Background: Lung cancer is the most common cancer in the world and is the main cause of cancer-related death. Revealing the potential mechanism of malignant characteristics of lung cancer is urgent for treating this disease effectively. Zinc finger protein 671 (ZNF671) is a member of the largest transcription factor family in the human genome. The role of ZNF671 in non-small-cell lung cancer (NSCLC) remains unknown. The purpose of this study was to investigate the function and mechanism of ZNF671 in NSCLC. Methods: ZNF671 expression in NSCLC cells and tissues were detected by Real-Time PCR, Western blot and TCGA databases. Then, we evaluated the prognostic value of ZNF671 expression in NSCLC using the Kaplan-Meier plotter (KM plotter) and TCGA databases. Moreover, the function of ZNF671 in the proliferation and metastasis of lung cancer was investigated by MTT assay, colony formation assay, in vivo experiment, EdU assay, wound healing assay, transwell assay, and 3D culture assay. Luciferase reporter and subcellular fractionation assays were performed to determine the underlying mechanism of ZNF671-mediated proliferation and metastasis of NSCLC. Results: ZNF671 expression was significantly reduced in both NSCLC cell lines and clinical specimens compared to that in normal controls. The survival analysis results indicated that the downregulation of ZNF671 significantly correlates with poor prognosis and predicts a shorter overall survival and post-progression survival among NSCLC patients. Ectopic overexpression of ZNF671 dramatically restrains, whereas silencing ZNF671 enhanced, cell proliferation and metastasis of NSCLC. Mechanically, gene set enrichment analysis (GSEA) showed that the expression of ZNF671 was significantly correlated with Wnt/beta-catenin signaling. Simultaneously, our results confirm that the overexpression of ZNF671 inhibits cell cycle progression and metastasis by weakening the Wnt/beta-catenin pathway, and then downregulating the expression of downstream target genes CyclinD1 and MMP9. Conclusion: This study found that the overexpression of ZNF671 restrains the proliferation and metastasis of lung cancer through inhibiting Wnt/ss-catenin signaling pathway. Furthermore, our current results provide important insights into ZNF671 as an excellent predictive biomarker for NSCLC, thus providing a novel perspective for the treatment of NSCLC.

Background: Lung cancer is the most common cancer in the world and is the main cause of cancer-related death. Revealing the potential mechanism of malignant characteristics of lung cancer is urgent for treating this disease effectively. Zinc finger protein 671 (ZNF671) is a member of the largest transcription factor family in the human genome. The role of ZNF671 in non-small-cell lung cancer (NSCLC) remains unknown. The purpose of this study was to investigate the function and mechanism of ZNF671 in NSCLC. Methods: ZNF671 expression in NSCLC cells and tissues were detected by Real-Time PCR, Western blot and TCGA databases. Then, we evaluated the prognostic value of ZNF671 expression in NSCLC using the Kaplan-Meier plotter (KM plotter) and TCGA databases. Moreover, the function of ZNF671 in the proliferation and metastasis of lung cancer was investigated by MTT assay, colony formation assay, in vivo experiment, EdU assay, wound healing assay, transwell assay, and 3D culture assay. Luciferase reporter and subcellular fractionation assays were performed to determine the underlying mechanism of ZNF671-mediated proliferation and metastasis of NSCLC. Results: ZNF671 expression was significantly reduced in both NSCLC cell lines and clinical specimens compared to that in normal controls. The survival analysis results indicated that the downregulation of ZNF671 significantly correlates with poor prognosis and predicts a shorter overall survival and post-progression survival among NSCLC patients. Ectopic overexpression of ZNF671 dramatically restrains, whereas silencing ZNF671 enhanced, cell proliferation and metastasis of NSCLC. Mechanically, gene set enrichment analysis (GSEA) showed that the expression of ZNF671 was significantly correlated with Wnt/beta-catenin signaling. Simultaneously, our results confirm that the overexpression of ZNF671 inhibits cell cycle progression and metastasis by weakening the Wnt/beta-catenin pathway, and then downregulating the expression of downstream target genes CyclinD1 and MMP9. Conclusion: This study found that the overexpression of ZNF671 restrains the proliferation and metastasis of lung cancer through inhibiting Wnt/ss-catenin signaling pathway. Furthermore, our current results provide important insights into ZNF671 as an excellent predictive biomarker for NSCLC, thus providing a novel perspective for the treatment of NSCLC.

Lactate dehydrogenase (LDH) is a key enzyme in glycolysis process. It catalyzes the interconversion between pyruvic acid and lactic acid. Schistosoma japonicum adult worms largely rely on glycolysis for energy production when they parasitize in human. S. japonicum may be killed if energy production is suppressed. So, we wonder whether antibody against S. japonicum LDH is a harmful factor for S. japonicum surviving. In this study, we cloned and characterized S. japonicum lactate dehydrogenase B (SjLDHB) to evaluate its role in parasite survival. We found SjLDHB was highly similar to S. japonicum lactate dehydrogenase A (SjLDHA) which is another LDH subtype in S. japonicum in amino acid sequence. The optimal temperature of SjLDHB catalytic activity was 37 degrees C, the optimal pH values for pyruvate reduction and lactate oxidation were 7.0 and 6.0 and Km values of pyruvate and lactate were 0.2752 and 0.2339 mM respectively. Then, we identified SjLDHB expression in male and female S. japonicum. Finally, we evaluated the influence of antibodies on SjLDHB enzymatic activity. Interestingly, we found anti-SjLDHA antibody suppressed SjLDHB enzymatic activity, while anti-SjLDHB antibody and mixed antibody enhanced SjLDHB enzymatic activity in vitro. Although further investigation is needed, we suggest that anti-SjLDHB antibody may be not a negative factor, but a valuable compensation for S. japonicum adult worm surviving and pathogenicity.

[目的]研究多西他赛对野百合碱诱导的大鼠肺动脉高压的作用及可能机制.[方法]50只雄性SD大鼠随机分为5组:正常对照组(control)、多西他赛组(control+DTX)、野百合碱组(MCT)、野百合碱+溶媒组(MCT+SOL)和野百合碱+多西他赛组(MCT+DTX).后3组大鼠一次性腹腔注射野百合碱(60 mg/kg)建立肺动脉高压模型.野百合碱注射后第21天和第28天,经尾静脉注射多西他赛(5 mg/kg)或溶媒进行干预.多导生理记录仪测定大鼠右心血流动力学,计算右心室肥厚指数(RVHI);左肺病理切片行van Geison染色,光镜下观察肺内小动脉病理改变,并计算肺小动脉中膜厚度与血管直径比值.Western blotting检测右肺组织中p-PDGFR和PDGFR的表达水平.[结果]与control组相比,MCT和MCT+SOL组大鼠的RVSP、RVHI、肺小动脉中膜厚度与血管直径比值、p-PDGFR和PDGFR的表达均显著增加(P＜0.05);与MCT+SOL组相比,MCT+DTX组RVSP、RVHI、肺小动脉中膜厚度与血管直径比值、p-PDGFR和PDGFR的表达均显著下降(P＜0.05);Control+DTX组与control组相比,以上指标的差异均无显著性(P＞0.05).[结论]多西他赛可降低野百合碱诱导的大鼠肺动脉高压、减轻肺血管重构,其机制可能与抑制PDGFR的表达及其磷酸化有关.

The proliferation and migration of pulmonary artery smooth muscle cells (PASMCs) play an important role in the pathogenesis and progression of pulmonary hypertension. The purpose of this study was to investigate the effect of docetaxel on proliferation and migration of PASMCs induced by transforming

Tight junctions (TJs) are a critical component in maintaining the intestinal mucosal barrier function and gastrointestinal health of animals. Gut barrier dysfunction contributes to the initiation and development of sepsis which induces an uncontrollable systemic inflammatory response and gives rise to life-threatening clinical conditions. Excretory-secretary antigens from Trichimella spiralis (T. spiralis) have been reported to protect from sepsis in a mouse model, however the mechanism remains to be elucidated. Mice were treated with recombinant T. spiralis 53-kDa glycoprotein (rTsP53) at 2 or 6 h following lipopolysaccharide (LPS) injection. Survival rate, serum systemic inflammation, Chiu's score, D-lactic acid (D-LA) and diamine oxidase (DAO) as intestinal injured biomarkers, bacterial translocation and growth in peritoneal fluid (PF) and mesenteric lymph nodes (MLN), intestinal tight junction structure and protein zona occludens (ZO)-1 expression were investigated. In LPS-induced septic mice, rTsP53 was demonstrated to protract the survival and inhibit serum systemic inflammatory response, and then, allayed morphological alteration, decreased the release of D-LA and DAO from intestines. Furthermore, LPS-induced intestinal permeability, bacterial translocation and growth in PF, MLN and vital organs were significantly suppressed by rTsP53 treatment. Notably, rTsP53 treatment markedly improved the intestinal tight junction damaged in sepsis via promoting ZO-1 expression. These results demonstrated that rTsP53 ameliorated LPS-induced intestinal injury and is a potential protective agent for treatment of sepsis.

[目的]探讨诱导型多能干细胞(iPS-MSC)对脓毒症小鼠肠黏膜通透性的改善作用和对肠道菌群移位的影响.[方法]采用尾静脉注射脂多糖(LPS,10 mg/Kg)建立小鼠脓毒症模型.常规培养及传代iPS-MSC.在脓毒症建立2h和6h经小鼠尾静脉注射进行治疗干预(1×106/只).利用基因重组技术制备新质粒pET28b(+)-EGFP,转染大肠杆菌,并在脓毒症后连续2d予小鼠进行灌胃处理.在脓毒症发生72 h后,取各组小鼠腹水及肠系膜淋巴结匀浆于Kan抗性的LB培养基培养鉴定,计算和比较菌群负荷.通过透射电镜观察小鼠小肠黏膜上皮细胞超微结构的变化.Western blotting法检测各组小鼠肠黏膜ZO-1蛋白的表达.荧光显微镜下观察带有GFP绿色荧光蛋白的ips-MSC在损伤肠黏膜的移行和归巢情况.[结果]成功构建表达绿色荧光的重组大肠杆菌pET-28b(+)-EGFP作为实验用示踪菌.灌胃处理后,ips-MSC治疗的小鼠腹水和肠系膜淋巴结的示踪菌的菌负荷较脓毒症组明显降低,其中ips-MSC 2 h治疗组较6h治疗组降低的更明显.透射电镜观察发现脓毒症小鼠肠系膜上皮细胞间紧密连接结构破坏,细胞间缝隙增宽,而经iPS-MSC治疗的小鼠细胞间紧密连接结构破坏明显改善,在2h治疗组表现更为明显,伴随紧密连接蛋白ZO-1的表达水平升高.[结论]静脉注射iPS-MSC能够向脓毒症小鼠损伤的肠黏膜移行,通过提高连接蛋白ZO-1的表达,修复紧密连接,改善脓毒症小鼠肠黏膜的通透性,减少脓毒症时肠道菌群的移位.

目的:分析与评价针对长学制医学生开展团队为基础的学习(Team-based Learning,TBL)结合典型病例情境模拟教学法改进急诊见习教学的效果.方法:将2010年至2011年期间由中山大学附属第一医院急诊医学教研室承担教学的长学制医学生共120名作为研究对象,其中将2010年期间60名设为对照组,按照传统临床观摩结合专题讲座的方法进行教学;将2011年期间60名设为实验组,采用TBL结合典型病例情境模拟教学法进行教学.见习前后进行书面理论测试、操作技能考核和模拟临床情境考核,见习结束时作教学满意度调查,对所有数据进行统计学处理.结果:见习后两组各项考核成绩较见习前有显著提高(P＜0.05),实验组书面理论考核成绩与对照组无显著差异,但实验组操作技能及模拟临床情境考核成绩明显优于对照组(P＜0.05),实验组教学满意度高于对照组(P＜0.05).结论:采用TBL结合典型病例情境模拟教学法比传统临床观摩结合专题讲授教学法明显提高长学制医学生急诊见习的教学成效,尤其在培养解决临床实际问题能力上有明显优势.

AIM: To evaluate the immune state in rats with chronic Clonorchis sinesis(Cs) infestation by investigating the effects of Cs on macrophage polarization and inflammatory reactions.METHODS: Sprague-Dawley rats were used in the study.Chronic Cs infestation model was reproduced by intragastric perfusion with Cs eggs.Twenty rats were randomly divided into normal group(n=10) and Cs infestation group(n=10).The serum levels of interleukin(IL-4) and IL-10,tumor necrosis factor α(TNF-α) and interferon γ(IFN-γ) were detected by ELISA.The macrophages were harvested by peritoneal lavage.The differentiation proportion of M1 and M2 macrophages were detected by flow cytometry.The macrophages were divided into control group,normal group and chronic Cs infestation group according to the sources of macrophages.The levels of TNF-α and IL-10 in the culture supernatants were detected by ELISA at 0,2,12 and 24 h after lipopolysaccharide(LPS,10 μg/L) stimulation in vitro.RESULTS: Compared with normal group,chronic Cs infestation increased the serum levels of TNF-α,IFN-γ,IL-4 and IL-10.The differentiation proportion of M1 detected by flow cytometry was 92.1% in normal group and that of M2 macrophages was 93.8% in Cs infestation group.The levels TNF-α and IL-10 in culture supernatants were increased at 2~24 h after LPS stimulation both in normal group and Cs infestation group,but the levels of TNF-α were lower in chronic Cs infestation group than that in normal group at 2 h,12 h and 24 h after LPS stimulation.The level of anti-inflammatory cytokine IL-10 was higher in Cs infestation group than that in normal group at 2 h,12 h and 24 h after LPS stimulation.CONCLUSION: Chronic Cs infestation increases the serum levels of both pro-inflammatory cytokines and anti-inflammatory cytokines,thus inducing the polarization of M2 macrophages.The macrophages derived from chronic Cs-infected rats produce tolerance in the inflammatory process against LPS in vitro.

OBJECTIVE:The purpose of this study was to investigate the neuroprotective effects of intraperitoneal injection of hydrogen (H2) in rabbits with cardiac arrest (CA).METHODS:A rabbit model of CA was established by the delivery of alternating current between the esophagus and chest wall to induce ventricular fibrillation. Before CA, the animals were randomly divided into four groups: a sham group (no CA), a CA group, a CA + low dose (10 ml/kg) H2 group (CA + H2 group 1), and a CA + high dose (20 ml/kg) H2 group (CA + H2 group 2). In the first experiment, animals were observed for 72 h after the restoration of spontaneous circulation (ROSC). The neurological scores were assessed at 24, 48 and 72 h after ROSC. The rabbits that survived until 72 h were sacrificed using an overdose of anesthetic, and the brain tissues were collected and Nissl-stained to observe nerve cell damage in the hippocampal CA1 area. In addition, TUNEL assay was performed to detect apoptosis. In the second experiment, animals were observed for 6h after ROSC. Blood samples and brain hippocampal tissues were collected, and differences in oxidative stress indicators were compared among the four groups.RESULTS:Intraperitoneal injection of H2 improved the 72-h survival rate and neurological scores, reduced neuronal injury and inhibited neuronal apoptosis. Intraperitoneal injection of H2 reduced oxidative stress indicators in the plasma and hippocampal tissues and enhanced antioxidant enzyme activity. No significant difference was observed between the two CA groups treated with different doses of H2.CONCLUSIONS:Intraperitoneal injection of H2 is a novel hydrogen administration method and can reduce cerebral ischemia-reperfusion injury and improve the prognosis of cardiopulmonary cerebral resuscitation in a rabbit model of CA.

Objectives As a novel anti-inflammationary and immuno-regulatory factor, Mesenchymal Stem Cells (MSCs) have recently been applied to treat septic animals in experimental research. Our previous results have shown that MSCs decreased the mortality caused by sepsis, but the exact mechanisms underlying its beneficial effects are not well defined. Since inflammationary injury induced by Migration Inhibitory Factor (MIF), as a late-stage pro-inflammationary factor, is significantly expressed in septic myocardium, we hypothesised that intervention of MSCs could down-regulate its expression on myocardium in septic mice, contributing to its protective outcomes on sepsis. In present study, we aimed to investigate the influence of MSCs on cardiomyocytic MIF expression during sepsis in BALB/c mice. Methods One hundred and Eighty BALB/c mice were randomly assigned into three groups: the sham group (sham group, n = 60), the sepic control group (septic group, n = 60) and the septic MSCs interventing group (septic + MSCs group, n = 60). Sepsis was induced by cecal ligation puncture in mice of the later two groups, while the mice in septic + MSCs group were treated intravenously with 2 x 106 MSCs once a day for three days before cecal ligation puncture. Serum MIF levels, macroscopic and microscopic cardiomyocytic changes were evaluated 12 h (n = 10), 24 h (n = 10), 36 h (n = 10), 48 h (n = 10), 60 h (n = 10) and 72 h (n = 10) post puncture. The levels of MIF mRNA and protein expression in myocardium were detected at the same time points as above by RT-PCR, Immunohistochemical staining and Western Blot, respectively. Results Sepsis caused apparent damages to myocardium in mice with cecal ligation puncture. Compared with sham group and septic group, MSCs attenuated the macroscopic and microscopic injuries in myocardium of septic mice, while serum MIF concentrations at 12 h, 24 h, 36 h, 48 h, 60 h and 72 h post puncture were significantly suppressed following MSCs intervention. The mRNA and protein expression of MIF in myocardium were significantly lower in the septic + MSCs group than in the septic group at the same time points as above, but still higher than the sham group (p < 0.05). Conclusions It is concluded that elevated MIF expression in myocardium may play an important role in pathogenesis of sepsis; MSCs may be taken as a protective option for sepsis treatment; Transcriptional down-regulation of MIF in cardiomyocytes may be one of the molecular mechanisms contributing to the beneficial outcomes following MSCs intervention.

BACKGROUND: Different ways to supply hydrogen have curative effect on ischemia-reperfusion injury. But the relevant metabolism studies are rare to compare the different ways of supplying hydrogen. OBJECTIVE: To investigate the effect of intraperitoneal or intravenous saturated hydrogen saline and intraperitoneal injection of hydrogen on hydrogen metabolism in rabbits, providing a more optimal hydrogen treatment proposal. METHODS: Twenty New Zealand white rabbits were tested the basis concentration of exhaled hydrogen. Then all of them were supplied saturated hydrogen saline or hydrogen gas 10 mL/kg via intraperitoneal injection and saturated hydrogen saline 10 mL/kg via intravenous injection within 10 minutes, respectively. Exhaled hydrogen concentrations were monitored continuously. When the exhaled concentration declined to the baseline and stabilized for more than 30 minutes, hydrogen was supplied by another way. Time to maximal exhaled hydrogen concentration and max exhaled hydrogen concentration were recorded, as well as half-life and area under the curve were calculated to compare the effects of three different ways of hydrogen supply on hydrogen metabolism in rabbits. RESULTS AND CONCLUSION: The time to maximal exhaled hydrogen concentration was (3.25±1.80), (17.8±6.48) and (7.45±1.39) minutes in three ways, respectively, and there were significant differences among the three ways (P < 0.01). The half-life was (7.40±2.09), (141.50±85.01) and (1.20±0.37) minutes, respectively, and there were significant differences among the three ways (P < 0.01). The increment in the area under the curve was (302.17±221.90), (5 234.29±2 681.18), (209.51± 104.49) ppmomin, respectively, and there were significant differences among the three ways (P < 0.01). Hydrogen supply by intraperitoneal injection of saturated hydrogen saline or pure hydrogen both can rapidly increase exhaled hydrogen concentration in rabbits. Intraperitoneal hydrogen can maintain a high exhaled hydrogen concentration for a long time.

Objectives Glucagon-like peptide-1 (GLP-1) was a hormone predominately synthesised and secreted by intestinal L-cells. Pharmacological modulation of the GLP-1 had emerged as an important treatment target for diabetes mellitus. In addition to its glucose lowering properties, GLP-1 was found to have multiple cardioprotective effects. Impaired cardiac microvascular function is thought to contribute greatly to the diabetes cardiovascular disease. Yet the effects of GLP-1 on cardiac microvessels remained unclear, this study was aim to investigate the protective effects of GLP-1 on cardiac microvessels injury and the underlying regulatory mechanism in diabetes mellitus. Methods Streptozocin (STZ)-induced diabetic rats (n=45) were randomised to 12 weeks of treatment with vehicle, LAF237 (DPP-IV inhibitor, 1 mg/kg/d) or Exenatide (GLP-1 analogue, 1 nmol/kg/d). Before and after treatment, blood glucose levels and weight were assessed. Cardiac function was examined by echocardiographic measurements; cardiac energetics was examined by 18F-FDG PET/CT. Scanning electron microscopy was used to analyse changes in morphology of cardiac microvessels. Transmission electron microscopy was used to assay cardiac microvascular permeability via lanthanum nitrate tracer. Adult rat cardiac microvascular endothelial cells (CMECs) were isolated and cultured in medium alone (control) or medium containing glucose (25 mmol/l), GLP-1 (10−7 mmol/l), high glucose (25 mmol/l) plus GLP-1 (10−7 mmol/l). First, GLP-1 receptor (GLP-1R) was detected by immunofluorescence and western blot. Then lucigenin-enhanced chemiluminescence assay and dihydroethidine (DHE) staining were used to assess oxidative stress. Tunnel staining and caspase-3 expression were used to assess apoptosis of CMECs. H89 was used to inhibit cAMP/PKA pathway; fasudil was used to inhibit Rho/Rho-kinase (ROCK) pathway; Rho siRNA was transfected into CMECs to silence Rho. The protein expression of Rho, ROCK, p22phox, p47phox and rac-1 was examined by western blot analysis. Results After 12 weeks of treatment with LAF237 or Exetinade, the cardiac function and energetics were improved significantly compared with the vehicle treated groups. Cardiac microvascular barrier function was also improved. We demonstrated that GLP-1R was expressed on CMECs. Compared with vehicle treated groups, ROS production (relative light unit, RLU) (4.06±0.36 vs 2.13±0.31, p<0.05) and apoptotic index (33.95%±5.49% vs 24.39%±3.39%, p <0.05) were significantly decreased by GLP-1 treatment in high glucose-induced CMECs. There were also significant reductions in NADPH oxidase such as p22phox, p47phox and rac-1 expression. However, no difference was found in ROS production (RLU) (0.45±0.57 vs 0.53±0.07, p<0.05), apoptotic index (9.15%±1.33% vs 10.87%±1.65%, p<0.05) and NADPH oxidase expression between non-glucose induced groups. Western blot assay showed that the cAMP/PKA activity was increased and the Rho expression was decreased in high glucose induced CMECs after treatment with GLP-1, which reproduced the same effect as PKA inhibitor H89. Fasudil and transfection with Rho siRNA significantly decreased p22phox, p47phox and rac-1 expression in high-glucose induced CMECs Conclusions GLP-1 could protect the cardiac microvessels against oxidative stress injury, apoptosis and the resultant microvascular barrier dysfunction in diabetic rats, which contribute to the improvement of cardiac function and energetics. The protective effects of GLP-1 are dependent on downstream inhibition of Rho, which is through cAMP/PKA pathway, resulting in subsequent decreased expression of NADPH oxidase.

Objectives To explore effect of continuous opening airway in emergence cardiopulmonary resuscitation which can hopefully lead to the development of more effective ways to open airway in short period of time. Methods 94consecutive cases of patients with acute cardiac-pulmo arrest that require emergency cardiopulmonary resuscitation at the EICU and emergency observation room of our hospital during 11 May 2010 and. 2 September 2012 all cases were randomly divided into continuous opening airway implementation group and conventional group. The studies was performed in accordance with guidelines as prescribed in the International cardiopulmonary resuscitation 2010 guidelines, in applying cardiopulmonary resuscitation, monitoring and recording recovery process and the physical signs, as well as observing the general progress and use of respirator. Results Evidently more patients in the implementation group had iris shrinking to normal during the resuscitation process than those in the conventional group p<0.05). This group also requires less time in returning to natural breathing than the conventional group. Additionally, the same group required more frequent use of SIMG+PSV or PEEP p<0.05). Conclusions Applying continuous opening airway in an effective and well-organised manner positively contribute to cardiopulmonary resuscitation and prognosis of patients.

Objectives Cardiopulmonary resuscitation is the most important technique for the first-aid in the rescue of the patients with cardiac arrest. Many aspects in basic life supporting has been adjusted in 2010 CPR guideline. This research aims to evaluate and analyse the training effectiveness improvements of cardiopulmonary resuscitation skills based on 2010 CPR guideline in emergency medicine. Methods Sixty clinical training doctors in the First Affiliated Hospital of Sun Yat-sen University, who were trained in the emergency department from August, 2010 to March, 2011, were taken as the research groups. Among them, 30 doctors assigned into control group, entered emergency department before 2010 CPR guideline was published and were supposed to be trained based on 2005 CPR guideline and the other 30 doctors assigned into experimental group, were trained after 2010 CPR guideline was published and were trained based on 2010 CPR guideline. Theory and skill- practice tests were employed to evaluate the training effectiveness after the training course was finished in both groups. Results Total scores of the experimental group are higher than those of the control group (p<0.05). The theory test scores have no significant difference between the two groups (p>0.05), while the experimental group acts better in skill-practice test (p<0.05). More prompt initiating of chest-pressing and defibrillation, higher rates and superior quality of chest-pressing, as well as better self-evaluation among trainees, are obtained in the experimental group (p<0.05). However, other items including self-protection awareness, airway-opening skills and ventilation quality, are similar between the two groups (p>0.05). Conclusions It seems helpful to improve training effectiveness of basic life-support procedures in medical staff based on the adjustment of 2010 CPR guideline.

Objectives Most cardiac arrests occur outside the hospital, so it is really necessary to begin cardiopulmonary resuscitation skills training for the publics. The publics can participate in the rescue at once as the first witnesses of the cardiac arrest to improve the survival rate of the sufferer. The purpose of this research is to explore the teaching effectiveness of team-based learning teaching in cardiopulmonary resuscitation skills training for the publics. Methods Between 15 September 2011 to 30 October 2011, 160 college students that are not medical profession participated in this research. They were trained for cardiopulmonary resuscitation skills based on 2010 CPR guidelines. Eighty students assigned into the experimental group, were trained with TBL teaching. Another 80 students assigned into the control group, were trained with traditional lecture teaching. Theory, skill-practice and cardiac arrest scene simulation, three tests were employed to evaluate the training effectiveness before the training course started and after the training course finished in two groups. Results After training, both groups got higher scores than before training in all the tests (p<0.05). College students in experimental group acted better than those in contol group in skill-practice and cardiac arrest scene simulation tests (p<0.05). Better group cooperation, superior quality and higher rates of chest compression, as well as more prompt initiation of chest compression, are obtained in the experimental group (p<0.05). However, there was no difference in theory test between them (p>0.05). The experimental group to teaching satisfaction was also higher than those in the control group (p<0.05). Conclusions Teaching with team-based learning seems more helpful than traditional lecture teaching in training of the cardiopulmonary resuscitation skills for the publics.

【Objective】 To establish a simple,stable and high success rate cardiac arrest(CA) model in rabbits.【Methods】Cardiac ventricular fibrillation(VF) was induced in 15 New Zealand rabbits by transoesophageal-chest wall electrode with 35mA alternating current.Five minutes after onset of CA,conventional cardiopulmonary resuscitation(CPR) was initiated.The time spent on inducing cardiac arrest,the cardiac rhythm when the electric stimulation was stopped,the cardiac rhythm when the CPR was started,the time spent on CPR,the defibrillation frequency,the administration frequency,the rate of restoration of spontaneous circulation(ROSC),the mechanical ventilation time after ROSC,the life time after ROSC and the 72 h survival rate of 15 rabbits were recorded respectively.【Results】 All of 15 rabbits were successfully induced cardiac arrest.The inducing time was 26.47 ± 10.36 s.When the electric stimulation was stopped,all cardiac rhythm was ventricular fibrillation(15/15),no pulseless electrical activity and asystole occurred.During the observation of nonintervention,no automatic cardioversion phenomenon occurred.When the CPR was started,electrocardiogram indicated VF occurred in 73.3% of the rabbits(11/15)and pulseless electrical activity occurred in 26.7% of the rabbits(4/15).The time spent on CPR was 200.07 ± 136.00 s.The defibrillation frequency was 1.00 ± 0.76.The frequency of intravenous injection of adrenaline was 2.40 ± 1.12.The rate of ROSC was 93.3%(14/15).The mechanical ventilation time after ROSC was 40.46 ± 17.05min.The death rate within 6h after ROSC was 6.7%(1/15) and the 72h survival rate was 26.6%(4/15).【Conclusion】 The model of cardiac arrest in rabbits induced by transoesophageal-chest wall electric stimulation is very simple operation,and has a stable result and high success rate.It is a ideal animal model for cardiopulmonary resuscitation study.

Objective:To investigate the clinical effects of ulinastain on Soluble Triggering Receptor Expressed on Myeloid Cells-1(sTREM-1) expression in septic patients.Methods:Sixty patients with sepsis were divided randomly into two groups:classical treatment group with regular therapy and the other group was classical treatment plus ulinastain 200kU iv bid for 10 days,and 30 healthy individuals as control group The concentration of sTREM1 in plasma was measured by enzyme-linked immunosorbent assay and the level of serum CRP was detected by spectrophotometer in all patients.The acute physiology and chronic health evaluation M scoring system was applied to assess the severity of sepsis at the 3rd,7th and 10th days after treatment.The survival and dead patients in two sepsis groups were observed.Results:The plasma concentration of sTREM-1 and CRP are significantly higher in septic patients than those in the control group before treatment(P < 0.05 ),and there was no difference between patients of the two groups(P > 0.05).At the 3rd,7th and 10th days after treatment,the serum levels of sTREM1 and CRP decreased gradually in the two groups(P < 0.05 ).In the ulinastain treatment group,the concentration of sTREM-1 and CRP and APACHEⅢscoring were much lower than the routine treatment group(P <0.05).The mortality at 28th day decreased significantly in the ulinastain treatment group(P <0.05).Conclusion:The treatment with ulinastain could reduce the serum level of sTREM-1 and CRP,alleviate the inflammatory reaction and decrease the occurrence of MODS in septic patients,so as to relieve the clinical symptoms and improve the prognosis of sepsis.