least six other people were treated for injuries caused by the accident, which left rubble and thick dust strewn over a wide area near Rio's famed Teatro Municipal and the Fine Arts Museum.
One of those pulled out alive was Marcelo Moreira, a janitor in an eight-story building that fell.
"He stayed behind to finish a little bit of work," said Rosalvo Alves, the building's main doorman, who had spent the night in a local hospital with his friend. "We shut down at 8. I left, and he was supposed to come too. Now this; he's hurt, our jobs are gone, everything is gone."
Alves worked in the building for 38 years, and said he had never noticed any problems.
A cloud of dust was still drifting from the building the next as rescue crews dug through tons of brick and twisted metal, hoping to find survivors.
"Firefighters and others are working to find the missing," said Moises Torres, a spokesman with the Fire Department who confirmed the numbers of dead and missing. "We have hopes of finding people alive."
Relatives and friends of the missing gathered inside a nearby government building, taking shelter from from the scorching sun as they waited for news.
Francisco Adir was trying to get information about a friend who had been attending a computer course in the in the largest of the three buildings.
"We think he's alive. At 3 a.m. he managed to call his girlfriend and say, 'Hello, love," before his phone went dead," Adir said. "The rescuers haven't given us any information, but the family is hanging all their hopes on that phone call."
A building inspector told the Globo television network that a survivor from the collapse was a worker on a construction project being performed in the first building that went down, and that illegal projects could have led to the collapse.
"Two projects were happening in the building, on the 16th floor," said Luiz Cosenza, head of the accident prevention unit of Rio's Regional Council of Engineering, in charge of building inspections. "They were illegal works; they were not registered with the council."
He didn't provide details on what sort of construction work was being carried out, but said that it was not being supervised by any registered professional.
Shortly after the collapse, there was a strong smell of natural gas in the area, but Mayor Paes said that probably did not cause the problem.
"There apparently was not an explosion. The collapse occurred because of structural damages," he said. "I don't think there was a gas leak."
GREAT FALLS, Mont. ? University of Montana economists say energy development may be the industry that helps improve Montana's economy.
Patrick Barkey is director of UM's Bureau of Business and Economic Research. He says a full recovery from the nationwide recession could still take several years.
Barkey made his comments during recent economic outlook presentations in Helena and Great Falls.
Montana's economic growth slowed from 1.5 percent in 2010 to 0.7 percent in 2011. But experts say they're expecting 2 percent growth this year and 2.4 percent growth in each of the following three years.
Barkey says energy has potential for strong growth and the outlook for the agriculture economy is reasonably good. Growth in the health care industry slowed last year, while housing and construction continued to struggle along with retail and tourism.
How do you propose to the ultimate Indy fan? Not with snakes or crystal skulls, that's for sure. You pop the question with the snap of a whip. Or at least a whip ring. More »
Philadelphia, PA, January 25, 2012 A significant obstacle to progress in understanding psychiatric disorders is the difficulty in obtaining living brain tissue for study so that disease processes can be studied directly. Recent advances in basic cellular neuroscience now suggest that, for some purposes, cultured neural stem cells may be studied in order to research psychiatric disease mechanisms. But where can one obtain these cells outside of the brain?
Increasingly, schizophrenia research is turning to the nose. Strange as it may seem, the idea makes sense because the olfactory mucosa, the sense organ of smell in the nose, is continually regenerating new sensory neurons from "adult" stem cells. These neurons are among the very few nerve cells outside of the skull that connect directly to nerve cells in the brain.
Over several decades, researchers found that these cells can be collected directly by obtaining a small tissue sample, called a biopsy. By taking small pieces of olfactory tissue from the nose, researchers of this new study were able to gain access to the stem cells from patients with schizophrenia and compare them to cells from healthy individuals.
"We have discovered that patient cells proliferate faster - they are running with a faster speed to their clock controlling the cell cycle - and we have identified some of the molecules that are responsible," explained Dr. Alan Mackay-Sim from the National Centre for Adult Stem Cell Research in Brisbane, Australia, an author of the study. The findings clearly indicate that the natural cell cycle is dysregulated in individuals diagnosed with schizophrenia.
"This is a first insight into real differences in patient cells that could lead to slightly altered brain development," Mackay-Sim added. This is an important finding, as scientists are already aware of many developmental abnormalities in the 'schizophrenia brain'.
Dr. John Krystal, editor of Biological Psychiatry, commented: "The current findings are particularly interesting because when we look closely at the clues to the neurobiology of psychiatric disorders, we find new and often unexpected mechanisms implicated."
###
The article is "Altered Cell Cycle Dynamics in Schizophrenia" by Yongjun Fan, Greger Abrahamsen, John J. McGrath, and Alan Mackay-Sim (doi: 10.1016/j.biopsych.2011.10.004). The article appears in Biological Psychiatry, Volume 71, Issue 2 (January 15, 2012), published by Elsevier.
Notes for editors
Full text of the article is available to credentialed journalists upon request; contact Rhiannon Bugno at +1 214 648 0880 or Biol.Psych@utsouthwestern.edu. Journalists wishing to interview the authors may contact Dr. Alan Mackay-Sim at +61 7 373 57563 or a.mackay-sim@griffith.edu.au.
The authors' affiliations, and disclosures of financial and conflicts of interests are available in the article.
John H. Krystal, M.D., is Chairman of the Department of Psychiatry at the Yale University School of Medicine and a research psychiatrist at the VA Connecticut Healthcare System. His disclosures of financial and conflicts of interests are available here.
About Biological Psychiatry
Biological Psychiatry is the official journal of the Society of Biological Psychiatry, whose purpose is to promote excellence in scientific research and education in fields that investigate the nature, causes, mechanisms and treatments of disorders of thought, emotion, or behavior. In accord with this mission, this peer-reviewed, rapid-publication, international journal publishes both basic and clinical contributions from all disciplines and research areas relevant to the pathophysiology and treatment of major psychiatric disorders.
The journal publishes novel results of original research which represent an important new lead or significant impact on the field, particularly those addressing genetic and environmental risk factors, neural circuitry and neurochemistry, and important new therapeutic approaches. Reviews and commentaries that focus on topics of current research and interest are also encouraged.
Biological Psychiatry is one of the most selective and highly cited journals in the field of psychiatric neuroscience. It is ranked 4th out of 126 Psychiatry titles and 15th out of 237 Neurosciences titles in the Journal Citations Reports published by Thomson Reuters. The 2010 Impact Factor for Biological Psychiatry is 8.674.
About Elsevier
Elsevier is a world-leading provider of scientific, technical and medical information products and services. The company works in partnership with the global science and health communities to publish more than 2,000 journals, including The Lancet and Cell, and close to 20,000 book titles, including major reference works from Mosby and Saunders. Elsevier's online solutions include SciVerse ScienceDirect, SciVerse Scopus, Reaxys, MD Consult and Nursing Consult, which enhance the productivity of science and health professionals, and the SciVal suite and MEDai's Pinpoint Review, which help research and health care institutions deliver better outcomes more cost-effectively.
A global business headquartered in Amsterdam, Elsevier employs 7,000 people worldwide. The company is part of Reed Elsevier Group PLC, a world-leading publisher and information provider, which is jointly owned by Reed Elsevier PLC and Reed Elsevier NV. The ticker symbols are REN (Euronext Amsterdam), REL (London Stock Exchange), RUK and ENL (New York Stock Exchange).
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
In schizophrenia research, a path to the brain through the nosePublic release date: 25-Jan-2012 [ | E-mail | Share ]
Philadelphia, PA, January 25, 2012 A significant obstacle to progress in understanding psychiatric disorders is the difficulty in obtaining living brain tissue for study so that disease processes can be studied directly. Recent advances in basic cellular neuroscience now suggest that, for some purposes, cultured neural stem cells may be studied in order to research psychiatric disease mechanisms. But where can one obtain these cells outside of the brain?
Increasingly, schizophrenia research is turning to the nose. Strange as it may seem, the idea makes sense because the olfactory mucosa, the sense organ of smell in the nose, is continually regenerating new sensory neurons from "adult" stem cells. These neurons are among the very few nerve cells outside of the skull that connect directly to nerve cells in the brain.
Over several decades, researchers found that these cells can be collected directly by obtaining a small tissue sample, called a biopsy. By taking small pieces of olfactory tissue from the nose, researchers of this new study were able to gain access to the stem cells from patients with schizophrenia and compare them to cells from healthy individuals.
"We have discovered that patient cells proliferate faster - they are running with a faster speed to their clock controlling the cell cycle - and we have identified some of the molecules that are responsible," explained Dr. Alan Mackay-Sim from the National Centre for Adult Stem Cell Research in Brisbane, Australia, an author of the study. The findings clearly indicate that the natural cell cycle is dysregulated in individuals diagnosed with schizophrenia.
"This is a first insight into real differences in patient cells that could lead to slightly altered brain development," Mackay-Sim added. This is an important finding, as scientists are already aware of many developmental abnormalities in the 'schizophrenia brain'.
Dr. John Krystal, editor of Biological Psychiatry, commented: "The current findings are particularly interesting because when we look closely at the clues to the neurobiology of psychiatric disorders, we find new and often unexpected mechanisms implicated."
###
The article is "Altered Cell Cycle Dynamics in Schizophrenia" by Yongjun Fan, Greger Abrahamsen, John J. McGrath, and Alan Mackay-Sim (doi: 10.1016/j.biopsych.2011.10.004). The article appears in Biological Psychiatry, Volume 71, Issue 2 (January 15, 2012), published by Elsevier.
Notes for editors
Full text of the article is available to credentialed journalists upon request; contact Rhiannon Bugno at +1 214 648 0880 or Biol.Psych@utsouthwestern.edu. Journalists wishing to interview the authors may contact Dr. Alan Mackay-Sim at +61 7 373 57563 or a.mackay-sim@griffith.edu.au.
The authors' affiliations, and disclosures of financial and conflicts of interests are available in the article.
John H. Krystal, M.D., is Chairman of the Department of Psychiatry at the Yale University School of Medicine and a research psychiatrist at the VA Connecticut Healthcare System. His disclosures of financial and conflicts of interests are available here.
About Biological Psychiatry
Biological Psychiatry is the official journal of the Society of Biological Psychiatry, whose purpose is to promote excellence in scientific research and education in fields that investigate the nature, causes, mechanisms and treatments of disorders of thought, emotion, or behavior. In accord with this mission, this peer-reviewed, rapid-publication, international journal publishes both basic and clinical contributions from all disciplines and research areas relevant to the pathophysiology and treatment of major psychiatric disorders.
The journal publishes novel results of original research which represent an important new lead or significant impact on the field, particularly those addressing genetic and environmental risk factors, neural circuitry and neurochemistry, and important new therapeutic approaches. Reviews and commentaries that focus on topics of current research and interest are also encouraged.
Biological Psychiatry is one of the most selective and highly cited journals in the field of psychiatric neuroscience. It is ranked 4th out of 126 Psychiatry titles and 15th out of 237 Neurosciences titles in the Journal Citations Reports published by Thomson Reuters. The 2010 Impact Factor for Biological Psychiatry is 8.674.
About Elsevier
Elsevier is a world-leading provider of scientific, technical and medical information products and services. The company works in partnership with the global science and health communities to publish more than 2,000 journals, including The Lancet and Cell, and close to 20,000 book titles, including major reference works from Mosby and Saunders. Elsevier's online solutions include SciVerse ScienceDirect, SciVerse Scopus, Reaxys, MD Consult and Nursing Consult, which enhance the productivity of science and health professionals, and the SciVal suite and MEDai's Pinpoint Review, which help research and health care institutions deliver better outcomes more cost-effectively.
A global business headquartered in Amsterdam, Elsevier employs 7,000 people worldwide. The company is part of Reed Elsevier Group PLC, a world-leading publisher and information provider, which is jointly owned by Reed Elsevier PLC and Reed Elsevier NV. The ticker symbols are REN (Euronext Amsterdam), REL (London Stock Exchange), RUK and ENL (New York Stock Exchange).
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Jennifer Diley auditioned for American Idol in San Diego Sunday - on an episode that will be replayed at 8 p.m. tonight on Fox - and did not make the Hollywood cut. Case closed, right?
Not so much.
The aspiring singer, who donned a tube top and very short shorts, has gone public with complaints over producers forcing her to choose from a list of "flirty" songs. (She ended up covering "With You" by Jessica Simpson and "Hero" by Mariah Carey, neither of which she had rehearsed.).
Diley is also apparently mad at Steven Tyler because he supposedly told her off-air that he loved her outfit... and then remained silent while she was mocked for it during the audition. The nerve!
Informed off this random complaint, Tyler's manager told TMZ: "You are telling me some provocatively dressed woman is claiming Steven Tyler flirted with her? I am shocked."
As for auditions of people who can actually sing, we recommend fans keep an eye on Ashley Robles. She has serious potential.
WASHINGTON ? Rick Santorum says he's under no pressure to quit the GOP presidential race so conservative voters can coalesce around Newt Gingrich.
The former Pennsylvania senator tells CNN's "State of the Union" that his campaign is building momentum even after a third-place finish in South Carolina. He says he expects to run well in Florida's Jan. 31 primary.
Santorum says the suggestion that conservatives will have to coalesce to beat former Massachusetts Gov. Mitt Romney is "objectively false."
Santorum points out that he beat Romney in Iowa and says Gingrich "smoked him here in South Carolina."
Santorum says that while Romney has more campaign money, he has the better ideas and message to inspire voters.
A study published this week in the journal Leukemia identifies a mechanism that acute myeloid leukemia (AML) cells use to evade chemotherapy ? and details how to close this escape route.
"Introducing chemotherapy to cells is like putting a curve in front of a speeding car," says Christopher Porter, MD, investigator at the University of Colorado Cancer Center and assistant professor of pediatrics at the University of Colorado School of Medicine. "Cells that can put on the brakes make it around the corner and cells that can't speed off the track."
Porter and colleagues collaborated with James DeGregori, PhD, CU Cancer Center investigator and professor of biochemistry and molecular genetics at the CU School of Medicine to define a molecular braking process that AML cells use to survive the curves of chemotherapy. They also showed that when this molecular brake is removed, AML cells (but not their healthy neighbors) die on the corners.
The discovery of this escape route and how to plug it provides hope for survival for a greater proportion of the estimated 12,950 people diagnosed with AML every year in the United States.
The group's findings rely on the relatively new technique of functional genomic screening of AML cells, accomplished by the CU Cancer Center Functional Genomics Shared Resource at the University of Colorado Boulder.
Using techniques they developed, the group turned off a different gene in each of a population of AML cells all at once. Then they hit all cells with chemotherapy traditionally used for AML. The goal: to see which genes, when turned off, would make the cells especially susceptible to chemo.
In this study, which generated over 30 million data points, cells that lacked a gene to make something called WEE1 died in disproportionate numbers. When you turn off WEE1, cancer cells die.
"WEE1 is the brakes," Porter says. "With chemotherapy we introduce DNA damage in cancer cells ? we push them toward the curve hopefully at a greater rate than healthy cells. If WEE1 is there, cancer cells can round the curve. Without it, they flip."
Hidden in Porter's words is an element that makes this an especially exciting finding: AML cells may be more dependent than are healthy cells on WEE1. And so when you inhibit WEE1, you strip the brakes from cancer cells but not their healthy neighbors, killing AML cells but leaving healthy cells able to corner on rails.
"I'm optimistic that this will eventually lead to a therapeutic regimen that allows us to target AML cells that have escaped conventional therapies," Porter says.
Porter calls the team's initial results combining a drug that inhibits WEE1 with chemotherapy in mouse models of AML, "extremely promising."
"In light of these data, we are already early in the clinical trial planning process," Porter says.
###
University of Colorado Denver: http://www.ucdenver.edu
Thanks to University of Colorado Denver for this article.
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[unable to retrieve full-text content]Changes to the way autism is diagnosed may make it harder for many people who would no longer meet the criteria to get health, educational and social services, researchers say.
In this film image released by Sundance Film Festival, Melanie Lynskey is shown in a scene from "Hello I Must Be Going," a love story between a 19-year-old man and a 35-year-old divorcee that will be featured at the Sundance Film Festival, opening Thursday, Jan. 19, 2012. (AP Photo/Sundance Film Festival)
In this film image released by Sundance Film Festival, Melanie Lynskey is shown in a scene from "Hello I Must Be Going," a love story between a 19-year-old man and a 35-year-old divorcee that will be featured at the Sundance Film Festival, opening Thursday, Jan. 19, 2012. (AP Photo/Sundance Film Festival)
In this image released by Sundance Film Festival, Jackie Siegel is shown with her children during the filming of a documentary, "The Queen of Versailles," being shown at the Sundance Film Festival. The festival begins Thursday, Jan. 19, 2012. (AP Photo/Sundance Film Festival, Lauren Greenfield)
PARK CITY, Utah (AP) ? A fresh dusting of snow over Park City heralded the opening of the Sundance Film Festival on Thursday.
For 11 days every January, Sundance becomes the focal point of the independent film world as established directors and stars mix with up-and-coming talent, while theatrical distributors prowl the festival looking for the next indie hit and film lovers have a good time being the first audiences to see new movies.
"You can't make a film with a festival in mind, and it's not something I would have expected or taken for granted. But it's always kind of the dream in the back of your mind," said Lauren Greenfield, who premiered her debut documentary "Thin" at Sundance in 2006 and returns this time with one of the opening-night films, "The Queen of Versailles." It chronicles the housing-bust story of a couple that tried to build a palatial mansion.
"I think it's this really magical environment, a place that's such a nurturing, supportive influence for independent films. Even when you're out there making your film, I think that you think about Sundance, and it just kind of gives you motivation."
Also opening Thursday is "Hello I Must Be Going," actor-turned-director Todd Louiso's U.S. dramatic entry, which centers on a love story between a 19-year-old man and a 35-year-old divorcee that stars Melanie Lynskey.; the world-cinema drama "Wish You Were Here," a dark story of a vacation gone wrong from Australian filmmaker Kieran Darcy-Smith that stars Joel Edgerton and Teresa Palmer; and Swedish director Malik Bendjelloul's world-cinema documentary "Searching for Sugar Man," a portrait of promising 1970s singer-songwriter Rodriguez and his fade into obscurity.
Sundance also is a launch place for films that already have distributors, who show off their films hoping to build buzz among audiences and the legions of cinema journalists and bloggers who attend the festival.
"All the film press in North America is at Sundance to discover films," said Michael Barker, co-president of Sony Pictures Classics, which is showing director Nadine Labaki's Lebanese drama "Where Do We Go Now?" and Gareth Huw Evans' Indonesian action tale "The Raid" at the festival. "
Among the more established filmmakers showcasing their work at the festival are Spike Lee with his urban drama "Red Hook Summer," in which he reprises the character he played in "Do the Right Thing"; Stephen Frears with his sports-wagering caper "Lay the Favorite," starring Bruce Willis, Catherine Zeta-Jones and Rebecca Hall; documentary veteran Joe Berlinger with his Paul Simon portrait "Under African Skies"; and Julie Delpy with her relationship comedy "2 Days in New York," in which she stars with Chris Rock.
The Sundance Film Festival continues through Jan. 29.
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AP Movie Writer David Germain contributed to this report.
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AP Entertainment Writer Sandy Cohen is on Twitter: www.twitter.com/APSandy .
ScienceDaily (Jan. 17, 2012) ? A natural enzyme derived from human blood plasma showed potential in significantly reducing the effects of graft-vs.-host disease, a common and deadly side effect of lifesaving bone marrow transplants.
Researchers from the University of Michigan Comprehensive Cancer Center looked at the drug alpha-1-antitrypsin, which is approved by the U.S. Food and Drug Administration for use in people who have a genetic mutation that makes them deficient in a certain enzyme. This drug has been used in many of these patients over extended periods of time and is known to cause minimal side effects.
More important, there are no known reports of increased susceptibility to infections. This is key for people with graft-vs.-host disease, where existing treatment options tend to suppress the immune system, putting patients at risk of infection. Graft-vs.-host disease is a major complication of bone marrow transplants using marrow from a donor, called an allogeneic transplant. This often-deadly side effect is what makes the procedure so risky.
"If we can get graft-vs.-host disease under control, we can more effectively use allogeneic bone marrow transplant to treat people with leukemia and lymphoma as well as other blood disorders. It would be a curative therapy for people who otherwise have no hope," says senior study author Pavan Reddy, M.D., associate professor of hematology/oncology at the U-M Medical School.
In this study, which appears in the Proceedings of the National Academy of Sciences, researchers used alpha-1-antitrypsin in mice that received allogeneic bone marrow transplants. The drug significantly reduced mortality from graft-vs.-host disease, compared to control mice who did not receive the drug.
In addition, alpha-1-antitrypsin reduced the number of inflammatory cells called T Effector cells that are known to be present in graft-vs.-host disease. It also increased the number of T-regulatory cells, which immunologists believe play a positive role in immune responses.
"It's likely the balance between the T-regulatory cells and the T Effector cells that leads to graft-vs.-host disease. Alpha-1-antitrypsin appears to have tipped that balance favorably," says lead study author Isao Tawara, M.D., Ph.D., a research investigator at the U-M Medical School.
The U-M researchers collaborated on this work with researchers from the University of Colorado and from Ben Gurion University of the Negev in Israel. The researchers are beginning to discuss a possible clinical trial using alpha-1-antitrypsin in post-transplant patients with graft-vs.-host disease for whom conventional therapies are no longer working.
Additional authors include Yaping Sun, Tomomi Toubai, Rebecca Evers and Evelyn Nieves, all from U-M; Eli C. Lewis, from Ben-Gurion University of the Negev in Israel; Tania Azam and Charles A. Dinarello, from the University of Colorado.
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The above story is reprinted from materials provided by University of Michigan Health System.
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Journal Reference:
I. Tawara, Y. Sun, E. C. Lewis, T. Toubai, R. Evers, E. Nieves, T. Azam, C. A. Dinarello, P. Reddy. Alpha-1-antitrypsin monotherapy reduces graft-versus-host disease after experimental allogeneic bone marrow transplantation. Proceedings of the National Academy of Sciences, 2011; 109 (2): 564 DOI: 10.1073/pnas.1117665109
Note: If no author is given, the source is cited instead.
Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.
High risk oesophageal cancer gene discoveredPublic release date: 19-Jan-2012 [ | E-mail | Share ]
Contact: Kerry Noble k.noble@qmul.ac.uk 44-020-788-27943 Queen Mary, University of London
New research from Queen Mary, University of London has uncovered a gene which plays a key role in the development of oesophageal cancer (cancer of the gullet).
The researchers studied families who suffer a rare inherited condition making them highly susceptible to the disease and found that a fault in a single gene was responsible.
Initial studies suggest that the gene could play a role in the more common, non-inherited form of the disease, revealing a new target for treating this aggressive type of cancer.
Oesophageal cancer affects more than 8,000 people each year in the UK and rates are rising. It is more common in the UK than anywhere else in Europe.
Survival rates are poor compared to other types of cancer with only eight per cent of people alive five years after diagnosis. Scientists know little about how oesophageal cancer develops and very few drugs for targeting the disease are currently available.
The new study was led by Professor David Kelsell from Queen Mary, University of London with collaborators from the University of Dundee and the University of Liverpool.
The research concentrated on three families with a hereditary condition called tylosis with oesophageal cancer. This condition affects the skin and mouth and sufferers have a 95 per cent chance of developing oesophageal cancer by the age of 65.
The research revealed that all three families carried a faulty version of a gene called RHBDF2.
Experiments showed that this gene plays an important role in how cells that line the oesophagus, and cells in the skin, respond to injury. When the gene is functioning normally it ensures that cells grow and divide in a controlled fashion to help heal a wound.
However, in tylosis patients' cells, and in cells from oesophageal cancers, the gene malfunctions. This allows cells to divide and grow uncontrollably, causing cancer.
Professor Kelsell explains: "In studying this relatively rare condition, we have made an important dicovery about a cancer that is all too common. Finding a genetic cause for this aggressive cancer, and understanding what that gene is doing, is an enormous step forward.
"By analysing the complex biology which causes a particular type of cancer we begin to understand which treatments might be effective and also which treatments are unlikely to help."
###
The study was funded by Queen Mary Innovations and Cancer Research UK. Professor Kelsell has also received new funding from Barts and The London Charity to continue this research.
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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
High risk oesophageal cancer gene discoveredPublic release date: 19-Jan-2012 [ | E-mail | Share ]
Contact: Kerry Noble k.noble@qmul.ac.uk 44-020-788-27943 Queen Mary, University of London
New research from Queen Mary, University of London has uncovered a gene which plays a key role in the development of oesophageal cancer (cancer of the gullet).
The researchers studied families who suffer a rare inherited condition making them highly susceptible to the disease and found that a fault in a single gene was responsible.
Initial studies suggest that the gene could play a role in the more common, non-inherited form of the disease, revealing a new target for treating this aggressive type of cancer.
Oesophageal cancer affects more than 8,000 people each year in the UK and rates are rising. It is more common in the UK than anywhere else in Europe.
Survival rates are poor compared to other types of cancer with only eight per cent of people alive five years after diagnosis. Scientists know little about how oesophageal cancer develops and very few drugs for targeting the disease are currently available.
The new study was led by Professor David Kelsell from Queen Mary, University of London with collaborators from the University of Dundee and the University of Liverpool.
The research concentrated on three families with a hereditary condition called tylosis with oesophageal cancer. This condition affects the skin and mouth and sufferers have a 95 per cent chance of developing oesophageal cancer by the age of 65.
The research revealed that all three families carried a faulty version of a gene called RHBDF2.
Experiments showed that this gene plays an important role in how cells that line the oesophagus, and cells in the skin, respond to injury. When the gene is functioning normally it ensures that cells grow and divide in a controlled fashion to help heal a wound.
However, in tylosis patients' cells, and in cells from oesophageal cancers, the gene malfunctions. This allows cells to divide and grow uncontrollably, causing cancer.
Professor Kelsell explains: "In studying this relatively rare condition, we have made an important dicovery about a cancer that is all too common. Finding a genetic cause for this aggressive cancer, and understanding what that gene is doing, is an enormous step forward.
"By analysing the complex biology which causes a particular type of cancer we begin to understand which treatments might be effective and also which treatments are unlikely to help."
###
The study was funded by Queen Mary Innovations and Cancer Research UK. Professor Kelsell has also received new funding from Barts and The London Charity to continue this research.
[ | E-mail | Share ]
?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
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Public release date: 25-Jan-2012
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