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神经毒性
    group B 26 cases, nerve toxicity of 1~3 grade occurred in 9,4,3 cases respectively ,develop ratc was 61.5%.
    3级1例,总发生率28.5%。 B组26例,发生神经毒性1级9例;
    Study on Nerve Toxicity and Oxidation Damage to Antioxidant Defenses of Mice Induced by Pentachloronitrobenzene (PCNB)
    五氯硝基苯对小鼠的神经毒性和抗氧化防御系统损伤研究
    Conclusion GIK can lighten the nerve toxicity of Glu,Asp and NO,and protect on the ischemic organisation.
    应用GIK后较缺血组有明显降低。 结论GIK能减轻Glu、Asp、NO的神经毒性,起到对缺血脑组织的保护作用。
    The diversity of the two groups’(Ⅰ,Ⅱ) perisensory nerve toxicity is also obvious. 62.9 percent toxicity group and 31.6 percent of HCPT group appear the toxicity (P< 0.05), but the diversity of adverse reaction is not obvious (P> 0.05).
    毒副反应两组Ⅰ~II外周神经毒性有显著性差异,Oxaliplatin组为62.9%,HCPT组为31.6%(P<0.05),其他毒副反应的差异无显著性(P>0.05)。
    Clincal observation of the prevention and treatment of the nerve toxicity by combining potassium aspartate and magnesium aspartate and calcium gluconate
    门冬氨酸钾镁与葡萄糖酸钙联用防治奥沙利铂神经毒性的临床观察
    Conclusion:QiLeng decoction plays the nerve protective effect by reducing the nerve toxicity of EAA, the content of NO and the activity of iNOS, and increasing the expression of Hsp70. It is maybe the mechanism of benef itvital energy (BVE), nourishing yin (NY), activating blood circulation (ABC) treating ischemic stroke.
    芪棱汤通过降低兴奋性氨基酸(excitatory amino acid,EAA)神经毒性和NO含量,降低iNOS活性,增加Hsp70的蛋白表达,发挥神经保护作用,可能是益气养阴活血法改善缺血性中风的作用机理。
    This paper selected disinfectant pentachloronitrobenzene (PCNB) as research object,studied its nerve toxicity and the damage on oxidize defend system on mice withacetylcholinesterase(AChE), catalase(CAT), acetylcholine(ACh) and lipid peroxidation(LPO)at the molecular level of toxicity. Moreover, this paper tried to probe into the effectmechanisms of its nerve toxicity and oxidation damage, which provided the basis for the fullyestimate of ecological toxicology on mammals.
    本文以有机氯杀菌剂五氯硝基苯(PCNB)为研究对象,从分子毒理学水平,以乙酰胆碱酯酶(AChE)、过氧化氢酶(CAT)、乙酰胆碱(ACh)和脂质过氧化(LPO)为指标,研究了 PCNB 对小鼠的神经毒性和抗氧化防御系统损伤作用,并对 PCNB 致神经毒性和氧化损伤的毒作用机理进行了初步探讨,为全面评价 PCNB 对哺乳动物的生态毒理效应提供科学依据。
    The results showedthat with the concentration increasing, the activities of CAT in brain descended, the level ofACh in liver had a tendency to increase, and showed an evident dependence on dose and time,indicated that PCNB had nerve toxicity.
    研究结果表明,随着染毒剂量的增加,小鼠脑乙酰胆碱酯酶活性不断降低,肝乙酰胆碱含量总体上呈升高趋势,并表现为明显的剂量和时间依赖性,说明 PCNB 对神经递质乙酰胆碱产生了作用,表明其可能具有神经毒性;
    WBC and PLT occurred in a rate of 37%? 76.6% and 33.3% respectively,side effect mostly including nausea, vomiting, constipation,bellyache, nerve toxicity,phlebitis,alopecia, skin rash, fever,oral sore of mucous membrane,damage of liver and kidney function. Conclusion A better response rate is obtained by combination chemotherapy with NVB for treating the advanced tumor,including NSCLC?
    血红蛋白减少发生率为 37% ,白细胞为 76 .6 % ,血小板为 33.3% ,恶心呕吐发生率为 70 % ,便秘为 5 6 .6 % ,腹痛为 16 .6 % ,神经毒性为 13.3% ,静脉炎为30 % ,脱发为 33.4% ,皮疹为 6 .6 % ,发热为 10 % ,口腔黏膜溃疡为 10 % ,肝功损害为 13.3% ,肾功损害为 6 .6 %。
    Conclusion The results confirmed profoundly that aluminum had nerve toxicity and might play an important role in increasing the risk of GVD,and suggested that nerve toxicity might be related to the number decreasing and structure changing of neurons due to the dosage of aluminum.
    结论 本实验结果进一步证实了铝的神经毒性 ,其中海马GVD可能起重要作用 ,并提示该毒性与铝导致神经细胞结构改变及细胞数减少有关
    Conclusion:PCB had strong nerve toxicity to hippocampal neuronic cells.
    结论 :PCB对海马神经元细胞可产生明显的神经毒性
    The main side effects were myelosppression, GI and peripheral nerve toxicity and phlebitis.
    腺癌疗效比鳞癌稍好 ,主要毒副反应为骨髓抑制、消化道反应、周围神经毒性及静脉炎。
    The major toxicity included nerve toxicity,neutropenia,nausea vomiting and mucositis.
    主要不良反应为神经毒性 ,骨髓抑制 ,恶心 /呕吐 ,腹泻 ,粘膜炎等。
    Also, nerve toxicity induced by exceeding NO during stress may be one of the causes of damage to neurons in the limbic system of the stressed rats.
    应激过程中大鼠脑边缘系统过量增多的NO产生的神经毒性可能是应激导致大鼠脑边缘系统神经元受损的原因之一
    The main toxic reaction showed slight sensory nerve toxicity, marrow restraint and gastrointestinal reactions.
    主要毒性反应为感觉神经毒性、骨髓抑制和胃肠道反应,均较轻微。
    Conclusions:The inhibitory effect on 20s proteasome activity may play a role in the nerve toxicity which induced by manganese.
    结论:蛋白酶体20s活性的抑制可能在锰所诱导的神经毒性过程中发挥着一定的作用。
    The major toxicity included bone suppression,gastrointestinal reaction,nerve toxicity and phlebitis.
    主要毒性有骨髓抑制、消化道反应、神经毒性、静脉炎。
    The major side-effects included nerve toxicity,nausea/vomiting,neutropenia,mucositis and losing hair et al.
    主要不良反应为神经毒性、恶心/呕吐、腹泻、黏膜炎、脱发等。
    The main side effects were myelosuppresion,gastrointestinal reation and peripheral nerve toxicity and phlebitis.
    主要毒副反应为骨髓抑制、胃肠道反应、周围神经毒性及静脉炎。
    Less patients of oxaliplatin group developed nausea and vomiting than the patients of cisplatin group and nerve toxicity was stronger in oxaliplatin group than in cisplatin group(P<0.05).
    奥铂组恶心、呕吐发生低于顺铂组,奥铂组神经毒性明显高于顺铂组,而且比较差异有显著性(P<0.05)。
 

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