Differential regulation of the alpha 2-adrenergic receptor by Na+ and guanine nucleotides

Many hormones interact with receptors which stimulate the enzyme adenylate cyclase. Less well characterized ar those receptors which mediate an inhibition of adenylate cyclase activity. However, guanine nucleotides are clearly important in the regulation of both stimulatory and inhibitory receptors. Monovalent cations, notably Na+, regulate many inhibitory receptor systems but apparently not stimulatory receptors. We investigate here the effects of Na+ and guanine nucleotides on the adenylate cyclase-coupled inhibitory alpha 2-adrenergic receptor of the rabbit platelet. Computer modelling of adrenaline competition curves with 3H-dihydroergocryptine (3H-DHE) indicates that adrenaline induces two distinct affinity states of the alpha 2 receptor--one of higher (alpha 2H) and the other of lower (alpha 2L) affinity. Guanyl-5'-yl-imidodiphosphate (Gpp(NH)p) seems to reduce adrenaline affinity to converting the high-affinity state into the low-affinity form of the receptor. In contrast, Na+ reduces adrenaline affinity at both the high- and low-affinity states of the alpha 2 receptor while preserving receptor heterogeneity. Thus, guanine nucleotides and Na+ differ in the manner by which each reduces agonist affinity for the alpha 2-adrenergic receptor.     

关于Fibonacci数列的两点注记

注记给出了Fibonacci数列两个重要公式的组合表达式,以及Fibonacci数与级数有关的两个新结果。     

序列空间lp（Xn）中的两个提升问题

主要讨论了序列空间ｌｐ（Ｘｎ）中的性质提升问题。证明了：（１）性质（ｕ）可以提升到ｌｐ（Ｘ）（１≤ｐ〈＋∞）上；（２）弱Ｂａｎａｃｈ－Ｓａｋｓ性质可以提升到Ｌ１（Ｘｎ）上。     

激发态鸟嘌呤无辐射失活的动力学模拟

为了研究DNA碱基在紫外辐射下损伤-修复的机理,采用半经典动力学方法模拟了激发态的鸟嘌呤分子无辐射失活过程.模拟发现了一条新的失活通道,即N7-C8解离,释放的键能转化为分子动能.C8-H的强烈振动会导致无辐射跃迁,使分子在600 fs以内返回基态,从而避免了鸟嘌呤的光损伤.     

多项式序列一致逼近连续函数的两个结论

对用多项式序列一致逼近有界区间的连续函数进行了讨论并得到两个结果:1.这种逼近可以进行的充分必要条件为函数是一致连续的;2.多项式序列的阶数的极限为正无穷.     

Computational roles for dopamine in behavioural control

Neuromodulators such as dopamine have a central role in cognitive disorders. In the past decade, biological findings on dopamine function have been infused with concepts taken from computational theories of reinforcement learning. These more abstract approaches have now been applied to describe the biological algorithms at play in our brains when we form value judgements and make choices. The application of such quantitative models has opened up new fields, ripe for attack by young synthesizers and theoreticians.     

鸟嘌呤对B-Z振荡体系扰动的研究

研究了鸟嘌呤对B-Z化学振荡体系的扰动.结果表明,鸟嘌呤的浓度在2.5×10-8~1.4×10-4mol.L-1范围内时,体系周期的变化量与所加入鸟嘌呤浓度的负对数呈良好的线性关系,相关系数为0.998 7,检出限为2.5×10-9mol.L-1.同时,对可能的反应机理进行了简要讨论.     

依靠互联网平台,探索体育理论课的教学新模式

本文意在探讨通过互联网技术,借助多媒体中集动画、图片、影象、声音与文字与一体的功能,改变高校体育理论课的传统授课模式,激发学生学习体育理论的兴趣,利用搜索引擎GOOGLE与离线浏览器TLTEPORT PRO两款软件,将互联网中与体育有关的理论知识与体育常识以及最新的体育动态下载制作成课件,便于体育理论课中随时调用,丰富体育理论课的内容,利用互联网的魅力激发学生对体育理论课的兴趣。     

关于单形外接球半径的两个结果

研究了n维欧氏空间E^n中n维单形与其子单形的外接球半径之间的关系，获得单形外接球的两个不等式，推广了已有的结果．     

Involvement of guanine nucleotide-binding protein in the gating of Ca2+ by receptors

The introduction of impermeant aqueous solutes into individual cells by microinjection has long been established but the difficulties of manipulating the cytosol composition of large populations of microscopic cells have only recently been overcome. Successful techniques include a dielectric breakdown procedure, treatment with micromolar concentrations of ATP4- (ref. 7) and also with very small (that is nonagglutinating, non-fusogenic) amounts of Sendai virus. So far, attention has been concentrated on the behaviour of the cells (generally their response to applied Ca2+ buffers) at the time when the membrane permeability lesions are open, and thus cytosol and external medium are in contact. I now report a novel technique for monitoring the state of molecular solute permeability in cell membranes and show that the lesions generated by ATP4- in the membrane of mast cells can be closed within seconds of adding Mg2+ so that a cycle of permeabilization and resealing can be used to explore the effect of foreign compounds trapped in the cytosol of effectively intact cells. I show that non-hydrolysable GTP analogues, introduced into the cytosol of mast cells, cause them to undergo exocytotic secretion in response to addition of extracellular Ca2+. This finding is discussed in the light of previous experience relating guanine nucleotide regulatory proteins as intermediaries between receptors and the transducers which they control.     

Jacobian的两个积分估计

在空间W1,n(Ω,Rn)中映射的Jacobian的研究已有了很大的进展,其结果也广泛应用到拟正则及拟共形分析领域,本文利用H lder不等式和Hadamard不等式等工具,推导出了在广义空间W1,P(Ω,Rn),P=(p1,p2,…,pn),1相似文献   

Abolition of the expression of inhibitory guanine nucleotide regulatory protein Gi activity in diabetes

Many cell-surface receptors for hormones appear to exert their effects on target cells by interacting with specific guanine nucleotide binding regulatory proteins (G-proteins) which couple receptors to their second-messenger signal generation systems. A common intracellular second messenger, which is used by many hormones, is cyclic AMP. This is produced by adenylate cyclase, whose activity is controlled by two G-proteins, Gs which mediates stimulatory effects and Gi inhibitory effects on adenylate cyclase activity. In liver, the hormone glucagon increases intracellular cAMP concentrations by activating adenylate cyclase by a Gs-mediated process. This effect of glucagon is antagonised by the hormone insulin, although the molecular mechanism by which insulin elicits its actions is obscure. However, insulin receptors exhibit a tyrosyl kinase activity and appear to interact with G-proteins, perhaps by causing phosphorylation of them. In type I diabetes, circulating insulin levels are abnormally low, giving rise to gross perturbations of metabolism as well as to a variety of complications such as ionic disturbances, neuropathies of the nervous system, respiratory and cardiovascular aberrations and predisposition to infection. We show here that experimentally-induced type I diabetes leads to the loss of expression of Gi in rat liver. As it has been suggested that Gi may couple receptors to K+-channels as well as mediating the inhibition of adenylate cyclase, aberrations in the control of expression of this key regulatory protein in type I diabetes may be expected to lead to pleiotropic effects.