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Objective To investigate the residents' acceptance and the influencing factors of the hierarchical medical system in Xuzhou, and to suggest on effective system implementation. Methods Xuzhou residents free of cognitive impairment and over 18 years old were sampled for questionnaire survey in July-August 2016, to study their acceptance of their basics and acceptance of the system. 1 550 questionnaires were distributed, and 1 473 valid ones were recovered. The count data were expressed as constituent ratio, and χ2test was used for single-factor analysis, with binary logistic regression analysis for multi-factor analysis. Results 71. 0% of the residents embraced this system. Their acceptance varies significantly with their age, place of residence, education, annual average monthly income, self-rated health status, physical examination experience, conditions of chronic diseases, medical visit experience at primary healthcare institutions, and their awareness of the system (P<0.05). Conclusions The acceptance of the system by Xuzhou residents needs to be elevated, by means of greater promotional efforts, capacity building for primary institutions, so as to fully leverage the system to serve the residents.
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Objective To investigate the effects of salidroside on proliferation and invasive ability of glioma U87-MG cells; To discuss the its mechanism to induce apoptosis of U87-MG cells. Methods U87-MG cells were cultured in vitro for 24 h under different concentrations of salidroside and camptothecin. The proliferation of U87-MG cells was detected by MTT assay. The apoptosis rate of U87-MG cells was detected by flow cytometry. Transwell assay was used to detect the invasive ability of U87-MG cells. ROS was detected by indirect fluorescent labeling. The expressions of Caspase-3, Bcl-2, Bax, E-cadherin, N-cadherin and matrix metalloproteinase-9 (MMP-9) in U87-MG cells were detected by Western blot. Results Compared with the blank control group, U87-MG cells had significant inhibitory effect on the growth of U87-MG cells in each administration group, and the invasive ability of U87-MG cells was significantly reduced after 10, 50, 100 μg/mL salidroside was intervened, and 10, 50, 100 μg/mL salidroside for 48 h for U87-MG cells could induce apoptosis of the cells; the level of ROS was positively correlated with the concentration of salidroside; 10, 50, 100 μg/mL salidroside up-regulated the expressions of Caspase-3, Bax and E-cadherin, and down-regulated the expressions of Bcl-2, N-cadherin and MMP-9. Conclusion Salidroside can induce apoptosis of U87-MG cells and inhibit the invasive ability of U87-MG cells.
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Objective·To explore effects of pCPT-cAMP on proteinuria and dedifferentiation of podocytes in adriamycin (ADR)-induced nephropathy mice. Methods·Male BALB/c mice were divided into three groups. The control group did not make any intervention, and the other mice were administrated with ADR in a dose of 10 mg/kg by intravenous injection (ADR group). Some ADR-injected mice were treated with pCPT-cAMP [50 mg/(kg·d)] by intraperitoneal injection everyday (A+P group). Albumin urine was detected by Coomassie blue stain. Urine creatinine concentration was estimated by ELISA. The expression of WT-1 was detected by immunohistochemical staining. Immunofluorescence staining and Western blotting were used to evulate the dedifferentiation of podocytes. Results·Compared with the control group, the ratio of urinary albumin/creatinine in ADR nephropathy mice was significantly increased. WT-1 immunohistochemical staining showed that the number of podocytes was significantly decreased, while immunofluorescence double staining of podocyte-specific protein synaptopodin and podocalyxin remarkably reduced, and the expression of desmin was increased. pCPT-cAMP intervention decreased the ratio of albumin/creatinine in ADR mice, elevated the quantity of WT-1 positive cells and the expression of synaptopodin and podocalyxin, while desmin expression decreased. Conclusion·pCPT-cAMP activates the PKA signaling and protects ADR nephropathy mice by preventing the loss of podocytes and ameliorating the urine albumin/creatinine ratio, which may be mediated by pCPT-cAMP-prevented dedifferentiation of podocytes.
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AIM:To investigate the role of B cells in CD45RB antibody-induced transplantation immune toler-ance.METHODS:Single cell suspension was made from the spleen of BALB/c nude mice disposed by CD45RB antibod-y, then mixed cultured with T cells of BALB/c mice and spleen cells of C57BL/6 mice.The Th1, Th2, Treg and Tm cells were monitored by flow cytometry during the culture process .The skin graft model was set up with B 6.μMT-/-mice as re-ceptors and BALB/c mice as donors.CD45RB antibody was intraperitoneally injected into the receptors after transplantation and then CD3+CD45RBhi cells were detected by flow cytometry .In another mixed lymphocyte culture , CD45RB antibody was added, and then B cells were isolated and injected into B6.μMT-/-mice through the tail vein.The heart transplanta-tion model was established with B 6.μMT-/-mice as receptors and BALB/c mice as donors, and then the survival and the migration of B cells to the thymus were observed .RESULTS:When T lymphocytes were co-cultured with B lymphocytes treated with anti-CD45RB monoclonal antibody (mAb) in vivo, the percentages of Th2 and Treg cells were up-regulated and Th1 cells were down-regulated, but Tm cells were not altered as compared with the control .In vivo without B lympho-cytes, anti-CD45RB mAb also down-regulated the expression of CD45RB in T lymphocytes.The reduction was faster and the percentage of CD3 +CD45RBhi T cells was not altered as compared with the control .The B lymphocytes treated with an-ti-CD45RB mAb in vitro prolonged the lifetime of receptor in heart transplantation model but failed to induce complete toler -ance.After recieving B cells treated with anti-CD45RB mAb and allogeneic heart transplantation , B cells migrated to the thymus in B6.μMT-/-mice.CONCLUSION:B lymphocytes play a definite role in the transplantation immune tolerance induced by anti-CD45RB mAb through their affection on T-cell subgroups and also in the central tolerance .However, the induction of immune tolerance can not only rely on B cells .
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BACKGROUND:In recent years a large number of studies have suggested that bone marrow mesenchymal stem cells can ease hyperglycemia of diabetic rats, but the related mechanism is unclear and controversial. OBJECTIVE:To investigate the relevant mechanism of bone marrow mesenchymal stem cells on pancreas microenvironment in vivo in diabetic rats. METHODS:Bone marrow mesenchymal stem cells were transfected with enhanced green fluorescent protein (EGFP) and administered to diabetic rats via the subcapsular pancreas. Blood glucose levels were monitored. The expressions of the key genes in islet development in these EGFP positive pancreatic cells were analyzed by Real-time quantitative PCR at different times. EGFP and insulin double-positive cells were detected by immunofluorescence. Flow cytometry was performed to analyze cellcycle and DNA ploidy. RESULTS AND CONCLUSION:Blood glucose levels were effectively reduced after transplantation. The expressions of the key genes in islet development reached their own peak values at different times after transplantation:Nestin at week 1, Nkx 2.2 at week 3, Pax 4 and Ngn 3 at week 4, insulin and glucagon at week 12, PDX-1 at week 8 until week 12. The cells double-positive for EGFP and insulin cells were observed. In the pancreas, EGFP positive cells at S+G 2/M phase were significantly increased, and there were no polyploid and aneuploid cells. In pancreas microenvironment, the bone marrow mesenchymal stem cells transplanted into the diabetic pancreas can differentiate into isletβ-like cells under gene control, but not through the fusion with tissue cells.