Objective:To investigate the effects of celastrol (CSR) on dendritic cell (DC) and T follicular helper cell (Tfh) subsets in the mouse of ulcerative colitis (UC) .Methods:Forty-eight male BALB/c mice were randomly divided into healthy control group, model group, and CSR intervention group, with 16 mice in each group. The healthy control group was fed with normal purified water, while the mice in model group and CSR intervention group were fed with 3% DSS solution to induce UC model. Since the induction, the mice in CSR intervention group were gavaged with 1mg/kg of CSR, and the mice in UC group were gavaged with equal volume of saline once a day. The weight and stool characteristics of the mice were recorded, and disease activity index (DAI) were evaluated. After the 8-day intervention, the length of the mouse colon was measured, the histopathological changes were observed, and the histopathological score was evaluated. Flow cytometry was used to detect the percentage of DC, conventional DC (CD8α + cDC1, CD103 + cDC1, cDC2), plasmacytoid DC (pDC), and Tfh subsets in colon lamina propria, mesenteric lymph nodes and spleen. Cytometric bead array kit was used to detect the expression levels of DC and Tfh related cytokines [interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), interleukin 21 (IL-21) ] in colon tissue. The influence of CSR on naive CD4 +T cell proliferation and Tfh differentiation were validated in vitro experiments. Results:The modelling success rate was 100% and all mice survived. Compared with model group, mice in CSR intervention group had heavier weight, lower DAI, and ameliorated colonic length shortening, with all differences being statistically significant (all P < 0.05). The intestinal mucosal structure of mice in model group was disordered, with a large number of inflammatory cell infiltration; the intestinal mucosal barrier of mice in CSR intervention group approached normal structure, with fewer inflammatory cells, and the histopathological scores were significantly decreased ( P<0.05). In the colon lamina propria, compared with model group, the percentages of DC, CD8α + cDC1 and Tfh decreased, while the percentage of CD103 + cDC1 increased in CSR intervention group, and these differences were all statistically significant (all P<0.05). In mesenteric lymph nodes, the percentage of CD8α + cDC1 decreased, while the percentages of DC, CD103 + cDC1, cDC2 and Tfh increased in CSR intervention group compared with model group, and these differences were all statistically significance (all P<0.05). In the spleen, compared with model group, the percentage of pDC was significantly reduced in CSR intervention group ( P<0.05) .The expression levels of IL-6, TNF-α and IL-21 in colon tissues of CSR intervention group were lower, while IL-10 was higher than those of model group, and these differences were statistically significant (all P<0.05). In vitro experiments, CSR could inhibit naive CD4 + T cell proliferation and Tfh differentiation, with statistically significant differences (all P < 0.05) . Conclusion:CSR can alleviate intestinal damage in UC mice, potentially by modulating the local immune microenvironment through regulating DC and Tfh subsets.

Objective:To investigate the effects of celastrol (CSR) on dendritic cell (DC) and T follicular helper cell (Tfh) subsets in the mouse of ulcerative colitis (UC) .Methods:Forty-eight male BALB/c mice were randomly divided into healthy control group, model group, and CSR intervention group, with 16 mice in each group. The healthy control group was fed with normal purified water, while the mice in model group and CSR intervention group were fed with 3% DSS solution to induce UC model. Since the induction, the mice in CSR intervention group were gavaged with 1mg/kg of CSR, and the mice in UC group were gavaged with equal volume of saline once a day. The weight and stool characteristics of the mice were recorded, and disease activity index (DAI) were evaluated. After the 8-day intervention, the length of the mouse colon was measured, the histopathological changes were observed, and the histopathological score was evaluated. Flow cytometry was used to detect the percentage of DC, conventional DC (CD8α + cDC1, CD103 + cDC1, cDC2), plasmacytoid DC (pDC), and Tfh subsets in colon lamina propria, mesenteric lymph nodes and spleen. Cytometric bead array kit was used to detect the expression levels of DC and Tfh related cytokines [interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), interleukin 21 (IL-21) ] in colon tissue. The influence of CSR on naive CD4 +T cell proliferation and Tfh differentiation were validated in vitro experiments. Results:The modelling success rate was 100% and all mice survived. Compared with model group, mice in CSR intervention group had heavier weight, lower DAI, and ameliorated colonic length shortening, with all differences being statistically significant (all P < 0.05). The intestinal mucosal structure of mice in model group was disordered, with a large number of inflammatory cell infiltration; the intestinal mucosal barrier of mice in CSR intervention group approached normal structure, with fewer inflammatory cells, and the histopathological scores were significantly decreased ( P<0.05). In the colon lamina propria, compared with model group, the percentages of DC, CD8α + cDC1 and Tfh decreased, while the percentage of CD103 + cDC1 increased in CSR intervention group, and these differences were all statistically significant (all P<0.05). In mesenteric lymph nodes, the percentage of CD8α + cDC1 decreased, while the percentages of DC, CD103 + cDC1, cDC2 and Tfh increased in CSR intervention group compared with model group, and these differences were all statistically significance (all P<0.05). In the spleen, compared with model group, the percentage of pDC was significantly reduced in CSR intervention group ( P<0.05) .The expression levels of IL-6, TNF-α and IL-21 in colon tissues of CSR intervention group were lower, while IL-10 was higher than those of model group, and these differences were statistically significant (all P<0.05). In vitro experiments, CSR could inhibit naive CD4 + T cell proliferation and Tfh differentiation, with statistically significant differences (all P < 0.05) . Conclusion:CSR can alleviate intestinal damage in UC mice, potentially by modulating the local immune microenvironment through regulating DC and Tfh subsets.

Using the concept and method of evidence-based medicine,the paper systematically analyzes the functions and shortage of intelligent health Application (App) in disease diagnosis,treatment and self-management,and describes the functions of health and disease management App,so as to promote the development of App and enable App to better assist in health management.

Objective To establish the median equation of second trimester Down′s syndrome (DS) screening maternal serum markers ,alpha-fetoprotein (AFP) and human chorionic gonadotrophin (HCG) ,in Xiangxi area and to investigate the influence of new median values on the local screening results .Methods The electrochemiluminescence immunoassay (ECLIA ) was applied to detect the serum AFP and HCG levels in 2619 second-trimester normal pregnant women ,the medians of AFP and HCG in each gestational week were calculated ,and the regression equation between gestational period and the medians of AFP and HCG were es-tablished by using the statistical software ,then the results were compared with the evaluation results of software built-in medians . Results Serum AFP level was positively correlated with the gestational week (P<0 .01) ,the HCG level was negatively correlated with the gestational week (P< 0 .01);the AFP and HCG levels were negatively correlated with the body weight of pregnant woman (P<0 .01) .Before correcting the body weight ,compared with software built-in human source serum markers ,the average levels of serum AFP and HCG in Xiangxi area increased by 6 .73% and 31 .54% respectively ,the differences were statistically sig-nificant ,after correcting the software ,the screening false positive rate was remarkably decreased .Conclusion The establishment of serum maker medians for second trimester pregnant woman in Xiangxi area can increase the efficiency of the second trimester DS screening ,thus effectively screens out the DS fetus in local area .

Medullary thyroid cancer is a kind of rare malignancy arising from unregulated replication of parafollicular C cells of the thyroid gland. Therapeutic approaches to patients with medullary thyroid cancer have their own features,which are different from those to patients with papillary thyroid cancer,the most com-mon type of thyroid cancer. The targeted therapy using tyrosine kinase inhibitors has brought new hope for the management of aggressive medullary thyroid cancer in recent years.

Objective To observe the effects of subretinal transplantation of rat mesenchymal stem cells (rMSCs) on Sodium Iodate (SI)-induced retinal degeneration.Methods One hundred and twenty Brown-Norway (BN) rats were divided into three groups including SI injection group,rMSCs transplantation group and normal control group,each with 40 rats.The retinal degeneration was induced by caudal vein injection of SI.The retinal pigment epithelium(RPE)and neural retinal were evaluated by ocular fundus photograph,fluorescein fundus angiography (FFA),electroretinogram (ERG) and histological approach,and TUNEL(terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling).CM-Dilprelabeled primary rMSCs were transplanted into the subretinal space of Sl-induced rats.The survival,integration,and differentiation of rMSCs were observed between 14 day to 60 day after the transplantation.Results The rat retinal function was gradually reduced afterl4 days of SI injection,with a time-dependent manner.After the RPE cells were damaged,the outer segments of photoreceptors became disrupted and shortened until karyopyknosis.The nuclear morphology and positive TUNEL labeling indicated that the death of photoreceptor cells was apoptosis.After rMSCs transplantation,CM-DiI labeled donor cells were observed to be scattered in the subretinal space and expressed RPE cell markers.Average amplitude of bwave and Ops (oscillation potential) in ERG improved 27.80%,59.38% respectively after rMSCs transplantation.Conclusions Transplanted rMSCs can survive in subretinal space and differentiate into RPE cells,thus cure SI- induced retinal degeneration.