Objective To investigate the clinical effect of coagulation therapy in patients with gastric ulcer bleeding.Methods From January 2013 to January 2016 in Xiaoshan First People's hospital 150 cases of gastric ulcer patients with bleeding,using SPSS16.0 software to generate randomly divided into hemocoagulase group(basic treatment + hemocoagulase injection therapy)and control group(basic treatment)of the 75 cases,compared two groups of hemostatic time,hemostatic effect.Results After 72h treatment,the average hemostasis time of hemocoagulase group were significantly lower than the control group(P<0.05),the blood coagulation enzyme in patients with serum VEGF,EGF levels higher than the control group(P<0.05),gastrin and somatostatin levels lower than the control group(P<0.05),hemocoagulase group cure rate is 64％,effective in 22.67％,effective 9.33％,invalid 4％,the control group were 46.67％,25.33％,18.67％,9.33％,two groups compare difference was statistically significant(P<0.05).Conclusion Treatment of gastric ulcer bleeding patients with coagulation enzyme can shorten the hemostatic time,improve the clinical effect of hemostasis.

Objective To investigate the effect of radiation-induced heart injury on cardiac troponin I (cTnI)and endothelin-1(ET-1) and observe the preventive and therapeutic effect of fluvastatin. Methods Healthy female SD rats were randomly divided into three groups: control group(c), irradiation alone group(R) and fluvastatin therapeutic group (F). Rats of F group had been gastrogavaged with fluvastatin at dose of 20mg?kg -1?d -1 from 1week before irradiation to the end of the experiment. In C group and R group, rats were gastrogavaged with the same volume isotonic sodium chloride. The rats of R and F group were irradiated with accelerator linear at a dose of 20Gy thoracically. Rats were executed at 5,15,30d and 60d after irradiation, then cTnI in serum and ET-1 in blood plasma were detected. Results On 5d, the content of cTnI in R group increased significantly than that in C group(P

A large number of studies have shown that long non-coding RNAs (IncRNAs) display abnormallity in organisms exposed to toxic chemicals,carcinogens and heavy metals.In this paper,the relationships between IncRNAs and microRNAs (miRNAs),the expressions of IncRNAs in organisms exposed to different exogenous toxic chemicals and the related toxicological mechanism are reviewed in order to provide reference for biological monitoring with IncRNAs in environmental toxicology.

Objective To investigate the anti-fibrosis effect of a 5-lipoxygenase (5-LO)specific inhibitor AA-861 on liver fibrosis. Methods Liver fibrosis was induced in male Sprague Dawley rats by intraperitoneal injection of carbon tetrachloride(CCI4).AA-861(0.2 mg/100 g/d)was administrated by intraperitoneal injection starting 2 days before the first dosage of CCI4 and rats were killed at weeks 2,4,and 6.Liver specimens were obtained from each animal and fixed with 4%formaldehyde for histological analysis. The Mrna expression of 5-LO,smooth muscle-alpha(α-SMA),Collagen-1,matrix metalloproteinase-2(MMP-2)and tissue inhibitors of metalloproteinase-1(TIMP-1),the protein expression of 5-LO were evaluated by real time PCR and Western blot respectively. Histological analysis was performed by microscopy observation. Fibrosis conditions in rat liver in each group were evaluated according to the semi-quantitative scoring system (SSS), Hyp in rat livers and the hepatic functional biochemistry were also detected. Results Along with the aggravation of liver fibrosis, the gene expression of 5-Lo,α-SMA,Collagen-1,MMP-2 and TIMP-1 increased gradually, and the level of ALT, TBA, Hyp and SSS score also increased gradually. With the administration of AA-861,the Mrna expression of 5-LO,α-SMA,Collagen-1,MMP-2,TIMP-1 and the protein expression of 5-LO decreased remarkably, and the reduction in TIMP-1 Mrna expression was more significant than that in MMP-2.Six weeks after AA-861 treatment, the level of ALT, TBA, Hyp and SSS score were also decreased significantly. Conclusion AA-861 ameliorates CCI4 induced rat liver fibrosis by inhibiting the 5-LO pathway and decreasing the expression of 5-LO,α-SMA,Collagen-1,MMP-2 and TIMP-1.

Objective To observe the effects of cystamine, a tissue transglutaminase (tTG) inhibitor, on the development of rat liver fibrosis induced by carbon tetrachloride. Methods One hundred male SD rats were randomly divided into control group (n=20), hepatic fibrosis group (n=40) and cystamine group (n=40) . Liver fibrosis model was induced by intraperitoneal injection of carbon tetrachloride. Cystamine (112 mg·kg-1·d-1) was administered by intraperitoneal injection 2 days before injection of carbon tetrachloride. The rats were sacrificed at weeks 4 and 8, and the liver tissues and serum specimens were obtained. The mRNA expression of tTG, smooth muscle-alpha (α-SMA), collagen-Ⅰ and tissue inhibitors of metalloproteinase-1 (TIMP-1) were detected by real time PCR. The protein expression of tTG and α-SMA, liver function and content of hydroxyproline in liver tissues were determined by Western blot. Histological changes of the liver was observed under microscope. The fibrosis conditions of rat liver in each group were evaluated according to the semi-quantita-tive scoring system. All the data were analyzed by one-way ANOVA. Results Eight weeks after the injection of carbon tetrachloride, obvious injury of the liver in liver fibrosis group was observed. The levels of alanine trans-aminase (ALT), total bile acid, total bilirubin, hydroxyproline, tTG, α-SMA, collagen-Ⅰ and TIMP-1 were (1313±157)U/L, (99.9±18.5)μmol/L, (10.9±1.6)μmoL/L, (55±12)μg/g, 145.6±51.2, 130.3±44.6, 211.3±75.1 and 162.4±53.5. After administration of cystamine, the levels of ALT, total bile acid, total bilirubin, hydroxyproline, tTG, α-SMA, collagen-Ⅰ and TIMP-1 were (378±87) U/L, (61.0±12.7) μmol/L, (9.8±1.7) μmol/L, (70±14 ) μg/g, 48.6±12.3, 40.7±12.3, 63.9±16.0, 59.2μ23.4. Conclusion Cystamine can alleviate the carbon tetrachloride-induced rat liver fibrosis by inhibiting the tTG pathway.

Objective To construct short hairpin RNA (shRNA) expression plasmids against the inhibitor of differentiation 2 (Id2) gene and establish a suitable cell model for the role of Id2 in proliferation and differentiation of human Ewing sarcoma cell.Methods Three shRNA sequences targeting Id2 gene were designed and inserted into the pGPU6/GFP/Neo (-shRNA-Id2) expression vectors.The recombinant pGPU6/GFP/Neo-shRNA-Id2 plasmids were introduced into Ewing sarcoma RD-ES cells by liposome-mediated transfection.The knock-down efficiency of Id2 in infected RD-ES cells was verified by Western blot assay.The cell growth and cell cycle changes were evaluated by cell counting and flow cytometry between transfected cells and control cells.Results The Id2 expression decreased 54 ％ and 57 ％,respectively,in RD-ES cell line which were transfected with the shRNA-Id2-543 and shRNA-Id2-593 plasmids compared with the control group cells by Western blot analysis.The cell growth assay demonstrated that the cell number in transfected cells was significantly decreased during 6-7 d compared with the control group (P ＜ 0.05).The cells at the S-phase of cell cycle were increased [(36.60±1.53) ％ and (44.89E2.46) ％ vs (29.73±2.03) ％,P ＜ 0.05],and no significant changes at the G2 phase or even reduction in the transfected cells.Conclusions Id2 stable knock-down cell lines are successfully established.The reduced expression of Id2 is related with decreased cell growth and cell cycle arrest in the S-phase.Id2 maybe plays an important role in proliferation of Ewing sarcoma cell.

Objective To evaluate the effects of endothelial nitric oxide synthase (eNOS) gene transfer on intrahepatic vascular resistance (IHVR) and portal venous pressure (PVP) in cirrhotic rats. Methods (1) 5 days after eNOS gene transfer, the in situ liver perfusion system (ISLP) was prepared and in different groups of controls and eNOS treated rats, the followings were analyzed: portal perfusion pressure (PP) dose-response curve to norepinephrine (NE); the effects on PP caused by specific nitric oxide synthase (NOS) inhibitor N-monomethyl-L- arginine (L-NMMA) or the nitric oxide (NO) synthesis substrate L-arginine (L-Arg). (2) The experiment of perfusion via portal vein in vivo was performed and the effects of L-NMMA on the PVP was observed. Results (1) In ISLP model, after L-NMMA was added into the perfusate of the control rats, PP dose-respose to NE increased remarkably and the peak of PP increased to (26.7?0.9) mm?Hg. The increased PP response to NE caused by L-NMMA was offsetted by L-Arg and the peak of PP decreased to (23.2?0.9) mm?Hg. In eNOS treated rats, PP response to NE was significantly lower than that in controls (P

Objective To develop a method for rapid and accurate detection and identification of bacterial pathogens directly from body fluid specimens and to evaluate its application in clinical laboratory.Methods Bacteria DNA was extracted from 205 body fluid specimens with column-based kit,and the high variable V1 and V3 regions of bacterial 16S rRNA gene were amplified with broad-range primers.Amplicons were analyzed by pyrosequencing and the generated sequences were searched in the bacterial identification database.Traditional culture-biochemical method was also used for these specimens and the results were taken as the golden standard.SPSS 11.0 was used to calculate the sensitivity,specificity,false positive/negative rate,positive/negative predictive value and positive/negative likelihood rate of pyrosequencing method.Results The positive rate of bacteria culture was 39.5％ (81/205),among which 71 were infected with single bacterium,and 10 were infected with two species of bacteria.Compared with the culture identification results,pyrosequencing had a 100.0％ (71/71) concordance when applied to detect and identify bacterial pathogens from specimens with single specie bacterium infected.To specimens with two species bacteria infected,7 out of 10 specimens were in concordance with the culture identification results.Besides,pyrosequencing detected 10 positive specimens and identified bacterial pathogens infected in the 124 culture-negative specimens.Taken bacteria culture as the standard method,the sensitivity of pyrosequencing for identifying bacterial pathogen in body fluid was 100.0％,and with a specificity of 91.9％,the false positive rate was 8.1％,the false negative rate was 0.0％,the positive predictive value was 89.0％,the negative predictive value was 100.0％,and the positive and the negative likelihood rate were 12.4 and 0,respectively.Conclusion Pyrosequencing can be used to detect and identify bacterial pathogens directly from body fluid specimens with the advantages of rapidity,high sensitivity,high accuracy and high throughput.

Aim To determine the effects of high-fat meal and ABCB1 C3435 T polymorphism on the phar-macokinetics of nifedipine in the healthy Chinese sub-jects. Methods A total of 90 unrelated healthy Han subjects were divided into two groups:fasting group ( n=45 ) and high-fat meal group ( n=45 ) and then they received a single oral dose of 90 mg extended release tablet. Multiple blood samples were collected after 48 h, and the plasma concentrations of nifedipine were determined by high performance liquid chromatogra-phy- mass spectrometry ( LC-MS ) . PCR-restriction fragment length polymorphism ( RFLP ) analysis was performed to detect the C3435 T polymorphism in AB-CB1 gene. Results The numbers of individuals carry-ing C/C, C/T and T/T genotypes in fasting group were 13, 24 and 8, respectively. The mean area under the curve ( AUC0-∞) in subjects carrying T/T genotype distinctly increased by 46. 34% compared with subjects with C/C genotype, but there was no statistically sig-nificant difference (P=0. 066). In addition, pharma-cokinetic parameters including Tpeak, Cmax and AUC0-48 had statistically significant differences between fasting group and high-fat meal group ( all P<0. 05 ) . Con-clution High-fat meal can speed the absorption and increase the extent of nifedipine absorption; ABCB1 C3435 T polymorphism almost does not affect the phar-macokinetics of nifedipine.

BACKGROUND:Although vitamin C has an anti-oxidation role and can promote cell proliferation, there is a lack of research about the promoting effect of vitamin C on the proliferation of adipose-derived stem cells under high glucose conditions and the related molecular mechanisms.OBJECTIVE:To explore the promoting effect of vitamin C on the proliferation adipose-derived stem cells treated by the high glucose and the related molecular mechanisms.METHODS:Passage 3 human adipose-derived stem cells were cultured under high glucose conditions and then treated with different concentrations of vitamin C (0, 100, 150, 200, 250, 300 μmol/L). Cells cultured under low glucose conditions acted as controls. The expression levels of p-ERK and p-AKT proteins were detected by western blot. MTT method was used to choose the optimal concentration and time of vitamin C for all the subsequent tests. Human adipose-derived stem cells cultured under high glucose conditions were divided into four groups, and cells in blank control group had no treatment. Cells in the other three groups were treated with the optimal concentration of vitamin C (vitamin C group), LY294002+the optimal concentration of vitamin C (LY294002 group), or U0126+the optimal concentration of vitamin C (U0126 group) for 48 hours.EdU staining assay was used to detect the cell proliferation of human adipose-derived stem cells.RESULTS AND CONCLUSION:(1) Cell counting kit detection:We found that high glucose reduced the proliferation of human adipose-derived stem cells, and vitamin C promoted the proliferation of these cells. The best concentration of vitamin C was 200 μmol/L and the optimal effect time was 48 hours. (2) Western blot detection:Compared with the 0 μmol/L vitamin C group, the level of p-ERK in the 200 μmol/L vitamin C group was upregulated significantly (P < 0.01),while no significant expression change in p-AKT protein was found in control, 0 and 200 μmol/L vitamin C groups.(3) EdU test:the number of EdU positive cells was significantly higher in the vitamin C, LY294002, and control groups compared with the blank control group (P < 0.01). Moreover, compared with the vitamin C group, the EdU positive cells in the U0126 group were decreased significantly in number (P < 0.01). In conclusion, the ERK/MAPK signaling pathway is involved in the promotion effect of vitamin C on the proliferation of human adipose-derived stem cells under high glucose conditions.