糖皮质激素受体基因第4内含子G1666T多态性与脑出血的相关性

目的 探讨糖皮质激素受体(GR)基因第4内含子G1666T(GR G1666T)多态性与脑出血(ICH)的相关性.方法 应用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)方法检测48例ICH患者(ICH组)、48例ICH伴高血压(EH)患者(ICH+EH组)、46例单纯高血压患者(EH组)及71名健康对照者(NC组) GR G1666T基因型和等位基因频率;比较不同基因型ICH患者的性别、体质量指数(BMI)、血压、血管紧张素原、肾素、血糖、血脂水平的差异.结果 4组间GR G1666T的基因型和等位基因频率差异无统计学意义; ICH组、ICH+EH组及EH组女性患者G等位基因频率明显高于NC组(均P<0.05).GG、GT、TT基因型女性ICH组患者的BMI、血管紧张素原水平和血压依次显著降低(均P<0.05);GG基因型ICH组患者中,女性上述指标明显高于男性(均P<0.05).结论 GR G1666T G等位基因可能是中国女性ICH的易感基因之一.     

学术交流新型平台的形成

20世纪80年代,邓小平同志提出了“科学技术是第一生产力”的科学论断,此后江泽民同志提出了“科教兴国”的战略构想,胡锦涛总书记提出了“科学发展观”的治国纲领。可见,我党从改革开放以来,始终坚持以科技兴国为主轴。尤其是胡锦涛担任总书记以来,一直重点强调要以和谐、创新、科学发展为主轴。因此,全国上下各部门和各行业都应积极认真地考虑如何在实际工作中切实体现和谐和科学发展观的落实。学术界如何创新,即学术原生态建设问题。学术争鸣是学术生态建设的灵魂,也是科学创新的源头之一。能证伪的问题就是科学问题。科学的本质是批判,应…     

眼脉冲幅度增加提示动脉反流

目的:报道1例因双眼脉冲幅度(OPA)增加发现动脉反流的病例,而后者正是引起OPA增加的原因。设计:病例报道。方法:偶然发现双眼OPA增高,由此发现脉压增高和动脉反流。患者接受动脉瓣膜手术,待动脉脉压恢复正常后评价OPA。结果:动脉脉压高时的双眼OPA为9mmHg,动脉脉压恢复正常后的双眼OPA为3mmHg。结论:动脉脉压增高可以导致OPA增高。眼脉冲幅度增加提示动脉反流@McKee H.D.R.$Hull and East Yorkshire Eye Hospital, Fountain Street, Hull, Uni ted Kingdom @Saldaa M. @Ahad M.A. @张少娟…     

组织工程的研究现状

组织工程的研究现状张晨＊张东＊高景恒＊十九世纪和二十世纪中叶，生物学的两大发现是细胞和ＤＮＡ的双螺旋结构，标志着细胞生物学和分子生物学的形成，它们是现代医学发展的两个重要里程碑。近二十年来，在国际上兴起了一门由生物医学和工程学技术相结合的边缘学科，即...     

中国狂热的美容外科——小腿延长术增高会使患者跛行

长期以来，经常用“不劳无获”与美容外科相关联，但它用在当今的中国恐怕是再合适不过了，那里无论男人、女人都愿意承受昂贵和痛苦的手术来改变他们的外形。     

Peripheral Nerve Injury Sensitizes the Response to Visceral Distension but Not Its Inhibition by the Antidepressant Milnacipran

Background: Manipulations that cause hypersensitivity to visceral stimuli have been shown to also result in hypersensitivity to somatic stimuli coming from convergent dermatomes, but the converse has not been examined. The authors tested whether lumbar spinal nerve ligation in rats, a common model of neuropathic pain that results in hypersensitivity to somatic stimuli, also leads to hypersensitivity to visceral stimuli coming from convergent dermatomes and whether pharmacology of inhibition differed between these two sensory modalities.

Methods: Female Sprague-Dawley rats were anesthetized, and the left L5 and L6 spinal nerves were ligated. Animals received either intrathecal saline or milnacipran (0.1-3 [mu]g), and withdrawal thresholds to mechanical testing in the left hind paw, using von Frey filaments, and visceral testing, using balloon colorectal distension, were determined.

Results: Nerve ligation resulted in decreases in threshold to withdrawal to somatic mechanical stimulation (from 13 +/- 1.8 g to 2.7 +/- 0.7 g) and also in decreases in threshold to reflex response to visceral stimulation (from 60 mmHg to 40 mmHg). Intrathecal milnacipran increased withdrawal threshold to somatic stimulation in a dose-dependent manner but failed to alter the response to noxious visceral stimulation.     

Nuclear Factor κB and Anesthetic Preconditioning during Myocardial Ischemia-Reperfusion

Background: Volatile anesthetic preconditioning (APC) protects against myocardial ischemia-reperfusion (IR) injury, but the precise mechanisms underlying this phenomenon remain undefined. To investigate the molecular mechanism of APC in myocardial protection, the activation of nuclear factor (NF) [kappa]B and its regulated inflammatory mediators expression were examined in the current study.

Methods: Hearts from male rats were isolated, Langendorff perfused, and randomly assigned to one of three groups: (1) the control group: hearts were continuously perfused for 130 min; (2) the IR group: 30 min of equilibration, 15 min of baseline, 25 min of ischemia, 60 min of reperfusion; and (3) the APC + IR group: 30 min of equilibration, 10 min of sevoflurane exposure and a 5-min washout, 25 min of global ischemia, 60 min of reperfusion. Tissue samples were acquired at the end of reperfusion. NF-[kappa]B activity was determined by electrophoretic mobility shift assay. The NF-[kappa]B inhibitor, I[kappa]B-[alpha], was determined by Western blot analysis. Myocardial inflammatory mediators, including tumor necrosis factor [alpha], interleukin 1, intercellular adhesion molecule 1, and inducible nitric oxide synthase, were also assessed by Western blot analysis.

Results: Nuclear factor [kappa]B-DNA binding activity was significantly increased at the end of reperfusion in rat myocardium, and cytosolic I[kappa]B-[alpha] was decreased. Supershift assay revealed the involvement of NF-[kappa]B p65 and p50 subunits. APC with sevoflurane attenuated NF-[kappa]B activation and reduced the expression of tumor necrosis factor [alpha], interleukin 1, intercellular adhesion molecule 1, and inducible nitric oxide synthase. APC also reduced infarct size and creatine kinase release and improved myocardial left ventricular developed pressure during IR.     

Morphine Enhances Pharmacological Preconditioning by Isoflurane: Role of Mitochondrial KATP Channels and Opioid Receptors

Background: Adenosine triphosphate-regulated potassium channels mediate protection against myocardial infarction produced by volatile anesthetics and opioids. We tested the hypothesis that morphine enhances the protective effect of isoflurane by activating mitochondrial adenosine triphosphate-regulated potassium channels and opioid receptors.

Methods: Barbiturate-anesthetized rats (n = 131) were instrumented for measurement of hemodynamics and subjected to a 30 min coronary artery occlusion followed by 2 h of reperfusion. Myocardial infarct size was determined using triphenyltetrazolium staining. Rats were randomly assigned to receive 0.9% saline, isoflurane (0.5 and 1.0 minimum alveolar concentration [MAC]), morphine (0.1 and 0.3 mg/kg), or morphine (0.3 mg/kg) plus isoflurane (1.0 MAC). Isoflurane was administered for 30 min and discontinued 15 min before coronary occlusion. In eight additional groups of experiments, rats received 5-hydroxydecanoic acid (5-HD; 10 mg/kg) or naloxone (6 mg/kg) in the presence or absence of isoflurane, morphine, and morphine plus isoflurane.

Results: Isoflurane (1.0 MAC) and morphine (0.3 mg/kg) reduced infarct size (41 +/- 3%; n = 13 and 38 +/- 2% of the area at risk; n = 10, respectively) as compared to control experiments (59 +/- 2%; n = 10). Morphine plus isoflurane further decreased infarct size to 26 +/- 3% (n = 11). 5-HD and naloxone alone did not affect infarct size, but abolished cardioprotection produced by isoflurane, morphine, and morphine plus isoflurane.     

面型动态美的研究与进展

人的面型(面部)即是人的形态与形态美的象征,也是人的思维、情绪的表型.面型美既往研究以静态美型为主体,如额型、眶型、睑型、鼻型、唇型、颏型、颌型的静态美和比例协调美的研究与实施.然而人的面型美不仅仅是单一的静态美,还包含有更加重要的动态美.人的表情在表达中体现出动态美,即是在解剖静态美的基础上体现出功能上的动态美.如此才是完整的面型美或称之美上加美.笔者将以下问题[1,2]作一综述.