June 16, 2009, 5:03 AM CT

RNA snippet suppresses spread of aggressive breast cancer

A low cellular level of a tiny fragment of RNA appears to increase the spread of breast cancer in mouse models of the disease, as per scientists at Whitehead Institute for Biomedical Research.

Measuring levels of this so-called microRNA, which is also linked to metastatic breast cancer in humans, may more accurately predict the likelihood of metastasis (which accounts for 90% of cancer-related deaths) and ultimately help determine patient prognoses.

In the study, whose results are published in the June 12 issue of Cell, Scott Valastyan, a graduate student in Whitehead Member Robert Weinberg's laboratory, screened patient breast cancer samples for microRNAs with potential roles in metastasis. MicroRNAs are single strands of RNA about 21-23 nucleotides long. Within a cell, a single microRNA can fine-tune the expression of dozens of genes simultaneously. This capability could be especially important in metastasis, a multi-step process that could be influenced by a single microRNA at several points.

The screened samples were classified as either metastatic cancer or non-metastatic cancer. After analysis, the microRNA miR-31 stood out because of its inverse correlation with metastasis. In samples where a patient's original tumor had not metastasized, the cancer cells retained high levels of the microRNA. But where the tumor had metastasized, the cancer cells came to possess lower levels of miR-31......... Posted by: Janet      Read more         Source

June 12, 2009, 5:22 AM CT

Gene therapy technique for cancer by cutting off blood supply

University of Florida scientists have come up with a new gene treatment method to disrupt cancer growth by using a synthetic protein to induce blood clotting that cuts off a tumor's blood and nutrient supply.

In mice implanted with human colorectal cancer cells, tumor volume decreased 53 percent and cancer cell growth slowed by 49 percent in those treated with a gene that encodes for the artificial protein, compared with those that were untreated.

The research team, led by Dr. Bradley S. Fletcher, an assistant professor of pharmacology and therapeutics in the College of Medicine, created the so-called fusion protein to target another protein called tumor endothelial marker 8, or TEM8, which was recently found to be preferentially expressed in the inner lining of tumor vessels. Such differences in protein expression enable delivery of drug molecules to the cells that harbor these proteins.

"The protein we created did a very good job of homing to the tumor and binding," said Stephen Fernando, who recently completed his doctoral studies. "By targeting TEM8, we can potentially create a treatment against cancer".

The Fletcher group is the first to target cancer cells through protein binding to TEM8. The findings, now available online, are featured on the cover of the June 15 edition of Cancer Research........ Posted by: Janet      Read more         Source

June 12, 2009, 5:20 AM CT

Simple chemical system that mimics DNA

A team of Scripps Research researchers has created a new analog to DNA that assembles and disassembles itself without the need for enzymes. Because the new system comprises components that might reasonably be expected in a primordial world, the new chemical system could answer questions about how life could emerge.

The work, published in the June 11, 2009 issue of Science Express, an advance, online publication of the journal Science, might also be a starting point on the way to exotic new materials that repair themselves or transform in response to their environment.

Researchers are both bemused and fascinated by the question of how life could have arisen on Earth. One of the most prominent theories is that, before the emergence of DNA, the earliest forms of life used RNA to transmit their genetic codes. The late Leslie Orgel, a co-author of the new paper, first suggested this idea, known as the "RNA World".

One of the theory's challenges is that RNA is still so complex that a number of scientists believer something still simpler must have preceded it. "I have been working for years to learn what replicators and genetic systems might have come before the advent of the RNA World," says team leader of the new research Professor Reza Ghadiri, a Scripps Research chemist......... Posted by: Scott      Read more         Source

June 11, 2009, 5:15 AM CT

What causes multiple sclerosis?

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

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

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

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

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

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

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

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

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

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

May 19, 2009, 5:02 AM CT

DNA patterns of cancer and genetic disorders

A new tool will help scientists identify the minute changes in DNA patterns that lead to cancer, Huntington's disease and a host of other inherited disorders. The tool was developed at North Carolina State University and translates DNA sequences into graphic images, which allows scientists to distinguish genetic patterns more quickly and efficiently than was historically possible using computers.

David Cox, a Ph.D. student in computer science at NC State, devised the "symbolic scatter plot" tool to provide a visual representation of a DNA sequence. Cox explains, "The human visual system is more adept at identifying patterns, and differentiating between patterns, than existing computer programs such as those that try to identify repetitions of DNA sequences." In other words, the naked eye sees patterns better than computers can.

Identifying patterns in a sequence of DNA is important because it can help scientists identify the minute genetic variations between subjects that suffer from a disease, such as cancer, and subjects that do not. "Improved identification of relevant DNA sequences will hopefully expedite the development of successful therapy for a range of diseases," Cox says, "by allowing scientists to focus on the components of DNA that are correlation to the disease and improving our understanding of the genetic mechanisms of these diseases. For example, what turns specific genes on and off?"......... Posted by: Janet      Read more         Source

April 30, 2009, 5:14 AM CT

Tiny differences in our genes make the big picture

By examining very small differences in people's genes, researchers from Cornell University have developed a new tool for identifying big events in human history and pinpointing the origins of specific gene mutations. This research, reported in the recent issue of the journal GENETICS (http://www.genetics.org), helps shed light on times when the human population moved close to extinction and helps researchers close in on gene mutations that make some demographic groups more likely to develop diseases such as cancer, heart disease, diabetes, among others.

"We know that a number of diseases are caused by a combination of genetic and environmental factors," said Kirk E. Lohmueller, one of the scientists involved in the work from Cornell University. "To find the genes that contribute to disease, it's very helpful to know the demographic history of the population being studied. Accurate estimates of population events help inform the search for mutations that might have been helpful and necessary for survival at the time, but no longer necessary and potentially harmful today".

In their work, Lohmueller and his colleagues confirmed the existence of a major decline in European populations (called a "bottleneck") 32,500-47,500 years ago. They used computer simulations to model the expected correlation among segments of DNA containing very small genetic mutations that only involve a single letter of the genetic code (called "single nucleotide polymorphisms" or SNPs). Previous to this development, methods used to identify major population events relied on the frequency patterns of individual SNPs, while ignoring the patterns of specific groups of SNPs. This work shows that looking at groups of SNPs helps us better understand what happened long before there was a human historical record......... Posted by: Janet      Read more         Source

April 29, 2009, 5:23 AM CT

New gene variant for autism

UCLA scientists, in partnership with 30 research institutions across the country, have identified a new gene variant that is highly common in autistic children. And when scientists scrutinized the activity of the gene, known as CDH10, in the fetal brain, they discovered that it is most active in key regions that support language, speech and interpreting social behavior.

Published April 28 in the advance online edition of the journal Nature, the two findings suggest that CDH10 plays a critical role in shaping the developing brain and may contribute to a prenatal risk of autism.

A variant is a gene that has undergone subtle changes from the normal DNA yet is shared by a significant portion of the population.

"While this gene variant is common in the general population, we discovered that it occurs about 20 percent more often in children with autism," said study author Dr. Daniel Geschwind, director of the UCLA Center for Autism Treatment and Research. "A major change like this in the genetic code is too common to be a simple mutation it is a risk factor in the origin of the disease."

Using the largest population sample to date, the researchers systematically scanned the DNA of 3,100 individuals from 780 families nationwide. Each family had at least two autistic children......... Posted by: Scott      Read more         Source

April 29, 2009, 5:02 AM CT

Preventing migraine

When migraine strikes, because of severe pain, often accompanied by nausea and sensitivity to light and sound, sufferers are effectively disabled for up to 72 hours. Since they are forced to stop what they are doing until the pain and other symptoms subside, migraine causes a significant loss in productivity at work and the personal lives of those affected. Migraineurs particularly the 25% of migraineurs who experience more than three migraine attacks per month are looking to drug developers to provide new drugs to prevent migraine attacks before they start. In the U.S. alone, approximately 30 million people suffer from migraines and the cost to employers has been estimated at $13 billion annually in lost productivity. Currently, several types of drugs, like generic beta blockers, calcium channel blockers, tricyclic antidepressants and anti-epileptic drugs, some of which are used off-label, are given to prevent migraines. However, a number of patients have only a partial response to these products, a number of of which have troubling side effects. Nevertheless, a number of migraine patients use existing drugs, illustrating how badly new drugs are needed.

Given the role of glutamate in the pathophysiology of migraine, the future of migraine prophylaxis, may lie in modulating one of the receptors in the glutamate system, mGluR5......... Posted by: Daniel      Read more         Source

April 28, 2009, 5:23 AM CT

Novel role of protein in generating amyloid-beta peptide

A defining hallmark of Alzheimer's disease is the accumulation of the amyloid β protein (Aβ), otherwise known as "senile plaques," in the brain's cortex and hippocampus, where memory consolidation occurs. Scientists at the University of California, San Diego School of Medicine have identified a novel protein which, when over-expressed, leads to a dramatic increase in the generation of Aβ. Their findings, which indicate a potential new target to block the accumulation of amyloid plaque in the brain, would be reported in the May 1 issue of the Journal of Biological Chemistry

"The role of the multi-domain protein, RANBP9, suggests a possible new therapeutic target for Alzheimer's disease," said David E. Kang, PhD, assistant professor of neurosciences at UC San Diego and director of this study.

The neurotoxic protein Aβ is derived when the amyloid precursor protein (APP) is "cut" by two enzymes, β-secretase (or BACE) and γ-secretase (or Presenilin complex.) However, inhibiting these enzymes in order to stop the amyloid cascade has a number of negative side effects, as these enzymes also have various beneficial uses in brain cells. So the scientists looked for an alternative way to block the production of amyloid beta.

In order for cleavage to occur, the APP needs to travel to cholesterol-enriched sites within the cell membrane called RAFTS, where APP interacts with the two enzymes. It is this contact that the scientists sought to block......... Posted by: Daniel      Read more         Source

April 24, 2009, 5:12 AM CT

Major advance in cell reprogramming

In a paper publishing online April 23rd in Cell Stem Cell, a Cell Press journal, Dr. Sheng Ding and his colleagues from the Scripps Research Institute in La Jolla, California, report an important step forward in the race to make reprogrammed stem cells that appears to be better suited for use in clinical settings.

Ding and colleagues show that mouse cells can be reprogrammed to form stem cells with a combination of purified proteins and a chemical additive, thus avoiding the use of genetic material.

The discovery three years ago that adult cells could be reprogrammed to form induced pluripotent stem cells, or iPS cells, with similar properties to embryonic stem cells was a major scientific breakthrough. These cells hold enormous potential for drug development and even cell treatment processes, and this promise has garnered significant attention from researchers and the media worldwide. However, a major caveat to the eventual application of iPS cells is that until now all the methods used to generate them have mandatory the introduction of genetic material to make the transcription factors needed for reprogramming. Eventhough some research groups have recently generated iPS cells that lack genetic modifications, even the most advanced methods used genes in the form of plasmids, and thus the risk of genetic mutations caused by the introduced sequences remained......... Posted by: Scott      Read more         Source

April 24, 2009, 5:08 AM CT

Stem cells obtained from a patient's own adipose tissue for MS treatment

A preliminary study on the use of stem cells obtained from a patient's own adipose tissue in the therapy of multiple sclerosis (MS) has shown promising results. The three case studies, described in BioMed Central's open access Journal of Translational Medicine support further clinical assessment of stromal vascular fraction (SVF) cells in MS and other autoimmune conditions.

Thomas Ichim, from Medistem Inc., and Dr. Boris Minev, from the Division of Neurosurgery, University of California San Diego, worked with a team of scientists to demonstrate the possible effectiveness of SVF cells in MS therapy. Minev said, "All three patients in our study showed dramatic improvement in their condition after the course of SVF treatment. While obviously no conclusions in terms of therapeutic efficacy can be drawn from these reports, this first clinical use of fat stem cells for therapy of MS supports further investigations into this very simple and easily-implementable therapy methodology".

MS is an autoimmune condition, in which the body's own defences attack nerve cells, resulting in loss of their fatty myelin sheath. The first symptoms commonly occur in young adults, most usually in women. It is believed that SVF cells, and other stem cells, appears to be able to treat the condition by limiting the immune reaction and promoting the growth of new myelin. As per Minev, "None of the presently available MS therapys selectively inhibit the immune attack against the nervous system, nor do they stimulate regeneration of previously damaged tissue. We've shown that SVF cells may fill this therapeutic gap"......... Posted by: Daniel      Read more         Source

April 21, 2009, 5:28 AM CT

We're all pot heads deep inside

U.S. and Brazilian researchers have just proven that one of Bob Dylan's most famous lines"everybody must get stoned" is correct. That's because they've discovered that the brain manufactures proteins that act like marijuana at specific receptors in the brain itself. This discovery, published online in The FASEB Journal (http://www.fasebj.org), may lead to new marijuana-like drugs for managing pain, stimulating appetite, and preventing marijuana abuse.

"Ideally, this development will lead to drugs that bind to and activate the THC receptor, but are devoid of the side effects that limit the usefulness of marijuana," said Lakshmi A. Devi of the Department of Pharmacology and Systems Therapeutics at Mount Sinai School of Medicine in New York and one of the senior scientists involved in the study. "It would be helpful to have a drug that activated or blocked the THC receptor, and our findings raise the possibility that this will lead to effective drugs with fewer side effects".

Researchers made their discovery by first extracting several small proteins, called peptides, from the brains of mice and determining their amino acid sequence. The extracted proteins were then compared with another peptide previously known to bind to, but not activate, the receptor (THC) affected by marijuana. Out of the extracted proteins, several not only bound to the brain's THC receptors, but activated them as well......... Posted by: JoAnn      Read more         Source

April 21, 2009, 5:17 AM CT

How does lithium work in bipolar disease?

Lithium has been established for more than 50 years as one of the most effective therapys for bipolar mood disorder.

However, researchers have never been entirely sure exactly how it operates in the human brain.

Now, new research from Cardiff University researchers suggests a mechanism for how Lithium works, opening the door for potentially more effective therapys.

Laboratory tests on cells have shown that Lithium affects a molecule called PIP3 that is important in controlling brain cell signalling. Lithium suppresses the production of inositol, a simple sugar from which PIP3 is made.

Lithium inhibits inositol monophosphatase (IMPase) an enzyme mandatory for making inositol. Importantly, this research shows that increasing the amount of IMPase causes higher levels of PIP3. This can then be reduced by lithium therapy.

High levels of IMPA2, a gene for a variant of IMPase, has previously been associated with bipolar mood disorder. This new result suggests that Lithium could counteract the changes in IMPA2.

Professor Adrian Harwood of Cardiff School of Biosciences, who led the research, said: "We still cannot say definitively how Lithium can help stabilise bipolar disorder. However, our research does suggest a possible pathway for its operation. By better understanding Lithium, we can learn about the genetics of bipolar disorder and develop more potent and selective drugs......... Posted by: JoAnn      Read more         Source

April 16, 2009, 5:07 AM CT

How Alzheimer's destroy brain cells

For a decade, Alzheimer's disease scientists have been entrenched in debate about one of the mechanisms thought to beresponsible for brain cell death and memory loss in the illness.

Now scientists at the University of Michigan and the University of California, San Diego have settled the dispute. Resolving this controversy improves understanding of the disease and could one day lead to better therapys.

Michael Mayer, an assistant professor in the U-M departments of Biomedical Engineering and Chemical Engineering, and Jerry Yang, an assistant professor in the Department of Chemistry and Biochemistry at UCSD, and their colleagues found a flaw in earlier studies supporting one side of the debate. Their findings are published online in the Journal of Neurotoxicity Research They will appear in the May print edition.

Their results clarify how small proteins called amyloid-beta peptides damage brain cell membranes, allowing extra calcium ions to enter the neurons. An ion is an electrically-charged particle. An ion imbalance in a cell can trigger its suicide.

Amyloid-beta peptides are the prime suspects for causing cell death in Alzheimer's, eventhough other mechanisms could also be to blame. The disease is not well understood.

The scientists confirmed evidence found by others that amyloid-beta peptides prick pores into brain cell membranes, opening channels where calcium ions can rush in. This was one mechanism the field had contemplated, but other evidence suggested a different scenario. Some scientists believed that the peptide caused a general thinning of the cell membranes and these thinned membranes lost their ability to keep calcium ions out of brain cells. Mayer and Yang disproved this latter theory......... Posted by: Daniel      Read more         Source