NEW YORK (Reuters) - New Jersey Governor Chris Christie responded angrily on Wednesday to a former White House physician's comment that he could die in office if he does not lose weight, calling the doctor a "hack" for offering advice without examining him.
Connie Mariano, a doctor in the White House medical unit from 1992 to 2001, said in an interview on CNN that Christie, a blunt-spoken Republican who is seen as a strong contender if he decides to run for president in 2016, risks a heart attack or a stroke if he does not slim down.
"It's almost like a time bomb waiting to happen unless he addresses those issues before running for office," Mariano said.
Asked about the comments on Wednesday, Christie, who has spoken openly about his struggle to lose weight, said Mariano was out of line.
"I find it fascinating that a doctor in Arizona who has never met me, never examined me, never reviewed my medical history or records, knows nothing about my family history, could make a diagnosis from 2,400 miles away. She must be a genius," Christie said, adding: "My children saw that."
He called Mariano "just another hack who wants five minutes on TV."
Mariano's comments came after Christie appeared on the Late Show with David Letterman and poked fun at his own size - producing a donut while Letterman was mid-joke.
"I'm basically the healthiest fat guy you've ever seen in your life," Christie said.
But Mariano, who helped former President Bill Clinton during his White House years, said her advice was not partisan.
"I'm a Republican. I like Chris Christie. I want him to run. I just want him to lose weight," Mariano said. "I'm a physician more than I'm a Democrat or Republican. And I'm worried about this man dying in office."
In a follow-up interview on CNN on Wednesday, Mariano said she and Christie had spoken by phone.
"The words gracious and appreciative don't come to mind," she said, adding that Christie had asked her not to share the specifics of their conversation.
"You don't have to be a doctor to look at him and see that he has a problem with weight," she said. "I have patients who suffer with obesity, and it is not a laughing matter."
(Reporting By Edith Honan; Editing by Andre Grenon, Cynthia Johnston and Paul Simao)
Stroke damage in mice overcome by training that 'rewires' brain centersPublic release date: 5-Feb-2013 [ | E-mail | Share ]
Contact: Stephanie Desmon sdesmon1@jhmi.edu 410-955-8665 Johns Hopkins Medicine
Study findings suggest physical and pharmacological solutions for human stroke victims
Johns Hopkins researchers have found that mice can recover from physically debilitating strokes that damage the primary motor cortex, the region of the brain that controls most movement in the body, if the rodents are quickly subjected to physical conditioning that rapidly "rewires" a different part of the brain to take over lost function.
Their research, featuring precise, intense and early treatment, and tantalizing clues to the role of a specific brain area in stroke recovery, is described online in the journal Stroke.
"Despite all of our approved therapies, stroke patients still have a high likelihood of ending up with deficits," says study leader Steven R. Zeiler, M.D., Ph.D., an assistant professor of neurology at the Johns Hopkins University School of Medicine. "This research allows us the opportunity to test meaningful training and pharmacological ways to encourage recovery of function, and should impact the care of patients."
With improved acute care for stroke, more patients are surviving. Still, as many as 60 percent are left with diminished use of an arm or leg, and one-third need placement in a long-term care facility. The economic cost of disability translates to more than $30 billion in annual care.
For their study, the researchers first trained normal but hungry mice to reach for and grab pellets of food in a precise way that avoided spilling the pellets and gave them the pellets as a reward. The task was difficult to master, the researchers say, but the mice reached maximum accuracy after seven to nine training days.
Then the researchers created experimental small strokes that left the mice with damage to the primary motor cortex. Predictably, the reaching and grasping precision disappeared, but a week of retraining, begun just 48 hours after the stroke, led the mice to again successfully perform the task with a degree of precision comparable to before the stroke.
Subsequent brain studies showed that although many nerve cells in the primary motor cortex were permanently damaged by the stroke, a different part of the brain called the medial premotor cortex adapted to control reaching and grasping. Zeiler says the function of the medial premotor cortex is not well-understood, but in this case it seemed to take over the functions associated with the reach-and-grab task in his experimental mice.
The researchers also report that otherwise healthy mice trained to reach and grasp pellets did not lose this ability after experiencing a stroke in the medial premotor cortex, which suggests that this part of the brain typically plays no role in those activities, and the existence of untapped levels of brain plasticity might be exploited to help human stroke victims.
Zeiler says another key finding in his research team's mouse model was a reduction of the level of parvalbumin, a protein that marks the identity and activity of inhibitory neurons that keep the brain's circuitry from overloading. With lower levels of parvalbumin in the medial premotor cortex, it appears the "brakes" are essentially off, allowing for the kind of activity required to reorganize and rewire the brain to take on new functions in this case the ability to reach and grasp.
To prove that the learned functions had moved to the medial premotor cortex in the mice, the researchers induced strokes there. Again, the new skills were lost. And again, the mice could be retrained.
The research team's next steps with their mouse model include evaluating the effect of drugs and timing of physical rehab on long-term recovery. The research could offer insight into whether humans should receive earlier and more aggressive rehab.
"In people left with deficits after a stroke, we have been asking how we can encourage the rest of the nervous system to adapt to allow true recovery," Zeiler says. "This research begins to provide us some answers."
###
The research was supported by a startup fund from the Johns Hopkins University School of Medicine's Department of Neurology as well as grants from the National Institutes of Health's National Institute of Neurological Disorders and Stroke (R01 NS052804-05 and R01 NS 39156) and the NIH's National Institute of Mental Health (MH084020).
Other Johns Hopkins researchers involved in the study include Ellen M. Gibson, B.S.; Robert E. Hoesch, M.D., Ph.D.; Ming Y. Li, B.A.; Paul F. Worley, M.D.; Richard O'Brien, M.D., Ph.D.; and John W. Krakauer, M.D.
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.
Stroke damage in mice overcome by training that 'rewires' brain centersPublic release date: 5-Feb-2013 [ | E-mail | Share ]
Contact: Stephanie Desmon sdesmon1@jhmi.edu 410-955-8665 Johns Hopkins Medicine
Study findings suggest physical and pharmacological solutions for human stroke victims
Johns Hopkins researchers have found that mice can recover from physically debilitating strokes that damage the primary motor cortex, the region of the brain that controls most movement in the body, if the rodents are quickly subjected to physical conditioning that rapidly "rewires" a different part of the brain to take over lost function.
Their research, featuring precise, intense and early treatment, and tantalizing clues to the role of a specific brain area in stroke recovery, is described online in the journal Stroke.
"Despite all of our approved therapies, stroke patients still have a high likelihood of ending up with deficits," says study leader Steven R. Zeiler, M.D., Ph.D., an assistant professor of neurology at the Johns Hopkins University School of Medicine. "This research allows us the opportunity to test meaningful training and pharmacological ways to encourage recovery of function, and should impact the care of patients."
With improved acute care for stroke, more patients are surviving. Still, as many as 60 percent are left with diminished use of an arm or leg, and one-third need placement in a long-term care facility. The economic cost of disability translates to more than $30 billion in annual care.
For their study, the researchers first trained normal but hungry mice to reach for and grab pellets of food in a precise way that avoided spilling the pellets and gave them the pellets as a reward. The task was difficult to master, the researchers say, but the mice reached maximum accuracy after seven to nine training days.
Then the researchers created experimental small strokes that left the mice with damage to the primary motor cortex. Predictably, the reaching and grasping precision disappeared, but a week of retraining, begun just 48 hours after the stroke, led the mice to again successfully perform the task with a degree of precision comparable to before the stroke.
Subsequent brain studies showed that although many nerve cells in the primary motor cortex were permanently damaged by the stroke, a different part of the brain called the medial premotor cortex adapted to control reaching and grasping. Zeiler says the function of the medial premotor cortex is not well-understood, but in this case it seemed to take over the functions associated with the reach-and-grab task in his experimental mice.
The researchers also report that otherwise healthy mice trained to reach and grasp pellets did not lose this ability after experiencing a stroke in the medial premotor cortex, which suggests that this part of the brain typically plays no role in those activities, and the existence of untapped levels of brain plasticity might be exploited to help human stroke victims.
Zeiler says another key finding in his research team's mouse model was a reduction of the level of parvalbumin, a protein that marks the identity and activity of inhibitory neurons that keep the brain's circuitry from overloading. With lower levels of parvalbumin in the medial premotor cortex, it appears the "brakes" are essentially off, allowing for the kind of activity required to reorganize and rewire the brain to take on new functions in this case the ability to reach and grasp.
To prove that the learned functions had moved to the medial premotor cortex in the mice, the researchers induced strokes there. Again, the new skills were lost. And again, the mice could be retrained.
The research team's next steps with their mouse model include evaluating the effect of drugs and timing of physical rehab on long-term recovery. The research could offer insight into whether humans should receive earlier and more aggressive rehab.
"In people left with deficits after a stroke, we have been asking how we can encourage the rest of the nervous system to adapt to allow true recovery," Zeiler says. "This research begins to provide us some answers."
###
The research was supported by a startup fund from the Johns Hopkins University School of Medicine's Department of Neurology as well as grants from the National Institutes of Health's National Institute of Neurological Disorders and Stroke (R01 NS052804-05 and R01 NS 39156) and the NIH's National Institute of Mental Health (MH084020).
Other Johns Hopkins researchers involved in the study include Ellen M. Gibson, B.S.; Robert E. Hoesch, M.D., Ph.D.; Ming Y. Li, B.A.; Paul F. Worley, M.D.; Richard O'Brien, M.D., Ph.D.; and John W. Krakauer, M.D.
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.
Adding a little alcohol to your dishes can boost their flavor, and even though much of the alcohol will eventually cook out, not all of it does. If you have guests over while you're cooking, or you're just feeling flashy, you might be tempted to flamb? your dish and set your dish alight after you've added a flavorful wine or spirit. Here's how to do it safely.
First of all, don't think you have to flamb? your dish for any culinary reason. It's largely for show, although it can (slightly) speed up the process of burning away excess alcohol. If your dish calls for it as part of the preparation though, or you're just feeling flashy, go for it. This video from the folks at America's Test Kitchen shows you how. It uses a Bananas Foster recipe as a demonstration, but the same rules apply for any dish: roll up your sleeves, pull your hair back, and turn off the other burners and the overhead fan or hood over your stove. You don't want to burn yourself or set fire to your clothing, and the hood can draw a flame up, while other lit burners can flare up.
Then, turn off the heat, pour in your alcohol, and give it a little time to soak into the dish. (Do not use the TV chef method of tipping the pan over a gas flame to ignite it.) Then use a long lighter to light up the dish. Shake your now-flaming pan over the stove to evenly distribute the alcohol (and the flames) and wait about 15-30 seconds for the flames to die out naturally. It looks impressive, and is a fun kitchen trick if you can do it safely.
How to Set Bananas on Fire Safely | America's Test Kitchen
First time accepted submitter ras writes "The Reserve Bank of Australia did some investigation into the accuracy of their economic predictions ? the ones they use to run the country ? with less than flattering results. '70 per cent of the RBA's forecasts for underlying inflation for the year ahead were close to the mark, but its predictions of economic growth were less accurate, and its unemployment rate estimates no better than [chance] ... The Reserve Bank employs numbers of people on very high pay and what they're admitting now is that their ? all of this so-called science ? has produced nothing more than what a roll of the dice could produce.'"
The Republican Party may be dealt another far-right candidate in a potentially competitive U.S. Senate race if a poll released Tuesday is any indication.
Rep. Steve King (R-IA) is the favorite among Iowa Republicans to run in next year's contest to replace retiring Sen. Tom Harkin (D-IA), according to the latest survey from Democratic-leaning Public Policy Polling. The poll showed 41 percent of usual GOP primary voters in the state identifying King as their preferred candidate over three other Republicans. Rep. Tom Latham (R-IA) was a distant second with 22 percent support among Hawkeye State Republicans. Neither King nor Latham so far has declared an intention to run.
Some conservatives, including a new group backed by political operative Karl Rove, have warned recently that nominating King would put Republicans in the same bind they found themselves in the previous two cycles, when the party squandered prime pick-up opportunities in Senate races by fielding candidates who turned out to be too extreme for voters.
In 2008, King said that electing President Barack Obama would be bad "optics" in the Muslim world. And last August, King seemingly backed up the now-infamous argument made by embattled Rep. Todd Akin (R-MO), saying he's never never heard of a woman getting pregnant from statutory rape or incest.
PPP's findings suggested that King could face the same fate in a general election as Akin. In four hypothetical matchups tested by PPP, King trailed by seven to 11 points against notable Democrats, including a 10-point deficit to former Iowa Gov. Tom Vilsack (D). The poll indicated that Latham would fare much better in a general election.
While 63 percent of Republicans in Iowa have a favorable opinion of King, only 32 percent of all registered voters feel the same way. Forty-one percent of Iowa voters have an unfavorable opinion of King (compared with just 12 percent of GOP voters), while more than a quarter of all voters said they have no opinion of the conservative firebrand.
Along with PPP's release, a survey released Tuesday from GOP pollster Wenzel Strategies also pegged King as the clear favorite among Republicans in the state. In that poll, 34 percent of GOP primary voters said they would vote for King in a prospective eight candidate intra-party contest, while 19 percent said they would vote for Latham.
Jan. 31, 2013 ? New design guidelines from researchers in Singapore simplify the development of targeted therapies for muscular dystrophy and other diseases.
The dystrophin protein offers critical support to muscle fibers. Mutations affecting dystrophin's expression cause the muscle-wasting disease muscular dystrophy. In Duchenne muscular dystrophy (DMD), these mutations take the form of small sequence changes that make much of the dystrophin gene (DMD) untranslatable, yielding nonfunctional protein or no protein at all.
Therapies based on a strategy known as 'exon skipping' could undo the damage from these mutations. Development of such treatments is set to accelerate, thanks to research by a team led by Keng Boon Wee of the A*STAR Institute of High Performance Computing and Zacharias Pramono of the National Skin Centre in Singapore.
Proteins are translated from messenger RNA transcripts of genes; however, only certain RNA regions -- known as exons -- actually encode protein, and these are enzymatically spliced together prior to translation. Several clinical studies have demonstrated that small 'antisense oligonucleotide' (AON) molecules that bind mutated DMD exons can induce elimination of those defective exons during splicing, yielding shorter but largely functional versions of dystrophin. "We are cautiously optimistic that AON-induced exon skipping could be the first effective therapy for DMD patients," says Wee.
Unfortunately, DMD arises from many different mutations, and targeted AON design remains a time-consuming, trial-and-error process. To address this challenge, Wee and Pramono sought to define the characteristics of AONs that efficiently promote exon-skipping. They used computational analysis to zoom in on exonic sequences that coordinate splicing. They also identified regions of suitable length within dystrophin RNA transcripts that span these sequences and would be accessible to AONs in living cells.
The researchers thus derived a set of guidelines enabling them to effectively design AONs that targeted nine different exons affected in DMD patients. For each exon, at least one AON proved capable of boosting dystrophin expression to clinically relevant thresholds in cultured muscle cells (see image). "Our proposed set of factors resulted in a reasonable success rate of designing efficient AONs -- 61% versus 38% using semi-empirical methods," says Wee. Clinical studies have already demonstrated the promise of efficient exon skipping in treating DMD patients.
Wee notes that other diseases arising from abnormal RNA processing could also benefit from this approach. However, his team is also exploring this method as a general strategy to abort production of disease-causing proteins in cancer and other conditions. "In contrast to small-molecule inhibitor drugs that can target only about 10% of the human genome, this approach could downregulate most human genes," Wee says.
Share this story on Facebook, Twitter, and Google:
Other social bookmarking and sharing tools:
Story Source:
The above story is reprinted from materials provided by The Agency for Science, Technology and Research (A*STAR).
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
Pramono, Z. A. D., Wee, K. B., Wang, J. L., Chen, Y. J., Xiong, Q. B. et al. A prospective study in the rational design of efficient antisense oligonucleotides for exon skipping in the DMD gene. Human Gene Therapy, 2012 DOI: 10.1089/hum.2011.205
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.
Distribution is a hell of a drug. In a product-obsessed town, it's distribution that often proves most elusive, and when a person or platform can tap into it, they oftentimes move quickly to lock-in those advantages. However, not all distribution is created equal. In today's technology landscape, while thousands of startups pursue the dream of massive distribution, a few platforms and companies hold tremendous advantages in their own special, elite tier: Apple's iOS, Google's Android, Facebook, Twitter, and Amazon.
![[ Back to EurekAlert! ]](https://lh3.googleusercontent.com/blogger_img_proxy/AEn0k_tWCm6SSI2DD7SjQ5Gbq4zx8ixWS9LpGVDehc9jYIOIMeBBxnnOJPjwK_Pi_dMh9G_6wQVUWH2F64uTeXcyfWV5hVtwAZl18Y_yebzMmcQ=s0-d){kind=small}
Public release date: 5-Feb-2013
Share ] 
Adding a little alcohol to your dishes can boost their flavor, and even though much of the alcohol will eventually cook out, not all of it does. If you have guests over while you're cooking, or you're just feeling flashy, you might be tempted to flamb? your dish and set your dish alight after you've added a flavorful wine or spirit. Here's how to do it safely. 
Distribution is a hell of a drug. In a product-obsessed town, it's distribution that often proves most elusive, and when a person or platform can tap into it, they oftentimes move quickly to lock-in those advantages. However, not all distribution is created equal. In today's technology landscape, while thousands of startups pursue the dream of massive distribution, a few platforms and companies hold tremendous advantages in their own special, elite tier: Apple's iOS, Google's Android, Facebook, Twitter, and Amazon.