Objective To find out the immunologic mechanism of complete Freud's adjuvant (CFA) when used for preventing from streptozotocin (STZ)-insulitis and STZ-induced diabetes mellitus. Methods 20 healthy Kunming mice were equally and randomly divided into A and B groups. The animals in group A was respectively injected once into the pad of hind foot and intraperitoneally injected with 50?L CFA, and the animals in group B was injected with 50?L sodium chloride. After 2 weeks, all mice in both groups were i.p. injected with STZ (40 mg?kg-1/d) for 5 days. All mice were killed 6 weeks after administration of CFA or sodium chloride. Diabetes was diagnosed if blood glucose level was more than 16.7mmol/L after 2 consecutive days. The incidence of diabetes was compared between the two groups before mice were killed. The expression of Fas/FasL on ? cells as well as on infiltrating T cells of islets was investigated by immunochemistry method. Results The incidences of diabetes mellitus and insulitis in group A and group B were 0 % vs 80% (P

Objective To detect the expression of apoptotic inhibitor protein Livin in different esophageal epithelial lesions and to analyze the relation between the expression of Livin with pathologic characteristics. Methods The expressions of Livin mRNA and Livin protein were detected by real- time fluorescence quantitative PCR and western blot in 40 patients with different esophageal epithelial lesions including normal, atypical hyperplasia, carcino-ma in stiu and invasive carcinoma. Results The expressions of Livin mRNA were progressively increased from nor-mal to invasive carcinoma( 1.00 ± 0. 00,2.26 ± 0.79,7.24 ± 1.06,12.21 ± 2.47 ). There was statistical signifi-cance in Livin mRNA expression among carcinoma in stiu and invasive carcinoma and normal tissues ( P < 0.05 ). Conclusion The expression of Livin is significantly related to the progression of esophageal cancer,which may be a new target for diagnosis and gene treatment of esophageal carcinoma.

Objective: To determine the expression of TAZ and its role in angiogenesis in gastric carcinoma. Methods: Immunohistochemical staining was performed to investigate the expression of TAZ and to determine whether a direct relationship exists between TAZ and β-catenin. Transfection with TAZ overexpression plasmid in MKN28 cells was conducted to induce exogenous expression of TAZ and a TAZ knockdown plasmid was transfected into MGC803 cells to reduce TAZ levels. The effects on endothelial cell formation, proliferation, and migration were determined by Matrigel three-dimensional culture, MTT proliferation assay and Transwell migration assay. In addition, the expression of TAZ and β-catenin in transfected gastric cancer cells was detected by Western blot. Results: Immunohistochemistry showed that TAZ protein was expressed in 64 of 150 gastric cancer sample tissues (43%), TAZ was localized in the nucleus, and its expression was associated with tumor grade, TNM stage, metastasis, and microvessel density (MVD) (P<0.05). In addition, the expression frequency of β-catenin in the TAZ positive group was 67.2%, which was significantly higher than that in the TAZ negative group, and the expression of TAZ was positively correlated with β-catenin. After transfection, TAZ overexpression increased the expression of β-catenin and enhanced HUVECs tube formation, proliferation, and migration. In the MGC803 cells transfected with the knockdown plasmid, β-catenin levels were decreased and HUVECs motility was inhibited. Conclusions: TAZ may promote angiogenesis in gastric cancer by promoting β-catenin expression.

Objective:To explore the relationship between marital status and mild cognitive impairment in older adults.Methods:This study is a cluster random sampling.From January to December 2020, a questionnaire survey was conducted among older adults aged 60 years and over in four cities of Hebei Province.Finally, 2690 older adults with mild cognitive impairment and normal cognitive function were enrolled.The older adults were divided into 2 groups according to their marital status: married and living with their spouses(group E1), divorced or living alone(group E2). The mini-mental state examination(MMSE)scores of older adults in the two groups were compared.Moreover, the cognitive differences of older adults between the two groups and the interaction of marital status, social activities and life events on cognitive outcomes were analyzed.Results:The married older adults with partners had better cognitive preservation( P<0.01). The more life events were more likely to cause cognitive impairment( P<0.01), and the interaction of marital status, social activities and life events had a significant impact on cognition( P<0.01). Older men who were married and lived with spouse had better cognition than older women who were married and lived with spouse( P<0.05 in Model 3). The cognition of widowed elderly women was better than those of widowed elderly men( P<0.1 in Model 1; P<0.1 in Model 2). Among elderly men, the cognition of those married and living with spouse was better than that those of widowed( P<0.01 in models 1 and 2, P<0.1 in model 3). Among elderly women, those married and living with spouse had better cognitive outcomes than those widowed( P<0.01 in Model 1, P<0.01 in Model 2). Conclusions:Marital companionship is a protective factor for the cognition of older adults, and there are gender differences in the impact of marital status on cognition in late life.

Uridine is one of the essential nutrients in organisms. To maintain normal cell growth and intracellular metabolism, the uridine must be maintained at certain concentration. Recent studies have shown that uridine can reduce inflammatory response in organisms, participate in glycolysis, and regulate intracellular protein modification, such as glycosylation and acetylation. Furthermore, it can protect cells from hypoxic injury by reducing intracellular oxidative stress, promoting high-energy compounds synthesis. Previous studies have shown that the protective effects of uridine are closely related to its effect on mitochondria. This review summarizes the effect of uridine on mitochondrial function.
Uridine/metabolism* ; Mitochondria/metabolism*