Fas-mediated gastric mucosal apoptosis is gaining attention as a cause of tissue damage due to

Polysaccharides from the roots of Panax ginseng were extracted by hot water and fractionated by using ethanol precipitation and ion exchange chromatography. Fractions FC (crude extract), F1 (fraction precipitated by ethanol), F1N (fraction unbound to DEAE-Sepharose CL-6B), and F1A (bound fraction) were obtained. Their carbohydrate analyses showed that acidic fraction F1A contains higher amounts of galactose, arabinose and uronic acids, in comparison to FC and F1. Fraction F1N mainly consists of glucose. The inhibition of Helicobacter pylori-induced hemagglutination revealed different inhibitory activities of these fractions. In particular, acidic fraction F1A showed a remarkable inhibitory activity (minimum inhibition concentration was 0.25 mg/ml) among the polysacharide fractions. However, digestion of the fraction F1A with pectinase resulted in a lower molecular weight oligosaccharide fraction F1AP which was non-inhibitory at the concentration of 4 mg/ml. Comparison of inhibitory activities and carbohydrate compositions of isolated fractions indicates that the activity correlated with the contents of galactose, arabinose, and uronic acids. These data suggest that acidic polysaccharides may be responsible for the inhibitory activity.

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It is generally accepted that intestinal-type gastric adenocarcinoma arises through a multistep process originating with chronic gastritis, progressing through stages of atrophy, intestinal metaplasia, and dysplasia and finally invasive carcinoma. This sequential process, known as the "Correa cascade" is in many instances initiated by Helicobacter pylori infection and perpetuated by a number of environmental and host factors. Given that the development of carcinoma can be the end point of this sequential process, there is great interest in determining which if any of these steps may be reversible. Clinical studies have shown that the eradication of H. pylori can lead to resolution of chronic gastritis, and a few studies have suggested some improvement in gastric atrophy. Intestinal metaplasia, however, does not appear to be as reversible. Nevertheless, results of several intriguing studies of high-risk populations support the notion that eradication of H. pylori may decrease or delay progression to gastric carcinoma despite the inability to reverse all mucosal damage. The applicability of these findings to low-risk countries such as the United States and the United Kingdom remain uncertain. Currently, in the United States, there is no widely accepted screening program for H. pylori infection in asymptomatic individuals, and consensus regarding surveillance for gastric intestinal metaplasia or dysplasia is lacking. The purpose of this report is to evaluate the available data regarding the epidemiology of H. pylori and associated carcinoma, discuss relevant human and animal data that address eradication strategies in the prevention of gastric carcinoma, and finally discuss current recommendations regarding screening programs aimed at high-risk populations.