Renji Hospital

About: Renji Hospital is a healthcare organization based out in Shanghai, China. It is known for research contribution in the topics: Medicine & Biology. The organization has 1112 authors who have published 714 publications receiving 15442 citations. The organization is also known as: Rénjì Yīyuàn.

Osteopontin expression in oral lichen planus

Abstract: To explore circulation levels of osteopontin (OPN), tumour necrosis factor (TNF)-alpha and transforming growth factor (TGF)-beta1 from patients with oral lichen planus (OLP) for clinical application. A group of 26 subjects with OLP were compared with 26 sex- and age-matched control (NC) subjects. Local lesion tissue was examined for OPN by immunohistochemical analysis. And, serum OPN, proinflammatory TNF-alpha and TGF-beta1 levels were measured by enzyme-linked immunoabsorbent assay. The serum concentrations of OPN and TNF-alpha were significantly higher in OLP patients than the NC group (P < 0.05). Although serum concentrations of TGF-beta1 increased slightly, they were not statistically significant. Erosive-form OLP exhibited significantly elevated TGF-beta1 serum levels, compared with reticular-form OLP. The above results suggest that the production of OPN is associated with the inflammatory process of OLP development, and may serve as a potential disease marker of OLP.

Tissue Factor-Factor VIIa Complex Induces Epithelial Ovarian Cancer Cell Invasion and Metastasis Through a Monocytes-Dependent Mechanism

Abstract: Objective: Tumor-associated macrophage infiltration and up-regulation of tissue factor-factor VII (TF-FVIIa) complex have been observed in the peritoneum and stroma of epithelial ovarian cancer (EOC). However, it is not clear how tumor-associated macrophage and TF-FVIIa complex promotes EOC invasion. In the present study, we aimed to determine the mechanism by which interaction of TF-FVIIa and monocytes (MOs) promotes EOC metastasis. Method: Matrigel invasion assay was used to analyze the potential of EOC metastasis. Enzyme-linked immunosorbent assay and real-time polymerase chain reaction were used to detect expressions of cytokines and chemokines. Fluorescence-activated cell sorting was used to count the percentage of CD14, CD68, and CD163 of MOs. Results: We found that the TF-FVIIa complex caused dynamic changes in MOs cytokine and chemokine expression. CD14 and CD163 were also upregulated on MOs by TF-FVIIa. Epithelial ovarian cancer cells were cocultured with TF-FVIIa-stimulated MOs, demonstrating increased invasion potential. Interleukin 8 (IL-8) was proposed as the major chemoattractant mediating EOC invasion based on MOs messenger RNA and protein expression profiles. Anti-IL-8 monoclonal neutralizing antibody attenuated EOC cell invasion in a concentration-dependent manner, and tumor necrosis factor α from TF-FVIIa-stimulated MOs was observed to amplify IL-8 production. The following transcription factors in MOs were activated by TF-FVIIa and inhibited by the tissue factor pathway inhibitor: oncogenes HIF-1α, HIF-1β, Oct I, Oct II, and Egr-1; inflammatory mediators c-Fos and c-Rel; and STAT family members STAT5A and STAT5B. Conclusions: Our study suggested that the interaction between the TF-FVIIa complex might play a role in mediating EOC invasion and metastasis depending on MOs mechanism.

[Prophylactic and therapeutic effect of oxymatrine on D-galactosamine-induced rat liver fibrosis].

Abstract: OBJECTIVE To investigate the prophylactic and therapeutic effect of oxymatrine on experimental liver fibrosis and to reveal its mechanism. METHODS By establishing D-galactosamine-induced rat liver fibrosis model, we observed the effect of oxymatrine on serum and tissue biochemical indexes, content of liver hydroxyline, expression of TGF?1 mRNA and changes of tissue pathology. RESULTS There was a decline of liver hydroxyline and serum AST and ALT in oxymatrine group compared to those of the D-GalN group. The hydroxyline content in oxymatrine pretreatment group was (0.50 0.11)mug/mg compared with (0.99 0.14)mug/mg in D-GalN group (t=8.366, P<0.01). The content in oxymatrine treatment group was (0.44 0.04)mug/mg compared with 0.70 0.06 in D-GalN group (t=9.839, P<0.01). The SOD activity was (149.81 15.28) NU/mg in oxymatrine pretreatment group and (95.22 16.33) NU/mg in the model group (t=7.309, P<0.01); (157.68 19.54) NU/mg in the treatment group compared with (119.88 14.94) NU/mg in the model group (t=4.348, P<0.01). MDA in the pretreatment group was (2.06 0.17) nmol/mg, lower than (4.57 0.37) nmol/mg in the model group (t=17.529, P<0.01). In the treatment group, it was (1.76 0.24)nmol/mg, lower than (3.10 0.17) nmol/mg in the model group (t=12.697, P<0.01). TGF?1 mRNA reduced in the pretreatment and treatment groups as compared with that in the model group (0.21 0.01 vs 0.50 0.01, t=48.665, P<0.01; 0.18 0.02 vs 0.38 0.01, t=22.464, P<0.01). Electron microscopy showed that oxymatrine group had milder hepatocyte degeneration and less fibrosis accumulation than did the model group. Microscopy revealed wide septa expansion from the portal area to the central venous, piecemeal and confluent necrosis and pseudo-nodular formation in part of the lobular in the model group. While in oxymatrine group these lesions were much improved. CONCLUSIONS Oxymatrine shows prophylactic and therapeutic effect in D-galactosamine induced rat liver fibrosis. This is partly by protecting hepatocyte and suppressing fibrosis accumulation through anti-lipoperoxidation.

Comparison of D&C and hysterectomy pathologic findings in endometrial cancer patients

Abstract: The objective of this study is to compare the accuracy of tumor grade in endometrial cancer between fractional dilatation and curettage (DC grade 3 ~ grade 1, P=0.005). Fourteen out of 52 (26.9%) patients diagnosed with atypical endometrial hyperplasia by DC thus, the diagnosis of endometrial disorders by D&C should not be overlooked.

Effects of DNA methylation on expression of tumor suppressor genes and proto-oncogene in human colon cancer cell lines.

Abstract: AIM: To investigate the effects of DNA methylation on the expression of tumor suppressor genes and proto-oncogene in human colon cancer cell lines. METHODS: Three colon cancer cell lines (HT-29, SW1116 and Colo-320) treated with different concentrations of DNA methyltransferase inhibitor, 5-aza-2’-deoxycytidine (5-aza-dC) were used to induce DNA demethylation. The expressions of p16INK4A, p21WAF1, APC and c-myc genes were observed by using RT-PCR. The methylation status of p16INK4A promoter in HT-29 cells was also determined by methylation-specific PCR (MSP). RESULTS: Weak expressions of p16INK4A and APC in the three colon cancer cells were detected, and p21WAF1 expression was not found in SW1116 and Colo-320 cells before treatment. After treatment of 1 μmol/L but not 10 μmol/L of 5-aza-dC, the methylation level of p16INK4A gene promoter decreased significantly, and the hypomethylation led to the up-regulation of p16INK4A gene transcription in HT-29 cells. In the cell lines of SW1116 and Colo-320, p16INK4A and APC mRNA expressions were obviously enhanced after treatment of either 10 μmol/L or 5 μmol/L 5-aza-dC for 24 h. However, no evidence was found that methylation regulated the expression of p21WAF1 and c-myc genes in human colon cancer cell lines. CONCLUSION: Expression of p16INK4A and APC genes is regulated by DNA methylation in three human colon cancer cell lines.