从著作权角度剖析逢甲大学校园数位内容经营服务管理计画

在数位化与网路化的学术典藏传播大趋势下 ,建构一个完整、方便、迅速与合理使用的校园数位内容经营服务体系 ,是兼具教育与研究两大使命的大学机构必须进行的工作 ,特别是对身负知识典藏与传播责任的图书馆来说 ,更是刻不容缓的任务 .本文介绍逢甲大学图书馆所规划推动的校园数位内容经营服务管理计画 ,探讨其征集服务范围以及提交、互评、加值典藏、传播与版权管理等作业流程 ,并说明所需要的支援团队和人力配置、所产出的产品形式和应用方式 .最后从著作权的角度分析校园数位内容经营服务所涉及的合理使用、著作财产权和著作授权使用问题     

Memory

Memories become stabilized through a time-dependent process that requires gene expression and is commonly known as consolidation. During this time, memories are labile and can be disrupted by a number of interfering events, including electroconvulsive shock, trauma and other learning or the transient effect of drugs such as protein synthesis inhibitors. Once consolidated, memories are insensitive to these disruptions. However, they can again become fragile if recalled or reactivated. Reactivation creates another time-dependent process, known as reconsolidation, during which the memory is restabilized. Here we discuss some of the questions currently debated in the field of memory consolidation and reconsolidation, the molecular and anatomical requirements for both processes and, finally, their functional relationship.     

Common deletion polymorphisms in the human genome

The locations and properties of common deletion variants in the human genome are largely unknown. We describe a systematic method for using dense SNP genotype data to discover deletions and its application to data from the International HapMap Consortium to characterize and catalogue segregating deletion variants across the human genome. We identified 541 deletion variants (94% novel) ranging from 1 kb to 745 kb in size; 278 of these variants were observed in multiple, unrelated individuals, 120 in the homozygous state. The coding exons of ten expressed genes were found to be commonly deleted, including multiple genes with roles in sex steroid metabolism, olfaction and drug response. These common deletion polymorphisms typically represent ancestral mutations that are in linkage disequilibrium with nearby SNPs, meaning that their association to disease can often be evaluated in the course of SNP-based whole-genome association studies.     

Wnt-beta-catenin signaling initiates taste papilla development

Fungiform taste papillae form a regular array on the dorsal tongue. Taste buds arise from papilla epithelium and, unusually for epithelial derivatives, synapse with neurons, release neurotransmitters and generate receptor and action potentials. Despite the importance of taste as one of our five senses, genetic analyses of taste papilla and bud development are lacking. We demonstrate that Wnt-beta-catenin signaling is activated in developing fungiform placodes and taste bud cells. A dominant stabilizing mutation of epithelial beta-catenin causes massive overproduction of enlarged fungiform papillae and taste buds. Likewise, genetic deletion of epithelial beta-catenin or inhibition of Wnt-beta-catenin signaling by ectopic dickkopf1 (Dkk1) blocks initiation of fungiform papilla morphogenesis. Ectopic papillae are innervated in the stabilizing beta-catenin mutant, whereas ectopic Dkk1 causes absence of lingual epithelial innervation. Thus, Wnt-beta-catenin signaling is critical for fungiform papilla and taste bud development. Altered regulation of this pathway may underlie evolutionary changes in taste papilla patterning.     

Chronobiology of sleep in humans

Periodic circadian (24-h) cycles play an important role in daily hormonal and behavioural rhythms. Usually our sleep/wake cycle, temperature and melatonin rhythms are internally synchronized with a stable phase relationship. When there is a desynchrony between the sleep/wake cycle and circadian rhythm, sleep disorders such as advanced and delayed sleep phase syndrome can arise as well as transient chronobiologic disturbances, for example from jet lag and shift work. Appropriately timed bright light is effective in re-timing the circadian rhythm and sleep pattern to a more desired time, ameliorating these disturbances. Other less potent retiming effects may also be obtained from the judicious use of melatonin and exercise.     

Der Einfluß der Temperatur auf die Giftwirkung des DDT bei Honigbienen (Apis mellifica L.)

Summary The action of DDT on honey-bees depends to a high extent on the temperature (see graph). At 36°C (breeding temperature) DDT has a far weaker insecticidal action than at 20°C (laboratory temperature). This shows that the insecticidal properties of DDT diminish with the raise of temperature.This resistance to DDT at higher temperature is most propitious for bee-keeping and also explains the fact why in agricultural practice there has been no corroborated case of poisoning of bees, though in laboratory tests DDT avered itself to be toxic to bees.