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May 11, 2007, 5:06 PM CT

Dynamin's Role in Nerve Cell Function

Dynamin's Role in Nerve Cell Function
An unexpected finding on how nerve cells signal to one another could rewrite the textbooks on neuroscience, says a collaborative team of scientists at Weill Cornell Medical College and Yale University.

Their study, published as a high-profile research article in the journal Science, suggests that a key cellular enzyme called dynamin 1 is not essential to all synaptic transmission, as experts had previously assumed.

Dynamin has long been a focus of research for its role in packaging chemical signals, called neurotransmitters, into tiny synaptic vesicles within the cell.

The new study finds that the enzyme is not always necessary for this process. Instead, dynamin 1 goes into action only when the synapse enters moments of particularly high activity.

"In that sense, dynamin 1 remains crucial, allowing the synapse the freedom to function under all conditions," explains co-senior author Dr. Timothy Ryan, professor of biochemistry at Weill Cornell Medical College.

The discovery is a potentially important new piece of the puzzle for researchers investigating neurological injury and disease.

"In the long run, what we're trying to achieve here is a kind of biochemical 'repair manual' for the brain and brain cells," Dr. Ryan explains. "So, in the future, if we find out that a particular illness is caused by a flaw in dynamin 1 function or proteins that interact with dynamin 1, we'll have answers on hand to help fix that".........

Posted by: Daniel      Read more         Source


May 9, 2007, 11:23 PM CT

DNA repair monitored at double-strand break

DNA repair monitored at double-strand break
Investigators at St. Jude Children's Research Hospital had a molecules eye view of the human cells DNA repair kit as it assembled on a double-strand break to link together the broken ends. Double-strand breaks are ruptures that cut completely across the twisted, ladder-like structure of DNA, breaking it into two pieces.

Using a technique developed specifically for this project, the St. Jude scientists could determine when repair proteins arrived at or around the DNA break and evaluate its repaireven when particular proteins shifted away from the break to make room for others. A report on this work appears in the May 7 online issue of "Nature Cell Biology." .

The findings are important because disruption of the precise movement of these repair proteins can cause mutations, cell death or cancer, and the ability to track the process so closely will give scientists critical insights into what can go wrong with DNA repair. This could lead to novel ways to make cancer cells more sensitive to treatment by blocking their ability to repair double-stranded breaks caused by chemotherapy or radiation. It could also suggest new strategies for enhancing repair of double-stranded DNA caused by radiation, natural oxidants in food or the body and other toxins that can cause disease and aging.........

Posted by: Scott      Read more         Source


May 7, 2007, 11:00 PM CT

immune dysfunction in melanoma patients

immune dysfunction in melanoma patients
Scientists at the Stanford University School of Medicine have begun to shed light on why the human immune system isn't able to stop such cancers as melanoma, suggesting answers that could pave the way for better therapy of this often-fatal illness.

In a small study, the researchers observed that the immune cells in a majority of people with this deadly skin cancer fail to respond properly to a molecule called interferon, which normally activates the immune system. Without the ability to respond to interferon, the cells are less able to fend off the cancer, as per the study that would be reported in the recent issue of Public Library of Science-Medicine.

These results help explain a decade of research showing that people with cancer often have dysfunctional immune systems. Until now, scientists could tell that the immune system wasn't working properly but didn't know which genes or pathways were involved in that failure. Finding the disruption in the cancer cells' interferon response could help in the development of vaccines to treat cancers.

"We think this is a dominant way that immune dysfunction occurs in people with cancer," said senior author Peter Lee, MD, associate professor of medicine.

Lee was interested in melanoma rather than other forms of cancer in part because of the deadly nature of the disease, which will kill about one in six of the 47,700 people it is expected to strike this year. Unless melanoma is caught early and removed, there is no effective therapy, eventhough research groups have been testing vaccine therapies for the disease. However, Lee worried that unless scientists better understood immune dysfunctions in those people, the vaccines would have a low probability of success. "If you don't address the underlying immune defects, then vaccines won't do any good," Lee said.........

Posted by: George      Read more         Source


May 7, 2007, 10:41 PM CT

Diabetes Drug With Chemotherapy

Diabetes Drug With Chemotherapy
A widely used diabetes drug dramatically boosted the potency of platinum-based cancer drugs when administered together to a variety of cancer cell lines and to mice with tumors, researchers from Dana-Farber Cancer Institute report.

Combining a platinum chemotherapy agent and the diabetes drug rosiglitazone halted or shrank mouse tumors as much as three times more effectively than either of the drugs given alone, as per the article in the recent issue of Cancer Cell.

If pairing the drugs has the same synergistic effect in humans, the scientists say, it could improve control of ovarian, lung and other cancers routinely treated with platinum-based chemotherapy, to which tumors eventually become resistant. Moreover, the experiments suggest the combination might extend the use of platinum drugs to other cancers where they haven't previously been shown to be effective.

"There's still a huge gulf between these experiments and human cancers," said Bruce Spiegelman, PhD, senior author of the report. "But it's worked in every animal model of cancer weve looked at, and I think theres a fair chance it will help people".

Dana-Farber scientists are already drawing up plans for initial clinical trials, which could begin sometime this year.

"We really see a way forward here to improve the chemotherapy's effectiveness for multiple forms of cancer," said George Demetri, MD, a Dana-Farber researcher who is preparing a proposal for a pilot study of rosizitaglone and platinum chemotherapy drugs in lung and ovary cancer and sarcomas.........

Posted by: Janet      Read more         Source


May 6, 2007, 5:20 PM CT

Antidepressants stimulate new nerve cells

Antidepressants stimulate new nerve cells
In adult monkeys, an antidepressant therapy has induced new nerve cell growth in the hippocampus, a brain area responsible for learning and memory. A similar process may occur in humans, the research suggests, and may help explain the effectiveness of antidepressant therapys.

The results, the first from nonhuman primates, are similar to those previously seen in rodents. They suggest that creation of new nerve cells, a process known as neurogenesis, is an important part of antidepressant treatment. Researcher Tarique Perera, MD, at Columbia University, and his colleagues observed changes in the number of brain cells in the dentate gyrus region of the hippocampus. The study is reported in the May 2 issue of The Journal of Neuroscience

The growth of new nerve cells in the hippocampus has been suggested as the way antidepressants work in rodents, says Eric Nestler, MD, PhD, of the University of Texas Southwestern Medical Center. "However, the clinical relevance of this action has remained controversial, in part, because of uncertainty as to whether similar neurogenesis occurs in humans," he says. "This finding further supports the potential clinical relevance of changes in neurogenesis seen in rodent models."

Perera and the team treated a group of monkeys with electroconvulsive shock (ECS), an animal version of the highly effective clinical antidepressant electroconvulsive treatment. They saw an increase in new nerve cells in the hippocampus. Over four weeks, a majority of these cells became mature neurons.........

Posted by: Daniel      Read more         Source


May 2, 2007, 10:00 PM CT

Later-life diseases resulting from fetal and infant toxicity

Later-life diseases resulting from fetal and infant toxicity Janice and Rodney Dietert display herbal and fungal medicinal sources that show promise for addressing developmental immunotoxicity (DIT) and DIT-associated diseases.
A Cornell researcher and his wife have conducted the first comprehensive review of later-life diseases that develop in people who were exposed to environmental toxins or drugs either in the womb or as infants. They have observed that most of the diseases have two things in common: They involve an imbalanced immune system and exaggerated inflammatory reactions (at the cellular level).

In an invited, peer-evaluated article on developmental immunotoxicity (DIT), published in a recent issue of Current Medicinal Chemistry, Rodney Dietert, professor of immunotoxicology at Cornell's College of Veterinary Medicine, and Janice Dietert of Performance Plus Consulting in Lansing, N.Y., observed that almost all the chronic diseases that are linked to DIT share the same type of immunological damage.

The diseases associated with DIT include asthma, allergy, suppressed responses to vaccines, increased susceptibility to infections, childhood neurobehavioral conditions, autoimmunity, cancer, cerebral palsy, atherosclerosis, high blood pressure and male sterility.

Toxins that are known to cause developmental immune problems in fetuses and neonates, as per the Dieterts, include herbicides, pesticides, alcohol, heavy metals, maternal smoking, antibiotics, diesel exhaust, drugs of abuse and PCBs.........

Posted by: Scott      Read more         Source


May 2, 2007, 9:56 PM CT

New clues for treatment of disease that causes accelerated aging

New clues for treatment of disease that causes accelerated aging Boy with progeria
There is renewed hope for therapy of a rare genetic condition that causes rapidly accelerated aging and leads to an average life expectancy of 13 years.

Researchers studying the genes of two infants who died of mysterious illnesses found the infants had mutations in LMNA, the same gene altered in patients with the premature aging condition progeria. But the infants' unusual mutations caused them to make a number of more bad copies of the gene's primary protein, lamin A, than progeria patients.

Both infants died very young and before scientists could fully unravel the cause of their disorders. But when scientists treated cell samples from one of the patients with a drug targeted for progeria, they saw signs that the cells were improving.

"Our success in treating these cells, which had uncommonly high levels of bad lamin A, suggest that progeria therapy may not be as distant as we thought," says senior author Jeffrey Miner, Ph.D., associate professor of medicine and cell biology and physiology. "If physicians can reduce production of bad lamin A by as little as half in progeria patients, we might see significant improvement".

Progeria therapy also has potential implications for larger populations. The LMNA gene is involved in several other more prevalent disorders including forms of muscular dystrophy and heart disease.........

Posted by: Scott      Read more         Source


April 30, 2007, 8:24 PM CT

Google technology to track avian flu spread

Google technology to track avian flu spread Credit: CU-Boulder, Ohio State University
An interactive "supermap" that portrays the mutations and spread of the avian flu around the globe over time should help scientists and policy makers better understand the virus and anticipate further outbreaks, as per a new study involving University of Colorado at Boulder and Ohio State University researchers.

The research team used data from the known evolution and spread of the avian flu, known as H5N1, to create a roadmap of viral spread in time and space, said CU-Boulder ecology and evolutionary biology Assistant Professor Robert Guralnick, a co-author of study. The team projected genetic and geographic information onto an interactive globe using Google Earth technology, allowing users to fly virtually around the planet and analyze movements and changes in the genomes, or genetic blueprints, of known avian flu sub-strains that have been sequenced since the virus was first detected in Guangdong, China, in 1996.

The scientists used the novel technology to chart the spread of H5N1 through Asia, Indonesia, the Middle East and Europe by various hosts, including its transport by specific orders of birds and mammals, said CU-Boulder graduate student Andrew Hill, a co-author of study. They also used the supermap to track key genetic traits prevalent in some avian flu genomes that appear to confer the ability of H5N1 to more readily infect mammals, including humans, he said.........

Posted by: Mark      Read more         Source


April 29, 2007, 7:22 PM CT

Creating a Molecular Nose

Creating a Molecular Nose Image: Max-Planck-Institut für Polymerforschung
The senses of living organisms function using various mechanisms, among other things utilizing membrane proteins as receptors. Scientists at the Max Planck Institute for Polymer Research and the Max Planck Institute of Biochemistry have now succeeded in creating biosensors by incorporating such proteins into artificial structures. The membrane proteins are synthesized in-vitro directly from the genetic information introduced to the cell extract.

Prior attempts to create biosensors from membrane proteins failed due to an idiosyncrasy of these proteins: they are not water soluble. In the past, scientists tried to remove the proteins from their biological membranes by solubilising the latter using detergents. However, this destroys the natural folding structure of the protein membranes, which is precisely what makes the proteins so special. "We quickly realized how difficult it is to isolate such membrane proteins. Neither we, nor other research groups, were able to work with them using conventional methods," explains Dr. Eva-Kathrin Sinner of the Max Planck Institute for Polymer Research in Mainz.

Yet the Max Planck scientists found a way around this: they succeeded in incorporating the proteins in an artificial matrix, just as they would be integrated in a natural cell membrane. They achieved this by introducing the developing membrane proteins to artificial lipid membrane systems that mimic natural cell membranes from a statu nascendi, and the membrane proteins actually did simply insert themselves into the artificial membranes. The odorant receptors selected by the scientists were a type of G-protein coupled receptor taken from brown rats. The researchers were also able to prove that the odorant receptors maintained their biological functions by demonstrating the binding of odorants to the receptors. "We now have something akin to an instruction manual on how membrane proteins that were previously difficult to access can be produced and analyzed in their active structure," says Sinner.........

Posted by: Scott      Read more         Source


April 29, 2007, 7:15 PM CT

Concealed Intentions In Human Brain

Concealed Intentions In Human Brain Image: Bernstein Center for Computational Neuroscience Berlin
Our secret intentions remain concealed until we put them into action -so we believe. Now scientists have been able to decode these secret intentions from patterns of their brain activity. They let subjects freely and covertly choose between two possible tasks - to either add or subtract two numbers. They were then asked to hold in mind their intention for a while until the relevant numbers were presented on a screen. The scientists were able to recognize the subjects intentions with 70% accuracy based alone on their brain activity - even before the participants had seen the numbers and had started to perform the calculation.

Participants made their choice covertly and initially did not know the two numbers they were supposed to add or subtract. Only a few seconds later the numbers appeared on a screen and the participants could perform the calculation. This ensured that the intention itself was being read out, rather than brain activity correlation to performing the calculation or pressing the buttons to indicate the response. "It has been previously assumed that freely selected plans might be stored in the middle regions of the prefrontal cortex, whereas plans following external instructions could be stored on the surface of the brain. We were able to confirm this theory in our experiments", Haynes explained.........

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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