Radioprotective effects of cimetidine on rats irradiated by long-term, low-dose-rate neutrons and ^(60)Coγ-rays

Background: Cimetidine, an antagonist of histamine type II receptors, has shown protective effects against γ-rays or neutrons. However, there have been no reports on the effects of cimetidine against neutrons combined with γ-rays. This study was carried out to evaluate the protective effects of cimetidine on rats exposed to long-term, low-dose-rate neutron and γ-ray combined irradiation(n-γ LDR).Methods: Fifty male Sprague-Dawley(SD) rats were randomly divided into 5 groups: the normal control group, radiation model group, 20mg/(kg·d) cimetidine group, 80mg/(kg·d) cimetidine group and 160mg/(kg·d) cimetidine group(10 rats per group). Except for the normal control group, 40 rats were simultaneously exposed to fission neutrons(^(252)Cf, 0.085 m Gy/h) for 22 h every day and γ-rays(^(60)Co, 0.097Gy/h) for 1.03 h once every three days, and the cimetidine groups were administered intragastrically with cimetidine at doses of 20, 80 and 160mg/kg each day. Peripheral blood WBC of the rats was counted the day following exposure to γ-rays. The rats were anesthetized and sacrificed on the day following exposure to ^(252)Cf for 28 days. The spleen, thymus, testicle, liver and intestinal tract indexes were evaluated. The DNA content of bone marrow cells and concanavalin A(Con A)-induced lymphocyte proliferation were measured. The frequency of micronuclei in polychromatic erythrocytes(f MNPCEs), superoxide dismutase(SOD), malondialdehyde(MDA), and glutathione peroxidase(GSH-Px) in the serum and liver tissues were detected.Results: The peripheral blood WBC in the cimetidine groups was increased significantly on the 8th day and the 26 th day compared with those in the radiation model group. The spleen, thymus and testicle indexes of the cimetidine groups were higher than those of the radiation model group. The DNA content of bone marrow cells and lymphocyte proliferation in the cimetidine groups were increased significantly, and fMNPCE was reduced 1.41-1.77 fold in cimetidine treated groups. The activities of SOD and GSH-Px in the cimetidine groups were increased significantly, and the content of MDA in the cimetidine groups was decreased significantly.Conclusions: The results suggested that cimetidine alleviated damage induced by long-term, low-dose-rate neutron and γ combined irradiation via antioxidation and immunomodulation. Cimetidine might be useful as a potent radioprotector for radiotherapy patients as well as for occupational exposure workers.

The influence of diabetes enhanced inflammation on cell apoptosis and periodontitis

Aim: Diabetes mellitus is a metabolic disorder leading to hyperglycemia and exhibiting altered fat and protein metabolism. Diabetes altered cellular microenvironment caused myriad untoward effects. Periodontitis is chronic inflammatory disease. Diabetes and periodontitis had higher prevalence in populations. The objective studied the relationship between diabetes and periodontitis associated with cell apoptosis and the influence of diabetes enhanced inflammation on apoptosis and periodontitis. Methods: This paper studied and analyzed the papers which published in the worldwide associated with the influence of diabetes enhanced inflammation on cell apoptosis and periodontitis, and reviewed the probably mechanism associated with apoptosis. Results: Diabetes induced hyperglycemia enhanced inflammation related to cell apoptosis. Periodontitis had a higher morbidity on diabetes patients. Periodontal intervention may be benefit to controlling the diabetes. The bidirectional efficiency happened between diabetes and periodontitis. Anti-apoptotic and anti-inflammation option can improve the therapeutic effects on diabetes and periodontitis. The finding included following several aspects. 1) Advanced glycation end products enhanced inflammatory response;2) Hyperglycemia induced cell apoptosis;3) inflammatory cytokines caused cell apoptosis;4) Mutuality between cell apoptosis and periodontitis;5) Diabetes induce periodontitis and bone loss;6) Periodontitis induced insulin resistance. 7) TNFα induce prostaglandins elicited cell apoptosis;8) periodontal therapies had effects on diabetes. Conclusion: Diabetes can enhance inflamemation leading to apoptosis and periodontitis. Effective periodontal therapy and control glucose may produce better effects on diabetes or periodontitis. Further research required to investigate the bidirectional mechanism between diabetes and periodontitis.

Origin,migration,and accumulation of carbon dioxide in the East Changde Gas Field,Songliao Basin,northeastern China

CO2reservoirs are widely distributed within the Yingcheng Formation in the Songliao Basin, but the extreme horizontal heterogeneity of CO2content causes difficulties in the exploration and exploitation of methane. Former studies have fully covered the lithology, structure, and distribution of the reservoirs high in CO2content, but few are reported about migration and accumulation of CO2. Using the East Changde Gas Field as an example, we studied the accumulation mechanisms of CO2 gas. Two original types of accumulation model are proposed in this study. The fault-controlled accumulation model refers to gas accumulation in the reservoir body that is cut by a basement fault(the West Xu Fault), allowing the hydrocarbon gas generated in the lower formation to migrate into the reservoir body through the fault, which results in a relatively lower CO2content. The volcanic conduit-controlled accumulation model refers to a reservoir body that is not cut by the basement fault, which prevents the hydrocarbon gas from being mixed in and leads to higher CO2contents. This conclusion provides useful theories for prediction of CO2distribution in similar basins and reservoirs.