细胞坏死

xì bāo huài sǐ
  • cell necrosis;cellular necrosis;necrocytosis;meronecrosis
细胞坏死细胞坏死
  1. 肝内HBVdna与血清HBV复制标志及肝细胞坏死关系的探讨

    The implication of cytoplasmic HBV-DNA : HBV replication and hepatic cell necrosis

  2. 肿瘤细胞坏死因子(TNF)含量也明显大于对照组(0.02

    The number of tumor cell necrosis factor ( TNF ) is greater than that of control group ( 0.02

  3. 和田当地的医生告知小孩父亲,手术需要在6小时之内完成,否则细胞坏死后将无法治疗。医院的骨科医生检查完手臂后,建议由于伤势严重,需要将手臂切断,然后再复位,将骨片正确对齐,否则孩子将终身残疾。

    After the orthopedists in the hospital examined the arm , they suggested that as the injury was so severe that the arm would need to be severed the bone fragments , otherwise the child would be disabled for life .

  4. 外源性bFGF明显抑制颅脑损伤后神经细胞坏死、凋亡过程。

    Exogenous bFGF could prevent the neurons necrosis and apoptosis obviously .

  5. 目的:探讨T淋巴细胞在中毒性表皮坏死松解症(TEN)早期角质形成细胞坏死中的作用。

    Objective : To investigate the role of T lymphocytes in the pathogenesis of early keratinocyte necrosis in toxic epidermal necrolysis ( TEN ) .

  6. 降脂、抗凝药物预防激素所致股骨头骨细胞坏死、凋亡及对Bcl-2表达的影响

    Study on Antilipemic and Anticoagulant Preventing Necrosis and Apoptosis of Osteocytes in Steroid-induced Osteonecrosis of the Femoral Head

  7. TNF-α(1000ng/ml)诱导K562细胞坏死。

    TNF α( 1 000 ng / ml ) induced K 562 cells ' necrosis .

  8. 背景:心肌梗死(myocardialinfarction,MI)是心肌严重缺血所导致的心肌细胞坏死。

    Introduction : Myocardial infarction ( myocardial infarction , MI ) is necrosis of the myocardium as a result of severe ischaemia .

  9. 重型乙型病毒性肝炎患者血清IL-1、IL-6、TNF-α水平与肝细胞坏死程度密切相关,检测血清中IL-1、IL-6、TNF-α对判断病情危重程度和预后有重要意义。

    Detect serum IL-1 , IL-6 and TNF - α is helpful for judging the degree hepatitis and its prognosis .

  10. IL-6可以反映肝细胞坏死程度,可以作为判断肝功能的又一实验室指标。

    IL-6 level can reflect the hepatocellular necrosis degree and can be used as a laboratory marker to determine the liver function .

  11. 结论新生大鼠HI迟发性神经元死亡中,不仅存在细胞坏死和细胞凋亡,而且还存在III型细胞死亡。

    Conclusions The type III cell death was mainly involved in the delayed cell death following HI injury in addition to the necrosis and apoptosis .

  12. 瞬间表达的研究结果表明,ROS能够被外源的乙烯和ACC诱导,持续的乙烯刺激和应用高浓度的ACC能够导致细胞坏死并伴随着ROS的产生。

    Ethylene-sustainable stimulation and high concentration ACC application could cause necrotic cell death accompanied by ROS generation on transient expression .

  13. 结果:心肌缺血再灌注后心肌梗死范围明显,血浆CK活性增高,心肌细胞坏死增多。

    Results : Myocardial infarct size enlarged and serum CK level elevated and the number of myocyte necrotic cell in creased in MIR group .

  14. 脑缺血24h,脑损伤侧梗死区内广泛细胞坏死,部分细胞自溶;

    After 24 hours , many cells necrosis in the infarction area of the injured side were found , part of cells autolysis ;

  15. 3研究超声辐射微泡剂引起小鼠H22腹水瘤细胞坏死的效应。

    To study the biological effects of tumor cell necrosis by ultrasound irradiation microbubble agent .

  16. 病理学检查结果表明浕-MSH可以减轻LPS引起的肝脏、脾脏及肺脏瘀血及细胞坏死。

    The results of pathologic inspection showed that α - MSH could lighten the blood stasis and the cytonecrosis of livers , spleens or lungs caused by LPS .

  17. 软骨细胞坏死,早期化骨是大骨节病(KBD)病因发病机制的核心。

    The cartilage necrosis , early ossification were the core of pathogenic mechanism in Kaschin-Beck disease ( KBD ) .

  18. 结论TNFα、IL6和NO水平与肝细胞坏死程度、内毒素血症和自发性细菌性腹膜炎肾损害(SBPRI)密切相关。

    Conclusion The results showed TNF - α, IL-6 and NO were closely associated with the degree of hepatocyte necrosis , endotoxemia and SBP-RI .

  19. 体内实验中,DHA高、中剂量组主要引起H22癌细胞坏死,低剂量组主要诱导细胞凋亡。

    In vivo higher or medium dose of DHA compound mainly caused H 22 cells necrosis and the lower dose mainly induced apoptosis .

  20. 5%酒精作用30h则可引起细胞坏死。

    5 % alcohol may cause necrosis .

  21. 结论EPO能够显著降低脑组织含水量,抑制脑水肿,缩小脑梗死体积及减少神经细胞坏死,对脑缺血再灌注损伤有良好的保护作用。

    Conclusion EPO could reduce the neurons necrosis and the cerebral infarction volume and decrease the cerebral water content . So EPO has a protective effect on ischemia-reperfusion injury .

  22. 结果表明,TnT可以作为判定心肌细胞坏死程度及左室功能障碍的良好指标,优于传统心肌酶学测定。

    These results show that TnT may be a more useful and valuable indicator than cardiac enzymes in evaluating the degree of myocardial cell damage and the function of left cardiac ventricle .

  23. 目的通过对9例小儿组织细胞坏死性淋巴结炎(HNL)进行总结分析,探讨其诊断和治疗方法。

    Objective To summary 9 cases of histiocytic necrotizing lymphadenitis ( HNL ) of children and discuss the diagnosis and therapy .

  24. 分离、鉴定蛋白质有益和有害的功能区域,更有利于我们将harpin相关蛋白应用于农作物,而不产生诸如细胞坏死之类的负面效应。

    Identification of beneficial and deleterious regions might facilitate the advantageous use of harpin-related proteins on crops without causing negative effects like cell death .

  25. 经皮乙醇注射(PEI)可导致肝癌细胞坏死从而减少肝癌细胞数,坏死的瘤体形成自身瘤苗可以诱导机体产生抗肝癌免疫反应。

    Percutaneous ethanol injection ( PEI ) can induce the hepatoma cells necrosis , and thus can reduce the number of the tumor cells and self-tumor vaccines help the organism generate immune responses against hepatocellular carcinoma .

  26. 光镜下检查显示,BDL组及PTX组均可见肝细胞坏死及增生,汇管区可见胆管扩张、胆汁淤积,肝坏死程度以BDL组为重。

    Microscope examination showed that liver cell necrosis was heavier in BDL group than that in PTX group . Bile was filled up in bile duck in both group .

  27. Harpin蛋白是由植物病原菌hrp基因编码的非特异性蛋白激发子,能够激发非寄主植物的过敏性细胞坏死,诱导植物抗病。

    Harpin protein is nonspecific protein elicitor coded by hrp genes of plant pathogen , and it can elicit hypersensitive cell death ( HCD ) in nonhost plants and induce resistance to pathogens in many plants .

  28. 乙型肝炎病毒(HBV)所致的肝细胞坏死,被认为是与人类白细胞抗原(HLA)有关的MHC限制的T细胞为主的免疫应答的结果。

    Hepatocellular injury during hepatitis B virus ( HBV ) infection is postulated ^ to result from an human leucocyte antigen ( HLA ) restricted T-cell host immune response against HBV antigens . However , it is not known if HBV itself can induce HLA expression on infected hepatocytes .

  29. 结论:dti技术与体视学对照分析,能提供急性心肌缺血、心肌梗死发生后在不同时间内心肌细胞坏死的动态变化规律,为临床早期评价局部心肌缺血及功能异常提供可靠依据。

    Conclusions : comparative analysis with DTI and stereology can provide the rule of the dynamic changes in the necrosis of myocytes during different time after ami ; and can provide the theory accordant with clinical evaluating local myocytic ischemia and abnormal function .

  30. 结果A组注药后48h血清天冬氨酸氨基转移酶、总胆红素、血氨和凝血酶原时间达最高峰,1周年生存率为17%,肝脏病理检查显示大量肝细胞坏死伴出血。

    Results In group A , the level of aspartate transaminase , total bilirubin , ammonia and prothrombin time reached to peak at 48h , and the 7-day survival rate was only 17 % . The postmortem liver specimens showed a severe hepatocellular necrosis with hemorrhage .