应用高分子材料整治铁路桥梁支座病害

分析了铁路桥梁支座病害的成因,介绍了应用高分子材料整治桥梁支座病害的施工工艺和取得的效果.     

可吸入颗粒污染物在下呼吸道运动和沉积规律的数值模拟

为研究受慢性阻塞性肺病影响的呼吸道内气固流动特性,建立了基于Weibel模型的5～8级三维肺部模型.气相采用标准k-ε湍流模型,颗粒相采用离散颗粒模型.三级呼吸道内模拟的气固流动特性与实验结果进行了对比验证.在呼吸强度为30,60和90 L/min条件下,模拟了稳态、非稳态吸气时第7级内侧呼吸道受慢性阻塞性肺病影响收缩...     

“花柳病”概念探源补遗

当今我国学者普遍将花柳病等同于性病,认为花柳病是性病在旧社会的称谓或者是一种民间称法。本文通过对花柳病概念进行溯源,认为这种看法是缺乏历史依据的:花柳一词作为对妓女等的雅称始于唐代,但是作为一种疾病的名称则始于日本,自19世纪中后期被引入中国之后,它又经历了近代医学的洗礼和改造,成为了一个充满本土感的近代词汇。     

浅谈红层地区小型水库的常见地质病害

根据对自贡地区300余座小一型及小二型水库病害的分析、统计,列出红层地区小型水库的普遍性地质病害,为川南、川北以及川东地区的水库病害整治提供一点借鉴作用。     

淋巴囊肿病病毒主要衣壳蛋白1.3 kb基因片段的原核表达

取淋巴囊肿病病毒感染牙鲆组织,蛋白酶K裂解,PCR法成功获得了淋巴囊肿病病毒主要衣壳蛋白1.3 kb基因片段.构建其原核表达载体,IPTG诱导表达.结果表明,该融合蛋白分子量约70 kD,可与抗LCDV多克隆血清特异反应.为LCDV基因工程疫苗的研制奠定了实验基础.     

Phytanic acid impairs mitochondrial respiration through protonophoric action

Refsum disease is a rare, inherited neurodegenerative disorder characterized by accumulation of the dietary branched-chain fatty acid phytanic acid in plasma and tissues caused by a defect in the alphaoxidation pathway. The accumulation of phytanic acid is believed to be the main pathophysiological cause of the disease. However, the exact mechanism(s) by which phytanic acid exerts its toxicity have not been resolved. In this study, the effect of phytanic acid on mitochondrial respiration was investigated. The results show that in digitonin-permeabilized fibroblasts, phytanic acid decreases ATP synthesis, whereas substrate oxidation per se is not affected. Importantly, studies in intact fibroblasts revealed that phytanic acid decreases both the mitochondrial membrane potential and NAD(P)H autofluorescence. Taken together, the results described here show that unesterified phytanic acid exerts its toxic effect mainly through its protonophoric action, at least in human skin fibroblasts. Received 4 August 2007; received after revision 26 September 2007; accepted 10 October 2007 J. C. Komen, F. Distelmaier: These authors contributed equally to this work.     

<Emphasis Type="Italic">Legionella pneumophila</Emphasis> — a human pathogen that co-evolved with fresh water protozoa

The bacterial pathogen Legionella pneumophila is found ubiquitously in fresh water environments where it replicates within protozoan hosts. When inhaled by humans it can replicate within alveolar macrophages and cause a severe pneumonia, Legionnaires disease. Yet much needs to be learned regarding the mechanisms that allow Legionella to modulate host functions to its advantage and the regulatory network governing its intracellular life cycle. The establishment and publication of the complete genome sequences of three clinical L. pneumophila isolates paved the way for major breakthroughs in understanding the biology of L. pneumophila. Based on sequence analysis many new putative virulence factors have been identified foremost among them eukaryotic-like proteins that may be implicated in many different steps of the Legionella life cycle. This review summarizes what is currently known about regulation of the Legionella life cycle and gives insight in the Legionella-specific features as deduced from genome analysis. Received 1 September 2006; received after revision 10 October 2006; accepted 22 November 2006     

Developing pharmacological therapies for Alzheimer disease

Alzheimer disease (AD), while chronic and progressive with an average progression of 7 – 10 years, is both multifactorial and heterogeneous. Thus, AD offers a large window of opportunity and a large number of therapeutic targets to inhibit it. The selection of a therapeutic target, however, is one of the biggest challenges in developing a pharmacological treatment of this multifactorial disease. Inhibition of a pivotal downstream event is likely to benefit more patients than inhibition of an upstream event in AD pathogenesis. Neurofibrillary degeneration of abnormally hyperphosphorylated tau offers such a pivotal therapeutic target. Abnormal hyperphosphorylation of tau and not its aggregation into filaments appears to be the most deleterious step in neurofibrillary degeneration. Tau can be abnormally hyperphosphorylated by downregulation of protein phosphatase-2A activity or by upregulation of more than one tau kinase. Restoration of the phosphatase activity which is downregulated in AD brain or inhibition of GSK-3β and cdk5, which are required for AD-type abnormal hyperphosphorylation of tau, are among the most promising therapeutic strategies.     

黄芪注射液治疗肺心病急性加重期73例疗效观察

目的:探讨黄芪注射液静脉注射治疗肺心病急性加重期的疗效.方法:对照组67例,采用常规的抗感染、平喘、强心及利尿等治疗;治疗组73例,在常规治疗的基础上同时加用黄芪注射液40mL溶于5%葡萄糖250mL中静脉滴注,每日一次,10d为一疗程.结果:治疗组和对照组的有效率分别为91.78%和74.63%(P<0.01);两组治疗后心输出量(CO,L/minm2)、心脏指数(CI)、左室射血分数(LVEF)、左室短轴缩短率(FS)、每搏输出量(SV)、二尖瓣快速充血期和心房收缩期血流速度(E/A)均较治疗前明显改善(P<0.05,P<0.01),但治疗组更优于对照组(P<0.05).两组动脉血气治疗后均有改善,但治疗组改善程度优于对照组(P<0.05).结论:黄芪注射液对肺心病急性加重期具有较好疗效.     

腹部消化器官病变部位与两类腹痛部位的关系

目的:探讨腹部消化器官疾病所致内脏痛及腹膜痛的部位与病变部位的关系.方法:收集1226例有腹痛表现的腹部消化器官疾病患者的临床资料,分别统计分析内脏痛部位及腹膜痛部位与内脏病变部位的关系.结果:内脏痛平面与病变内脏起源的原肠的平面呈正相关(rs=0.87,P<0.01).腹膜痛最先出现或最明显的部位与病变内脏的解剖部位一致(=0.96,P<0.01).结论:腹部消化器官疾病所致内脏痛及腹膜痛的部位均与病变部位显著相关.依据腹痛部位定位诊断,需要分清腹痛类型,分别根据内脏痛及腹膜痛部位推测病变内脏的胚胎起源及解剖部位.