Objective To investigate the relation between the prognosis and complication of patients with severe viral hepatitis (SVH) Methods The incidences of different complications in 573 patients with SVH were analyzed The survival rates of SVH patients with different complications were compared Results Complications were diagnosed in 77 8% SVH patients The incidences of hepatic encephalopathy, infection, brain edema, gastrointestinal hemorrhage, and hepatorenal syndrome were 50 4%, 34 6%, 30 2%, 22 2%, and 21 8%, respectively The survival rate of SVH patients without complications was 78 7%, significantly higher than that of patients with complications (13 7%, P

Objective To investigate and compare the effects of etomidate or propofol on spatial cognitive,exploring,learning and memory abilities and hippocampus tissue in rapid development period of rats.Methods Thirty-nine SD rats with anage from 17 to 18 days were randomly divided into group C(10 ml/kg of normal saline),group E(5 mg/kg of etomidate),group P(50 mg/kg of propofol)(n=13).They were all single injected intraperitoneally.The tests of cognitive function were performed in Open Field Test(OFT),Hole Board Test and Ymaze Test at 3 hours postanesthesia awake.HE staining method was uesed to observe the morphology of hippocampus neuron tissue and immunohistochemistry(IHC) method was uesed to detect the expression of aspartic acid specificity cysteine protease (caspase-3) in hippocampal neurons.Results In the OFT,there was no significant difference between group C((3.70 ± 1.06)s,(39.10 ± 11.89)s)and group E,P((4.40 ±2.01)s and (4.60 ± 1.96) s,(37.90 ± 11.88) s and (36.30 ± 15.68) s) about the retention time in central check and the locomotion (P ＞ 0.05).In the Hole Board Test,the rats of groups E and P(12.00 ± 3.13,10.00 ± 2.79) about the times of rats stretch into the hole were significant different comparing with group C(16.30 ±4.62) (P＜0.05).In the Ymaze Test,compared with group C,the group E in the right number and total reaction time were no significant differences (P ＞ 0.05).The right number of group P (9.80 ± 2.39) were obviously decreased as compared with group C(13.30 ±2.00)(P ＜ 0.01),and there also had significant difference between group E and group C (P ＜0.05).In addition,the total reation time between group P ((82.30 ± 10.20) s) and group C ((67.70 ± 12.18) s) was significant difference(P ＜ 0.05).In HE staining,there were obvious changes in group E and P.In IHC,the expression of caspase-3 between groups C,E and P,there were no significant differences (P ＞ 0.05).Conclusion Single intraperitoneal injection of etomidate can make a transient effects for the rapid development period of rats ' ability of exploration,but have no obvious influence of the spatial cognition and learning and memory abilities.And etomidate lead less influence on newborn rat behavior and hippocampal tissue than propofol.

OBJECTIVEThe aim of this study was to explore the effect of SPARC on the anti-cancer effect of gemcitabine and underlying mechanism in pancreatic cancer.

METHODSAfter treating with gemcitabine, the proliferation rate of MIA PaCa2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells was detected by MTT assay. The cell cycle distribution and cell apoptosis in each group were examined by flow cytometry, and the capability of clone formation was tested by adhesion-dependent clone formation assay. The apoptosis-related proteins were analyzed by Western blot.

RESULTSThe growth of pancreatic cancer cells was inhibited by gemcitabine in a time-dependent and dose-dependent manner. Its IC50 at 24, 48, and 72-h was (40.1 ± 2.5) µmol/L, (15.0 ± 0.5) µmol/L and (6.6 ± 0.1) µmol/L, respectively. The overexpression of SPARC increased the inhibitory effect of gemcitabine on growth of pancreatic cancer MIA PaCa2/SPARC69 cells, presenting a dose- and time- dependent manner. Its IC50 at 24, 48, 72 h was (24.3 ± 1.5) µmol/L, (7.7 ± 0.3) µmol/L and (4.8 ± 0.2) µmol/L, respectively. The clone formation assay showed that before gemcitabine treatment, the clone numbers of MIA PaCa2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells were (2350 ± 125), (2130 ± 120) and (1567 ± 11), respectively. After gemcitabine treatment, the clone numbers of MIA PaCa2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells were ( 1674 ± 79) , (1587 ± 94) and (557 ± 61), respectively. The overexpression of SPARC enhanced the chemosensitivity of MIA PaCa2 cells to gemcitabine chemotherapy. After treating with 10 µmol/L gemcitabine for 48 h, the ratio of G0/G1 cells in MIA PaCa2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells were (56.0 ± 5.5)%, (55.0 ± 4.5)% and (68.0 ± 7.0)%, respectively. The cells arrested at G0/G1 phase were significantly increased in the MIA PaCa2/SPARC69 cells. The apoptosis rates of MIA PaCa2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells were (22.4 ± 2.5)%, (19.9 ± 2.0)% and (37.7 ± 3.9)%, respectively, indicating that overexpression of SPARC enhanced the gemcitabine-induced apoptosis in MIA PaCa2 cells. The Western blot analysis showed that, compared with MIA PaCa2 and MIA PaCa2/V cells, the expression of caspase-2, -8, -9 and cleaved PARP protein was significantly increased, while the expression of Bcl-2 was not changed significantly in the MIA PaCa2/SPARC69 cells.

CONCLUSIONSPARC can enhance the chemosensitivity of pancreatic cancer cells to gemcitabine via regulating the expression of apoptosis-related proteins.

Antimetabolites, Antineoplastic ; administration & dosage ; pharmacology ; Apoptosis ; drug effects ; Caspase 2 ; metabolism ; Caspase 8 ; metabolism ; Caspase 9 ; metabolism ; Cell Cycle ; drug effects ; Cell Cycle Checkpoints ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Cysteine Endopeptidases ; metabolism ; Deoxycytidine ; administration & dosage ; analogs & derivatives ; pharmacology ; Dose-Response Relationship, Drug ; Drug Resistance, Neoplasm ; Humans ; Osteonectin ; metabolism ; Pancreatic Neoplasms ; metabolism ; pathology ; Poly(ADP-ribose) Polymerases ; metabolism ; Time Factors

Objective The aim of this study was to explore the effect of SPARC on the anti-cancer effect of gemcitabine and underlying mechanism in pancreatic cancer . Methods After treating with gemcitabine, the proliferation rate of MIA PaCa2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells was detected by MTT assay .The cell cycle distribution and cell apoptosis in each group were examined by flow cytometry, and the capability of clone formation was tested by adhesion-dependent clone formation assay . The apoptosis-related proteins were analyzed by Western blot .Results The growth of pancreatic cancer cells was inhibited by gemcitabine in a time-dependent and dose-dependent manner .Its IC50 at 24, 48, and 72-h was (40.1 ±2.5) μmol/L, (15.0 ±0.5) μmol/L and (6.6 ±0.1) μmol/L, respectively.The overexpression of SPARC increased the inhibitory effect of gemcitabine on growth of pancreatic cancer MIA PaCa2/SPARC69 cells, presenting a dose-and time-dependent manner .Its IC50 at 24, 48, 72 h was (24.3 ±1.5) μmol/L, (7.7 ±0.3) μmol/L and (4.8 ±0.2) μmol/L, respectively.The clone formation assay showed that before gemcitabine treatment , the clone numbers of MIA PaCa 2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells were ( 2350 ±125 ) , ( 2130 ±120 ) and ( 1567 ±11 ) , respectively . After gemcitabine treatment, the clone numbers of MIA PaCa2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells were ( 1674 ±79) , (1587 ±94) and (557 ±61), respectively.The overexpression of SPARC enhanced the chemosensitivity of MIA PaCa 2 cells to gemcitabine chemotherapy .After treating with 10 μmol/L gemcitabine for 48 h, the ratio of G0/G1 cells in MIA PaCa2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells were (56.0 ±5.5)%, (55.0 ±4.5)% and (68.0 ±7.0)%, respectively.The cells arrested at G0/G1 phase were significantly increased in the MIA PaCa 2/SPARC69 cells.The apoptosis rates of MIA PaCa2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells were (22.4 ±2.5)%, (19.9 ±2.0)% and (37.7 ± 3.9)%, respectively, indicating that overexpression of SPARC enhanced the gemcitabine-induced apoptosis in MIA PaCa2 cells.The Western blot analysis showed that , compared with MIA PaCa2 and MIA PaCa2/V cells, the expression of caspase-2,-8,-9 and cleaved PARP protein was significantly increased , while the expression of Bcl-2 was not changed significantly in the MIA PaCa 2/SPARC69 cells.Conclusion SPARC can enhance the chemosensitivity of pancreatic cancer cells to gemcitabine via regulating the expression of apoptosis-related proteins .

Objective The aim of this study was to explore the effect of SPARC on the anti-cancer effect of gemcitabine and underlying mechanism in pancreatic cancer . Methods After treating with gemcitabine, the proliferation rate of MIA PaCa2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells was detected by MTT assay .The cell cycle distribution and cell apoptosis in each group were examined by flow cytometry, and the capability of clone formation was tested by adhesion-dependent clone formation assay . The apoptosis-related proteins were analyzed by Western blot .Results The growth of pancreatic cancer cells was inhibited by gemcitabine in a time-dependent and dose-dependent manner .Its IC50 at 24, 48, and 72-h was (40.1 ±2.5) μmol/L, (15.0 ±0.5) μmol/L and (6.6 ±0.1) μmol/L, respectively.The overexpression of SPARC increased the inhibitory effect of gemcitabine on growth of pancreatic cancer MIA PaCa2/SPARC69 cells, presenting a dose-and time-dependent manner .Its IC50 at 24, 48, 72 h was (24.3 ±1.5) μmol/L, (7.7 ±0.3) μmol/L and (4.8 ±0.2) μmol/L, respectively.The clone formation assay showed that before gemcitabine treatment , the clone numbers of MIA PaCa 2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells were ( 2350 ±125 ) , ( 2130 ±120 ) and ( 1567 ±11 ) , respectively . After gemcitabine treatment, the clone numbers of MIA PaCa2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells were ( 1674 ±79) , (1587 ±94) and (557 ±61), respectively.The overexpression of SPARC enhanced the chemosensitivity of MIA PaCa 2 cells to gemcitabine chemotherapy .After treating with 10 μmol/L gemcitabine for 48 h, the ratio of G0/G1 cells in MIA PaCa2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells were (56.0 ±5.5)%, (55.0 ±4.5)% and (68.0 ±7.0)%, respectively.The cells arrested at G0/G1 phase were significantly increased in the MIA PaCa 2/SPARC69 cells.The apoptosis rates of MIA PaCa2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells were (22.4 ±2.5)%, (19.9 ±2.0)% and (37.7 ± 3.9)%, respectively, indicating that overexpression of SPARC enhanced the gemcitabine-induced apoptosis in MIA PaCa2 cells.The Western blot analysis showed that , compared with MIA PaCa2 and MIA PaCa2/V cells, the expression of caspase-2,-8,-9 and cleaved PARP protein was significantly increased , while the expression of Bcl-2 was not changed significantly in the MIA PaCa 2/SPARC69 cells.Conclusion SPARC can enhance the chemosensitivity of pancreatic cancer cells to gemcitabine via regulating the expression of apoptosis-related proteins .

OBJECTIVETo explore the clinical effect of L-ornithine L-aspartate (LOLA) granules in treating chronic liver disease in patients with high-level serum gamma-glutamyltransferase (G-GT) using a 24-week treatment course.

METHODSTwo-hundred patients with chronic liver disease and above normal G-GT were given a 12-week course of LOLA granules (9 g/d) and then classified into the following three groups according to the change in serum Gamma-GT:group I:patients with Gamma-GT level returned to normal;group II:patients with serum Gamma-GT level that was reduced during the treatment; group III:patients with serum Gamma-GT level that did not decrease or that increased to a higher level than at start of treatment.After the 12-week treatment course, the patients in group I were divided into three subgroups for receipt of a control drug (compound glycyrrhizin, 50mg/d) or an additional 12-week course of Gamma-GT at a reduced dose (LOLA granules 3 g/d) or at the original dose; groups II and III were maintained on the initial dose for an additional 12 weeks.The groups were reassessed at the end of the second 12-week course (at the end of week 24 of the study's observation period).Count data were compared using the x2 test and measurement data were compared using the t-test.

RESULTSIn group I, the serum Gamma-GT level was 90.9% at the end of the first 12-week course and dropped to a mean level of 52.2% for both of the subgroups that received the reduced and original dose after the additional 12 weeks of LOLA granules treatment; the difference from week 12 to week 24 was significant (x2=8.213, P less than 0.05).The 24-week change in serum Gamma-GT levels for the group I reduced and original dose subgroups vs.the control subgroup were also significantly different from those seen in groups II and III (P less than 0.05).The percentage of patients in group I who achieved normal level serum Gamma-GT after 24 weeks of treatment (78.6%) was significantly higher than that for the control group (vs.55.0%, x2=11.452, P less than 0.05).When the patients in group 1 who had received the 12 additional weeks of LOLA granules treatment were measured again at two weeks after the treatments had been discontinued (end of week 26), the percentage of patients with normal serum Gamma-GT level was 92.7%, with only three cases showing obviously abnormal levels; in contrast, the group I patients in the control group of the second 12-week study period had on 66.7% of patients with normal-level serum Gamma-GT.The difference in change between the treated groups (both reduced and original dose) and the control group was significant (x2=14.964, P less than 0.05).

CONCLUSIONPatients whose serumGamma-GT levels returned to normal after receipt of LOLA granules for 12 weeks benefitted from an additional 12 weeks of consolidation treatment, and those given the treatment at the original dose benefitted most.Compared with the compound glycyrrhizin, LOLA granules provided a better maintenance of resolved Gamma-GT level.Therefore, the effect of LOLA appears to be reliable and stable as well as safe for clinical use.

Chronic Disease ; Dipeptides ; therapeutic use ; Humans ; Liver Diseases ; drug therapy ; Liver Function Tests ; gamma-Glutamyltransferase ; blood

Objective To explore the effects of information-motivation-behavioral (IMB) skills model based WeChat education on the treatment compliance, the self-efficacy and the quality of life of diabetic nephropathy patients.Methods A total of 92 patients with diabetic nephropathy treated in Danyang People's Hospital from January 2015 to June 2016 were selected as the research object by convenient sampling method and randomly divided into observation group and control group according to the random number table, with 46 cases in each. The control group received conventional WeChat health education, and the observation group implemented WeChat health education based on IMB model. The treatment compliance, the self-efficacy and the quality of life were compared between the two groups 6 months after the nursing intervention. Results There was no statistically significant difference between the two groups of all dimensions and the total scores of treatment compliance before intervention (P>0.05). All the dimensions of treatment compliance of the observation group were higher than those of the control group after intervention, and the differences were statistically significant (t=3.365, 3.258, 3.989, 2.655, 3.513, 4.674, 3.747, 4.187,3.578;P<0.01). The change degree of the 10 dimensions of self-efficacy and total scores were all greater than those of control group, the differences were statistically significant (t=4.854, 5.632, 4.854, 4.241,3.896, 3.785, 3.789, 3.325, 3.314, 3.817,4.123;P<0.01). The improvement of all the dimensions of patients' life quality and its total score were all higher than the control group after intervention, with significant statistical difference (t=5.965, 4.763, 4.746, 4.547, 3.869;P<0.01).Conclusions Application of IMB model based WeChat health education on diabetic nephropathy patients can significantly improve the patient's treatment compliance, self-efficacy and quality of life.

Objective: To detect differentially expressed microRNAs in chronic hepatitis B (CHB) before being treated with pegylated interferon (PegIFN) and the relationship between their target genes and HBsAg loss. Methods: Pretreatment differentially expressed microRNAs between different response groups were screened using high throughput microarrays and validated by quantitative reverse-transcription polymerase chain reaction (RT-qPCR). Bioinformatics analysis was performed to determine their target genes potential mechanistic roles. Results: A total of 417 microRNA were differentially expressed between different response groups, among which 342 were up-regulated and 75 were down-regulated. miR-3960, miR-126-3p, miR-23 a-3p and miR-335-5p were verified to be down-regulated by RT-qPCR result in HBsAg loss group. Bioinformatic analysis result show that the relevant pathways of microRNAs include AMPK signal pathway, NOD-like signal pathway, NF-kappa B signal pathway and mTOR signal pathway. Conclusions HBsAg loss is probably achieved as the result of genes expression regulated in association with immune response, further enhance the immune response of HBV elimination and acquire HBsAg loss.

【Objective】 To study the mechanism of Apocynum leaves in the treatment of sepsis by network pharmacology method in order to explore the multi-dimensional research method of Xinjiang ethnic medicine treatment of infectious diseases and provide scientific theoretical basis for clinical medication. 【Methods】 TCMSP and literature collection were used to screen the main active components of Apocynum venetum leaf, and target prediction analysis was conducted by SwissTarget Prediction database. We used Genecards database to screen relevant targets for sepsis, used Omicshare to calculate Venn figure of the intersection targets, constructed the protein-protein interaction network diagram in the STRING database, used Ensembl for name conversion of protein targets, then entered Omicshare server for Go function and KEGG pathway enrichment of dynamic analysis. Last we used Cytoscape3.6.0 software to construct "Apocynum venetum leaf-the active ingredients-targets-Go-KEGG-sepsis" network to explore the mechanism of action of Apocynum’s resistance to sepsis. 【Results】 Kaferol, luteolin, proanthocyanidin B1 and phytosterol in Apocynum venetum leaves may treat sepsis by controlling signal transduction, regulating hormone level and anti-infection through predictive biological targets such as Akt1, VEGFA, MAPK3, EGFR, Src and PTGS2. They can play an important role through VEGF, EGFR, erbB, HIF-1, RAS and other enrichment pathways. 【Conclusion】 The active components of Apocynum venetum leaves can fight against sepsis through multiple targets and multiple pathways.