نتایج جستجو برای: airway hyper

تعداد نتایج: 107108  

2017
Becky J. Buelow Michelle Rohlfing Françoise Jung Garry J. Douglas Mitchell H. Grayson

INTRODUCTION Asthma is major health burden throughout the world, and there are no therapies that have been shown to be able to prevent the development of disease. A severe respiratory paramyxoviral infection early in life has been demonstrated to greatly increase the risk of developing asthma. We have a mouse model of a severe respiratory paramyxoviral infection (Sendai virus, SeV) that mimics ...

Journal: :Advances in medical sciences 2013
M Gruchała-Niedoszytko S Małgorzewicz M Niedoszytko M Gnacińska E Jassem

Obesity and asthma are both important public health issues. Increasing number of studies suggest the association between obesity and asthma which may be causal or accidental. The studies on animal models show innate enhancement of airway hyper-responsiveness which suggest that chronic airway hyper-responsiveness may be related to chronic low-grade systemic inflammation occurring in obesity. The...

Journal: :Pulmonary pharmacology & therapeutics 2011
Graham M Donovan

Loss of lung function in airway disease frequently involves many complex phenomena and interconnected underlying causes. In many conditions, such as asthmatic airway hyper-responsiveness, hypothesised underlying causes span multiple spatial scales. In cases like this, it is insufficient to take a reductionist approach, wherein each subsystem (at a given spatial scale) is considered in isolation...

Journal: :The Journal of pharmacology and experimental therapeutics 2010
Miao Wang Philip R Cooper Meiqi Jiang Hengjiang Zhao Yiqun Hui Yubing Yao Joshua C Tate Gautam Damera John A Lawson William F Jester Angela Haczku Reynold A Panettieri Garret A FitzGerald

Nonsteroidal anti-inflammatory drugs ameliorate pain and fever by inhibiting cyclooxygenase (COX) and suppressing prostanoid formation. Microsomal prostaglandin E synthase-1 (mPGES-1) catalyzes formation of PGE(2) from the COX product PGH(2) and has emerged as a therapeutic target. Inhibition of mPGES-1, however, renders the PGH(2) substrate available for diversion to other PG synthases. To add...

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