Objeetive To explore the relationship among the glomerular mesangium components,degree of renal lesion and glomerulosclerosis in patients with type 2 DM.Method A quantitative study of type Ⅳ collagen in kidneys taken from twenty-one patients with type 2 DM and ten-two control autoptical renal tissue specimens were investigated by immunochemical techniques,computer image analysis system.Results The amounts of type Ⅳ collagen were increased parallel with advances of glomerulosclerosis and renal arteriolosclerosis in patients with type 2 DM,but the collagen had not obviously elevation in renal failure patients.Conclusions The increased type Ⅳ collagen is a characteristic manifestation of early and moderate lesions of glomerulosclerosis in type 2 DM.Quantitative determination of glomerular mesangium components could be a good index to judge the lesion degree of kidney.

Objective To evaluate the clinical curative efficacy and to explore the leaking pathway of bone cement to verte‐bral canal through treating osteoporotic vertebral burst fractures (OVBF) by using percutaneous kyphoplasty(PKP) .Methods Ac‐cording to AO classification ,45 OVBF patients with 45 vertebras in the Erdos Central Hospital from October 2005 to May 2013 were treated by using PKP .The pathway of bone cement leaking to spinal canal and intervertebral space was determined by postop‐erative CT plain scan .The postoperative vertebral height ,Cobb angle and spinal stenosis improvement were measured .The change of VAS were compared between before and after operation .Results There were 2 cases of bone cement leaking to spinal canal .The leaking passway was mainly through basivertebral foramen .The leakage of bone cement to superior intervertebral space was higher than that to lower intervertebral space .The recovery of the vertebral height ,correction of Cobb angle and pre‐and post‐operative VAS scores had statistically significant differences (P<0 .05) .The spinal stenosis rate had no statistical difference between before and after operation(P>0 .05) .Conclusion PKP for treating OVBF is not a contraindication .The main pathway of bone cement lea‐king to spinal canal is basivertebral foramen after the treatment of OVBF by using PKP ,the leakage to intervertebral space is relat‐ed with the endplate damage .

Objective To observe the effect of Ginkgolide B of various consistency on the differentiation of neuron stem cells (NSCs).MethodsNSCs were cultured in differentiation medium containing Ginkgolide B of various consistency for 3 and 7 days, the neurites length and cell body area were measured by inverted phase-contrast micrograph, then neurofilament-200 (NF-200), glial fibrillary acidic protein (GFAP), adenomatus polyposis coli (CC-1) expression were detected and counted by fluorescence microscope. The suppressor of cytokine signaling-2 (SOCS2), inhibitor of DNA binding-2 (Id2) were alsoimmunostained. The percentage of positive cells were counted respectively.ResultsThe neurites length and cell body area in Ginkgolide B groups were obviously larger than that in the control group. The percentage of NF, GFAP positive cells in Ginkgolide B groups increased with dosage increasing of Ginkgolide B. Compared with the normal control group, the percentage of SOCS2 positive cells increased significantly ( P<0.01) and the percentage of Id2 positive cells decreased significantly ( P<0.01) in Ginkgolide B groups.ConclusionGinkgolide B can promote NSCs to differentiate into neuron and astrocyte, the percentage of astrocyte is increased with a dosage-dependent relationship with Ginkgolide B.

Objective To evaluate the therapeutic effect of Huangqin Decoction(HQD)on ulcerative colitis(UC)in mice and explore its mechanism.Methods Male Balb/c mice were randomly divided into normal control group,model group,mesalazine group(5-ASA,200 mg/kg),and low-,medium-and high-dose HQD groups(2.275,4.55 and 9.1 g/kg,respectively).With the exception of those in the normal control group,all the mice were exposed to 3%DSS solution in drinking water for 7 days to establish UC models.After treatment with the indicated drugs,the mice were assessed for colon injury and apoptosis using HE,AB-PAS and TUNEL staining,and the expression levels of inflammatory factors were detected with ELISA.Western blotting,immunohistochemistry and qRT-PCR were used to detect the changes in protein expressions associated with the intestinal chemical barrier,mechanical barrier and endoplasmic reticulum stress(ERS).Results HQD treatment significantly reduced DAI score and macro score of UC mice,decreased colonic epithelial cell apoptosis,lowered expressions of IL-6,TNF-α,IL-1β and IL-8,and enhanced the expressions of MUC2 and TFF3.HQD treatment also upregulated the protein expressions of claudin-1,occludin and E-cadherin,reduced the expressions of GRP78,CHOP,caspase-12 and caspase-3,decreased the phosphorylation levels of PERK,eIF2α and IRE1α,and increased the Bcl-2/Bax ratio in the colon tissues of UC mice.Conclusion HQD inhibits colonic epithelial cell apoptosis and improves intestinal barrier function in UC mice possibly by reducing ERS mediated by the PERK and IRE1α signaling pathways.

Objective To evaluate the therapeutic effect of Huangqin Decoction(HQD)on ulcerative colitis(UC)in mice and explore its mechanism.Methods Male Balb/c mice were randomly divided into normal control group,model group,mesalazine group(5-ASA,200 mg/kg),and low-,medium-and high-dose HQD groups(2.275,4.55 and 9.1 g/kg,respectively).With the exception of those in the normal control group,all the mice were exposed to 3%DSS solution in drinking water for 7 days to establish UC models.After treatment with the indicated drugs,the mice were assessed for colon injury and apoptosis using HE,AB-PAS and TUNEL staining,and the expression levels of inflammatory factors were detected with ELISA.Western blotting,immunohistochemistry and qRT-PCR were used to detect the changes in protein expressions associated with the intestinal chemical barrier,mechanical barrier and endoplasmic reticulum stress(ERS).Results HQD treatment significantly reduced DAI score and macro score of UC mice,decreased colonic epithelial cell apoptosis,lowered expressions of IL-6,TNF-α,IL-1β and IL-8,and enhanced the expressions of MUC2 and TFF3.HQD treatment also upregulated the protein expressions of claudin-1,occludin and E-cadherin,reduced the expressions of GRP78,CHOP,caspase-12 and caspase-3,decreased the phosphorylation levels of PERK,eIF2α and IRE1α,and increased the Bcl-2/Bax ratio in the colon tissues of UC mice.Conclusion HQD inhibits colonic epithelial cell apoptosis and improves intestinal barrier function in UC mice possibly by reducing ERS mediated by the PERK and IRE1α signaling pathways.