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December 13, 2006, 4:48 AM CT

Gene That Causes Familial Pancreatic Cancer

Gene That Causes Familial Pancreatic Cancer
An international group of scientists has discovered that the mutated form of a gene called Palladin causes familial pancreas cancer. The findings, published online today (Dec. 12) in the peer-evaluated journal PLoS-Medicine, may help explain why the disease is so deadly. The research project was led by Dr. Teri Brentnall, University of Washington associate professor of medicine, and supported by The Lustgarten Foundation, Canary Foundation, and other private sources.

Pancreas cancer is commonly a fatal diagnosis. One of the deadliest types of cancer, it is the fourth leading cause of cancer deaths overall, and third-leading cause of cancer deaths for people aged 40 to 60 in the United States. Most people with the disease die within a year of diagnosis; about 95 percent of patients die within five years. Scientists estimate that at least ten percent of all pancreas cancer cases are inherited.

The discovery also reveals that the Palladin gene behaves abnormally in both the hereditary and non-hereditary, or sporadic, forms of pancreas cancer. Prior studies by co-author Dr. Carol Otey, associate professor of physiology at the University of North Carolina, have revealed that when the Palladin gene is functioning properly, it gives a cell its shape and enables the cell to move. In the case of pancreas cancer, a mutation in Palladin allows the cell to move much more quickly than normal, essentially invading the surrounding, healthy tissue.........

Posted by: Sue      Permalink         Source


December 12, 2006, 4:50 AM CT

'ZIP Code' Spurs Cargo Transport in Neurons

'ZIP Code' Spurs Cargo Transport in Neurons Highly prized in the kitchen and the lab Squid have a giant axon that is 1,000 times wider than the average human.
Image: Russell Jacobs, Elaine Bearer/MBL
For the first time, scientists have identified a peptide that can spur cargo transport in nerve cells, a discovery that could help researchers better understand nerve cell function and test possible therapies for neurodegenerative diseases.

Elaine Bearer, a professor at Brown Medical School, led the research, which was conducted at the MBL (Marine Biological Laboratory) in Woods Hole, Mass., where Bearer was a Dart Scholar and is a Whitman investigator. Reported in the Proceedings of the National Academy of Sciences online early edition, the research shows that a peptide, or protein bit, can hitch biological material onto molecular motor machinery, acting as a "ZIP Code" that directs the shipment to the synapse.

The peptide comes from amyloid precursor protein, or APP, a principal component of plaques found in the brains of people with Alzheimer's disease. Researchers have long known that APP can break down and form these plaques and that mutations in this protein lead to early onset of Alzheimer's disease. Until now, however, little was understood about the function of APP in healthy nerve cells.

The research also sheds light on the complex intracellular transport system inside nerve cells. This transport system is critical to nervous system function, bringing proteins and RNA from the cell body down a neuron's spindly axon to the synapse, the major site of information exchange and storage in the nervous system. Without this precious cargo, neurons can't communicate. Memories can't be made. Learning can't take place. And neurons die.........

Posted by: Daniel      Permalink         Source


December 11, 2006, 4:57 AM CT

Challenging The Theory Of Memory Storage

Challenging The Theory Of Memory Storage The brain’s neocortex (blue) and the hippocampus (red)
Image: Mayank Mehta/Brown Universit
Daily events are minted into memories in the hippocampus, one of the oldest parts of the brain. For long-term storage, researchers think that memories move to the neocortex, or "new bark," the gray matter covering the hippocampus. This transfer process occurs during sleep, particularly during deep, dreamless sleep.

A number of neuroresearchers have embraced and built upon this theory of memory storage, or consolidation, for a generation. But the theory is difficult to test. New research led by Brown University neuroscientist Mayank Mehta, conducted with Nobel Prize-winning physiologist Bert Sakmann, shows the best evidence yet of the sleep dialogue between the old brain and the.

Their work, published in Nature Neuroscience, also shows that this interaction occurs in a startling way. Instead of the hippocampus uploading information to the neocortex in a burst of brain cell communication, Mehta found the opposite: the neocortex seems to drive the dialogue with the hippocampus.

The findings may give researchers a new understanding of how the brain manages memories in health and during dementia, offering up a fresh look at the causes of diseases such as Alzheimer's, as well as potential therapys.

"Long-term memory making may be a very different process than we previously thought," said Mehta, an assistant professor in the Department of Neuroscience at Brown. "Either this reversed dialogue is, somehow, a part of memory storage or this transfer of information from the old to the new brain may not occur during sleep. Either way, the results call into question usually held theories about the role of cortico-hippocampal dialogue in sleep".........

Posted by: Daniel      Permalink         Source


December 10, 2006, 9:13 PM CT

Reduced Body Temperature Extends Lifespan

Reduced Body Temperature Extends Lifespan
Scientists at The Scripps Research Institute have found that reducing the core body temperature of mice extends their median lifespan by up to 20 percent. This is the first time that changes in body temperature have been shown to affect lifespan in warm-blooded animals.

The findings appear in a paper in the journal Science on November 3.

"Our study shows it is possible to increase lifespan in mice by modest but prolonged lowering of core body temperature," said Bruno Conti, an associate professor at Scripps Research who led the study. "This longer lifespan was attained independent of calorie restriction".

Prior to this study, researchers had known that core body temperature and aging were related in cold-blooded animals. Scientists had also known that lifespan could be extended in warm-blooded animals by reducing the number of calories they consumed, which also lowered core body temperature. But the degree of calorie restriction needed to extend lifespan is not easy to achieve, even in mice.

Prior to the current study, critical questions about the relation between calorie restriction, core body temperature, and lifespan remained unanswered. Was calorie restriction itself responsible for longer lifespan, with reduced body temperature simply a consequence? Or was the reduction of core body temperature a key contributor to the beneficial effects of calorie restriction? Conti and colleagues wanted to find out.........

Posted by: Janet      Permalink         Source


December 8, 2006, 4:39 AM CT

Data From Robotic Medical Tools Could Improve Surgery Skills

Data From Robotic Medical Tools Could Improve Surgery Skills Da Vinci Robotic System (Credit: Will Kirk/JHU)
When a surgeon operates the controls of a da Vinci robotic system, the device records these hand movements
Borrowing ideas from speech recognition research, Johns Hopkins computer researchers are building mathematical models to represent the safest and most effective ways to perform surgery, including tasks such as suturing, dissecting and joining tissue.

The team's long-term goal is to develop an objective way of evaluating a surgeon's work and to help doctors improve their operating room skills. Ultimately, the research also could enable robotic surgical tools to perform with greater precision.

The project, supported by a three-year National Science Foundation grant, has yielded promising early results in modeling suturing work. The scientists performed the suturing with the help of a robotic surgical device, which recorded the movements and made them available for computer analysis.

"Surgery is a skilled activity, and it has a structure that can be taught and acquired," said Gregory D. Hager, a professor of computer science in the university's Whiting School of Engineering and principal investigator on the project. "We can think of that structure as 'the language of surgery.' To develop mathematical models for this language, we're borrowing techniques from speech recognition technology and applying them to motion recognition and skills assessment".

Complicated surgical tasks, Hager said, unfold in a series of steps that resemble the way that words, sentences and paragraphs are used to convey language. "In speech recognition research, we break these down to their most basic sounds, called phonemes," he said. "Following that example, our team wants to break surgical procedures down to simple gestures that can be represented mathematically by computer software".........

Posted by: Scott      Permalink         Source


December 7, 2006, 9:57 PM CT

New Approach To Melanoma Treatment

New Approach To Melanoma Treatment
While investigating a fungus known to cause an infection in people with AIDS, two grantees of the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health (NIH), unexpectedly discovered a potential strategy for treating metastatic melanoma, one of the deadliest forms of skin cancer. The therapy approach, which involves combining an antibody with radiation, has since been further developed and is expected to enter early-stage human clinical studies in 2007.

"This is an excellent example of how scientific research in one discipline may have payoffs in a completely unpredictable way," says NIAID Director Anthony S. Fauci, M.D. "This important AIDS-related research has led to the development of a promising therapeutic strategy for a terrible cancer that affects thousands of people each year."

Arturo Casadevall, M.D., Ph.D., of the Albert Einstein College of Medicine at Yeshiva University, in New York City, and his research team began studying the biology of the skin pigment melanin to better understand why its synthesis plays a role in the process whereby certain yeast-like fungi, specifically Cryptococcus neoformans, cause disease in some people. C. neoformans can cause cryptococcosis, a potentially fatal fungal infection that can lead to inflammation of the brain and death in people with AIDS and other immunocompromised individuals.........

Posted by: George      Permalink         Source


December 7, 2006, 9:49 PM CT

Blood Pressure Drugs Could Halt Pancreatic Cancer Spread

Blood Pressure Drugs Could Halt Pancreatic Cancer Spread
Common blood pressure medications might help block the spread of pancreas cancer, scientists at the Kimmel Cancer Center at Thomas Jefferson University in Philadelphia have found. The researchers showed in laboratory studies that two types of pressure-lowering drugs - ACE inhibitors and AT1R blockers - may help reduce the development of tumor-feeding blood vessels, a process called angiogenesis. Such drugs, they say, may become part of a novel strategy to control the growth and spread of cancer.

As per Hwyda Arafat, M.D., Ph.D., assistant professor of surgery at Jefferson Medical College, prior studies have linked a lower cancer incidence with the inhibition of the pancreas hormone angiotensin II (Ang II) by either ACE (Angiotensin I converting enzyme) inhibitors or AT1R (Ang II type 1 receptor) blockers. Ang II increases the production of VEGF, a vascular factor that promotes blood vessel growth in many cancers. High VEGF levels have been correlated with poor cancer prognosis and early recurrence. ACE is the enzyme that converts Ang I to Ang II.

Dr. Arafat and her co-workers examined the protein of both invasive pancreas cancer and normal pancreatic tissue, analyzing the expression of ACE and AT1R in relation to VEGF. They also looked at the effects of blood pressure drugs captopril, an ACE inhibitor, and losartan, an AT1R blocker, on VEGF production in cancer cell lines.........

Posted by: Sue      Permalink         Source


December 7, 2006, 9:47 PM CT

Growing Heart Muscle

Growing Heart Muscle A length of bioengineered heart muscle, or BEHM, grown at the University of Michigan
Credit: Ravi Birla, University of Michiga
It looks, contracts and responds almost like natural heart muscle - even though it was grown in the lab. And it brings researchers another step closer to the goal of creating replacement parts for damaged human hearts, or eventually growing an entirely new heart from just a spoonful of loose heart cells.

This week, University of Michigan scientists are reporting significant progress in growing bioengineered heart muscle, or BEHM, with organized cells, capable of generating pulsating forces and reacting to stimulation more like real muscle than ever before.

The three-dimensional tissue was grown using an innovative technique that is faster than others that have been tried in recent years, but still yields tissue with significantly better properties. The approach uses a fibrin gel to support rat cardiac cells temporarily, before the fibrin breaks down as the cells organize into tissue.

The U-M team details its achievement in a new paper published online in the Journal of Biomedical Materials Research Part A.

And while BEHM is still years away from use as a human heart therapy, or as a testing ground for new cardiovascular drugs, the U-M scientists say their results should help accelerate progress toward those goals. U-M is applying for patent protection on the development and is actively looking for a corporate partner to help bring the technology to market.........

Posted by: Daniel      Permalink         Source


December 6, 2006, 8:46 PM CT

Statin Users Risk Heart Attacks By Dropping Treatment

Statin Users Risk Heart Attacks By Dropping Treatment
Thousands of statin users worldwide are suffering preventable heart attacks, simply because they are not complying with their therapy or are taking too low a dose, as per new research published on-line (Thursday 7 December) in European Heart Journal[1].

These life-saving drugs, used to lower cholesterol levels in people who are at risk of coronary heart disease (CHD), can only be optimally effective if patients use them properly - and a number of are not.

That is the conclusion by the research team, who followed the prescription records of nearly 60,000 patients in the Netherlands for up to 14 years.

Dr Fernie Penning-van Beest and his colleagues from the PHARMO Institute[2], the Utrecht Institute of Pharmaceutical Sciences and the Academic Hospital in Amsterdam, analysed 548,084 prescriptions of statin therapy issued over the first two years of therapy[3] in 59,094 new users in the period January 1991-December 2004, and followed the patients until their first hospital admission for heart attack, death, or the end of the study in December 2004.

The aim was to see how effective robust statin therapy was for primary and secondary CHD in the 'real world' - as opposed to in clinical trials. Their results enabled them to calculate the absolute number of avoidable heart attacks that occurred because patients had stopped taking their drugs or were not taking them consistently. They were also able to compare the preventive effects of different doses and types of statins.........

Posted by: Daniel      Permalink         Source


December 6, 2006, 8:13 PM CT

New Treatment Approaches For Glaucoma

New Treatment Approaches For Glaucoma
New research from Children's Hospital Boston and the Massachusetts Eye and Ear Infirmary (MEEI) may help explain how glaucoma causes blindness, revealing the chain of cellular and molecular events that ultimately damage the optic nerve, preventing visual information from traveling from the eye to the brain. The study, done in mice, indicates possible targets for intervention, including an inflammatory molecule called tumor necrosis factor-alpha (TNF-alpha), which is already targeted by some existing drugs.

"These findings give a whole new approach to thinking about glaucoma treatment," says Joan Miller, MD, chief of Ophthalmology at the MEEI and a coauthor of the study, which will appear online December 6 in the Journal of Neuroscience.

Glaucoma affects an estimated 3 million Americans, and it's speculated that an equal number of people are affected but undiagnosed. The disease is six to eight times more common in African-Americans (in whom it is the leading cause of blindness) than in Caucasians, and six times more common in people over age 60 than in younger people. The primary risk factor for glaucoma is increased pressure in the eye, measured by the familiar "puff" test and other screening examinations. If glaucoma is diagnosed early, eyedrops or surgery to lower intraocular pressure can often prevent further optic-nerve damage and halt vision loss. However, it has not been understood how the increased pressure leads to optic-nerve damage.........

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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