نتایج جستجو برای: antitrypsin deficiency
تعداد نتایج: 139573 فیلتر نتایج به سال:
Dawn L DeMeo, Robert A Sandhaus, Alan F Barker, Mark L Brantly, Edward Eden, N Gerard McElvaney, Stephen Rennard, Esteban Burchard, James M Stocks, James K Stoller, Charlie Strange, Gerard M Turino, Edward J Campbell, Edwin K Silverman . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ....
Chronic obstructive pulmonary disease (COPD) is a prevalent and preventable disease associated with high morbidity and mortality. Severe and intermediate alpha1-antitrypsin (AAT) deficiency (serum levels <11 and 11-20 micromol.L(-1), respectively) increase the risk of COPD in active smokers. However, little is known about the interaction of severe and intermediate AAT deficiency with modifiable...
As in hereditary alpha 1-antitrypsin deficiency, protease-antiprotease and oxidant-antioxidant balances play a significant role in the pathogenesis of ARDS. However, the disease processes and possibilities for therapeutic intervention differ markedly.
MATERIAL AND METHODS: At the Institute of Immunobiology and Human Genetics, part of the Faculty of Medicine in Skopje, in the previous 7 years, total of 361 patients with suspected alpha-1-antitrypsin (AAT) deficiency were referred for analysis of AAT concentration using nephelometry (Dade Behring) and subsequent AAT genotyping of individuals with alpha-1antytripsin deficiency at protein level,...
Alpha-1 antitrypsin deficiency (AATD) is a hereditary disorder characterised by low circulating levels of the key antiprotease alpha-1 antitrypsin (AAT) and is associated with the development of chronic obstructive pulmonary disease (COPD), often by the 3rd or 4th decade, and liver disease. The two most common SERPINA1 mutations associated with AATD are the Z and S mutations, and the vast major...
CHRONIC OBSTRUCTIVE PULMONARY DISEASE Decreased expression of interleukin 13 in human lung emphysema
Background: The overexpression of interferon (IFN)c or interleukin (IL)-13 in the adult murine lung induces the development of changes that mirror human lung emphysema. Methods: IL-13 and IFNc expression was determined in lung samples from five groups of patients: severe emphysema without a1-antitrypsin deficiency (SE+, n = 10); severe emphysema with a1-antitrypsin deficiency (SE2, n = 5); mild...
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