Regional variation of non-Hodgkin’s Lymphoma (NHL) in Mongolia and its association with Ki-67 expression

Background: The prevalence of non-Hodgkin’s lymphoma (NHL) varies worldwide in association with demographic and environmental factors. The analysis of these associations in Asia, Africa, and less developed countries is limited by low absolute numbers and unknown etiologic factors such as in Mongolia. The geographic variations in NHL incidence and mortality rates may induce by differences in case ascertainment and registration, or disease diagnosis and classification. The interpretation of NHL patterns and trends remains difficult. Therefore, an attempt was made to test the correlation between Ki-67 expression and clinical parameters on one hand, and geographical or ethnic differences on the other. Research purpose: The objectives of this study are to examine the geographic distribution of non-Hodgkin's disease more in detail for high incidence Mongolian prefectures, and to evaluate the association between the distribution of NHL and Ki-67 expression. Methods: Expression of Ki-67 was examined using an immunohistochemical technique in archival paraffin-embedded sections taken from (n=35) both National pathology center of Mongolia and Etemo clinic previously. Geo-processing was conducted with the aide of the software R Studio [under the Mapping plots] (1.0.136 version). The analyzed geographic incidence rates of NHL include locations of the central and east provinces Orkhon, Uvurhangay, Khuvsgul, Ulaanbaatar and Dornod The age-specific incidence and mortality rates were compared to those for all regions in Mongolia and those for the combined high mortality localities within the high-risk prefectures. Results: Expression of Ki-67 protein was noted in 71.8% of the tumor cases. Average Ki-67 expression was associated with regions of high incidence. Conclusion: We found that provinces with a high incidence and mortality from non-Hodgkin's disease were aggregated in the eastern-central parts of Mongolia, particularly in the areas along Ulaanbaatar capital city

Protective Effect of Anar-5 Herbal Treatment on Experimental Chronic Atrophic Gastritis in Wistar Rats

BACKGROUND: Chronic gastritis is a slowly progressive disease. It includes atrophy of gastric mucosa, impairment of epithelial regeneration, formation of lymphoid tissue/germinal center, loss of gastric secretion and movement. The Mongolian traditional medicine used Anar-5 recipes for the treatment of stomachache, emesis, and improvement of gastric digestion. Based on these observations, we implemented a rat model of Anar-5 treatment in artificial chronic gastritis in order to elucidate its potential protective mechanisms scientifically. METHODS AND MATERIAL: We established an experimental rat model of chronic gastritis by use of ammonia water. We divided the rat cohorts in an Anar-5–treated test group, an untreated cohort, and a control group. The untreated group was fed with 0.1% ammonia water and the treated group with both 0.1% ammonia water and administered Anar-5 100 mg/kg/day for 6 weeks. Gastric lesions were evaluated microscopically. The Prostaglandin E2 levels, cyclooxygenase COX-2 expression and the cellular proliferation marker Ki67 were in addition asessed. RESULTS: The Anar-5 cohort displayed with an increased thickness of the antrum mucosa, number (р˂0.05) and regeneration zones of gastric mucous epithelial cells when compared to the results of the untreated cohort (693.1±63.8 μm versus 429.6±43.5 μm). The untreated cohort displayed with decreased PGE2 levels (14.8±0.62 ng/dl) when compared to those of the control group and Anar-5 cohort (19.5±1.22 ng/dl and 18.7+0.32 ng/dl protein, respectively). The Ki67-Associated proliferation rate of the antrum mucosa was enhanced and measured 19.75% in the untreated cohort in comparison to a proliferation rate of 6.58% in the Anar-5 cohort. CONCLUSION: The data of our rat experiment indicate that a contemporary application of Anar-5 herbs acts as a gastric mucosal protective agent. In addition it induces an overexpression of COX 2 and maintenance of the PGE2 level