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Objective:To investigate the effect of BMSC transplantation on the recovery of neurological function in rats with cerebral infarction,and to explore the related mechanism.Methods:90 rats were randomly divided into 3 groups:sham operation group,control group,BMSC transplantation group,30 rats in each group.The control group and BMSC transplantation group established middle cerebral artery occlusion (MCAO) model,the sham operation group only need to separate the cervical tissue of rats,and MCAO model in the MCAO model operation.After 1 days of BMSC transplantation group by intravenous injection of 1 mL 3× 106 BMSC,the control group was injected with the same dose of NS in MCAO after 1 D,3 D,7 d,14 d,21 d,28 d,35 d,42 d,49 D respectively,the neurological function score of rats (mNSS),after 2 months of transplantation BMSC group and control group of brain tissue for immunohistochemical staining,detection of MAP2,TUJ1,Ⅷ factor,the expression of GFAP.Results:In seventh to thirty-fifth days after treatment,BMSC mNSS transplantation group were significantly lower than the control group (P < 0.05).2 months after BMSC transplantation group MAP2,TUJ1,Ⅷ expression level was significantly higher than the control group,while the control group,the expression of GFAP was significantly higher than that of BMSC group (P < 0.01).Conclusion:BMSC transplantation in order to promote the recovery of neurological function in cerebral infarction.
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Purpose To investigate the role of S3I-201 on tubular interstitial lesion in lupus nephritis.Methods MRt/MpJ mice were designated as the control group.MRL/lpr nice were randomly divided into LN group,S3I-201 group and DMSO group.The serum and 24 h-urine were collected to detect the serum creatinine,blood urea nitrogen and urine protein.Immunohistochemistry was used to detect the expression of FN.Western blotting analysis was used to determine the expression of E-cadherin,α-SMA,MCP-1,ICAM1,STAT3 and p-STAT3.Results Compared with the expression level in control group,the protein level of α-SMA,MCP-1,ICAM1 and FN were increased in renal tissue of MRL/lpr mice,while the expression of E-cadherin was markedly decreased.And the STAT3 was activated in renal tissue of MRL/lpr mice.The administration of S3I-201 could inhibite the activation of STAT3 and ameliorate the expression of E-cadherin,α-SMA,MCP-1,ICAM-1 and FN.Conclusion S3I-201 can relieve the tubular interstitial leison,which maybe concerned with the phosphorylation of STAT3.
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Objective To investigate healthcare-associated infection(HAI)in patients in a cancer hospital,provide reference for controlling HAI in cancer patients,and guide rational use of antimicrobial agents.Methods Clinical data of patients in a cancer hospital between August 2006 and July 2012 were analyzed retrospectively.Results The incidence of HAI case was 1 .53% (2 060/134 389),and annual incidence showed a downward trend.The main in-fection site was lower respiratory tract (46.46%,n=957),followed by bloodstream (15.63%,n=322),abdominal and pelvic (14.03%,n=289).The main pathogens were Pseudomonas aeruginosa (16.16%,n=350),Staphylo-coccus aureus (9.97%,n=216),Klebsiella pneumoniae (9.79%,n=212),Escherichia coli (9.65%,n=209), and Candida albicans (6.51 %,n=141 ).Gram-negative bacilli,including Klebsiella pneumoniae and Escherichia coli ,were sensitive to carbapenems and β-lactamase inhibitors.Conclusion Lower respiratory tract is the major HAI site in patients with cancer,and gram-negative bacteria are the main pathogens.Carbapenems andβ-lactamase inhibitors are recommended for the empirical treatment of HAI in cancer patients.
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Purpose To investigate the role of SOCS3 on diabetic renal injury. Methods Male CD-1 mice were randomly divided into four groups:control group, diabetic group, empty plasmid vector transfection group and SOCS3 plasmid transfection group. The diabet-ic mice were induced by intraperitoneal injection of STZ at a dose of 150 mg/kg body weight. The mice of transfection group were re-ceived an injection of SOCS3 plasmid or empty vector at every 7 days thereafter. Specimens were collected at 12 week after STZ injec-tion. The morphological changes of tubular epithelial cells were observed by transmission electron microscope. RT-PCR and immuno-histochemistry were used to determine the mRNA and protein expression of CK18 and α-SMA. Western blotting analysis was used to determine the protein expression of SOCS3, p-STAT3, CK18 and α-SMA. Results SOCS3 overexpression in kidney down-regulated the levels of p-STAT3 andα-SMA but up-regulated the expression of CK18. Conclusion Overexpression of SOCS3 can ameliorate the tubular epithelial-mesenchymal transdifferentiation of diabetic mice via inhibiting the phosphorylation of STAT3.