Friday, 9 February 2007

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Biology, Health and Medicine for the Third World is our motto!

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What we expect from you people is suggestions regarding uplift of the health sector in the third world, development of Scientific community and of course your write-ups, if you can contribute to us.


Wednesday, 3 January 2007

Hypertension, alcohol OK in small doses

A drink or two a day shouldn't increase the risk of heart attack for men with high blood pressure, U.S. and Dutch researchers said.
"We could not find any increased risk of heart disease or death due to heart disease for moderate drinkers. Moderate drinkers may even have a reduced risk for heart attack," Joline Beulens, University Medical Center Utrecht in the Netherlands.
Beulens said the study is the first to examine whether men who drink moderately and have high blood pressure are more prone to heart attacks than non-drinkers, USA Today reported.
Researchers analyzed data from 11,711 men with hypertension in the Health Professionals Study, begun in 1986. Participants completed surveys noting how often they consumed alcohol.
From 1986 to 2002, subjects reported 653 heart attacks, of which 279 were fatal, researchers said in the Annals of Internal Medicine. Men who drank up to two drinks a day reduced their heart attack risk by about a third.
"Moderate consumption of alcohol seems to be associated with a lower risk of heart attack, similar to the association seen in healthy men in general," says co-author Dr. Kenneth Mukamal, Beth Israel Deaconess Medical Center, Boston.
Copyright 2007 by United Press International. All Rights Reserved.
UTRECHT, Netherlands
via Sciencedaily

Newly Identified Strains Of Chlamydia Trachomatis Could Produce New Diseases

A new study led by a scientist at Children's Hospital Oakland Research Institute (CHORI) is the first to conclude that Chlamydia trachomatis is evolving at a rate faster than scientists first thought or imagined. Chlamydia trachomatis is a bacterium that is the leading cause of sexually transmitted diseases and the second leading cause of blindness worldwide. Scientists believe the bacterium is evolving through a process called recombination where genes from one or more strains combine to create new strains and -- theoretically -- new diseases. The study is featured in the November issue of Genome Research and was led by Dr. Deborah Dean MD, MPH, senior scientist at Children's Hospital Oakland Research Institute (CHORI). Her research suggests that since Chlamydia trachomatis evolves through recombination where one or more strains combine, the traditional method of studying a single gene to track the transmission of the bacterium is wrong. "What we found is an organism that not only evolves rapidly, but in ways that we thought were rare. We also discovered that this organism can customize its attack," said Dr. Dean. "Consequently, the constant flux of the bacterium could serve as a gateway for new emerging diseases, but more research needs to be conducted to understand if and how this is happening."
600 million people are infected across the globe with Chlamydia trachomatis and 8 million are already blind or severely visually impaired. In some parts of third-world countries, more than 90% of the population is infected. Chlamydia trachomatis has a variety of strains; different strains are responsible for different diseases. Some strains cause sexually transmitted diseases while others cause eye infections. Blinding trachoma is caused by repeated eye infections that cause scarring, which result in the eyelashes turning in-wards. Bacterial infection develops as the eyelashes scratch the surface of the eye, which eventually heals by scarring, resulting in blindness.
Previously, the organism was identified using a single gene, ompA, and the protein encoded by that gene, MOMP. In this study, the clinical strains, which are samples of Chlamydia trachomatis currently responsible for human disease today, were compared to standard reference strains that have been laboratory adapted over the last few decades. By studying multiple strains, the researchers discovered that the strains that were identified as the same strain were actually different.
The next step will be to study clinical strains in comparison with laboratory reference strains to decipher exactly how different strains cause disease and whether new diseases are emerging as a result of the emergence of new strains. "Large-scale comparative genomics will be necessary to understand the precise mechanisms underlying Chlamydia trachomatis recombination and how other species of chamydiae may evolve and transfer from animals to humans."

Note: This story has been adapted from a news release issued by Children's Hospital & Research Center at Oakland. via Science Daily

Regulatory Pathway In Brain Development Possible Basis For Malformations

Researchers at the University of California, San Diego (UCSD) School of Medicine have identified a genetic regulator of brain development that sheds new light on how immature neural cells choose between proliferation and differentiation. Defects in regulating this choice result in brain malformations. Their research will be published on line the week of December 4, in advance of publication in the Proceedings of the National Academy of Sciences (PNAS.)

Animals that lack the Zfp423 gene (right) have a malformed cerebellum (cbm), including a complete loss of the midline structure (vermis). This structure is important for postural control and coordinated movement. The protein encoded by Zfp423 regulates the expression of other genes and is required for normal levels of proliferation by neural precursor cells in the cerebellum. (Credit: UCSD Medical Center)
Bruce Hamilton, Ph.D., associate professor in the Department Medicine, and his colleagues have identified a genetic regulatory pathway that controls a neural precursor cell's decision to self-renew as a dividing precursor or differentiate into a non-dividing neuron. Cells that are unable to differentiate appropriately and continue to proliferate may give rise to brain cancers. On the other hand, cells that differentiate too soon or make too few cells can result in malformations of critical brain structures.
"Development of the brain requires intricate coordination to control the proliferation, differentiation, and connections among different groups of cells," said Hamilton. "We have found a gene in mice, mutated in one kind of malformation, which appears both to promote proliferation and to help coordinate differentiation of immature precursor cells."
The work in Hamilton's lab, led by UCSD Biomedical Sciences graduate students Wendy Alcaraz and David Gold, discovered a specific transcription factor called Zfp423. When Zfp423 is mutated in mice, developmental defects in the cerebellum occur that resemble Dandy-Walker malformations seen in human patients.
Dandy-Walker malformations occur in about one in 25,000 human births. Patients have a congenital malformation in the cerebellum, an area of the brain that controls movement, which can significantly slow motor development and cause progressive enlargement of the skull. Dandy-Walker malformation is frequently associated with disorders of other areas of the central nervous system and malformations of the heart, face, limbs, fingers and toes. Study of the Zfp423 mouse model in Hamilton's lab provides an important genetic clue in Dandy-Walker malformations, whose causes are not well understood.
"Loss of Zfp423 in mice results in diminished proliferation by precursor cells at a key time in the development of the cerebellum, resulting in its malformation," said Alcaraz.
The protein encoded by Zfp423 regulates the expression of other genes and is required for normal levels of proliferation by neural precursor cells in the cerebellum. This gene had previously been identified as a co-factor in two distinct signaling or regulatory pathways that mediate neuronal differentiation. The new work proposes that Zfp423 actually acts as a bridge between the two pathways.
"This means that external signals used in cell-cell communication could affect the developing neurons in ways we hadn't previously realized," Hamilton said. "In particular, cell lineage pathways that are often thought of as independent of signaling once they are initiated may really be under tight regulation by signaling-dependent pathways that compete with them for access to factors like Zfp423." He added that development of this mouse could lead to targeted therapies for some genetic brain disorders.
Additional contributors to this paper include Eric Raponi and Dorothy Concepcion of the UCSD Department of Medicine and Peter M. Gent, of the UCSD Biomedical Sciences Graduate Program. The research was funded in part by grants from the National Institutes of Health.
Note: This story has been adapted from a news release issued by University of California - San Diego. via Science Daily

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