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 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.

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.

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.

The satorius muscle,its blood vessels and nerves have been dissected and examinedin 20 Chinese adult cadavers.It was found,on the average,that the length of thesatorius muscle is 529?8.48mm;the breadth,25.30?0.82mm;and the thickness,10.5?0.66mm.The arteries of the satorius muscle may arise from the surperficial circumflex iliacartery (0.66%?0.46),the femoral artery(58.36%?2.82),the deep femoral artery(3.93?1.11),the lateral circumflex femoral artery and its branches(13.44%?1.95),the supreme genicular artery(20.98%?2.33)and the popliteal artery(2.62%?0.91).There may be 5～13 arterial branches,averaging 7.6,in each satorius muscle,distributing roughly and evenly to the whole muscle,with an interval of about 7cmbetween two adjacent arteries and showing segmental distribution.The upper one third of the satorius muscle is mainly supplied by the branchesof the deep femoral artery and the lateral circumflex femoral artery while theinferior one third,by the branches of the supreme genicular artery.Therefore twoisolated flaps may be planned depending on the arteries mentioned above.The satorius muscle is innervated by the femoral nerve.70% of the cases arewith 1～2 branches of nerves,which,before entering the muscle,may give out 1～7twigs.

Objective To investigate the changes of Notch signaling pathway activity in human pancreatic cancer cell lines (SW1990, BxPC3 )after gemcitabine induction, and to study its relationship with pancreatic cancer resistant to gemcitabine chemotherapy. Methods The pancreatic cancer cell lines SW1990 and BxPC3 were cultured with different concentrations of gemcitabine for 48 hours. The Notch signaling pathway receptors ( Notch1, Notch2, Notch3, Notch4), ligands (Jagged1, Jagged2) and downstream target Hesl mRNAs expression were detected by quantitative real-time PCR (Q-PCR). Protein levels of Hes1 were determined by Western blotting. Results After treatment with 2 μmol/L gemcitabine for 48 hours, the expression of Notch1, Notch2, Notch3, Jagged1, Jagged2 and Hes1 mRNAs in SW1990 cells were 8.26 ±0.48, 39.12 ±4.87, 0.84 ±0.06, 105.8 ± 17.92, 6.59 ±0.32 and 17.30 ±2.96, which were significantly elevated when compared with those without gemcitabine treatment ( 1.02 ± 0. 15, 15.25 ± 1.28, 0. 12 ± 0.02,32.66 ± 1.98, 1.88 ± 0.29 and 5.02 ± 0.64, P < 0.05 or P < 0. 01 ); the expression in BxPC3 cells was 7.87 ±0.59, 109.4 ± 10.98, 0.74 ±0.19, 62.73 ± 13.50, 2.09 ±0.16 and 15.38 ± 1.06, which were significantly elevated when compared with those without gemcitabine treatment ( 1.14 ±0.43, 58.96 ±2.63,0.10 ± 0.02, 16.95 ± 3.79, 0.98 ± 0.02 and 2.04 ± 0.16, P < 0.05 or P < 0.01 ). The expressions of Hes1protein in SW1990 cells after 1, 2 μmol/L gemcitabine treatment for 48 h were 0.30 ±0.03, 0.42 ±0.03;and the expressions in BxPC3 cells were 0.33 ± 0.02, 0.45 ± 0.03, which were significantly increased when compared with those without gemcitabine treatment (0.13 ± 0.01, F = 33.71,0.09 ± 0.02, F = 38.54, P <0.01 ). Conclusions The Notch signaling pathway is significantly activated in pancreatic cancer cells SW1990 and BxPC3 by gemcitabine, which may be one of the mechanisms of chemoresistance.

Objective To evaluate the clinical efficacy of vertebroplasty using vertebral pedicle screw technique combined with calcium sulfate cement injection in the treatment of thoracolumbar vertebrae fractures.Methods Twenty-eight patients with thoracolumbar vertebrae fractures admitted in our department in recent 2 years were enrolled in this study,including 21 cases of type A,3 cases of type B,and 4 cases of type C.All patients were fixed with vertebral pedicle screw,and then verteplasty was performed using calcium sulfate cement injection.Results All patients were followed up for an average time of 16 months.Within the follow-up,there was no complication noted,such as loosening or breakage of internal fixation,chronical lumbar back pain,and loss of effected vertebral height.Artificial bones injected into vertebrae were absorbed in about 3 months.Conclusion Vertebroplasty using vertebral pedicle screw technique combined with calcium sulfate cement injection is an effective and safe procedure for thoracolumbar vertebrae fractures,which renders it possible to bear weight early and to maintain corrected vertebral height postoperatively.

The blood vessels, nerves and the size of the gracilis muscle were studied in 50 adult Chinese cadavers (43 males and 7 females).In average, the length of the gracilis muscles is 325 mm the breadth is 26.18mm the thickness is 6.56mm. The length of its tendon is 112.78 mm.The nutrient arteries of the gracilis muscle may arise from the profund femoral artery, medial circumflex femoral artery, the first perforating artery, femoral artery, popliteal artery, supreme genicular artery or obturator artery. Among them, the profund femoral artery and femoral artery give off constant branches to the gracilis muscle.The dominant nutrient artery of the gracilis muscle arises from the profund femoral artery in 94 cases (94％), from the medial circumflex femoral artery in 5 cases (5％). There is only one case (1％) arising from the first perforating artery.The average length of the dominant nutrient artery is 83.6mm. Its diameter in the origin is 2.24mm. and outside the hilum, 1.44mm. The distance from the vascular hilum to the pubic tubercle is 142.48mm. The surface respresentation of the dominant neuro-vascular hilum is situated at the junction point of the upper and middle thirds of the line joining the pubic tubercle to the adductor tubercle.There are 72.5％ of the dominant nutrient arteries of the gracilis muscle accompanying with two veins and 27.5％, with only one vein.The gracilis muscle is innervated by the anterior branch of the obturator nerve which accompanies the dominant nutrient artery entering the muscle. Its average diameter is 1.78mm.

Objective: To investigate epidermal growth factor receptor (EGFR) and thymidylate synthase (TS) expression in primary liver cancer, and analyze its clinicopathological features and prognostic significance. Methods: Immunohistochemistry was performed using EnVision method to detect EGFR and TS expression in 41 cases of liver cancer. Correlation coefficient between EGFR and TS was calculated by Spearman method. Fisher's exact probability method or χ² test was used to analyze the clinicopathological features of EGFR and TS. Kaplan-Meier method was used to calculate the survival rate of patients in conjunction with the log-rank test.COX proportional hazard regression model was used to analyze the prognostic factors of patients. ROC curve was used to analyze the predictive accuracy of EGFR and TS for prognosis. Results: The positive rates of EGFR and TS in liver cancer tissues were 34.15% and 39.02%, respectively. There was a positive correlation between EGFR and TS expressions, and the difference was statistically significant (P < 0.05). EGFR was associated with tumor size and tissue differentiation (P < 0.05) in HCC patients, whereas TS was associated with tissue differentiation (P < 0.05). There was no significant difference in prognostic effect of EGFR on survival rate (P > 0.05). TS prognostic effect on survival rate was statistically significant (P < 0.05). HR of EGFR was 0.210 with 95% CI, 0.052-0.852, P = 0.029; indicating that the risk of death in patients with negative EGFR was 0.210 times higher than that in patients with positive EGFR. HR of TS was 2.496, with 95% CI, 1.325-4.701, P = 0.005, indicating that the risk of death increased by 2.496 times with the same level of EGFR. The area under the EGFR curve was 0.553 and its approximate reference confidence interval was 95% (0.355, 0.751), indicating that EGFR was a risk factor for death and the area under the TS curve was 0.695, and its approximate reference confidence interval was 95% (0.513, 0.878), indicating that TS was a risk factor for death. Conclusion EGFR and TS were equally expressed in primary liver cancer, and EGFR and TS expressions were positively correlated. EGFR and TS had an effect on the degree of tissue differentiation in patients with liver cancer. EGFR and TS were risk factors for prognosis, and TS may assist EGFR.