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内毒

nèi dú
  • Endotoxin;endogenous toxic material
内毒内毒
内毒[nèi dú]
  1. 肺表面活性蛋白A、B在内毒素性急性肺损伤时变化的研究

    Changes of Surfactant Proteins A and B After Lipopolysaccharide-Induced Acute Lung Injury in Rats

  2. 异丙嗪对家兔内毒素性发热及血清SOD和MDA含量的影响

    Effect of promethazine on endotoxic fever and contents of superoxide dismutase and malondialdehyde in rabbits serum

  3. Fas在内毒素致大鼠肝细胞凋亡中的作用

    Effect of Fas on endotoxin-induced hepatocyte apoptosis in rat

  4. 湛江市静脉内毒瘾者感染HCV和肝功能分析

    AN Analysis of HCV Infection and ALT Alteration in Intravenous Drug Addicts in Zhanjiang City

  5. 目的研究亲和免疫吸附清除循环肿瘤坏死因子(TNF)对内毒素性急性肺损伤动物的保护作用。

    Objective To study the protective effect of removing circulatory TNF by immunoadsorption on endotoxin induced acute lung injury in rabbits .

  6. 肝星形细胞CD14表达变化在内毒素肝损伤中的作用

    Dynamic Expression of CD14 on Kupffer Cells in Endotoxin-induced Hepatic Injury

  7. 内毒素性发热家兔血浆、不同脑区组织cAMP含量的变化及电针的影响

    The cAMP levels of the plasma and the different tissues of different brain regions in ET-induced fever in rabbits with the influence of the electric acupuncture

  8. 目的:观察大黄对家兔内毒素性急性肺损伤(ALI)的保护作用。

    Objective : To observe the protective effect of rhubarb on lipopolysaccharide induced acute lung injury ( ALI ) in rabbits .

  9. 目的观察肿瘤坏死因子(TNFα)在内毒素血症大鼠急性肝损伤中的作用及抗肿瘤坏死因子单抗(antiTNFαMcAb)保护效应。

    Objective To observe the effect of TNF α on acute liver injury in rats with endotoxemia and the protective effect of anti TNF α McAb .

  10. 吸入一氧化碳对内毒素性急性肺损伤大鼠肺组织TNF-α和IL-10表达的影响及意义

    Effects of carbon monoxide inhalation on the expression of TNF - α and IL-10 in rats with acute lung injury induced by lipopolysaccharide

  11. PAF受体拮抗剂SRI63-411可抑制内毒素引起的PLA2活性升高,减轻内毒素性低血压和肺损伤。

    Pretreatment with PAF receptor antagonist SRI 63-441 blocked the increase in PLA , activity and attenuated endotoxin-induced hypotension and acute lung injury .

  12. 在失血性与内毒性休克家兔中,利用免疫单扩和双扩法分别测定家兔休克前后不同时间血浆内Fn含量。

    The changes of plasma Fn content in rabbits of hemorrhagic and endotoxic shock has been assayed by means of single and double immunodiffusion tests .

  13. 已有研究表明,ALI本质是一种炎症;多种炎症介质和细胞因子在内毒素性ALI病理过程中发挥着关键作用。

    The previous studies had indicated that ALI is a kind of inflammation , in which many inflammation mediators and cytokines play key roles in the pathological process .

  14. 目的:观察异丙嗪对家兔内毒素性发热及血清超氧化物歧化酶(SOD)和脂质过氧化物丙二醛(MDA)含量的影响。

    AIM and METHOD : The effects of intravenous injection of endotoxin ( ET ) and promethazine ( PMZ ) on superoxide dismutase ( SOD ) and malondialdehyde ( MDA ) in serum were studied .

  15. 结论:PTX对内毒素性ALI的保护作用可能与其抑制肺组织iNOS活性和减少NO生成有关。

    Conclusion : The protection of PTX on endotoxin induced lung injury is related to the inhibition on iNOS activity and NO lever in rat lungs .

  16. 亚临床HRS在内毒素血症、利尿过度、消化道出血等诱因作用下,很快即发展为HRS。

    The subclinical HRS will soon develop to be the HRS when it is affected by the endotoxemia , excess diuresis and the bleeding-out of the digestive tract .

  17. 结果LDH活性在内毒素达到0.4μg/ml并作用12小时后才有显著升高(P<0.05),而6-酮-PGF1a含量在各组内毒素损伤中变化均不显著。

    The HUVECs morphologic changes were also observed with microscope and scanning electron microscope . Results The LDH activity in medium increased obviously when the endotoxin reached 0.4 μ g / ml and incubated over 12 hours ( P 0.05 ) .

  18. TNF-α和CINC在内毒素耐受大鼠肺部炎症中的动态变化

    Pulmonary TNF - α Production and CINC mRNA Expression During LPS-initiated Lung Inflammation in Endotoxin Tolerant Rats

  19. 方法:在内毒素刺激人THP-1细胞分泌细胞因子TNF-α模型上,观察合成肽、多黏菌素B、合成肽和多黏菌素B对内毒素激活THP-1细胞的影响。

    METHODS : By model of LPS-induced TNF - α secretion in human THP-1 cells , the affects of anti-endotoxin capability of the peptide , polymyxin B , and the peptide plus polymyxin B were examined .

  20. 模拟肽可改善内毒素性ALI大鼠的氧合,减轻肺损伤,其减少大鼠肺泡巨噬细胞与LPS的结合可能是对大鼠内毒素性ALI保护作用的机制之一。

    The mimic peptide improves oxygenation and attenuates lung injury in rats . It inhibits the conjugation between LPS and alveolar macrophages , suggesting that the mimic peptide could protect rats from endotoxin-induced ALI .

  21. 本研究旨在观察IL10对肺泡巨噬细胞(AM)、清道夫受体(SR)、CD14表达的影响,探讨IL10在内毒素血症时防止AM由免疫防御向炎症效应转变中的作用。

    To study the effects of IL 10 on expression of CD14 and scavenger receptor ( SR ) in alveolar macrophages ( AM ) .

  22. IRAK-M在内毒素耐受形成机制中作用的实验研究

    The Role of IRAK-M in the Development Mechanisms of Endotoxin Tolerance

  23. 结论内毒素性休克大鼠α1-AR的基因表达普遍下调,抗氧化剂的抗休克作用机制与α1-AR基因表达上调有关。

    The therapeutic effects of antioxidant on the endotoxic shock is partly due to up-regulation of α 1-AR gene expression .

  24. 表明内毒素致伤后,体内尤其是肺内合成TXA2和PGI2增加,在内毒素肺损伤的反应中具有重要作用。

    The results indicated that TXA2 and-PGI2 synthesis increased in the lung after injury and that TXA2 and PGI2 were important media in the lung injury .

  25. 结论肺组织HO-1表达增强是内毒素性ALI的重要应激保护机制,赤芍对内毒素性ALI的防治作用可能与诱导HO-1的表达和抑制肺组织iNOS异常高表达有关。

    Conclusion High expression of HO-1 is important stress protective mechanism . While protective effect of RPR on LPS-induced ALI is related to the inhibition of iNOS expression and the inducement of HO-1 expression .

  26. 目的:观察赤芍对内毒素性急性肺损伤(ALI)时肺iNOS和eNOS表达的影响,并探讨其保护作用机制。

    Objective : To investigate the effect of Radix Paeoniae Rubra ( RPR ) on expression of iNOS and eNOS in lipopolysaccharide-induced acute lung injury ( ALI ) and to explore it 's protective mechanism .

  27. 二苯羟乙酸-3-喹咛环酯(QNB)等与大白鼠脑内毒蕈碱样乙酰胆碱受体的作用

    The binding activity of quinuclidinyl benzilate ( qnb ) and some cholinergic agents on muscarinic cholinergic receptor in rat brain

  28. 结论LPS在体内外对Akt蛋白磷酸化作用不同,体外Akt蛋白磷酸化水平增高,但在内毒素血症小鼠体内出现Akt蛋白磷酸化水平异常减低。

    Conclusion The phosphorylation level of Akt protein is different after LPS attack in vitro and in vivo . The Akt protein phosphorylation is increased obviously in vitro , but decreased in mice model of endotoxemia .

  29. 结果脑热清对家兔内毒素性发热有显著的解热作用(P001),能够明显降低下丘脑中IL1β及cAMP的含量(P001)。

    Results NOS showed marked antipyretic effects on the endotoxin-induced fever ( P0.01 ) and remarkably decreased the contents of IL-1 and cAMP in the hypothalamus ( P0.01 ) .

  30. 结论IL-1β与TNF-α是脑缺血级联反应的重要环节,参与了脑缺血病理损害,其动态变化和毒性效应体现了内毒形成及作用过程。

    Conclusion The expressions of IL1 β and TNF - α are the important points of cascade reaction of cerebral ischemia . They are involved in the pathological lesion of cerebral ischemia and their dynamic changes and toxic effects reflect the formation and actions of endogenetic toxins .