Objective To explore short term curative effects and adverse reactions of two different kinds of intraperitoneal hyperthermic chemotherapy (IPHC) drugs in the treatment of advanced ovarian cancer after cytoreductive surgery.Methods 76 patients with advanced ovarian cancer in the Second Affiliated Hospital of Zhengzhou University from July 2013 to November 2015 were divided into two groups:single-drugs group of 36 patients (IPHC with 5-fluorouracil after cytoreductive surgery combined with intravenous chemotherapy),combined treatment group of 40 patients(IPHC with 5-fluorouracil and carboplatin after cytoreductive surgery combined with intravenous chemotherapy).Short term curative effects,postoperative clinical indicators and adverse reactions of chemotherapy in two groups were compared and analyzed.Results The CA125 effective rates in single-drugs and combined treatment group were 86.11％ and 95％,and the difference showed statistically significant differences (P ＞ 0.05).The ascites remission rates in single-drugs and combined treatment group were 97.22％ and 97.5％,and the difference between two groups showed no statistically significant differences (P ＞ 0.05).Adverse drug reactions showed statistical difference in distribution of the bone marrow,liver damage and gastrointestinal toxicity.No statistical difference were found between the two groups in terms of distribution of renal damage and cardiovascular system damage.Conclusion IPHC after cytoreductive surgery in the treatment of advanced ovarian cancer is an effective means as adjuvant chemotherapy.The short-term curative effect of combined treatment group is obvious and adverse reactions can be tolerated.IPHC can be applied according to the patient's specific clinical situation.

Objective To study the rules of circumferential margin invasion(CMI)in middle and(or)lower rectal cancers by pathological large slices stained with HE and labeled with CK20,and provide a pathological basis for clinical therapy of rectal cancer.Methods Forty-one patients with middle or low rectal cancer were randomly selected in 8 months.The surgically resected specimens were detected after they were made into the pathological large slices stained with HE and labeled with CK20.Results The mesentery CMI positive rate in the pathological slices with HE staining and CK20 labeling was 21.95%,and 29.27% respectively.The mesentery CMI positive rate in moderately-and well-differentiated group was lower than in poorly-differentiated group(P＜0.05).Moreover,the mesentery CMI rate was higher in the specimens with lower edge less than 5 cm away from the dentate line than that in those with lower edge more than 5 cm away from the dentate line(P＜0.05).There was no significant correlation between CMI with the factors such as gender,age,pathological general types,tumor infiltration depth,lymph node metastasis,and surgical procedures(all P＞0.05).Conclusion There were risk factors for the CMI such as low location,poor differentiation and so on.The CMI patients should be treated with standardized adjunctive therapy after operation.

Objective To investigate the distribution of hepatitis B virus (HBV) genotypes in patients with chronic HBV infections and the correlations of genotypes with liver fibrosis and hepatocellular carcinoma (HCC).Methods Serological,virological and pathological data of 190 patients with chronic HBV infections admitted to Hangzhou First People's Hospital during June 2007 and June 2012 were retrospectively analyzed.The series included 62 cases of chronic hepatitis B (CHB),60 cases of liver cirrhosis and 68 cases of HCC.HBV was genotyped by multiplex PCR,and subgenotyped by restriction fragment length polymorphism (RFLP).SPSS 11.0 was used for statistical analysis.Results Among 190 patients,61 were HBV genotype B (32.1％),126 were genotype C (66.3％),and 3 were B + C hybrid.HBV B2 (61/61,100.0％) and C2 (123/126,97.6％) were the major subgenotypes.HBV genotype B was more prevalent in CHB patients (46.8％,29/62) than in liver cirrhosis (20.0％,12/60) and in HCC patients (29.4％,20/68) (x2 =8.73 and 4.16,P＜0.01 or P＜0.05),whereas the prevalence of genotype C was higher in liver cirrhosis and HCC than that in CHB (x2 =9.54 and 4.17,P ＜0.01 or P ＜ 0.05).Patients with genotype C2 had higher serum hyaluronic acid level than with genotype B2 in 3 groups (t =2.685,2.433 and 2.015,P ＜ 0.01 or P ＜ 0.05).CHB patients with C2 infections had higher liver fibrosis grade than those with B2 (x2 =6.726,P =0.010),while there was no statistical difference in liver inflammation grade (x2 =0.601,P ＞ 0.05).HCC patients with B2 infection tended to have larger tumor diameter (≥5 cm) (x2 =7.231,P ＜ 0.01) and those with C2 infection were prone to be more serious cirrhosis (x2 =4.910,P ＜ 0.05).Conclusions HBV genotypes C2 and B2 are predominant in patients with chronic HBV infections in Hangzhou.HCC patients infected with HBV C2 may be complicated with more severe liver fibrosis,and those with HBV B2 infections may tend to have larger liver tumor.

This article analyzes the factors of influencing practice quality from such aspects as hospital management,medical reform,clinical teachers and students and points out that only by enhancing the management of practice hospital as well as the system of examining and assessment,raising the teacher guidance and teaching consciousness and guiding the students to properly handle with the relations between employment,entrance exam for postgraduate and practice can we guarantee the clinical practice quality.

Objective To investigate the expression and the clinical significance of meningioma-association protein（MAC30）mRNA and protein in colorectal carcinomas.Methods MAC30 was immunohistochemically examined in 130 primary tumours,73 distant normal mucosa specimens and 34 lymph node metastases from rectal cancer patients＇paraffin embedded blocks.MAC30 mRNA expression was detected by RT-PCR in primary tumors,adjacent and distal normal mucosa of 50 rectal cancer patients underwent colectomy.Results MAC30 cytoplasmic expression level in colorectal primary tumors and lymph node metastases was significantly higher than that in distant normal mucosa.MAC30 mRNA expression was upregulated in primary tumor,and the expression level was related to the histologic type of the tumor.Three-year survival rate of the colorectal carcinomas patients with strong expression of MAC30 was significantly lower than that of the patients with weak MAC30 expression（P 0.05）.Conclusion MAC30 overexpression might be involved in the development of colorectal carcinomas and seemed to be a prognostic factor.

ObjectiveTo explore the feasibility, safety and clinical value of laparoscopic Rouxen-Y cystojejunostomy in the treatment of pancreatic pseudocyst. Method Four patients with pancreatic pseudocyst received totally laparoscopic pancreatic pseudocystojejunostomy. The data on intraoperative bleeding, operative time, postoperative time to get out of bed, time of first flatus/bowel motion, complication and duration of hospital stay were collected and analyzed retrospectively. ResultsAll operations were carried out successfully with laparoscopic surgery. The mean operative time was 90 min. The average intraoperative blood loss was 40 ml. The mean postoperative time to get out of bed was 1.5 d, and the mean time of first flatus/bowel motion was 2. 3 d. All patients recovered smoothly without any pancreatic fistula. The average hospital stay was 7 days. Fever, pancreatitis,adhesive intestinal obstruction and other complications did not occur. ConclusionsTotally laparoscopic Roux-en-Y pancreatic pseudocystojejunostomy was an efficacious, safe, and minimally invasive procedure.

Objective To investigate the expression of pSTAT5 in 7 pancreatic carcinoma cell lines,and the change of expression of pSTAT5 in pancreatic carcinoma cells SW1990 after growth hormone (GH) treatment, and explore its molecular mechanism. Methods Human pancreatic carcinoma cell lines (SW1990, Cap-1, Colo, Mia, AsPc, P3, PANC1) were cultured in vitro, and Western blotting was used to detect the expression of pSTAT5 in these cell lines. SW1990 in exponential growth phase was collected and nude Balb/c mice were inoculated with SW1990 cells. When tumors became palpable after inoculation, mice (normal saline group). 1 h, 2 h and 24 h after the last dose of GH treatment, the mice were sacrificed.Western blotting was used to detect the expression of pSTAT5 in SW1990 and inoculation tumor cells after GH injection. Results Positive expression of pSTAT5 was observed in all human pancreatic carcinoma cell lines (SW1990, Cap-1, Colo, Mia, Aspc, P3, PANC1). 5 minutes after GH (50 ng/ml) stimulation, the expression of pSTAT5 in SW1990 was 0.57 ±0.05, which was significantly increased; and it reached 0.64 ±0.04 at 10 minutes, then decreased to 0.39 ±0.03 at 15 minutes, however, it remained higher than that in the control group at 1 h (0.33 ± 0.02 vs 0.25 ± 0.06), and its expression at 2 h was 0.26 ± 0.03 and returned to the normal level. The expression of pSTAT5 in xenograft was not significantly changed. Conclusions GH could rapidly up-regulate the expression of pSTAT5 in SW1990 but the effect lasted for a relatively short period. GH had no significant effect on the expression of pSTAT5 in xenograft.

Objective To investigate the effect of GH on proliferation of pancreatic cancer cells and observe the features of IGF-IGFBP3 pathway in the host after GH administration. Methods Pancreatic cancer cells (SW-1990,PANC-1 and P3) during exponential growth stage were harvested and cultured in medium containing growth hormone (50 ng/ml). After 24, 48 and 72 hours, cells were counted using a Coulter Counter. Thirty-five Athymic nude Balb/c mice were inoculated with SW-1990cells. When tumors became palpable after inoculation, animals were randomized to receive GH points (1 h, 2 h, 6 h, 24 after the last injection), plasma samples were gathered for subsequent ELISA determination and liver was rapidly incised for immune blotting analysis. Results The results revealed that GH stimulated cell growth in vitro. GH elevated levels of IGF-Ⅰ , Ⅱ at the 1st , 2nd , 6th hour after the last injection. GH augmented the expression of IGFBP3 in the liver of the host in vivo (1 h, 2 h, 6 h, 24 h, respectively). Conclusion Such proteins as IGF- Ⅰ and Ⅱ might be associated with mechanism of last effect of GH on tumor host. The up-regulation of IGFBP3 by GH administration in the host may help to explain the phenomena that GH doesn't accelerate growth of pancreatic tumor in vivo.

Objective To study the impact of exogenous growth hormone (GH) on the levels of insulin-like growth factor-Ⅰ and -Ⅱ (IGF-Ⅰ, -Ⅱ) of the pancreatic cancer tissue and the small intestine mucosa of the host. Methods In situ hybridization was performed on pancreatic cancer cell lines (SW-1990) and inoculation tumor of the host to determine the location of the mRNA transcript encoding IGF R-Ⅰ,-Ⅱ. Athymic nude Balb/c mice were inoculated with SW-1990 cells. After inoculated tumors have become palpable, animals were randomized to receive GH (4 mg/kg once daily for 2 weeks) versus saline control. After the animals were killed at time point, tissues (tumor and small intestine) were rapidly incised for subsequent immune blotting analysis. Results Strong IGF R-Ⅰ,-Ⅱ mRNA hybridization signal could be detected in pancreatic cancer cell. There was no statistically significant difference between the level of IGF-Ⅰ, Ⅱ in the tumor of the GH and NS groups after 1 hours of GH injection (P>0.05). GH augmented the expression of IGF-Ⅰ(1 h : 0.33±0.05, P<0.05 ; 2 h : 0.34±0.04, P<0.05 ; 6 h:0.34±0.05, P<0.05), -Ⅱ(1 h : 0.36±0.05, P<0.05) in the small intestine mucosa of the host. Conclusions The expression of IGF-Ⅰ, Ⅱ in the small intestine mucosa of the host was elevated by GH, but not in the inoculation tumor in vivo. The discrepancy of GH-IGF pathway between inoculation tumor and small intestine of the host may help to explain the phenomena that GH doesn't accelerate growth of pancreatic tumor in vivo.

Objective To inVestigate the effect of emodin on hyPertroPhic scar fibroblasts ( HSFs ) and exPlore the underlying mechanism. Methods HSFs were treated by emodin at final concentrations of 0,20,40,and 80 μmol·L-1, resPectiVely,in the cultural media. Forty_eight hours later,the cells were subjected to MTS assay and flow cytometry assay with annexin V and ProPidium iodide as dyeing indicators. Whole cell lysates from the cells of eVery grouP were subjected to Western blotting to measure the Protein exPression leVels of ERK1∕2,Bcl_2,Mcl_1 and RIP1. Results The cell Viability of HSFs was inhibited by emodin in a dose dePendent manner. The mortality rate of HSFs treated with emodin for 48 h at the concentrations of 40 and 80 μmol·L-1 were 28. 6%and 68. 0%,resPectiVely,which was significantly higher than that of the control grouP ( P<0.01).Pretreatmentwith Z_VAD_FMK could Partially reduce the mortality caused by emodin (P<0.05).PhosPhorylation of ERK1∕2 and the exPression of RIP1 and Mcl_1 were inhibited by emodin. Conclusion Down regulation of ERK1∕2,RIP1 and Mcl_1 by emodin may account for the inhibited Proliferation and increased cell death of HSFs.