利手与注意偏向对双耳分听汉字大脑功能优势的影响

对24名左利手和24名右利手被试在三种注意条件（刺激驱动、注意左耳和注意右耳）下进行双耳分听汉字测验,检查中国人利手与汉字听觉词汇加工大脑两半球功能优势的关系,同时考察被试的注意偏向对优势效应的影响.结果表明：（1）汉语母语左利手被试加工汉字听觉词汇的大脑功能偏侧化组织明显不同于右利手;（2）右利手被试在刺激驱动条件下的右耳（左半球）优势易受注意偏向的调节出现明显波动;（3）注意偏向对左利手被试的影响主要表现为优势的左耳（右半球）成绩的下降与非优势的右耳（左半球）成绩的提高,这暗示汉语母语左利手者可能存在汉字听觉词汇加工的潜在两半球表征.     

Pathogenesis of Plasmodium falciparum malaria: the roles of parasite adhesion and antigenic variation

Malaria results in up to 2.5 million deaths annually, with young children and pregnant women at greatest risk. The great majority of severe disease is caused by Plasmodium falciparum. A characteristic feature of infection with P. falciparum is the accumulation or sequestration of parasite-infected red blood cells (RBCs) in various organs, such as the brain, lung and placenta, and together with other factors is important in the pathogenesis of severe forms of malaria. Sequestration results from adhesive interactions between parasite-derived proteins expressed on the surface of infected RBCs and a number of host molecules on the surface of endothelial cells, placental cells and uninfected RBCs. Some receptors for parasite adhesion have been implicated in particular malaria syndromes, such as intercellular adhesion molecule 1 in cerebral malaria and chondroitin sulfate A and hyaluronic acid in placental infection. The principal parasite ligand and antigen on the RBC surface, P. falciparum erythrocyte membrane protein 1 encoded by a multigene family termed var, is clonally variant, enabling evasion of specific immune responses. An understanding of these host-parasite interactions in the context of clinical disease and immunity may reveal potential targets to prevent or treat severe forms of malaria. Received 25 June 2001; received after revision 22 August 2001; accepted 24 August 2001     

体外反搏对犬动脉剪切应力参数的影响

为研究体外反搏对不同情况下剪切应力参数的影响，对18条开胸犬实时测量颈主动脉，头臂干和胸主动脉等处的血流量，计算出各处剪切应力的变化，结果表明，急性心肌缺血和体外反搏可以使剪切应力的平均值，变化范围和变化速率发生变化，即改变了剪切应力的脉动性。     

大鼠不完全性视网膜缺血的组织学变化

采用双侧颈总动脉阻断血流（２ＶＯ）的方法，造成大鼠不完全性视网膜缺血，用组织学方法观察了不同缺血时间（３０、９０ｍｉｎ，４、７、３０ｄ）的缺血后再灌注与不再灌流对视网膜变化的影响。结果显示：缺血３０和９０ｍｉｎ再灌流４ｄ后，内炕网膜（包括外网层、内核层、内网层、节细胞层、神经纤维怪和内界膜）明显增厚；其他不再灌流的缺血组，厚度趋向减少。节细胞计数随缺血时间延长逐渐减少；缺血４ｄ后明显减少。提示不完     

不同生理状态时脑电时间序列的皮层信息传输

引用一种“信息传输”理论来研究不同生理状态时的脑电时间序列，比较了正常人和在急性缺氧条件下、睡眠条件下及局灶性癫痫病患者的大脑皮层信息传输，发现在各种情况下的大脑皮层信息传输有非常特殊的现象：在急性缺氧时，人的大脑皮层信息传输量各导联均较正常人高；当深睡时，各导联的信息传输量均较正常人低；局灶性癫痫病人痫性导联与其他导联间的皮层信息传输量有明显增加，而非痫性导联信息传输量 对降低，用脑皮层信息传输量来分析在不同生理状态下的脑电信号是一个极有潜力的方法，可能为研究和理解大脑的活动机理提供一条新的途径。     

Cerebral ischemia revisited: New insights as revealed using in vitro brain slice preparations

Summary The elucidation of the pathophysiological mechanisms of cerebral ischemia/hypoxia dictates the use of experimental models which mimic this disabling brain condition. In vivo experimental models have been available for many decades and are responsible for the bulk of, though incomplete, knowledge we have about these mechanisms. Since study in isolation of each postulated mechanism is impossible in vivo, the need for an in vitro experimental model has intensified in recent years. Consequently, rat and guinea pig hippocampal slice preparations have emerged as the models of choice. This review attempts to highlight some of the results obtained using brain slices in the study of cerebral ischemia/hypoxia and compare them to those obtained in vivo. Both the biochemical and the physiological correlates of energy metabolism, ion homeostasis, neurotransmission and neuromodulation of this brain condition are reviewed. The agreements, and especially the disagreements, between the in vivo and in vitro findings are emphasized. Details are given of the possible roles of both lactic acid, Ca²⁺ and excitotoxins in the neuronal damage inflicted by cerebral ischemia/hypoxia. Recent attempts to protect brain slices against experimental cerebral ischemic/hypoxic damage are also reviewed here briefly.     

脉络膜血流图及其临床诊断价值

阐明了利用激光干涉度量术测定眼底脉胳膜血流图的原理和数据判读方法,并且以实例说明脉胳膜血流图对于多发性大动脉炎的诊断价值和在预报缺血性脑血管病方面的潜在的重要意义。     

Conduction of the impulse in the ischemic myocardium — implications for malignant ventricular arrhythmias

Summary Ventricular arrhythmias occurring consequent to regional disturbances of myocardial perfusion are the most frequent cause of sudden cardiac death. They are related to marked changes of impulse propagation in the ischemic region, which consist of circulating excitation with re-entry. Mapping of the impulse during ventricular tachycardias and ventricular fibrillation shows that the circus movements change their shape and localization from beat to beat. Zones of tissue which block the impulse during one beat may conduct the impulse at a fast rate during the next beat. The main cause underlying this behavior is the depression of the ischemic action potential. This depression is caused by the partial inactivation and the prolonged recovery of the rapid sodium inward current. In addition to the decrease in resting potential, other factors, such as acidosis, contribute to the inactivation of the inward currents generating the upstroke of the action potential. An increase of coupling resistance between myocardial cells and/or an increase of extracellular resistance appear to be less important for explaining conduction disturbances in acute ischemia.     

Ventricular fibrillation threshold during acute ischemia in hypertrophied rat hearts

Summary Ventricular fibrillation threshold was significantly lower in hypertrophied hearts than in normal hearts. Ischemia produced by coronary occlusion reduced fibrillation threshold in both normal and hypertrophied hearts, but the maximum reduction in fibrillation theshold was observed earlier in hypertrophied hearts.