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July 7, 2010, 7:26 AM CT

It takes more than antioxidants to slow aging

It takes more than antioxidants to slow aging
Don't put down the red wine and vitamins just yet, but if you're taking antioxidants because you hope to live longer, consider this: a newly released study reported in the June 2010 issue of the journal GENETICS (http://www.genetics.org) casts doubt on the theory that oxidative stress to our tissues shortens lifespan. That's because scientists from McGill University in Canada have identified mutations in 10 different genes of worms (genes believed to have counterparts in humans) that extend their lifespan without reducing the level of oxidative stress the worms suffer. The results contradict the popular theory that production of toxic reactive oxygen species in tissues is responsible for aging.

"We hope that our study will help in tempering the undue emphasis put on the notion that oxidative stress causes aging and thus that antioxidants could combat aging," said Siegfried Hekimi, Ph.D, the senior author of the study from the Department of Biology at McGill University in Montreal. "We also hope that the genes we have discovered can be used in the future to modulate energy metabolism in a way that can help delay the health issues associated with aging, and possibly increase lifespan itself."

To make their discovery, the researchers exposed a passel of worms (Caenorhabditis elegans) to a chemical that causes random changes in its DNA, and looked among the mutagenized worms for those appearing to have a slow rate of metabolism, manifested in their slow development and slow behavioral responses. They then identified the mutations in these worms that caused this effect, revealing 10 distinct genes involved in metabolism. The scientists' expected that the slowly metabolizing worms would have less oxidative stress, but to the investigators' surprise that was not the case. This suggests that a slow rate of living and reduced energy metabolism is sufficient to increase longevity, even when oxidative stress is not reduced.........

Posted by: Scott      Read more         Source


July 2, 2010, 7:23 AM CT

DNA mutation as cause of cancer

DNA mutation as cause of cancer
What if we could understand why cancer develops? We know that certain risk factors, such as smoking or excessive sun exposure, can increase the chances of developing this terrible disease, but cancer can form in any tissue, and the cause is not always clear. One idea that has emerged is that for a cell to transform into a cancer cell it must suffer a large number of mutations affecting different genes needed to control cell growth. As per a research findings published this week in Science, Brandeis University scientists have observed that the process of repairing DNA damage also unexpectedly increases the rate of mutations and changes the kinds of mutations that arise.

Surprisingly, as cells progress toward full-blown cancer they begin to suffer alterations of the normal DNA replication process, leading to an increased amount of DNA damage, particularly chromosome breaks. Thus there is an increased need for cells to accurately repair these breaks.

Biologist James Haber, graduate student Wade Hicks and undergraduate Minlee Kim report that the repair of damaged strands of DNA, specifically by a process known as gene conversion, can cause higher-than-normal levels of mutation; in fact, 1,400 times as high as spontaneous mutations in cells.

"It has been hard to imagine how cells could accumulate so a number of mutations in the few generations that they undergo cell division on the way to becoming malignant," Haber said. "We believe that the elevated rate of mutation at sites where DNA has been broken appears to be an important source of these gene changes." .........

Posted by: Janet      Read more         Source


July 2, 2010, 7:20 AM CT

Loss of key protein promotes aggressive form of leukemia

Loss of key protein promotes aggressive form of leukemia
Cold Spring Harbor, NY New research by researchers at Cold Spring Harbor Laboratory (CSHL) has illuminated in fine detail one of the genetic paths that leads to a especially aggressive form of leukemia.

CSHL Professor Scott W. Lowe. Ph.D., an Investigator of the Howard Hughes Medical Institute, led a team of researchers who wanted to know more about how the absence of an important tumor-suppressing protein called p53 combines with another genetic "hit" in immature blood cells to give rise to acute myeloid leukemia, or AML. In experiments in living mice, the team discovered that if p53 is disabled in immature blood-cell "precursors" in which a mutation in a gene called Kras is also present, a built-in braking mechanism fails to engage and the cells proliferate out of control.

Mutations in p53, the gene that encodes the p53 "master tumor-suppressor" protein, had previously been linked to drug resistance and adverse outcome in AML. The mechanism, however, was a matter of conjecture previous to the new results, which are reported in the July 1 issue of Genes & Development

"Our team has shown how mutations in Kras and p53 act to reinforce one another to change the character of blood precursor cells, transforming them into cells that can renew themselves and thus proliferate indefinitely, somewhat as cancer stem cells are theorized to do," says Lowe.........

Posted by: Janet      Read more         Source


June 30, 2010, 7:08 AM CT

Turning Back the Cellular Clock

Turning Back the Cellular Clock
method for tracking adult stem cells as they regress
Cell reprogramming calls The Curious Case of Benjamin Button to mind.

It's a new technology that uses molecular treatment to coax adult cells to revert to an embryonic stem cell-like state, allowing researchers to later re-differentiate these cells into specific types with the potential to treat heart attacks or diseases such as Parkinson's. But at this point in the technology's development, only one percent of cells are successfully being reprogrammed.

Now, for the first time, researchers at Tel Aviv University in collaboration with scientists at Harvard University have succeeded in tracking the progression of these cells through live imaging to learn more about how they are reprogrammed, and how the new cells evolve over time.

Dr. Iftach Nachman of TAU's Department of Biochemistry says that this represents a huge stride forward. It will not only allow scientists to develop techniques and choose the right cells for replacement treatment, increasing the efficiency of cell reprogramming, but will give invaluable insight into how these cells will eventually react in the human body. Results from the research project were recently reported in the journal Nature Biotechnology.

Looking at your cell's family tree

Dr. Nachman and his fellow scientists used flourescent markers to develop their live imaging approach. During the reprogramming process, the team was able to visually track whole lineages of a cell population from their single-cell point of origin.........

Posted by: Scott      Read more         Source


June 24, 2010, 11:07 PM CT

Antihypertensive against Alzheimer's disease

Antihypertensive against Alzheimer's disease
Scientists at Mount Sinai School of Medicine have observed that the drug carvedilol, currently prescribed for the therapy of hypertension, may lessen the degenerative impact of Alzheimer's disease and promote healthy memory functions. The new findings appear in two studies in the current issues of Neurobiology of Aging and the Journal of Alzheimer's Disease

"These studies are certainly very exciting, and suggest for the first time that certain antihypertensive drugs already available to the public may independently influence memory functions while reducing degenerative pathological features of the Alzheimer's disease brain," said study author Giulio Maria Pasinetti, MD, PhD, Saunders Family Professor of Neurology and Director of the Center of Excellence for Novel Approaches to Neurotherapeutics at Mount Sinai School of Medicine.

Dr. Pasinetti's team found for the first time that carvedilol, a blood pressure lowering agent, is capable of exerting activities that significantly reduce Alzheimer's disease-type brain and memory degeneration. This benefit was achieved without blood pressure lowering activity in mice genetically modified to develop Alzheimer's disease brain degeneration and memory impairment. These data were published in Neurobiology of Aging.........

Posted by: Daniel      Read more         Source


June 24, 2010, 10:23 PM CT

Gene Therapy A Step Closer

Gene Therapy A Step Closer
EUREKA project E! 3371 Gene Transfer Agents has made great advances in the development of novel non-viral carriers able to introduce genetic material into the target cells. These new agents, derivatives of cationic amphiphilic 1,4-dihydropyridine (1,4-DHP), avoid the problems of the recipient's immune system reacting against a viral carrier. The project partners have developed methods to produce them in large amounts, which solves another of the problems with viral delivery. But the greatest advantage is that the new compounds are significantly more effective at delivering DNA into cell nuclei than other standard synthetic carriers; increasing the chance of the DNA successfully controlling the defective genes, and the disease.

Gene treatment involves the insertion of DNA into human cells within the body to treat disease. The technique is still in its early days, and has been demonstrated successfully only in the last decade. Most investigation has been into the possibilities for treating hereditary diseases correlation to a genetic defect, and the technique also has potential uses in treating the early stages of cancer, and in cardiovascular and neurodegenerative diseases.

Gene treatment faces a number of difficulties as a practical method; not the least of which is that DNA is a large and complicated structure which needs to be delivered and attached to the correct section of the recipient's set of DNA. Many methods are in use or under investigation for introducing DNA into cells (a process known as transfection) - using viruses, chemical agents or physical injection.........

Posted by: Scott      Read more         Source


June 21, 2010, 7:18 AM CT

Therapeutic potential of embryonic stem cells

Therapeutic potential of embryonic stem cells
The therapeutic potential of embryonic stem cells has been an intense focus of study and discussion in biomedical research and has resulted in technologies to produce human induced pluripotent stem cells (hiPSCs). Derived by epigenetic reprogramming of human fibroblasts, these hiPSCs are believed to be almost identical to human embryonic stem cells (hESCs) and provide great promise for patient-tailored regenerative medicine therapies. However, recent studies have suggested noteworthy differences between these two stem cell types which require additional comparative analyses.

Researchers at Children's Memorial Research Center at Northwestern University Feinberg School of Medicine investigated the expression of key members of the Nodal embryonic signaling pathway, critical to maintaining pluripotency, in hiPSC and hESC cell lines. Nodal is an important morphogen a soluble molecule that can regulate cell fate in embryological systems that requires tight regulatory control of its biological function.

The group's results demonstrated slightly lower levels of Nodal and Cripto-1 (Nodal's co-receptor) and a dramatic decrease in Lefty (Nodal's inhibitory regulator) in hiPSCs compared with hESCs, suggesting less regulatory control of cell fate in reprogrammed stem cells. Based on these findings, additional work addressed the implications linked to the epigenetic reprogramming of hiPSCs and examined a global comparative analysis of 365 microRNAs (miRs) in hiPSC vs. hESC lines.........

Posted by: Scott      Read more         Source


June 16, 2010, 7:19 AM CT

How does that taste to you?

How does that taste to you?
Low-salt foods appears to be harder for some people to like than others, as per a research studyby a Penn State College of Agricultural Sciences food scientist. The research indicates that genetics influence some of the difference in the levels of salt we like to eat.

Those conclusions are important because recent, well-publicized efforts to reduce the salt content in food have left a number of people struggling to accept fare that simply does not taste as good to them as it does to others, pointed out John Hayes, assistant professor of food science, who was lead investigator on the study.

Diets high in salt can increase the risk of hypertension and stroke. That is why public health experts and food companies are working together on ways to help consumers lower salt intake through foods that are enjoyable to eat. This study increases understanding of salt preference and consumption.

The research involved 87 carefully screened participants who sampled salty foods such as broth, chips and pretzels, on multiple occasions, spread out over weeks. Test subjects were 45 men and 42 women, reportedly healthy, ranging in age from 20 to 40 years. The sample was composed of individuals who were not actively modifying their dietary intake and did not smoke cigarettes. They rated the intensity of taste on a usually used scientific scale, ranging from barely detectable to strongest sensation of any kind.........

Posted by: Janet      Read more         Source


June 8, 2010, 7:05 AM CT

Protein may repair damage from multiple sclerosis

Protein may repair damage from multiple sclerosis
A protein that helps build the brain in infants and children may aid efforts to restore damage from multiple sclerosis (MS) and other neurodegenerative diseases, scientists at Washington University School of Medicine in St. Louis have found.

In a mouse model of MS, scientists observed that the protein, CXCR4, is essential for repairing myelin, a protective sheath that covers nerve cell branches. MS and other disorders damage myelin, and this damage is associated with loss of the branches inside the myelin.

"In MS patients, myelin repair occurs inconsistently for reasons that aren't clear," says senior author Robyn Klein, MD, PhD, associate professor of medicine and of neurobiology. "Understanding the nature of that problem is a priority because when myelin isn't repaired, the chances that an MS flare-up will inflict lasting harm seem to increase."

The findings appear online in The Proceedings of the National Academy of Sciences

Mouse models typically mimic MS symptoms by causing chronic immune cell infiltration in the brain, but, as per Klein, the ongoing immune damage caused by the cells makes it difficult for scientists to focus on what the brain does to repair myelin.

For the study, Klein and first author and postdoctoral fellow Jigisha Patel, PhD, used a non-inflammatory model that involves giving mice food containing cuprizone, a compound that causes the death of cells that form myelin in the central nervous system. After six weeks, these cells, known as oligodendrocytes, are dead, and the corpus callosum, a structure that connects the left and right hemispheres of the brain, has lost its myelin. If cuprizone is then removed from the mouse diet, new cells migrate to the area that restore the myelin by becoming mature oligodendrocytes.........

Posted by: Daniel      Read more         Source


May 21, 2010, 7:27 AM CT

First drug to demonstrate therapeutic effect in a type of autism

First drug to demonstrate therapeutic effect in a type of autism
Scientists from Mount Sinai School of Medicine have identified a drug that improves communication between nerve cells in a mouse model of Phelan-McDermid Syndrome (PMS). Behavioral symptoms of PMS fall under the autism spectrum disorder category. The research will be presented Friday at the International Meeting for Autism Research (IMFAR) in Philadelphia.

Prior research has shown that a gene mutation in the brain called SHANK3 can cause absent or severely delayed language abilities, intellectual disability, and autism. Mount Sinai scientists developed mice with a mutant SHANK3 gene and observed a lapse in communication between nerve cells in the brain, which can lead to learning problems. This communication breakdown indicated that the nerve cells were not maturing properly.

The scientists then injected the mice with a derivative of a compound called insulin-like growth factor-1 (IGF1), which is FDA-approved to treat growth failure in children. After two weeks of therapy, nerve cell communication was normal and adaptation of nerve cells to stimulation, a key part of learning and memory, was restored.

"The result of IGF1 therapy of these mice is an exciting development on the road to ultimate therapies for individuals with PMS," said Joseph Buxbaum, PhD, Director of the Seaver Autism Center for Research and Treatment at Mount Sinai School of Medicine. "If these data are further verified in additional preclinical studies, individuals with a SHANK3 mutation appears to benefit from therapys with compounds like this one".........

Posted by: JoAnn      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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