血小板活化因子在烧伤合并内毒素血症早期肺损伤中的作用及意义

目的　探讨血小板活化因子（ＰＡＦ） ,肿瘤坏死因子（ＴＮＦ）等在烧伤合并内毒素血症早期肺损伤中的作用及意义。方法　采用２０ ％ ＴＢＳＡⅢ度烧伤合并内毒素注射复制大鼠早期肺损伤模型,检测血浆ＰＡＦ、ＴＮＦ含量等,观察肺组织病理形态学变化并应用ＰＡＦ受体拮抗剂防治早期肺损伤。结果　ＰＡＦ是烧伤合并内毒素血症早期先于ＴＮＦ出现变化的炎症介质,血浆ＰＡＦ浓度与早期肺损伤程度呈正相关,注射ＰＡＦ受体拮抗剂ＢＮ５０７３９ 可使肺损伤程度减轻。结论　ＰＡＦ在烧伤合并内毒素血症早期肺损伤中起重要致病作用     

血小板活化因子在烧伤合并内毒素血症早期肺损伤中的作 …

目的 探讨血小板活化因子（ＰＡＦ）肿瘤坏死因子（ＴＮＦ）等在烧伤合并内毒素血症早期肺损伤中的作用及意义。方法 采用２０％ＴＢＳＡⅢ度烧伤合并内毒素注射复制大鼠早期肺损伤模型,检测血浆ＰＡＦ、ＴＮＦ含量等,观察肺组织病理形态学变化并应用ＰＡＦ受体拮抗剂防治早期肺损伤。结果 ＰＡＦ是烧伤合并内毒素血症早期先于ＴＮＦ出现变化的炎症介质,血浆ＰＡＦ浓度与早期肺操作程度呈正相关,注射ＰＡＦ受体拮抗剂ＢＮ５０     

TNFα、NO在烧伤复合内毒素血症早期肾损害中的作用及其意义

目的 探讨肿瘤坏死因子α(TNFα)、一氧化氮(NO)在烧伤合并内毒素血症早期肾脏损害中的作用及其意义。方法 以大鼠体表烧伤Ⅲ度20％TBSA合并小剂量内毒素(1mg／kg体重)腹腔注射造成多脏器损害模型,按设计分组并在致伤后不同时相点进行肾脏病理形态学观察、TNFα和NO血清浓度测定、TNFα mRNA原位杂交和iNOS免疫组化染色。结果 烧伤后注射内毒素组诱导型一氧化氮合酶(iNOS)的表达和NO的合成以及TNFα mRNA的表达和TNFα的血浆水平均显高于和早于单纯烧伤组和单纯注射内毒素组。结论 烧伤合并内毒素血症时肾组织中NO和TNFα的水平显升高,两的升高可能是导致肾脏损害和引起肾脏血流动力学改变的重要因素之一。     

烧伤合并内毒素血症TNFαmRNA原位表达与早期心肌损害的实验研究

目的观察TNFαmRNA及其蛋白在心肌细胞的原位表达,探讨烧伤合并内毒素血症早期心肌损害的可能机制。方法采用20％TBSAⅢ度烧伤复合内毒素血症多脏器损害模型,时相点设为伤后0.5、1、3、6、12、24和48h。将178只大鼠随机分为烧伤复合内毒素注射组(烧注组)、单纯烧伤(单烧组)、单纯内毒素注射组(单注组)和正常对照组。采用光、电镜观察,ELISA及免疫组化,原位杂交染色,等观察大鼠心肌形态功能变化、血清TNFα含量变化、TNFαmRNA及其蛋白在心肌细胞的定位及分布。结果烧注组致伤早期心肌出现一系列损害性改变,如波浪变性、收缩带形成、肌纤维断裂和灶性胞浆内溶解等。左室收缩压(LVSP)及室内压最大变化速率(±dp/dtmax)显著下降(P＜0.01)。血清TNFα水平于1h明显升高(P＜0.01),3～6h达高峰。TNFαmRNA主要定位于心肌细胞和部分炎细胞。而单因素组病变程度轻,心肌损害不明显,血清TNFα峰值滞后以及心肌组织TNFαmRNA表达相对较弱。结论烧伤合并内毒素血症状态下,心肌本身可表达TNFαmRNA及其蛋白,并可能作为机体TNFα产生来源之一,参与早期心肌结构与功能损害的发生发展。     

烧伤并发内毒素血症早期肝损害与TNF—αmRNA表达的实验研究

目的 观察TNF－αmRNA及其蛋白的组织分布和细胞定位,探讨烧伤并发内毒素血症早期肝损害的发生机理。方法 选用20％Ⅲ度TBSA烧伤大鼠合并腹腔内毒素（LPS）注射造成烧伤复合内毒素血症肝损害模型,采用光镜,电镜及免疫组化原位杂交染色观察产肝脏的形态功能变化、血清TNF－α含量变化、肝组织TNF－α和TNF－α mRNA的细胞定位及其分布。结果 烧伤复合内毒素血症组,光镜下主要表现肝窦反应,枯否细胞（KCs)激活与增生以及肝细胞（HCs)变性坏死等;电镜下主要表现肝窦内血小板聚集、纤维素沉积与中性粒细胞（PMNs)扣押以及KCs、肝细胞退变溶解等。血清丙氨酸氨基转氨酶（ALT）显著升高（P＜0．01）和白蛋白（ALB）轻度下降。组织TNF－α主要定位于肝窦内皮细胞（SECs)、KCs。TNF－αmRNA主要定位于KCs、PMNs、巨噬细胞（MPs)。而在单因素组主要特点为病变程度轻,肝功能损害不明显,血清TNF－α峰值滞后以及组织TNF－α和TNF－αmRNA表达相对较弱等。结论 TNF－α是参与烧伤复合内毒素血症早期肝脏损害的重要细胞因子。     

PGE2及cAMP在烧伤合并内毒素血症骨髓粒单系造血变化中作用的实验研究

目的　探讨前列腺素E2 (PGE2 )、环磷酸腺苷 (cAMP)在烧伤合并内毒素血症骨髓粒单系造血变化中的作用。　方法　 178只昆明种小鼠随机分为烧伤合并内毒素注射组、单纯烧伤组、单纯内毒素注射组和等渗盐水对照组。应用放射免疫分析和免疫组化法 ,动态检测各组小鼠致伤后 1周内 ,骨髓细胞环氧酶 2 (COX 2 )表达及PGE2 、cAMP含量 ,并对粒单系造血变化进行了动态观察。　结果　烧伤合并内毒素血症早期骨髓粒单系略呈增生反应 ,继而呈现造血抑制。骨髓细胞COX 2表达、骨髓细胞上清PGE2 和细胞内cAMP在 12h～ 5d显著升高 ,且cAMP与PGE2 呈显著正相关 (r=0 .978,P <0 .0 1) ,而与粒 巨噬细胞集落形成单位 (CFU GM)呈显著负相关 (r =- 0 971,P <0 .0 1)。　结论　PGE2 在烧伤合并内毒素血症骨髓粒单系抑制中起重要作用 ,抑制效应是通过其与特异性受体结合 ,激活腺苷酸环化酶 ,使骨髓细胞内cAMP升高     

肿瘤坏死因子mRNA在严重烫伤大鼠小肠中的表达及细胞定位的研究

为探讨严重烫伤后肿瘤坏死因子(TNF)在大鼠小肠中的表达及细胞定位,应用斑点杂交及原位杂交方法,结合血浆 TNF、内毒素浓度的变化,探讨了 TNF mRNA 的表达及细胞定位规律。结果发现,烧伤后小肠 TNF mRNA 的表达量迅速升高,在伤后6小时达峰值,是正常值的5.56倍。门静脉血浆TNF、内毒素的变化与之类似。正常大鼠小肠有少量的细胞表达 TNF mRNA,主要是小肠固有层内的单核吞噬细胞。烧伤后固有层内的阳性细胞明显增多,而且固有层毛细管内皮细胞表达也是阳性,隐窝内也出现大量的阳性细胞。提示 TNF 的表达分泌,在烧伤早期与肠源性内毒素血症有非常密切的联系。固有层及粘膜下层间质中的内皮细胞及单核吞噬细胞是肠道分泌 TNF 的主要细胞。TNF 分泌量明显增加,其结果是造成小肠局部微循环障碍或诱导自由基的产生,从而导致肠粘膜屏障的破坏。     

烧伤并发内毒素血症早期肝损害与TNF-α mRNA表达的实验研究

目的观察 TNF-α mRNA 及其蛋白的组织分布和细胞定位,探讨烧伤并发内毒素血症早期肝损害的发生机理。方法选用20%Ⅲ度 TBSA 烧伤大鼠合并腹腔内毒素(LPS)注射造成烧伤复合内毒素血症肝损害模型,采用光镜,电镜及免疫组化原位杂交染色观察大鼠肝脏的形态功能变化、血清 TNF-α含量变化、肝组织 TNF-α和 TNF-α mRNA 的细胞定位及其分布。结果烧伤复合内毒素血症组,光镜下主要表现肝窦反应,枯否细胞(KCs)激活与增生以及肝细胞(HCs)变性坏死等;电镜下主要表现肝窦内血小板聚集、纤维素沉积与中性粒细胞(PMNs)扣押以及 KC_s、肝细胞退变溶解等。血清丙氨酸氨基转氯酶(ALT)显著升高(P<0.01)和白蛋白(ALB)轻度下降。组织TNF-α主要定位于肝窦内皮细胞(SECs)、KCs。TNF-α mRNA 主要定位于 KCs、PMNs、巨噬细胞(MPs)。而在单因素组主要特点为病变程度轻,肝功能损害不明显,血清 TNF-α峰值滞后以及组织TNF-α和 TNF-α mRNA 表达相对较弱等。结论 TNF-α是参与烧伤复合内毒素血症早期肝脏损害的重要细胞因子。     

生长抑素应用于急性轻型胰腺炎时血浆内毒素和TNFα水平变化

目的　观察生长抑素 (施他宁 )对急性轻型胰腺炎的治疗效果及其对急性轻型胰腺炎患者血浆内毒素和TNFα水平的影响。方法　 5 8例急性轻型胰腺炎患者随机分为A、B两组 ,A组采用施他宁治疗 (治疗组 ) ,B组给予一般常规治疗 (对照组 ) ,于第 1、3、5、7天抽血测定血闪内毒素和TNFα。结果　急性轻型胰腺炎患者入院第 1天的血浆内毒素和TNFα水平均明显高于健康人 ;治疗组患者血浆内毒素和TNFα水平下降速度明显快于对照组。结论　急性轻型胰腺炎患者早期均存在不同程度的内毒素血症及血浆TNFα水平升高 ,生长抑素治疗急性轻型胰腺炎疗效肯定 ,治疗组患者血浆内毒素和TNFα水平下降均明显快于对照组。     

内毒素血症时肝组织中脂多糖受体CD14的表达及其意义

目的 观测内毒素血症时大鼠肝组织中脂多糖受体CD14 mRNA的表达及其在内毒素介导Kupffer细胞（KCs)激活中的作用。方法 经大鼠尾静脉注入内毒素（剂量按5mg/kg计算）建立内毒素血症动物模型，测定血浆中内毒素、脂多糖结合蛋白（LBP)、TNF－α及IL－6含量变化，同时观测不同时相点肝组织中CD14 mRNA的表达及肝组织形态学变化，并与生理盐水组大鼠相比较。结果 在内毒素血症组大鼠中，随着血浆LPS浓度升高和时间延长，肝组织中CD14 mRNA的表达明显增强；血浆中LBP、TNF－α和IL－6含量也明显增加，与对照组相比较有显著差异（P＜0．01）。伴随KCs激活和肝细胞损伤的形态学改变，表现为KCs数量增多、体积增大、噬功能增强，肝细胞出现变性、坏死等变化。结论 内毒素血症时，随着肝组织中CD14表达增强和血浆LBP增加，可介导KCs激活，产生和释放多种细胞因子，诱导或加重肝组织及其它器官的损害。     

2015年乳腺癌辅助化疗进展

【摘要】〓乳腺癌是危害我国女性健康的头号杀手,尽管近年来辅助化疗的研究进展突飞猛进,但临床中仍有不少问题未能明确,如辅助化疗的合适人群、化疗的开始时间、蒽环及紫杉类的地位和用法、强化维持治疗的作用、疗效及预后的生物标志物等。本文结合乳腺癌辅助化疗在临床上的常见问题和2015年各大乳腺癌会议阐述乳腺癌辅助化疗的最新进展。     

Alterations in T-Cell Subset Frequency in Peripheral Blood in Obesity

Background: Obesity affects the regulation of immune and inflammatory responses. This study characterizes differences in peripheral blood lymphocyte phenotype in obese humans. Methods: Frequencies of lymphocyte subsets among peripheral blood mononuclear cells were compared between 10 obese (BMI ≥35) and 10 lean subjects, as determined by antibodies directed against cluster differentiation (CD) markers. Results: Obese patients demonstrated an increased frequency of CD3+CD4+ T-cells (mean difference 12%, P=0.004), a decreased frequency of CD3+CD8+ T-cells (mean difference 9.4%, P=0.016) and an increased frequency of CD3+CD8+CD95+ T-cells (mean difference 13.3%, P=0.032). No other differences among T-cell or monocyte subsets were noted. Conclusions: Obesity is associated with alterations in frequencies of peripheral CD4+ and CD8+ T-cells and aberrations in the expression of CD95 among CD8+ T-cells. These data suggest both CD4+ and CD8+ T-cell compartments, as well as the regulation of CD95 expression on CD8+ T-cells, as targets for further study into obesity's effects on the immune system.     

西宁地区烧伤病人动脉血气分析观察

对高海拔地区的27例烧伤病人动脉血气变化进行了分析和观察。结果证明:无论是存活病人还是死亡病人伤后均存在有低氧血症问题。并且在死亡病人和烧伤合并吸入性损伤病人其低氧血症的发生早于单纯烧伤病人。提示:吸入性损伤病人应立即行气管切开术以保障氧气供给,单纯烧伤病人可常规吸氧以维持正常血 PaO_2,ARDS 均发生在合并吸入性损伤的病人,高频喷射通气技术对纠正低氧血症有一定效果。     

Controversies in Fistula in Ano

Managing a complex fistula in ano can be a daunting task for most surgeons; largely due to the two major dreaded complications—recurrence & fecal incontinence. It is important to understand the anatomy of the anal sphincters & the aetiopathological process of the disease to provide better patient care. There are quite a few controversies associated with fistula in ano & its management, which compound the difficulty in treating fistula in ano. This article attempts to clear some of those major controversies.     

β-半乳糖苷酶在体内外成骨细胞中的表达

目的 研究β—半乳糖苷酶(β—gal)在成骨细胞中的表达状况，为阐明MorquioB综合征的发病机制提供依据。方法 裸鼠各器官和骨组织标本行X-gal染色检测。抽取羊和人骨髓行骨髓基质细胞(BMSCs)培养，分为4组：I：Adv-hBMP-2转染组；Ⅱ：Adv—β—gal转染组；Ⅲ：未转染组；Ⅳ：地塞米松诱导组。分别行X-gal染色和RT-PCR检测β—gal的表达。结果 裸鼠骺板两侧、骨膜内面及松质骨的成骨细胞和破骨细胞可见多量β—gal的表达。未转染BMSCs组有少量β—gal的表达，其他3组细胞的β—gal表达增高。结论成骨细胞和破骨细胞可表达多量β—gal，该两种细胞的β—gal缺乏可能是MorquioB综合征骨骼异常的直接原因。     

Smoking-Attributable mortality in Spain in 2016

IntroductionSmoking-attributable mortality (SAM) is a valuable indicator that can be used to characterize the course and health burden of the smoking epidemic. The aim of this paper was to estimate SAM in Spain in 2016 in the population aged 35 and over, using the best available evidence.MethodsA smoking prevalence-dependent analysis based on the estimation of population-attributable fractions was performed. Smoking prevalence (never, former, and current smokers) was calculated from a combination of the Spanish Health Survey (2016) and the European Health Survey (2014); the relative risk of death among current and former smokers was taken from the follow-up of various cohorts; and mortality rates were obtained from National Center for Statistics data. SAM estimates are presented globally, and by sex, age groups, and major disease categories: cancer, cardiometabolic diseases and respiratory diseases.ResultsIn 2016, 56,124 deaths were attributed to tobacco consumption, 84% in men (47,000), and 50% in the population aged over 74 (27,795). Overall, 50% of SAM was due to cancer (28,281), 65% of which was lung cancer. One in 4 attributable deaths (13,849) occurred before the age of 65.ConclusionsOne in 7 deaths in Spain in 2016 were attributable to smoking. This estimation of SAM clearly highlights the great impact of smoking on mortality in Spain, mainly due to lung cancer and chronic obstructive pulmonary disease.     

MicroRNAs in hepatic pathophysiology in diabetes

MicroRNAs(miRNAs or miRs) are small approximately 22 nucleotide RNA species that are believed to regulate diverse metabolic and physiological processes.In the recent past,several reports have surfaced that demonstrate the role of miRNAs in various biological processes and numerous disease states.For a disease as complex as diabetes,the emergence of miRNAs as key regulators leading to the disease phenotype has added a novel dimension to the area of diabetes research.On the other hand,the liver,a metabolic hub,contributes in a major way towards maintaining normal glucose levels in the body as it can both stimulate and inhibit hepatic glucose output.This equilibrium is frequently disturbed in diabetes and hence,the liver assumes special significance considering the correlation between altered hepatic physiology and diabetes.While the understanding of the mechanisms behind this altered hepatic behavior is not yet completely understood,recent reports on the status and role of miRNAs in the diabetic liver have further added to the complexities of the knowledge of hepatic pathophysiology in diabetes.Here,we bring together the various miRNAs that play a role in the altered hepatic behavior during diabetes.     

Fluid-phase transcytosis in the primate epididymis in vitro and in vivo

Ligated tubules from the corpus epididymidis of men and monkeys were incubated in medium containing horseradish peroxidase (HRP) as a marker for fluid-phase endocytosis. HRP was localized by light and electron microscopy after 0, 15, 30 and 60 min of incubation. Movement between the cells was prevented by tight junctions, but bypass of this barrier was apparently achieved by an intracellular vesicular mechanism leading to a time-dependent appearance of HRP in the lumen. Uptake of HRP into basal cells and capture by the lysosomal apparatus of principal cells were also observed. HRP-filled vesicles also appeared in the basal, mid and apical cytoplasm of epithelial cells in the caput 1 h after injection of the tracer into the epididymal circulation of the monkey, suggesting that this pathway also operates in vivo.