s Objective To observe the enhancement of sensitivity of human gastric cancer cell MKN-74 to anticancer drugs by administration of 5-aza-2'-deoxycytidine(5-Aza-CdR)and trichostatin A(TSA)with anticancer drugs.Methods Growth inhibition of MKN-74 with treatment of 5-Aza-CdR and/or TSA together with anticancer drugs,including fluorouracil(5-FU),paclitaxel(PTX),oxaliplatin(OXA),SN38 or gemcitabine(GEM),was detected by MTT method.Induction of apoptosis was analyzed by flow cytometry.Expressions of p21,caspase3,Rb and p16 gene were studied by RT-PCR.The gray scale of the genes was analyzed by gel analysis software Bandscan 4.3,and the ratio of gray scale of targeted genes and GAPDH gene were calculated.Results Compared with 5-Aza-CdR alone,combined administration of 5-Aza-CdR and TSA enhanced the chemosensitivity of MKN-74 to 5-FU,PTX,OXA and GEM.Compared with TSA alone,the combined administration enhanced its osensitivity to OXA and GEM.The apoptosis rates in MKN-74 cells in TSA+OXA group,5-Aza-CdR+OXA group and 5-Aza-CdR+TSA+OXA group were 28.067%,25.333% and 38.367%,respectively(P

Objective To observe the effects of aerobic training on plasma tissue plasminogen activator/plasminogen activator inhibitor-1 and postaglandin I2/thromboxanes A2 in rats fed a high methionine diet. Methods Ninetysix male Wistar rats were randomly divided into a normal diet control group (CR), a high methionine diet group (MR)and a high methionine diet plus 90 min aerobic training intervention group (T + MR). After 8 weeks of training, the plasma level of homocysteine (Hcy) 6-keto-PGF1α, TXB2, t-PA and PAI-1 were measured. Results Plasma Hcy in the MR group increased two-fold as compared with the CR group, whereas t-PA/PAI-1 and 6-keto-PGF1α/TXB2 of the MR group decreased significantly. Plasma Hcy in the T + MR group significantly decreased, while plasma t-PA/PAI-1 and 6-ketoPGF1α/TXB2 increased significantly compared with the MR group. The above parameters were not different in the T + MR group from those of the CR group. Conclusions Hyperhomocysteinemia could be induced by a high methionine diet.Proper training can decrease the plasma Hcy level of rats fed with a high methionine diet, and correcting the imbalance of t-PA/PAI-1 and 6-Keto-PGF1α/TXB2 could prevent the development of hyperhomocysteinemia.

Objective To investigate the effects of exercise on the activity of heme oxygenase-1 ( HO-1 ) and the expression of HO-1 mRNA and the mechanisms involved in the vascular smooth muscle tissue of rats with spontaneous hypertension (SHR). Methods Twelve male Wistar rats with normal blood pressure were used as control group ( group C ).Another 24 male rats with SHR were randomly assigned to one of 2 experimental groups ( 12 rats per group):an SHR group (group S) and an SHR treated group (group T).Rats in group T were treated with 60 minutes of unloaded swimming exercise 6 times a week for 9 weeks.Their blood pressure was measured once a week.After the nine weeks HO-1 activity as well as the expression of HO-1 mRNA in vascular smooth muscle and the concentration of carbon monoxide in plasma were measured. Results After the 9 weeks of training,average systolic blood pressure in group T was close to that of group C.The systolic blood pressure of group S continued to rise,and was significantly higher than that of the other 2 groups at each time point.Average HO-1 activity in group S (637.94 ± 73.637 ) reduced significantly compared with that of group C (786.20 ± 74.698) or with that of group T ( 1036.53 ± 140.63 ).That of group T was significantly higher than that of group C.The average expression of HO1 mRNA in group S (80.85 ± 6.953 ) was significantly higher than that of group C (45.15 ± 7.651 ) and lower than that of group T (90.70 ± 11.20),and the differences were statistically significant at the 5％ level of confidence.The average level of expression of HO-1 mRNA in the T group was significantly higher than that of group C.The plasma carbon monoxide content of S group was significantly lower than that of groups C and T. Conclusions Exercise can enhance the activity of HO-1 and the expression of HO-1 mRNA in vascular smooth muscle in rats with SHR to reduce blood pressure.

Objective:To improve the medical equipment timely filing rate.Methods: Through the literature reference and practical work experience, based on the research of medical equipment archives management content, problems, solutions.Results: According to the comprehensive analysis of the literature in recent years is introduced and all levels of hospital medical equipment archives management and practice management work experience, summarizes the paper, summarized and further improve the management of medical equipment archives.Conclusion:To improve the timely filing rate, improve the utilization of archives, and find out the existing problems of hospital medical equipment archives management, the medical equipment archives play a major role in the practical work.

Adult ; Aged ; Aged, 80 and over ; Carbon Monoxide Poisoning ; complications ; Female ; Humans ; Interleukins ; blood ; Male ; Middle Aged ; Neurotoxicity Syndromes ; blood ; etiology

BACKGROUND:Proto-oncogene c-Src plays an important role in regulating cardiovascular diseases such as hypertension. At present, there were no studies concerning exercise intervention effects on c-Src expression in aortic endothelial cels so as to regulate hypertension. OBJECTIVE: To observe the effects of aerobic exercise on c-Src mRNA expression and c-Src activity in the aorta blood vessel endothelial cels of spontaneous hypertensive rats. METHODS: A total of 8 male Wistar rats were considered as normal control group. Sixteen spontaneous hypertensive rats were randomly assigned to 8 rats as spontaneous hypertension group and 8 rats as spontaneous hypertension exercise group. Rats in the spontaneous hypertension exercise group carried on 90 minutes unloaded aerobic swimming every day, 6 days a week, for 8 weeks. The rats in the normal control group and spontaneous hypertension group did not swim. Blood pressure of rats was measured once a week. 8 weeks later, the c-Src mRNA expression and c-Src activity were determined in aortic vascular endothelial cels of rats in each group. RESULTS AND CONCLUSION: Compared with spontaneous hypertension group, blood pressure was lower, but c-Src mRNA expression and c-Src activity were significantly higher in the spontaneous hypertension exercise group. The c-Src activity and c-Src mRNA expression were higher in the spontaneous hypertension exercise group than normal control group and spontaneous hypertension group (P < 0.01). Results indicated that aerobic exercise can promote the increase in c-Src activity and c-Src mRNA expression in aortic endothelial cels of spontaneous hypertensive rats.

Objective:To evaluate dendritic cells induced immune response against hepatocellular carcinoma by pulsed CD34+ hematopoietic stem cells originated dendritic cells with p53 gene.Methods:CD34+ hematopoietic stem cells were harvested after mobilization by chemotherapy and G-CSF.CD34+ hematopoietic stem cell apheresis was induced to differentiate into dendritic cells by cytokine cocktail IL-4,GM-CSF and TNF-?.On day 7,dendritic cells were transfected with plasmid pEGFP-C3/p53 DNA.The CTL response triggered by p53 pulsed dendritic cells was assayed by MTT method.Results:Dendritic cells originated from CD34+ cell apheresis had typical dendritic stick and expressed high level CD1a,CD11c,CD80,CD86,and HLA-DR molecules.After being pulsed with p53 gene,dendritic cells expressed green fluorescence protein and immunofluorescence assay(Cy3 labeled anti-P53 antibody)showed that transfected dendritic cells emitted red fluorescence.Dendritic cells inducing CTL response against HMCC97 cells(P53 positive)and HepG2 cells(P53 negative)were assessed by MTT method.P53 pulsed dendritic cells could induce P53 specific immune response against HMCC97 cells and the cytotoxin rate was(49.3?4.6)% compared with pEGFP-C3 transfection group [(25.4?4.1)%] and control group[(24.8?3.8)%](P0.05).Conclusion:P53 gene transfecting hematopoietic stem cell apheresis originated dendritic cells could induce specific CTL response against P53-expressing hepatocellular carcinoma cells.P53 may be a potential candidate for dendritic cell based immunotherapy of cancer.

Objective:The relative expression of miR-4698 in liver cancer tissues and cell lines was detected, and its effect on the proliferation and migration of liver cancer cells and its molecular mechanism were analyzed.Methods:Real-time fluorescence quantitative polymerase chain reaction (qRT-PCR) was used to analyze the relative expression of miR-4698 in liver cancer tissues and liver cancer cell lines. Among the lowest-expressing hepatocellular carcinoma cell lines, miR-4698 mimic and control mimic were transfected with liposome transfection method, and named as experimental group and control group. qRT-PCR was used to detect transfection efficiency. Cell counting kit-8 (CCK-8) and transwell migration experiments were used to detect the effects of overexpressing miR-4698 on the proliferation and migration ability of liver cancer cells. Bioinformatics and dual luciferase reporter gene experiments were used to predict and verify the binding of miR-4698 to target gene. qRT-PCR and Western blot were used to detect the relative expression of target gene at mRNA and protein levels, respectively.Results:Compared with the adjacent tissues, miR-4698 was significantly lower in the liver cancer ( P<0.01). Compared with normal hepatocytes, miR-4698 was significantly lower in hepatoma cell lines ( P<0.05), and the lowest in Huh7 cells ( P<0.01). After transfection, the expression of miR-4698 in Huh7 cells in experimental group was significantly increased compared with that in the control group ( P<0.01). Overexpression of the miR-4698 can inhibit the proliferation and migration of Huh7 cells ( P<0.05). Bioinformatics showed that the target gene of miR-4698 was polypeptide-n-acetylgalactosamine transferase 4 (GALNT4), and the double luciferase reporter gene confirmed that miR-4698 could bind to GALNT4 ( P<0.01). qRT-PCR showed that overexpression of miR-4698 could inhibit the expression of GALNT4 gene ( P<0.01). Western blot results showed that overexpression of miR-4698 decreased the protein expression of GALNT4, cyclin B and CDK1, and increased the protein expression of N-cadherin and ZEB-2. Conclusions:The expression of miR-4698 in liver cancer tissues and cell lines is significantly reduced. Overexpression of miR-4698 can inhibit the expression of GALNT4 gene and reduce the proliferation and migration ability of liver cancer Huh7 cells.

OBJECTIVE:To observe the clinical effect of Shu’nao capsules for cerebral edema.METHODS:42preoperative patients with glioma above tentorium of cerebellum and meningioma complicated with cerebral edema were randomly divided into control group and treatment group:the control group was assigned to receive carbamazepine and VitB 6 ,and the treatment group to receive Shu’nao Capsules in combination with the drugs as stated in the control group for an average of4.5d,during which the clinical symptoms and urine volume changes were monitored.RESULTS:The effective rates of the treatment group and the control group against headache or dizziness were85.00%and27.27%,respectively(P

[ ABSTRACT] AIM:To investigate the effects of BARF1 down-regulation on EBV-positive gastric carcinoma cell apoptosis, and the molecular mechanisms by BARF1 silencing-mediated apoptosis.METHODS: After NUGC3 and SNU719 cells were transfected with NCsiRNA and siRNA, respectively, the protein levels of BARF1, Bcl-2, Bax, cyto-chrome C, caspase 3 and capase 9 were detected by Western blot, and the mRNA expression of BARF1, Bcl-2 and Bax was determined by RT-PCR.The cell viability was measured by the method of Trypan blue exclusion and the cell apoptosis was analyzed by flow cytometry analysis with Annexin V-FITC/PI staining.The expression of the apoptosis-related proteins in the cells transfected with siRNA and NCsiRNA was examined by human apoptosis antibody arrays.Mitochondrial mem-brane potential was determined by flow cytometry.The interaction between Apaf-1 and caspase 9 was confirmed by immuno-precipitation.RESULTS: Compared with untreated and NCsiRNA groups, BARF1 gene silencing significantly inhibited the cell viability, induced apoptosis, and reduced the mitochondrial membrane potential in the NUGC3 and SNU719 cells transfected with siRNA.BARF1 gene silencing up-regulated the expression of pro-apoptotic proteins and down-regulated the expression of anti-apoptotic proteins, and the Bcl-2/Bax ratio was significantly decreased.In BARF1 gene silencing cells, the caspase inhibitor z-VAD-fmk inhibited BARF1 silencing-mediated apoptosis, and significantly increased the levels of cleaved caspase 3 and caspase 9.The concentration of cytochrome C significantly increased as compared with NCsiRNA group, and Apaf-1 interacted with caspase 9 in the cytoplasm.CONCLUSION:BARF1 silencing induces apoptosis via the mitochondrial pathway through regulating the expression of Bcl-2 and Bax proteins in a caspase-dependent manner in the NUGC3 and SNU719 cells.