Wednesday, August 1, 2012
In Mice, Alzheimer's-Linked Protein Shows Promise Against MS
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Tuesday, July 10, 2012
Keeping the flu away: Synthetic protein activates immune system within two hours
A new study published July 6 in the Public Library of Science journal PLoS ONE, finds that EP67, a powerful synthetic protein, is able to activate the innate immune system within just two hours of being administered.
Prior to this study, EP67 had been primarily used as an adjuvant for vaccines, something added to the vaccine to help activate the immune response. But Joy Phillips, Ph.D. a lead author of the study with her colleague Sam Sanderson, Ph.D. at the University of Nebraska Medical Center, saw potential for it to work on its own.
"The flu virus is very sneaky and actively keeps the immune system from detecting it for a few days until you are getting symptoms," Phillips said. "Our research showed that by introducing EP67 into the body within 24 hours of exposure to the flu virus caused the immune system to react almost immediately to the threat, well before your body normally would."
Because EP67 doesn't work on the virus but on the immune system itself, it functions the same no matter the flu strain, unlike the influenza vaccine which has to exactly match the currently circulating strain.
Phillips said while this study focuses on the flu, EP67 has the potential to work on other respiratory diseases and fungal infections and could have huge potential for emergency therapeutics.
"When you find out you've been exposed to the flu, the only treatments available now target the virus directly but they are not reliable and often the virus develops a resistance against them," Phillips said. "EP67 could potentially be a therapeutic that someone would take when they know they've been exposed that would help the body fight off the virus before you get sick."
It could even be used in the event of a new strain of infectious disease, before the actual pathogen has been identified, as in SARS or the 2009 H1N1 influenza outbreak, Phillips said.
Right now, the testing has been done primarily in mice by infecting them with a flu virus. Those that were given a dose of EP67 within 24 hours of the infection didn't get sick (or as sick) as those that were not treated with EP67.
The level of illness in mice is measured by weight loss. Typically, mice lose approximately 20 percent of their weight when they are infected with the flu but mice treated with EP67 lost an average of just six percent. More importantly, mice who were treated a day after being infected with a lethal dose of influenza did not die, Phillips said.
She said there are also huge implications for veterinary applications, since EP67 is active in animals, including birds.
Future research will examine the effect EP67 has in the presence of a number of other pathogens and to look closer at exactly how EP67 functions within different cells in the body.
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Monday, July 9, 2012
Sunday, June 24, 2012
Role of cellular protein demonstrated in regulation of binge eating
The research, which is published online in Neuropsychopharmacology, was led by Pietro Cottone, PhD, and Valentina Sabino, PhD, both assistant professors in the pharmacology and psychiatry departments at BUSM.
Binge eating disorder, which affects approximately 15 million Americans, is believed to be the eating disorder that most closely resembles substance dependence. In binge eating subjects, normal regulatory mechanisms that control hunger do not function properly. Binge eaters typically gorge on "junk" foods excessively and compulsively despite knowing the adverse consequences, which are physical, emotional and social in nature. In addition, binge eaters typically experience distress and withdrawal when they abstain from junk food.
The researchers developed an experimental model of compulsive binge eating by providing a sugary, chocolate diet only for one hour a day while the control group was given a standard laboratory diet. Within two weeks, the group exposed to the sugary diet exhibited binge eating behavior and ate four times as much as the controls. In addition, the experimental binge eaters exhibited compulsive behavior by putting themselves in a potentially risky situation in order to get to the sugary food while the control group avoided the risk.
The researchers then tested whether a drug that blocks the Sigma-1 receptor could reduce binge eating of the sugary diet. The experimental data showed the drug successfully reduced binge eating by 40 percent, caused the binge eaters to eat more slowly and blocked the risky behavior.
The abnormal, risky behavior exhibited by the binge eating experimental group suggested to the researchers that there could be something wrong with how decisions were made. Because evaluation of risks and decision making are functions executed in the prefronto-cortical regions of the brain, the researchers tested whether the abundance of Sigma-1 receptors in those regions was abnormal in the binge eaters. They found that Sigma-1 receptor expression was unusually high in those areas, which could explain why blocking its function could decrease both compulsive binge eating and risky behavior.
"These findings suggest that the Sigma-1 receptor may contribute to the neurobiological adaptations that cause compulsive-like eating, opening up a new potential therapeutic treatment target for binge eating disorder," said Cottone, who also co-directs the Laboratory of Addictive Disorders at BUSM with Sabino.
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Tuesday, May 15, 2012
Scientists identify protein that stimulates brown fat to burn calories
Unlike white fat, which functions primarily to store up fat, brown fat (also known as brown adipose tissue) burns fats to generate heat in a process known as thermogenesis. The research, led by scientists at the University of Cambridge Metabolic Research Laboratories at the Institute of Metabolic Science, discovered that the protein BMP8B acts on a specific metabolic system (which operates in the brain and the tissues) to regulate brown fat, making it a potential therapeutic target.
The scientists believe that activating brown fat could help to support current weight loss programmes, which individuals often struggle to maintain.
Dr Andrew Whittle, one of the authors of the paper from the Institute of Metabolic Science, said: "Other proteins made by the body can enhance heat production in brown fat, such as thyroid hormone but often these proteins have important effects in other organs too. Therefore they are not good targets for developing new weight loss treatments. However, BMP8B seems to be very specific for regulating the heat producing activity of brown fat, making it a more ideal mechanism for new therapies."
The experiments showed that when mice lacked the protein BMP8B they found it more difficult to maintain their normal body temperature. They also became much more obese than normal mice, particularly when fed a high-fat diet. Additionally, when the researchers treated brown fat cells with BMP8B they responded more strongly to activation by the nervous system. Furthermore, when BMP8B was administered to specific parts of the brain it increased the amount of nervous activation of brown adipose tissue. The result was that these BMP8B-treated brown fat cells burned more fat and mice given BMP8B in the brain lost weight.
Professor Toni Vidal-Puig, lead author of the study from the Institute of Metabolic Science and a member of the MRC Centre for Obesity and Related Metabolic Diseases, said: "A major feature of current weight-loss strategies is that people lose a lot of weight early on, but then reach a plateau despite continuing to follow the same diet regime. This is because the human body is incredibly good at sensing a reduction in food consumption and slows the metabolic rate to compensate. A strategy to increase brown fat activity could potentially be used in conjunction with current weight loss strategies to help prevent the typical decrease in a person's metabolic rate.
"One could be sceptical that techniques to increase metabolic rate might just be compensated by the body trying to make you want to eat more, to fuel this increased metabolism. But our findings showed that treating mice with Bmp8b did not have this effect, it simply made them lose weight by burning more fat in their brown adipose tissue.
"There are obvious differences between mice and humans, and from a therapeutic perspective this work is preliminary. Validation will be necessary to see if manipulating BMP8B would be safe and effective in humans."
The research was funded by the Medical Research Council (MRC), the Wellcome Trust, and the Biotechnology and Biological Sciences Research Council (BBSRC).
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Tuesday, April 17, 2012
Try Quality Bariatric Protein Bars For Change
Health
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