阻塞性黄疸患者血清EGF测定的临床意义

目的：探讨阻塞性黄疸病人手术前后血清表皮生长因子（ＥＧＦ）水平的变化及其在胃粘膜病变中的作用。方法：采用放射免疫分析法检测３１例阻塞性黄疸病人手术前后血清ＥＧＦ水平。结果：与正常对照组相比,阻塞性黄疸病人血清ＥＧＦ术前即降低,术后降低更明显。结论：阻塞性黄疸患者手术前后血清ＥＧＦ均减少,ＥＧＦ不能发挥对胃粘膜的保护作用,致使胃粘膜保护性因素减弱,可能是阻塞性黄疸时胃粘膜病变及术后应激性溃疡的发病机     

门脉高压时胃粘膜病变发生机制的实验研究

为探讨门脉高压时胃粘膜病变的发生机制，本文对四氯化碳所致的肝硬变伴门脉高压大鼠的胃粘膜主要防御和损伤因子进行了测定，并观察了胃粘膜超微结构。结果表明，门脉高压大鼠的胃粘膜前列腺素Ｆ２含量、胃粘膜血流量和胃壁结合粘膜量明显低于正常大鼠（均为Ｐ＜０．００１），而胃液ｐＨ值，胃酸浓度、胃酸分泌量和胃蛋白酶活性与正常比较无明显差异（均为Ｐ＞０．０５）。门脉高压大鼠的胃粘膜毛细血管组织结构的完整性破坏，毛细     

实验性急性肝衰竭时门脉高压发生机制的研究

目的：阐明急性肝衰竭时门脉高压的发生与肠源性内毒素血症和肝内微循环障碍的关系。方法：动态观察皮下注射硫代乙酰胺大鼠门脉血流动力学、血浆内毒素、内皮素－１、肿瘤坏死因子－α及台盼蓝肝脏原位灌流等。结果：随着给注射时间的延长,血浆内毒素水平、ＡＬＴ和ＬＤＨ明显升高,血浆及肝组织ＴＮＦ－α和ＥＴ－１显著增多,台盼蓝灌流时间明显延长。肝组织可见肝窦直径显著变窄,肝细胞肿胀变性坏死使肝窦被挤压。结论：肠源性内毒素血症及其引发的肝微循环障碍在急性门脉高压形成中具有重要作用。     

胸液中一氧化氮及细胞因子的检测

对结核性胸液及癌性胸液中一氧化氮（ＮＯ）、白细胞介素－８（ＩＬ－８）、肿瘤坏死因子α（ＴＮＦα）、表皮生长因子（ＥＧＦ）含量进行测定。结果发现结核性胸液中ＮＯ－２／ＮＯ－３（间接反映体内ＮＯ合成状况）浓度及ＩＬ－８、ＴＮＦα、ＥＧＦ含量均较正常人血清显著增高，且结核性胸液中ＩＬ－８、ＴＮＦα及ＥＧＦ含量均较癌性胸液明显增高。结果提示胸膜腔局部释放产生的大量ＮＯ、ＩＬ－８及ＴＮＦα参与了胸膜组织免疫损伤及胸液渗出过程，ＥＧＦ则可能与损伤修复有关。ＩＬ－８、ＴＮＦα、ＥＧＦ检测对良性或恶性胸液的鉴别有一定参考价值。     

慢性肺心病患者血清ET、TNF-α与NO含量变化及意义

慢性肺原性心脏病 (ＣＰＨＤ)是慢性支气管炎、肺气肿、支气管哮喘的慢性阻塞性肺疾病、肺胸疾病或肺血管病变引起肺循环阻力增加、肺动脉高压 ,进而右心室增大或右心功能不全。近年来 ,关于ＥＴ、ＴＮＦ -α和ＮＯ在心血管疾病发生发展中的作用日益受到重视。本文选择 4 0例ＣＰＨＤ患者 ,检测不同时期血清中ＥＴ、ＴＮＦ -α、ＮＯ含量 ,探讨其相关性及临床意义。对象和方法一、对象 :(一 )病例组 :4 0例 (男 2 4 ,女 16 )均为本院住院者 ,年龄4 2～ 6 9岁 ,所有病例均经历了ＣＰＨＤ急性发作期和缓解期两个阶段。(二 )正常对照组 :30例 (…     

生长因子对培养的肺泡Ⅱ型细胞分泌功能及形态的影响

目的：探讨表皮生长因子（ＥＧＦ）、转化生长因子α和β１（ＴＧＦα，ＴＧＦβ１） 对肺泡Ⅱ型细胞（ＡＴⅡ） 磷脂分泌功能及细胞形态（ 肥大） 的影响。方法：原代培养的成年大鼠ＡＴⅡ中，加入生长因子作用４８ ｈ，应用化学测定法测定培养介质中总磷脂含量，采用图像分析技术测量细胞体积参数。结果：ＥＧＦ、ＴＧＦα均可使总磷脂含量增加，而ＴＧＦβ１ 则使总磷脂含量降低；随ＥＧＦ、ＴＧＦα浓度增加，ＡＴⅡ平均直径（ＤＱ） 、体积（ＶＱ） 和表面积（ＳＱ） 均逐渐增大，ＴＧＦβ１ 对细胞体积变化无明显影响；ＴＧＦα和ＴＧＦβ１ 同时加入培养体系中，总磷脂含量及细胞体积均无明显改变。结论：ＥＧＦ、ＴＧＦα能促进ＡＴⅡ磷脂分泌和细胞肥大；ＴＧＦβ１ 对ＴＧＦα的作用有抑制效应。     

肿瘤坏死因子及磷脂酶A2在实验性急性肝衰竭中的作用

应用Ｄ－ＧａｌＮ＋ＥＴ复制急性肝衰竭（ＡＨＦ）动物模型，检测肝衰竭鼠血清中肿瘤坏死的子（ＴＮＦ）含量及肝组织匀浆中磷脂酶Ａ２（ＰＬＡ２）活性，探讨二者在ＡＨＦ的作用，结果发现，ＡＨＦ组鼠血清中ＴＮＦ含量及肝组织匀浆中ＰＬＡ２活性明显高于正常对照组（Ｐ〈０．０５，Ｐ〈０．０１），提示ＴＮＦ可能激活ＰＬＡ２后者与ＴＮＦ所致的肝损伤有关。     

前列腺素E1对肿瘤坏死因子水平及磷脂酶A2活性的影响

为探讨前列腺素Ｅ１（ＰＧＥ１）保护肝细胞作用机制。本实验应用Ｄ－氨基半乳糖及内毒素复制急性肝衰竭（ＡＨＦ）模型，观察ＰＧＥ１对血清肿瘤坏死因子（ＴＮＦ）水平及肝组织匀浆磷脂酶Ａ２（ＰＬＡ２）活性的影响，结果显示：ＰＧＥ１治疗组鼠血清ＴＮＦ含量及肝组织匀浆ＰＬＡ２活性明显低于对照组（Ｐ〈０．０１），肝组织坏死面积也小于对照组（Ｐ〈０．０１）。提示ＰＧＥ１保护肝细胞作用与降低ＴＮＦ合成及抑制ＰＬＡ２活     

促炎症细胞因子、T细胞亚群在小儿过敏性紫癜不同病期的变化

目的：探讨促炎症细胞因子（ＩＬ－６１、ＩＬ－８、ＴＮＦ－α）以及Ｔ细胞亚群在小儿过敏性紫癜发病中的作用。方法：采用双抗体夹心ＥＬＩＳＡ法检测３０例急性期２１例恢复期及２８例健康儿童血清及外周血单个核细胞（ＰＢＭＣ）培养上清液ＩＬ－６、ＩＬ－８及ＴＮＦ－α水平,以及外周血Ｔ细胞及其亚群的变化。结果：急性期血清及ＰＢＭＣ上清液ＩＬ－６、ＩＬ－８、ＴＮＦ－α水平明显高于恢复期和对照,且以ＩＬ－８、ＴＮＦ     

可溶性TNF受体及膜TNF受体检测方法的初步应用

本文采用竞争结合法测定了血清中可溶性ＴＮＦ受体（ＳＴＮＦＲ）。４９例ＳＬＥ病人血清中ｓＴＮＦＲ水平明显高于正常人。用放射受体分析法测定６例正常对照及４例肾脏肿瘤患者远离肿瘤的肾实质细胞膜表面的ＴＮＦ受体数目（Ｂｍａｘ）及亲和力（ＫＤ值）。结果Ｓｃａｔｃｈａｒｄ作图为曲线，人肾实质组织细胞膜表面存在高、低两种亲和力ＴＮＦ受体。     

热休克蛋白70对内毒素致门静脉高压性胃病大鼠胃黏膜损伤的保护作用研究

目的: 探讨热休克蛋白70(HSP70)对内毒素诱导的肝硬化门静脉高压性胃病(PHG)大鼠胃黏膜损伤的作用及机制。方法: 以CCl₄制备肝硬化PHG大鼠模型。热处理诱导HSP70表达,注射内毒素及其拮抗剂BPI21,酶联免疫吸附测定(ELISA)检测HSP70和TNF-α水平,HE染色观察胃黏膜病理变化。实验分为正常对照组、PHG组、PHG+热处理组、PHG+内毒素组及PHG＋BPI21组。结果: (1) PHG时胃黏膜HSP70表达明显减少,血浆内毒素及胃黏膜TNF-α表达明显增加,胃黏膜损伤明显;(2) 外源性内毒素增加PHG大鼠胃黏膜TNF-α表达,加重其胃黏膜损伤;BPI21则显著减少其TNF-α表达,减轻胃黏膜损伤;(3)热处理增加PHG大鼠胃黏膜HSP70表达,减少TNF-α表达,减轻胃黏膜损伤。结论: HSP70减轻PHG胃黏膜损伤,其机制可能与降低胃黏膜TNF-α水平有关。     

内源性一氧化氮预防大鼠乙醇性胃粘膜损伤的研究

目的：探讨内源性一氧化氮在大鼠乙醇性胃粘膜损伤时保护胃粘膜作用及机制。方法：大鼠７２ 只,随机分为４ 组,正常对照组,单纯乙醇灌胃（Ｅｔｈ） 组,Ｌ－ 精氨酸＋ 乙醇（Ｌ－ ａｒｇ ＋ Ｅｔｈ） 组,Ｌ－ 硝基精氨酸＋ 乙醇（Ｌ－ ＮＮＡ＋Ｅｔｈ） 组,观察其血浆ＮＯ 含量对胃粘膜的大体及组织学损伤程度、胃粘膜血流量（ｇａｓｔｒｉｃ ｍｕｃｏｓａｌ ｂｌｏｏｄ ｆｌｏｗ ,ＧＭＢＦ） 和胃粘液分泌量的影响。结果：Ｅｔｈ 组血浆ＮＯ 含量,ＧＭＢＦ 和粘液分泌量明显少于对照组（ Ｐ 均＜ ０－０５） ,Ｌ－ ａｒｇ ＋ Ｅｔｈ 组血浆ＮＯ 含量,ＧＭＢＦ 和粘液分泌量明显多于Ｅｔｈ 组（ Ｐ 均＜ ０ ．０５） ,而乙醇对胃粘膜损伤明显减轻（ Ｐ＜ ０－０５） ,Ｌ－ ＮＮＡ ＋ Ｅｔｈ组血浆ＮＯ 含量ＧＭＢＦ 和粘液分泌量明显少于前３ 组（ Ｐ 均＜ ０－０５） ,而胃粘膜损伤程度明显较重（ Ｐ＜ ０－０５） 。结论：内源性ＮＯ 保护胃粘膜对抗乙醇引起的损伤,是通过增加胃粘膜血流量和促进粘液分泌而实现的。     

神经肽Y、降钙素基因相关肽、肿瘤坏死因子在先天性心脏病肺动脉高压中作用的研究

目的 本文着重阐述两种心血管调节肽-降钙素基因相关肽（CGRP）、神经肽Y（NPY）和先天性心脏病肺动脉高压（简称先心病肺高压）的关系;同时对先心病肺高压患儿测定肿瘤坏死因子（TNF）水平,以判断其与肺高压严重程度的关系;对部分病例外周血NPY、CGRP水平行术前,术后对照,以观察分流被纠正后其变化情况;另外,对外周血CGRP、NPY浓度作相关分析。以判断它们是否具有相关性。方法 运用放射免疫分析方法测定80例先天性心脏病患儿血清NPY、CGRP及TNF浓度,其中13例为非肺高压组,67例为肺高压组,将两组进行比较,进行方差分析,t检验。结果 非肺高压组与轻、中、重度肺高压组血浆NPY及CCRP浓度均存在显著性差异;非肺高压组与中、重度肺高压组血浆TNY存在显著性差异。与轻度肺高压组无显著性差异;手术前后轻,中度肺高压组NPY和CGRP浓度存在显著性差异。而重度肺高压组差异不明显;NPY与CGRP存在负相关关系。结论 三种活性物质在先天性心脏病肺动脉高压的发生机制中有重要作用。NPY/CGRP比值的升高参与和促进了肺动脉高压的形成和发展。     

Morphological features of the gastric mucosa capillary network in patients with portal hypertension

The pathogenesis of portal hypertension (PH) involves venous congestion with gastric mucosal capillary dilatation. The formation of new blood vessels, as was shown in experimental models of PH, is pathological hallmark of PH. Generation of new blood vessels is stimulated by vascular endothelial growth factor (VEGF), the regulator of angiogenesis. The aim of the study was to investigate changes in gastric microvessels in patients with liver cirrhosis complicated with PH in different stages, and the factors influencing the development of portal hypertensive gastropathy. We studied the relation between gastric mucosal capillary parameters, measured morphometrically, and endoscopic appearances in 56 patients with PH. The gastric biopsy was obtained from antrum and corpus of the stomach. We determined expression and localization of Fit-1 receptor for VEGF in human gastric mucosa by immunohistochemistry. Mucosal capillary network assessed on histological sections immunostained for CD34, a specific marker for endothelial cells and revealed proliferating endothelial cells by Ki-67 antibodies. Nicon CP 995 camera and digital image analyzing system (DMI-1) was used for morphometry. The number, size and relative volume of vessels in gastric mucosa were evaluated. Helicobacter pillory-positive patients were excluded from study. The number of vessels in gastric mucosa was significantly higher in groups with PH (p < 0.05) compared with patients without PH. The mean size of vessels in gastric mucosa was decreased in patients with PH (212 +/- 20 vs 282 +/- 25 mkm2, p < 0.05) in atrum and (155 +/- 12 vs 198 +/- 13 mkm2, p < 0.039) in corpus. The majority of the vessels were presented by newly formed small sized capillaries. Meanwhile the relative volume of vessels in gastric mucosa was not changed significantly in groups with PH. These observations have not supported the view that PH is usually associated with a prominent dilatation of gastric mucosal capillaries. Our data have shown intensifying of neoangiogenesis in human gastric mucosa at PH. The anti-angiogenic therapeutic approach could be taken into consideration for patients suffering from PH.     

实验高压电烧伤胃黏膜微循环动态变化及意义

目的探索高压电对家兔胃黏膜微循环的影响及其发生机制。方法将20只家兔随机分为高压电烧伤组(实验组)和假高压电烧伤组(对照组),每组10只。用实验高压电击系统复制家兔高压电烧伤模型,采用WX-9B型多部位微循环显微镜及其图像分析系统,通过胃黏膜下层微循环观测窗,观察高压电烧伤后胃黏膜微血管形态、血流动力学及微血管周围状态的早期变化及规律,并大体观察6h胃黏膜损伤情况。结果与对照组比较,实验组电击后微动脉即刻收缩,1h扩张,以后逐渐恢复;微静脉即刻收缩,并较快恢复为电前状态,4~6h再次出现收缩现象。致伤即刻微动静脉血流速度明显减慢,1h以后加快,2h再次减慢。致伤即刻黏膜层毛细血管网扩张,渗出明显,1h缓解,2h以后随时间逐渐加重。结论高压电烧伤导致家兔胃黏膜微循环障碍。     

慢性乙型肝炎患者胃粘膜HBV-DNA检测及临床意义

目的:检测慢性乙型肝炎(乙肝)患者乙肝病毒脱氧核糖核酸(HBV-DNA),探讨HBV与胃粘膜病变的关系。方法:选择慢性乙肝并伴有慢性胃炎的患者58例(H组)及慢性胃炎但其血清HBV标志物(HBVM)和HBV-DNA均阴性对照组52名(C组),两组均进行胃镜检查,同时取胃粘膜,H组取空腹静脉血液,采用荧光定量聚合酶链反应(FQ-PCR)方法进行血清、胃粘膜HBV-DNA含量和血清HBVM检测。结果:H组血清和胃粘膜HBV-DNA阳性例数分别为38例(65.52%)和46例(79.31%),两者相比有显著性差异(χ2=6.125,P<0.05);两者HBV-DNA含量显著正相关。H组32例血清HBeAg阳性患者的血清和胃粘膜HBV-DNA均为阳性,而26例血清HBeAg阴性患者的血清和胃粘膜HBV-DNA阳性只有6例(23.1%)和14例(53.8%)。C组胃粘膜HBV-DNA全部阴性。胃镜下观察H组患者广泛存在胃窦炎,C组以慢性浅表性胃炎为主。结论:HBV存在于胃粘膜中,可能引起胃部的炎性损伤。     

白内障患者手术治疗前后血浆ET和TNF-α检测的临床意义

目的：探讨了白内障患者手术治疗前后血浆内皮素（ET）和血清肿瘤坏死因子（TNF-α）水平的变化及临床意义。方法：应用放射免疫分析对32例白内障患者进行了血浆ET和血清TNF-α测定，并与30名正常健康人作比较。结果：手术前白内障患者血浆ET和血清TNF-α水平非常显著地高于正常人组（P〈0．01），术后1个月则与正常人比较无显著性差异（P〉0．05）。结论：测定白内障患者血浆ET和血清TNF-α水平的变化与患者的病情和预后密切相关。     

Association between Helicobacter pylori infection and serum pepsinogen concentrations in gastroduodenal disease.

AIM: To investigate the association between Helicobacter pylori infection and serum pepsinogen (PG) 1 and 2 concentrations in various gastroduodenal diseases. METHODS: Serum PG1 and 2 concentrations and antibodies to H pylori were measured by enzyme linked immunosorbent assay (ELISA); gastric mucosal pH was assessed and urease activity in biopsy tissue was determined. A comparison of the ELISA and urease test results permitted division of the cases into positive, false positive, false negative and negative categories for control, gastritis, and ulcer groups. RESULTS: The gastric mucosal pH and serum PG2 in cases positive for H pylori were significantly increased in ulcer and gastritis cases compared with H pylori negative cases. Similar tendencies were observed for the false positive and false negative categories. CONCLUSIONS: A positive ELISA reaction for antibodies and an increased serum PG2 concentration are reliable indicators of H pylori infection.     

Comparative diagnostic value of phenyla-lanine challenge and phenylalanine hydroxylase activity in phenylketonuria

Serum phenylalanine (phe) concentrations during and following phe challenges and liver phenylalanine hydroxylase (PH) activity were compared in 13 phenylketonuric (PKU) patients. These patients were separated into two groups: eight patients with no detectable PH activity (PH°) and five patients with residual PH activity (PH^-) ranging from 9 to 24% of the activity obtained in 10 non-PKU subjects. The rise in serum phe concentration during 3 days of oral loading did not differentiate the two groups. However, the difference in serum phe concentration of the PH° and PH^- groups reached statistical significance at 24 h postloading (p<0.01). We concluded that combined results from multiple measurements during the oral challenge, namely serum phe concentration after termination of loading, serum phe clearance rate, post-loading phe tolerance index and urinary metabolite excretion, make a better indicator for predicting residual PH activity for the majority of PKU subjects than peak phe concentrations during phe challenge.     

The increased gastroprotective effect of pioglitazone in cholestatic rats: role of nitric oxide and tumour necrosis factor alpha

The prevalence of gastric ulcers is high in cholestatic patients, but the exact mechanism of this increased frequency remains uncertain. It has been shown that pioglitazone accelerates the healing of pre‐existing gastric ulcers. The present study was designed to investigate the effect of pioglitazone, on the gastric mucosal lesions in cholestatic rats. Cholestasis was induced by surgical ligation of common bile duct and sham‐operated rats served as control. Different groups of sham and cholestatic animals received solvent or pioglitazone (5, 15, 30 mg/kg) for 7 days. On the day eight rats were killed after oral ethanol administration and the area of gastric lesions was measured. The serums of rats were also collected to determine serum levels of tumour necrosis factor alpha (TNF‐α), IL‐1β and bilirubin. The ethanol‐induced gastric mucosal damage was significantly more severe in cholestatic rats than sham‐operated ones. Pretreatment with pioglitazone dose‐dependently attenuated gastric lesions induced by ethanol in both sham and cholestatic rats, but this effect was more prominent in cholestatic ones. The effect of pioglitazone was associated with a significant fall in serum levels of TNF‐α in cholestatic rats. L‐NAME, a non‐selective nitric oxide synthase (NOS) inhibitor, and decreased pioglitazone‐induced gastroprotective effect in cholestatic rats, while aminoguanidine, a selective inducible NOS inhibitor, potentiated pioglitazone‐induced gastroprotective effect in the cholestatic rats. Chronic treatment with pioglitazone exerts an enhanced gastroprotective effect on the stomach ulcers of cholestatic rats compared to sham rats probably due to constitutive NOS induction and/or inducible NOS inhibition and attenuating release of TNF‐α.