Objective To investigate the effect of no-tonch harvesting technique in reducing vein graft intimal hyperplasin. A4othods This longitudinal trial compared graft ungiestenosis of two groups undergoing jugular vein to carotid artery interposition grafting in rabbit model. Conventional group: 12 rabbits had their veins stripped, distended, and stored in heparinized saline solution. No-touch group: 12 rabbits had veins removed with surrounding tissues, but were not distended, and stored in heparinized blood. The grafts were removed 4 weeks following grafting, and morphometry and immunohistochemistry assessment were performed. Results The intimal thickness, degree of anginstennsis and proliferation index of vascular smooth muscle cells of no-touch group were significantly reduced (P< 0.01) compared with those of the conventional group. The proliferating cell nuclear antigen pnsitive-staining cells were significantly increased (P<0.01) in the conventional group compared with whose in the no-touch group. Conclusion Harvesting the vein graft with no-touch harvesting technique could significantly reduce intimul hyperpinsin of the vein graft.

OBJECTIVE:To strengthen application management of antibiotics in outpatients,promote rational use of antibiot-ics,and to provide reference for scientific management and decision-making in the hospital. METHODS:The proportion of outpa-tients receiving antibiotics in total outpatients was analyzed statistically during Jan. 2008-Jun. 2016. Utilization rate data of antibiot-ics in outpatients during 2008-2015 were used to establish Autoregressive integrated moving average model(ARIMA),and the data of the first half of 2016 was used to validate established model;the utilization rate trend of antibiotics in outpatients in the second half of 2016 was predicted. SPSS 20.0 statistical software was adopted for statistical analysis. RESULTS:Established ARIMA(2,1, 0)(2,1,0)12 model has higher fitting degree. There was a small difference between measured value and fitted value of utilization rate of antibiotics in outpatients in 2016. Average absolute error was 0.72%,and average relative error was 4.20%,within 95%confidence interval of fitted value. Dynamic trend of model predicted value was basically consistent with measured value. CONCLU-SIONS:ARIMA model simulates utilization rate trend of antibiotics in outpatients well,can be used for short-term prediction and dynamic analysis of utilization rate trend of antibiotics. However,for long-term prediction,various factors should be considered.

Objective To investigate the expression of stromal cell-derived factor-1(SDF-1)and its clinical significance in blood plasma of patients with breast tumor.Methods The level of SDF-1 protein was examined by enzyme linked immunosorbent assay(ELISA)in blood plasma of 26 patients with breast benign tumor and 52 patients with breast cancer.Results The SDF-1 protein in blood plasma was detected in both breast benign tumor patients and breast cancer ones.The level of SDF-1 protein in patients with breast cancer was higher than that in ones with breast benign tumor,and there was a statistical difference between them(P=0.000).In patients with breast cancer,the level of SDF-1 protein in axillary lymph node(ALN)metastasis positive patients was significantly higher than that in ALN metastasis negative ones(P=0.036).Conclusion The level of SDF-1 protein in blood plasma may be a specific tumor marker.Its level is correlated with lymph node involvement in breast cancer.

Objective To evaluate the role of c?Jun N?terminal kinase ( JNK) and p38 mitogen?ac?tivated protein kinase ( p38MAPK) signaling pathways in attenuation of myocardial ischemia?reperfusion ( I∕R) injury by morphine postconditioning. Methods Healthy adult male Sprague?Dawley rats, weighing 180-240 g, were used in the study. Their hearts were excised and retrogradely perfused in a Langendorff apparatus with Krebs?Ringer ( K?R) buffer saturated with 95% O2?5% O2 at 37℃. After 15 min of equili?bration, 52 isolated hearts were divided into 4 groups ( n=13 each) using a random number table: control group (group C), I∕R group, morphine postconditioning group (group MP), and morphine postcondition?ing plus anisomycin group ( group MP+A) . The hearts were continuously perfused with K?R buffer for 105 min in group C. In group I∕R, the hearts were subjected to 45 min of global ischemia by stopping perfusion with K?R buffer, followed by 60 min of reperfusion by restoration of perfusion with K?R buffer. In group MP, the hearts were subjected to 45 min of global ischemia, followed by 10 min of reperfusion with K?R buffer containing 3?0 μmol∕L morphine and then by 50 min of reperfusion with K?R buffer. In group MP+A, the hearts were subjected to 45 min of global ischemia, followed by 10 min of reperfusion with K?R buffer containing 3?0 μmol∕L morphine and 1?0 μmol∕L anisomycin ( an activator of JNK and p38MAPK) and then by 50 min of reperfusion with K?R buffer. At 60 min of reperfusion, 8 hearts in each group were selected for measurement of the myocardial infarction and amount of creatine kinase?MB ( CK?MB) released from the myocardium, and the myocardial infarct size was calculated. At 20 min of reperfusion, 5 hearts in each group were selected to detect the expression of phosphorylated JNK ( p?JNK ) , phosphorylated p38MAPK ( p?p38MAPK) and cytochrome c ( Cyt c) in myocardial tissues ( by Western blot) and content of nicotinamide adenine dinucleotide ( NAD+) in myocardial tissues ( by spectrophotometry ) . Results Compared to group C, the myocardial infarct size and amount of CK?MB released from the myocardium were significantly increased, the expression of p?JNK, p?p38MAPK and Cyt c was significantly up?regulated, and the content of NAD+ was significantly decreased in I∕R, MP and MP+A groups ( P<0?05) . Compared to group I∕R, the myocardial infarct size and amount of CK?MB released from the myocardium were signifi?cantly decreased in MP and MP+A groups, and the expression of p?JNK, p?p38MAPK and Cyt c was sig?nificantly down?regulated, and the content of NAD+ was significantly increased in group MP (P<0?05). Compared to group MP , the myocardial infarct size and amount of CK?MB released from the myocardium were significantly increased, the expression of p?JNK, p?p38MAPK and Cyt c was significantly up?regula?ted, and the content of NAD+ was significantly decreased in group MP+A (P<0?05). Conclusion The mechanism by which morphine postconditioning attenuates myocardial I∕R injury is related to inhibition of activation of JNK and p38MAPK signaling pathways in rats.

Objective To observe the expression of connective tissue growth factor (CTGF) in pancreas, and discuss its significance. Methods The pancreatic fibrosis model was induced by high fat diets. The rats were sacrificed 16 weeks later, and the pancreatic tissue was harvested for routine pathologic examinations. Pancreatic collagen fibrosis I was determined by HE and Sirius red staining;α-SMA and CTGF expression were detected by immunohistochemistry. Results After pancreatic fibrosis, pancreatic lobules and acinar atrophy was observed, lobules gap was widened, interstitial fibrous tissue was significantly proliferated, the synthesis of pancreatic collagen fibrosis I was significantly increased when compared with normal pancreas ( 1500.2 + 255.8 vs. 57.4 ± 23.2, P ＜ 0. 01 ), the expression of α-SMA was significantly increased when compared with normal pancreas( 1500.2 + 255.8 vs. 57.4 + 23.2, P ＜ 0. 01 ), and the expression of CTGF was significantly increased when compared with normal pancreas (2950.5 ± 431.9 vs. 382.2 + 190.8, P ＜0.01 ), and there were abundant activated PSCs. Conclusions CTGF participated in the regulation of pancreatic fibrosis development; the function of CTGF was closely related to PSCs activation.

ObjectiveTo explore the sensitivity of cancer stem cells to chemotherapy in human pancreatic carcinoma.MethodsPANC-1 ceils were cultured in an incubator filled with 5％ CO2 at a temperature of 37℃,and were labeled with Hoechst 33342.The SP analysis and sorting were performed using a FACSVantage SE.RT-PCR was performed to detect the expression of human CD133 ABCG2 and Notch1.SP and non-SP cells from the PANC-1 cell line were treated with 5-fluorouracil (5-FU; 1,10,or 100 μg/ml) or gemcitabine (10,100,or 1000μg/ml),and the cell viability was determined using the MTT assay.The sensitivity of sorted tumor cells to chemotherapeutics was determined in NOD/SCID mice model.ResultsSP cells were found to have higher drug-resistance both in vivo and in vitro and higher levels of mRNA expression for CD133,ABCG2 and Notch1,when compared to non-SP ceils.The xenografted tumors derived from injected SP cells and treated with gemcitabine had more CD133± cells than the untreated group.ConclusionsThe SP of PANC-1 pancreatic carcinoma cells are enriched with highly gemcitabine-resistant CSCs and determine the carcinogenesis of the PANC-1 pancreatic carcinoma cells.

Objective To investigate the factors influencing the incidence of acute pancreatitis (AP) in patients with organophosphorus poisoning and explore the effectiveness of measures for its prevention and treatment. Methods Clinical data of 50 patients with organophosphorus poisoning were reviewed retrospectively in our center between January 2001 and December 2006. Results The incidence of AP in patients with organophosphorus poisoning was 30% (15/50), and 14 patients suffered from MAP, while one patient occurred SAP. 13 of 15 AP patients underwent gastric lavage with cold normal saline; gastric tube was placed in 14 patients; toxic doses over 50 ml were observed in 10 patients; atropine overdose were observed in 11 patients. There were 35 cases of organophosphorus poisoning alone, and 2 of them underwent gastric lavage with cold normal saline; gastric tube was not placed in 1 patient; toxic doses over 50 ml were not observed in all the patients. The toxic dose, water temperature for gastric lavage, gastric tube placement, duration from poisoning to treatment between the two groups were significantly different (P＜0.01). All the patients with organophosphorus poisoning alone survived, while in these 15 patients with AP, 14 patients were cured, 1 patient died. Conclusions Organophosphorus poisoning can induce AP and development of AP was possibly related to organophosphorus poisoning and improper treatment.

Hyperlipidemia is one of the most important risk factors of human atherosclerosis and cardiaccerebral vascular disease.The number of hyperlipidemia in China increased year by year and showed a younger trend.The current treatments for hyperlipidemia include drug therapy,physical exercise,diet prevention,liposuction surgery and low-energy laser therapy,etc.Many researches showed that low intensity laser irradiation has a certain curative effect on hyperlipidemia.The aim of this paper is to provide a new idea and method for the future treatment of dyslipidemia by reviewing the anti-hyperlipidemia methods and mechanism of low energy laser irradiation treatment.

ObjectiveTo investigate the effects of sleep deprivation on expressions of Mir-132,mir-134 in the different regions of rat brain.MethodsAll the male SD rats were divided into control group ( normal sleep group),sleep deprivation (SD).The modified multiple platform method (MMPM) was used to establish sleep deprivation model.Mir-132,mir-134 level was detected by real time PCR.ResultsMir-132 were significantly increased in SD groups in hippocampus compared with the control groups ( 51.87 ± 8.13 vs 67.25 ± 7.59 ) (P ＜0.01 ).Mir-134 were significantly decreased in SD groups compared with the control groups( 1.82 ±0.15 vs 1.45± 0.12 )(P ＜ 0.01 ).There were no statistically significant differences in cortex and thalamus (P ＞ 0.05 ).Cortex mir-132 level in SD group and control group was 1.57 ±0.10,1.48 ±0.11 respectively,and it was 1.37 ±0.09,1.36 ±0.11 in thalamus;Cortex mir-134 level in SD group and control group was 98.26 ± 5.17,100.80 ±4.15respectively,and it was 97.56 ± 6.28,91.01 ± 4.07 in thalamus.ConclusionThe upregulation of mir-132 and downregulation of mir-134 implies that two miRNAs did opposite actions in the processes of sleep deprivation.This findings indicate that hippocampus mir-132,mir-134 levels in the SD rat may reflect associated depressive patho-physiological processes.

ObjectiveTo investigate the morphological and ultrastructural characteristics of pancreatic stellate cells (PSCs) in a chronic pancreatitis murine model.MethodsSprague-Dawley rats were divided into experimental group (n=12) and control group (n=12).The experimental group was fed with a high-fat diet (HFD) for 16 weeks whereas the control group received regular rat feed.Pathologic changes in the pancreas were observed by several morphological studies including a Sirius Red staining method,as well as immunostaining for desmin and a smooth muscle actin (a-SMA).TEM and immunoelectron microscopy were performed to study the ultrastructure of the PSCs.Results The number of desmin and α-SMA positive cells significantly increased in the HFD groups compared to the control group.The quiescent and activated PSC cells both coexisted in the pancreas in the HFD group.ConclusionsThe morphology and ultrastructural study of pancreatic stellate cells may be helpful for further functional studies on chronic pancreatic fibrosis.