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August 20, 2009, 7:03 AM CT

Stem Cells Repair the Human Brain

Stem Cells Repair the Human Brain
There is no known cure for neurodegenerative diseases such as Huntington's, Alzheimer's and Parkinson's. But new hope, in the form of stem cells created from the patient's own bone marrow, can be found - and literally seen - in laboratories at Tel Aviv University.

Dr. Yoram Cohen of TAU's School of Chemistry has recently proven the viability of these innovative stem cells, called mesenchymal stem cells, using in-vivo MRI. Dr. Cohen has been able to track their progress within the brain, and initial studies indicate they can identify unhealthy or damaged tissues, migrate to them, and potentially repair or halt cell degeneration. His findings have been published in the journal Stem Cells.

"By monitoring the motion of these cells, you get information about how viable they are, and how they can benefit the tissue," he explains. "We have been able to prove that these stem cells travel within the brain, and only travel where they are needed. They read the chemical signalling of the tissue, which indicate areas of stress. And then they go and try to repair the situation".

Tracking live cells in the brain

To test the capabilities of this innovative new stem cells, Dr. Cohen created a study to track the activity of the live cells within the brain using the in-vivo MRI at the Strauss Centre for Computational Neuro-Imaging. Watching the live, active cells has been central to establishing their viability as a treatment for neurodegenerative disease.........

Posted by: Scott      Read more         Source


August 19, 2009, 7:19 AM CT

Neurons that control obesity in fruit flies

Neurons that control obesity in fruit flies
A team of researchers from the California Institute of Technology (Caltech) have pinpointed two groups of neurons in fruit fly brains that have the ability to sense and manipulate the fly's fat stores in much the same way as do neurons in the mammalian brain. The existence of this sort of control over fat deposition and metabolic rates makes the flies a potentially useful model for the study of human obesity, the scientists note.

Their findings were reported in the August 13 issue of the journal Neuron

By manipulating neural activity in fruit fly brains using transgenic techniques, the scientists observed that, "just as in mammals, fly fat-store levels are measured and controlled by specific neurons in the brain," says Caltech postdoctoral scholar Bader Al-Anzi, the Neuron paper's first author. "Silencing these neurons created obese flies, while overactivating them produced lean flies".

Mammalian brains are given information about the body's fat stores by hormones such as leptin and insulin, and respond to that information by inducing changes in food intake and metabolism to maintain a constant body weight. The scientists observed that similar behavioral and metabolic changes occurred in the fruit flies, though which changes occurred depended on which of the two sets of newly identified neurons was silenced.........

Posted by: Scott      Read more         Source


August 14, 2009, 7:19 AM CT

Brain innately separates living and non-living objects

Brain innately separates living and non-living objects
For unknown reasons, the human brain distinctly separates the handling of images of living things from images of non-living things, processing each image type in a different area of the brain. For years, a number of researchers have assumed the brain segregated visual information in this manner to optimize processing the images themselves, but new research shows that even in people who have been blind since birth the brain still separates the concepts of living and non-living objects.

The research, published in today's issue of Neuron, implies that the brain categorizes objects based on the different types of subsequent consideration they demandsuch as whether an object is edible, or is a landmark on the way home, or is a predator to run from. They are not categorized entirely by their appearance.

"If both sighted people and people with blindness process the same ideas in the same parts of the brain, then it follows that visual experience is not necessary in order for those aspects of brain organization to develop," says Bradford Mahon, postdoctoral fellow in the Department of Brain and Cognitive Sciences at the University of Rochester, and main author of the study. "We think this means significant parts of the brain are innately structured around a few domains of knowledge that were critical in humans' evolutionary history".........

Posted by: Daniel      Read more         Source


August 14, 2009, 7:17 AM CT

Gene implicated in regulating length of human sleep

Gene implicated in regulating length of human sleep
Researchers have discovered the first gene involved in regulating the optimal length of human sleep, offering a window into a key aspect of slumber, an enigmatic phenomenon that is critical to human physical and mental health.

The team, reporting in the Aug. 14, 2009 issue of Science, identified a mutated gene that allows two members of an extended family to thrive on six hours of sleep a day rather than the eight to eight-and-a-half hours that studies have shown humans need over time to maintain optimal health. Working from this discovery, the researchers genetically engineered mice and fruit flies to express the mutated gene and study its impact.

While most Americans obtain less than eight hours of sleep a night (the average on non-work days is 7.4 hours), and some may feel they succeed with less when engaged in exhilarating work, domestic life or recreation, scientific evidence indicates that, over time, the body suffers from this regimen, the scientists say.

"Short term and chronic disruptions in the length of optimal sleep can have serious consequences on cognition, mood and physical health, including cancer and endocrine function," says the senior author of the study, Ying-Hui Fu, PhD, UCSF professor of neurology. However, teasing out this impact can be challenging, she says, given access to such stimuli as coffee and chocolate.........

Posted by: Scott      Read more         Source


August 11, 2009, 11:19 PM CT

Taking dex can improve high altitude exercise capacity

Taking dex can improve high altitude exercise capacity
Taking dexamathasone prophlyactically may improve exercise capacity in some mountaineers, as per Swiss researchers. Dexamathasone, known popularly to climbers as "dex," has been used for years to treat altitude-related symptoms in mountaineers, but has never been tested for its ability to improve exercise capacity at high altitude.

"We have known that both tadalafil and dexamethasone are good for preventing high altitude pulmonary edema (HAPE) and dex for treating symptoms of acute mountain sickness (AMS). But we did not know whether they could also improve exercise capacity at altitude by reducing pulmonary hypertension, one of the important factors in altitude- related exercise limitations," said main authors Manuel Fischler, MD, of the University Hospital in Zurich, Switzerland, and Hans-Peter Brunner-La Rocca, of the University Hospital in Basel, Switzerland.

The results were reported in the August 15th issue of the American Journal of Respiratory and Critical Care Medicine, the journal of the American Thoracic Society.

The scientists recruited 23 mountaineers with a history of HAPE and administered baseline cardiopulmonary exercise tests a low elevation (490 meters, or 1607 feet). Subjects were tested for oxygen uptake kinetics by pedaling a stationary bike at a constant rate for six minutes, and then for exercise capacity by pedaling at 50 percent of their predicted maximum workload for one minute, then increasing output by 25 percent each additional minute until exhaustion, commonly after 8 to 12 minutes.........

Posted by: Scott      Read more         Source


August 11, 2009, 11:17 PM CT

Toxic levels of Alzheimer's clusters in brain

Toxic levels of Alzheimer's clusters in brain
Researchers have long suspected that Alzheimer's disease (AD) is caused by a small protein called the amyloid β-protein (Aβ). This protein clumps or binds to itself, eventually changing chemically to create brain protein deposits (plaques) that are characteristic of AD. However, recent studies have suggested that it is not the plaques that cause AD but rather these small, grape-like clusters of Aβ. These clusters vary in size, and the relationship between cluster size and their ability to kill nerve cells (toxicity) has never been determined accurately.

Until now. By creating various sizes of Aβ clusters in the lab that exactly match what forms in brains of those afflicted with AD, neurologists at UCLA have determined that toxicity increases dramatically as clusters increase in size from two to three to four Aβs. The scientists also report that eventhough the larger clusters are more toxic than smaller ones, the larger formations are relatively rare; smaller versions are numerous and thus are an inviting target for the development of new therapeutic drugs.

In addition, said David Teplow, senior author and a professor of neurology, developing the ability to make Aβ clusters in a very pure and precise way that duplicates what forms in AD brains will enable researchers to make detailed studies of their structures. This too will make development of future therapeutic drugs much easier and likely more successful. The research appears in the early on line edition of the Proceedings of the National Academy of Sciences (PNAS).........

Posted by: Daniel      Read more         Source


August 11, 2009, 11:10 PM CT

Powerful new therapy for asthma

Powerful new therapy for asthma
University of Texas Medical Branch at Galveston scientists have observed that a single enzyme is apparently critical to most allergen-provoked asthma attacks and that activity of the enzyme, known as aldose reductase, can be significantly reduced by compounds that have already undergone clinical trials as therapys for complications of diabetes.

The discovery, made in experiments conducted with mice and in human cell cultures, opens the way to human tests of a powerful new therapy for asthma, which today afflicts more than 20 million Americans. Such a development would provide a badly needed alternative to current asthma treatment, which primarily depends on hard-to-calibrate inhaled doses of corticosteroids and bronchodilators, which have many side effects.

"Oral administration of aldose reductase inhibitors works effectively in experimental animals," said UTMB professor Satish Srivastava, senior author of a paper on the discovery appearing in the Aug. 6 issue of the journal PLoS One "If these drugs work as well in humans as they do in animals you could administer them either orally or in a single puff from an inhaler and get long-lasting results."

Srivastava and colleagues (postdoctoral fellows Umesh Yadav and Leopoldo Aguilera-Aguirre, associate professor Kota Venkata Ramana, professor Istvan Boldogh and LSU Health Sciences Center assistant professor Hamid Boulares) focused on aldose reductase inhibition as a possible asthma treatment after establishing an essential role for the enzyme in other diseases also characterized by inflammation. In disorders such as colon cancer, atherosclerosis, sepsis and uveitis, the Srivastava team has found, cells are hit by a sudden overload of reactive oxygen species (varieties of oxygen and oxygen compounds that are particularly eager to react with other molecules). The result is a chain of biochemical reactions that leads the cells' genetic machinery to crank out a barrage of inflammatory signaling proteins. These summon immune system cells and generate even more reactive oxygen species, producing a vicious cycle of ever-increasing inflammation.........

Posted by: JoAnn      Read more         Source


August 11, 2009, 11:10 PM CT

No-Needle Approach to Prevent Blood Clots

No-Needle Approach to Prevent Blood Clots
The dean of the University of Oklahoma College of Public Health and a team of researchers worldwide have found a better way to prevent deadly blood clots after joint replacement surgery - a major problem that results in thousands of unnecessary deaths each year. The research appears this week in the New England Journal (NEJM).

The research team, which includes researchers from Oklahoma, Denmark, Australia and Canada, set out to find a better way to prevent blood clots without increasing the risk of bleeding. Blood clots, known as deep-vein thrombosis (DVT), affect the large veins in the lower leg and thigh. If the clot breaks free and moves through the bloodstream, it can lodge in the lungs, a condition known as pulmonary embolism (PE), which is often fatal. Pulmonary embolism is the most common preventable cause of sudden death after surgery.

Current preventive therapys include uncomfortable injections and one oral anti-clotting medicine that is difficult for patients and physicians to manage. Scientists wanted to find something better.

In a double-blind study of more than 3,000 patients, scientists tested a new type of anti-clotting drug called Apixaban, which is an oral medication. The medicine proved just as effective at preventing blood clots and reduced the risk of bleeding by half. Most importantly for patient convenience, it was much easier to use.........

Posted by: Scott      Read more         Source


August 6, 2009, 11:35 PM CT

Tumor mutations can predict chemo success

Tumor mutations can predict chemo success
New work by MIT cancer biologists shows that the interplay between two key genes that are often defective in tumors determines how cancer cells respond to chemotherapy.

The findings should have an immediate impact on cancer therapy, say Michael Hemann and Michael Yaffe, the two MIT biology professors who led the study. The work could help doctors predict what types of chemotherapy will be effective in a particular tumor, which would help tailor therapys to each patient.

"This isn't something that's going to take five years to do," says Yaffe, who, along with Hemann is a member of the David H. Koch Institute for Integrative Cancer Research at MIT. "You could begin doing this tomorrow".

The work could also guide the development of new chemotherapy drugs targeted to tumors with specific genetic mutations.

Hemann, Yaffe, and their colleagues report their results in the Aug. 15 issue of the journal Genes and Development Koch Institute postdoctoral associates Hai Jiang and H. Christian Reinhardt are main authors of the study, which the scientists say is one of the first examples of how genetic profiling of tumors can translate to improvements in patient therapy.

"There's a huge amount of genetic information available, but it hasn't made its way into clinical practice yet," says Hemann.........

Posted by: Janet      Read more         Source


July 29, 2009, 11:15 PM CT

Chemo directly to ovarian cancer cells

Chemo directly to ovarian cancer cells
Anil K. Sood, M.D. is a professor and in the Departments of Gynecologic Oncology and Cancer Biology at M. D. Anderson.
With a novel therapeutic delivery system, a research team led by researchers at The University of Texas M. D. Anderson Cancer Center has successfully targeted a protein that is over-expressed in ovary cancer cells. Using the EphA2 protein as a molecular homing mechanism, chemotherapy was delivered in a highly selective manner in preclinical models of ovary cancer, the scientists report in the July 29 issue of the Journal of the National Cancer Institute

EphA2 is attractive for such molecularly targeted treatment because it has increased expression in ovarian and other cancers, including breast, colon, prostate and non-small cell lung cancers and in aggressive melanomas, and its expression has been linked to a poor prognosis.

"One of our goals has been to develop more specific ways to deliver chemotherapeutic drugs," said senior author Anil K. Sood, M.D., professor and in the Departments of Gynecologic Oncology and Cancer Biology at M. D. Anderson. "Over the last several years we have shown that EphA2 is a target that is present quite frequently in ovarian and other cancers, but is either present in low levels or is virtually absent from most normal adult tissues. EphA2's preferential presence on tumor cells makes it an attractive therapeutic target".

The scientists used a carrier system to deliver chemotherapy directly to ovary cancer cells. The immunoconjugate contains an anti-EphA2 monoclonal antibody associated with the chemotherapy drug monomethyl auristatin phenylalanine (MMAF) through the non-cleavable linker maleimidocaproyl. Research has shown that auristatins induce cell cycle arrest at the G - M border, disrupt microtubules and induce apoptosis (programmed cell death) in cancer cells.........

Posted by: Emily      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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