Objective To explore the quality of life (QOL) and its influential factors among patients with 3 major rheumatic diseases. Methods A total of 216 patients with rheumatic diseases (84 patients with systemic lu- pus erythematosus, SLE, 83 with rheumatoid arthritis, RA, and 49 with ankylosing spondylitis, AS) were recruited. The information with regard to their quality of life, sociopsychological factors and the evaluation of disease activity were obtained by using the medical outcomes study short form-36 (SF-36) and clinic documents. Results Patients with rheumatic diseases scored significantly lower with each subscale of SF-36 as compared to those of a healthy popu- lation in China (P

The megakaryocyte and platelet lineage may be one of the major sites of human cytomegalovirus (HCMV) infection. However, whether HCMV aggravates apoptosis in normal megakaryocytes was not well investigated. Megakaryocytic cell line CHRF-288-11 and HCMV AD 169 strain were co-cultured in this study. PCR was used to detect the direct infection of the cells by HCMV IEA expression. The apoptotic cells were analyzed by morphologic observation, DNA ladder formation, annexin V/PI and PI assay with flow cytometry. The results showed that HCMV significantly inhibited the growth of CHRF cells in three different concentrations of viral infection groups (10(-3), 10(-2), 10(-1)). The viability levels in each infection groups were 77%, 73% and 68% respectively after incubation for 7 days, compared with 98% in the control group. Using annexin V/PI with flow cytometry, it was shown that the percentages of apoptotic cells viral infection in groups (10(-3), 10(-2), 10(-1)) were (21.3 +/- 2.49)%, (25.8 +/- 3.65)% and (31.4 +/- 3.91)% at 7 days after infection, while the control was (3.68 +/- 1.47)%. The apoptotic cells were further confirmed by morphologic observation and DNA ladder formation. Furthermore, PCR detection also showed the direct infection by identification of HCMV IEA expression in CHRF cells. This study suggested that HCMV could directly infect megakaryocytes and aggravated apoptosis in HCMV-infected megakaryocytes.
Apoptosis ; Cell Survival ; Cells, Cultured ; Cytomegalovirus ; pathogenicity ; DNA, Viral ; analysis ; Humans ; Megakaryocytes ; cytology ; virology ; Polymerase Chain Reaction

Objective: To study retrovirus (RV)-mediated transduction of gastric carcinoma cells with the herpes simplex virus thymidine kinase (HSV-tk) gene and the subsequent treatment with ganciclovir(GCV). Methods: The TK gene was transfected into human gastric carcinoma cell line MKN28 using HSV-TK that packed with PA317 cell, the sensitivity of MKN28TK cells to GCV was examined in vitro. Results: The retroviral-mediated HSV-TK gene can be transfected to MKN28 cells. The growth rate of MKN28 cells transfected with HSV-TK gene did not change. MKN28TK cells became significantly sensitive to GCV and had bystander effect. Conclusion: Transfection of gastric carcinoma with HSV-TK has higher transfection efficiency. MKN28TK cells are significantly sensitive to GCV.

Objective: To study retrovirus (RV)-mediated transduction of gastric carcinoma cells with the herpes simplex virus thymidine kinase (HSV-tk) gene and the subsequent treatment with ganciclovir(GCV). Methods: The TK gene was transfected into human gastric carcinoma cell line MKN28 using HSV-TK that packed with PA317 cell, the sensitivity of MKN28TK cells to GCV was examined in vitro. Results: The retroviral-mediated HSV-TK gene can be transfected to MKN28 cells. The growth rate of MKN28 cells transfected with HSV-TK gene did not change. MKN28TK cells became significantly sensitive to GCV and had bystander effect. Conclusion: Transfection of gastric carcinoma with HSV-TK has higher transfection efficiency. MKN28TK cells are significantly sensitive to GCV.

OBJECTIVETo study the effect of hepatitis C virus core protein (HCV-C) on human normal biliary epithelial cells (BEC) transformation and tumor development.

METHODSBEC cells were transfected with plasmid pcDNA HCV-C (expressing HCV-C) by lipofectamine and selected in G418. The expression of HCV-C gene and protein was determined by PCR and immunohistochemical staining, respectively. Biological effect of transfected cells was observed through cell proliferation assay, anchor independent growth, and tumor development in nude mice. The expression of HCV-C protein in the induced tumor was evaluated by immunohistochemistry.

RESULTSHCV-C was strongly expressed in BEC cells transfected with plasmid pcDNA HCV-C and the positive signal was located in cytoplasm. The HCV-C expression protein in the induced cytoplasm. Cell proliferation assay showed that the population doubling time in the pcDNA HCV-C transfected cells was much shorter than that in the pcDNA3 and non-transfected cells (14 h, 28 h, 30 h respectively). The cloning efficiencies of transfected cells with pcDNA HCV-C, pcDNA3 and non-transfected cells were 36%, 2.5% and 1.5%, respectively (P < 0.01). Tumor developed in nude mice inoculated with pcDNA HCV-C transfected cells after the inoculation. HE staining showed bile duct carcinoma character and immunohistochemistry confirmed HCV-C expression in the tumor tissue. The positive control group also showed tumor development, while no tumor mass obtained in the nude mice inoculated with pcDNA3 and non-transfected cells even 36 days after the injection.

CONCLUSIONHCV-C protein showed human normal biliary epithelial cells transformation and tumorigenic features.

Animals ; Bile Duct Neoplasms ; etiology ; Bile Ducts ; cytology ; Cell Transformation, Neoplastic ; Cell Transformation, Viral ; Cells, Cultured ; Epithelial Cells ; pathology ; Female ; Hepacivirus ; Humans ; Mice ; Mice, Nude ; Plasmids ; Transfection ; Viral Core Proteins ; physiology

OBJECTIVETo improve the therapeutic results of patients with glandular cystitis.

METHODSOne hundred and twenty-seven patients with glandular cystitis were treated according to their different etiological factors. The therapeutic methods included anti-infection, obstruction relief, bladder irrigation, transurethral resection, partial cystectomy, total cystectomy.

RESULTSThe patients who were associated stones and foreign bodies (50%) were cured spontaneously with an effective rate of 94%. The effective rate in patients with low urinary tract obstruction was 84%. Patients with simple urinary tract infection (53%) were cured spontaneously after anti-infection therapy. The effective rate, recurrence rate and malignancy rate in patients without associated diseases were 71%, 46% and 21% respectively.

CONCLUSIONSCystitis glandularis should be treated according to different etiological factors.

Adolescent ; Adult ; Aged ; Combined Modality Therapy ; Cystitis ; pathology ; therapy ; Female ; Follow-Up Studies ; Humans ; Male ; Middle Aged ; Treatment Outcome ; Young Adult

BACKGROUND:No retrievable and repositionable second generation transcatheter aortic valve is available in China. Here, we report the first-in-man implantation of the retrievable and repositionable VenusA-Plus valve. METHODS:A 76-year-old patient with symptomatic severe aortic stenosis and high surgical risk (STS 13.8％) was recommended for transcatheter aortic valve replacement (TAVR) by heart valve team. Type 0 bicuspid aortic valve with asymmetric calcification was identified by dual source computed tomography, and the unfavorable anatomies increased the possibility of malposition and paravalvular leakage during TAVR. Therefore, we used the retrievable and repositionable VenusA-Plus valve for the patient. RESULTS:Transfemoral TAVR was performed under local anesthesia with sedation, and a 26-mm VenusA-Plus valve was successful y implanted. No transvalvular pressure gradient and trace paravalvular leakage were found. CONCLUSION:The successful first-in-man implantation indicates the retrievable and repositionable VenusA-Plus valve is feasible in complicated TAVR cases such as bicuspid aortic valve.

Background: In acute and chronic renal inflammatory diseases, the activation of inflammatory cells is involved in the defect of erythropoietin (EPO) production. Ras guanine nucleotide-releasing protein-4 (RasGRP4) promotes renal inflammatory injury in type 2 diabetes mellitus (T2DM). Our study aimed to investigate the role and mechanism of RasGRP4 in the production of renal EPO in diabetes. Methods: The degree of tissue injury was observed by pathological staining. Inflammatory cell infiltration was analyzed by immunohistochemical staining. Serum EPO levels were detected by enzyme-linked immunosorbent assay, and EPO production and renal interstitial fibrosis were analyzed by immunofluorescence. Quantitative real-time polymerase chain reaction and Western blotting were used to detect the expression of key inflammatory factors and the activation of signaling pathways. In vitro, the interaction between peripheral blood mononuclear cells (PBMCs) and C3H10T1/2 cells was investigated via cell coculture experiments. Results: RasGRP4 decreased the expression of hypoxia-inducible factor 2-alpha (HIF2A) via the ubiquitination–proteasome degradation pathway and promoted myofibroblastic transformation by activating critical inflammatory pathways, consequently reducing the production of EPO in T2DM mice. Conclusion RasGRP4 participates in the production of renal EPO in diabetic mice by affecting the secretion of proinflammatory cytokines in PBMCs, degrading HIF2A, and promoting the myofibroblastic transformation of C3H10T1/2 cells.

Background: In acute and chronic renal inflammatory diseases, the activation of inflammatory cells is involved in the defect of erythropoietin (EPO) production. Ras guanine nucleotide-releasing protein-4 (RasGRP4) promotes renal inflammatory injury in type 2 diabetes mellitus (T2DM). Our study aimed to investigate the role and mechanism of RasGRP4 in the production of renal EPO in diabetes. Methods: The degree of tissue injury was observed by pathological staining. Inflammatory cell infiltration was analyzed by immunohistochemical staining. Serum EPO levels were detected by enzyme-linked immunosorbent assay, and EPO production and renal interstitial fibrosis were analyzed by immunofluorescence. Quantitative real-time polymerase chain reaction and Western blotting were used to detect the expression of key inflammatory factors and the activation of signaling pathways. In vitro, the interaction between peripheral blood mononuclear cells (PBMCs) and C3H10T1/2 cells was investigated via cell coculture experiments. Results: RasGRP4 decreased the expression of hypoxia-inducible factor 2-alpha (HIF2A) via the ubiquitination–proteasome degradation pathway and promoted myofibroblastic transformation by activating critical inflammatory pathways, consequently reducing the production of EPO in T2DM mice. Conclusion RasGRP4 participates in the production of renal EPO in diabetic mice by affecting the secretion of proinflammatory cytokines in PBMCs, degrading HIF2A, and promoting the myofibroblastic transformation of C3H10T1/2 cells.

Background: In acute and chronic renal inflammatory diseases, the activation of inflammatory cells is involved in the defect of erythropoietin (EPO) production. Ras guanine nucleotide-releasing protein-4 (RasGRP4) promotes renal inflammatory injury in type 2 diabetes mellitus (T2DM). Our study aimed to investigate the role and mechanism of RasGRP4 in the production of renal EPO in diabetes. Methods: The degree of tissue injury was observed by pathological staining. Inflammatory cell infiltration was analyzed by immunohistochemical staining. Serum EPO levels were detected by enzyme-linked immunosorbent assay, and EPO production and renal interstitial fibrosis were analyzed by immunofluorescence. Quantitative real-time polymerase chain reaction and Western blotting were used to detect the expression of key inflammatory factors and the activation of signaling pathways. In vitro, the interaction between peripheral blood mononuclear cells (PBMCs) and C3H10T1/2 cells was investigated via cell coculture experiments. Results: RasGRP4 decreased the expression of hypoxia-inducible factor 2-alpha (HIF2A) via the ubiquitination–proteasome degradation pathway and promoted myofibroblastic transformation by activating critical inflammatory pathways, consequently reducing the production of EPO in T2DM mice. Conclusion RasGRP4 participates in the production of renal EPO in diabetic mice by affecting the secretion of proinflammatory cytokines in PBMCs, degrading HIF2A, and promoting the myofibroblastic transformation of C3H10T1/2 cells.