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Paper Information

Journal:   TANAFFOS   SUUMMER 2012 , Volume 11 , Number 3; Page(s) 7 To 8.
 
Paper: 

EDITORIAL NOTE: LIMITATION OF COPD STUDIES IN ANIMAL MODELING

 
 
Author(s):  MORTAZ ESMAEIL, ADCOCK IAN A.
 
* 
 
Abstract: 

Chronic obstructive pulmonary disease (COPD) is a major health problem and cigarette smoke is the main risk factor for the development of COPD. The characteristic changes in airway morphology, inflammatory cell infiltration and mediator expression in COPD may result from direct effects of cigarette smoke (CS) on airway cells. CS causes lung damage through oxidative stress either by itself or due to oxidants released by inflammatory cells that are recruited as a result of smoke-induced injury. CS is a major source of oxidants/free radicals and a complex of over 4, 700 chemical compounds. This huge amount of oxidants from CS and those formed endogenously cause an imbalance between oxidants and antioxidants which are considered to be important in the pathogenesis of COPD.

 
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+ Click to Cite.
APA: Copy

MORTAZ, E., & ADCOCK, I. (2012). EDITORIAL NOTE: LIMITATION OF COPD STUDIES IN ANIMAL MODELING. TANAFFOS, 11(3), 7-8. https://www.sid.ir/en/journal/ViewPaper.aspx?id=274104



Vancouver: Copy

MORTAZ ESMAEIL, ADCOCK IAN A.. EDITORIAL NOTE: LIMITATION OF COPD STUDIES IN ANIMAL MODELING. TANAFFOS. 2012 [cited 2021May16];11(3):7-8. Available from: https://www.sid.ir/en/journal/ViewPaper.aspx?id=274104



IEEE: Copy

MORTAZ, E., ADCOCK, I., 2012. EDITORIAL NOTE: LIMITATION OF COPD STUDIES IN ANIMAL MODELING. TANAFFOS, [online] 11(3), pp.7-8. Available: https://www.sid.ir/en/journal/ViewPaper.aspx?id=274104.



 
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