viernes, 21 de septiembre de 2012

Scientists Focus on Factors Behind Asthma Attacks: MedlinePlus

Scientists Focus on Factors Behind Asthma Attacks: MedlinePlus

 
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Scientists Focus on Factors Behind Asthma Attacks

Findings could pave way to reducing 2 major airway symptoms, researchers say

By Robert Preidt
Thursday, September 20, 2012
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THURSDAY, Sept. 20 (HealthDay News) -- Blocking two particular biological processes might help provide relief to people with asthma, according to a new study.
The University of California, San Francisco-led team found that a specific calcium-activated chloride channel called TMEM16A plays a role in the severity of asthma. The channel regulates airway secretions and smooth-muscle contraction: the major factors that lead to an asthma attack.
"Maybe if we could inhibit both of these processes by blocking this one channel, then we could affect the two symptoms of asthma," study senior author Jason Rock, an assistant professor at the UCSF anatomy department, said in a university news release.
People with asthma have a higher-than-normal number of mucus-producing cells in the lining of the airway tubes that lead to the lungs, and they also have an abnormal amount of smooth muscle surrounding the airway tubes. The slightest stimulus can cause the tubes to contract.
"The overabundance of mucus plugging the airways combined with hyper-contractility of the smooth muscle -- when the tubes get really small -- make it difficult to move air in or out," Rock explained. "A lot of people equate that with breathing through a straw."
In laboratory tests, the researchers identified three chemicals that inhibited the activity of TMEM16A and led to reduced mucus production and smooth muscle contraction.
The study was published Sept. 17 in the journal Proceedings of the National Academy of Sciences.
The next step is to test the safety and effectiveness of these chemical blockers in animals, the researchers say. If that goes well, human clinical trials could follow.
SOURCE: University of California, San Francisco, news release, Sept. 14, 2012
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