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June 11, 2009, 5:15 AM CT

What causes multiple sclerosis?

What causes multiple sclerosis?
Multiple sclerosis is a very complex disease of the nervous system. Thanks to the development of the new animal model, significantly improved insights into its emergence and progress are now possible.

Credit: Image: Max Planck Institute of Neurobiology
Over 100,000 people suffer from multiple sclerosis in Gera number of alone. Despite intensive research, the factors that trigger the disease and influence its progress remain unclear. Researchers from the Max Planck Institute of Neurobiology in Martinsried and an international research team have succeeded in attaining three important new insights into the disease. It would appear that B cells play an unexpected role in the spontaneous development of multiple sclerosis and that especially aggressive T cells are activated by different proteins. Furthermore, a new animal model is helping the researchers to understand the emergence of the most common form of the disease in Gera number of. (Nature Medicine, May 31, 2009 & Journal of Experimental Medicine, June 1, 2009).

Multiple Sclerosis (MS) poses enormous problems for both patients and doctors: it is the most common inflammatory disease of the central nervous system in our part of the world and often strikes patients at a relatively young age. In some patients it leads to severe disability. Moreover, despite decades of research on MS, the causes and course of the disease are still largely unclear.

There is much evidence to support the fact that MS is triggered by an autoimmune reaction: immune cells that should actually protect the body against threats like viruses, bacteria and tumours, attack the body's own brain tissue. New therapys now available can attenuate the harmful immune reaction and thus delay the progress of the disease. However, the more effective the therapy, the more serious its side effects. Therefore, it is a matter of extreme urgency that new forms of therapy be developed which can differentiate in a targeted way between the immune cells that cause the disease and those that should be protected. A better understanding of the disease is mandatory in order to achieve this.........

Posted by: Daniel      Read more         Source


June 10, 2009, 9:32 PM CT

HIV-1's 'hijacking mechanism

HIV-1's 'hijacking mechanism
Scientists at McGill University and the affiliated Lady Davis Institute for Medical Research at Montreal's Jewish General Hospital along with colleagues at the University of Manitoba and the University of British Columbia may have found a chink in the armour of the human immunodeficiency virus type 1 (HIV-1), the microorganism which causes AIDS. They have pinpointed the key cellular machinery co-opted by HIV-1 to hijack the human cell for its own benefit. Their study was published in May in the Journal of Biological Chemistry

Once a cell is infected with HIV-1, activation of the virus's gene generates a large HIV-1 RNA molecule known as the RNA genome. This is then transported from the cell nucleus to the inner surface of the plasma membrane. The RNA genome can produce both structural proteins and enzymes, but once it arrives at the plasma membrane it can also assemble into new copies of the virus that actually bud out of the cell. Dr. Andrew J. Mouland and colleagues have discovered how the RNA genome gets transported or trafficked from the nucleus to the plasma membrane.

"There is a highway inside the human cell," explained Dr. Mouland, Associate Professor at McGill's Departments of Medicine and Microbiology and Immunology and head of the HIV-1 RNA Trafficking Laboratory at the Lady Davis Institute. "When you drive your car to Toronto you're 'trafficking' the items in your trunk. Similarly, what we have shown is that HIV-1 commandeers the host cell's endosomal machinery to traffic its structural proteins and RNA genome. Imagine that it's essentially jumping on board for the ride and directing it to where it needs to go. This trafficking can occur very fast in cells; so this is how these key components of HIV-1 so efficiently get to the plasma membrane, where the virus can begin to assemble.........

Posted by: Mark      Read more         Source


June 9, 2009, 5:00 AM CT

Dynamic stroma microenvironment in prostate cancer

Dynamic stroma microenvironment in prostate cancer
As stroma the supportive framework of the prostate gland react to prostate cancer, changes in the expression of genes occur that induce the formation of new structures such as blood vessels, nerves and parts of nerves, said scientists at Baylor College of Medicine in a report that appears in the current issue of the journal Clinical Cancer Research

In this study, using special techniques and gene chips that allowed them to sample the entire genome, the scientists found changes in 1,141 genes. They were either upregulated meaning that there was more of the protein with which they were associated than expected or downregulated, which meant the opposite, said Dr. Michael Ittmann, professor of pathology at BCM and a senior author of the report. These gene changes may explain why men with reactive stroma face a more aggressive disease, said Ittmann and Dr. Gustavo Ayala, professor in the departments of pathology and urology at BCM and another senior author.

"Often in prostate cancer, you don't see much change in the stromal cells," said Ittmann. "However, in this subgroup of patients (in which the stroma become visibly reactive), you see a histologically recognizable change in the appearance of the stroma. Dr. Ayala has shown previously that this correlates with a bad prognosis. We know the stroma are doing something to promote bad behavior in cancer cells".........

Posted by: Mark      Read more         Source


June 5, 2009, 4:44 AM CT

Risks of sharing personal genetic information online

Risks of sharing personal genetic information online
With just $399 and a bit of saliva in a cup, consumers can learn about their genetic risk for diseases from breast cancer to diabetes. Now, thanks to social networking sites set up by personal genomics companies, they can also share that information with family, friends and even strangers on the Internet.

Bonding over a similar genetic background sounds relatively harmless. But as per bioethicists from the Stanford University School of Medicine, sharing genetic information online raises a host of ethical questions.

"Genetic information is unique in that it's not only relevant for the individuals who receive the information, but also for their family members, their children and even their children's children," said Sandra Soo-Jin Lee, PhD, senior research scholar at the school's Center for Biomedical Ethics.

Because genetic information applies to more than one person, issues of privacy and consent become complicated. "For example," Lee said, "if you receive information on your breast cancer risk and share it with others, you might also be sharing information about your daughter's risk for breast cancer even though she never consented to have that information shared".

In cooperation with assistant professor of pediatrics and bioethicist LaVera Crawley, MD, MPH, Lee has been studying the potential implications of exchanging genetic information online. To fully understand the effects of sharing, the scientists say we need more data on who's giving out information and how it's being used. Their recommendations will be published in a special double-issue of the American Journal of Bioethics on June 5.........

Posted by: Scott      Read more         Source


June 1, 2009, 7:07 PM CT

Genes, smoking and rheumatoid arthritis

Genes, smoking and rheumatoid arthritis
Recent genetic studies have revealed several new sites of genes that are risk factors for developing rheumatoid arthritis (RA). The strongest association with anti-citrullinated protein antibody (ACPA)-positive RA (ACPAs are autoantibodies detected in RA that are used as a major diagnostic tool) has been found for the HLA-DRB1 gene, and this site seems to play a central role in susceptibility to the disease in Caucasian populations. Prior studies have shown a high increase in the risk of ACPA-positive RA linked to smoking in those who have certain variations of the HLA-DRB1 gene. There are several types of such alleles correlation to a particular amino acid sequence known as shared epitope (SE). ACPAs occur in about 60 percent of RA patients and are closely associated with the presence of SE alleles. In fact, SE alleles are the strongest genetic risk factor for ACPA-positive RA.

Of several environmental factors that predispose people toward developing RA, smoking has been found to be the main risk factor and a strong gene-environment interaction between smoking and SE alleles for ACPA-positive patients has been shown in prior studies in Europe. Results in North America have not been as conclusive, however. A new large population-based study examined the gene-environment interaction between smoking and SE alleles in RA and observed that all SE alleles strongly interact with smoking in conferring an increased risk of ACPA-positive RA. The study was reported in the recent issue of Arthritis & Rheumatism (http://www3.interscience.wiley.com/journal/76509746/home).........

Posted by: Mark      Read more         Source


June 1, 2009, 5:17 AM CT

Predicting response to melanoma treatment

Predicting response to melanoma treatment
Genes that help predict a melanoma patient's response to therapy. The new findings are being presented at the 45th annual meeting of the American Society of Clinical Oncology (ASCO), May 29 to June 2, in Orlando, Fla.

"Approximately 70,000 people will be diagnosed with metastatic melanoma this year," said principal investigator Hussein Tawbi, M.D., M.Sc., assistant professor of medicine, University of Pittsburgh School of Medicine, and with UPCI's Melanoma Program. "This form of cancer is aggressive and often resistant to chemotherapy. In fact, only 7 to 10 percent of patients are likely to respond to the current standard of care. We wanted to see if there was a way to predict which patients would respond to therapy and which ones would not".

Dr. Tawbi and colleagues examined the tumor tissues of 21 patients with metastatic melanoma, some of whom responded to chemotherapy and some who did not. Once the cases were divided, the scientists used a mathematical tool called Neural Network Analysis to survey over 25,000 genes and the regulators that turn the genes on and off to see if they could identify ones that could distinguish responders from nonresponders.

"Cancer cells contain massive amounts of information that, if analyzed appropriately, may inform us how to kill them," said Dr. Tawbi. "They contain thousands of genes, and every gene has a switch that turns it on or off. Neural Network Analysis, which utilizes pattern recognition algorithms, helped us identify a signature of eight genes and their switches that predict a patient's likelihood of responding to therapy for metastatic melanoma".........

Posted by: George      Read more         Source


June 1, 2009, 5:07 AM CT

Stem cell-gene therapy approach cures human genetic disease

Stem cell-gene therapy approach cures human genetic disease
Shown in green are genetically-corrected fibroblasts from Fanconi anemia patients are reprogrammed to generate induced pluripotent stem cells, which, in turn, can be differentiated into disease-free hematopoietic progenitors, capable of producing blood cells in vitro.

Credit: Courtesy of Dr. Juan-Carlos Belmonte, Salk Institute for Biological Studies

A study led by scientists at the Salk Institute for Biological Studies, has catapulted the field of regenerative medicine significantly forward, proving in principle that a human genetic disease can be cured using a combination of gene treatment and induced pluripotent stem (iPS) cell technology. The study, reported in the May 31, 2009 early online edition of Nature, is a major milestone on the path from the laboratory to the clinic.

"It's been ten years since human stem cells were first cultured in a Petri dish," says the study's leader Juan-Carlos Izpisa Belmonte, Ph.D., a professor in the Gene Expression Laboratory and director of the Center of Regenerative Medicine in Barcelona (CMRB), Spain. "The hope in the field has always been that we'll be able to correct a disease genetically and then make iPS cells that differentiate into the type of tissue where the disease is manifested and bring it to clinic".

Eventhough several studies have demonstrated the efficacy of the approach in mice, its feasibility in humans had not been established. The Salk study offers the first proof that this technology can work in human cells.

Belmonte's team, working with Salk colleague Inder Verma, Ph.D., a professor in the Laboratory of Genetics, and his colleagues at the CMRB, and the CIEMAT in Madrid, Spain, decided to focus on Fanconi anemia (FA), a genetic disorder responsible for a series of hematological abnormalities that impair the body's ability to fight infection, deliver oxygen, and clot blood. Caused by mutations in one of 13 Fanconi anemia (FA) genes, the disease often leads to bone marrow failure, leukemia, and other cancers. Even after receiving bone marrow transplants to correct the hematological problems, patients remain at high risk of developing cancer and other serious health conditions.........

Posted by: Scott      Read more         Source


May 22, 2009, 5:13 AM CT

Identifying Alzheimers disease early

Identifying Alzheimers disease early
Analyzing MRI studies of the brain with software developed at the Martinos Center for Biomedical Imaging at Massachusetts General Hospital (MGH) may allow diagnosis of Alzheimer's disease and of mild cognitive impairment, a lesser form of dementia that precedes the development of Alzheimer's by several years. In their report that will appear in the journal Brain and has been released online, the MGH/Martinos team show how their software program can accurately differentiate patients with mild cognitive impairment or Alzheimer's disease from normal elderly individuals based on anatomic differences in brain structures known to be affected by the disease.

"Traditionally Alzheimer's has been diagnosed based on a combination of factors such as a neurologic exam, detailed medical history and written tests of cognitive functioning with neuroimaging used primarily to rule out other diseases such as stroke or a brain tumor," says Rahul Desikan MD, PhD, of the Martinos Center and Boston University School of Medicine, main author of the Brain paper. "Our findings show the feasibility and importance of using automated, MRI-based neuroanatomic measures as a diagnostic marker for Alzheimer's disease."

The scientists note that mild cognitive impairment occurs in about 20 percent of elderly individuals as a number of as 40 percent of those over 85 80 percent of whom develop Alzheimer's within five or six years. Since drugs that may slow the progression of Alzheimer's are in development, the ability to treat patients in the earliest stages of the disease may significantly delay progression to dementia. To investigate whether MR imaging can produce diagnostic markers for mild cognitive impairment and Alzheimer's disease, the research team used FreeSurfer an openly available imaging software package developed at the Martinos Center and the University of California at San Diego to examine many neuroanatomic regions across a range of normal individuals and patients with mild cognitive impairment and Alzheimer's disease.........

Posted by: Daniel      Read more         Source


May 20, 2009, 5:23 AM CT

Satiation solution

Satiation solution
Have you ever gotten sick of pizza, playing the same computer game, or had a song stuck in your head for so long you never wanted to hear it again? If you have, you may suffer from variety amnesia. In new research, Joseph Redden, professor of marketing at the University of Minnesota's Carlson School of Management, may have found a cure for your satiation blues. "People forget about the abundance of different experiences they have had and tend to focus on the repetition," said Redden. "Simply thinking about the variety of songs they have listened to or meals they have eaten will make people enjoy the activity again." .

Satiation, the process of consuming products and experiences to the point where they are less enjoyable, is a big problem for consumers and retailers. In the past, time and variety have been seen as the only ways to cure satiation. In their new article forthcoming in the Journal of Consumer Research, Redden and co-authors find that just recalling variety may cure satiation faster. "Intuition says that if time passes we will like something again: we call this 'spontaneous recovery,' " said Redden. "This isn't the whole story. People don't fully recover on their own with the mere passage of time. If I'm sick of chocolate, simply thinking about all the other desserts I've had since the last time I had chocolate helps cure my satiation. Time doesn't seem to do that very well".........

Posted by: JoAnn      Read more         Source


May 20, 2009, 5:09 AM CT

A new way of treating the flu

A new way of treating the flu
Dr. Robert Linhardt's new compound (green spheres) blocks both the N (pink spikes) and H (blue spikes) portion of the flu virus. The compound prevents the infection of the cell and the spread of the flu to other cell like no other compound before.

Credit: Melissa Kemp/Rensselaer Polytechnic Institute

What happens if the next big influenza mutation proves resistant to the available anti-viral drugs? This question is presenting itself right now to researchers and health officials this week at the World Health Assembly in Geneva, Switzerland, as they continue to do battle with H1N1, the so-called swine flu, and prepare for the next iteration of the ever-changing flu virus.

Promising new research announced by Rensselaer Polytechnic Institute could provide an entirely new tool to combat the flu. The discovery is a one-two punch against the illness that targets the illness on two fronts, going one critical step further than any currently available flu drug.

"We have been fortunate with H1N1 because it has been responding well to available drugs. But if the virus mutates substantially, the currently available drugs might be ineffective because they only target one portion of the virus," said Robert Linhardt, the Ann and John H. Broadbent Jr. '59 Senior Constellation Professor of Biocatalysis and Metabolic Engineering at Rensselaer. "By targeting both portions of the virus, the H and the N, we can interfere with both the initial attachment to the cell that is being infected and the release of the budding virus from the cell that has been affected".

The findings of the team, which have broad implications for future flu drugs, will be featured on the cover of the June edition of European Journal of Organic Chemistry........

Posted by: Mark      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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