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December 23, 2005

How Brain Replenishes Memory-making Molecules

How Brain Replenishes Memory-making Molecules Image credit: Credit: Pamela England, UCSF
New research on living neurons has clarified how the brain refreshes the supply of molecules it needs to make new memories.

The discovery by researchers at UCSF is reported today in the December 22 issue of the journal Neuron and is featured on the journal's cover.

Memory formation is thought to involve a strengthening of the communication between neurons in the part of the brain known as the hippocampus. Scientists know that this increased communication results from a surge in the number of receptors on one neuron that is available to bind to the neurotransmitter glutamate released from another neuron. The two neurons meet at a synapse.

But how and from where the brain gains fresh supplies of these crucial receptors has remained unclear. Known as AMPA receptors, they are essential for the rapid connections made between nerves during learning.

The researchers sought to answer this question by studying the basal trafficking of receptors -- the normal process by which receptors are replaced from fresh stores that are synthesized and located inside the cell. Focusing on live neurons cultured from rats, they discovered clear evidence to dispel the prevailing view that receptors at the synapse are constantly being replaced by stores inside the cell. Rather, the researchers found that the synaptic receptors are relatively stable, lasting about 16 hours before they are replaced.

The study also supports an unsuspected route by which new receptors make their way to the synapse: Fresh AMPA receptors appear to be placed on the cell surface at the cell body and then migrate along the arms or dendrites of the cell to synapses, rather than moving within the cell to the synapse as had been thought.

The researchers suspect the trafficking process their research revealed also occurs during learning and memory formation, but at a much faster rate. The study may provide insight into how to treat memory disorders, said Pam England, PhD, assistant professor of pharmaceutical chemistry at UCSF and senior author on the study.........

Daniel      Permalink


December 21, 2005

Genes Related To Alcoholism

Genes Related To Alcoholism
Scientists have found in a study of tobacco users that their drinking behavior is linked to some of the same chromosome regions associated with alcohol addiction.

The study, published in the January issue of the journal Alcoholism: Clinical and Experimental Research, offers evidence that the interaction between smoking and alcohol consumption may partly be due to overlapping genetic risk factors.

The results also provide further confirmation that alcoholism is a complex behavior drawing from both environmental and genetic factors.

"Since we know that people who drink often smoke and that smokers often drink, we thought it reasonable to collect some information about the drinking behavior in these families," said lead study author Dr. Kirk C. Wilhelmsen, associate professor in the departments of genetics and neurology at the University of North Carolina at Chapel Hill's School of Medicine.

He also is a member of the Carolina Center for Genome Sciences, the Bowles Center for Alcohol Studies and the UNC Lineberger Comprehensive Cancer Center.

The research team studied 158 families that had at least two first-degree relatives who had smoked 100 or more cigarettes in their lifetime. These included any combination of parents, siblings and offspring who had smoked.

A detailed questionnaire was used to search for alcohol-related behavioral traits, or phenotypes, shared within each family. Questions concerned the quantity of alcohol consumed, such as the number of alcohol drinks per month for six consecutive months and the number of alcohol of drinks consumed in a typical week and typical day.

DNA from blood samples taken from each family participant was analyzed for particular genetic variations. "We looked for excess chromosome sharing of regions that had genes that affect patterns of drinking behavior," Wilhelmsen said.........

JoAnn      Permalink


December 21, 2005, 9:09 PM CT

Beta Blockers Not Effective in Cirrhosis

Beta Blockers Not Effective in  Cirrhosis Roberto Groszmann, M.D
Beta blockers are not effective in preventing development of varices-veins in the esophagus that can rupture and bleed-as a consequence of cirrhosis, according to a recent study by Yale School of Medicine scientists in the New England Journal of Medicine.

Cirrhosis of the liver is the seventh leading cause of death in persons between the ages of 25-65. One of the main consequences of cirrhosis is the development and rupture of varices, which account in large part for the mortality associated with cirrhosis.

One of the lead authors of the study, Roberto Groszmann, M.D, professor in the Department of Internal Medicine, Section of Digestive Diseases, said beta blockers are routinely prescribed to prevent rupture of the varices, but some practitioners also prescribe beta blockers to all patients with cirrhosis, whether or not they have varices. This study examined the effects of beta blockers in the latter situation.

The study enrolled 213 patients of which 108 received the beta blocker timolol and 105 received a placebo. The patients were followed for five years. Forty percent of the patients developed varices, but there were no differences between the beta blocker and the placebo groups.

"Additionally, patients that received the beta blocker had more side effects, a number of of which were serious," Groszmann said. "The findings of this study clearly do not support the use of beta blockers in patients who have cirrhosis without varices since the risks far outweigh the benefits".

He said another important finding of the study was that the development of varices depended on how high the portal vein pressure was at the beginning of the study and how much it could be lowered. The portal vein takes blood to the liver. The pressure is elevated in cirrhosis and leads to the development of varices.........

Scott      Permalink


December 21, 2005

Novel mechanism for blood disease

Novel mechanism for blood disease
Approximately 80,000 to 100,000 people in the United States suffer from myeloproliferative disease, a broad category of ailments characterized by overproduction of different types of blood cells. Often these diseases lead to cancers of blood cells. Scientists at Whitehead Institute for Biomedical Research and Brigham and Women's Hospital have discovered an unusual mechanism underlying this condition, and their findings may lay the foundation for future drug development.

As people age, their genes acquire mutations. In a patient with myeloproliferative disease, a mutation occurs in a specific kind of protein called a kinase, that is, a protein that adds a small molecule called a phosphate to other proteins, in this case proteins involved in blood-cell growth. But the mutation alone will not produce the disease. The mutant kinase, named JAK2V617F, causes the condition only after binding to another molecule. This makes myeloproliferative disease an unusual disease of overproduction of cells, since a number of other kinase mutations lead directly to cell proliferation.

"Surprisingly, this mutant kinase is completely dependent on a cell-surface protein for its transforming potential," says Whitehead Member Harvey Lodish, whose lab made the discovery in collaboration with D. Gary Gilliland of Brigham and Women's. Their results will be published online in Proceedings of the National Academy of Sciences during the week of December 19.

"This paper provides new and important insights into how this gene contributes to the development of myeloproliferative disease and it should provide an important foundation for subsequent development of new drugs," says Gilliland, who is also a Howard Hughes Medical Institute investigator.

Gilliland's lab was one of several to identify the precise genetic mutation responsible for myeloproliferative disease when they discovered that the exact same genetic mutation in a kinase called JAK2 causes many distinct disorders that fall under the myeloproliferative disease umbrella. After publishing this finding in Cancer Cell in April, Gilliland turned to Lodish lab researchers, who designed experiments that shed light on the mechanism behind the disease.........

Daniel      Permalink


December 20, 2005

Promise For Mending Broken Heart

Promise For Mending Broken Heart
More Stem Cell research news from UW-MadisonWorking with heart attack-stricken mice, a team of UW-Madison researchers has shown that embryonic stem cells may one day live up to their clinical promise.

In a paper would be published in the January 2006 issue of the Journal of Molecular and Cellular Cardiology, a team led by UW-Madison stem cell researcher and heart specialist Timothy J. Kamp reports that all-purpose embryonic stem cells, transplanted into mouse hearts damaged by experimentally induced heart attacks, shift gears and morph into functional forms of the major types of cells that compose the healthy heart.

The study's results are important because they demonstrate that blank-slate embryonic stem cells can be introduced to damaged heart tissue, develop into heart muscle and into cells that form the heart's blood vessels. If perfected, such treatment could provide a practical, less-invasive alternative to current therapies such as surgery, improve the quality of life for a number of patients and reduce the number of deaths attributed to heart disease, now estimated at about 700,000 deaths per year in the United States.

"Typically, when that heart muscle dies (as the result of heart attack), it is gone for good," says Kamp, a professor of medicine and physiology in the UW-Madison School of Medicine and Public Health.

In their experiments, when stem cells were introduced directly to tissue damaged by a heart attack, three critical types of cells formed: cardiomyocytes or heart muscle; vascular smooth muscle, the muscle that forms the bulk of the walls of blood vessels; and endothelial cells, the flat cells that line the interior surfaces of blood vessels in the heart and throughout the body's circulatory system.

"There are multiple components," Kamp explains. "But (in these experiments) we see the three most important types of cells forming. It didn't completely repair the heart, but it was encouraging."........

Scott      Permalink


December 20, 2005

Sneaking Drugs Into The Brain

Sneaking Drugs Into The Brain
One of the great challenges for treating Parkinson's diseases and other neurodegenerative disorders is getting medicine to the right place in the brain.

The brain is a complex organ with a number of different types of cells and structures, and it is fortified with a protective barrier erected by blood vessels and glial cells - the brain's structural building blocks - that effectively blocks the delivery of most drugs from the bloodstream.

But now researchers have found a new way to sneak drugs past the blood-brain barrier by engineering and implanting progenitor brain cells derived from stem cells to produce and deliver a critical growth factor that has already shown clinical promise for treating Parkinson's disease.

Writing today in the journal Gene Therapy, UW-Madison neuroscientist Clive Svendsen and colleagues describe experiments that demonstrate that engineered human brain progenitor cells, transplanted into the brains of rats and monkeys, can effectively integrate into the brain and deliver medicine where it is needed.

The Wisconsin team obtained and grew large numbers of progenitor cells from human fetal brain tissue. They then engineered the cells to produce a growth factor known as glial cell line-derived neurotrophic factor (GDNF). In some small but promising clinical trials, GDNF showed a marked ability to provide relief from the debilitating symptoms of Parkinson's. But the drug, which is expensive and hard to obtain, had to be pumped directly into the brains of Parkinson's patients for it to work, as it is unable to cross the blood-brain barrier.

In an effort to develop a less invasive strategy to effectively deliver the drug to the brain, Svendsen's team implanted the GDNF secreting cells into the brains of rats and elderly primates. The cells migrated within critical areas of the brain and produced the growth factor in quantities sufficient for improving the survival and function of the defective cells at the root of Parkinson's.........

Daniel      Permalink


December 20, 2005

Protein Responsible For Shaping The Nervous System

Protein Responsible For Shaping The Nervous System
A team of scientists led by The Hospital for Sick Children (SickKids), the University of Toronto (U of T) and Cold Spring Harbor Laboratory have discovered a protein that is responsible for shaping the nervous system. This research was made possible with the support of a $1.5-million NeuroScience Canada Brain Repair Program team grant that enabled researchers from across Canada to work together and fast track their research. This research is reported in the December 8, 2005 issue of the journal Neuron.

"We discovered that p63 is the major death-promoting protein for nerve cells during fetal and post-natal development," said Dr. David Kaplan, the paper's senior author, senior scientist at SickKids, professor of Molecular Genetics, Medical Genetics and Microbiology at U of T, Canada Research Chair in Cancer and Neuroscience, and co-team leader on the NeuroScience Canada Brain Repair Program grant with Dr. Freda Miller of SickKids. "Proteins such as p63 that regulate beneficial cell death processes during development may cause adverse affects later in life by making us more sensitive to injury and disease".

At birth, the nervous system has twice the number of nerve cells than needed. The body disposes of the excess cells by eliminating those that go to the wrong place or form weak or improper connections. If this process does not happen, the nervous system cannot function properly. The expression of the p63 protein guides the nervous system in disposing of the ineffective nerve cells. The protein is from the p53 family of tumour suppressor proteins that is mutated in a number of human cancers.

While p63 is involved in determining which nerve cells die, the research team also suspects that it determines whether nerve cells die when injured or in neurological and neurodegenerative diseases such as Alzheimer's and Parkinson's diseases.........

Daniel      Permalink


December 20, 2005

Genetics May Guide New Infertility Therapies

Genetics May Guide New Infertility Therapies
Rutgers geneticists have reported groundbreaking research on the genetics of fertility. They have discovered two genes, aptly named egg-1 and egg-2, mandatory for fertilization to take place. The proteins encoded by these genes are similar to low density lipoprotein (LDL) receptors, known from cholesterol and fat metabolism but never before specifically implicated in fertilization.

One in six couples is experiencing fertility problems worldwide, and people are asking why. This is a question of great medical, social and economic importance - one that cannot be answered until the process of fertilization is more fully understood.

A team led by Andrew Singson, an assistant professor and Pavan Kadandale, a graduate student in the Singson lab at the Waksman Institute of Microbiology at Rutgers, The State University of New Jersey, has taken a new and productive approach in this quest. The scientists found that in the absence of these two genes, the vital process of fertilization came to a halt. "What we learn in studying fertilization is not only important for this event, but also for the functioning of other cells in our bodies and for understanding a number of of those processes," Singson said.

Fertilization can be a paradigm for gaining insight into how cells interact over the life and development of multicellular organisms because it is one of the most basic of cell-cell interactions. The underlying cell biology is going to be universal with applications even in infectious diseases, such as AIDS, where the virus passes its genetic material to the cells it infects just as fertilization transmits sperm DNA to the egg, Singson explained.

Fertilization has primarily been studied in mammals or select marine invertebrates; but Singson and his group have instead turned to the lowly roundworm Caenorhabditis elegans (C. elegans), the first multicellular organism to have had its genome completely sequenced.........

Emily      Permalink


December 19, 2005

New Look At Gene Regulation

New Look At Gene Regulation
Researchers at the University of North Carolina at Chapel Hill have purified a novel protein and have shown it can alter gene activity by reversing a molecular modification previously thought permanent.

In the study, the authors showed that a protein called JHDM1A is able to remove a methyl group from histone H3, one of four histone proteins bound to all genes. Until just last year, the addition of a methyl group to a histone had been regarded as irreversible.

"That histones can become methylated has been known for over three decades, and just now we're learning that those methyl groups can also be removed," said Dr. Yi Zhang, the lead author.

Zhang is professor of biochemistry and biophysics at UNC's School of Medicine and the university's first Howard Hughes Medical Institute investigator. He also is a member of the UNC Lineberger Comprehensive Cancer Center.

The new study is now online in the journal Nature.

"Human genes are so tightly compact within the nucleus that if the DNA of a single cell were unwound and stretched, it would be a line of about two meters in length," said Zhang. "Histones are necessary to package the DNA so that it fits inside a cell's nucleus".

Because they are so intimately associated with DNA, even slight chemical alterations of histones can have profound effects on nearby genes. Depending on the precise location and how a number of methyl groups are added, their presence can either switch affected genes on or off.

The first enzyme to remove methyl groups from histones, or histone demethylase, was identified last year. This was a breakthrough in the study of histone modifications, but Zhang thought pieces of the puzzle were still missing.

"We hypothesized that there were more demethylase enzymes out there for two reasons," Zhang said. "For one, the prior demethylase identified, called LSD1, could not remove a chain of three methyl groups from a histone, or a trimethyl group. Secondly, common baker's yeast does not have LSD1, eventhough it does have proteins adding methyl groups to histones".........

Scott      Permalink


December 18, 2005

Eye Cell Implants Improve Motor Symptoms

Eye Cell Implants Improve Motor Symptoms
A preliminary study suggests that implants of cells from the human retina improved motor symptoms in patients with Parkinson disease, and they appear to be safe and well tolerated, according to a report in the recent issue of the Archives of Neurology, one of the JAMA/Archives journals.

Parkinson disease (PD) is a neurodegenerative disorder characterized by tremor, rigidity, postural instability, and slowed ability to start and continue movements. Most patients with PD require treatment with the medicine levodopa to control symptoms three to five years after a diagnosis of PD. However, disease progression and long-term oral therapy with levodopa may lead to the development of motor fluctuations and dyskinesias (difficulty or distortion in performing voluntary movements). Human retinal pigment epithelial (RPE) cells produce levodopa and can be isolated from post mortem human eye tissue, grown in culture, and implanted into the brain attached to microcarriers. These implants have ameliorated the motor deficits in animal models of Parkinson disease, according to background information in the article. (The retinal pigment epithelium is the pigment cell layer found in the inner layer of the retina of the eye.)

Natividad P. Stover, M.D., of the University of Alabama at Birmingham, and his colleagues conducted an open-label pilot study to evaluate the effect of unilateral implantation of human RPE cells attached to gelatin microcarriers. Six patients with advanced Parkinson disease received cell implants, which were inserted into the brain tissue. The scientists performed efficacy evaluations at one and three months after surgery, and then at six, nine, 12, 15, 18 and 24 months. Yearly follow-up visits are ongoing and will continue.

"The implants were well tolerated," the authors report. "We observed an average improvement of 48 percent at 12 months after implantation in the Unified Parkinson's Disease Rating Scale motor subscore with the patient in the off state, which was sustained through 24 months." .........

Mike      Permalink



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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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