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March 4, 2008, 5:28 PM CT

Cholesterol-lowering power of dietitian visits

Cholesterol-lowering power of dietitian visits
Worried about your cholesterol? You may want to schedule a few appointments with a registered dietitian, to get some sound advice about how to shape up your eating habits, as per a new national study led by University of Michigan Health System researchers.

Not only are you likely to lower your cholesterol levels, you may be able to avoid having to take cholesterol medication, or having to increase your dose if youre already taking one. And youll probably lose weight in the process, which also helps your heart.

The new results, reported in the recent issue of the Journal of the American Dietetic Association, are based on data from 377 patients with high cholesterol who were counseled by 52 registered dietitians at 24 sites in 11 states.

In the group of 175 patients who started the study with triglycerides less than 400 milligrams per deciliter of blood (mg/dL), and who had their cholesterol measured before they changed or added medication, 44.6 percent either reduced their levels of bad cholesterol by at least 15 percent, or reached their cholesterol goal.

The results reflect progress in approximately eight months, after three or more appointments with a dietitian. But the results add further evidence that medical nutrition treatment, as it is called, can make a big difference in a patients life.........

Posted by: Scott      Read more         Source


March 4, 2008, 5:26 PM CT

Gene mutations linked to longer lifespans

Gene mutations linked to longer lifespans
Mutations in genes governing an important cell-signaling pathway influence human longevity, researchers at the Albert Einstein College of Medicine of Yeshiva University have found. Their research is described in the March 4 issue of the Proceedings of the National Academy of Sciences.

The report is the latest finding in the Einstein scientists ongoing search for genetic clues to longevity through their study that by now has recruited more than 450 Ashkenazi (Eastern European) Jews between the ages of 95 and 110. Descended from a small founder group, Ashkenazi Jews are more genetically uniform than other groups, making it easier to spot gene differences that are present. In 2003, this study resulted in the first two longevity genes ever identifiedfindings that have since been validated by other research.

The present study focused on genes involved in the action of insulin-like growth factor (IGF-I), a hormone that in humans is regulated by human growth hormone. Affecting virtually every cell type in the body, IGF-I is crucially important for childrens growth and continues contributing to tissue synthesis into adulthood. The IGF-I cell-signaling pathway is triggered when IGF-I molecules circulating in blood plasma latch onto receptors on the surface of cells, causing a signal to be sent to the cells nucleus that may, for example, tell that cell to divide.........

Posted by: Scott      Read more         Source


March 2, 2008, 8:45 PM CT

Mouse model for speed drug hunt

Mouse model for speed drug hunt
Frustrated by the slow pace of new drug development for a condition that causes pediatric brain tumors, a neurologist at Washington University School of Medicine in St. Louis decided to try to fine-tune the animal models used to test new drugs.

Instead of studying one mouse model of the disease causing the brain tumors, the laboratory of David Gutmann, M.D., Ph.D., the Donald O. Schnuck Family Professor of Neurology, reviewed three. They "auditioned" the three models to see which was the best match for neurofibromatosis 1, a genetic condition that increases the risk of brain tumors and afflicts more than 100,000 people in the United States.

Animal models have long been used to explore the basic physiology underlying disease and to tentatively try out new remedies, but Gutmann believes that creating a tighter match between the animal models and the human disorder will allow more extensive and more accurate preclinical testing of potential therapies.

"If you think of how we move drugs from testing in the laboratory to testing in humans, this is an exciting step that's likely to speed the translation from bench to bedside," says Gutmann, the senior author of a report in the March 1 Cancer Research. "With more extensive preclinical testing in the mice, we can make sure a new drug is reaching its target protein in tumor cells, we can learn whether the drug is killing tumor cells or shutting off their growth, and we can get some indication of whether the drug is likely to have an adverse effect on the developing brain."........

Posted by: JoAnn      Read more         Source


March 2, 2008, 7:37 PM CT

Novel way to develop tumor vaccines

Novel way to develop tumor vaccines
Scientists at the University of Southern California (USC) have uncovered a new way to develop more effective tumor vaccines by turning off the suppression function of regulatory T cells. The results of the study, titled A20 is an antigen presentation attenuator, and its inhibition overcomes regulatory T cell-mediated suppression, will be published in Nature Medicine on March 2, 2008.

Under normal circumstances, regulatory T cells inhibit the immune system to attack its own cells and tissues to prevent autoimmune diseases. Cancer cells take advantage of regulatory T cells' suppressor ability, recruiting them to keep the immune system at bay or disabling the immune systems attack provoked by tumor vaccines. says Si-Yi Chen, M.D., Ph.D., professor of immunology and molecular microbiology at the USC/Norris Comprehensive Cancer Center and the Keck School of Medicine of USC. Our study provides a new vaccination strategy to overcome the regulatory T cells immune suppression while avoiding non-specific overactivation of autoreactive T cells and pathological autoimmune toxicities.

The study identified a new molecular player called A20, an enzyme that restricts inflammatory signal transduction in dendritic cells. When it is inhibited, the dendritic cells overproduce an array of cytokines and co-stimulatory molecules that triggers uncommonly strong immune responses that cannot be suppressed by regulatory T cells. The resulting hyperactivated immune responses triggered by A20-deficient dendritic cells are capable of destroying various types of tumors that are resistant to current tumor vaccines in mice.........

Posted by: Janet      Read more         Source


February 26, 2008, 10:24 PM CT

Bacterial 'battle for survival' leads to new antibiotic

Bacterial 'battle for survival' leads to new antibiotic
Biologists have provoked soil-dwelling bacteria into producing a new type of antibiotic by pitting them against another strain of bacteria in a battle for survival.

The antibiotic holds promise for therapy of Helicobacter pylori, which causes stomach ulcers in humans. Also, figuring out the still murky explanation for how the new antibiotic was produced could help researchers develop strategies for finding other new antibiotics.

The work is published in the recent issue of the Journal of the American Chemical Society.

A combination of luck, patience and good detective work contributed to the discovery of the new antibiotic, as per Philip Lessard, research scientist in Professor Anthony Sinskey's laboratory at MIT.

Sinskey's lab has been studying Rhodococcus, a type of soil-dwelling bacteria, for a number of years. While sequencing the genome of one Rhodococcus species, the scientists noticed that a large number of genes seemed to code for secondary metabolic products, which are compounds such as antibiotics, toxins and pigments.

However, Rhodococcus does not normally produce antibiotics. A number of bacteria have genes for antibiotics that are only activated when the bacteria are threatened in some way, so the scientists suspected that might be true of Rhodococcus.........

Posted by: Mark      Read more         Source


February 14, 2008, 10:29 PM CT

Novel approach strips staph of virulence

Novel approach strips staph of virulence
An international team of scientists supported by the National Institutes of Health (NIH) has blocked staph infections in mice using a drug previously tested in clinical trials as a cholesterol-lowering agent. The novel approach, described in the February 14 online edition of Science, could offer a new direction for therapies against a bacterium thats becoming increasingly resistant to antibiotics.

By following their scientific instinct about a basic biological process, the scientists made a surprising discovery with important clinical implications, said NIH Director Elias A. Zerhouni, M.D. Eventhough the results are still very preliminary, they offer a promising new lead for developing drugs to treat a very timely and medically important health concern.

This work was supported by three NIH components: the National Institute of General Medical Sciences, the National Institute of Allergy and Infectious Diseases, and the National Institute of Child Health and Human Development.

A pigment similar to the one that gives carrots their color turns Staphylococcus aureus (staph) golden. In the bacterium, this pigment acts as an antioxidant to block the reactive oxygen molecules the immune system uses to kill bacteria.

Scientists had speculated that blocking pigment formation in staph could restore the immune systems ability to thwart infection. While perusing a magazine on microbial research, Eric Oldfield, Ph.D., of the University of Illinois at Urbana-Champaign read how in 2005 University of California, San Diego scientists knocked out a gene in staphs pigment-making pathway to create colorlessand less pathogenicbacteria.........

Posted by: Mark      Read more         Source


February 12, 2008, 9:20 PM CT

Gene research to explain autistic savants

Gene research to explain autistic savants
From left, postdoctoral associate Albert Y. Hung and Menicon Professor of Neuroscience Morgan H. Sheng report gene research that may explain the phenomenon of autistic savants. Photo / Donna Coveney
Mice lacking a certain brain protein learn some tasks better but also forget faster, as per new research from MIT that may explain the phenomenon of autistic savants in humans. The work could also result in future therapys for autism and other brain development disorders.

Scientists at the Picower Institute for Learning and Memory at MIT report in the Feb. 13 issue of the Journal of Neuroscience that mice genetically engineered to lack a key protein used for building synapses--the junctions through which brain cells communicate--actually learned a spatial memory task faster and better than normal mice. But when tested weeks later, they couldn't remember what they had learned as well as normal mice, and they had trouble remembering contexts that should have provoked fear.

"These opposite effects on different types of learning are reminiscent of the mixed features of autistic patients, who may be disabled in some cognitive areas but show enhanced abilities in others," said Albert Y. Hung, a postdoctoral associate at the Picower Institute, staff neurologist at Massachusetts General Hospital and co-author of the study. "The superior learning ability of these mutant mice in a specific realm is reminiscent of human autistic savants."

Autism is one of a group of developmental disabilities known as autism spectrum disorders (ASDs), in which a person's ability to communicate and interact with others is impaired. The Centers for Disease Control and Prevention estimate that one in 150 American children have an ASD. Occasionally, an autistic person has an outstanding skill, such as an incredible rote memory or musical ability. Such individuals--like the character Dustin Hoffman played in the film "Rain Man"--may be referred to as autistic savants.........

Posted by: JoAnn      Read more         Source


February 11, 2008, 10:36 PM CT

Mechanism leading to cleft palate

Mechanism leading to cleft palate
Zebrafish face with cleft palate.

Credit: Courtesy of John Postlethwait

By creating a genetic mutation in zebrafish, University of Oregon scientists say they've discovered a previously unknown mechanism for cleft palate, a common birth defect in humans that has challenged medical professionals for centuries.

Many molecular pathways in zebrafish are present in humans and other vertebrates. By studying the induced mutation in zebrafish, the 10-member research team isolated a disruption in early developmental signaling involving Pdgf, a platelet-derived growth-factor protein, and a microRNA known as Mirn140, the researchers write in a paper posted online in advance of regular publication the monthly journal Nature Genetics.

Mutant zebrafish lacking Pdgf had cleft palate similar to many human babies, showing that this growth factor helps to organize cells that make the palate. It came as a surprise that zebrafish into which the scientists had injected too much Mirn140 also had cleft palate.

MicroRNAs are small gene products, found to be involved in gene expression, that were first described in 1993 by researchers at Harvard University. The term microRNA was introduced in when these single-strand RNA molecules about nucleotides in length were more fully detailed in Science in October 2001 by Gary Ruvkun of Massachusetts General Hospital in Boston.........

Posted by: Scott      Read more         Source


February 7, 2008, 10:04 PM CT

Effort To Sequence 1,000 Human Genomes

Effort To Sequence 1,000 Human Genomes
Washington University School of Medicine in St. Louis will play a leading role in an international collaboration to sequence the genomes of 1,000 individuals. The ambitious 1000 Genomes Project will create the most detailed picture to date of human genetic variation and likely will identify a number of genetic factors underlying common diseases.

Drawing on the expertise of research teams in the United States, China and England, the project will develop a new map of the human genome that will provide a close-up view of medically relevant DNA variations at a resolution unmatched by current technology. As with other major human genome reference projects, data from the 1000 Genomes Project will be made swiftly available to the worldwide scientific community through free public databases.

"A project like this would have been unimaginable only a few years ago," says Elaine Mardis, Ph.D., co-director of the University's Genome Sequencing Center, and one of the project's lead investigators. "We now have the ability to examine in intimate detail variations in the genetic code that differ from person to person."

At the genetic level, any two humans are more than 99 percent alike. However, it is important to understand the small fraction of genetic material that varies among people because it can help explain differences in individuals' risk of disease, response to drugs or reaction to environmental factors. Common variation in the human genome is organized into local neighborhoods called haplotypes, which commonly are inherited as intact blocks of information.........

Posted by: Scott      Read more         Source


February 4, 2008, 10:24 PM CT

Key interaction in cholesterol regulation

Key interaction in cholesterol regulation
Scientists at UT Southwestern Medical Center have determined the specific way in which a destructive protein binds to and interferes with a molecule that removes low-density lipoproteins (LDL), the so-called bad cholesterol, from the blood.

The practical benefit of this finding is that we can now search for new ways to lower cholesterol by designing targeted antibodies to disrupt this interaction, said Dr. Jay Horton, professor of internal medicine and molecular genetics and a senior author of the study, which appears online this week in the Proceedings of the National Academy of Sciences.

The protein, called PCSK9, has emerged as an important regulator of bad cholesterol in the blood, said Dr. Horton, whose research focuses in part on understanding the proteins function.

PCSK9 disrupts the activity of a key molecule called the low-density lipoprotein receptor, or LDLR. This molecule, which juts out from the surface of cells, latches on to bad cholesterol in the bloodstream and removes it by drawing it into the cells.

The PCSK9 protein also can latch on to the LDL receptor. This binding, however, triggers a chain of biochemical reactions that leads to the destruction of the LDL receptor. With fewer receptors available, more bad cholesterol remains in the bloodstream.........

Posted by: Daniel      Read more         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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