Objective To investigate the relationship between serum Golgi protein-73 (GP73)level and related indexes of he-patic fibrosis in patients with hepatitis B cirrhosis diseases and discuss the clinical value of GP73.Methods The level of GP73 was detected by ELISA;the levels of type Ⅳ precollagen (Ⅳ-C)and hyaluronic acid (HA)were measured by radio-immunity in serum from 11 patients with acute hepatitis B (AHB),31 patients with chronic hepatitis B (CHB),71 patients with Hepatitis B Cirrhosis (LC),23 patients with primary hepatic carcinoma (PHC)and 34 healthy people with check-up. The clinical changes and relationship between the GP-73 level and the parameter of fibrous degeneration were studied.Re-sults The GP73 level in CHB group was 118.0±82.2μg/L;the GP73 level in LC group was 154.4±87.7μg/L and the GP73 level in PHC group was 196.5±89.6μg/L.Compared with the normal control group,statistically significant differ-ence were found in GP73 level of CHB group,LC group and PHC group (t values were -7.284,-7.909 and -9.609,re-spectively;P<0.01).As the progress of liver cirrhosis,the levels of GP73,Ⅳ-C and HA all increased gradually and the level of GP73 was significantly positively correlated to Ⅳ-C and HA (r valves were -0.212 and 0.487,respectively;P<0.01). Conclusion The GP73 was high expressed in chronic liver disease,especially in liver cirrhosis.The GP73 was significantly associated with the occurrence of hepatitis b liver fibrosis.There fore,GP73 could be used as a better index to monitor the fi-brosis degree.

Background:Gemcitabine is the main drug for chemotherapy of advanced pancreatic cancer,however,the prognosis of pancreatic cancer patients has not been changed obviously because of the high innate and acquired resistance of cancer cells to gemcitabine. Aims:To investigate the correlation of DNA repair and expression of human APE1 / Ref-1(apurinic/apyrimidinic endonuclease 1 / redox factor-1),the key enzyme in base excision repair pathway,with the resistance of pancreatic cancer to gemcitabine. Methods:A gemcitabine-resistant human pancreatic cancer cell line SW1990-0. 5 with a resistance index of 9. 32 and its parental cell line SW1990 were treated with gemcitabine. DNA injury was assessed by comet assay. Expressions of APE1 / Ref-1 mRNA and protein were determined by real-time PCR and Western blotting, respectively. Results:In comet assay,after treated with gemcitabine for 24 hours,OTM value of SW1990-0. 5 and SW1990 cells were 0. 32 ± 0. 13 and 26. 96 ± 6. 83,respectively. Expression level of APE1 / Ref-1 mRNA in SW1990-0. 5 cells was 2. 48 ± 0. 49;and expression levels of APE1 / Ref-1 protein in SW1990-0. 5 and SW1990 cells were 1. 57 ± 0. 08 and 0. 84 ± 0. 06,respectively. Statistically significant differences were existed in all these parameters between SW1990-0. 5 and SW1990 cells(P all < 0. 05). Conclusions:DNA repair might be correlated with the resistance of pancreatic cancer to gemcitabine,and up-regulation of APE1 / Ref-1 might contribute to this resistance by its function on DNA repair.

Purpose:To investigate whether NSAIDs can induce apoptosis of gastric cancer cell lines,to observe the effect of different p53 genotype on NSAIDs induced apoptosis,to elucidate the regulation of NSAIDs on expression of apoptosis related genes. Methods:The anti-proliferative effect of NSAIDs was measured by MTT assay.Apoptosis was determined by acridine orange(AO) staining,Annexin-V/PI double staining,laser scanning cytometry(LSC) and flow cytometry (FCM).Alteration of bcl-2 and bax genes was detected by reverse transcription polymerase chain reaction (RT-PCR).Protein expression was determined by Western-blotting.Results: Indomethacin (Indo) and Aspirin (Asp) inhibited both AGS(wild-type p53)and MKN28(mutant p53) gastric cancer cell lines growth in a time/dose dependent manner.AGS cell line was more sensitive to NSAIDs,which apoptosis percentage was significantly higher than MKN28 under the same condition. The percentages of apoptosis of MKN28 were somewhat higher among NSAIDs treated groups compared with the normal control group,but these slight differences were not statistically significant. The bax mRNA kept increasing since NSAIDs treatment accompanied by a decrease of bcl-2 gene.The Bax protein increased after treatment while the Bcl-2 protein was undetectable, which tendency was more obvious during 6-24hs.Conclusion: Both Indo and Asp could induce apoptosis in gastric cancer cell lines,which adds further theoretical foundation to the anti-cancer use of NSAIDs.NSAIDs could not induce notable apoptosis of MKN28,which indicated the mutant p53 gene perhaps blocked NSAIDs induced apoptosis.One of the major pathways that mediated the anti-tumour response of NSAIDs in gastric cancer cells was through up-regulation of bax and down-regulation of bcl-2 genes and/or proteins.[

Background:Gemcitabine is the first-line drug for chemotherapy of pancreatic cancer. However,owing to the inherent and acquired resistance,gemcitabine does not change obviously the prognosis of patients with pancreatic cancer. Exploration of the mechanism of acquired resistance to gemcitabine is of great clinical importance. Aims:To establish a gemcitabine-resistant human pancreatic cancer cell subclone and to explore preliminarily the resistance mechanism. Methods:Human pancreatic cancer cell line SW1990 was stimulated continuously with 0. 5 μmol/ L gemcitabine in vitro to establish the gemcitabine-resistant subclone SW1990-0. 5. The resistance index of SW1990-0. 5 cells was counted by CCK-8 assay. Proliferation and invasion of SW1990 and SW1990-0. 5 cells were detected by cell doubling time assay and scratch wound healing assay in vitro;cell cycle and cell apoptosis were detected by flow cytometry;expressions of multidrug-resistance related genes(MDR-1,MRP-1,and BRCP)and gemcitabine metabolic enzyme related genes(dCK,RRM1, and RRM2)were determined by real-time PCR. Results:The resistance index of SW1990-0. 5 cells was 9. 32. Compared with the parental SW1990 cells,the proliferation capacity but not the invasion capacity of SW1990-0. 5 cells in vitro was reduced. When treated with gemcitabine,the cell cycle of SW1990-0. 5 cells was similar to that of parental cells,whereas the cell apoptosis was significantly inhibited;expressions of MRP-1,BRCP and dCK mRNA were down-regulated,while expressions of MDR-1,RRM1 and RRM2 mRNA did not change. Conclusions:A stable gemcitabine-resistant human pancreatic cancer cell subclone SW1990-0. 5 was successfully established. Inhibition of cell apoptosis and down-regulation of dCK expression might contribute to the acquired resistance to gemcitabine of pancreatic cancer.

Objective To analyze the effect of total parenteral nutrition (TPN) and enteral nutrition (EN) in patients with acute pancreatitis. Methods Randomized controlled trials of TPN and EN in patients with acute pancreatitis were searched in Medline and China Biological Medicine Disk from Jan 1966 to June 2004. Eight studies were enrolled into the analysis. The detail about the trial design, characters of the subjects, results of the studies were reviewed by two independent authors and analysed by using Revman 4.2 software. Results Compared with TPN, EN was associated with a significantly lower incidence of secondary infections (RR 0.45, 95% CI 0.29-0.68, P=0.0002) and other complications(RR 0.67, 95% CI 0.47-0.96, P=0.03), fewer surgical interventions (RR 0.47, 95%CI 0.24-0.94, P=0.03) and shorter hospitalization. However, there was no significant difference in mortality (RR 0.61, 95%CI 0.32-1.18, P=0.14) between patients with TPN and EN. Conclusion EN could be the preferred nutrition feeding method in patients with acute pancreatitis.

0.05).②Gabexate mesilate significantly reduced the frequency of contraction (P0.05).③High dose gabexate mesilate could markedly reduce the motility index ( P

Objective To compare the effect of parenteral nutrition and enteral nutrition with different start time on acute pancreatitic patients.Methods Randomized controlled trials comparing enteral and parenteral nutrition in acute pancreatitic patients published from January 1996 to January 2011 were searched in MEDLINE,EMBASE,Cochrane databases,Wanfang science library,and China National Knowledge Infrastructure.The information about study design,patient characteristics,and outcomes were extracted by two independent analysers before processed with RevMan 4.2 software.Results Altogether 14 trials were included.When started after 24 hours of admission,enteral nutrition,in comparison with total parenteral nutrition,resulted in a statistically significant reduction in the risks of infections (P =0.0004),surgical intervention (P =0.0200),organ failure (P =0.0400),and morality (P =0.0002) in acute pancreatitic patient.When started within 48 hours of admission,enteral nutrition,in comparison with total parenteral nutrition,resulted in a statistically significant reduction in the risks of infections (P =0.0000),surgical intervention (P =0.0001),organ failure (P =0.0006),and mortality (P =0.0300) in acute pancreatitic patients.Conclusions The time of the commencement of nutriton has an influence on the benefits of enteral nutrition.Enteral nutrition started between 24 hours and 48 hours of admission is more effective than within 24 hours or after 48 hours of admission.

Objective To examine the relationship between inflammatory response induced by cardiopulmonary bypass and postoperative cognitive dysfunction.Methods Twenty-five patients undergoing elective cardiac valve replacement under cardiopulmonary bypass were randomly divided into two groups:ulinastatin group(group U,n=13) and control group(group C,n=12).In group U,ulinastatin 12 000 U/kg Was given intravenously immediately after induction of anesthesia,6 000 U/kg ulinastatin Was added to the priming solution,and 6000 U/kg ulinastatin was given at 5 min before the aortic decamping.In group C,normal saline was given instead of ulinastatin.Venous blood samples were taken after induction of anesthesia,at the end of CPB,and 24 h after operation for determination of plasma IL-6 concentration and neutrophils NF-kB expression.The cognitive function of the patients was evaluated by Mini-Mental State Examination(MMSE) before and 3 d,7 d after operation.Results The concentraion of IL-6 and neutrophils NF-kB expression were lower in group U than in group C(P<0.05 or 0.01).There wag no significant difference in the incidence of postoperative cognitive dysfunction between group C and U.Conclusion Inflammatory response induced by cardiopulmonary bypass is not related to postoperative cognitive dysfunction.

The college has been keeping its characteristics in the 7-year medical students training program in the pastten years. It is emphasized that the cultivating target in this program is to make the students become creative medicalprofessionals with lifelong study capacity by applying the humanistic spirit as the forerunner, and placing emphasis onthe practical and advanced feature, The training mode should fully incarnate the consistent characteristics of the bach-elor-and-master courses and the three-phrase tutor system, which aims to improve the practical and research competenceof the students. And the training outcome has been approved to be identical with the target set in advance.[

Objective To establish the animal model of cervical pain induced by formalin injection and explore the effect of cervical pain on cervical vertigo.Methods Formalin of 40 mL/L was injected near the nerve root of left side of neck to establish the model of cervical pain in rabbits.A total of 30 rabbits were divided randomly into two groups.Formalin-induced pain group(15 rabbits): indexes related to the vertebral artery were observed respectively before 2 mL of formalin injection and after it at 5,10 and 30 minutes.Lidocaine-blocking pain group(15 rabbits): pain induced by formalin was blocked by lidocaine of 10 g/L after 15-minute drug administration and the same indexes were observed at the same time and position of the neck.Results In formalin-induced pain group,vertebral artery systolic velocity,diastolic velocity and pulsatility indexes were decreased whereas resistance index was increased(P