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        e-Learning, Gender Sensitive

        Britta Schinzel 숙명여자대학교 아시아여성연구원 2008 Asian Women Vol.24 No.4

        With the introduction of new media in education the possibilities for using technological means in didactics, organization of learning and content presentation have extended. But the appropriation of these devices and possibilities, like all artefacts, also is a cultural means and it makes culture. Thereby also symbolic connection between gender and technology come into play. In fact sometimes effects on inclusion versus exclusion of groups of people, as women have been observed. On the other hand it can be expected that with growing intensity and broader use of the technical means these barriers are sinking. This for two reasons: Once the rising diversity of user groups requires possibilities for adapting technological means and media didactics to their wishes. On the other hand also more diversified groups of users become more familiar with the technical means thereby mediated education. The text deals with changes mediated education has to take in order to include diverse groups, respecting especially gender and other cultural, ethnical and age diversities. The effects of e-learning on these groups have been analyzed in several investigations, many of them also showing gender and other differences in one or the other category. Concerning gender and all other diversities, in this text the intentions are deconstructive, that is we do not presuppose biologically essential gender (or other) differences in competences, attitudes, motivations etc., but only socially constructed ones. This brings about difficulties: The analysis of gender and other differences can easily turn into self referential results and facilitate essentialist beliefs. This paradoxical situation has to be handled and we will present possibilities for it. To this aid we present empirical results, which are refined with respect to gender together with other items, such that gender differences can be deconstructed by dissolving them into other differentiated categories.

      • Alzheimer's disease - synergistic effects of glucose deficit, oxidative stress and advanced glycation endproducts

        Vlassara, H.,Li, J. J.,Loske, C.,Perry, G.,Wong, A.,Munch, G.,Durany, N.,Schinzel, R.,Smith, M. A.,Riederer, P. 한림대학교 한림과학원 부설 환경ㆍ생명과학연구소 1998 국제학술회의 Vol.1998 No.-

        Many approaches have been undertaken to understand Alzheimer's disease(AD) but the heterogeneity of the etiologic factors makes it difficult to define the clincally most important factor determining the onset and progression of the disease. However, there is increasing evidence that the previously so-called "secondary factors" such as a disturbed glucose metabolism, oxidative stress and formation of "advanced glycation endproducts" (AGEs) and their interaction in a vicious cycle are also important for the onset and progression of AD. AGEs are protein codifications that contribute to the formation of the histopathological and biochemical hallmarks of AD: amyloid plaques, neurofibrillary tangles and activated microglia. Oxidative modifications are formed by a complex cascade of dehydration, oxidation and cyclisation reactions, subsequent to a non-enzymatic reaction of sugars with amino groups of proteins. Accumulation of AGE-crosslinked proteins throughout life is a general phenomenon of ageing. However, AGEs are more that just markers of ageing since they can also exert adverse biologic effects on tissues and cells, including the activation of intracellular signal transduction pathways, leading to the upregulation of cytokine and free radical production (oxidative stress). Oxidative stress is involved in various divergent events leading to cell damage, including an increase in membrane rigidity, DNA strand breaks and an impairment in glucose uptake. In addition, other age-related metabolic changes such as depletion of antioxidants or decreased energy production by a disturbed glucose metabolism diminish the ability of the cell to cope with the effects of radical-induced membrane, protein and DNA damage. With our improving understanding of the molecular basis for the clinical symptoms of dementia, it is hoped that the elucidation of the etiologic causes, particularly the positive feedback loops involving radical damage and a reduced glucose metabolism, will help to develop novel "neuroprotective" treatment strategies able to interrupt this vicious cycle of oxidative stress and energy shortage in AD.

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