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December 4, 2007, 9:48 PM CT

Protein controls blood vessel formation

Protein controls blood vessel formation
Image courtesy of people.bath.ac.uk
After an injury, the body grows new blood vessels to repair damaged tissue. But sometimes too much growth causes problems, as when new blood vessels in the eyes leak, causing diabetic retinopathy and blindness if not treated.

A protein called CIB1 discovered by scientists at the University of North Carolina at Chapel Hill School of Medicine appears to play a major role in controlling new blood vessel growth, offering a target for drug therapys to help the body repair itself after injury and control unwanted blood vessel growth.

In the future, this knowledge may help our ability to control blood vessel growth in disease situations such as wound healing, retinal diseases and diabetes, said Leslie Parise, Ph.D., senior study author and professor and chair of biochemistry and biophysics in the UNC School of Medicine.

The results will appear in an upcoming print issue of the journal Circulation Research and were published online Nov. 1, 2007. The research was funded by the National Institutes of Health.

Parises lab first discovered the protein, called CIB1 in 1997. It was originally found in blood platelets. CIB1 keeps blood platelets from sticking together, acting as a natural anti-coagulant to prevent clots that might lead to heart attacks or strokes. But further research showed CIB1 appears in almost every cell type in the body, Parise said. For example, male mice bred without both copies of the CIB1 gene are infertile.........

Posted by: Scott      Read more         Source


December 3, 2007, 10:18 PM CT

Novel genes for schizophrenia

Novel genes for schizophrenia
Researchers at the Zucker Hillside Hospital campus of the Feinstein Institute for Medical Research have identified nine genetic markers that can increase a persons risk for schizophrenia. As per a research findings published this week in the Proceedings of the National Academy of Sciences, the research team uncovered original evidence that this disabling brain disease can be inherited in a recessive manner. A recessive trait is one that is inherited from both parents.

If a person inherits identical copies of these markers from each parent, his or her risk for schizophrenia increases substantially, said Todd Lencz, PhD, associate director of research at Zucker Hillside and the lead author of the study. If these results are confirmed, they could open up new avenues for research in schizophrenia and severe mental illness, said Anil Malhotra, MD, director of psychiatric research at Zucker Hillside and senior investigator of the study.

The researchers developed a complex mathematical approach called whole genome homozygosity association (WGHA) that provides a new way of analyzing genetic information. It enables researchers to simultaneously look at genetic information derived from the patients mother and father, and identify pieces of chromosomes that are identical. They tested genetic material from 178 patients and 144 controls.........

Posted by: JoAnn      Read more         Source


December 2, 2007, 8:47 PM CT

Broccoli against devastating genetic skin disorder

Broccoli against devastating genetic skin disorder
The compound sulforaphane whose natural precursors are found at high levels in broccoli and other cruciferous vegetables has been hailed for its chemopreventive powers against cancer. Now sulforaphane has demonstrated new skills in treating a genetic skin blistering disorder called epidermolysis bullosa simplex (EBS), Pierre Coulombe and his colleagues at the Johns Hopkins University School of Medicine in Baltimore report at the American Society for Cell Biology 47th Annual Meeting.

EBS is a rare but devastating inherited condition in which fluid-filled lesions called bullae appear at sites of frictional trauma to the skin. Unfortunately, therapy options for EBS are limited and palliative in nature. Much work remains to be done before sulforaphane can be tested clinically with EBS patients, but Coulombe notes that extracts from broccoli sprouts rich in sulforaphane have already been shown to be safe for use in human skin.

In EBS patients, the bottom layer of the epidermis, which is made of cells called keratinocytes, is uncommonly fragile and ruptures readily. Molecularly, most cases of EBS result from mutations in genes that produce the proteins keratin 5 (K5) and keratin 14 (K14). These proteins co-polymerize to form the intermediate filament cytoskeleton in basal keratinocytes. Since the discovery in 1991 that EBS is a keratin-based disease, more than 40 additional disorders affecting a broad range of tissues have been traced to defects in genes that encode intermediate filament proteins.........

Posted by: George      Read more         Source


December 2, 2007, 8:43 PM CT

Leading cause of death in 'preemies' might be controlled

Leading cause of death in 'preemies' might be controlled
Blocking signals from a key molecular receptor that normally switches on the intestines immune response but instead becomes too intense in the presence of stress and toxins may help reverse necrotizing enterocolitis (NEC), a leading cause of death in premature newborns, as per researchers at the American Society for Cell Biology 47th annual meeting.

David J. Hackam and his laboratory team at the Childrens Hospital of Pittsburgh report that neonatal mice with inactivating mutations in the Toll-like receptor 4 (TLR4) are protected from NEC. Its a case of defenders becoming unwitting attackers, says Hackam.

Toll-like receptors are key players in the innate immune system. Protruding from enterocytes that form the innermost barrier-like layer of the small and large intestines, TLR4 receptors are primed to recognize pathogenic bacteria and sound the alarm.

But Hackams group observed that the stresses of oxygen deprivation and bombardment by bacterial toxins, conditions that can occur in premature infants with underdeveloped lungs, stimulate too much production of TLR4. Like an unstoppable alarm, the increased numbers of TLR4 blare out signals that eventually tip the cells into cellular suicide. They also stop enterocytes from migrating to close wounds in the intestines.........

Posted by: JoAnn      Read more         Source


December 2, 2007, 8:39 PM CT

Embryonic stem cell closes massive skull injury

Embryonic stem cell closes massive skull injury
There are mice in Baltimore whose skulls were made whole again by bone tissue grown from human embryonic stem cells (hESCs).

Healing critical-size defects (defects that would not otherwise heal on their own) in intramembraneous bone, the flat bone type that forms the skull, is a vivid demonstration of new techniques devised by researchers at John Hopkins University to use hESCs for tissue regeneration.

Using mesenchymal precursor cells isolated from hESCs, the Hopkins team steered them into bone regeneration by using scaffolds, tiny, three-dimensional platforms made from biomaterials.

Physical context, it turns out, is a powerful influence on cell fate. Nathaniel S. Hwang, Jennifer Elisseeff, and colleagues at Hopkins demonstrated that by changing the scaffold materials, they could shift mesenchymal precursor cells into either of the bodys osteogenic pathways: intramembraneous, which makes skull, jaw, and clavicle bone; or endochondral, which builds the long bones and involves initial formation of cartilage, which is then transformed into bone by mineralization.

Mesenchymal precursor cells grown on an all-polymer, biodegradable scaffold followed the endochondral lineage. Those grown on a composite scaffold made of biodegradable polymers and a hard, gritty mineral called hydroxyapatite went to the intramembraneous side.........

Posted by: Scott      Read more         Source


November 29, 2007, 10:42 PM CT

New treatment for age-related macular degeneration

New treatment for age-related macular degeneration
With 8 million people at high risk for advanced age-related macular degeneration, scientists from Harvard and Japan discovered that the experimental drug, endostatin, may be the cure. A research report reported in the December 2007 issue of The FASEB Journal, describes how giving endostatin to mice significantly reduced or eliminated abnormal blood vessel growth within the eye, which is ultimately why the disease causes blindness.

Our study provides intriguing findings that may lead to a better therapy of age-related macular degeneration, said Alexander Marneros, the first author of the report, but clinical studies in patients with age-related macular degeneration are still necessary.

In this study, scientists describe testing the effects of endostatin on mice lacking this naturally occurring substance. The mice without endostatin were about three times more likely to develop advanced age-related macular degeneration (AMD) than normal mice. Then the scientists administered endostatin to both sets of mice. In the mice lacking endostatin, the number of abnormal blood vessels that cause AMD were reduced to normal levels. In control mice with normal levels of endostatin, the number of abnormal blood vessels were practically undetectable.

With Baby Boomers reaching advanced ages, new therapys are desperately needed to keep age-related macular degeneration from becoming a national epidemic, said Gerald Weissmann, MD, Editor-in-Chief of The FASEB Journal. This research provides hope for those at risk for blindness, and it gives everyone another glimpse of how investments in molecular biology will ultimately pay off in terms of new therapys and cures.........

Posted by: Mike      Read more         Source


November 28, 2007, 9:47 PM CT

A molecular map for aging in mice

A molecular map for aging in mice
Scientists at the National Institute of Aging and Stanford University have used gene arrays to identify genes whose activity changes with age in 16 different mouse tissues. The study, published November 30 in PLoS Genetics, uses a newly available database called AGEMAP to document the process of aging in mice at the molecular level. The work describes how aging affects different tissues in mice, and ultimately could help explain why lifespan is limited to just two years in mice.

As an organism ages, most tissues change their structure (for example, muscle tissues become weaker and have slow twitch rather than fast twitch fibers), and all tissues are subject to cellular damage that accumulates with age. Both changes in tissues and cellular damage lead to changes in gene expression, and thus probing which genes change expression in old age can lead to insights about the process of aging itself.

Prior studies have studied gene expression changes during aging in just one tissue. The new work stands out because it is much larger and more complete, including aging data for 16 different tissues and containing over 5.5 million expression measurements.

One noteworthy result is that some tissues (such as the thymus, eyes and lung) show large changes in which genes are active in old age whereas other tissues (such as liver and cerebrum) show little or none, suggesting that different tissues may degenerate to different degrees in old mice.........

Posted by: Scott      Read more         Source


November 27, 2007, 9:56 PM CT

Decoding Genomes Of Tuberculosis Bacteria

Decoding Genomes Of Tuberculosis Bacteria
An international collaboration led by scientists in the US and South Africa announced Nov. 20 the first genome sequence of an extensively drug resistant (XDR) strain of the bacterium Mycobacterium tuberculosis, one associated with more than 50 deaths in a recent tuberculosis (TB) outbreak in KwaZulu-Natal, South Africa.

As part of this work, genomes of multi-drug resistant (MDR) and drug sensitive isolates were also decoded. Initial comparisons of the genome sequences reveal that the drug-resistant and drug-sensitive microbes differ at only a few dozen locations along the four-million-letter DNA code, revealing some known drug resistance genes as well as some additional genes that may also be important to the spread of TB.

The scientists have taken an unusual step of immediately sharing both the genome sequence and their initial analysis far in advance of submitting a scientific paper, in order to accelerate work on drug-resistant TB by scientists around the world.

"Tuberculosis is a major threat to global public health that demands new approaches to disease diagnosis and therapy," said Megan Murray, one of the project's principal investigators, an associate member of the Broad Institute of MIT and Harvard and an associate professor at the Harvard School of Public Health. "By looking at the genomes of different strains, we can learn how the tuberculosis microbe outwits current drugs and how new drugs might be designed".........

Posted by: Mark      Read more         Source


November 26, 2007, 10:06 PM CT

Mathematician works to make virtual surgery a reality

Mathematician works to make virtual surgery a reality
A surgeon accidently kills a patient, undoes the error and starts over again. Can mathematics make such science fiction a reality? .

The day is rapidly approaching when your surgeon can practice on your "digital double" a virtual you before performing an actual surgery, as per UCLA mathematician Joseph Teran, who is helping to make virtual surgery a viable technology. The advantages will save lives, he believes.

"You can fail spectacularly with no consequences when you use a simulator and then learn from your mistakes," said Teran, 30, who joined UCLA's mathematics department in July. "If you make errors, you can undo them just as if you're typing in a Word document and you make a mistake, you undo it. Starting over is a big benefit of the simulation.

"Surgical simulation is coming, there is no question about it," he said. "It's a cheaper alternative to cadavers and a safer alternative to patients." .

How would virtual surgery work? .

"The ideal situation would be when patients come in for a procedure, they get scanned and a three-dimensional digital double is generated; I mean a digital double you on the computer, including your internal organs," Teran said. "The surgeon first does surgery on the virtual you. With a simulator, a surgeon can practice a procedure tens or hundreds of times. You could have a patient in a small town scanned while a surgeon hundreds or thousands of miles away practices the surgery. The patient then flies out for the surgery. We have to solve mathematical algorithms so what the surgeon does on the computer mimics real life." .........

Posted by: Scott      Read more         Source


November 19, 2007, 8:32 PM CT

Gene therapy normalizes brain function in Parkinson's patients

Gene therapy normalizes brain function in Parkinson's patients
Brain scans used to track changes in a dozen patients who received an experimental gene treatment show that the therapy normalizes brain function - and the effects are still present a year later.

Andrew Feigin, MD, and David Eidelberg, MD, of The Feinstein Institute for Medical Research collaborated with Michael Kaplitt, MD, of Weill Cornell Medical Center in Manhattan and others to deliver genes for glutamic acid decarboxylase (or GAD) into the subthalamic nucleus of the brain in Parkinsons patients. The study was designed as a phase I safety study, and the genes were delivered to only one side of the brain to reduce risk and to better assess the therapy.

A recently published study included the clinical results of the novel gene treatment trial, but this new report from the same study focuses on the power of modern brain scans to show that the gene treatment altered brain activity in a favorable way. This latest study is published this week in the Proceedings of the National Academy of Sciences.

The patients only received the viral vector-carrying genes to the side of the brain that controls movement on the side of their body most affected by the disease. It was a so-called open-label study -- everybody received the gene treatment so the researchers knew that there could be a placebo effect. That is why brain scans were so critical to the experiment. Dr. Eidelberg and colleagues pioneered the technology and used it to identify brain networks in Parkinsons disease and many other neurological disorders.........

Posted by: Daniel      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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