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81.
82.
目的:探讨丙种球蛋白(IVIG)和不同剂量维生素C(VitC)对实验性自身免疫性心肌炎(EAM)的保护作用。方法:Balb/c小鼠52只,随机分为6组:空白组不予任何处理;其余小鼠分别于第1天和第7天在双测腹股沟皮下注射充分乳化的猪心肌肌凝蛋白,剂量为每次每只100μg;从免疫的当天开始给每只小鼠腹腔注射所给药物。小剂量VitC组:150mg/kg·d^-1 VitC;大剂量VitC组:300mg/kg·d^-1 VitC;IVIG组:1g/kg·d^-1 IVIG;IVIG+VitC组:1g/kg·d^-1 IVIG和150mg/kg·d^-1 VitC;对照组:与干预组等量的生理盐水。小鼠于第21天给予称重,麻醉后处死,并摘眼球取血,用Elisa法测定血清肿瘤坏死因子α(TNF—α)水平;取心脏、脾脏和肾脏分别称重,得心脏、脾脏和肾脏与体重之比(C/W、S/W、R/W);脾脏在肉眼观察后作病理切片和H—E染色。心脏分为三部分:一部分作病理切片和H—E染色,一部分作冰冻切片,在荧光显微镜下用直接免疫荧光法测定心肌组织中沉积的IgG水平,一部分作电镜检查。结果:(1)心脏的病理改变:大、小剂量VitC组心肌炎性细胞的浸润及心包钙化有所减轻;IVIG组和IVIG+VitC组心肌偶有淋巴细胞浸润,无心包钙化。(2)脾脏的病理改变:除空白组外,其余脾脏均明显增大,IVIG组和IVIG+VitC组更是明显,镜检表现为红髓充血和白髓增生。(3)心脏、脾脏、肾脏与体重之比:各干预组C/W明显低于对照组;各干预组和对照组S/W明显高于空白组,IVIG组和IVIG+VitC组S/W明显高于大、小剂量VitC组;R/W各组无差异。(4)TNF—α水平:大、小剂量VitC组的TNF—α水平略低于对照组,IVIG组和IVIG+VitC组的TNF—α水平明显低于对照组。(5)心肌的免疫荧光检测:对照组比较粗的荧光条带主要集中在心肌间质,大、小剂量VitC组荧光的密度和强度有所降低,而IVIG组和IVIG+VitC组的荧光条带增宽,在心肌间质中呈宽大的条索状分布,亮度明显增强。(6)心肌的电镜检测:对照组心肌肌丝排列紊乱,肌节断裂严重,线粒体肥大,并出现空泡变性;大、小剂量VitC组病变比对照组有所减轻;IVIG组和IVIG+VitC组肌丝排列紊乱明显减轻,肌节断裂比对照组减少,线粒体基本正常。结论:IVIG和VitC对EAM都有一定的保护作用,可以减轻心脏的病理改变,抑制TNF—α的产生;但IVIG或IVIG+VitC作用更为明显,并可刺激机体的免疫反应,增加心肌中IgG的沉积。 相似文献
83.
表皮生长因子与肿瘤坏死因子在胸腔积液中的表达 总被引:1,自引:0,他引:1
采用RIA法对58例良、恶性胸腔积液中EGF与TNF进行含量检测。结果显示22例良性胸水中EGF与TNF含量分别为2.03±0.35μg/L,1.63±0.54μg/L。36例恶性胸水中EGF与TNF含量分别为1.25±0.32μg/L,1.02±0.24μg/L。良性胸水组EGF与TNF浓度均明显高于恶性胸水组,两组间有显著性差异,(P<0.05)。结果表明EGF与TNF均参与了良、恶性胸腔积液的免疫病理生理过程。 相似文献
84.
行坏死肠管切除小肠单口造瘘术,延期行肠吻合术治疗重症小儿肠坏死10例。待病儿休克纠正后,再做Ⅱ期肠吻合术,此术式可及早缓解腹胀,减轻中毒症状,有利于休克纠正,未出现大量肠液丢失及切口裂开等并发症。 相似文献
85.
Oxidative stress, mitochondrial permeability transition, and cell death in Cu-exposed trout hepatocytes 总被引:11,自引:0,他引:11
We have previously shown that, in trout hepatocytes, exposure to a high dose of copper (Cu) leads to disruption of Ca(2+) homeostasis and elevated formation of reactive oxygen species (ROS), with the latter ultimately causing cell death. In the present study, we aimed at identifying, using a lower Cu concentration, the role of mitochondria in this scenario, the potential involvement of the mitochondrial permeability transition (MPT), and the mode of cell death induced by the metal. Incubation with 10 muM Cu resulted in a strong stimulation of ROS formation, and after 2 h of exposure a significant increase of both apoptotic and necrotic cells was seen. Co-incubation of Cu-treated hepatocytes with the iron-chelator deferoxamine significantly inhibited ROS production and completely prevented cell death. The origin of the radicals generated was at least partly mitochondrial, as visualized by confocal laser scanning microscopy. Furthermore, ROS production was diminished by inhibition of mitochondrial respiration, but since this also aggravated the elevation of intracellular Ca(2+) induced by Cu, it did not preserve cell viability. In a sub-population of cells, Cu induced a decrease of mitochondrial membrane potential and occurrence of the MPT. Cyclosporin A, which did not inhibit ROS formation, prevented the onset of the MPT and inhibited apoptotic, but not necrotic, cell death. Cu-induced apoptosis therefore appears to be dependent on induction of the MPT, but the prominent contribution of mitochondria to ROS generation also suggests an important role of mitochondria in necrotic cell death. 相似文献
86.
BACKGROUND: Identifying factors that can contribute to a better understanding of tumor progression in stage III colon cancer patients continues to be an important task. Necrotic changes in metastatic lymph nodes have not been previously analyzed in English literature. METHODS: The study included 48 consecutive colon and rectosigmoid cancer patients with stage III disease who underwent radical surgery. After reviewing the diagnostic slides, a pathologist developed a scale describing the extent of necrotic changes. Results were evaluated using Kaplan-Meier method and log-rank test. RESULTS: Thirty-four (70%) patients had necrotic changes in metastatic lymph nodes. Patients with necrotic changes in metastatic lymph nodes had more risk factors than patients without necrosis. The 5-year survival rate for patients with necrotic changes in metastatic lymph nodes was 85% and for patients without necrosis was 50% (P = 0.02). CONCLUSIONS: The survival of patients with necrotic changes in metastatic lymph nodes was higher (P = 0.02). These necrotic changes can help us to understand body-tumor relations. 相似文献
87.
Remes-Troche JM Duarte-Rojo A Morales G Robles-Díaz G 《World journal of gastroenterology : WJG》2005,11(44):7018-7023
AIM: To determine whether the hematocrit (Hct) at admission or at 24 h after admission was associated with severe acute pancreatitis (AP), organ failure (OF), and pancreatic necrosis. METHODS: A total of 336 consecutive patients with a first AP episode were studied. Etiology, Hct values at admission and at 24 h, development of severe AP according to Atlanta's criteria, pancreatic necrosis, OF and mortality were recorded. Hemoconcentration was defined as Hct level >44% for males and >40% for females. The t-test and X2 test were used to assess the association of hemoconcentration to the severity, necrosis and OF. Diagnostic accuracy was also determined. RESULTS: Biliary disease was the most frequent etiology (n = 148). Mean Hct levels at admission were 41±6% for females and 46±7% for males (P<0.01). Seventy-eight (23%) patients had severe AP, and OF developed in 45 (13%) patients. According to contrast-enhanced computed tomography scan, 36% (54/150) patients showed pancreatic necrosis. Hct levels were elevated in 58% (55/96) and 61% (33/54) patients with interstitial and necrotizing pancreatitis, respectively. Neither Hct levels at admission nor hemoconcentration at 24 h were associated with the severity, necrosis or OF. Sensitivity, specificity and positive predictive values for both determinations were very low; and negative predictive values were between 61% and 86%, being the highest value for OF. CONCLUSION: Hct is not a useful marker to predict a worse outcome in acute pancreatitis. In spite of the high negative predictive value of hemoconcentration, the prognosis gain is limited due to an already high incidence of mild disease. 相似文献
88.
Summary Chandipura virus was inoculated intraperitoneally into 9-day old mice. Rising viral titers were detected in blood, skeletal muscle and viscera, beginning 3 to 6 h post-inoculation. Significant quantities of virus were initially noted in the brain at 24 h, and titers in that region rose precipitously during the succeeding 72 h. Detectable clinical signs, including neurologic dysfunctions began 48 h post-inoculation. Death was common at 72 and 96 h. The most significant and consistently observed lesions were in the central nervous system and included necrosis of neurons and ependymal cells.Supported by U.S. Public Health Service Grants PHS-FR-05358-08 and PHS 2 PO 6 RR 00393. 相似文献
89.
Grossmayer GE Munoz LE Gaipl US Franz S Sheriff A Voll RE Kalden JR Herrmann M 《Modern rheumatology / the Japan Rheumatism Association》2005,15(6):383-390
Systemic lupus erythematosus (SLE) is a very heterogeneous systemic autoimmune disease, in which autoantibody synthesis against
nuclear constituents is the main immunological characteristic. These autoantibodies underwent affinity maturation and isotype
switching. Additionally, T-cell tolerance against nuclear autoantigens should be affected in these autoimmune patients. Nuclear
material derived from apoptotic and/or necrotic cells may serve as an important source of autoantigens. However, dead and
dying cells as well as cellular debris are rapidly removed from tissues by phagocytes without eliciting inflammation or immune
responses under healthy conditions. During apoptosis nuclear components are strongly modified through enzymatic reactions.
If these cells are not timely cleared, those autoantigens may be released, taken up, and presented by dendritic cells in tissues
or presented by follicular dendritic cells in lymph nodes to T and B cells, respectively. This could be a mechanism for breaking
the peripheral self-tolerance. In this article we focus on the deficient clearance of apoptotic cells in SLE patients and
its importance in development of this autoimmune disease.
G.E.G. and L.E.M. contributed equally to this work 相似文献
90.
Necrotic cells are generally considered to stimulate inflammation, whereas apoptotic cells should not. However, apoptotic cells have pro-inflammatory properties since they can activate complement. To what extent this activation compares to that by necrotic cells is not known. We compared complement activation by necrotic cells and apoptotic cells in plasma. Jurkat cells were made apoptotic or necrotic by incubation with etoposide or by heat shock, respectively. Cells incubated in recalcified plasma were tested for C3 and C4 fixation and fluid phase generation of complement activation products. Fixation of C3 and C4 to necrotic cells occurred mainly via the classical pathway, independent from the method of necrosis induction and the cell type. Depletion of IgM from plasma almost completely abrogated complement fixation by necrotic cells, which was restored by supplementation with purified IgM. Complement activation by late apoptotic cells was comparable to that by necrotic cells regarding the extent and dependence on IgM. Moreover, incubation of plasma with necrotic or late apoptotic cells led to the generation of comparable amounts of complement activation products. These results indicate that late apoptotic and necrotic cells employ similar complement activation mechanisms in the plasma environment. 相似文献