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July 15, 2007, 9:15 PM CT

Mechanism Behind Fear

Mechanism Behind Fear
Scientists from MIT's Picower Institute for Learning and Memory have uncovered a molecular mechanism that governs the formation of fears stemming from traumatic events. The work could lead to the first drug to treat the millions of adults who suffer each year from persistent, debilitating fears - including hundreds of soldiers returning from conflict in Iraq and Afghanistan.

The team will report their results in the July 15 advance online publication of Nature Neuroscience.

A study conducted by the Army in 2004 observed that one in eight soldiers returning from Iraq reported symptoms of post-traumatic stress disorder (PTSD). As per the National Center for PTSD in the United States, around eight percent of the population will have PTSD symptoms at some point in their lives. Some 5.2 million adults have PTSD during a given year, the center reports.

Li-Huei Tsai, Picower Professor of Neuroscience in the Department of Brain and Cognitive Sciences, and his colleagues show that inhibiting a kinase (kinases are enzymes that change proteins) called Cdk5 facilitates the extinction of fear learned in a particular context. On the other hand, the learned fear persisted when the kinase's activity was increased in the hippocampus, the brain's center for storing memories.........

Posted by: JoAnn      Read more         Source


July 12, 2007, 5:44 AM CT

Up To 10 Percent Of Human Genome May Have Changed Very Recently

Up To 10 Percent Of Human Genome May Have Changed Very Recently
A Cornell study of genome sequences in African-Americans, European-Americans and Chinese suggests that natural selection has caused as much as 10 percent of the human genome to change in some populations in the last 15,000 to 100,000 years, when people began migrating from Africa.

The study, reported in the June 1 issue of PLoS (Public Library of Science) Genetics, looked for areas where most members of a population showed the same genetic changes. For example, the scientists found evidence of recent selection on skin pigmentation genes, providing the genetic data to support theories proposed by anthropologists for decades that as anatomically modern humans migrated out of Africa and experienced different climates and sunlight levels, their skin colors adapted to the new environments.

However, the study found no evidence of differences in genes that control brain development among the various geographical groups, as some scientists have proposed in the past.

"We undertook a very careful study of genetic differences within and among major human groups, and aimed to explain why certain parts of the genome differed," said Scott Williamson, the study's lead author and a Cornell assistant professor of biological statistics and computational biology. "We aimed to eliminate as a number of possible confounding variables as possible, and when all is said and done, we find that as much as 10 percent of the genome may have been affected by one of these bouts of recent selection".........

Posted by: Scott      Read more         Source


July 12, 2007, 5:35 AM CT

How the brain and an iPhone differ

How the brain and an iPhone differ
UO psychologist Edward Awh and colleagues have found that people with high IQs may be able to remember more than the four objects an average person can store in short-term memory, but they may not be able to recall the objects with clarity.
Credit: Photo by Jim Barlow
How many simple objects can you think about at once? Even though people feel they have rich visual experiences, researchers have found that the average person is only aware of about four items at a time.

This ability, say researchers at the University of Oregon, varies from person to person, and theyve found that an individuals capacity of short-term memory is a strong predictor of IQ and scholastic achievement. People with high IQs can think about more things at once.

Because the capacity of the short-term memory system seems to underlie a core aspect of intelligence, cognitive psychologists have been interested in determining what causes a four-item limit for most people. One reasonable idea, which researchers have been tossing about, is that memory capacity might be influenced by the complexity of items being stored.

For example, a four-gigabyte iPhone, the popular new Apple cell phone, might be able to hold about 1,000 four-minute songs, but, of course, far fewer songs would fit in storage if the songs were all 20 minutes in length, explained UO psychology professors Edward Awh and Edward Vogel, co-authors with recent UO graduate Brian Barton on a study published in the July issue of Psychological Science.

Does human memory work the same way? Their study drew some surprising conclusions on the topic. Even when very complex objects had to be remembered by subjects participating in laboratory experiments, participants, who ranged in age from 18 to 30, still were able to hold four items in active memory. However, Awh said, the clarity of those items was not perfect, and some people had much clearer memories than others.........

Posted by: Daniel      Read more         Source


July 8, 2007, 10:11 PM CT

obesity drug and new cancer treatments

obesity drug and new cancer treatments
Based on their surprising discovery that an obesity drug can kill cancer cells, researchers at Wake Forest University School of Medicine have made a new finding about the drugs effects and are working to design more potent cancer therapys.

Published online today in Nature Structural and Molecular Biology, the study is the first to report how the drug orlistat (Xenical or Alli) binds and interacts with a protein found in tumor cells. The drug blocks the proteins function and causes cell death.

The project started five years ago when Steven Kridel, Ph.D., an assistant professor in the Department of Cancer Biology, analyzed prostate cancer cells to see which enzymes were expressed at high levels. His hope was that therapys to inhibit those enzymes could also stop tumor growth.

We observed that a protein known as fatty acid synthase is expressed at high levels in prostate tumor cells, and is fairly absent in normal cells, said Kridel.

Other research has shown that the protein is found in a number of tumor cells including breast, colon, ovarian, liver, lung and brain.

High levels of fatty acid synthase correlate with a poor prognosis so it is a great therapy target, said Kridel. This makes an exciting therapy target because theoretically you dont have to worry about harming nearby healthy tissue.........

Posted by: Scott      Read more         Source


July 8, 2007, 10:09 PM CT

A gene that protects from kidney disease

A gene that protects from kidney disease
Scientists from the European Molecular Biology Laboratory (EMBL) and the University of Michigan have discovered a gene that protects us against a serious kidney disease. In the current online issue of Nature Genetics they report that mutations in the gene cause nephronopthisis (NPHP) in humans and mice. NPHP is a disease marked by kidney degeneration during childhood that leads to kidney failure requiring organ transplantation. The insights might help develop effective, noninvasive therapies.

The kidneys are the organs that help our body dispose of potentially harmful waste. Diseases that affect this fundamental function are very serious but so far only poorly understood. NPHP is such a disease; it causes the kidneys to degenerate and shrink starting early on in childhood often leading to renal failure before the age of 30. So far, kidney transplantation in early age has been the only way to save patients suffering from NPHP. With a new mouse model Mathias Treier and his group at EMBL have shed new light on the molecular mechanisms underlying NPHP opening up novel ways to treat the disease.

Our mice show striking similarities with NPHP patients, says Mathias Treier, group leader at EMBL. Very early on in their lives their kidney cells start to die and the mice develop all the characteristic disease symptoms. It is the first time that a mouse model reveals increased cell death as the mechanism underpinning kidney degeneration in NPHP. The genetic cause is a mutation in a gene called GLIS2.........

Posted by: Mark      Read more         Source


July 8, 2007, 10:06 PM CT

Genetic Risk Factor For Colorectal And Prostate Cancer

Genetic Risk Factor For Colorectal And Prostate Cancer
A study led by scientists at the Keck School of Medicine of the University of Southern California (USC) has observed that one of seven genetic risk factors previously identified as increasing the probability of developing prostate cancer also increases the probability of developing colorectal cancer. As in the prior prostate cancer study, which was also conducted by USC scientists and reported in the April 2007 edition of Nature Genetics, the colorectal cancer risk factor is located in a region of the human genome devoid of known genes on chromosome 8. The studys complete findings would be reported in the July 8 online edition of Nature Genetics.

This is an important finding because, for the first time, a common genetic risk factor for multiple cancers has been identified, says lead author Christopher Haiman, assistant professor of preventive medicine at the Keck School of Medicine of USC. Adding, There appears to be something fundamental occurring in this region that influences not only colorectal and prostate cancer, but perhaps cancers in general. (Another recently published study, in which USC scientists also were involved, identified variants in this same chromosomal region as playing a predictive role relative to the risk of developing breast cancer.).

For the current colorectal cancer study, the USC team genotyped six of the seven variants previously identified as increasing the risk of prostate cancer development. The samples analyzed totaled 1,807 invasive colorectal cancer cases and 5,511 controls. These samples were drawn from five populations (African Americans, Japanese Americans, Native Hawaiians, Latinos, and European Americans) included in the Multiethnic Cohort Study, an epidemiological study of more than 215,000 people from Los Angeles and Hawaii created in 1993 by Brian Henderson, dean, Keck School of Medicine of USC, and Laurence Kolonel of the University of Hawaii.........

Posted by: Sue      Read more         Source


July 5, 2007, 9:06 PM CT

Engineered Blood Vessels Function

Engineered Blood Vessels Function
Blood vessels that have been tissue-engineered from bone marrow adult stem cells may in the future serve as a patient's own source of new blood vessels following a coronary bypass or other procedures that require vessel replacement, as per new research from the University at Buffalo Department of Chemical and Biological Engineering.

"Our results show that bone marrow is an excellent source of adult stem cells containing smooth muscle and endothelial cells, and that these stem cells can be used in regenerative medicine for cardiovascular applications," said Stelios T. Andreadis, Ph.D., associate professor in the UB Department of Chemical and Biological Engineering in the School of Engineering and Applied Sciences.

Andreadis co-authored the paper, published recently in Cardiovascular Research, with Jin Yu Liu, Ph.D., lead author and a post doctoral researcher in Andreadis' lab.

The research demonstrates the potential for eventually growing tissue-engineered vessels out of stem cells harvested from the patients who need them, providing a desirable alternative to the venous grafts now routinely done in patients undergoing coronary bypass operations.

Disadvantages with venous grafts include limited availability of vessels, pain and discomfort at the donor site and a high 10-year failure rate.........

Posted by: Scott      Read more         Source


July 3, 2007, 5:01 AM CT

Fat kills cancer

Fat kills cancer
Scientists in Slovakia have been able to derive mesenchymal stem cells from human adipose, or fat, tissue and engineer them into suicide genes that seek out and destroy tumors like tiny homing missiles. This gene treatment approach is a novel way to attack small tumor metastases that evade current detection techniques and therapys, the scientists conclude in the July 1 issue of Cancer Research, a journal of the American Association for Cancer Research.

These fat-derived stem cells could be exploited for personalized cell-based therapeutics, said the studys lead investigator, Cestmir Altaner, Ph.D., D.Sc., an associate professor in the Cancer Research Institute of the Slovak Academy of Sciences in Bratislava. Nearly everyone has some fat tissue they can spare, and this tissue could be a source of cells for cancer therapy that can be adapted into specific vehicles for drug transport.

Mesenchymal stem cells help repair damaged tissue and organs by renewing injured cells. They are also found in the mass of normal cells that mix with cancer cells to make up a solid tumor. Scientists believe mesenchymal stem cells see a tumor as a damaged organ and migrate to it, and so might be utilized as a vehicle for therapy that can find both primary tumors and small metastases. These stem cells also have some plasticity, which means they can be converted by the micro environment of a given tissue into specialized cells, Altaner says.........

Posted by: Janet      Read more         Source


June 28, 2007, 11:49 PM CT

Critical protein prevents DNA damage

Critical protein prevents DNA damage
A protein long known to be involved in protecting cells from genetic damage has been found to play an even more important role in protecting the cell's offspring. New research by a team of researchers at Rockefeller University, Howard Hughes Medical Institute and the National Cancer Institute shows that the protein, known as ATM, is not only vital for helping repair double-stranded breaks in DNA of immune cells, but is also part of a system that prevents genetic damage from being passed on when the cells divide.

Early in the life of B lymphocytes -- the immune cells responsible for hunting down foreign invaders and labeling them for destruction -- they rearrange their DNA to create various surface receptors that can accurately identify different intruders, a process called V(D)J recombination. Now, in an study published online today in the journal Cell, Rockefeller University Professor Michel Nussenzweig, in collaboration with his brother Andr Nussenzweig at NCI and their colleagues, shows that when the ATM protein is absent, chromosomal breaks created during V(D)J recombination go unrepaired, and checkpoints that normally prevent the damaged cell from replicating are lost.

Normal lymphocytes contain many restorative proteins, whose job it is to identify chromosomal damage and repair it or, if the damage is irreparable, prevent the cell from multiplying. Earlier research by Andr and Michel Nussenzweig, who is an investigator at HHMI, had identified other DNA repair proteins that are important during different phases of a B lymphocyte's life. It was during one of these studies, which examined genetic damage late in the life of a B cell, that they came across chromosomal breaks that could not be explained.........

Posted by: Scott      Read more         Source


June 27, 2007, 6:44 PM CT

Gene That Spurs Development Of The Epididymis

Gene That Spurs Development Of The Epididymis
Photo courtesy H. Yao
Human sperm cells travel up to 6 meters in their transit from testes to penis, and most of that journey occurs in the epididymis, a tightly coiled tube that primes the cells for their ultimate task: fertilization. In a paper released this week in the Proceedings of the National Academy of Sciences, scientists at the University of Illinois report that they have discovered a gene - and related mechanism - essential to the embryonic development of the epididymis.

The findings are the result of a serendipitous discovery, said professor of veterinary biosciences Humphrey Hung-Chang Yao. His graduate student, Jessica Tomaszewski, was examining the testes of mouse embryos when she noticed something odd: In one specimen the normally convoluted coil of the epididymis was instead a stunted, straight tube.

The lack of coiling had serious implications for the fertility of the mouse, Yao said.

"If you take sperm directly from the testis and put it into the female reproductive tract, it won't swim. It won't be able to fertilize the egg," he said. Going through the epididymis changes the biochemical properties of the sperm and helps it develop the energy-generating machinery that allows it to swim. "So without this structure, under normal circumstances a male cannot be fertile".........

Posted by: Scott      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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