Monday, August 06, 2012

Malaria vaccine comes closer to reality

Two multi-national research teams have newly sequenced malaria genomes revealing new challenges in efforts to eradicate the parasite.
It also offers a clearer and more detailed picture of its genetic composition, providing an initial roadmap in the development of pharmaceuticals and vaccines to combat malaria.
They focus on Plasmodium vivax (P. vivax), a species of malaria that afflicts humans and the most prevalent human malaria parasite outside Africa, and Plasmodium cynomolgi (P. cynomolgi), a close relative that infects Asian Old World monkeys.
"The bad news is there is significantly more genetic variation in P. vivax than we'd thought, which could make it quite adept at evading whatever arsenal of drugs and vaccines we throw at it," said Professor Jane Carlton, senior author on both studies and part of New York University's Center for Genomics and Systems Biology.
"However, now that we have a better understanding of the challenges we face, we can move forward with a deeper analysis of its genomic variation in pursuing more effective remedies," Professor Carlton added.
In one study, the researchers examined P. vivax strains from different geographic locations in West Africa, South America, and Asia, providing the researchers with the first genome-wide perspective of global variability within this species.
Their analysis showed that P. vivax has twice as much genetic diversity as the world-wide Plasmodium falciparum (P. falciparum) strains, revealing an unexpected ability to evolve and, therefore, presenting new challenges in the search for treatments.
The second study, performed jointly with Professor Kazuyuki Tanabe at Osaka University, Japan, sequenced three genomes of P. cynomolgi. The researchers compared its genetic make-up to P. vivax and to Plasmodium knowlesi (P. knowlesi), a previously sequenced malaria parasite that affects both monkeys and humans in parts of Southeast Asia.
Their work marked the first time P. cynomolgi genomes have been sequenced, allowing researchers to identify genetic diversity in this parasite. Its similarity to P. vivax means that their results will also benefit future efforts to understand and fight against forms of malaria that afflict humans.
"We have generated a genetic map of P. cynomolgi, the sister species to P. vivax, so we can now push forward in creating a robust model system to study P. vivax. This is important because we can't grow P. vivax in the lab, and researchers desperately need a model system to circumvent this," explained Tanabe.
The research appears in two studies published in the latest issue of the journal Nature Genetics.

Does your DNA make you nice?

Why are people nice? or have you ever wondered what makes people nice? Money, happiness, fame, wealth...all hogwash! it's in their DNA! Well..partly at least...a new study suggests, but genes don’t tell the whole story.

The new research adds to the evidence linking specific genes to kindness and generosity, but these traits were also influenced by views about whether the world was a threatening or non-threatening place.

So although DNA may influence behavior, people do not come pre-programmed to be kind or mean or altruistic or selfish, says lead researcher Michael Poulin, PhD, of the University at Buffalo.

“We are not just puppets of our genes,” Poulin tells WebMD. “Genes influence niceness in combination with perceptions of social threat, which come from our past and present experiences.”

Oxytocin, Vasopressin: Niceness Genes?

Poulin and colleagues from the University at Buffalo and the University of California, Irvine, focused their research on the closely related hormones oxytocin and vasopressin, which have previously been linked to social behaviors, including love, generosity, and empathy.

They wanted to find out how expression of the two genes interacted with people’s experiences and feelings to affect behavior.

To do this, they surveyed people via the Internet about their views on civic responsibility, such as whether they considered it their duty to report crimes or pay taxes, and whether they participated in charitable activities such as giving blood or attending PTA meetings.

The study participants were also asked if they viewed other people as basically “good” or “bad,” and if they saw the world as more “threatening” or “non-threatening.”

About 700 of those who participated also provided saliva samples for DNA analysis, which showed whether they had the specific genetic receptors for oxytocin and vasopressin that have been linked to traits associated with niceness.

People who reported finding the world to be a threatening place were generally less likely to exhibit social behaviors linked to niceness, such as charitable giving — unless they had these versions of the genes.The study appears in this month’s issue of the journal Psychological Science.Poulin says the fact that the genes predicted behavior only in combination with people’s experiences and feelings about the world isn’t surprising, because most connections between DNA and social behavior are complex.

‘Love Hormone,’ ‘Cuddle Chemical’

Oxytocin has long been known to play a major role in childbirth and lactation, but over the last decade numerous studies have linked it more broadly to mother-child bonding and to other aspects of social interactions.Because of this, it has variously been referred to as the “love hormone” and “cuddle chemical.”

Cute names aside, University of Maryland School of Medicine professor and chair Margaret McCarthy, PhD, says the evidence that oxytocin and vasopressin play major roles in human social interaction is now quite strong.

“Humans are intensely social, and these hormones may have a lot to do with why we have evolved to be so social and so cooperative,” McCarthy tells WebMD. “It is interesting that a hormone that exists for the purposes of giving birth and lactation has been co-opted to facilitate increased trust and cooperation with strangers.”

She says the new research, like previous studies, highlights the interaction between genes and environment in determining behavior.

SOURCES:Poulin, M.J. Psychological Science, April 2012.Michael Poulin, PhD, assistant professor of psychology, University at Buffalo, SUNY, Buffalo, N.Y.Margaret McCarthy, PhD, professor of physiology and psychiatry, University of Maryland School of Medicine, Baltimore, Md.News release, University at Buffalo, SUNY.

This article is from WebMD. 

why women live longer - It's in the DNA

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.