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July 26, 2006, 4:54 PM CT

how much the eye tells the brain

how much the eye tells the brain
Scientists at the University of Pennsylvania School of Medicine estimate that the human retina can transmit visual input at about the same rate as an Ethernet connection, one of the most common local area network systems used today. They present their findings in the recent issue of Current Biology. This line of scientific questioning points to ways in which neural systems compare to artificial ones, and can ultimately inform the design of artificial visual systems.

Much research on the basic science of vision asks what types of information the brain receives; this study instead asked how much. Using an intact retina from a guinea pig, the scientists recorded spikes of electrical impulses from ganglion cells using a miniature multi-electrode array. The researchers calculate that the human retina can transmit data at roughly 10 million bits per second. By comparison, an Ethernet can transmit information between computers at speeds of 10 to 100 million bits per second.

The retina is actually a piece of the brain that has grown into the eye and processes neural signals when it detects light. Ganglion cells carry information from the retina to the higher brain centers; other nerve cells within the retina perform the first stages of analysis of the visual world. The axons of the retinal ganglion cells, with the support of other types of cells, form the optic nerve and carry these signals to the brain.........

Posted by: Daniel      Permalink         Source


July 25, 2006, 8:25 PM CT

Unlocking the Deadliest Malaria Parasite

Unlocking the Deadliest Malaria Parasite
Scientists at the Albert Einstein College of Medicine of Yeshiva University have leveraged the results of their research into tuberculosis to craft a tool for unlocking the secrets of another of the world's leading infectious killers-malaria.

These findings, reported in the recent issue of Nature Methods, "should substantially speed up research efforts to bring malaria under control," says Dr. David Fidock, senior author of the paper and an associate professor of microbiology & immunology at Einstein.

Malaria is caused by a single-celled parasite, Plasmodium, which is transmitted through the bite of the Anopheles mosquito. The disease kills an estimated 1.2 million people every year.

The Einstein researchers focused on the most deadly Plasmodium strain-P. falciparum-which is proving increasingly resistant to therapy. Their research has led to the first efficient technique for inserting any gene of interest into the P. falciparum genome to gain biological information that could lead to more effective therapys.

"This opens up a whole new window into the genetic manipulation of this lethal parasite," says Dr. William Jacobs, Jr., who is a Howard Hughes investigator and professor of molecular genetics and microbiology & immunology at Einstein and a major author of the Nature Methods paper. "Malaria scientists finally have an efficient way to shuffle genes into P. falciparum, which should lead to valuable information about the parasite's virulence, how it's transmitted from mosquito to humans and how it develops resistance to antimalarial drugs".........

Posted by: Mark      Permalink         Source


July 25, 2006, 8:17 PM CT

Identical Twins Be Genetically Different

Identical Twins Be Genetically Different
They sleep together, eat together, and most people find it impossible to tell them apart. Identical twins who grow up together share just about everything, including their genes. But sometimes only one twin will have health problems when genetics predicts both of them should.

Researchers at the University of Michigan Medical School are just beginning to understand how two people who are so similar biologically can be so different when it comes to the development of diseases like rheumatoid arthritis.

U-M scientists have discovered three genes that are over-expressed in rheumatoid arthritis, or RA, that were not known to be linked to the disease before. They also observed that non-genetic factors influenced the expression of these genes and that the expression patterns varied between identical twins where only one twin had RA. Results of the U-M study were reported in the recent issue of Arthritis and Rheumatism.

RA is a chronic inflammatory disease that damages joints. RA causes pain, loss of movement, and bone deformities. It affects 2.1 million Americans. There are a number of genetic factors that put people at a high-risk for developing RA, yet only 15 percent of identical twins will both develop it.

Researchers compared gene expression patterns of 11 pairs of monozygotic twins, who shared the same egg and were genetically identical, but only one of them had RA. They found three new genes that were significantly over-expressed in the twin with RA in comparison to the one without the disease. This is the first report for RA that examines gene expression patterns in monozygotic twins.........

Posted by: JoAnn      Permalink         Source


July 25, 2006, 8:13 PM CT

Nerve-stimulation Epilepsy Treatment

Nerve-stimulation Epilepsy Treatment
A unique nerve-stimulation therapy for epilepsy developed at UCLA offers a potential new alternative for tens of thousands of individuals unable to control their seizures with medicine and ineligible for surgery.

Developed by neuroresearchers at the David Geffen School of Medicine at UCLA and Valencia, Calif.-based Advanced Bionics Corp., trigeminal nerve stimulation (TNS) uses a "brain pacemaker" to stimulate a nerve involved in inhibiting seizures.

The trigeminal nerve extends into the brain from the face and forehead, and is known to play a role in seizure inhibition. The stimulator and electrodes used to transmit an electrical current to the nerve can be worn externally or implanted.

A study reported in the July edition of the peer-evaluated journal Epilepsia reports that four of seven subjects who used an external stimulator for at least three months in a pilot human clinical trial enjoyed a 50 percent or better reduction in seizure frequency.

"Most people with chronic epilepsy who have continuing seizures are drug-resistant," said Dr. Christopher DeGiorgio, vice chair and professor in residence of neurology at UCLA, and co-developer of TNS and lead author of the study. "In addition, anti-seizure drugs can have significant side effects on behavior, thinking and alertness. Women taking anti-seizure drugs and their unborn children are at special risk because of the effect of these drugs on fetal growth and development.........

Posted by: Daniel      Permalink         Source


July 25, 2006, 6:48 PM CT

Inflammation Disease Link

Inflammation Disease Link Chemistry of inflammation
New research at MIT may help researchers better understand the chemical associations between chronic inflammation and diseases such as cancer and atherosclerosis. The work could lead to drugs that break the link between the two.

When an infection occurs, immune cells flock to the area and secrete large amounts of highly reactive chemicals to combat the invader. But, these inflammatory chemicals also attack normal tissue surrounding the infection and damage critical components of cells, including DNA. During chronic inflammation, that damage may lead to mutations or cell death and even to cancer and other diseases.

MIT researchers, led by toxicology graduate student Yelena Margolin of the Biological Engineering Division, have discovered that the DNA damage produced by one of these inflammatory chemicals, nitrosoperoxycarbonate, occurs at unexpected locations along the DNA helix. The finding counters the prevailing theory about where the DNA damage occurs and may shed light on new ways to diagnose and combat inflammation.

"We need to understand the mechanisms of inflammation in order to make new drugs that will break the link between inflammation and disease and to develop predictive biomarkers," said Dr. Peter Dedon, professor of toxicology and biological engineering and associate director of the Biological Engineering Division at MIT. "One of our goals is to develop biomarkers that can tell if you have inflammation and to define its extent, severity and location".........

Posted by: Scott      Permalink         Source


July 25, 2006, 0:20 AM CT

Risk Of Estrogen Plus Testosterone Therapy

Risk Of Estrogen Plus Testosterone Therapy
Women who take a combination of estrogen and testosterone to treat the symptoms of menopause may have an increased risk of breast cancer, as per an article in the July 24 issue of Archives of Internal Medicine, one of the JAMA/Archives journals.

As women age, their natural levels of the hormone testosterone tend to decrease, as per background information in the article. Some evidence suggests that a number of of the symptoms of menopause--including decreased sex drive, worse moods and poorer quality of life--are correlation to this decline in testosterone. Clinical trials have shown that taking testosterone in combination with estrogen may reduce these symptoms and also promote bone health. Only one estrogen plus testosterone treatment is currently available to U.S. women, but the number and prevalence of such therapys are expected to increase in coming years, the authors write.

Rulla M. Tamimi, Sc.D., Brigham and Women's Hospital and Harvard Medical School, Boston, and his colleagues studied the long-term effects of estrogen plus testosterone treatment in 121,700 women who were part of the Nurses' Health Study. The study enrolled female nurses between the ages of 30 and 55 years beginning in 1976. The women completed an initial questionnaire and follow-up surveys every two years that included questions about menopausal status, medical conditions and the use of postmenopausal hormone treatment. For those who reported a diagnosis of breast cancer, medical records were evaluated for verification.........

Posted by: Janet      Permalink         Source


July 24, 2006, 6:34 AM CT

Slowing Alzheimer's disease

Slowing Alzheimer's disease
Scientists have uncovered the pathways behind the protection offered by environmental stimulation in Alzheimer's disease, further confirming that enhanced mental and physical activity slows neurological decline. The paper by Ambre et al., "Reduction of amyloid angiopathy and Aβ plaque burden after enriched housing in TgCRND8 mice: involvement of multiple pathways," appears in the recent issue of The American Journal of Pathology.

Alzheimer's disease, the leading cause of senile dementia, presents with cognitive and behavioral deficiencies resulting in part from accumulation of -amyloid (A) deposits within the brain (A plaques) and its blood vessels (amyloid angiopathy). Eventhough prior studies have shown that increased mental and physical activity can slow the progression of the disease, how such deceleration occurs has been unclear until now.

Dr. Kathy Keyvani's group at University Hospital Muenster examined the effects of environmental stimulation on the brain pathology of TgCRND8 mice. These mice, which express a mutant form of A found in some Alzheimer's patients, develop Alzheimer-like features including A plaques and cognitive deficits. To study the effects of enrichment, mice were housed in either standard cages or enriched cages, similar to the standard but with access to a stimulus cage containing permanent fixtures (rope and gnawing wood) as well as removable items (tunnels, balls, ladders, ramps, and exercise wheels) that were changed on a rotating basis.........

Posted by: Daniel      Permalink         Source


July 22, 2006, 10:38 PM CT

Watching Real-time Chemical Activity In Cells

Watching Real-time Chemical Activity In Cells
Attempts to identify potential drugs that interfere with the action of one particular enzyme associated with heart disease and similar health problems led researchers at Johns Hopkins to create a new tool and new experimental approach that allow them to see multiple, real-time chemical reactions in living cells. Their report on the work is published July 21 in the journal ACS Chemical Biology.

Most current drug development operations test chemicals on enzymes isolated from their normal environs and then take further steps to see if the chemical can get into the cell to do its work, and figure out how poisonous the chemical is to a cell.

"Living cells are critical to our work because they show us how and what is actually happening in a normal context and time span when a chemical is added," says Jin Zhang, Ph.D., an assistant professor of pharmacology and molecular sciences in Hopkins' Institute for Basic Biomedical Sciences.

Testing chemicals on enzymes in living cells provides the opportunity to find potential drugs that work in new ways. For example, using living cells allows scientists to "see" where in the cell chemicals do their work. Researchers could then design new drugs to go to specific places within cells to work more efficiently. Also, streamlining the one-at-a-time approach offers the chance to study - and rule out or in - a number of potentially useful chemicals at once.........

Posted by: Scott      Permalink         Source


July 19, 2006, 10:40 PM CT

Developing Safer Anti-obesity Drugs

Developing Safer Anti-obesity Drugs Dr. Joel Elmquist, professor of internal medicine
A study led by a UT Southwestern Medical Center researcher sheds light on how the brain chemical serotonin, when spurred by diet drugs such as Fen-phen, works to curb appetite.

That knowledge could aid in the design of safer anti-obesity drugs nearly a decade after Fen-phen was banned for causing harmful side effects.

The study, which tested the effect of several drugs that alter serotonin levels in the brain, observed that serotonin activates some neurons and melanocortin-4 receptors, or MC4Rs, to curb appetite and at the same time blocks other neurons that normally act to increase appetite.

The dual effect helps explain how such drugs, including Fen-phen, spur weight loss.

The finding, available online and in the July 20 issue of Neuron, also reinforces the role of serotonin - a regulator of emotions, mood and sleep - in affecting the brain's melanocortin system, a key molecular pathway that controls body weight.

"The more we understand about the pathways and the way serotonergic drugs regulate body weight, the more it one day might lead to harnessing beneficial properties of anti-obesity therapys like Fen-phen and minimizing the harmful side effects," said Dr. Joel Elmquist, professor of internal medicine at UT Southwestern and co-senior author of the study.........

Posted by: JoAnn      Permalink         Source


July 19, 2006, 10:08 PM CT

Antioxidants May Slow Vision Loss

Antioxidants May Slow Vision Loss
Researchers at Johns Hopkins have successfully blocked the advance of retinal degeneration in mice with a form of retinitis pigmentosa (RP) by treating them with vitamin E, alpha-lipoic acid and other antioxidant chemicals.

"Much more work needs to be done to determine if what we did in mice will work in humans," said Peter Campochiaro, the Eccles Professor of Ophthalmology and Neuroscience at The Johns Hopkins University School of Medicine. "But these findings have helped to solve a mystery".

In patients with RP, rod photoreceptors die from a mutation, but it has not been known why cone photoreceptors die. After rods die, the level of oxygen in the retina goes up, and this work shows that it is the high oxygen that gradually kills the cones. Oxygen damage is also called "oxidative damage" and can be reduced by antioxidants. So for the first time, researchers have a therapy target in patients with RP, added Campochiaro. His team's findings appeared in the July online edition of the Proceedings of the National Academy of Sciences.

Retinas in all mammals, from mouse to man, are made up of light-sensitive cells known as cones and rods, named for their shapes, which convert light into nerve signals that are then transmitted to the brain via the optic nerve. Cones are needed to see colors and make vision possible in bright light, whereas the far more numerous rods permit sight in low light. The human retina contains approximately 125 million rod cells and six million cone cells. In diseases like RP and age-related macular degeneration (AMD), these cells die off and eventually lead to blindness (in the case of RP) or legal blindness (in the case of AMD).........

Posted by: Mike      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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