灯盏乙素介入IP3R-Ca2+途径抑制β淀粉样蛋白诱导的神经细胞凋亡

目的：观察灯盏乙素（Scu）对β淀粉样蛋白（Aβ）诱导的细胞模型中1，4，5-三磷酸肌醇受体（IP₃R）-Ca²⁺途径的影响，探讨其在阿尔茨海默病（AD）病程中可能发挥的积极作用。方法：选用神经母细胞瘤细胞分为对照组、Scu处理组、Aβ处理组、Aβ+Scu （高、中、低）处理组及Aβ+IP₃R拮抗剂组，用CCK-8法筛选药物浓度并检测各组细胞生存率；用酶联免疫吸附法检测各组细胞中1，4，5-三磷酸肌醇（IP₃）的含量；用蛋白印迹和实时荧光定量聚合酶链反应方法检测各组细胞IP₃R和凋亡相关因子Caspase-3、Bcl-2、Bax的蛋白及mRNA的表达水平；用激光共聚焦显微镜观察各组细胞内Ca²⁺浓度的变化；用AnnexinV/PI双染法测定各组细胞的凋亡率。结果：与对照组和Scu处理组相比，Aβ处理组细胞存活率下降，IP₃含量升高，IP₃R、Bax和Caspase-3的蛋白及mRNA表达上调，Bcl-2蛋白及mRNA的表达下调，细胞胞浆内Ca²⁺浓度及细胞凋亡率升高；Aβ+Scu处理组细胞中各检测指标的变化与Aβ处理组的结果正好相反，IP₃R通道下游指标的变化与Aβ+IP₃R拮抗剂组基本一致。结论：Scu能够下调通路蛋白IP₃、IP₃R的表达，抑制Aβ介导的Ca²⁺内流所致的细胞凋亡，可能通过对IP₃R-Ca²⁺途径的调控来影响AD病程。     

前后挤压型骶骨Ⅱ区骨折与骶丛神经损伤的关系

目的 探讨前后挤压致骶骨Ⅱ区骨折造成骶丛神经损伤的机制。方法 经甲醛短期（1年内）浸泡固定的国人尸体6具，12侧。解剖保护骶丛神经，制成前后挤压型暴力致骶Ⅱ区骨折模型，定量测量不同骨折移位时骶丛神经被拉长的距离。另外，利用X线片观察骶从神经受压情况。结果 随耻骨联合分离逐渐增大，骶丛神经张应变呈直线相关逐渐加大，以S1，S4为最显著，且可造成神经的刺伤，多见于L5和S1，X线未发现骶丛神经受压表现。结论 前后挤压型暴力致骶骨Ⅱ区骨折神经损伤以牵拉伤为丰，以S1，S4为主，且与骨折移位程度成正相关关系。神经的刺伤，多见于骨折移位较大的L5和S1。     

健康教育个体化对预防急性冠脉综合征的应用研究

目的研究健康教育预防急性冠脉综合征(ACS)的临床治疗效果.方法将62例老年ACS患者分为A组 (常规教育)和B组 (个体化教育),B组通过指导患者制定合适的活动度、掌握缓解疼痛的方式、改善遵医行为、减少冠心病强危险因素以及改变A型行为等方法对患者进行个体化健康教育;A组分小组实施教育.对2组患者康复效果进行对照比较.结果 2组患者的康复有效率:A组低于B组,经统计学分析差异有显著性.结论在ACS患者的诊疗过程中,实施个体化教育对促进患者恢复,减少危险因素的发生具有重要辅助作用.     

肥胖类型与脑卒中亚型的相关性研究

目的探讨肥胖类型与脑卒中亚型的相关性。方法将573例急性脑卒中患者分为脑出血组126例,脑梗死组447例,脑梗死组再分为脑血栓形成组(215例)和腔隙性脑梗死组(232例),另外选择277例无脑卒中者为对照组。测量腰围、臀围和体重,计算体重指数和腰臀比(WHR),分析肥胖参数与脑卒中各亚组的关系。结果脑卒中各亚组与对照组肥胖发生率差异无显著性意义(P>0.05);各组WHR明显大于对照组(P<0.05)。WHR增大明显增加脑卒中各亚组的危险性(P<0.05);女性腹围增大患腔隙性脑梗死危险性升高(P<0.05);男性体重增加患脑出血的危险性升高(P<0.01)。结论腹型肥胖是脑出血、脑血栓形成和腔隙性脑梗死的危险因素之一。     

兔肢体爆炸伤合并海水浸泡后在不同复温速率及维持浅低体温下机体炎症反应的特征

Objective To investigate effects of different rewarming rates and maintenance of light hypothermia on inflammatory response in rabbits after limb blast injury, coupled with seawater immersion. Methods First, the model of limb blast injury coupled with seawater immersion was reproduced [the animals were immersed to low body temperature of (31.0±0.5℃)]. Then, 24 adult rabbits were randomly divided into group Ⅰ [the rapid rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (8.94±0.93)℃/h], group Ⅱ [the slow rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (3.88±0.22)℃/h], group Ⅲ [another slow rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (2.18±0.12)℃/h], and the H group [the hypothermia group, n =6, rewarmed to (34 - 35)℃ at a rate of (4.49±0.66)℃/h and kept at that temperature till termination of the experiment]. Regulation of ambient temperature and warm transfusion were used to restore body temperature to target levels and maintained there for 6 hours. Blood samples were taken at 5 different times, I.e. Pre-injury time(T0), post-immersion time (T1), the time when rewarming started (T2), 3 h after rewarming (T3), and 6 h after rewarming (T4). Tissue samples from heart, liver, intestinum, lung and kidney were also collected. Levels of TNF-α (tumor necrosis factor-α), IL-1β (interleukin-1β) and IL-6 (interleukin-6) in plasma and MPO (myeloperoxidase) in homogenate were detected. Results Following rewarming, TNF-α, IL-1β, IL-6 concentrations in the plasma of the animals in group Ⅰ and group H were significantly higher when compared with those of the animals in group Ⅱ and group Ⅲ (P<0.05, P<0.01), and MPO activity in homogenate was significantly higher when compared with that of the animals in group Ⅱ and group Ⅲ(P<0.01, P<0.05), and no statistical difference could be seen between group Ⅱ and Ⅲ (P>0.05). Conclusions Rapid rewarming and maintenance of light hypothermia could obviously elevate TNF-α, IL-1β, IL-6 concentrations in plasma and MPO activity in homogenate, following limb blast injury coupled with hypothermia induced by seawater immersion, while slow rewarming (with a rewarming rate of 2-4℃/h) could significantly inhibit TNF-α, IL-1β, IL-6 levels and PMN activity.     

心脏机械膜瓣置换术后血浆蛋白C和蛋白S活性变化及其与INR的关系

目的:探讨机械瓣膜置换术后口服华法令抗凝的患者血浆蛋白C(PC)、蛋白S(PS)活性改变的意义及其与国际标准IL比值(INR)的关系。方法:动态监测15例心脏机械瓣膜置换术后口服抗凝药初期患者服药1-2 d、3~10 d及1个月的PC、PS活性及INR值。结果:患者组PC、PS活性低于正常对照组(P<0.05),特别是术后3-10 d PC、PS活性明显低于正常对照组(P<0.01),已下降到正常的50％左右,而此时INR尚未达到治疗范围,提示口服抗凝药治疗初期在人体凝血功能未下调时,抗凝系统功能已经开始下降,有发生血栓的倾向;并且,随着抗凝强度的增高(INR低于1.5-高于2.5),PC、PS活性明显下降。结论:口服华法令抗凝患者在监测INR的同时,需要进行血浆PC、PS活性监测,以更好地预防血栓的发生。     

局麻胸腔镜清创术治疗脓胸实用性研究

目的探讨脓胸患者经局麻胸腔镜清创术治疗的实用价值。方法在局麻下用硬质电视胸腔镜行脓胸清创术，介绍操作方法及清创步骤，观察患者的耐受性及疗效。结果总有效率为90．6％，早、中、晚期治疗有效率分别是100．0％、90．9％、50．0％。术中监测患者对操作的反应及血氧饱和度、呼吸、脉搏、心电图改变均无统计学意义。结论局麻胸腔镜清创术在患者清醒状态下操作，除抽净黏稠脓液外尚可取出团块状脓苔及坏死组织，打穿包裹性脓腔，充分冲洗，可迅速控制感染。方法简单，避免全麻气管插管带来的并发症，术后恢复快，适应证广，患者易耐受，是治疗脓胸的实用方法。     

匹罗卡品致(癎)大鼠海马中表达生长抑素的中间神经元数目变化及其轴突出芽

Objective To investigate the roles of somatostatin(SS)positive intemeurons in the development and compensation of temporal lobe epilepsy.Methods Piloearpine-induced epilepsy rat model was established.Immunohistochemistry method was used to detect number changes and axonal sprouting of SS positive intemeurons in different domains of the hippocampus at difierent time points.Degeneration of SS positive interneurons and their neurophils were detected by the double immunofluorescence staining with SS and Fluoro-Jade B(FJB)at 7 and 60 days after status epilepticus (SE).Results In the exoerimental rat group,the number of SS positive neurons decreased in each hippocampal domain,and it reached the lowest at 7 days post-SE(There were 11.1±3.3 in hilus,2.8±0.9 in CA1region and 1.8±0.7 in CA1region,t=13.519,9.644 and 8.808,all P<0.01).In chronic phase,the number of SS neurons gradually recovered,and exceeded the control group in CA1 area at 60 days post-SE(12.8±1.5 vs 8.8±1.3,t=-4.506,P<0.01),however,the number of SS neurons in the hilus(25.5±4.6)and CA1 area(4.8±0.8)remained significantly less than normal levels(t value were 4.691 and 3.953.both P<0.01).Increased SS positive fibers were found in the lacunosum-molecular (1m)layer and outer molecular layer of dentate gyrus after 30 days post-SE,and numerous SS positive fibers were seen threnghout the layers of area CA1 at 60 days post-SE.Double immunofluuorescence revealed that a few SS positive interneurons and fibers were also labeled by FJB in area CA1 at 7 days post-SE and in CA domain/hilus at 60 days post-SE.Conclusions SS intemeurons loss plays an important role in the development of temporal lobe epilepsy.The loss is partially caIlsed by the degeneration and death of neurons;SS positive neurophils increase within area CA1 in chronic phase may play a significant role in the generation and compensation of temporal lobe epilepsy.