Port site infection in laparoscopic surgery: A review of its management

Laparoscopic surgery(LS), also termed minimal access surgery, has brought a paradigm shift in the approach to modern surgical care. Early postoperative recovery, less pain, improved aesthesis and early return to work have led to its popularity both amongst surgeons and patients. Its application has progressed from cholecystectomies and appendectomies to various other fields including gastrointestinal surgery, urology, gynecology and oncosurgery. However, LS has its own package of complications. Port site infection(PSI), although infrequent, is one of the bothersome complications which undermine the benefits of minimal invasive surgery. Not only does it add to the morbidity of the patient but also spoils the reputation of the surgeon. Despite the advances in the field of antimicrobial agents, sterilization techniques, surgical techniques, operating room ventilation, PSIs still prevail. The emergence of rapid growing atypical mycobacteria with multidrug resistance, which are the causative organism in most of the cases, has further compounded the problem. PSIs are preventable if appropriate measures are taken preoperatively, intraoperatively and postoperatively. PSIs can often be treated non-surgically, with early identification and appropriate management. Macrolides, quinolones and aminoglycosides antibiotics do show promising activity against the atypical mycobacteria. This review article highlights the clinical burden, presentations and management of PSIs in LS as shared by various authors in the literature. We have given emphasis to atypical mycobacteria, which are emerging as a common etiological agent for PSIs in LS. Although the existing literature lacks consensus regarding PSI management, the complication can be best avoided by strictly abiding by the commandments of sterilization techniques of the laparoscopic instruments with appropriate sterilizing agent.     

带免疫佐剂CEA基因疫苗的构建及其稳定同步表达的研究

背景与目的：基因疫苗是目前肿瘤免疫基因治疗研究的热点。目前癌胚抗原阳性肿瘤的治疗效果不佳,本研究拟利用质粒pVAX1构建带有免疫佐剂白细胞介素2同步表达的癌胚抗原(carcinoembryonic antigen,CEA)基因疫苗,探讨一种新的肿瘤生物治疗方法。方法：利用RT-PCR从患者肿瘤组织中钓取CEA目的基因cDNA;运用分子克隆技术,通过内部核糖体进入位点(IRES),将CEA cDNA和hIL-2 cDNA连接于质粒pVAX1中,采用化学发光免疫法和ELISA双抗体夹心法分别检测CEA抗原和hIL-2因子的表达;同时用蛋白质分析软件分析和预测目的抗原的特性。结果：测序结果证实本实验所构建的重组质粒插入DNA序列无错配,质粒上所接入的CEAcDNA与GenBank公布的M29540和M17303的序列99．8％同源,经蛋白质分析软件预测,其抗原性、跨膜结构片段、信号肽位点和二、三级结构特征与同源癌胚抗原基本一致。hIL-2 cDNA与母本序列100％同源。检测结果说明该重组质粒在体外CHO细胞株中可同步表达CEA和hIL-2分子。结论：从肿瘤组织中成功地获取了CEA cDNA,所构建的pVCEA2重组质粒能在体外细胞中同步表达CEA和IL-2蛋白分子,这为进一步体内实验研究基因治疗CEA阳性肿瘤提供了新的可能途径。     

14071例住院患者医院感染调查分析

目的探讨某医院医院感染临床特点,为医院感染控制提供依据。方法采用前瞻性与回顾性调查相结合的方法,对医院2009年1月1日-12月31日14 071例住院患者进行医院感染调查分析。结果医院感染491例,509例次,感染率为3.5%,例次感染率3.6%;其中呼吸肾病科、儿科、干保科、脑外科、神经内科感染率位居前列,医院感染共检出78株病原菌,以革兰阴性杆菌为主,占66.8%,居前3位的依次为大肠埃希菌、阴沟肠杆菌、铜绿假单胞菌,分别占23.1%、14.1%、9.0%,革兰阳性菌中以金黄色葡萄球菌检出最多,占12.8%;接受侵入性操作者4598例,占32.7%,其中发生医院感染319例,感染率6.9%;未接受侵入性操作的医院感染率为1.8%,两组医院感染率比较,差异有统计学意义(P<0.05);使用抗菌药物10 136例,使用率72.0%;治疗用抗菌药物病原学送检率34.5%,491例医院感染病例,在发生医院感染前就使用抗菌药物453例,使用率92.3%;有235例医院感染病例进行病原学检查,送检率47.9%。结论医院感染的危险因素较多,应针对重点科室加强管理,尽量减少并规范指导侵入性操作,临床医师合理规范使用抗菌药物,以有效预防控制医院感染的发生。     

甲壳胺敷料促进创面愈合的临床观察

目的观察甲壳胺敷料对烧伤患者供皮区创面的愈合影响。方法设立同体对照,将56例取皮创面分成治疗组和对照组,治疗组创面用甲壳素敷料覆盖,对照组创面用凡士林油纱覆盖,两组均定期换药至创面愈合,观察治疗期间两组创面局部变化、细菌计数及愈合时间。结果 56例供皮区创面,平均愈合时间治疗组(9.5±1.6)d,对照组(12.4±2.6)d,两组比较,差异有统计学意义(P<0.05);创面细菌检测率治疗组3.1%,对照组6.5%,差异无统计学意义。结论甲壳胺敷料不加重供皮区创面的感染,有显著的加速创面愈合的作用。     

脑室镜引起手术后颅内感染暴发的监测与控制

目的调查神经外科手术后颅内感染暴发,找出传染源、传播途径,并采取有效感染控制措施。方法利用医院感染实时监测预警系统对颅脑手术患者进行目标性监测,对发生术后颅内感染患者进行流行病学调查分析。结果 2010年8月神经外科共开展颅内手术165例,术后颅内感染患者14例(开颅手术9例,脑室镜辅助手术5例),感染率为8.5%,超出本科室月平均感染率3.0%～5.0%;某主刀医师当月完成颅内手术15例,6例术后发生颅内感染,感染率为40.0%;其中脑室镜手术共9例,5例术后发生颅内感染,感染率为55.6%。结论脑室镜损坏导致低温等离子灭菌失败,可能是造成此次神经外科手术颅内感染流行的重要原因,更换新脑室镜、严格检测消毒灭菌效果、提高医护人员无菌操作技术有效控制此次医院感染暴发。     

膨润土对垃圾填埋场天然土壤衬垫的改性研究

通过对垃圾填埋场天然土壤中添加不同比例的膨润土,击实后进行变水头渗透试验得出膨润土改性土样的最佳配比为8%.改性土样压实膨润土的渗透系数≤1.0×10-7 cm/s,符合GB 16889-2008生活垃圾填埋场污染控制标准,可作为填埋场防渗衬层.     

生活垃圾填埋场甲烷自然减排的新途径——厌氧与好氧的共氧化作用

通过证实生活垃圾填埋场中甲烷厌氧氧化与好氧氧化的共存,提出了甲烷自然减排的新途径.分别选取暴雨过后垃圾填埋表层30～60 cm的覆土、1.5 m以下的垃圾以及底层矿化垃圾做硫酸盐还原菌阳性反应实验,结果表明:生活垃圾填埋体不同填埋层都存在不同数量级的硫酸盐还原菌,且底层矿化垃圾中的硫酸盐还原菌的数量最多,表层覆土中最少...     

Development and characterization of a stable luciferase dengue virus for high-throughput screening

To facilitate dengue virus (DENV) drug discovery, we developed a stable luciferase reporter DENV-2. A renilla luciferase gene was engineered into the capsid-coding region of an infectious cDNA clone of DENV-2. Transfection of BHK-21 cells with the cDNA clone-derived RNA generated high titers (>10⁶ PFU/ml) of luciferase reporter DENV-2. The reporter virus was infectious to a variety of cells, producing robust luciferase signals. Compared with wild-type virus, the reporter virus replicated slower in both mammalian Vero and mosquito C6/36 cells. To examine the stability of the reporter virus, we continuously passaged the virus on Vero cells for five rounds. All passaged viruses stably maintained the luciferase gene, demonstrating the stability of the reporter virus. Furthermore, we found that the passaged virus accumulated a mutation (T108M) in viral NS4B gene that could enhance viral RNA replication in a cell-type specific manner. Using the reporter virus, we developed a HTS assay in a 384-well format. The HTS assay was validated with known DENV inhibitors and showed a robust Z′ factor of 0.79. The Luc-DENV-2 HTS assay allows screening for inhibitors of all steps of the viral life cycle. The reporter virus will also be a useful tool for studying DENV replication and pathogenesis.     

Arf nucleotide binding site opener [ARNO] promotes sequential activation of Arf6, Cdc42 and Rac1 and insulin secretion in INS 832/13 β-cells and rat islets

Glucose-stimulated insulin secretion [GSIS] involves interplay between small G-proteins and their regulatory factors. Herein, we tested the hypothesis that Arf nucleotide binding site opener [ARNO], a guanine nucleotide-exchange factor [GEF] for the small G-protein Arf6, mediates the functional activation of Arf6, and that ARNO/Arf6 signaling axis, in turn, controls the activation of Cdc42 and Rac1, which have been implicated in GSIS. Molecular biological [i.e., expression of inactive mutants or siRNA] and pharmacological approaches were employed to assess the roles for ARNO/Arf6 signaling pathway in insulin secretion in normal rat islets and INS 832/13 cells. Degrees of activation of Arf6 and Cdc42/Rac1 were quantitated by GST-GGA3 and PAK-1 kinase pull-down assays, respectively. ARNO is expressed in INS 832/13 cells, rat islets and human islets. Expression of inactive mutants of Arf6 [Arf6-T27N] or ARNO [ARNO-E156K] or siRNA-ARNO markedly reduced GSIS in isolated β-cells. SecinH3, a selective inhibitor of ARNO/Arf6 signaling axis, also inhibited GSIS in INS 832/13 cells and rat islets. Stimulatory concentrations of glucose promoted Arf6 activation, which was inhibited by secinH3 or siRNA-ARNO, suggesting that ARNO/Arf6 signaling cascade is necessary for GSIS. SecinH3 or siRNA-ARNO also inhibited glucose-induced activation of Cdc42 and Rac1 suggesting that ARNO/Arf6 might be upstream to Cdc42 and Rac1 activation steps, which are necessary for GSIS. Lastly, co-immunoprecipitation and confocal microscopic studies suggested increased association between Arf6 and ARNO in glucose-stimulated β-cells. These findings provide the first evidence to implicate ARNO in the sequential activation of Arf6, Cdc42 and Rac1 culminating in GSIS.     

New views of glutamate transporter structure and function: Advances and challenges

Neuronal and glial glutamate transporters limit the action of excitatory amino acids after their release during synaptic transmission. Recent structural and functional investigations have revealed much about the transport and conducting mechanisms of members of the sodium-coupled symporter family responsible for glutamate clearance in the nervous system. In this review we summarize emerging views on the general structure, binding sites for substrates and coupled ions, and transport mechanisms of mammalian glutamate transporters, integrating results from a large body of work on carrier structure-function relationships with several crystal structures obtained for the archaeal ortholog, Glt_Ph.