三腔二囊管的放置方法体会

一般采用三腔二囊管用于压迫上消化道出血止血,由于个体因素或技术因素往往造成失败。1987年以来,我们改进了三腔二囊管的一般放置方法,用于压迫上消化道出血止血13例,均获成功,现将体会介绍如下。 1 以前我们置入三腔二囊管时,只是在管上部擦少量的液体石腊油,这样病人往往有恶心、呕吐反应,插管不易成功。后来在插管前,先让患者喝10ml石腊油,使整个食道滑润、插管速度快,患者反应小,插管易成功。     

终末期糖基化终产物通过转化生长因子依赖和非依赖途径介导NRK52E细胞转分化和胶原Ⅰ的合成

目的探讨终末期糖基化终产物（AGEs）介导肾小管上皮细胞转分化和胶原（Col）Ⅰ合成的分子机制。方法体外培养正常大鼠近端肾小管上皮细胞系（NRK52E），应用自制的AGE-牛血清白蛋白（BSA）刺激NRK52E细胞。免疫细胞化学方法检测不同时间磷酸化（P）Smad2／3核转位情况。ELISA方法检测细胞培养上清TGF-β1的水平。RT-PCR方法检测α-平滑肌肌动蛋白（SMA）、E-钙黏着糖蛋白（cadherin）和ColⅠmRNA表达。Western印迹检测α-SMA、E-cadherin和ColⅠ蛋白的表达。同时观察TGF-β1中和抗体对AGE-BSA上述效应的阻断作用。结果基础状态下，NRK52E细胞存在低水平p-Smad2／3核表达（16％）。与BSA对照组比较，AGE—BSA以时间依赖方式上调NRK52E细胞p-Smad2／3核转位，其高峰出现在30min（68％比30.5％，P〈0．01）和24h（76％比31．3％，P〈0．01）。AGE—BSA显著上调α-SMA和ColⅠmRNA和蛋白表达；下调E-cadherin mRNA和蛋白的表达；并能促进NRK52E细胞合成和分泌TGF-β1。TGF-β1中和抗体能明显抑制AGE—BSA介导的24hp-Smad2／3核转位（25．2％，P〈0．01），但不能阻抑30min活化高峰；能明显抑制AGE-BSA介导的α-SMA和ColⅠmRNA和蛋白表达．以及显著地上调E-cadherin mRNA和蛋白的表达。结论AGEs通过TGF-β依赖和非依赖途径诱导肾小管上皮细胞Smads信号通路活化，促进其向肌成纤维母细胞转分化和ColⅠ的合成。     

表现为急性肾衰竭的IgA肾病11例临床与病理分析

目的：探讨IgA肾病并发急性肾衰竭(ARF)的临床与病理特点。方法：回顾分析11例IgA肾病并发ARF的临床与病理资料。结果：(1)本组11例IgA肾病患者并发ARF，占我院同期IgA肾病的1．28％(11／860)；(2)本组患者7例患者以浮肿、少尿为首发症状，3例以反复肉眼血尿为主诉、1例以恶性高血压为主要症状，6例患者蛋白尿≥2．0g／d；(3)肾活检示系膜增生性肾炎7例、新月体肾炎1例、增生硬化性肾炎伴新月体形成1例，余2例为In肾病的基础上伴发急性肾小管间质性肾炎。(4)本组资料中8例患者行激素加MP／CTX冲击治疗，4例予以单纯对症处理；8例肾功能恢复正常，1例肾功能部分缓解，2例患者肾功能进展行维持性透析治疗，总有效率为81．8％。结论：IgA肾病并发ARF发生率不低，病理可表现为多种病理类型，病理改变轻，预后好，多数患者肾功能可以恢复正常。     

尿红细胞在沉渣镜检中假阴性的因素探讨

在临床检验中 ,尿液分析是对临床治疗诊断提供重要依据。虽然现代科学技术的迅速发展 ,全自动尿沉渣分析仪的开发使用 ,尿液分析仪的普及 ,解决了尿液分析中的主要问题[1 ] 。但是 ,显微镜对尿沉渣的检查仍然有一定的作用。在实际工作中 ,由于主观或客观因素引起结果的误差 ,影响着尿液分析的准确性。本文根据近年来的资料 ,对 392例泌尿系疾病患者的尿检查结果作对比分析 ,仅就有关红细胞在尿沉渣镜检中假阴性的因素进行探讨。1　材料与方法　分析本科自 1 997年来的住院病人 ,均经过肾活检确诊和临床诊断为肾小球性血尿和非肾小球性血尿共…     

应用光学相干断层扫描量化评估糖尿病黄斑水肿的临床研究

目的 探讨糖尿病黄斑水肿患者在光学相干断层扫描(optical coherence tomography,OCT)中四个量化指标的变化.方法 纳入糖尿病视网膜病变患者89例(155眼),按照有无黄斑水肿分为阳性组(33例55眼)及阴性组(56例100眼),另收集正常志愿者23例(42眼)为正常对照组.所有试验对象经OCT检查,测量并分析各组黄斑中心凹视网膜厚度(central retinal thickness,CRT)、黄斑中心凹下脉络膜厚度(subfoveal choroidal thickness,SFCT)的差异,观察各组黄斑区外界膜(external limiting membrane,ELM)、椭圆体带(inner segment/outer segment,IS/OS)的连续性.结果 正常对照组、阴性组、阳性组CRT分别为(219.048±16.798) μm、(217.775±26.866) μm、(280.418±74.187)μm,3组间差异有统计学意义(P ＜0.001);3组SFCT分别为(312.893±140.559) μm、(302.080±125.287) μm、(293.745±140.517) μm,3组间差异无统计学意义(P=0.781);阴性组中黄斑区ELM连续97眼、中断3眼,阳性组连续47眼、中断8眼,两组间ELM连续性差异有统计学意义(P=0.019);阴性组中黄斑区IS/OS连续95眼、中断5眼,阳性组连续36眼、中断19眼,两组间IS/OS连续性差异有统计学意义(P＜0.001).结论 糖尿病黄斑水肿患者CRT增加,黄斑区ELM、IS/OS连续性遭到破坏,CRT、ELM连续性及IS/OS连续性可用于量化评估糖尿病黄斑水肿.     

Rosiglitazone down-regulates lipopolysaccharide-induced expression of CD40 and intercellular adhesion molecule 1 in rat peritoneal mesothelial cells through a NF-κB dependent mechanism

Objective To investigate the effect and mechanism by which PPARγ ligand, rosiglitasone, regulates the expression of CD40 and intercellular adhesion molecule 1 (ICAM-1) in the rat peritoneal mesothelial cells (RPMCs) induced by lipopolysaccharide (LPS). Methods RPMCs were harvested from Sprague-Dawley rat peritoneal cavity and maintained under defined in vitro conditions. The cells were randomly divided into groups as follows: medium, LPS (5 mg/L), LPS (5 mg/L)+BAY11-7085(5 μmol/L, NF-κB inhibitor), rosiglitazone (10 μmol/L or 20 μmol/L, peroxisome proliferator-activated receptor γ activator), LPS (5 mg/L)+rosiglitazone (10 μmol/L)+GW9662 (3 μmol/L, peroxisome proliferator-aetivatcd receptor γ antagonist), and LPS (5 mg/L)+vehicle (DMSO 0.2 ml/L). The expressions of CD40 and ICAM-1 RNA in RPMCs were examined by RT-PCR after 3 hour treatment, and the protein expressions of CD40, ICAM-1, p-NF-κB p65 and p-IκBα were examined by Western blot or immunofluorescence after 24 hour treatment. Results Following treatment with LPS, both the expressions of CD40 and ICAM-1 protein in RPMCs were up-regulated significantly (P<0.05), and the phosphoralation of p65 was increased greatly (1.10±0.17 vs 0.55±0.06, P<0.05). BAY11-7085 (5 μmol/L) significantly decreased the protein expression of p-p65 (0.22±0.11 vs 1.10±0.17, P<0.01), CD40 (0.34±0.02 vs 0.50±0.06, P<0.05) and ICAM-1 (0.35±0.16 vs 0.74±0.03, P<0.05). Pretreated with rosiglitazone for 3 h then added with LPS for 1 h, the levels of p-p65, CD40 and ICAM-1 in RPMCs were significantly decreased compared with those of LPS group (0.77±0.08 vs 0.90±0.10, P相似文献   

35例脑卒中偏瘫患者早期康复护理训练对瘫肢功能恢复的效果观察

目的探讨脑卒中偏瘫患者接受早期康复护理训练后肢体运动功能的恢复效果.方法将70例脑卒中偏瘫患者,分为观察组和对照组(各35例),对观察组实施早期康复护理训练.结果经早期康复护理训练后,2组肢体运动功能及日常生活能力的差别具有显著性意义(P＜0.05).结论早期实施康复护理训练,有利于提高运动功能和生活活动能力.     

消耗还原型谷胱甘肽抑制血管紧张素Ⅱ激活巨噬细胞c-Jun/ATF-2及NF-κB

目的:探讨还原型谷胱甘肽(GSH)在血管紧张素Ⅱ(AngⅡ)激活巨噬细胞转录因子c-Jun/ATF-2及NF-κB中的作用。方法:用荧光分光光度法测定细胞内GSH含量;用丁基硫堇硫氧胺(BSO)消耗细胞内GSH;用免疫印迹法测定细胞c-Jun/ATF-2磷酸化表达及NF-κBp65表达;用凝胶滞留法测定细胞NF-κB活性;用细胞免疫组化观察细胞c-Jun/ATF-2磷酸化表达的时间模式。结果:AngⅡ(1μmol/L)刺激30-60min可降低RAW264.7细胞内GSH;而后GSH逐渐适应性恢复。同时,AngⅡ刺激60min,呈剂量依赖性降低RAW264.7细胞内GSH。GSH特异性消耗剂BSO(0.5mmol/L)与RAW264.7细胞共同孵育18h,即可完全消耗细胞内GSH。AngⅡ(1μmol/L)可诱导RAW264.7巨噬细胞c-Jun/ATF-2磷酸化表达;BSO预先完全消耗细胞内GSH,AngⅡ(1μmol/L)不能诱导巨噬细胞c-Jun/ATF-2磷酸化。同样,AngⅡ(1μmol/L)可激活RAW264.7巨噬细胞NF-κB;BSO预先完全消耗细胞内GSH,AngⅡ(1μmol/L)不能激活巨噬细胞NF-κB。结论:还原型谷胱甘肽可能参与调控巨噬细胞转录因子c-Jun/ATF-2及NF-κB的转录活性。     

脂多糖通过NF-κB途径上调大鼠腹膜间皮细胞表达CD40和ICAM-1

目的 观察脂多糖(LPS)作用下大鼠腹膜间皮细胞NF-κB活性及其对CD40和细胞间黏附分子1(ICAM-1)表达的影响.方法 分离及培养大鼠腹膜间皮细胞.LPS不同浓度作用12 h 及LPS (5 μg/ml)作用不同时间点收集细胞;LPS(5 μg/ml)或BAY11-7085(一种IκBα的磷酸化抑制剂)不同浓度(1 μmol/L和5 μmol/L)预处理3 h加LPS,作用3 h后收集细胞;采用RT-PCR方法检测CD40和ICAM-1 mRNA表达.采用蛋白印迹检测NF-κB和磷酸化NF-κB(p-NF-κB)蛋白表达.结果 与常规培养基对照组相比,5 μg/ml LPS组CD40和ICAM-1 mRNA表达显著升高(P<0.05),10 μg/ml LPS组显著高于5 μg/ml LPS作用组(P<0.05).5 μg/ml LPS 作用下,ICAM-1 mRNA表达从1 h开始升高,3 h达到高峰,之后逐渐降低.CD40 mRNA表达在1 h无显著变化,3 h时迅速达到高峰,之后逐渐降低.常规培养的大鼠腹膜间皮细胞结构性表达p-NF-κB蛋白;加入LPS后,p-NF-κB蛋白表达显著增加,其中30 min～1 h表达最强,之后逐渐降低,至2 h仍显著高于常规培养组(P<0.05).加入5 μmol/L BAY11-7085后,LPS诱导的CD40和ICAM-1 mRNA表达显著降低(P<0.05),与正常对照组相比差异无统计学意义. 结论 LPS以时间依赖和浓度依赖模式上调CD40和ICAM-1的表达.NF-κB信号途径参与调节LPS诱导的大鼠腹膜间皮细胞CD40和ICAM-1的表达.     

Rosiglitazone down-regulates lipopolysaccharide-induced expression of CD40 and intercellular adhesion molecule 1 in rat peritoneal mesothelial cells through a NF-κB dependent mechanism

Objective To investigate the effect and mechanism by which PPARγ ligand, rosiglitasone, regulates the expression of CD40 and intercellular adhesion molecule 1 (ICAM-1) in the rat peritoneal mesothelial cells (RPMCs) induced by lipopolysaccharide (LPS). Methods RPMCs were harvested from Sprague-Dawley rat peritoneal cavity and maintained under defined in vitro conditions. The cells were randomly divided into groups as follows: medium, LPS (5 mg/L), LPS (5 mg/L)+BAY11-7085(5 μmol/L, NF-κB inhibitor), rosiglitazone (10 μmol/L or 20 μmol/L, peroxisome proliferator-activated receptor γ activator), LPS (5 mg/L)+rosiglitazone (10 μmol/L)+GW9662 (3 μmol/L, peroxisome proliferator-aetivatcd receptor γ antagonist), and LPS (5 mg/L)+vehicle (DMSO 0.2 ml/L). The expressions of CD40 and ICAM-1 RNA in RPMCs were examined by RT-PCR after 3 hour treatment, and the protein expressions of CD40, ICAM-1, p-NF-κB p65 and p-IκBα were examined by Western blot or immunofluorescence after 24 hour treatment. Results Following treatment with LPS, both the expressions of CD40 and ICAM-1 protein in RPMCs were up-regulated significantly (P<0.05), and the phosphoralation of p65 was increased greatly (1.10±0.17 vs 0.55±0.06, P<0.05). BAY11-7085 (5 μmol/L) significantly decreased the protein expression of p-p65 (0.22±0.11 vs 1.10±0.17, P<0.01), CD40 (0.34±0.02 vs 0.50±0.06, P<0.05) and ICAM-1 (0.35±0.16 vs 0.74±0.03, P<0.05). Pretreated with rosiglitazone for 3 h then added with LPS for 1 h, the levels of p-p65, CD40 and ICAM-1 in RPMCs were significantly decreased compared with those of LPS group (0.77±0.08 vs 0.90±0.10, P相似文献