Water vapour released into the air adds one degree Celsius to global warming for every one contributed by humanity through other greenhouse gas emissions.
The evidence for this phenomenon, long-debated among climate scientists, is now indisputable, according to a review of the evidence by Andrew Dessler of Texas A&M University and Steven Sherwood of the University of New South Wales (UNSW).
Known to science as water vapour feedback, it is responsible for a significant portion of the warming predicted to occur over the next century, according to Dessler and Sherwood. This is because water vapour itself is a greenhouse gas.
As a result of burning fossil fuels and other human activities, rising temperatures are increasing the volume of naturally occurring evaporation on our warm, watery planet, they point out. In turn, that evaporated water contributes additional global warming.
Dessler and Sherwood based their statement on studies of how atmospheric water vapour varies in line with the natural cycles that warm and cool the planet, such as the cyclical temperature change caused by the seasons and El Nino events.
'It's a vicious cycle: warmer temperatures mean higher humidity, which in turn leads to even more warming,' says Dessler, a professor.
Recent estimates suggest the earth will warm by between two to four degrees Celsius over the next century - a scenario that could have devastating long-term consequences, said an UNSW release.
The study was published in the latest issue of Science.
Friday, February 27, 2009
Scientists identify obesity gene
A group of researchers led by a scientist of Indian origin have determined that a specific gene plays a role in the weight-gain response to a high-fat diet.
The finding in an animal study suggests that blocking this gene could one day be a therapeutic strategy to reduce diet-related obesity and associated disorders, such as diabetes and liver damage, in humans.
Researchers found that a diet rich in fat induced production of this gene, called protein kinase C beta (PKC beta), in the fat cells of mice. These mice rapidly gained weight while eating a high-fat diet for 12 weeks.
On the other hand, mice genetically engineered to lack PKC beta gained relatively little weight and showed minimal health effects after eating the same high-fat diet.
'So we now know this gene is induced by a high-fat diet in fat cells, and a deficiency of this gene leads to resistance to fat-induced obesity and related insulin resistance and liver damage,' said Kamal Mehta, study co-author and professor of molecular and cellular biochemistry in Ohio State University College of Medicine.
'It could be that the high-fat diet is a signal to the body to store more fat. And when that gene is not there, then the fat storage cannot occur,' he said.
Research suggests that rather than storing fat, mice lacking the gene burn fat more rapidly than they would if the PKC beta were present, Mehta said, according to a Ohio release.
The research is available online in Hepatology and is scheduled for publication.
The finding in an animal study suggests that blocking this gene could one day be a therapeutic strategy to reduce diet-related obesity and associated disorders, such as diabetes and liver damage, in humans.
Researchers found that a diet rich in fat induced production of this gene, called protein kinase C beta (PKC beta), in the fat cells of mice. These mice rapidly gained weight while eating a high-fat diet for 12 weeks.
On the other hand, mice genetically engineered to lack PKC beta gained relatively little weight and showed minimal health effects after eating the same high-fat diet.
'So we now know this gene is induced by a high-fat diet in fat cells, and a deficiency of this gene leads to resistance to fat-induced obesity and related insulin resistance and liver damage,' said Kamal Mehta, study co-author and professor of molecular and cellular biochemistry in Ohio State University College of Medicine.
'It could be that the high-fat diet is a signal to the body to store more fat. And when that gene is not there, then the fat storage cannot occur,' he said.
Research suggests that rather than storing fat, mice lacking the gene burn fat more rapidly than they would if the PKC beta were present, Mehta said, according to a Ohio release.
The research is available online in Hepatology and is scheduled for publication.
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