缺血后处理与大鼠心肌能量代谢的关系

目的:探讨缺血后处理对大鼠体外心脏缺血再灌注损伤的作用。方法:48只Wistar大鼠,随机均分为2组;缺血后处理组、缺血再灌注组(对照组)。采用大鼠体外心脏Langendorff灌流模型,缺血后处理组全心缺血30 min后,再灌注30 s后,缺血30 s,反复3次,然后持续灌注57 min;对照组全心缺血30 min,再灌注60 min。TTC染色观察心肌梗死面积,高压液相色谱仪(HPLC)分析心肌组织中ATP的含量、灌流液腺苷(adenosine,ADO)含量,测定超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽还原酶(GR)活性。结果:缺血后处理可减少心肌梗死面积[(15.32±2.05)%],与对照组比较[(40.21±3.24)%],差异有统计学意义(P<0.05);减少ATP降解[(3.32±0.63)μmol/g],与对照组比较[(4.73±0.59)μmol/g]差异有统计学意义(P<0.05);心肌冠状动脉流出液中ADO清除速率[(4.33±1.87)nmol.min-1.g-1]小于对照组[(6.17±1.80)nmol.min-1.g-1],P<0.05;心肌SOD、CAT和GR酶活性均高于对照组(P<0.05),有更大的抗氧化能力。结论:缺血后处理可延缓ADO清除,减少ATP的降解,减轻活性氧的损伤作用而发挥心肌保护作用。     

人内源性反转录病毒也应该属于人体正常微生物群

人内源性反转录病毒( human endogenous retroviruses,herv)是反转录病毒如人类免疫缺陷病毒等感染哺乳动物后,将其遗传物质插入宿主的染色体中,经过数百万年的进化转化而来.herv参与了人体多项生理功能的调节,同时也可因herv基因转导、插入突变、点突变、扩增、染色体异位等方式活化而诱发一些疾病.herv的这些特征与我们认知的人体正常微生物群有很大的相似处,本文认为今后编写《医学微生物学》教材时,在有关正常微生物群的种类中应加入herv的内容,以适应本学科在此研究方面发展的需要.     

Mouse Models of Intracranial Aneurysm

Subarachnoid hemorrhage secondary to rupture of an intracranial aneurysm is a highly lethal medical condition. Current management strategies for unruptured intracranial aneurysms involve radiological surveillance and neurosurgical or endovascular interventions. There is no pharmacological treatment available to decrease the risk of aneurysm rupture and subsequent subarachnoid hemorrhage. There is growing interest in the pathogenesis of intracranial aneurysm focused on the development of drug therapies to decrease the incidence of aneurysm rupture. The study of rodent models of intracranial aneurysms has the potential to improve our understanding of intracranial aneurysm development and progression. This review summarizes current mouse models of intact and ruptured intracranial aneurysms and discusses the relevance of these models to human intracranial aneurysms. The article also reviews the importance of these models in investigating the molecular mechanisms involved in the disease. Finally, potential pharmaceutical targets for intracranial aneurysm suggested by previous studies are discussed. Examples of potential drug targets include matrix metalloproteinases, stromal cell‐derived factor‐1, tumor necrosis factor‐α, the renin‐angiotensin system and the β‐estrogen receptor. An agreed clear, precise and reproducible definition of what constitutes an aneurysm in the models would assist in their use to better understand the pathology of intracranial aneurysm and applying findings to patients.     

安贞小区脑卒中病人经济负担调查分析

于１９９２．１０．１－１９９２．１０．３１对安贞小区１９８８．１－１９９１．１２首发脑卒中（按照ＭＯＮＩＣＡ诊断标准）存活病人１６１例，进行了疾病经济负担调查。培训１０名调查员，采用统一问卷均入户调查。用历史性回顾询问法。直接经济负担部分作为本次调查分析重点。对结果用ＳＡＳ软件进行单因素及多因素分析。调查结果表明：１６１例脑卒中平均年龄６２．８岁，男性１００例，女性６１例。平均患病年限２．２６年。直接经济负担费用为６３０８．８元／２．２６年，２７９１元／年。其中医院保健花费中住院及门诊费用比例为８１．３５％，急诊、去单位医务室就诊及家庭病床的费用比例占６．７４％。非医院保健花费部分比例为１１．９％。６３０８．８元中由国家报销比例平均为８７．１％。分析表明：影响直接经济负担的主要因素有年龄、职业、医疗负担方式等。年龄低、在职、享受公费医疗的病人费用相对较高。此次调查的结果为脑卒中的预防效果的评价、健康保险的开展、卫生政策的制定等提供了可靠的数值依据。     

Knockdown of UCA1 inhibits viability and glycolysis by suppressing PKM2 expression through the mTOR pathway in non-small cell lung cancer cells

LncRNA urothelial carcinoma associated 1 (UCA1) was reported to be upregulated in non-small cell lung cancer (NSCLC) tissues and contributed to NSCLC progression. Additionally, it has been proposed that the oncogenic role of UCA1 may be related to glucose metabolism in bladder cancer. However, whether and how UCA1 regulates glucose metabolism in the progression of NSCLC remains unknown. Our results showed that knockdown of UCA1 inhibited the viability of NSCLC cells. UCA1 silencing suppressed glycolysis of NSCLC cells by reducing the glucose consumption and lactate production. Additionally, knockdown of UCA1 suppressed PKM2 expression and the mTOR pathway in NSCLC cells. Mechanistically, PKM2 knockdown suppressed the effects of UCA1 on viability and glycolysis of NSCLC cells and inhibition of the mTOR pathway suppressed the effects of UCA1 on viability, glycolysis, and PKM2 expression in NSCLC cells. In conclusion, knockdown of UCA1 inhibited viability and glycolysis by suppressing PKM2 expression maybe through the mTOR pathway in NSCLC cells, providing a novel insight into the molecular mechanism of UCA1 involved in the regulation of glucose metabolism in NSCLC cells.

LncRNA urothelial carcinoma associated 1 (UCA1) was reported to be upregulated in non-small cell lung cancer (NSCLC) tissues and contributed to NSCLC progression.     

国内社区护士压力性损伤新知识及培训现状

随着我国逐步进入人口老龄化社会,社区医疗作用日益突出,社区护理将成为我国健康管理的一个重要组成部分。压力性损伤是老年人的高发疾病,其不仅加重病人痛苦和经济负担,还造成医疗资源浪费。社区护士是社区压力性损伤管理的重要健康介入要素,社区护士对压力性损伤护理相关知识的掌握情况将影响社区护理的质量和发展。本文就国内社区护士的压力性损伤知识及培训现状进行综述,以期为今后社区护士压力性损伤知识培训作参考。     

纳络酮抗心律失常的机制不依赖于拮抗外周内源性阿片肽

为研究纳酪酮（Nal）的抗心律失常机制，制备大鼠缺血性心律失常模型，观察静脉注射Nal与3种内源性阿片肽（EOP）抗血清及小脑延髓池注射Nal对缺血性心律失常的影响，发现静脉及小脑延髓池注射Nal均有抗心律失常作用，而静脉注射3种EOP抗血清均无抗心律失常作用。提示Nal的抗心律失常的机制不依赖于拮抗外周内源性阿片肽EOP，而可能具有中枢机制。     

直肠癌内分泌样癌细胞分化与P^53蛋白表达关系的研究

目的：研究直肠癌内分泌样癌细胞分化与Ｐ＾５３蛋白表达的关系及意义。方法：采用免疫组织化学ＡＢＣ法检测４４例福尔马林固定、石蜡包埋的直肠癌手术切除及活检组织中的嗜铬蛋白Ａ（ＣＧＡ）及Ｐ＾５３蛋白的表达。结果：Ｐ＾５３、ＣＧＡ阳性表达率分别为６８．２％和３８．６％：ＣＧＡ阳性及阴性直肠癌Ｐ＾５３表达率分别为８８．２％和５５．６％，两者比较Ｐ〈０．０２５Ｘ＾２检测；Ｐ＾５３ＣＧＡ在分化差的直肠癌中的表达     

小儿脑性瘫痪脑血流动力学的研究

目的研究小儿脑性瘫痪(脑瘫)脑血流动力学的变化规律.方法应用经颅多普勒超声对347例脑瘫患儿与30例正常健康儿脑血流动力学参数进行对照检测.结果脑瘫患儿的大脑前动脉、大脑中动脉、大脑后动脉的平均血流较同年龄段的正常小儿显著下降(P＜0.05),而脑血管阻力指数则显著增高(P＜0.05).小于1岁年龄组的平均流速下降及脑血管阻力指数增高较其他年龄组更显著(P＜0.05).结论脑瘫患儿存在脑血流动力学的高阻力、低灌注障碍,早期应用改善脑微循环治疗对于小儿脑瘫的治疗有重要意义.