RSCRR空间5杆变角机构的结构和几种位置分析方法

本文对有名的 RSCRR 空间5杆变角机构进行了结构分析,进而用4种不同的方法对其进行位置分析,得出了相同的结论,证明了机构输出角δ与输入角α的关系是δ:arcsin[ctgλtg(arcctg((a/e)+cisa)/(sina))],并用实例证明了结论的正确。     

The failing heart.

Cardiomyopathies are disorders affecting heart muscle that usually result in inadequate pumping of the heart. They are the most common cause of heart failure and each year kill more than 10,000 people in the United States. In recent years, there have been breakthroughs in understanding the molecular mechanisms involved in this group of conditions, with knowledge of the genetic basis for cardiomyopathies perhaps seeing the largest advance, enabling clinicians to devise improved diagnostic strategies and preparing the stage for new therapies.     

广西农业科研院所科技开发现状、问题和对策研究

全面系统总结分析了广西农业科研院所科技开发现状，归纳出五大主要技术开发类型和目前科技开发存在的７个主要问题；提出了广西农业科研院所科技开发的十大措施与对策．     

The General Machining Process Simulator GMPS

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家兔膀胱动脉的解剖学研究

用血管铸型和透明方法观察了家兔膀胱的血供情况。膀胱动脉主要起自脐动脉，沿膀胱侧缘行向膀胱顶，沿途发出１～４支基本对称的分支分布于膀胱前面，两侧膀胱动脉的分支在其表面有吻合现象。膀胱动脉及其分支均呈不同程度的弯曲或弹簧状，可能是适应膀胱生理性增大的结构基础。     

相转移催化剂在合成苯乙哌啶中间体中的应用

用相转移催化剂的方法合成革乙哌啶的中间体,对原生产工艺进行了改进,摸索出中间体合成的最佳条件和最高收率,使改进前后的合成收率由34.6%提高到72.4%。     

用核磁共振量子计算机研究量子退相干问题

量子退相干理象是由系统与环境的纠缠所引起的系统相干性的消失，是一种纯粹量子力学效应[1].     

A Framework to Support Agility Strategy Formulation

In the last decade, turbulent times and uncertainti es in the business environment have made ground for a new business era, and “chang e“ has become a major characteristic of the new era. This has resulted in tirele ss evolution of business systems and the creation of new manufacturing and manag ement philosophies. Agile Manufacturing (AM) is a step forward in generation of new means for better performance and success of business, and in practice is a s trategic approach to manufacturing by considering ...     

量子搜索与两体弹性碰撞过程的相似性

量子搜索问题是由Grover首先提出的,其核心是利用量子相干性加速搜索过程[1].量子系统在外部条件和内部作用下演化,使待搜索本征态的系数接近于1,其他本征态的系数接近于0.通过对量子搜索过程的研究,我们发现了量子搜索与经典力学中两体弹性碰撞过程的相似性.利用这种相似性,可以讨论量子搜索的内在本质以及相关的问题.     

A calcium sensor in the sodium channel modulates cardiac excitability.

Sodium channels are principal molecular determinants responsible for myocardial conduction and maintenance of the cardiac rhythm. Calcium ions (Ca2+) have a fundamental role in the coupling of cardiac myocyte excitation and contraction, yet mechanisms whereby intracellular Ca2+ may directly modulate Na channel function have yet to be identified. Here we show that calmodulin (CaM), a ubiquitous Ca2+-sensing protein, binds to the carboxy-terminal 'IQ' domain of the human cardiac Na channel (hH1) in a Ca2+-dependent manner. This binding interaction significantly enhances slow inactivation-a channel-gating process linked to life-threatening idiopathic ventricular arrhythmias. Mutations targeted to the IQ domain disrupted CaM binding and eliminated Ca2+/CaM-dependent slow inactivation, whereas the gating effects of Ca2+/CaM were restored by intracellular application of a peptide modelled after the IQ domain. A naturally occurring mutation (A1924T) in the IQ domain altered hH1 function in a manner characteristic of the Brugada arrhythmia syndrome, but at the same time inhibited slow inactivation induced by Ca2+/CaM, yielding a clinically benign (arrhythmia free) phenotype.