ObjectiveTo determine whether simvastatin alleviates lower urinary tract symptoms (LUTS) in patients with metabolic syndrome (MS) coexisting with benign prostate hyperplasia (BPH) and explore an optimized scheme of treatment. MethodsFrom February to June in 2011,30 male subjects with MS and LUTS caused by BPH in out-patients and in-patients from geriatric department were recruited.The patients were randomly assigned to receive orally simvastatin (40 mg) and tamsulosin (0.2 mg) quaque noete as combination treatment group or only tamsulosin (0.2 mg,quaque nocte) as single treatment group for 8 weeks.International prostate symptoms score (IPSS),quality of life (QOL),maximum flow rate (MFR) and prostate volume (PV),liver enzymes,creatinine and routine urine test were monitored to evaluate the effectiveness and safety before and after the treatment.Results In the two groups,the significant differences were found in the levels of IPSS,QOL and MFR,while there was no difference in PV between pre-treatment and post-treatment.The scores of IPSS after treatment were (6.4 ± 4.4) in combination treatment group and(4.2±3.3)in single treatment group (P＜0.05),and there were significant difference in scores of IPSS before and after the treatment between two groups (P＜0.05),suggesting better improvement in combination treatment group than in single treatment group.In two groups,there were no adverse events,and no changes were found in liver and kidney function,muscle enzymes and routine urine test.Conclusions Combined tamsulosin and simvastatin treatment may alleviate LUTS caused by BPH and are well tolerated with no adverse events.

The source of seed cells has always been the major problem in cartilage tissue engineering.Bone marrow stromal cells (BMSCs) have gradually become an optimal source of seed cells for cartilage engineering due to their high proliferative potential,multi-lineage differentiation potential and easiness to be obtained with minute trauma.The great challenge is how to get abundant BMSCs with a high purity and how to induce them in vitro into chondrogenic phenotype.This review aims to discuss the various strategies that can induce BMSCs chondrogenic differentiation in vitro so as to offer beneficial reference for constructing cartilage with BMSCs as seed cells.

Articular cartilage defects are commonly found in clinics. It is always a great challenge for the repair of cartilage defects due to the limited self-regeneration after injury. Tissue engineering,a newly emerging biotechnique to regenerate cartilage with chondrogenic potential cells and biodegradable scaffolds in vivo and in vitro,provides a promising method to solve the challenge in cartilage defects repair. To regenerate cartilage with favourable structure and function,it is essential to gain a deep insight into the biochemical structure,biomechanical property and their relationship of articular cartilage. This article gives an introduction to the biochemical structure,biomechanical property and their relationship of both native and tissue-engineered cartilage.

Objective To investigate the effects of 15-deoxy-?12,14-prostaglandin J2(15d-PGJ2) and DDP on the growth of human pulmonary carcinoma PLA-801D cells and the mechanisms of apoptosis.Methods The human pulmonary carcinoma PLA-801D cells were selected and added to each well of 96-well place and cultivated for 24 h.Then the cells were treated with different concentrations of 15d-PGJ2(0,5,10,20,40 and 80 ?g?L-1) or 15d-PGJ2 combined with DDP(3 mg?L) for 24 h.0 ?g?L-1 15d-PGJ2 group was control group.The morphological changes of cells were observed under inverted microscope.Microculture tetrazolium(MTT)dye was applied to detect the proliferation of the human pulmonary carcinoma PLA-801D cells treated with 15d-PGJ2 and DDP.Diphenylamine assay(DPA) was used to evaluate the activation.Flow cytometry assay(FCM) was used to detect the apoptosis proportion and the changes of cell cycle.Results When the human pulmonary carcinoma PLA-801D cells were treated with low-concentration 15d-PGJ2 alone(5,10 and 20 ?g?L-1),no significant difference was observed in the inhibitory rate of cell growth and the apoptotic indexes such as the apoptosis proportion,the percent of DNA fragmentation and the activity of caspase-3 compared with control group(P

Aim To investigate the effects of rosiglitazone(ROZ)combined with cisplatin(DDP)on the growth of transplanted lung adenocarcinoma in mice and the corresponding mechanism.Methods The human lung adenocarcinoma mode was established with A549 cell in nude mice.Twenty eight female Balb/c-nu mice with lung adenocarcinoma were randomly divided into seven groups.① control group;② low-dose DDP group(1 mg?kg-1);③ high-dose DDP group(4 mg?kg-1);④ low-dose ROZ group(10 mg?kg-1);⑤ high-dose ROZ group(30 mg?kg-1);⑥ low-dose DDP plus low-dose ROZ group;⑦ low-dose DDP plus high-dose ROZ group;all the mice were sacrificed at 48 h after the last injection.Subcutaneous tumor was subjected to histological examination.Expressions of PPAR?、PTEN and pAkt in tumor tissues were detected by immunohistochemistry.Results ① In every treatment group tumor growth was suppressed significantly.Intraperitoneal injection of low and high-dose DDP,low and high-dose ROZ,low-dose DDP plus low-dose ROZ and low-dose DDP plus high-dose ROZ group resulted in a significant inhibition of the growth of A549 cells in vivo compared with that of control group(P

OBJECTIVETo investigate the in vitro proliferation of CD4(+)CD25(+) T cells from the peripheral blood mononuclear cells (PBMCs) of the chronic myelocytic leukemia patients and the inhibitory effect on CD4(+)CD25(-) T cells.

METHODSMagnetic-activated cell sorting (MACS) was used to separate CD4(+)CD25(+) T and CD4(+)CD25(-) T cells from the PBMCs of patients with chronic myelocytic leukemia, and the purity and activity of CD4(+)CD25(+) T cells were analyzed with flow cytometry. After stimulation with anti-CD3 mAb, anti-CD28 mAb and recombinant human interleukin-2 (rhIL-2), the CD4(+)CD25(-) and CD4(+)CD25(+) T cells were cocultured to observe the inhibitory effect of CD4(+)CD25(+)T on CD4(+)CD25(-)T cells using MTT assay.

RESULTSAfter cell sorting, the purity of CD4(+)CD25(+)T cells from healthy control and chronic myelocytic leukemia patients were (84.93-/+2.55)% and (86.32-/+2.40)%, respectively, showing no significant difference between them (P>0.05). The activity of CD4(+)CD25(+) and CD4(+)CD25(-) T cells from healthy control and the leukemic patients was also comparable [(98.12-/+0.68)% vs (97.33-/+0.78)%, P>0.05). In the coculture, CD4(+)CD25(+) T cells obviously inhibited CD4(+)CD25(-) T cell proliferation in vitro, and the maximum inhibition occurred when CD4(+)CD25(+)T cells were cocultured with CD4(+)CD25(-)T cells at the ratio of 1:1.

CONCLUSIONThe MACS system can effectively isolate CD4(+)CD25(+) and CD4(+)CD25(-) T cells. CD4(+)CD25(+) T cells obviously inhibit the proliferation of CD4(+)CD25(-)T cells in vitro, and the effect displays an effector-target ratio relationship.

Adult ; CD4 Antigens ; immunology ; Cell Proliferation ; Coculture Techniques ; Female ; Humans ; Interleukin-2 Receptor alpha Subunit ; immunology ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; blood ; immunology ; pathology ; Leukocytes, Mononuclear ; immunology ; pathology ; Male ; Middle Aged ; T-Lymphocyte Subsets ; immunology ; pathology ; T-Lymphocytes, Regulatory ; immunology ; pathology ; Young Adult

OBJECTIVETo study the effects of small interfering RNA (siRNA)-mediated silencing of CD158b expression on the efficiency of the natural killer (NK) cells in killing allogeneic dendritic cells.

METHODSAfter the knockdown of CD158b by CD158b -SiRNA, the CD158b mRNA expression in natural killer cells was examined by qRT-PCR and the CD158b protein expression by flow cytometer. The cytotoxic activity of RNAi-NK cells and normal NK cells against the allogeneic dendritic cells was detected by LDH release assay.

RESULTSThe CD158b mRNA expression and its protein expression were decreased significantly in the NK cells by CD158b siRNA (P/0.05). The cytotoxic activities of alloreactive NK cells generated by RNAi CD158b expression against allogeneic dendritic cells were increased significantly.

CONCLUSIONSilencing CD158b gene can inhibit the NK cell CD158B mRNA and protein expression. Alloreactive NK cells generated by RNAi CD158b expression have the potential for use in interventions of GVHD.

Bone Marrow Transplantation ; immunology ; methods ; Cytotoxicity, Immunologic ; immunology ; Dendritic Cells ; cytology ; immunology ; Flow Cytometry ; Gene Silencing ; Graft vs Host Disease ; immunology ; Humans ; Killer Cells, Natural ; cytology ; immunology ; RNA Interference ; RNA, Messenger ; biosynthesis ; genetics ; RNA, Small Interfering ; genetics ; Receptors, KIR ; metabolism ; Receptors, KIR2DL3 ; genetics ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction

Objective To evaluate the contrast-enhanced ultrasonography (CEUS) in quantitative diagnosis of chronic renal insufficiency. Methods Correlation of CEUS indexes with glomerular filtration rate (GFR) detected by 99mTc-DTPA renography was examined. Thirty-three cases of clinical chronic renal insufficiency were enrolled in the study. They were 15 males and 18 females with average age of (43.33±6.78) years. After intravenous bolus injection of 1 ml SonoVue,CEUS of renal cortex blood perfusion was performed successfully, and a time-intensity curve (TIC)was created with PHILIPS iU22 system's QLAB software. A 148 to 222 MBq dose of 99mTc-DTPA was injected as a bolus from antecubital vein. Renal scintigraphic images were collected immediately and GFR was obtained. Results The significant correlation coefficients between GFR and CEUS quantitative indexes were as follows: rAUC (area under curve)=0.886 (P＜0.05), rA (slope rate of ascending curve, A) =0.804(P＜0.05). However, rDPI (derived peak intensity, DPI)=0.021 (P＞0.05), rTTP (time to peak, TTP) =0.043 (P＞0.05), rα (slope rate of descending curve,α)=0.039 (P＞0.05). Conclusion CEUS can precisely display the hemodynamic change of chronic renal insufficiency, which is well correlated with GFR by 99mTc-DTPA renography.

Objective To evaluate the value of contrast-enhanced ultrasonography (CEUS) in quantitative diagnosis of chronic kidney dysfunction(CKD) by comparing it with color Doppler imaging (CDFI). Methods Tirty-three cases (15 males and 18 females) of clinical confirmed CKD (stage Ⅲ～Ⅴ)were included. Forty-five healthy volunteers were performed as control group. CEUS and CDFI were performed on each patient. After intravenous bolus injection of 1ml SonoVue each side,CEUS of renal cortex blood perfusion was collected successively,and a time-intensity curve(TIC) was created with Philips iU22 system's QLAB software. Resistance index(RI) and peak systolic velocity(PSV) of renal partial arteries were also tested. Results Compared with normal kidney,CKD patients had delayed perfusion and decreased intensity. Changes of area under curve(AUC), derived peak intensity(DPI), slope rate of ascending curve(A)and time to peak(TTP) were statistically significant ( P ＜0. 05). Sensitivities of AUC,DPI,A and TTP in diagnosis of CKD (stage Ⅲ～Ⅴ ) were 91.2% ,84. 9% ,90.9% and 85.3%, their specificities were 95.4%,88.9% ,93.3% and 90.9%, their accuracies were 93.6%, 87. 2%, 92.3% and 88. 5%, respectively. The results of CEUS were better than RI in CDFI (sensitivity 70.4%, specificity 37. 8%, accuracy 52.2%).Conclusions CEUS can precisely display the hemodynamic change in CKD ( stage Ⅲ～Ⅴ ), and is more sensitive than CDFI.

Objective To investigate the dynamic expressions of epidermal growth factor receptor (EGFR) in mice with liver fibrosis and the effect of bone morphogenetic protein-7 (BMP-7) intervention on the expression of EGFR,and to explore a new therapy target for fibrosis.Methods A total of 30 healthy male ICR mice were randomly divided into three groups:6 mice in control group,18 mice in hepatic fibrosis group and 6 mice in BMP-7 intervention group.The model of mice with liver fibrosis was established by subcutaneous injection of carbon tetrachloride (CCl4) for 12 weeks.After administration of CCl4 for 8 weeks,human recombinant BMP-7 was given into mice in intervention group by intraperitoneal injection for 4 weeks.Hematoxylin-Eosin and Masson staining of liver tissues were employed to observe the pathological changes,and the semi-quantitative analysis of liver fibrosis was performed.Blood withdrawn from inferior vena cava was detected for levels of alanine aminotransferase (ALT),aspartate aminotransferase (AST) and albumin (Alb).The expressions of transforming growth factor-β1 (TGF-β1)mRNA and TGF-β1,EGFR,phosphorylation EGFR (pEGFR) protein in each group were detected using quantitative real time polymerase chain reaction and Western blot.Measurement date was compared using analysis of variance and Pearson correlation analysis.Results The model of mice with liver fibrosis was successfully established.In model group,the serum levels of ALT and AST increased,while the level of Alb decreased gradually.All these biochemical index improved after intervention of BMP-7 (ALT:[153.9±18.1] U/L vs [191.3±24.5] U/L;AST:[177.8±19.2] U/L vs [206.6±25.0] U/L;Alb:[25.4±0.9] g/L vs [22.2±1.2] g/L; all P＜0.05).With the progress of fibrosis,TGF-β1,EGFR and pEGFR protein expressions increased gradually in model group and reached a peak at week 12,which was significantly different compared to the control group (all P＜0.05).In BMP-7 intervention group,the expressions of the three proteins decreased significantly compared to model group (TGF-β1:0.256 ± 0.006 vs 0.287±0.014,EGFR:1.061±0.017 vs 1.094±0.014,pEGFR:0.855±0.053 vs 1.007±0.063;all P＜0.05).Additionally,linear correlation analysis showed that expressions of both EGFR and pEGFR proteins were positively correlated with TGF-β1 protein (rs =0.895 and 0.859,respectively; both P＜0.05).Conclusions BMP-7 can suppress the pathogenesis of mouse liver fibrosis.The mechanism may rely on the regulation of EGFR and TGF-β1 expressions.