Low-cost pain killer can cure
resistant TB
A low-cost drug, which is widely used as a pain
killer in developing countries, can kill drug-resistant tuberculosis (TB) -- a feat few currently
approved TB drugs can accomplish, say researchers.
Weill Cornell Medical College researchers point to a potential new therapy for the more than half million people worldwide whose TB has become resistant to standard drug treatments.
But their main worry is that the effective drug, oxyphenbutazone, may never be tested in TB clinical trials.
Weill Cornell Medical College researchers point to a potential new therapy for the more than half million people worldwide whose TB has become resistant to standard drug treatments.
But their main worry is that the effective drug, oxyphenbutazone, may never be tested in TB clinical trials.
Weill Cornell's Carl Nathan and his team found what they called the "completely surprising" ability of oxyphenbutazone to kill drug-resistant TB after testing thousands of approved drugs against the bacteria.
This repurposing of the agent already in the market can lead to quicker testing for its new uses, the Publication of the National Academy of Sciences reports.
"This agent might help save lives if there was a way to test it in (sic) TB patients," says Nathan.
Oxyphenbutazone, best known by its trademark name of Tandearil, was introduced in the market as a patented drug for arthritis-like pain in the early 1950s, and lost its patent and market dominance by the 1970s, according to a Weill Cornell statement.
"It is difficult today to launch clinical studies on a medication that is so outdated in the United States, that it is mainly used here in veterinary medicine to ease pain," says senior study author Nathan, professor of microbiology.
"No drug firm will pay for clinical trials if they don't expect to make a profit on the agent. And that would be the case for an off-patent drug that people can buy over the counter for pain in most of the world," Nathan adds.
He says that oxyphenbutazone does have some established toxicities, "and is not a drug you should take for aches and pains if a safer alternative is available".
But the drug's major toxicities appear to be less frequent than the major side-effects of the drug regimens that are currently used to treat TB, he says.
Source: www.timesofindia.com
14.09.2012
Scientists find
protein responsible for heart failure!
Researchers
have unravelled how an out-of-tune protein precipitates heart failure by
causing its muscle to malfunction. Scientists have known for a while that
several heart proteins – troponin I is one of them – get “out of tune” in
patients with heart failure but the precise origin of the “bad notes” remained
unclear.Troponin I, found exclusively in heart muscle, is already used as the
gold standard marker in blood tests to diagnose heart attacks, but the new
findings reveal why and how the same protein is also altered in heart failure,
the journal “Circulation” reports.
The
discovery by Johns Hopkins researchers can pave the way to new and badly needed
diagnostic tools and therapies for heart failure, a condition marked by heart
muscle enlargement and inefficient pumping, believed to affect more than six
million adults in the US alone, the researchers say. ”Our findings pinpoint the
exact sites on troponin I’s molecule where disease-causing activity occurs, and
in doing so, they give us new targets for treatment,” says researcher Jennifer
Van Eyk, director of the Johns Hopkins Proteomics Innovation Centre in Heart
Failure.
Troponin
I acts as an on-off switch in regulating heart relaxation and contraction. In
response to adrenaline, this protein also triggers the “flight-fight” response,
according to a Johns Hopkins statement. But when altered, troponin I can start
acting as a dimmer switch instead, one that ever so subtly modulates cardiac
muscle function and reduces the heart’s ability to pump efficiently and fill
with blood, the researchers found.
The
Hopkins team used a novel method to pinpoint the exact sites, or epicentres,
along the protein’s molecule where disease-triggering changes occur. They found
14 such sites, six of them previously unknown. They said their work may spark
the development of tests that better predict disease risk and monitor
progression of the disease once the heart begins to fail.
Source: http://health.india.com
14.09.2012
Good, better, best.
Never let it rest. Until your good is better and your better is best
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