Aided and unaided decision making: Improving intuitive judgement

Intuitive judgement forms the basis of decision making both by experts, in professional settings, and by people in everyday life. Psychologists have studied the rationality of intuitive judgements. In this paper three approaches to decision making will be discussed: unqualified rationalism, qualified rationalism and irrationalism. The first approach holds that man is essentially rational, the second that serious cognitive biases exist, and the third that thinking is strongly influenced by non-cognitive sources of distortion, i.e. emotions and motives. Evidence on judgement is reviewed and found to support the last two approaches. Various ways of improving judgements, as suggested by the three basic viewpoints, are then presented.     

全球化与新的教育政策——欧洲高等教育面临的新挑战

社会的加速变化导致欧洲新教育政策的出台,里斯本战略提出了欧盟教育系统未来要实现的目标,即把欧盟建设成为世界上最具竞争力和多样性的知识经济体,高等教育在其中扮演着越来越重要的角色。分析过去10年欧洲颁布的相关政策文本可以发现,国家、市场和公民社会都对大学产生了新的期望,技术、经济和政治对劳动力市场以及大学的影响也越来越大。在全球化时代,大学应该建立起国际网络以促进国际合作、交流与竞争。     

Reversing EphB2 depletion rescues cognitive functions in Alzheimer model

Amyloid-β oligomers may cause cognitive deficits in Alzheimer's disease by impairing neuronal NMDA-type glutamate receptors, whose function is regulated by the receptor tyrosine kinase EphB2. Here we show that amyloid-β oligomers bind to the fibronectin repeats domain of EphB2 and trigger EphB2 degradation in the proteasome. To determine the pathogenic importance of EphB2 depletions in Alzheimer's disease and related models, we used lentiviral constructs to reduce or increase neuronal expression of EphB2 in memory centres of the mouse brain. In nontransgenic mice, knockdown of EphB2 mediated by short hairpin RNA reduced NMDA receptor currents and impaired long-term potentiation in the dentate gyrus, which are important for memory formation. Increasing EphB2 expression in the dentate gyrus of human amyloid precursor protein transgenic mice reversed deficits in NMDA receptor-dependent long-term potentiation and memory impairments. Thus, depletion of EphB2 is critical in amyloid-β-induced neuronal dysfunction. Increasing EphB2 levels or function could be beneficial in Alzheimer's disease.     

A network dysfunction perspective on neurodegenerative diseases

Patients with Alzheimer's disease or other neurodegenerative disorders show remarkable fluctuations in neurological functions, even during the same day. These fluctuations cannot be caused by sudden loss or gain of nerve cells. Instead, it is likely that they reflect variations in the activity of neural networks and, perhaps, chronic intoxication by abnormal proteins that the brain is temporarily able to overcome. These ideas have far-reaching therapeutic implications.