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Monday, August 6, 2012

புத்தர் ஞானம் பெற்ற போதிமரத்தை பாதுகாக்கும் முயற்சி !!!


New malaria vaccine target found


BURNET INSTITUTE   
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The researchers found people who are immune to malaria develop antibodies that primarily attack a protein known as PfEMP1, which could be a target for vaccines against malaria. 
Image: Henrik_L/iStockphoto
Researchers at the Burnet Institute have made a major breakthrough in the quest for a vaccine against malaria, which causes up to one million deaths each year.

Published in the Journal of Clinical Investigation, this research reveals a key target of the immune system’s attack against malaria. The findings show that people who are immune to malaria develop antibodies that primarily target a protein known as PfEMP1, which is produced by Plasmodium falciparum, the causative organism of most cases of malaria.

Head of Burnet’s Centre for Immunology and senior author of the study, Professor James Beeson, said that these findings are a major advance towards developing an effective vaccine because they unlock the mystery of which malaria proteins, known as variant surface antigens (VSAs), an effective vaccine could target to achieve immunity to malaria.

“The new findings support the idea that a vaccine could be developed that stimulates the immune system so that it specifically mounts a strong response (or attack) against the PfEMP1 protein that malaria produces,” Professor Beeson said.

“A vaccine against malaria is urgently needed to reduce this disease globally and currently there is no licensed malaria vaccine available.”

Co-first author, Jo-Anne Chan said the study also showed that when the immune system attacks other proteins that malaria produces, this is not as effective in protecting people. This emphasises that the immune system has to ‘get it right’ in order to fight malaria infection effectively.

“Our studies of Kenyan children showed that those with antibodies to the PfEMP1 protein had a significantly reduced risk of developing malaria, whereas antibodies to other surface antigens were not associated with protective immunity” she said.

Malaria is caused by a parasite that infects human red blood cells and replicates within them. While inside these cells, the malaria parasites produce specific proteins that enable infected cells to stick and clog-up blood vessels in the body. This clogging can occur in organs such as the brain and lungs, and the placenta in pregnant women, and causes severe illness and death.

People who recover from malaria develop antibodies that coat the malaria-infected red blood cells so that they are destroyed by white blood cells (the body’s killer immune cells). The new studies show that the PfEMP1 protein is the major target of these protective antibodies.

The research involved studies conducted at the Burnet Institute, Kenya Medical Research Institute, Walter and Eliza Hall Institute, and University of Melbourne.

Researchers involved included: Jo-Anne Chan, Katherine Howell, Linda Reiling, Ricardo Ataide, Claire Mackintosh, Freya Fowkes, Michaela Petter, Joanne Chesson, Christine Langer, George Warimwe, Michael Duffy, Stephen Rogerson, Peter Bull, Alan Cowman, Kevin Marsh, and James G. Beeson.

The study: ‘Targets of antibodies against Plasmodium falciparum–infected erythrocytes in malaria immunity’. Journal of Clinical Investigation, 2012
Editor's Note: Original news release can be found here.

DNA explains why women live longer


MONASH UNIVERSITY   
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Scientists are beginning to understand one of life's enduring mysteries - why women live, on average, longer than men.

Published in Current Biology, research led by Monash University describes how mutations to the DNA of the mitochondria can account for differences in the life expectancy of males and females. Mitochondria, which exist in almost all animal cells, are vital for life because they convert our food into the energy that powers the body.

Dr Damian Dowling and PhD student, Florencia Camus, both from the Monash School of Biological Sciences, worked with Dr David Clancy from Lancaster University to uncover differences in longevity and biological ageing across male and female fruit flies that carried mitochondria of different origins. They found that genetic variation across these mitochondria were reliable predictors of life expectancy in males, but not in females.

Dr Dowling said the results point to numerous mutations within mitochondrial DNA that affect how long males live, and the speed at which they age.

"Intriguingly, these same mutations have no effects on patterns of ageing in females. They only affect males,” Dr Dowling said.

“All animals possess mitochondria, and the tendency for females to outlive males is common to many different species. Our results therefore suggest that the mitochondrial mutations we have uncovered will generally cause faster male ageing across the animal kingdom.”

The researchers said these mutations can be entirely attributed to a quirk in the way that mitochondrial genes are passed down from parents to offspring.

“While children receive copies of most of their genes from both their mothers and fathers, they only receive mitochondrial genes from their mothers. This means that evolution’s quality control process, known as natural selection, only screens the quality of mitochondrial genes in mothers," Dr Dowling said.

"If a mitochondrial mutation occurs that harms fathers, but has no effect on mothers, this mutation will slip through the gaze of natural selection, unnoticed. Over thousands of generations, many such mutations have accumulated that harm only males, while leaving females unscathed.”

The study builds on previous findings by Dr Dowling and his team that investigated the consequences of maternal inheritance of mitochondria in causing male infertility.

“Together, our research shows that the mitochondria are hotspots for mutations affecting male health. What we seek to do now is investigate the genetic mechanisms that males might arm themselves with to nullify the effects of these harmful mutations and remain healthy,” Dr Dowling said.
Editor's Note: Original news release can be found here.