薄膜和表面的统计力学 第二版

本书的第一版是汇集1987年12月28日至1988年1月6日在耶路撒冷举行的第5届“薄膜和表面的统计力学”讲学会的所有演讲，于1989年出版。这次出版第2版更新了一些章的内容，并增加了最后三章。此书应用聚合物物理、微分几何、场论和临界现象等领域的工具来探讨几何和统计力学在一些材料中的微弱的相互作用。这些材料包括微乳状液、湿润的与生长的表面、易溶的液晶块、硫族化合物的眼镜和片状聚合物。     

宇宙中的暗物质

宇宙由什么组成？目前为止，我们还不知道。但是如果标准的引力理论成立，那么宇宙中的大部分物质是由一种无法被发现的形式存在，这些物质发出的光，当今的所有望远镜还不能观测到，这些看不见的物质就是暗物质。     

Book reviews

Affiliated to Astrophysics Div., Space Science Department, European Space Agency.     

Cortico-striatal synaptic defects and OCD-like behaviours in Sapap3-mutant mice

Obsessive-compulsive disorder (OCD) is an anxiety-spectrum disorder characterized by persistent intrusive thoughts (obsessions) and repetitive actions (compulsions). Dysfunction of cortico-striato-thalamo-cortical circuitry is implicated in OCD, although the underlying pathogenic mechanisms are unknown. SAP90/PSD95-associated protein 3 (SAPAP3; also known as DLGAP3) is a postsynaptic scaffolding protein at excitatory synapses that is highly expressed in the striatum. Here we show that mice with genetic deletion of Sapap3 exhibit increased anxiety and compulsive grooming behaviour leading to facial hair loss and skin lesions; both behaviours are alleviated by a selective serotonin reuptake inhibitor. Electrophysiological, structural and biochemical studies of Sapap3-mutant mice reveal defects in cortico-striatal synapses. Furthermore, lentiviral-mediated selective expression of Sapap3 in the striatum rescues the synaptic and behavioural defects of Sapap3-mutant mice. These findings demonstrate a critical role for SAPAP3 at cortico-striatal synapses and emphasize the importance of cortico-striatal circuitry in OCD-like behaviours.     

Basic fibroblast growth factor fused to a signal peptide transforms cells

Basic fibroblast growth factor (bFGF) is a potent growth and angiogenic factor that is found in abundance in tissues such as brain, hypothalamus, kidney and cartilage. Despite this copious production of bFGF, most of these tissues are not undergoing either active growth or angiogenesis, suggesting that bFGF activity must be regulated so as to prevent autostimulation of cell growth. In cultured cells, bFGF is associated mainly with cells and basement membranes and is not released into the medium. Prevention of release could be a mechanism for regulation of bFGF activity and may be a consequence of the apparent absence of a secretory-signal sequence in the bFGF protein. Here we investigate whether this regulation can be overridden through the forced secretion of bFGF. Such secretion might provide the bFGF access to its receptor and in turn lead to autocrine transformation of the cell. We report that bFGF, as specified by a recombinant plasmid, is itself unable to induce such transformation, but acquires this ability after fusion with a secretory-signal sequence. The resulting transformants undergo unusual morphological alteration and display tumorigenicity.