迁移·自立·融合--思想政治教育有效性概念探析

随着市场经济主体地位的确立,以信息和物质资源的合理流动为导向,在经济基础的相应调整和变动下,思想政治教育有效性已经成为思想政治教育研究的热点。思想政治教育有效性概念主要经历了迁移、自立和融合三个阶段,其中迁移指借鉴教育学基本理念进行界定,自立指立足于思想政治教育学科进行界定,融合指在思想政治教育学科的基础上借鉴多学科理论进行界定。     

Digital Library Service Initiative of the Hong Kong Institute of Education Library

Introduction　　ThemajorgoaloftheHongKongInstituteofEduca tion (HKIEd)Libraryistoprovidethebestservicestoli braryusersseamlesslyandefficiently.Sinceitsinception ,theHKIEdLibraryhasadoptedaninnovativedigitalli braryapproachtobuildupitsservicesandresources.Foralmostadecade,theHKIEdLibraryhasbeendevelopingitsmulti facetlibraryservicesarounditscoredigitalli brarycomponentsoftheINNOPACIntegratedLibrarySys tem ,LibraryWebsite,electronicresourcesfromvendors,andin housedevelopedknowledgeba…     

论WTO争端解决机制中赔偿救济制度的嵌入--基于发展中成员方的视角

WTO争端解决机制中赔偿救济制度的嵌入有助于多边贸易体制的有效运行,将使争端解决中胜诉方的经济权益得到更为现实地保障.发展中成员方在参与和变革WTO争端解决机制的过程中有了更多的话语权,发达成员方也有强化争端机制的需求,使得赔偿制度的嵌入有其现实和可行性.赔偿救济制度的构建内容包括明确其在整个救济措施体系中的地位和性质、赔偿制度的适用情形、赔偿范围和数额、赔偿方式等方面.     

The Kinematic Team Role Behavior in Work Team

Work-team has emerged as an important unit composi ng the organization today. The concepts relating to the properties of team-role t hat fit with today‘s business environment have attracted much attention from the theorists and researchers. A team having a balanced composition of team-ro les is called a balanced team. Theoretically, a balanced team usually renders a better team performance. Therefore, to improve the performance of the team, mana gement needs to ensure that their work teams are composed...     

Human metabolic phenotype diversity and its association with diet and blood pressure

Metabolic phenotypes are the products of interactions among a variety of factors-dietary, other lifestyle/environmental, gut microbial and genetic. We use a large-scale exploratory analytical approach to investigate metabolic phenotype variation across and within four human populations, based on 1H NMR spectroscopy. Metabolites discriminating across populations are then linked to data for individuals on blood pressure, a major risk factor for coronary heart disease and stroke (leading causes of mortality worldwide). We analyse spectra from two 24-hour urine specimens for each of 4,630 participants from the INTERMAP epidemiological study, involving 17 population samples aged 40-59 in China, Japan, UK and USA. We show that urinary metabolite excretion patterns for East Asian and western population samples, with contrasting diets, diet-related major risk factors, and coronary heart disease/stroke rates, are significantly differentiated (P < 10(-16)), as are Chinese/Japanese metabolic phenotypes, and subgroups with differences in dietary vegetable/animal protein and blood pressure. Among discriminatory metabolites, we quantify four and show association (P < 0.05 to P < 0.0001) of mean 24-hour urinary formate excretion with blood pressure in multiple regression analyses for individuals. Mean 24-hour urinary excretion of alanine (direct) and hippurate (inverse), reflecting diet and gut microbial activities, are also associated with blood pressure of individuals. Metabolic phenotyping applied to high-quality epidemiological data offers the potential to develop an area of aetiopathogenetic knowledge involving discovery of novel biomarkers related to cardiovascular disease risk.     

Towards a transgenic model of Huntington's disease in a non-human primate

Non-human primates are valuable for modelling human disorders and for developing therapeutic strategies; however, little work has been reported in establishing transgenic non-human primate models of human diseases. Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder characterized by motor impairment, cognitive deterioration and psychiatric disturbances followed by death within 10-15 years of the onset of the symptoms. HD is caused by the expansion of cytosine-adenine-guanine (CAG, translated into glutamine) trinucleotide repeats in the first exon of the human huntingtin (HTT) gene. Mutant HTT with expanded polyglutamine (polyQ) is widely expressed in the brain and peripheral tissues, but causes selective neurodegeneration that is most prominent in the striatum and cortex of the brain. Although rodent models of HD have been developed, these models do not satisfactorily parallel the brain changes and behavioural features observed in HD patients. Because of the close physiological, neurological and genetic similarities between humans and higher primates, monkeys can serve as very useful models for understanding human physiology and diseases. Here we report our progress in developing a transgenic model of HD in a rhesus macaque that expresses polyglutamine-expanded HTT. Hallmark features of HD, including nuclear inclusions and neuropil aggregates, were observed in the brains of the HD transgenic monkeys. Additionally, the transgenic monkeys showed important clinical features of HD, including dystonia and chorea. A transgenic HD monkey model may open the way to understanding the underlying biology of HD better, and to the development of potential therapies. Moreover, our data suggest that it will be feasible to generate valuable non-human primate models of HD and possibly other human genetic diseases.     

Going up in flames: necrotic cell injury and inflammatory diseases

Recent evidence indicates that cell death can be induced through multiple mechanisms. Strikingly, the same death signal can often induce apoptotic as well as non-apoptotic cell death. For instance, inhibition of caspases often converts an apoptotic stimulus to one that causes necrosis. Because a dedicated molecular circuitry distinct from that controlling apoptosis is required for necrotic cell injury, terms such as “programmed necrosis” or “necroptosis” have been used to distinguish stimulus-dependent necrosis from those induced by non-specific traumas (e.g., heat shock) or secondary necrosis induced as a consequence of apoptosis. In several experimental models, programmed necrosis/necroptosis has been shown to be a crucial control point for pathogen- or injury-induced inflammation. In this review, we will discuss the molecular mechanisms that regulate programmed necrosis/necroptosis and its biological significance in pathogen infections, drug-induced cell injury, and trauma-induced tissue damage.     

Membrane trafficking in neuronal maintenance and degeneration

Defects in membrane trafficking and degradation are hallmarks of most, and maybe all, neurodegenerative disorders. Such defects typically result in the accumulation of undegraded proteins due to aberrant endosomal sorting, lysosomal degradation, or autophagy. The genetic or environmental cause of a specific disease may directly affect these membrane trafficking processes. Alternatively, changes in intracellular sorting and degradation can occur as cellular responses of degenerating neurons to unrelated primary defects such as insoluble protein aggregates or other neurotoxic insults. Importantly, altered membrane trafficking may contribute to the pathogenesis or indeed protect the neuron. The observation of dramatic changes to membrane trafficking thus comes with the challenging need to distinguish pathological from protective alterations. Here, we will review our current knowledge about the protective and destructive roles of membrane trafficking in neuronal maintenance and degeneration. In particular, we will first focus on the question of what type of membrane trafficking keeps healthy neurons alive in the first place. Next, we will discuss what alterations of membrane trafficking are known to occur in Alzheimer’s disease and other tauopathies, Parkinson’s disease, polyQ diseases, peripheral neuropathies, and lysosomal storage disorders. Combining the maintenance and degeneration viewpoints may yield insight into how to distinguish when membrane trafficking functions protectively or contributes to degeneration.