In this paper, intelligent control of ultrasonic power during the process of thrombus ablation is realized through the combination of BP Neural Network and the expert system of ultrasonic thrombus ablation. One proper real-time power can be output correspondingly to different treatment circumstance according to expert ruler during the process of treatment.

Objective To study the use of laparoscopic cholecystectomy (LC) and laparoscopic common bile duct exploration (LCBDE) in patients with cholecystocholedocholithiasis.Methods From July 2006 to June 2010,127 patients with cholecystocholedocholithiasis were treated either by LC+LCBDE (n=78) or LC+endoscopic sphincterotomy (EST,n=49).The treatment success rate,complications,retained bile duct stones rate,recovery of gastrointestinal function and hospital-stay were retrospectively analyzed.Results The LCBDE+ LC group:The operative success rate was 94.87 ％.The incidence of postoperative complications was 5.41 ％.The EST+ LC group:Complete removal of bile duct stones was achieved in 46 of 48 patients (95.92％).The incidence of postoperative complications was 12.77％.There was a significant difference in the incidences of postoperative complications between the EST+ LC group and the LCBDE+ LC group (P＜0.05).The operative time and the cost for hospital stay between the two groups were significantly different (P＜0.05).After a follow-up of 3.2 years (mean,range 1-5 years),there was no significant difference in long-term complications such as bile duct recurrent stones,duodenal papilla stenosis and cholangitis between the two groups (P＜0.05).ConclusionsLCBDE was a safe,efficacious and feasible minimal invasiveness treatment for cholecystocholedocholithiasis.Primary closure of common bile duct in selected cases brought additional benefits to the minimal invasive technique.

Objective To establish the islet ? cell rat model by the ? cell-deleting technology.Methods Tweenty-four normal male SD rats and 12 weeks old were randomly divided into 3 groups,i.e,a normal diet group(NC,n=8),the model group 1(M1,n=8),and the model group 2(M2,n=8).The rats in M1 and M2 group were injected with 100 mg/kg and 150 mg/kg of streptozocin respectively.Five days later,the rats were sacrificed.The level of insulin(Ins)and Glucagon(Glc)in the pancreatic homogenate was measured.The tail of pancreas were obtained and fixed by Bolins liquid.Immunohistochemistry was performed to evaluate the expression of Ins and Glc in islet cells.Quantitative analysis was executed by image analyzer.Results Compared with the NC group,the total pancreas island areas of beta-cell deleting rats,M1 group and M2 group,are approximately 1/7 of normal control rats.Moreover,the percentages of beta-cell areas from total pancreas island areas decreased from 74.3% down to 5.4% and 5.2%,respectively.The Ins content in pancreas tissue homogenate of beta-cell deleting rats does not reach 3% of normal ones,While the Glc content unexpectedly increases.Less alpha cells distinguished by Glc positive dying through Immunohistochemistry are observed at periphery of pancreas islands of NC group.With beta cellsdeletion,the aggregation of alpha cells from periphery to centre of pancreas islands is found in M1 and M2 groups.Furthermore,the percentages of alpha cells area from total pancreas island areas are promoted from 16.4% to 76.5%、74.4%,respectively.Conclusion The islet ? cell rat model was established by injecting large dose STZ(100 mg/kg and 150 mg/kg).

Pancreatic stellate cell (PSC) activation in islet fibrosis of insulin-resistant rats induced by high-fat diet was investigated. After 20 weeks, the glucose infusion rate and glucose-stimulated insulin secretion in high-fat group were significantly decreased while fasting plasma glucose, fasting serum insulin, free fatty acid and the basal glucagon secretion were significantly increased compared with those parameters of the control rats (P< 0.05 or P<0.01). Activated PSC and collagen fiber ( type Ⅰ and Ⅲ) were found in islets of rats fed with high-fat. The result suggests that PSC activation, proliferation and migration to islet may contribute to islet fibrosis in insulin-resistant rats.

Objective To investigate the effects of chronic high glucose on α-cells glucagon releasing in relation to insulin resistance induced by high glucose. Methods TC1-6 cells, an α-cell line, were incubated separately in DMEM containing high (25.0 mmol/L), medium (11.1 mmol/L) and low (5.5 mmol/L) concentrations of glucose for 1 to 5 days. The secretion and gene expression of glueagon were measured. When TC1-6 cells had been cultured for 5 days, three different concentrations of insulin were added for 6 h and then glucagon secretion was detected. Western blot was used for 1 and 3 days to confirm the effect of high glucose on phosphorylation of Akt in TC1-6 cells. Results (1) Exposure of TC1-6 cells to 11.1 and 25.0 mmol/L glucose resulted in a slight increase of glucagon secretion compared with those incubated with 5.5 mmol/L. However, after 5 days in media containing 25.0 mmol/L glucose, glucagan secretion was significantly increased as compared to cells treated with low glucose [(136.80±10.94 vs 78.62±4.72 ) ng/106 cells, P<0.05]; moreover, in TC1-6 cell cultured with high glucose glucagon mRNA expression was increased significantly. (2) 10-7 mol/L insulin reduced significantly glucagon secretion of TC1-6 ceils exposed to low glucose [(21.59±1.30 vs 55.12±3.86) ng/106 cells], but just scarcely inhibited glucagon secretion of cells incubated with high glucose [(106.58±8.53 vs 117.18±10.55) ng/106 cells]. When insulin concentration was increased to 10-5 mol/L, glucagon secretion of TC1-6 cells in high glucose was also reduced [(46.55±3.72 vs 118.61±10.68 )ng/106 cells]. (3) After treated with 10-5 mol/L insulin for 2h, the levels of Akt phosphorylation in both groups of TC1-6 cells were increased by 180% and 70%, while the level in high glucose group was significantly lower than that in low glucose group. In the presence of phosphoinositide 3 kinase inhibitor, the levels of Akt phosphorylation were both lowered, but the inhibition in low glucose group was more significant than in high glucose group. Conclusion High glucose induces hypersecretion of glucagon, which may be due to the a-cell insulin resistance.

[Abstract ] Objective Clinically, the necessity of acid suppression treatment in vocal leukoplakia is still controversial .This paper aims to investigate the roles of LPR in the pathogenesis and pathological process of vocal leukoplakia , and to clear the signifi-cance of acid suppression in the treatment of this disease through observing the influence of laryngopharyngeal reflux ( LPR) on the symptoms of postoperative vocal leukoplakia . Methods We collected 97 cases underwent vocal leukoplakia surgery from June 2013 to December 2015 in the Department of Otorhinolarygology Head and Neck Surgery , Nanjing General Hospital of Nanjing Military Re-gion.According to the results of ambulatory 24-hour double probe ( simultaneous esophageal and pharyngeal ) pH monitoring ( pH-me-try), the patients with vocal leukoplakia were divided into LPR group (n=26, laryngopharyngeal reflux) and non-LPR group(n=71, non-laryngopharyngeal reflux).Meanwhile, the patients in LPR group were then randomly divided into acid-suppressing group(n=13, oral esomeprazole ) and non-acid-suppressing ( n=13, oral placebo ) . All patients received evaluation and compared by electrolaryngendo-scope, voice handicap index-10 ( VHI-10), reflux symptom index ( RSI) and reflux finding score ( RFS) before operation and 8 weeks after operation, and observe the effect of laryngopharyngeal reflux and acid suppression on the symptoms of postoperative vocal leukoplakia . Results RSI and RFS after operation were significantly lower than before operation in LPR group[(13.6±5.8) vs (18.2±6.2), (9.2±2.4) vs (10.6±2.8), P<0.05].The difference of RSI and RFS between before and after operation in LPR group was higher than the non-LPR group[(5.8±1.4) vs (2.3±0.8), (1.2±0.6) vs (0.5±0.2), P<0.05].The difference of RSI and RFS between before and after operation in acid-suppressing group was higher than the non-acid-suppressing group[(6.6±1.2) vs (0.8±0.6), (2.6±0.6) vs (0.5±0.3), P<0.05].VHI-10 after operation was significantly lower than before operation in acid-suppressing group[(12.6±3.6) vs (15.2±4.2), P<0.05] Conclusion Standard PPI administration to patients suffering from vocal leukoplakia accompanied with LPR can alleviate the symptoms of LPR and improve hoarseness .

Aims To study the effects of clenbuterol on anoxia/reoxygenation( A/R) injury in neonatal Wistar rat cardiomyocytes and to explore whether its mecha-nism is related to reperfusion injury salvage kinase ( RISK) or not. Methods The cultured primary neo-natal cardiomyocytes were randomly divided into eight groups: ①normal culture group; ②anoxia/reoxygen-ation( A/R) group;③ clenbuterol ( 1 μmol · L-1 ) +A/R;④ICI118,551(10 μmol·L-1) + clenbuterol ( 1 μmol · L-1 ) + A/R; ⑤Metoprolol ( 10μmol · L-1 ) + clenbuterol(1μmol·L-1 ) + A/R group;⑥Metoprolol ( 10 μmol · L-1 ) + A/R group; ⑦PD98059 ( 20 μmol · L-1 ) + clenbuterol ( 1 μmol · L-1 ) + A/R group;⑧ LY294002(10 μmol·L-1 ) +clenbuterol(1 μmol · L-1 ) + A/R group. Cell via-bility was determined by the conventional MTT reduc-tion assay. The content of LDH in cultured medium was measured with colorimetry. Cardiomyocyte apopto-sis was determined by Hoechst33342 . Intracellular re-active species( ROS) were monitored by the fluorescent DCFH-DA. Total ERK2 and phosphorylated ERK were detected by western blot. Results Compared with A/R group, clenbuterol significantly increased vaibility of cells, reduced LDH release, lowered the rate of apop-tosis and ROS production. When addedβ2 receptor an-tagonist ICI118 , 551 , PI3 K inhibitor LY294002 and ERK inhibitor PD98059 , the effects of clenbuterol a-bove were inhibited; but β1 receptor antagonist Meto-prolol protected the cardiomyocytes from A/R injury, as evidenced by decreased LDH release and increased cell viability. There were no synergistic effects in the combined use of clenbuterol and Metoprolol. Conclu-sion clenbuterol exerts cardioprotective effects against A/R injury by inhibiting oxidative stress and apopto-sis. The protection of clenbuterol is inhibited by ICI118 , 551 , LY294002 and PD98059 . clenbuterol protects cardiomyocytes against A/R injury via RISK pathway by activation of β2 receptor.

ObjectiveTo compare the results of laparoscopic and open radical operation for rectal cancer.MethodsThree hundred and twelve patients with laparoscopic operation and 226 cases with open operation during the period of June 2004 to August 2009 were included.The long-term survival,operative data,postoperative recovery and complications were compared between the two grougs.ResultsThere were no significant differences in age,sex,tumor stage and histologic types between the two groups.The 3 and 5- year-survival rate was 84.5％ and 66.7％ in laparoscopic group,83.3％ and 64.8％ in traditional operation group with no significant difference by Life-table method.The intraoperative blood loss in laparoscopic group was obviously less than that in open group (61 ± 13 nl vs 174 ±84 ml,t =23.24,P ＜0.05).The time of p assage of gas by anus and hospital stay in laparoscopic group were significantly shorter than those in openg roup (2.7 ±1.3 d vs 3.6 ±1.8 d,t =6.61,P ＜0.05;9.1 ±2.4 d vs 12.0 ±3.4 d,t =11.8,P ＜0.05).No significant difference was observed between the two groups in the lymph nodes clearance ( 11.0 ± 2.7 vs 12±3.6,t=1.72,P ＞0.05),specimen length (16.0 ±3.4 cm vs 16.0 ±4.3 cm,t =0,P＞0.05) and distal margin (3.2 ± 1.3 cm vs 3.2 ± 1.7 cm,t =0,P ＞0.05).Surgical site infection of incision developedin 28casesinopensurgerygroupandin8casesinlaparoscopicgroup(P＜ 0.05 ).ConclusionsLaparoscopic surgery for rectal cancer can achieve similar long-term survival as conventional laparotomy with minimal invasion,quicker recovery and less complications.

Objective To investigate the changes of peripheral insulin resistance after lipid infusion and the effect of N-acetylcystein(NAC) intervention.Methods Thirty-seven normal male SD rats,eight weeks old,were randomly divided into three groups,FFA group,NS group and NAC group(using into NAC 300 mg/(kg?d) two weeks before infusion).Catheters were implanted into right atrium via the jugular vein and left carotid artery.A technique for a 48-h infusion in unrestrained rats was used for triglyceride and heparin or saline infusion.The infusion period started on day 2 after surgery.48-h after infusion,we determined free fat acid(FFA),nitrotyrosine,malonaldehyde(MDA),reduced glutathione hormone(GSH) level in plasma.The glucose infusion rat(GIR) was measured by hyperinsulinemia euglycemic clamp to evaluated the perpherial insulin resistance.The expressions of IRS-1,IRS-2 gene in muscle were detected by real time PCR.Results(1)The FFA,nitrotyrosine and MDA con-centrations in FFA group were higher than that in NS group,but GSH level in plasma was lower.NAC intervention could reverse these effects.(2)GIR was decreased significantly in FFA group as compared with NS group[(8.34?1.8)mg/(min?kg)] vs[(13.56?1.7)mg/(min?kg)],(P

Objective:To observe the changes of arterial blood gas indexes in pigs with the free-field primary blast lung injury (PBLI) model, and to explore the value of arterial blood gas indexes in predicting moderate to severe PBLI.Methods:Nine adult healthy Landrace pigs were selected to construct the pig free-field PBLI model. Arterial blood samples were taken 15 minutes before the explosion (before injury) and 10, 30, 60, 120, and 180 minutes after the explosion (after injury). Arterial blood gas indexes and pulse oxygen saturation (SpO 2) were measured, compare the changes of blood gas analysis indexes and SpO 2 levels at different time points, and observe the changes of gross injury scores and pathological injury scores of lung tissue. Analyze the correlation between the blood gas indicators. Results:As time prolonged, at each time point, pH, arterial partial pressure of oxygen (PaO 2), and SpO 2 were lower than those before the injury, and blood lactic acid (Lac) and arterial partial pressure of carbon dioxide (PaCO 2) were higher than those before the injury. Compared with that before the injury, the pH value in the blood decreased significantly 10 minutes after the injury (7.39±0.06 vs. 7.46±0.02, P < 0.05), and the Lac increased significantly (mmol/L: 3.61±2.89 vs. 1.10±0.28, P < 0.05), and lasts until 180 minutes after injury (pH value: 7.37±0.07 vs. 7.46±0.02, Lac (mmol/L): 2.40±0.79 vs. 1.10±0.28, both P < 0.05); while PaO 2 and SpO 2 decreased significantly at 180 minutes after injury [PaO 2 (mmHg, 1 mmHg = 0.133 kPa): 59.40±10.94 vs. 74.81±9.39, P < 0.05; SpO 2: 0.75±0.11 vs. 0.89±0.08, P < 0.05], PaCO 2 increased significantly (mmHg: 56.17±5.38 vs. 48.42±4.93, P < 0.05). Correlation analysis showed that the gross injury score of lung blast injury animals was positively correlated with the pathological injury score ( r = 0.866, P = 0.005); PaO 2 and SpO 2 were positively correlated ( r = 0.703, P = 0.000); pH value and Lac were negative Correlation ( r = -0.400, P = 0.006); pH value is negatively correlated with PaCO 2 ( r = -0.844, P = 0.000). Conclusion:This study successfully established a large mammalian free-field PBLI model, arterial blood gas analysis is helpful for the early diagnosis of PBLI, whether SpO 2 can be used to evaluate the severity of lung injury remains to be further verified.