Hajime Sano

TL;DR: Investigation of the effect of systemic immunoneutralization of CRH in an experimental model of chemically induced aseptic inflammation in rats found suppression of both inflammatory exudate volume and cell concentration by approximately 50 to 60 percent.

TL;DR: Observations suggest that, in vivo, COX expression is upregulated in inflammatory joint diseases, the level of expression is genetically controlled and is a biochemical correlate of disease severity, sustained high level up-regulation is T cell dependent, and expression is down-regulated by antiinflammatory glucocorticoids.

TL;DR: Although LEW/N Rats have deficient hypothalamic CRH responses to inflammatory stimuli compared with F344/N rats, they express relatively high levels of CRH at the site of inflammation, providing further support for the concept that CRH not only triggers the pituitary-adrenal antiinflammatory cascade, but also functions as an antithetically active local mediator of acute and chronic inflammatory arthritis.

TL;DR: Observations implicate heparin binding growth factor (HBGF)-1 in a multitude of biological functions in inflammatory joint diseases.

TL;DR: Examination of the expression of CRH in the large bowel of patients with ulcerative colitis suggests that CRH may play a part in the modulation of intestinal immune and inflammatory system, and as a modulator in the pathogenesis of ulcers.