Acupuncture Points ; Adult ; Bloodletting ; Combined Modality Therapy ; Female ; Headache ; therapy ; Humans ; Male ; Middle Aged ; Moxibustion ; Neuralgia ; therapy ; Young Adult

Annexin A5 ; biosynthesis ; isolation & purification ; Escherichia coli ; metabolism ; Genetic Vectors ; Humans ; Recombinant Proteins ; biosynthesis ; isolation & purification

Animals ; Cyclic GMP ; metabolism ; Ischemic Preconditioning, Myocardial ; Myocytes, Cardiac ; metabolism ; Nitric Oxide ; biosynthesis ; Rats ; Rats, Sprague-Dawley

AIM:To investigate the inhibitory effects of recombinant human Mullerian inhibiting substance on cell proliferation in human ovarian carcinoma cells (OVCAR8 and SKOV3 cell lines). METHODS:The expression of MISIIR protein and the localization of MISIIR protein were analyzed by Western blotting and confocal spectral microscopy,respectively. Cell apoptosis and cell cycle were detected by flow cytometry (FCM). Cell viability was determined via MTT method. Clone formation test was used to detect oncogenicity in vitro.RESULTS:The MISIIR protein expression in OVCAR8 cells but not in SKOV3 cells was observed. MISIIR expression was seen on the OVCAR8 cell surface and in the cytoplasm with both antibodies. After treated with rhMIS for 48 h,the cell viability was significantly decreased in OVCAR8 cells. rhMIS inhibited the oncogenicity of OVCAR8 cells greatly. The cell apoptosis of OVCAR8 cell exposed to 10 mg/L rhMIS was (31.3±2.1)%,and OVCAR8 cells in the G_1 phase were increased by (70.4±3.0)%. Compared to SKOV3 cells the differences were significant (P<0.01). CONCLUSION:Recombinant human Mullerian inhibiting substance suppresses the growth of MISIIR-positive ovarian cancer cells by inducing apoptosis and cell cycle arrest. We predict that rhMIS might be a new target to treat human ovarian malignancies.

ADP-ribosyl Cyclase 1 ; metabolism ; Aged ; Epstein-Barr Virus Infections ; Herpesvirus 4, Human ; isolation & purification ; Humans ; Interferon Regulatory Factors ; metabolism ; Ki-67 Antigen ; metabolism ; Male ; Nasal Cavity ; Nose Neoplasms ; metabolism ; pathology ; surgery ; virology ; Plasmacytoma ; metabolism ; pathology ; surgery ; virology

Actins ; metabolism ; Female ; Glomus Tumor ; metabolism ; pathology ; surgery ; Humans ; Skin Neoplasms ; metabolism ; pathology ; surgery ; Thigh ; Vimentin ; metabolism ; Young Adult

Adult ; Antigens, CD20 ; metabolism ; Empyema, Pleural ; complications ; diagnostic imaging ; pathology ; virology ; Epstein-Barr Virus Infections ; Humans ; Ki-67 Antigen ; metabolism ; Lymphoma, Large B-Cell, Diffuse ; metabolism ; pathology ; surgery ; virology ; Male ; Pleural Neoplasms ; complications ; metabolism ; pathology ; surgery ; virology ; Radiography

Objective To investigate the effect of MDR1 and MDR3 gene silence by shRNA of human breast carcinoma cell line MCF-7/Adr,and explore the role of MDR1 and MDR3 in adriamycin-resistance of breast carcinoma cells. Methods shRNA plasmid vector specifically targeting MDR1 and MDR3 gene was transfected into cells. The control group was transfected with empty vector. The concentration of adriamycin was detected by the flow cytometry (FCM). Cell apoptosis was analysed by FITC-Annexin-V/PI double staining. Cell viability and the IC50 of adriamycin on MCF-7/Adr cells were determined by MTT method. MDR1 and MDR3 mRNA were assessed by RT-PCR. P-gp expression was detectedby immunochemistry. Results After treatment with ABCB1 and ABCB4 shRNA plasmid vector, the apoptosis of MCF-7/Adr cells was (30.21±1.65)%and (22.07±2.17)% respectively. Compared with untransfecedgroup and empty vector transfection group the difference was significant(P＜0.01). MDR1 and MDR3 shRNAcould increase cellular adriamycin accumulation of MCF-7/Adr cells. MCF-7/Adr cells viability and the IC50were significantly decreased after transfection. Compared with untransfeced group and empty vector transfectiongroup, the mRNA level of MDR1 and MDR3 in MCF-7/Adr cells were decreased by (89.5±0.8)%and(85.1±1.2)%, the reduction of MDR1 and MDR3 mRNA was in a time-dependent manner. Immunochemistry proved that the expression of p-gp was significantly inhibited. Compared with untransfeced group and empty vector transfection group the difference was significant (P＜0.05). Conclusion The shRNA can effectively and specifically silence the expression of MDR1 and MDR3 gene, reverse the adriamycin-resistance mediated by P-gp in MCF-7/Adr cells. The reversal effect of adriamycin-resistance by shRNA of MDR1 is more effective than that of MDR3.

Objective To research the effects of transcutaneous electrical stimulation (TES) on the expression of neurotrophin-3 (NT-3) and tumor necrosis factor-α (TNF-a) in the ventral horn of rats' spinal cords and in the injured region after spinal cord injury (SCI),and to explore the effects of TES on neuron reconstruction and functional recovery and their mechanisms. Methods Forty-eight Wistar rats were selected and divided using stochastic methods into a model group and a TES group.Using Allen's method,a complete SCI model was created at T9.Rats of the TES group were given TES treatment.Basso-Beattie-Brasnahan ( BBB ) ratings were used to evaluate locomotor function.Both groups were sampled at 1,3,5 and 7 days after the operation.Immunohistochemical techniques were used to detect the expression of NT-3 and TNF-α in the rats' spinal cords at the different time points. Results The post-operative BBB ratings of both groups showed an increasing trend.In the TES group the improvement was significantly better at 5 and 7 days than in the model group.The expression of NT-3 immuno-positive cells increased in both groups,peaking at 5 days post-operation,then declining at day 7.The expression of NT-3 positive cells at days 5 and 7 had increased significantly more in the TES group than in the model group.TNF-α immuno-positive expression increased with time in both groups,but in the TES group the expression increased substantially less than in the model group.At days 5 and 7 post-operation,the expression was significantly lower than in the model group. Conclusions TES can promote NT-3 expression in rats with SCI,inhibit the increase in TNF-α expression,and aid repair and reconstruction of neurons and related functional recovery.