茶叶细胞壁组分的分离及其稀土元素的分布与定位

本研究结果表明,细胞壁确实是稀土元素沉积的主要地方之一;茶叶细胞壁经无水乙二胺萃取处理后,得到了三种组分,组分A经SephadexG—100上柱分离后,表明它至少含有两种大分子化合物。分子量较小的大分子物质的分子量约为5.0×10~3。氧化稀土总量在三种组分中的含量,按组分A、B和C顺序依次降低,即132.6μg/g、87.8μg/g和12.3μg/g。组分A和B中的稀土元素含量比细胞壁中的要高,表现出富集。本研究基本实现了从细胞水平和分子水平上探索稀土元素在植物体中的分布与定位。     

精浆糖蛋白分析及其临床应用

本文报告了测定精浆糖蛋白总量及聚丙烯酰胺凝胶电泳分析糖蛋白组分的实验方法。对99例正常生育男性的精浆和96例男性不育症患者的精浆糖精浆糖蛋白总量蛋白总量进行了统计学处理。正常精浆糖蛋白总量为2.60±0.73g/dl,不育症患者为3.02±0 64g/dl,t=4.15.P<0.01。在96例不育症中有36例前列腺炎,18例小睾丸,10例副睾炎和6例精索静脉曲张,其糖蛋白总量分别为3.07±0.67g/dl,2.93±0.65g/dl,3.11±0.52g/dl 和2.63±0.92g/dl。与正常精浆相比,t 值显著性检验)分别为3.379(P<0.001),2.481(P<0.02),2.15(P<0.05)和0.095(P<0.05)。本文还对1例正常精浆和4例临床病因不同引起不育者的精浆进行了聚丙烯酰胺凝胶电脉分析,结果提示正常人与不育者在精浆糖蛋白组分上有很大差异,这种差异的临床意义还待进一步研究。     

Recent insights on biochemical and molecular basis for developing antihaemostatic agents: A review

The normal coagulation process is initiated by disruption and exposure of the subendothelial components of blood vessels. Platelets adhere to subendothelium-bound von Willebrand factor via glycoprotein (GP) Ib complex. This initial interaction per se and the release of platelet agonists transduce signals that leads to the rise in intracellular Ca2+ which induces shape change, prostaglandin synthesis, release of granular contents and conformational changes in platelet Gp IIb-IIIa. Gp IIb-IIIa in activated platelets binds fibrinogen and other adhesive proteins and mediates platelet cohesion the primary haemostatic plug. Furthermore, the activated platelets due to aggregation, result in the formation of fibrin (secondary hemostasis). Normally the haemostatic process plays a delicate balance between keeping the blood in the fluid state to maintain flow and rapidly forming an occluding plug following vessel injury. Thrombosis occurs because of alteration in this delicate balance. Arterial thrombosis occurs in the setting of previous vessel wall injury mostly because of atherosclerosis, while venous thrombosis occurs in areas of stasis. The recent advances in understanding of the haemostatic process have led to a better understanding of the mechanism of action of many antithrombotic drugs and identification of new targets for drug development. The molecular target of the ticlopidine has been identified. Large numbers of IIb-IIIa inhibitors have been developed. The mechanism of action of heparin has been defined at the molecular level. As a result, a synthetic pentasaccharide, based on antithrombin-binding domain of heparin, has been developed and tested successfully in clinical trials. New generation direct thrombin inhibitors are being developed. Factor Xa has a critical position at the convergence of intrinsic and extrinsic pathway. The clinical tolerability and the efficacy of low molecular weight heparins has established that inhibition of further thrombin generation, by blocking factor Xa alone can be an effective way of preventing thrombus growth without inactivating thrombin. A large number of specific factor Xa inhibitors are under development. Some of these are in preliminary clinical trials and appear to be promising. Future clinical trials will determine whether these new drugs will provide better risk-benefit ratio in treatment of thrombotic disorders. Similarly role of thrombolytics has been clearly established in many diseases including coronary artery disease.