Significados de asthmatic airway en inglés

Therefore, kaempferol may be a potential therapeutic agent targeting asthmatic airway constriction.

Background: S-nitrosothiols are potent endogenous bronchodilators depleted in asthmatic airway lining fluid.

Whether this deficiency can explain the increased bulk of muscle in the asthmatic airway remains to be established.

Here, we provide a clear picture of the events regulating NO synthesis in the human asthmatic airway in vivo.

Here, we demonstrated that increased metabolism sustains arginine availability in asthmatic airway epithelium with consequences for bioenergetics and inflammation.

In conclusion, these studies define multiple mechanisms that function coordinately to support high level NO synthesis in the asthmatic airway.

In this review, we discuss the paradigm of arginase and NOS competition for their substrate L-arginine in the asthmatic airway.

Here we report that PU.1 serves as a critical regulator of AAM polarization and promotes the pathological progress of asthmatic airway inflammation.

Thus surfactant dysfunction induced by an IL-4-driven SP-B deficiency after allergen provocation may be an important part of the late asthmatic airway response.

NOSII mRNA expression decreases in asthmatics receiving inhaled corticosteroid, treatment effective in reducing inflammation in asthmatic airways.

Therefore we suggest that MNK-1 inhibition may present a new target to limit inflammation and remodelling in asthmatic airways.

The aim was to address the hypothesis that RELM-β plays a role in extracellular matrix deposition in asthmatic airways.

Increased expression of arginase I and NOS2 occurs in murine models of allergic asthma and in biopsies of asthmatic airways.

Epithelial CCR3 participates in key functions for wound repair, amplifies the expression of profibrogenic and chemokine transcripts, and appears up-regulated in inflamed asthmatic airways.

In the present analysis, we sought to describe Th2 inflammation in human asthmatic airways quantitatively with respect to known mediators of inflammation and intercellular communication.