Elevated gaseous luminal nitric oxide and circulating IL-8 as features of -induced gastric inflammation.

Background: Gastric nitric oxide (NO) production in response to via inducible nitric oxide synthase (iNOS) is suggested as a biomarker of inflammation and cytotoxicity. The aim of this study was to investigate relationships between gastric [NO], immunological biomarkers and histopathology.

Materials And Methods: Esophagogastroduodenoscopy was done in 96 dyspepsia patients.

Utility of animal gastrointestinal motility and transit models in functional gastrointestinal disorders.

Alteration in the gastrointestinal (GI) motility and transit comprises an important component of the functional gastrointestinal disorders (FGID). Available animal GI motility and transit models are to study symptoms (delayed gastric emptying, constipation, diarrhea) rather than biological markers to develop an effective treatment that targets the underlying mechanism of altered GI motility in patients. Animal data generated from commonly used methods in human like scintigraphy, breath test and wireless motility capsule may directly translate to the clinic.

Drugs acting at the GABAA receptor attenuate ethanol-induced gastric mucosal damage in vitro.

1. Benzodiazepines (BZ) have been reported to protect against ethanol-induced gastric damage in rats in both in vivo and in vitro models. However, the effects of some drugs in the new in vitro model do not agree with results reported previously in in vivo studies.