Vancomycin-resistant enterococcal bacteremia: comparison of clinical features and outcome between Enterococcus faecium and Enterococcus faecalis.

BACKGROUND AND PURPOSE: Vancomycin-resistant enterococci (VRE) have emerged as important nosocomial pathogens. This study was conducted to clarify the clinical features and outcome of patients with vancomycin-resistant enterococcal bacteremia. METHODS: Patients with vancomycin-resistant enterococcal bacteremia treated at a medical center in northern Taiwan between November 1998 and July 2006 were reviewed. Clinical and bacteriological characteristics of Enterococcus faecium and Enterococcus faecalis were compared. RESULTS: Twelve patients (6 males and 6 females) were included for analyses. The mean age was 69.3 years (range, 40 to 86 years), and 8 cases (66.7%) were older than 65 years. All patients had underlying disease. Two patients received total hip replacement before development of VRE bacteremia. Twelve patients had prior exposure to broad-spectrum antimicrobial therapy. Ten patients had prior intensive care unit stay and prior mechanical ventilation before VRE bacteremia. All of the patients (n = 12) had an intravascular catheter in place. Bacteremia was caused by E. faecalis in 4 patients and by E. faecium in eight. The portals of entry included urinary tract (8.3%), skin, soft tissue and bone (41.7%) and unknown sources (50.0%). E. faecium showed a higher rate of resistance to ampicillin and teicoplanin than E. faecalis (87.5% vs 0.0%, p=0.01). The 60-day mortality rate was higher in patients with E. faecium bacteremia than E. faecalis bacteremia (62.5% vs 0.0%), although statistical significance was not obtained (p=0.08). CONCLUSIONS: VRE bacteremia may have an impact on the mortality and morbidity of hospitalized patients. Patients with bacteremia caused by vancomycin-resistant E. faecium had a grave prognosis, especially immunosuppressed patients. The prudent use of antibiotics and strict enforcement of infection control may prevent further emergence and spread of VRE.     

突变MyD88重组质粒的构建及其抑制绿脓杆菌诱导的A549细胞IL-8表达

构建突变MyD88真核表达质粒(MyD88 DN),转染人呼吸道上皮细胞株A549,探讨其对绿脓杆菌及其分泌产物刺激IL-8表达的影响.结果显示突变MyD88成功构建入pcDNA3.1/zeo真核表达质粒,转染A549细胞后,可降低绿脓杆菌培养上清或活菌刺激诱导的IL-8分泌.提示突变MyD88可阻断绿脓杆菌感染引起的呼吸道上皮细胞IL-8释放,为呼吸道炎症的基因治疗提供了新的靶基因.     

DICOM数据的三维重建与协同可视化系统的开发

复杂手术常需多科医生协商制定综合性治疗方案,网络协同三维可视化软件可使方案制定直观而精确。我们采用VTK工具包对DICOM格式CT图像数据进行三维重建并作网格简化,将结果所得多边形网格模型无缝集成到用HOOPS/3DAF所开发的图形系统进行显示,并用HOOPS/Stream工具包转成适合网络传输的HSF无损压缩流文件,再用HOOPS/NET工具包实现基于Client/Server架构的协同三维交互可视化系统。所得三维重建结果清晰,协同三维可视化操作实时度高。本研究实现了一个协同手术仿真开发平台,该架构易于进一步添加模拟手术操作与修复体设计功能。     

血脂测定结果的临床可接受性分析

目的:通过对不同检测系统血脂测定结果的偏倚评估,分析各系统间结果的可比性和临床可接受性。方法:参照CLSI文件相关要求,以可溯源的检测系统为目标检测系统,测定总胆固醇(TCH)、甘油三酯(TG)、载脂蛋白A1(APOA1)、载脂蛋白B(APOB)、高密度脂蛋白胆固醇(HDL-C)和低密度脂蛋白胆固醇(LDL-C),对本院3个不同检测系统进行朗道质控物(水平2和水平3)各测定21次和测定新鲜血清标本40份。结果:朗道质控物和新鲜血清标本TCH、TG、APOA1、APOB、HDL-C、LDL-C浓度在系统间的差异均有显著性(P<0.05)。除LDL-C在各检测系统间的相关系数为0.7859~0.9259之间外,其他项目各系统间的相关系数均大于0.975。各检测系统测定TCH、TG的不精密度CV均小于5%,其他项目的不精密度CV均小于10%;以可溯源检测系统1为目标检测系统,临床可接受性能评价:TCH、LDL-C在检测系统2和检测系统3超出临床接受范围,HDL-C在检测系统2超出临床接受范围,其他项目临床均可接受。结论:3个不同检测系统测定TG、APOA1、APOB结果具有可比性;测定HDL-C结果具有部分可比性,TCH、LDL-C结果不具有可比性,需采取整改措施。     

Cone beam volume CT image artifacts caused by defective cells in x-ray flat panel imagers and the artifact removal using a wavelet-analysis-based algorithm

The application of x-ray flat panel imagers (FPIs) in cone beam volume CT (CBVCT) has attracted increasing attention. However, due to a deficient semiconductor array manufacturing process, defective cells unavoidably exist in x-ray FPIs. These defective cells cause their corresponding image pixels in a projection image to behave abnormally in signal gray level, and result in severe streak and ring artifacts in a CBVCT image reconstructed from the projection images. Since a three-dimensional (3-D) back-projection is involved in CBVCT, the formation of the streak and ring artifacts is different from that in the two-dimensional (2-D) fan beam CT. In this paper, a geometric analysis of the abnormality propagation in the 3D back-projection is presented, and the morphology of the streak and ring artifacts caused by the abnormality propagation is investigated through both computer simulation and phantom studies. In order to calibrate those artifacts, a 2D wavelet-analysis-based statistical approach to correct the abnormal pixels is proposed. The approach consists of three steps: (1) the location-invariant defective cells in an x-ray FPI are recognized by applying 2-D wavelet analysis on flat-field images, and a comprehensive defective cell template is acquired; (2) based upon the template, the abnormal signal gray level of the projection image pixels corresponding to the location-invariant defective cells is replaced with the interpolation of that of their normal neighbor pixels; (3) that corresponding to the isolated location-variant defective cells are corrected using a narrow-windowed median filter. The CBVCT images of a CT low-contrast phantom are employed to evaluate this proposed approach, showing that the streak and ring artifacts can be reliably eliminated. The novelty and merit of the approach are the incorporation of the wavelet analysis whose intrinsic multi-resolution analysis and localizability make the recognition algorithm robust under variable x-ray exposure levels between 30% and 70% of the dynamic range of an x-ray FPI.     

钙离子载体在诱导人外周血单核细胞分化为树突状细胞中的作用

目的研究钙离子载体(CI)能否诱导人外周血单核细胞(PBMC)分化为树突状细胞(DC)，并初步探讨其信号转导途径。方法分离健康献血者的PBMC，在体外用CI(A23187)或人重组粒细胞／巨噬细胞集落刺激因子(rhGM—CSF)和CI培养40h，或rhGM-CSF和白细胞介素4(IL-4)培养7d，部分PBMC预先用W-7或CsA或K35926处理30min后，再加入上述细胞因子或CI。相差显微镜下观察细胞形态，流式细胞仪检测细胞表面CD14、CD80、CD86、CD83等分子的表达，MTT比色法检测其对同种异体混合T淋巴细胞的刺激增殖作用。结果健康献血者的PBMC经CI培养40h，或rhGM—CSF与CI培养40h，或rhGM-CSF与IL-4培养7d，均可获得DC的典型形态和表面分子的表达，包括CD14表达下调、共刺激分子(CD80、CD86)表达上调，以及较强刺激同种异体混合T淋巴细胞增殖的作用；CI诱导的DC其CD14分子的下调及CD83分子的上调更明显，刺激混合T淋巴细胞的增殖能力更强；rhGM-CSF可协同CI诱导PBMC向DC的分化。经rhGM—CSF及CI处理的PBMC，其形态、表面标志物及对T细胞的刺激增殖能力，均受到W-7或CsA或KT5926不同程度的抑制；而rhGM-CSF及IL-4所诱导的PBMC其形态、表面分子的表达以及刺激T细胞增殖的作用却不受上述抑制剂的影响。结论CI可快速诱导PBMC向DC分化，其分化过程可能受控于Ca^2 /钙调蛋白及其下游的多个细胞信号转导途径的调节。     

Experimental determination of the anisotropy function for the model 200 103Pd "light seed" and derivation of the anisotropy constant based upon the linear quadratic model

Since the publication of the AAPM Task Group 43 report in 1995, Model 200 103Pd seed, which has been widely used in prostate seed implants and other brachytherapy procedures, has undergone some changes in its internal geometry resulting from the manufacturer's transition from lower specific activity reactor-produced 103Pd ("heavy seeds") to higher specific activity accelerator-produced radioactive material ("light seeds"). Based on previously reported theoretical calculations and measurements, the dose rate constants and the radial dose functions of the two types of seeds are nearly the same and have already been reported. In this work, the anisotropy function of the "light seed" was experimentally measured and an averaging method for the determination of the anisotropy constant from distance-dependent values of anisotropy factors is presented based upon the continuous low dose rate irradiation linear quadratic model for cell killing. The anisotropy function of Model 200 103Pd "light seeds" was measured in a Solid Water phantom using 1 X 1 x 1 mm micro LiF TLD chips at radial distances of 1, 2, 3, 4, 5, and 6 cm and at angles from 0 to 90 degrees with respect to the longitudinal axis of the seeds. At a radial distance of 1 cm, the measured anisotropy function of the 103Pd "light seed" is considerably lower than that of the 103Pd "heavy seed" reported in the TG 43 report. Our measured values at all radial distances are in excellent agreement with the results of a Monte Carlo simulation reported by Weaver, except for points along and near the seed longitudinal axis. The anisotropy constant of the 103Pd "light seed" was calculated using the linear quadratic biological model for cell killing in 30 clinical implants. For the model 200 "light seed," it has a value of 0.865. However, our biological model calculations lead us to conclude that if the anisotropy factors of an interstitial brachytherapy seed vary significantly over radial distances anisotropy constant should not be used as an approximation for anisotropy characteristics of a brachytherapy seed.     

肠系膜上静脉外科干及下腔静脉下段的应用解剖观察

本文解剖了30具成人尸体,对肠系膜上静脉外科干、下腔静脉下段的位置、长度、外径、两者的相互关系以及前者与肠系膜上动脉分支后者与腹主动脉分支的关系等进行了观察测量。认为国人的外科干至少80％能满足手术中行肠腔静脉吻合术应具备的四点要求。     

A mouse model of galactose-induced cataracts

Galactokinase (GK; EC 2.7.1.6) is the first enzyme in the metabolism of galactose. In humans, GK deficiency results in congenital cataracts due to an accumulation of galactitol within the lens. In an attempt to make a galactosemic animal model, we cloned the mouse GK gene (Glk1) and disrupted it by gene targeting. As expected, galactose was very poorly metabolized in GK-deficient mice. In addition, both galactose and galactitol accumulated in tissues of GK-deficient mice. Surprisingly, the GK-deficient animals did not form cataracts even when fed a high galactose diet. However, the introduction of a human aldose reductase transgene into a GK-deficient background resulted in cataract formation within the first postnatal day. This mouse represents the first mouse model for congenital galactosemic cataract.     

CCKB受体诱发的小鼠神经元蛋白质磷酸化的研究

目的：从蛋白质可逆磷酸化修饰的角度初步勾勒出CCK_B型受体介导的胞内信号转导途径。方法:培养的小鼠大脑皮质神经元分为实验组、对照组和受体拮抗剂组，在无磷培养基加入 ［32P］-NaH₂PO₄标记细胞中的磷蛋白后，刺激组给予CCK₈（10^-7 mol/L），对照组加入等量的无磷培养基，受体拮抗剂组在分别加入CCK_A型、CCK_B型受体拮抗剂L364 718、L365 260以及L364 718＋L365 260，浓度均为10^-8 mol/L，孵育10 min后，再加入10^-7 mol/L CCK₈，37 ℃作用60 min，液氮中终止磷酸化反应。裂解细胞提取蛋白质，双向电泳分离，放射自显影7d后，获得磷酸化蛋白的放射自显影双向电泳图谱。采用PDQuest 2D分析软件对图谱进行差异分析，并在Swiss-Prot蛋白质数据库和自建磷蛋白数据库中查询定性。结果:CCK₈作用60 min后，小鼠神经元CCK₈信号转导相关磷酸化蛋白有：多种蛋白激酶、细胞信号分子、生长因子受体、转录因子等。加入L364 718后，神经元中PKCδ、P55G等的磷酸化水平降低，加入L365 260后， PKCα、PKGβ、OGFR、EGFR等的磷酸化水平呈现不同程度的降低，表明皮质神经元中CCK_B受体介导的信号转导更复杂。结论:CCK_A型、GGK_B型受体均可介导CCK₈在神经元的信号转导，但CCK_B型受体可能发挥了更重要的作用，其介导的信号途径可能包括：肌醇磷脂信使系统、cAMP-PKA途径、MAPK途径、JNK途径、PI3K-PKB途径和cGMP-PKG途径。