Dissociation of dopamine release in the nucleus accumbens from intracranial self-stimulation

Mesolimbic dopamine-releasing neurons appear to be important in the brain reward system. One behavioural paradigm that supports this hypothesis is intracranial self-stimulation (ICS), during which animals repeatedly press a lever to stimulate their own dopamine-releasing neurons electrically. Here we study dopamine release from dopamine terminals in the nucleus accumbens core and shell in the brain by using rapid-responding voltammetric microsensors during electrical stimulation of dopamine cell bodies in the ventral tegmental area/substantia nigra brain regions. In rats in which stimulating electrode placement failed to elicit dopamine release in the nucleus accumbens, ICS behaviour was not learned. In contrast, ICS was acquired when stimulus trains evoked extracellular dopamine in either the core or the shell of the nucleus accumbens. In animals that could learn ICS, experimenter-delivered stimulation always elicited dopamine release. In contrast, extracellular dopamine was rarely observed during ICS itself. Thus, although activation of mesolimbic dopamine-releasing neurons seems to be a necessary condition for ICS, evoked dopamine release is actually diminished during ICS. Dopamine may therefore be a neural substrate for novelty or reward expectation rather than reward itself.     

Cytotoxic T-cell immunity to virus-infected non-haematopoietic cells requires presentation of exogenous antigen

Cytotoxic T lymphocytes (CTLs) are thought to detect viral infections by monitoring the surface of all cells for the presence of viral peptides bound to major histocompatibility complex (MHC) class I molecules. In most cells, peptides presented by MHC class I molecules are derived exclusively from proteins synthesized by the antigen-bearing cells. Macrophages and dendritic cells also have an alternative MHC class I pathway that can present peptides derived from extracellular antigens; however, the physiological role of this process is unclear. Here we show that virally infected non-haematopoietic cells are unable to stimulate primary CTL-mediated immunity directly. Instead, bone-marrow-derived cells are required as antigen-presenting cells (APCs) to initiate anti-viral CTL responses. In these APCs, the alternative (exogenous) MHC class I pathway is the obligatory mechanism for the initiation of CTL responses to viruses that infect only non-haematopoietic cells.     

Electrical conduction through DNA molecules

The question of whether DNA is able to transport electrons has attracted much interest, particularly as this ability may play a role as a repair mechanism after radiation damage to the DNA helix. Experiments addressing DNA conductivity have involved a large number of DNA strands doped with intercalated donor and acceptor molecules, and the conductivity has been assessed from electron transfer rates as a function of the distance between the donor and acceptor sites. But the experimental results remain contradictory, as do theoretical predictions. Here we report direct measurements of electrical current as a function of the potential applied across a few DNA molecules associated into single ropes at least 600 nm long, which indicate efficient conduction through the ropes. We find that the resistivity values derived from these measurements are comparable to those of conducting polymers, and indicate that DNA transports electrical current as efficiently as a good semiconductor. This property, and the fact that DNA molecules of specific composition ranging in length from just a few nucleotides to chains several tens of micrometres long can be routinely prepared, makes DNA ideally suited for the construction of mesoscopic electronic devices.     

Structural basis for self-association and receptor recognition of human TRAF2

Tumour necrosis factor (TNF)-receptor-associated factors (TRAFs) form a family of cytoplasmic adapter proteins that mediate signal transduction from many members of the TNF-receptor superfamily and the interleukin-1 receptor. They are important in the regulation of cell survival and cell death. The carboxy-terminal region of TRAFs (the TRAF domain) is required for self-association and interaction with receptors. The domain contains a predicted coiled-coil region that is followed by a highly conserved TRAF-C domain. Here we report the crystal structure of the TRAF domain of human TRAF2, both alone and in complex with a peptide from TNF receptor-2 (TNF-R2). The structures reveal a trimeric self-association of the TRAF domain, which we confirm by studies in solution. The TRAF-C domain forms a new, eight-stranded antiparallel beta-sandwich structure. The TNF-R2 peptide binds to a conserved shallow surface depression on one TRAF-C domain and does not contact the other protomers of the trimer. The nature of the interaction indicates that an SXXE motif may be a TRAF2-binding consensus sequence. The trimeric structure of the TRAF domain provides an avidity-based explanation for the dependence of TRAF recruitment on the oligomerization of the receptors by their trimeric extracellular ligands.     

模式识别与计算机视觉手册第三版

本书的第一、二、三版分别于1993、1999和2005年出版。书中全面提供了过去20年中在模式识别与计算机视觉领域中的进展和成就，作者都是这个领域的第一流专家，其中的两位Thomas　Huang和Jake　Aggarwal是权威的K．S．Fu奖金获得者，该项奖金是由国际模式识别协会（IAPR）授予。     

Galectin-7

Galectins are a family of animal lectins with an affinity for β-galactosides. They are differentially expressed by various tissues and appear to be functionally multivalent, exerting a wide range of biological activities both during development and in adult tissue. Galectin-7, a member of this family, contributes to different events associated with the differentiation and development of pluristratified epithelia. It is also associated with epithelial cell migration, which plays a crucial role in the re-epithelialization process of corneal or epidermal wounds. In addition, recent evidence indicates that galectin-7, designated as the product of the p53-induced gene 1 (PIG1), is a regulator of apoptosis through JNK activation and mitochondrial cytochrome c release. Defects in apoptosis constitute one of the major hallmarks of human cancers, and galectin-7 can act as either a positive or a negative regulatory factor in tumour development, depending on the histological type of the tumour. Received 30 October 2005; received after revision 15 November 2005; accepted 25 November 2005