Objective To design and manufacture the simple lower fixtures of WXX2000 field medical box group, the medical boxes ZT-4-1 as an example. The principle, instrument, process and the applying of the device were introduced. Methods Based on the guidance principle of the ZT-4-1 medical box, the size of lower space and ampoule of the ZT-4-1 medical box were measured and design its layout, and then suitable instruments and materials of the device was selected, and external fixed wooden box and foam stuffing were produced step by step. Results The simple lower fixture is available for fixed and transportation safety. Conclusion The simple device is effective for fixed effect and can be used extensively.

Objective:To study the effect of interleukin-18 on transdifferentiation in renal tubular epithelial cells(TECs).Methods:Human proximal tubular epithelial cell line(HK-2) was cultured in vitro.TECs were exposed to different concentrations(0,0.1,1,10 and 100 ng/ml) of IL-18 for 24,48 and 72 hours.At the end of each incubation,the expressions of the ?-SMA and TGF-?_1 mRNA were assessed by RT-PCR,the rate of ?-SMA expressing TECs was assessed by immunocytochemistry,and the expression of the ?-SMA protein was assessed by Western blotting.Results:(1)The expressions of ?-SMA and TGF-?_1 mRNA were increased significantly by a dose- and time-dependent manner when TECs were exposed to IL-18(P

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BACKGROUND:Previous study has found that hsa-miR-182 is probably related to the apoptosis-related genes such as cytochrome C (Cycs C) and calcineurin subunit CnB (PPP3R1) in nucleus pulposus cells.
OBJECTIVE:To determine whether miR-182 plays a regulatory role in nucleus pulposus cel apoptosis by detecting the relative gene expression levels after transfecting miR-182 with Cycs C and PPP3R1 into nucleus pulposus cel s via plasmid delivery.
METHODS:After a bioinformatics prediction about miR-182, miR-182 and target genes were transfected into the nucleus pulposus cel s, and at the same time, blank control group was established. Then the expression levels of the target genes were detected through cel lysis.
RESULTS AND CONCLUSION:miR-182 significantly inhibited the expression of Cycs C in nucleus pulposus cel s compared with the blank control group (P<0.05). Compared with the blank control group, miR-182 made no inhibitory effect on the expression of PPP3R1. These findings suggest that miR-182 may play a regulatory part in nucleus pulposus cel apoptosis by inhibiting the expression of Cycs C.

Objective To investigate the effects of Free fatty acids (FFAs) on extracellular matrix(ECM) mRNA expression and secretion.Methods Rat glomerular mesangial cells(HBZY-1 cells) were cultured in vitro and stimulated with OA in different concentration.The expression of collagen Ⅳ(Col Ⅳ) and fibronectin (FN) and transforming growth factor-beta1(TGF-?_1) mRNA were measured by semi-quantitative RT-PCR.The levels of Col Ⅳ and FN in cultured supernatant were determined by ELISA.Results The mRNA expression of Col Ⅳ, FN and TGF-?_1 of 25、100、400 ?mol/L stimulated OA groups were 0.94?0.17、1.16?0.15、1.28?0.19 and 0.82?0.11、0.97?0.07、1.09?0.08 and 1.15? 0.07、1.24?0.06、1.36?0.05 respectively , which increased significantly compared with their control group(0.73?0.16、0.53?0.09、 0.96?0.11 P

Aim To investigate the effects of Panax Notoginsenosides(PNS) on the gene expression and protein excretion of TGF-?_1 and CTGF of human renal tubular epithelial cell induced by uremic serum in vitro.Methods Forty sera from CRF patients and twenty sera from healthy volunteers were collected,gently mixed,inactived and separated respectively in steriled condition.HK-2 Cells were cultured in RPMI-1640 medium with 10% newborn calves serum and subcultured routinely.They were differentiated by phase contrast microscope and scanning electron microscope detection and cytokeratin18(CK-18) immunohistochemistry method.The protein levels of TGF-?_1 were examined by enzyme-linked immunoadsordent assay(ELISA).The protein levels of CTGF were examined by Western Bloting assay.The gene expression of TGF-?_1 and CTGF was detected by Semi-quantitative reverse trainscriptase polymerase chain reaction(RT-PCR).Results TGF-?_1 and CTGF gene expression and protein level were increased in 10% uremic serum groups compared with that of normal control group(P

10 000 D uremic toxin through promoting the gene and protein expression of CTGF in renal tubular epithelial cells in patients with chronic renal failure.

AIM: To investigate the effects of interleukin-13(IL-13) on the inflammatory reaction of glomerular mesangial cells. METHODS: TNF-? protein in the supernatant of cultured mesangial cells was determined with ELISA. ICAM-1 expression on the mesangial cells was determined with flow cytometry. The expression of TNF-? mRNA and ICAM-1 mRNA were semiquantatively tested with RT-PCR. RESULTS: Mesangial cells did not constitutively express TNF-? mRNA and TNF-? protein. Induced by LPS(10 mg/L) for 24 h, mesangial cells expressed TNF-? mRNA and TNF-? protein at a high level. At the concentration of 1 ?g/L and 10?g/L, IL-13 markedly inhibited LPS-induced TNF-? mRNA and protein expression in mesangial cells. At the concentration of 100?g/L, IL-13 completely inhibited LPS-induced TNF-? mRNA and protein expression in mesangial cells. ICAM-1 constitutively expressed on the surface of mesangial cells at very low level. Induced by TNF-?(100?g/L), mesangial cells expressed ICAM-1 mRNA and ICAM-1 cell surface molecule at high level. Costimulated mesangial cells with IL-13(10?g/L) and TNF-?(100?g/L), IL-13 inhibited TNF-?-induced ICAM-1 mRNA and cell surface molecule expression at every time course. CONCLUSION: IL-13 not only inhibits LPS-induced TNF-? expression but also inhibits TNF-?-induced ICAM-1 expression in mesangial cells. These data suggest that IL-13 inhibits the inflammatory reaction in mesangial cells.

V infection group than in no infection group,while positive rate of other autoantibodies was not statistically different between the two groups.Conclusion Renal EBV infection may involve in the pathogenesis of LN by inducing the production of anti-Sm-Ab.