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浅谈细胞保护和细胞凋亡 总被引:2,自引:0,他引:2
细胞作为生物体形态结构和生理机能的基本单位,它的发生、增殖、分化、衰老和死亡是多细胞生物体生存和发展的基础。细胞保护和细胞凋亡作为细胞正常生命活动机制,广泛存在于生物体中,对细胞自身结构的完整性和机体的稳定性来说都具有十分重要的意义。 1 细胞保护 细胞保护系指细胞分泌的某些物质或其某些结构具有防止或减轻有害物质对机体细胞损伤和导致坏死作用的一种能力,对它的研究虽起步比较晚,但它作为生命科学中极其重要的研究领域之一,引起了广泛关注。目前已发现某些胃肠肽类激素对胃肠粘膜细胞、胰腺内外分泌细胞和肝细胞… 相似文献
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护理本科专业的人才培养目标是培养具有临床护理能力和初步的护理管理、护理科研、护理教育能力的高素质应用型人才.为了培养护生的科研素质,在我国许多医学院校开设了<医学信息检索>、<护理科研方法>、<毕业论文设计>等课程,在护生的自学能力、信息检索技能、科研创新能力的培养过程中发挥着重要的作用. 相似文献
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目的 观察小鼠海马不饱和脂肪酸含量变化,分析其在铅致小鼠学习记忆能力受损可能机制中的作用.方法 48只ICR小鼠分为4组,分别饮用0.625、1.250、2.500 g/L醋酸铅溶液50 d,同时设立对照组(饮用去离子水),水迷宫法测定小鼠学习记忆能力后,颈椎脱臼处死,取海马,高效液相色谱法测定小鼠海马中油酸(C18:1)、亚油酸(C18:2)、亚麻酸(C18:3)、花生四烯酸(C20:4,AA)、二十碳五烯酸(C20:5,EPA)和二十二碳六烯酸(C22:6,DHA)等6种不饱和脂肪酸的含量.结果 (1)在训练的第1~4天,中、高染铅组小鼠逃避潜伏期均明显长于对照组,在训练的第4天,低染铅组小鼠逃避潜伏期亦明显延长,差异有统计学意义(P<0.05);第1~4天的逃避潜伏期均与染铅剂量呈明显的正相关,r值分别为0.973,0.985,0.929,0.936.(2)中、高剂量组小鼠海马C18:2和从较对照组明显上升;而C18:3、EPA、DHA较对照组明显下降,差异均有统计学意义(P<0.05);高剂量组小鼠海马C18:1含量减少,差异有统计学意义(P<0.01).逃避潜伏期与C18:1、C18:3、EPA、DHA呈负相关,与C18:2、AA呈正相关,r值分别为-0.901,-0.914,-0.893,-0.855,0.936,0.727.结论 铅导致海马细胞脂肪酸代谢紊乱,使膜功能正常行使受阻,从而影响递质的合成、代谢和释放,导致学习记忆力的下降,推测这可能是铅干扰学习记忆能力的机制之一. 相似文献
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大学生乙肝疫苗基础免疫及加强免疫效果观察 总被引:5,自引:0,他引:5
目的 比较5μg和10μg两种不同剂量重组酵母乙肝疫苗基础免疫后及基础免疫失败后加强免疫的效果分析。方法 1997~1999年入学的学生采用5μg×3剂量组,2000年入学的学生采用10μg×3剂量组,按0、1、6程序接种,在学生例行体检时用ELISA检测血清中抗-HBs。结果 10μg剂量组抗体阳性率明显高于接种5μg剂量组(X~2=261.71,P<0.01)。基础免疫失败后加强免疫的3组学生,其抗体阳转率有明显差异(X~2=9.74,P<0.01)。经Kendail's等级相关分析。有显著相关性,说明随着免疫接种次数增多,加强免疫后抗体阳转率越低。结论 10μg×3剂量组产生的保护性免疫效果比5μg×3剂量组好。加强免疫接种次数与抗体阳转率呈显著相关性,这可能与机体对HBsAg产生免疫耐受性有关。 相似文献
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目的:研究黄体生成素受体(LHR)基因Asp578Gly突变与女童特发性性早熟的关系。方法:从16例特发性性早熟女童的口腔拭子中提取DNA,5’-CAC TGC TGG CTT TTT CAC TGT ATT-3’和5’-TGA AGG CAG CTG AGA TGG CAAAAA-3’作引物,经常规PCR扩增后采用限制性内切酶MspI消化,检测LHR基因是否存在A1733G的单碱基突变。结果:16例性早熟女童的LHR基因均未检测到Asp578Gly突变。结论:Asp578Gly突变不是女童特发性性早熟的主要病因。 相似文献
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中药抑制剂逆转细菌耐药性的研究进展 总被引:1,自引:0,他引:1
蒋培余 《辽宁中医药大学学报》2008,10(10)
围绕细菌耐药性产生的分子机制,对近年来中药作为细菌耐药性逆转的抑制剂的研究情况作一综述,为解决细菌耐药性问题提供一条新途径。 相似文献
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Objective To study possible impairment mechanisms of learning and memory abilities from unsaturated fatty acids in hippocampus of mice exposed to lead.Methods Forty-eight healthy mice were divided into 4 groups:low dose(0.625 g/L),middle dose(1.250 g/L) and high dose(2.500 g/L) of lead solution in diet and control group (distilled water).The mice in treatment groups were fed with lead solution every day while the mice in control group were fed with distilled water for 50 days.After learning and memory abilities were measured,the mice were killed and contents of oleic acid (C 18:1),linoleic acid (C 18:2),linolenic acid (C18:3),arachidonic acid (AA,C20:4),eicosapentaenoic acid (EPA,C20:5) and docosabexaenoie acid (DHA,C22:6) in hippocampus of mice were determined by high performance liquid chromatography (HPLC).Results (1) In the four training days,the mice treated with lead in the middle dose group and high dose group significantly increased the escape latencies compared with the mice treated with distilled water (P<0.05) ,and on the 4th day,the low dosage mice' s escape latencies were delayed (P<O.05).The escape latencies of the I st,2nd,3rd and 4th day had significantly positive linear relation with lead dose.Their relative coefficient in turn is r=0.973,0.985,0.929 and 0.936,indicating that lead harmed spatial memory of mice in Morris water maze (MWM).(2)The contents of C18:2 and AA were obviously enhanced in hippocampus of middle and high dosage (P<0.05);while there was evident decrease in the contents of C 18:3,EPA and DHA (P<0.05);the content of C 18:1 was decreased significantly in high dosage group (P<0.01).The mice's escape latencies had significantly negative linear relation with contents of C 18:1,C 18:3,EPA and DHA,while there was positive linear relation significantly with contents of C18:2 and AA.Their relative coefficient in turn was r=-0.901,-0.914,-0.893,-0.855,0.936,0.727.Conclusion Lead interferes with the metabolism of hippocampus fatty acids and affects membrane function in hippocampus of mice,which might contribute to change of the synthesis,metabolism and release of central neurotransmitter and decrease of the learning and memory abilities. 相似文献