Turcot's syndrome: Case report and review of the classification

Summary We report a case of association of a brain tumor with multiple colorectal polyposis and offer an analysis of the relevant literature with a view to revising the classification of the syndrome in relation to familial multiple polyposis and Gardner's syndrome. Differences emerged, depending on the brain tumor type, which suggests that this association may be classified as two distinct syndromes.     

不同抗生素杀菌过程导致细菌内毒素释放的异质性

目的初步了解各类抗生素杀菌过程导致细菌内毒素释放的不同特点。方法采用鲎基质偶氮法检测各类不同抗生素２倍最低抑菌浓度下对大肠埃希氏菌杀菌时细菌内毒素的释放量,计算杀菌开始至活菌数基本稳定阶段,平均每减少１个对数数量级（ｌｇ）菌落形成单位（ＣＦＵ）所导致的内毒素释放量（杀菌释放率）。结果各类抗生素致内毒素释放能力大致可以分为低、中、高三类,杀菌释放率的界限值分别为１０ｎｇ／ｉｇＣＦＵ和３０ｎｇ／ｉｇＣＦＵ。多粘菌素Ｂ具有低于所有品种的释放率。β－内酰胺类抗生素中的羟氨苄青霉素、棒酸和亚胺硫霉素具低释放率,氨苄青霉素、头孢氨苄、头孢呋辛、头孢哌酮、头孢他啶、氨曲南具高释放率。喹诺酮类的环丙沙星具高释放率,氧氟沙星具中等释放率。氨基甙类均具中等释放率,品种间无显著差异。此外,磷霉素也具有中等释放率。结论具有相似临床杀菌作用的抗生素可以具有差异明显的致内毒素释放能力,此认识有助于指导全身炎症反应综合征时抗生素的选择     

大肠杆菌HX88108膜孔蛋白初步研究

为了解大肠杆菌ＨＸ８８１０８耐药机理中有无膜孔蛋白缺失参与,用十二烷基磺酸钠－聚丙烯酰胺凝胶电泳（ＳＤＳ－ＰＡＧＥ）检测了大肠杆菌ＨＸ８８１０８的膜孔蛋白,并与膜孔蛋白标准株进行比较分析。结果发现：大肠杆菌ＨＸ８８１０８具有膜孔蛋白ＯｍｐＦ、ＯｍｐＣ,其耐药与膜孔蛋白缺失所致的抗生素进入减少无关     

Growth of Escherichia coli in propofol, lidocaine, and mixtures of propofol and lidocaine

BACKGROUND: Microorganisms grow rapidly in propofol. Extrinsic contamination of propofol is thought to be a source of postoperative sepsis and wound infection. We studied growth of a strain of Escherichia coli in thiopental, propofol, lidocaine, and mixtures of propofol and lidocaine. METHODS: The pathogen was exposed to 2.5% thiopental; 1.0% propofol; 1.0%, 2.0% and 4.0% preservative-free lidocaine; and propofol solutions containing 0.25%, 0.5%, 1.0%, 2.0%, or 4.0% lidocaine for 2, 4, 6, 8, 10, 12, 14, 16, 18, 20, 22, and 24 h at room temperature, respectively. The inocula from these suspensions were cultured for 48 h at 37 degrees C after the antimicrobial activity of the local anesthetics in the inocula was inactivated by a 1:1000 dilution with distilled water. RESULTS: No organisms grew after exposure to 2.5% thiopental. The exposure of E. coli to propofol increased the colony count to approximately 90 times the control count. The colony counts of E. coli after exposure to 1.0%, 2.0% and 4.0% lidocaine and 0.25%, 0.5%, 1.0%, 2.0% and 4.0% lidocaine in 1.0% propofol were lower than the counts after exposure to 1.0% propofol (P = 0.0048, 0.0027, 0.0003, 0.0503, 0.0188, 0.0080, 0.0044, and 0.0001, respectively). The growth rate of the microorganism was significantly higher in cultures exposed to 1.0% propofol than that in cultures exposed to lidocaine alone or lidocaine-propofol mixtures (P < 0.0001, respectively). CONCLUSION: Lidocaine possesses bacteriostatic activity against E. coli. Addition of lidocaine to propofol confers its bacteriostatic activity to the mixture and may decrease the hazard of infection associated with the extrinsic contamination of propofol.     

采用定点基因缺失突变技术在大肠杆菌中分泌鲑鱼生长激素

目的：为获得与天然鲑鱼生长激素一致的基因工程产物,对已构建的鲑鱼生长激素基因分泌型表达质粒ｐＯｓＧＨ１５３进行改造,删除所编码表达产物氨基端多余的９个碱基,方法：采用ＰＡＬＴＥＲ系统进行寡聚核苷酸指导下的基因定点缺失突变。突变质粒ｐＯｓＧＨ１５８经限制性酶切图谱及Ｓｏｕｔｈｅｒｎ印迹杂交分析加以证,结果：含有表达质粒ｐＯｓＧＨ１５８的大肠杆菌株经ＩＰＴＧ诱导后提取周质帽白,经ＳＤＳ－ＰＡＧＥ及免疫     

(His)6-Arg-Arg-人胰岛素原在大肠杆菌中的高效表达

为了提高胰岛素原的表达量，用pQE-40质粒构建了(His)6-Arg-Arg-人胰岛素原[(His)6-Arg-Arg- human Proinsulin，RRhPI]的大肠杆菌表达系统。通过培养条件的优化，在摇瓶培养的条件下，目标产物：RRhPI以包涵体形式获得了高效表达，每升培养基收获湿菌体约27g，包涵体6g(干重1．8g)，RRhPI约540mg。该水平已超过现有文献报道的摇瓶培养的最高水平。     

三种细菌生物被膜中超广谱β-内酰胺酶的检测

目的检测肺炎克雷伯氏菌、大肠埃希氏菌、铜绿假单胞菌三种细菌的生物被膜(biofilm,BF)中超广谱β-内酰胺酶(Extended-spectrumβ-lactamases,ESBLs)的产生。方法用改良平板培养法在硅胶膜上建立肺炎克雷伯氏菌、大肠埃希氏菌、铜绿假单胞菌BF的体外模型。用银染法及扫描电镜对BF进行鉴定。用双纸片试验检测ESBLs,等电聚焦电泳测定β-内酰胺酶的等电点。结果三种细菌的各30株中,BF肺炎克雷伯氏菌组(A2组)中ESBLs的产生率最高(14株,46.7%),其浮游菌组(A1组)检出8株(26.7%);BF大肠埃希氏菌组(B2组)有10株(33.3%)产生ESBLs,其浮游菌组(B1组)检出6株(20.0%);BF铜绿假单胞菌组(C2组)有3株(10%)产ESBLs,其浮游组(C1组)为2株(6.7%)。浮游菌组中ESBLs的产生率低于BF菌组,其中肺炎克雷伯氏菌及大肠埃希氏菌的BF组和浮游菌组的检出率之间有显著差异(P<0.05)。A2组共检出14株产生ESBLs,有4种ESBLs,等电点分别为8.2(4株)、7.6(8株)、6.3(1株)和5.6(1株),A1组检出8株产生ESBLs,为3种ESBLs,等电点分别为8.2(2株)、7.6(5株)和5.6(1株);B2、B1组检出2种相同等电点分别为7.6(B1组4株,B2组6株)、8.2(B1组2株,B2组4株)的ESBLs;C1、C2组检出一种等电点为6.4的ESBLs(C1组2株,C2组3株)。以pI为7.6的β-内酰胺酶的检出率最高,其     

抗体夹心酶联免疫吸附法测定重组E.coli L-天冬酰胺酶及药代动力学研究

目的建立大鼠血浆中重组E.coli L-天冬酰胺酶的抗体夹心酶联免疫吸附测定法,并进行药代动力学研究。方法应用重组E.coli L-天冬酰胺酶免疫家兔,分离IgG,用DEAE-纤维素柱色谱纯化,辣根过氧化物酶标记抗体,建立抗体夹心酶联免疫吸附法,测定大鼠血浆中重组E.coli L-天冬酰胺酶浓度。结果方法的线性范围为1～64 U·L^-1,血药浓度与时间的关系符合二房室模型,初期和末端的T_1/2分别为0.50～0.57 h和2.45～3.02 h,AUC与剂量成正比。结论建立的抗体夹心酶联免疫吸附法在灵敏度、特异性、线性范围、精密度和回收率等方面,满足药代动力学研究要求。实验方法和重组E.coli L-天冬酰胺酶在大鼠中的药代动力学参数为临床研究提供了手段和依据。     

TRAIL基因原核表达载体的构建、表达与抗体制备

目的:获取抗肿瘤坏死因子相关凋亡诱导配体(TRAIL)抗体.方法:利用PCR技术和基因重组技术将TRAIL基因构建于原核表达载体pPreTMH-Tb中,经酶切、测序鉴定证实构建完全正确后,通过IPTG诱导在大肠杆菌DH-5α中获得表达,并将TRAIL蛋白免疫家兔,通过Dot blot及Western blot检测抗TRAIL抗体的产生.结果:成功构建TRAIL基因原核表达载体,并在大肠杆菌DH-5α中获得表达,TRAIL蛋白表达量占菌体蛋白质总量的11.8%,Dot blot及Western blot检测证实获得了抗TRAIL抗体.结论:成功制备抗TRAIL抗体,这为TRAIL在真核细胞水平研究奠定了实验基础.     

Escherichia coli-induced alterations of human spermatozoa. An electron microscopy analysis

This study evaluated if the negative influence of Escherichia coli on the motility of human spermatozoa is a consequence of E. coli-induced ultrastructural alterations. Suspensions of spermatozoa were artificially infected with E. coli from a serotyped, pathogenic strain and incubated at 37 degrees C for 6 h. After incubation, spermatozoa were fixed in glutaraldehyde, stained with osmium tetroxide and ruthenium red and embedded in Spurr(R)-resin followed by ultramicrotomy. The sections were analysed subsequently by use of transmission electron microscopy. Uninfected suspensions of spermatozoa in medium and bacterial suspensions served as controls. Negative contrast technique was performed to facilitate visualization of ultrastructural details of the bacterial capsule after experimental exposure to spermatozoa. Electron microscopic evaluation revealed multiple and profound alterations in the ultrastructure of spermatozoa such as membrane defects and cytoplasmic vacuoles exclusively in spermatozoa of infected samples (> 90%). Morphological alterations involved all superficial structures of spermatozoa, in particular the plasma membrane of the mid-piece and neck as well as the inner and outer acrosomal membrane of the acrosome, indicating that morphological defects account for the immobilization of spermatozoa by E. coli. The results suggest that E. coli infection of ejaculates results in immobilization and impaired acrosomal function in human spermatozoa, findings that support the indication for antimicrobial chemotherapy in symptomatic and silent infections that affect the ejaculate.