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May 27, 2006, 7:19 PM CT

New Images Of AIDS Virus

New Images Of AIDS Virus Envelope Spikes on Surface of HIV-1 virus.
Courtesy of Kenneth Roux
As the world marks the 25th year since the first diagnosed case of AIDS, groundbreaking research by researchers at Florida State University has produced remarkable three-dimensional images of the virus and the protein spikes on its surface that allow it to bind and fuse with human immune cells.

Findings from this AIDS research could boost the development of vaccines that will thwart infection by targeting and crippling the sticky HIV-1 spike proteins. In fact, said principal investigator and FSU Professor Kenneth H. Roux, at least two laboratories already are crafting vaccine candidates based on preliminary results uncovered by his team of structural biologists.

Those results are described in the online edition of the journal Nature.

Never before generated in such intricate detail, the super-sized images of the virus and its viral spikes have given scientists their first good look at the pathogen's complex molecular surface architecture that facilitates the infection process.

"Until now, despite intensive study by a number of laboratories, the design details of the spikes and their distribution pattern on the surface of the virus membrane have been poorly understood, which has limited our understanding of how the virus infection actually occurs and frustrated efforts to create vaccines," Roux said.........

Posted by: Mark      Permalink         Source


May 25, 2006, 0:21 AM CT

Switch For Skeletal-Muscle Atrophy

Switch For Skeletal-Muscle Atrophy Amber Pond, a research scientist at Purdue University's School of Veterinary Medicine, tests skeletal muscle and heart tissue as Xun Wang, a graduate student in basic medical sciences, takes notes. The two are part of a research team investigating treatments that arrest the muscle atrophy caused by cancer and other diseases. (Purdue photo/David Umberger)
Scientists in Purdue University's School of Veterinary Medicine have discovered genetic and drug-treatment methods to arrest the type of muscle atrophy often caused by muscle disuse, as well as aging and diseases such as cancer.

The findings might eventually benefit people who have been injured or suffer from diseases that cause them to be bedridden and lose muscle mass, or sometimes limbs, due to atrophy, said Amber Pond, a research scientist in the school's Department of Basic Medical Sciences.

"The weight loss and muscle wasting that occurs in patients with cancer or other diseases seriously compromises their well-being and is correlated with a poor chance for recovery," Pond said. "In addition, muscle weakness caused by atrophy during aging can lead to serious falls and bone loss. Exercise is the most beneficial strategy to treat atrophy. However, a number of individuals are too ill to adequately participate in exercise programs.

"We've found a chemical 'switch' in the body that allows us to turn atrophy on, and, from that, we also have learned how to turn atrophy off."

Findings based on the research, funded in large part by the American Heart Association, are detailed in a study available online today (Wednesday, May 24) in The FASEB Journal, published by the Federation of American Societies for Experimental Biology. The study will be in the journal's print edition in July.........

Posted by: Mark      Permalink         Source


May 21, 2006, 9:49 AM CT

Key Role For Vegf In Onset Of Sepsis

Key Role For Vegf In Onset Of Sepsis
A study led by scientists at Beth Israel Deaconess Medical Center (BIDMC) has found that the vascular endothelial growth factor (VEGF) protein is a key biomarker for sepsis, a severe inflammatory response that develops following a bacterial infection. The findings, which would be reported in the June 12, 2006, issue of The Journal of Experimental Medicine (JEM) and currently appear on-line, offer a promising new target for the development of drug therapies to treat this overwhelming - and often fatal -- condition.

"Sepsis represents a patient's response to severe infection," explains senior author William C. Aird, MD, Chief of the Division of Molecular Medicine and Associate Director of the Center for Vascular Biology at BIDMC. "We know that antibiotics will take care of the primary infection, but 30 percent of patients with severe sepsis will die in spite of successful antibiotic treatment because the body's host response is out of control and turns on its bearer."

Sepsis develops when the immune system becomes overactivated in response to an existing infection, setting in motion a cascade of dangerous inflammatory and coagulation responses throughout the body. A leading cause of organ failure and intensive care unit (ICU) hospitalizations, severe sepsis accounts for 200,000 deaths each year and poses a particular danger in hospital settings, where patients are more likely to come in contact with antibiotic-resistant pathogens, and when their immune systems have already been weakened by illness or therapys.........

Posted by: Mark      Permalink         Source


May 18, 2006, 9:40 PM CT

Giving Rest To Restless Legs

Giving Rest To Restless Legs
Life can be hard. Sometimes you feel sad or distracted or anxious. Or maybe you feel a compelling urge to move your legs. But does that mean you are sick? Does it mean you need medication?

Maybe, maybe not. For some people, symptoms are severe enough to be disabling. But for a number of others with milder problems, these "symptoms" are just the transient experiences of everyday life. Helping sick people get therapy is a good thing. Convincing healthy people that they are sick is not. Sick people stand to benefit from therapy, but healthy people may only get hurt: they get labeled "sick," may become anxious about their condition, and, if they are treated, may experience side effects that overwhelm any potential benefit.

"Disease mongering" is the effort by pharmaceutical companies (or others with similar financial interests) to enlarge the market for a therapy by convincing people that they are sick and need medical intervention [2]. Typically, the disease is vague, with nonspecific symptoms spanning a broad spectrum of severity-from everyday experiences a number of people would not even call "symptoms," to profound suffering. The market for therapy gets enlarged in two ways: by narrowing the definition of health so normal experiences get labeled as pathologic, and by expanding the definition of disease to include earlier, milder, and presymptomatic forms (e.g., regarding a risk factor such as high cholesterol as a disease in itself).........

Posted by: JoAnn      Permalink         Source


May 16, 2006, 0:04 AM CT

Exercise, Diet May Protect Against Colorectal Cancer

Exercise, Diet May Protect Against Colorectal Cancer
Voluntary exercise and a restricted diet reduced the number and size of pre-malignant polyps in the intestines of male mice and improved survival, as per a research studyby a University of Wisconsin-Madison research published May 13 in the journal Carcinogenesis.

The study is the first to suggest that a "negative energy balance" - produced by increasing the mice's energy output by use of a running wheel, while maintaining a restricted calorie intake - appeared to be the important factor in inhibiting the growth of polyps, which are the forerunners of colorectal tumors, says lead author Lisa H. Colbert, assistant professor in the UW-Madison department of kinesiology.

For the study, Colbert and her co-authors used mice with a genetic mutation that predisposed them to develop intestinal polyps.

"Our studies are relevant for humans in that these mice have a mutation in one of the same genes, APC, that is also mutated in human colon cancer," she explains. "The protective effect of exercise and lower body weight in our mice is consistent with epidemiological evidence in humans that suggests higher levels of activity and lower body weight reduces the risk of colon cancer."

Mutations in the APC gene in humans are responsible for an inherited condition called familial adenomatous polyposis (FAP). This condition affects about one in 10,000-15,000 people worldwide, and 95 percent of those affected develop polyps in the colon that eventually progress into cancer, commonly before age 40.........

Posted by: Janet      Permalink         Source


May 15, 2006, 11:48 PM CT

New Compound To Block Brain Cancer Growth

New Compound To Block Brain Cancer Growth
By determining how a class of compounds blocks signaling in cells, UCSF researchers have identified what is perhaps the most potent drug candidate yet against a highly lethal kind of brain tumor.

The compound, known as PI-103, shows unique potency against cancer cell proliferation in studies of mice with grafts of human glioma cells. Gliomas are the most common form of brain cancer, and have proven very difficult to treat.

The unique effectiveness of PI-103 stems from its ability to attack two separate steps in the series of signals that trigger the spread of cancer. The dual blockade proved to be a safe and effective inhibitor of cancer cell proliferation in mice with the human tumors, the researchers found.

The glioma research is being published online May 15 by the journal Cancer Cell. A description of the strategy used to identify the molecular level action of the inhibitors was published online by the journal Cell on April 27.

Food and Drug Administration approval five years ago of the cancer drug Gleevec marked a promising new strategy against cancer. Gleevec was the first drug on the market designed to block ubiquitous signaling molecules called protein kinases - enzymes known to trigger normal cell proliferation, and in the case of cancer, the growth of tumors. Another group of kinases, called lipid kinases are now emerging as important new targets, particularly PI3 alpha kinase, an enzyme often found to be overactive in brain, breast, colon and stomach cancers.........

Posted by: Janet      Permalink         Source


May 15, 2006, 11:43 PM CT

New Compound Reduces Stroke Damage

New Compound Reduces Stroke Damage
A group of German researchers has synthesized a new compound that dramatically decreases the damage to neurons in rats demonstrating stroke symptoms. The research appears as the "Paper of the Week" in the May 26 issue of the Journal of Biological Chemistry, an American Society for Biochemistry and Molecular Biology journal.

Stroke is the third leading cause of death in the United States and the most common cause of adult disability. An ischemic stroke occurs when a cerebral vessel occludes, obstructing blood flow to a portion of the brain. Currently, there is only one approved stroke treatment, tissue plasminogen activator, which targets the thrombus within the blood vessel. Because of the lack of available stroke therapys, neuroprotective agents have also generated as much interest as thrombolytic therapies.

The immunosuppressive drug FK506 (also known as Tacrolimus or Prograf®) is often administered to patients receiving transplants to prevent organ rejection. Dervatives of the drug are also usually used in the therapy of autoimmune diseases. FK506 inhibits T-cell activation by binding to members of the FK506-binding protein (FKBP) family. Interestingly, FK506, and several molecules with similar structures, also demonstrate neuroprotective and neuroregenerative effects in a wide range of animal models mimicking Parkinson's disease, dementia, stroke, and nerve damage.........

Posted by: Daniel      Permalink         Source


May 12, 2006, 6:55 AM CT

Mobile DNA Part of Evolution's Toolbox

Mobile DNA Part of Evolution's Toolbox
The repeated copying of a small segment of DNA in the genome of a primeval fish may have been crucial to the transition of ancient animals from sea to land, or to later key evolutionary changes in land vertebrates. The discovery is "tantalizing evidence" that copied DNA elements known as retroposons could be an important source of evolutionary innovations, says the director of the research, Howard Hughes Medical Institute investigator David Haussler.

"The big question is whether this is a special case or whether it's the tip of the iceberg," says Haussler, who is at the University of California, Santa Cruz. A report on the research is reported in the May 4, 2006, issue of the journal Nature.

Haussler and colleagues were led to the discovery through their work on what they call "ultraconserved elements"-segments of DNA hundreds of nucleotides long that are almost exactly the same in a wide variety of vertebrate organisms. Haussler and postdoctoral fellow Gill Bejerano discovered the ultraconserved elements in 2003, and since then they have been trying to figure out how they arose and what function they serve.

One ultraconserved element in particular caught their eye. "We were very interested in this sequence, because it had many copies elsewhere in the genome," says Bejerano, who is the first author of the study. Close copies of the sequence were ubiquitous in amphibians, birds, and mammals, indicating that it served an important function. "We found it in every species for which we have genomes, from frogs to humans," says Bejerano.........

Posted by: Scott      Permalink         Source


May 12, 2006, 6:52 AM CT

Epstein-Barr Virus And Multiple Sclerosis

Epstein-Barr Virus And Multiple Sclerosis
Scientists have found that patients with multiple sclerosis (MS) carry a population of immune cells that overreact to Epstein-Barr virus. The virus, which causes mononucleosis and may contribute to some cancers, has long been suspected to play a role in MS. However, the mechanism linking the virus to the disease was poorly understood.

Researchers believe that MS-which can cause vision problems, muscle weakness, and difficulty with coordination and balance-is a result of the immune system attacking the body's own nervous system. Not everyone who is infected with Epstein-Barr develops MS, but the results of the new study, reported in the June 2006, issue of the journal Brain, suggest that some individuals' uncommonly strong reaction to the virus may trigger the disease. The findings could lead to new therapeutic strategies for better control of the damage caused in this autoimmune disorder.

The culprit, the scientists say, may be a population of T cells that helps boost other components of the immune system in response to the virus. "What we discovered in the peripheral blood of the MS patients were T cells that appeared to be primed for action against EBV," said Nancy Edwards, an HHMI-NIH research scholar at the National Institutes of Health (NIH) and co-author of the paper, which was published in advance online.........

Posted by: Daniel      Permalink         Source


May 9, 2006, 11:52 PM CT

Stem Cell Fusion Occurs In Tumors

Stem Cell Fusion Occurs In Tumors
An Oregon Health & Science University study is adding credence to an increasingly popular theory that fusion is what bonds stem cells with bone marrow cells to regenerate organ tissue.

Researchers in the OHSU School of Medicine found that transplanted cells derived from adult bone marrow can fuse with intestinal stem cells of both normal and diseased tissue comprising the cellular lining of intestinal walls, known as the epithelium. The findings, reported recently in the Proceedings of the National Academy of Sciences, point to the integral role of bone marrow-derived cells in not only regeneration of damaged tissue, but also disease progression.

"It's the first observation that there's fusion at the level of stem cells," said the study's corresponding author, Melissa Wong, Ph.D., assistant professor of dermatology, and cell and developmental biology. "Second, we're seeing cell fusion in tumors and we think that this concept is an underappreciated mechanism for promoting tumor growth. Our findings have implications on how tissues regenerate and how, in the process of this regeneration, cells may become prone to future problems. ".

Eventhough the tumor in her study did not "initiate" tumors or become cancerous, Wong believes the fusion process is one explanation for how tumors acquire genetic instability and have the potential to give rise to cancerous cancer.........

Posted by: Janet      Permalink         Source



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Did you know?
Scientists at Yale have brought to light a mechanism that regulates the way an internal organelle, the Golgi apparatus, duplicates as cells prepare to divide, according to a report in Science Express.Graham Warren, professor of cell biology, and colleagues at Yale study Trypanosoma brucei, the parasite that causes Sleeping Sickness. Like a number of parasites, it is exceptionally streamlined and has only one of each internal organelle, making it ideal for studying processes of more complex organisms that have a number of copies in each cell.

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