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Worms may hold key to stroke

Worms that can survive with almost no oxygen are teaching scientists how to rescue oxygen-starved cells in humans who suffer a heart attack or stroke, US researchers said on Thursday.

They identified a gene that can help a cell slow down when oxygen levels get too low, protecting the cells from making fatal mistakes while starved of oxygen.

Researchers hope that some day drugs can be designed to help human cells survive without oxygen.

"In stroke and heart attack, cells die because they lack oxygen," said Dr Michael Crowder of Washington University School of Medicine in St Louis, whose study appears in the journal Science.

"We're trying to find novel approaches to understanding why cells die in low-oxygen conditions," Crowder said in a telephone interview.

Genetically engineered worms
Crowder's team used genetic engineering techniques on worms called Caenorhabditis elegans to find genes that help them survive better with little oxygen.

They identified a gene that they could "turn down" in the worms and help them survive with little oxygen. Normal worms all died when exposed to the same conditions.

The researchers think interfering with this gene, found in the mitochondria, or powerhouse of the cells, may protect the cells by putting them into a kind of hibernation so they do not need as much oxygen.

Study protein folding
In a second experiment, the team also interfered with how genes fold proteins, making them into the shapes they need to function best. Improperly folded proteins can die, and low-oxygen environments have been linked with high levels of unfolded proteins.

The researchers found that slowing down the cell also helps stop the damage caused by faulty proteins.

The next step for the team is to see if the same approach can help protect nerve cells in mammals. "If that happens, then I think there is hope that, eventually, we could target this process for therapy," Crowder said. – (Julie Steenhuysen/Reuters Health)

Read more:
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Myths and interesting facts about stroke

January 2009

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