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“Diarrheal illness is a significant cause of morbidity and mortality worldwide. It is the fifth leading cause of death worldwide and the second leading cause of death among children under 5. Nearly one in five childhood deaths – about 1.5 million each year – is due to diarrhea. In the developed world, acute gastroenteritis is a major cause of physician visits and absence from school or work. Diarrhea has also become a significant consequence of hospitalization and antibiotic use. The major causes of acute gastroenteritis are viruses, bacteria, and parasites. The etiology of infection is

based on epidemiological risk factors such as food consumption, antibiotic usage, sexual practices, and travel history. Norovirus is the leading cause of Pictilisib cost acute infectious gastroenteritis. The virus is highly infectious, results in a self-limited diarrheal illness, but has substantial morbidity. Clostridium difficile is the major cause of healthcare-associated diarrhea. The emergence of a hypervirulent strain of C. difficile has contributed to increasing morbidity and mortality. Ixazomib The primary steps in the evaluation and treatment of acute diarrhea are to recognize the severity of illness and maintain hydration and nutrition. Specific treatment is focused on the particular infectious agent and the elimination of any exacerbating factors.

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“Over the last 3 decades, the incidence of esophageal adenocarcinoma has dramatically increased in Western countries; a similar increase may be observed in Asian countries in the near future. Esophageal adenocarcinoma arises from

a sequential gastroesophageal reflux disease (GERD) spectrum from reflux erosive esophagitis, to Barrett’s learn more esophagus, and finally to esophageal adenocarcinoma. At present, gastric acid and bile are assumed to be primarily involved in the etiology of the GERD spectrum. We reported in 2002 that, at the gastroesophageal junction in humans, abundant amounts of nitric oxide (NO) are generated luminally through the entero-salivary re-circulation of dietary nitrate. Since then, we have carried out a series of experiments to demonstrate that NO diffuses into the adjacent epithelium at cytotoxic levels. This diffusion results in disruption of the epithelial barrier function, exacerbation of inflammation, acceleration of columnar transformation in the esophagus (Barrett’s esophagus) via the induction of caudal-type homeobox 2, and the shifting of carcinogenic N-nitroso compound formation from the luminal to epithelial compartment. These results suggest that, in addition to conventionally recognized causative factors, luminal NO could also be involved in the pathogenesis of the GERD spectrum. In addition, we recently showed that there is a prominent gender-related difference in NO-related cytotoxicity in the esophagus and that estrogen attenuated the esophageal tissue damage via the estrogen receptor in female rats.