Objective To explore the variation of the plasma high-sensitive C reactive protein (hs-CRP) levels and analyze the relationship between inflammation and malnutrition in the patients with stage V chronic kidney disease (CKD). Methods Ninety patients with stage V CKD were enrolled. The patients were divided into three groups according to their treatment, no dialysis (ND) group, hemodialysis (MHD) group and continuous ambulatory peritoneal dialysis (CAPD) group. Plasma hs-CRP, albumin and hemoglobin were detected. Results The levels of plasma hs-CRP were significantly increased in the patients with stage V CKD compared with normal individuals (P< 0.01). It showed a significant difference between MHD group, CAPD group and ND group (P < 0.05), while no significant difference was found between MHD group and CAPD group. The plasma hs-CRP levels increased in the patients with lower plasma albumin (< 35 g/L) or lower hemoglobin (< 90 g/L). Levels of plasma hs-CRP showed a negative relationship with plasma albumin and hemoglobin (r =- 0.535, P < 0.01 ;r =-0.220, P < 0.05). Conclusions Plasma hs-CRP levels increase in patients with stage V CKD, and there is a negative relationship between hs-CRP and plasma albumin and hemoglobin. Inflammation may be a factor of malnutrition in patients with CKD.

Objective To induce and identify the differentiation of rat bone marrow mesenchymal stem cells(MSCs)into cardiomyocytes in vitro,and observe the expression of Nesprin protein during the differentiation. Methods Rat MSCs were isolated and purified by Ficoll density gradient centrifugation,and adhered for serial subcultivation.Surface-associated antigens of MSCs of the second passage were dedected by flow cytometry.MSCs of the second passage were induced by 10μmol/L 5-azacytidine(5-Aza)to differentiate into cardiomyocytes,and the morphological changes were observed.The expression of Desmin,α-sarcomeric actin and cardiac Troponin I(cTnI) mRNA and protein was detected by RT-PCR,immunocytochemistIv and immunofluorescence staining, and the expression of Nesprin protein was detected by Western blotting. Results The morphology of MSCs induced by 5-Aza was bigger and longer,and the nuclei became bigger,exhibiting more consistent patterns.The expression of Desmin,α-sarcomeric actin and cTnI mRNA and protein of MSCs was positive.Immunofluorescence staining revealed that Nesprin protein positioned in the nuclear membrane,and Western blotting detection demonstrated that the expression of Nesprin protein significantly increased after differentiation(P<0.05).Conclusion MSCs may be successfully induced to differentiate into cardiomyocytes.The expression of Nesprin protein in the differentiated MSCs may significantly increase,indicating Nesprin may play a role in the differentiation from MSCs to cardiomyocytes.

Objective:To investigate the mechanism by which chronic psychological stress aggravates intestinal barrier damage and promotes the development of enteritis through inhibiting Wnt/β-catenin pathway, so as to provide a new therapeutic strategy for the clinical diagnosis and treatment of inflammatory bowel disease (IBD).Methods:A comorbidity model of chronic psychological stress and enteritis was established using C57BL/6J mice. HE staining was used to analyze the effects of chronic psychological stress on the intestinal pathological damage in mice with enteritis. ELISA was used to detect the expression of proinflammatory cytokines. The ultrastructural changes of colonic cells and the state of intestinal mucus layer were observed under transmission electron microscope and scanning electron microscope. The secretion of mucoprotein 2 (MUC2) and the expression of cell proliferation marker Ki67 were detected by immunofluo rescence staining. The numbers of goblet cells were detected by Alcian blue-periodic acid-Schiff (AB-PAS) staining. Western blot was performed to analyze the expression of tight junction protein between intestinal epithelial cells, β-catenin which was a key protein of Wnt/β-catenin pathway maintaining crypt proliferation, and downstream protein c-myc.Results:The sugar water consumption ratio decreased, but tail suspension immobility time, the swimming immobility time and the expression of corticotropin releasing hormone (CRH) in hypothalamus increased (all P<0.05) in the stress group as compared with those in the control group. Chronic psychological stress promoted weight loss and colonic shortening in mice with enteritis, exacerbated pathological damage and enhanced the release of pro-inflammatory factors. Moreover, increased disappearance of intestinal epithelial microvilli and severe cellular ultrastructural damage were also observed in the stress+ dextran sulfate sodium salt (DSS) group. There was no pathological damage in the control and stress groups. Chronic psychological stress aggravated intestinal barrier injury and inhibited intestinal barrier repair by inhibiting Wnt/β-catenin pathway. Conclusions:In the mouse model of DSS-induced enteritis, chronic psychological stress preconditioning inhibited the Wnt/β-catenin pathway, weakened the repair ability of intestinal epithelium, aggravated the loss of mucus layer of intestinal barrier and the damage of tight junction structure, and promoted the development of enteritis. In the absence of enteritis, chronic psychological stress had no significant effects on the Wnt/β-catenin pathway and the intestinal barrier.

Objective: To explore the mechanism of miR-19a-3p regulating cell adhesion molecule 2 (CADM2) to inhibit the proliferation and metastasis of renal carcinoma cells via the AKT signaling pathway. Methods: A total of 42 patients with renal cancer admitted to Department of Nephrology, the First Affiliated Hospital of Suzhou University from April 2012 to November 2017 were enrolled to collect samples of surgically resected renal carcinoma tissues and paracancerous tissues. Expression of miR-19a-3p was detected in renal carcinoma tissues and 4 types of renal carcinoma cell lines such as 786-O by quantitative Real-time polymerase chain reaction (qPCR). The effects of miR-19a-3p knockdown on proliferation, invasion and epithelial mesenchymal transition (EMT) of renal carcinoma 786-O cells were evaluated by CCK-8 assay, Transwell assay and immunofluorescence, respectively. Subsequently, dual luciferase reporter assay was used to verify whether CADM2 was a target gene of miR-19a-3p. Furthermore, Wb was applied to detect the regulatory effect of miR-19a-3p onAKT signaling pathway through CADM2. Results: miR-19a-3p expression was significantly up-regulated in renal carcinoma tissues and cell lines (all P<0.01). Knockdown of miR-19a-3p could inhibit proliferation, invasion and EMT process of 786-O cells; furthermore, the results indicated that CADM2 was a direct target of miR-19a-3p and its expression was down-regulated (P <0.05 or P<0.01). Additionally, knockdown of miR-19a-3p obviously suppressed proliferation, migration and EMT process of 786-O cells via up-regulating CADM2 and blocking AKT pathway (all P<0.05 or P<0.01), thus alleviating the occurrence and development of renal carcinoma. Conclusion: The study demonstrates that miR-19a-3p has a high expression level in renal carcinoma tissues; knockdown of miR-19a-3p could significantly inhibit the proliferation, migration and EMT process of renal carcinoma tissues, and its mechanism may be associated with miR-19a-3p/CADM2/AKT axis.