scispace - formally typeset
Y

Yasuo Shimizu

Researcher at Dokkyo Medical University

Publications -  90
Citations -  1913

Yasuo Shimizu is an academic researcher from Dokkyo Medical University. The author has contributed to research in topics: Asthma & Immunoglobulin E. The author has an hindex of 23, co-authored 85 publications receiving 1793 citations. Previous affiliations of Yasuo Shimizu include Gunma University & Dokkyo University.

Papers
More filters
Journal ArticleDOI

Resolvin E1 dampens airway inflammation and hyperresponsiveness in a murine model of asthma.

TL;DR: Findings provide evidence that RvE1 is a pivotal counterregulatory signal in allergic inflammation and offer novel multi-pronged therapeutic approaches for human asthma.
Journal ArticleDOI

Regulation of LPS induced IL‐12 production by IFN‐γ and IL‐4 through intracellular glutathione status in human alveolar macrophages

TL;DR: It is suggested that IFN‐γ and IL‐4 oppositely affect the GSH/GSSG balance, which may regulate IL‐12 secretion from AM in response to LPS.
Journal ArticleDOI

C-Jun-NH2-Terminal Kinase Mediates Expression of Connective Tissue Growth Factor Induced by Transforming Growth Factor-β1 in Human Lung Fibroblasts

TL;DR: The results suggest that TGF-beta1-induced CTGF mRNA expression is mediated through the JNK-dependent pathway, whereas p38 MAP kinase and ERK pathways minimally contribute.
Journal ArticleDOI

Evaluation of Y-27632, a rho-kinase inhibitor, as a bronchodilator in guinea pigs

TL;DR: Although Y-27632 is not as potent as a beta-adrenoceptor agonist, it is concluded that it may become an alternative inhaled bronchodilator, because Y- 27632 is more potent than theophylline, and the relaxant effect is independent of beta- adrenoceptors.
Journal ArticleDOI

Glutathione redox regulates airway hyperresponsiveness and airway inflammation in mice.

TL;DR: Changing glutathione redox balance, increase in GSH level, and the GSH/GSSG ratio by gamma-GCE, is suggested to ameliorate bronchial asthma by altering the Th1/Th2 imbalance through IL-12 production from APC and suppressing chemokine production and eosinophil migration itself.