0.05). TNF-? in group EK and EKM was lower than that in group E (P0.05). Conclusions Ketamine can inhibit the release of TNF-? caused by LPS and increase myocardial cAMP level, protecting myocardium from sepsis. This may be one of the anti-septic shock mechanisms of ketamine. Combination of midazolam with ketamine does not affect the anti-septic shock property of ketamine.

Adolescent ; Asthma ; psychology ; therapy ; Behavior Therapy ; Child ; Female ; Health Education ; Humans ; Male ; Massage ; Psychotherapy

Objective To systematically review the efficiency of 18 F-FDG PET in glioma grading by using Meta-analysis. Methods Retrieval in PubMed and China National Knowledge Infrastructure (CNKI)was performed. Relevant papers concerning with glioma diagnoses with 18 F- FDG PET were selected. Paper quality was evaluated according to the standard of diagnostic test recommended by Cochrane Workshop. The data of glioma malignancy degree defined as semi-quantitatively and qualitatively were extracted from the papers. Meta-analysis was conducted with the Meta-Disc software to calculate pooled weighted sensitivity and specificity with 95% confidence interval (CI). Summary receiver operating characteristic (SROC) curve was performed and the areas under the curve (AUC) were calculated. Results Seven hundred and fifty-three patients from 17 papers ( 16 in English, 1 in Chinese) were included. Two hundred and seventy-two patients from 11 papers were using semi-quantitative (tumor to cortex ratio, T/C; tumor to white matter ratio,T/W) method and 481 patients from 9 papers were using qualitative method (visual observation, some of the papers had 2 or more methods). After heterogeneity test was done, different effect models were selected. The pooled weighted sensitivity, specificity and diagnostic odds ratio (DOR) with 95% CI for T/C group was 0. 952 (95% CI: 0. 903 -0. 980), 0. 409 (95% CI: 0. 318-0. 504) and 11. 746 (95% CI:5. 368-25. 702) respectively. The pooled weighted sensitivity, specificity and DOR with 95% CI for T/W group was 0. 857 (95% CI: 0. 768-0. 922), 0. 538 (95% CI: 0. 431 -0. 642) and 22. 066 (95% CI:7. 077-68. 800) respectively. The pooled weighted sensitivity, specificity and diagnostic odds ratio (DOR)with 95% CI for qualitative method was 0.810 (95%CI: 0.757-0.855), 0.870 (95%CI: 0. 819-0.911 ) and 15.282 (95% CI: 3. 716-62. 851 ) respectively. The AUC for T/C group, T/W group and qualitative method was 0.8604, 0. 8373 and 0. 8724 respectively. Conclusions Grading glioma by 18 F-FDG PET with semi-quantitative method may provide high diagnostic sensitivity. If qualitative method is used, the diagnostic specificity may be higher.

Cell Line, Tumor ; Cell Proliferation ; drug effects ; Diterpenes, Kaurane ; pharmacology ; Humans ; Nasopharyngeal Neoplasms ; pathology

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.

Diabetes mellitus increases the risk of breast cancer and affects the prognosis of breast cancer patients. Metformin, an anti-diabetic drug, decreases blood glucose level and has a role in suppressing various cancers. In addition, metformin has a unique in-hibitory effect on breast cancer, i.e., it can inhibit breast cancer cells in vivo and in vitro. Moreover, metformin exerts its anti-tumor ef-fect on epidermal growth factor receptor 2 (HER-2) positive and monoclonal antibody trastuzumab-resistant breast cancer cell lines, breast cancer stem cells, and triple negative breast cancer cells. Metformin can reduce the risk of the breast cancer in patients with dia-betes, lower histologic grade, and increase expression of estrogen and progesterone receptors. Furthermore, metformin has certain effect on neo-adjuvant chemotherapy for breast cancer. This review aims to clarify the mechanism of metformin in restraining breast cancer based on basic and clinical study results.

Conventional diagnostic methods used for pathologic nipple discharge (PND) include color ultrasound, mammary mo-lybdenum target X-ray radiography (mammography), nipple cytologic smears, and ductography. Diagnosis of PND through inspection yields indirect signs and has low positive rate. Fiberoptic ductoscopy (FDS) allows direct visualization of intra-ductal lesions, evaluates etiology of PND, and accurately locates intraductal lesions through wire marking. FDS is a valuable test for the early diagnosis of breast cancer and can help identify appropriate location for surgical excision. Interventional treatment for ductal ectasia and inflamma-tion is also efficient. Our study discusses FDS as a novel diagnosis and treatment method for PND patients.

The purpose of this paper is to investigate the reversal effect of small interfering RNA (siRNA) targeting MDR1 and MDR3 genes on the resistance of MCF-7/ADR cells to adriamycin. siRNA plasmid vector targeting MDR1 and MDR3 genes was transfected into MCF-7/ADR cells, and then was stained with Annexin-V FITC (fluorescein isothiocyanate conjugated) to detect the early stage cell apoptosis by flow cytometry (FCM). 50% inhibition concentration (IC50) of adriamycin for MCF-7/ADR cells was determined by MTT method. MDR1 and MDR3 mRNA was assessed by RT-PCR. Treatment of MCF-7/ADR cells with the two kinds of siRNAs resulted in a reversal of adriamycin resistance of MDR to different extents. 1) The apoptosis efficiency of MDR1 and MDR3 siRNA vector after transfection was (18.21+/-1.65) % and (9.07+/-2.16) % respectively (P<0.05), and there was significant differences in the apoptosis efficiency between pSuppressor Neo vector and the MDR1siRNA or MDR3 siRNA vector (P<0.01); 2) The reversal effect of MDR1 siRNA is higher than that of MDR3 siRNA (P<0.05); 3) The expression of MDRI and MDR3 mRNA can be restrained by pSuppressor Neo MDR1 and MDR3 siRNA respectively, and the reduction in the mRNA level was in a time-dependent manner (P<0.01). MDR1 and MDR3 gene silencing can enhance intracellular adriamycin accumulation in MCF-7/ADR cells, improve sensitivity of MCF-7/ADR cells to adriamycin, and induce cell apoptosis. The reversal effect of adriamycin resistance by siRNA of MDR1 was more effective than that of MDR3.

To explore the role and possible mechanism of apoptosis and caspase-3 activity in the development of multicellular drug resistance of ovary cancer. Ovarian cancer cell A2780 multicellular spheroids (MCS) were obtained from three-dimensional culture. Drug sensitivity of monolayer cells (MC) and MCS were respectively tested by MTT staining and cytometry. The apoptosis of MC and MCS were determined by the flow cytometry (FCM). The expression of bcl-2 and caspase-3 in A2780/MC and A2780/MCS were detected by using Western blot and caspase-3 assay kit. A2780/MC was compacted into mass after 2 days in three-dimensional cell culture model, and MCS had more than two layers of cells growing within 5 days. Compared with A2780/MC, A2780/MCS were more resistant to the anticancer drug, and the apoptosis rate was significantly lower than those of A2780/MC. The activity of caspase-3 in A2780/MCS was significantly lower than the A2780/MC. But the expression of bcl-2 in A2780/MCS was significantly higher than that in A2780/MC. It was suggested that the drug resistance of MCS might be associated with the overexpression of anti-apoptosis protein bcl-2 and the down-regulation of caspase-3 activity.

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.