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[Baroreflex sensitivity: diagnostic importance, methods of determination and a model of baroreflex blood-pressure regulation]. [压反射敏感性:诊断的重要性,测定方法和压反射血压调节模型]。
Pub Date : 2013-01-01
J Svacinová, J Moudr, N Honzíková

Baroreflex regulation of blood pressure primarily moderates its fluctuations and also affects mean blood pressure. Heart rate baroreflex sensitivity is described as changes of the inter-beat interval induced by a change of blood pressure of 1 mmHg (BRS). BRS is decreased in many cardiovascular diseases (hypertension, diabetes mellitus, obesity, cardiac failure, etc.). Decreased BRS in disposed individuals, especially after myocardial infarction, increases the risk of sudden cardiac death. Therefore, early diagnosis of BRS decrease gains in importance. This article describes different methods of determination of baroreflex sensitivity. The methods are based on evaluation of the spontaneous fluctuation of heart rate and blood pressure (spectral, sequential or nonlinear methods), or of primary changes of blood pressure induced by a vasoactive substance or a physiological manoeuvre and corresponding changes of cardiac intervals (Valsalva manoeuvre, phenylephrine administration). Each method has its advantages and disadvantages resulting from a different difficulty of calculation or from inclusion of different deviations in the results, which are not directly linked with baroreflex. Baroreflex regulating total peripheral resistance is less described. A mathematical model of baroreflex blood pressure regulation by fluctuation of heart rate and peripheral resistance is presented in this paper.

血压反射调节主要是调节其波动,也影响平均血压。心率压反射敏感性被描述为由1 mmHg (BRS)的血压变化引起的心跳间隔的变化。BRS在许多心血管疾病(高血压、糖尿病、肥胖、心力衰竭等)中降低。处置个体的BRS降低,特别是心肌梗死后,会增加心源性猝死的风险。因此,早期诊断BRS减少的重要性增加。本文介绍了测定气压反射灵敏度的不同方法。这些方法是基于评估心率和血压的自发波动(光谱法、序列法或非线性法),或评估由血管活性物质或生理操作引起的血压的原发性变化以及相应的心间隔变化(Valsalva操作、苯肾上腺素给药)。每种方法都有其优点和缺点,这是由于计算难度不同或结果中包含不同的偏差,而这些偏差与气压反射没有直接联系。压力反射调节总外周电阻的描述较少。本文建立了基于心率波动和外周阻力调节血压的数学模型。
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引用次数: 0
[Jirí Procháska (1749-1820) II.: the structure of the nervous tissue]. [Jirí Procháska (1749-1820)][神经组织的结构]。
Pub Date : 2013-01-01
A Chvátal

The treatise "De structura nervorum" by Jirí Procháska was published in 1779 after his appointment as a professor in Prague. This work is remarkable not only for its anatomical and histological findings, but also for its historical introduction, which contains a very detailed bibliographical review of previous knowledge about the structure of the nervous tissue. The treatise "De structura nervorum" has never been translated from the Latin language, but as a historical document about the level of neuroscience research conducted by a famous Czech researcher, it deserves further analysis. The present article includes a historical overview of knowledge about the structure of nervous tissue up to the late 18th century from the perspective of today, a translation of the historical introduction about the medieval knowledge of the structure of the nervous tissue and documenting the way in which Jirí Procháska processed his bibliography, a translation and interpretation of his neurohistological observations and an analysis of the results in the light of current knowledge.

1779年,在他被任命为布拉格教授后,Jirí Procháska的专著《神经结构》出版了。这项工作不仅因其解剖和组织学发现而引人注目,而且因其历史介绍而引人注目,其中包含了对先前关于神经组织结构的知识的非常详细的参考文献综述。《神经结构》(De structura nervorum)这篇论文从未被翻译成拉丁文,但作为捷克著名研究者关于神经科学研究水平的历史文献,值得进一步分析。本文包括从今天的角度对18世纪晚期神经组织结构知识的历史概述,对中世纪神经组织结构知识的历史介绍的翻译,并记录Jirí Procháska处理其参考书目的方式,对他的神经组织学观察进行翻译和解释,并根据当前的知识对结果进行分析。
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引用次数: 0
[Mechanisms of growth of neuronal axons and dendrites]. 神经元轴突和树突的生长机制。
Pub Date : 2013-01-01
Z Lest'anová, Z Bacová, T Havránek, J Bakos

Brain development is determined by neuronal differentiation including changes of cell polarity and asymetric growth of neuronal processes. Although, there are many unkown factors contributing to changes of lenght of neuronal cones, mounting experimental and review papers focus on changes of growth conus and role of axonal transport. In particular, mechanisms of actin/microtubule polymerisation and depolymerisation are important. Role of intracellular calcium is also significant. Normal and properly timed changes of lenght of axons and dendrites are dependent on interaction of neurons and glia. Moreover, regeneration of injured axons is dependent on growth factors secreted from glial cells. The aim of the present study is characterisation of the most important mechanisms underlying changes of lenght of neurites.

大脑发育是由神经元分化决定的,包括细胞极性的改变和神经元突的不对称生长。虽然影响神经元锥体长度变化的因素尚不清楚,但越来越多的实验和综述都集中在生长锥体的变化和轴突运输的作用上。特别是,肌动蛋白/微管聚合和解聚合的机制是重要的。细胞内钙的作用也很重要。轴突和树突长度的正常和定时变化依赖于神经元和神经胶质的相互作用。此外,受损轴突的再生依赖于神经胶质细胞分泌的生长因子。本研究的目的是描述神经突长度变化的最重要机制。
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引用次数: 0
[Several remarks to the philosophy of modern science]. [对现代科学哲学的几点评论]。
Pub Date : 2013-01-01
R Rokyta
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引用次数: 0
[Role of reactive oxygen species and nitric oxide in development of the hypoxic pulmonary hypertension]. [活性氧和一氧化氮在低氧性肺动脉高压发展中的作用]。
Pub Date : 2013-01-01
Milan Chovanec

Pulmonary circulation is completely different compared to systemic circulation. Chronic hypoxia damages peripheral pulmonary arterioles and causes hypoxic pulmonary hypertension (HPH) which consists of vasoconstriction and remodelling of the arterioles. The release of reactive oxygen species (ROS)--mainly superoxide and nitric oxide (NO) contribute to the pathogenesis of HPH. During exposition to chronic hypoxia, the NO production is markedly elevated and it has two effects: the first, direct vasodilatory effect caused by NO, the second, contribution to remodelling of the peripheral pulmonary vessels by interaction with ROS. The interaction of superoxid and NO releases peroxynitrite which plays a role in the onset of collagen cleavage. A typical low molecular weight of collagen fragments induces remodelling of the peripheral pulmonary arterioles. These changes are typical for the first week of exposure to the chronic hypoxia which also correlates with sudden elevation of the mean pulmonary artery pressure. Continual exposition to the chronic hypoxia after first week does not cause progressive worsening of HPH.

肺循环与体循环完全不同。慢性缺氧损伤外周肺小动脉,引起低氧性肺动脉高压(HPH),包括血管收缩和小动脉重构。活性氧(ROS)——主要是超氧化物和一氧化氮(NO)的释放参与了HPH的发病机制。暴露于慢性缺氧时,一氧化氮的产生明显升高,其作用有两个:一是一氧化氮引起的直接血管扩张作用,二是通过与活性氧的相互作用促进肺外周血管的重塑。超氧化物和一氧化氮的相互作用释放过氧亚硝酸盐,它在胶原蛋白裂解的开始起作用。典型的低分子量胶原碎片诱导外周肺小动脉的重塑。这些变化在暴露于慢性缺氧的第一周是典型的,这也与平均肺动脉压的突然升高有关。第一周后持续暴露于慢性缺氧并不会导致HPH的进行性恶化。
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引用次数: 0
[Neuro-skeletal biology and its importance for clinical osteology]. [神经骨骼生物学及其对临床骨学的重要性]。
Pub Date : 2012-01-01
I Zofková

Bone remodeling is determined by function of two basic cell forms--bone resorbing osteoclasts and bone formation activating osteoblasts. Both cells are under control of a variety of endogenic and environmental factors, which ensure balance between bone resorption and bone formation. This article reviews the neuro-hormonal factors with osteoanabolic (central isoform of serotonin, melatonin, cannabinoids, beta 1 adrenergic system, oxytocin, ACTH and TSH) or osteocatabolic effects (neuropeptide Y, neuromedin U, beta2 adrenergic system). The dual effects of the beta-adrenergic system, serotonin and leptin are also discussed. The goal of studies focused on neuro-skeletal interaction is to synthesize new molecules, which can modify osteo-anabolic or osteo-catabolic pathways.

骨重塑是由两种基本细胞形态的功能决定的——骨吸收破骨细胞和骨形成激活成骨细胞。这两种细胞都受到多种内源性和环境因素的控制,这些因素确保了骨吸收和骨形成之间的平衡。本文综述了具有骨合成代谢作用的神经激素因子(血清素、褪黑素、大麻素、β 1肾上腺素能系统、催产素、促肾上腺皮质激素和TSH)或骨代谢作用(神经肽Y、神经素U、β 2肾上腺素能系统)。还讨论了-肾上腺素能系统、血清素和瘦素的双重作用。神经-骨骼相互作用研究的目标是合成可以改变骨合成代谢或骨分解代谢途径的新分子。
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引用次数: 0
[Degeneration and regeneration of the peripheral nerve]. [周围神经的退化和再生]。
Pub Date : 2012-01-01
R Kaiser, P Haninec

The peripheral nerve's degeneration and regeneration after its injury was described by Waller in 1850. The distal stump and small part of the proximal part of the transected fibre disintegrate. Proliferating Schwann cells create the band of Büngner for the guiding of the regrowing axon. Even if the suture of the nerve is quickly and well performed, the reinervation is never absolute. Regrowing axons can grow into wrong endoneurial tubes or outside the area of the suture and long-lasting denervation leads to progressive atrophy of the target organs. In the future, the neurotrophic factors might improve the outcome of the reinervation.

1850年,沃勒描述了周围神经损伤后的退化和再生。远端残端和近端截断纤维的一小部分碎裂。增殖的雪旺细胞会产生一条带状的 ngner,用于引导再生的轴突。即使神经的缝合迅速而良好,再神经支配也不是绝对的。再生长的轴突可以生长成错误的神经内膜管或在缝合区域外,长时间的去神经支配会导致目标器官的进行性萎缩。在未来,神经营养因子可能会改善再神经移植的结果。
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引用次数: 0
[Pathophysiology of development of pulmonary hypertension after acute pulmonary embolism]. [急性肺栓塞后肺动脉高压发生的病理生理学]。
Pub Date : 2012-01-01
Roman Mizera

Acute pulmonary embolism (PE) is the life-threatening condition with high incidence and mortality where the death is the result of pulmonary hypertension followed by right side heart failure. There are two important mechanisms concerned in the development of pulmonary embolism--induced pulmonary hypertension--mechanic obstruction of pulmonary vessels by the embolus and vasoconstriction. The effect of mechanic obstruction is quite clear, in contrast to the role of vasoconstriction. Activation of endothelial cells, thrombocytes and leucocytes, which release vasoconstricting substances (ET-1, 5-HT etc.) and production of reactive oxygen species (ROS) are the most important factors causing the vasoconstriction after PE. ROS are produced as a result of hypoxia, increased (and decreased) shear stress and are released from activated leukocytes. Vasoconstriction after PE is caused by change of conformation voltage-gated potassium channels, the decrease of vasodilatation effect of NO and activation of matrix metalloproteinases.. Most of the current therapeutic protocols in PE are focused on mechanic obstruction of pulmonary vessels. Thus, the research of the role of vasoconstriction in PE and potentially protective factors in vasocostriction--induced injury represent clinically highly important field.

急性肺栓塞(PE)是一种发病率和死亡率高、危及生命的疾病,其死亡是肺动脉高压和右侧心力衰竭的结果。肺栓塞的发生有两种重要的机制——肺动脉高压——栓子对肺血管的机械性阻塞和血管收缩。与血管收缩的作用相比,机械性阻塞的作用是相当明显的。内皮细胞、血小板和白细胞的活化释放血管收缩物质(ET-1、5-HT等)和活性氧(ROS)的产生是引起PE后血管收缩的最重要因素。活性氧是缺氧、剪应力增加(和减少)的结果,并从活化的白细胞中释放出来。PE后血管收缩主要是由于构象电压门控钾通道的改变、NO的血管舒张作用减弱和基质金属蛋白酶的激活所致。目前大多数PE的治疗方案都集中在肺血管的机械性阻塞上。因此,血管收缩在PE中的作用以及血管收缩损伤的潜在保护因素的研究是临床上非常重要的研究领域。
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引用次数: 0
[Regulation of receptors coupled to G proteins (GPCRs)]. [G蛋白偶联受体(gpcr)的调控]。
Pub Date : 2012-01-01
H Tománková, J Myslivecek

Regulation of G protein coupled receptors (GPCRs) looks to be not only classically lineary regulated but it is now discovered to be a complex network of interconnected proteins. Taking these in mind it is highly probable that there is multilevel system of regulation that is able to maintain control of signaling. We review here main mechanisms of GPCRs regulation.

G蛋白偶联受体(gpcr)的调控似乎不仅是经典的线性调控,而且现在发现它是一个相互连接的蛋白质的复杂网络。考虑到这些,很可能存在一个能够维持信号控制的多层调节系统。本文综述了gpcr调控的主要机制。
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引用次数: 0
[Selected problems of behavioral tests]. 【行为测试的问题选择】。
Pub Date : 2012-01-01
M Pometlová, K Nohejlova, R Slamberová

Changes in experimental animals' behavior as well as humans' behavior reflect even mild alterations in function of central nervous system. In order to detect those changes variety of tests' batteries were developed. With help of such unified tests it is possible to determine and differentiate individual behavioral parameters and establish their relation to specific CNS alterations. Behavioral tests results from animal studies thereafter can be linked to certain type of behavioral changes in humans, because biochemical composites and reactions of the brain are significantly alike in all of mammals. The advantages of behavioral tests include its non-invasive methods of detection and possibility to determine changes of function even before there are any morphological or biochemical representations. The following work overviews specific aspects of behavioral testing, e.g., animals' preparation to the test, behavioral categories, possibility of tests' measurements and their limitations.

实验动物和人类行为的变化反映了中枢神经系统功能的轻微改变。为了检测这些变化,开发了各种测试电池。在这种统一测试的帮助下,可以确定和区分个体行为参数,并建立它们与特定中枢神经系统改变的关系。此后,动物研究的行为测试结果可以与人类某些类型的行为变化联系起来,因为所有哺乳动物的大脑生化成分和反应都非常相似。行为测试的优点包括其非侵入性的检测方法和在有任何形态或生化表征之前确定功能变化的可能性。下面的工作概述了行为测试的具体方面,例如,动物对测试的准备,行为类别,测试测量的可能性及其局限性。
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引用次数: 0
期刊
Ceskoslovenska fysiologie
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