MECHANISM OF SYNCOPE AND ACTION OF DRUGS IN COMPLETE HEART BLOCK

The syncopal attacks of complete heart block may be due either to ventricular standstill or to ventricular acceleration including fibrillation. As treatment may be harmful unless the underlying mechanism in each case is determined, it is important to apply the available methods for differentiation.Epinephrine and certain related compounds (sympathomimetic amines) are the only effective substances in the therapy of ventricular arrest.Isopropyl nor-epinephrine is a most potent drug in the prevention and treatment of ventricular arrest and has the advantage that it does not dispose to fibrillation.Quinidine is unreliable and probably hazardous in the control of ventricular fibrillation in heart block as it appears to precipitate this arrhythmia.Preliminary observations indicate that ectopic ventricular rhythms are also induced by procaine amide in complete heart block.Isuprel® may be of value in the therapy of ventricular acceleration, by preventing the ventricular arrest which frequently follows the initial acceleration.     

中国第一个完整的锯齿龙头骨

中国已经命名了7种锯齿龙,但是没有一个有完整的头骨。本文描述一个产自鄂尔多斯盆地孙家沟组的新材料,包括一个近于完整头骨及关连的下颌。根据下列特征将其归入埃尔金龙科(Elginiidae):头骨的膜质骨突起形成长而尖的角,面颊上装饰有显著的锥型角,上颞骨角从头骨一角向侧后方伸出,副基蝶骨细长且腹面中间有凹沟,案骨加大并在中间相互接触,使后顶骨不参与形成头骨边缘。该标本与矮小三川龙(Sanchuansaurus pygmaeus)有下列共同特征:鼻孔后的上颌骨前背支有小的突起,上颌齿齿冠扇形,9—11个齿尖;但是有以下特征区别于后者:眶下神经两个外开口距离更近且更接近上颌骨腹缘,齿冠不重叠,只有14个牙槽。与柳林黄河龙(Huanghesaurus)共有以下特征:下颌腹缘直、光滑,隅骨突位于后缘,下颌齿有中脊,17个齿尖;不过其下颌前部厚度比后部大。新标本表明三川龙和黄河龙关系接近,两者都应可能属于埃尔金龙科。根据新标本建立一个新种并暂时归入石千峰龙属,即完整石千峰龙(Shitienfenia completus);但是目前不能排除这个标本属于二叠石千峰龙的可能性。     

A COMPARATIVE STUDY OF L-GLUTAMATE DECARBOXYLASE FROM MOUSE BRAIN AND BOVINE HEART WITH PURIFIED PREPARATIONS1

Abstract— L-Glutamate decarboxylase (EC 4.1.1.15) (GAD), the enzyme responsible for the formation of GABA, has been purified to homogeneity from mouse brain (Wu et at., 1973) and antibodies specific for neuronal GAD have been obtained (SAITO et al., 1974a). The present report describes the purification of GAD from bovine heart more than 2000-fold over the homogenate by initial solubilization with Triton X-100. subsequent fractionation with ammonium sulfate, column chromatography on DEAE cellulose, calcium phosphate gel, and DEAE-Sephadex, and gel filtration. At least two forms of GAD have been observed in bovine heart preparations; one of them appears as a high molecular weight form (Peak I, MW 360,000) and the other one as a low molecular weight form (Peak II, MW 105,000). Cysteine sulfinic acid and cysteic acid, both precursors of taurine, had no effect on the purified heart enzyme or on neuronal GAD at 10 mM, suggesting that cysteine sulfinic acid and cysteic acid probably are not substrates for any species of GAD described above. The heart enzyme and neuronal GAD differ in several respects. First, they are different immunochemically as judged by the lack of cross reactivity between the purified heart enzyme and the antibody against purified neuronal GAD. Second, they are different biochemically. 5,5′-Dithiobis[2-nitrobenzoic acid] (DTNB). one of the most potent inhibitors of neuronal GAD [K_i= 1.0 × 10^?8M] inhibits the heart enzyme only to a small extent at 1 mM. On the other hand, pyruvic acid, which inhibits the heart enzyme to an extent of 90% at 10 mM, only inhibits the neuronal enzyme slightly. Third, they are different in their substrate specificity. The neuronal enzyme can catalyze α-decarboxylation of both L-glutamate and L-aspartate while the heart enzyme can use only L-glutamate as substrate. Moreover, an unidentified product probably derived from L-glutamate is obtained in the reaction mixture of the heart enzyme but is not observed with the brain enzyme, suggesting that the heart enzyme may catalyze a reaction converting L-glutamate to products other than GABA. It is therefore concluded that heart GAD and neuronal GAD are two different entities. Work is in progress to determine whether the heart enzyme is related to the glial enzyme. Should the antibody against the heart enzyme cross-react with the glial enzyme, the role of the glial enzyme in GABA function can then be studied by immunochemical and immunocytochemical methods.