1000 resultados para Genotype theory


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This paper is part of a broader investigation on Epistemology of Biology carried out by a group of researchers from Cascavel/PR. It involves studies and research about biological thought on subjects such as the growing of the concepts of gene, genotype and phenotype. The aim of this research was to gather the undergraduate students of Biological Sciences’ views about the role played by the inclusion of a historical episode in the study group as a trigger for epistemological discussions and didactic reflections. Firstly, the students received Johannsen’s article “The genotype conception of heredity”, published in 1911 in the journal The American Naturalist, in which he proposed the concepts of genotype and phenotype, among other ones. After, there was a discussion held by group about the concepts proposed in the article taking into account the epistemological, historical and didactic aspects. Data collection occurred through the recording of the group discussions and individual interviews. The results suggest that the inclusion of this historical episode, enabled the participants to develop critical thinking through collective reflection on the meaning of biological knowledge in different contexts.

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Alzheimer's disease (AD) is probably caused by both genetic and environmental risk factors. The major genetic risk factor is the E4 variant of apolipoprotein E gene called apoE4. Several risk factors for developing AD have been identified including lifestyle, such as dietary habits. The mechanisms behind the AD pathogenesis and the onset of cognitive decline in the AD brain are presently unknown. In this study we wanted to characterize the effects of the interaction between environmental risk factors and apoE genotype on neurodegeneration processes, with particular focus on behavioural studies and neurodegenerative processes at molecular level. Towards this aim, we used 6 months-old apoE4 and apoE3 Target Replacement (TR) mice fed on different diets (high intake of cholesterol and high intake of carbohydrates). These mice were evaluated for learning and memory deficits in spatial reference (Morris Water Maze (MWM)) and contextual learning (Passive Avoidance) tasks, which involve the hippocampus and the amygdala, respectively. From these behavioural studies we found that the initial cognitive impairments manifested as a retention deficit in apoE4 mice fed on high carbohydrate diet. Thus, the genetic risk factor apoE4 genotype associated with a high carbohydrate diet seems to affect cognitive functions in young mice, corroborating the theory that the combination of genetic and environmental risk factors greatly increases the risk of developing AD and leads to an earlier onset of cognitive deficits. The cellular and molecular bases of the cognitive decline in AD are largely unknown. In order to determine the molecular changes for the onset of the early cognitive impairment observed in the behavioural studies, we performed molecular studies, with particular focus on synaptic integrity and Tau phosphorylation. The most relevant finding of our molecular studies showed a significant decrease of Brain-derived Neurotrophic Factor (BDNF) in apoE4 mice fed on high carbohydrate diet. Our results may suggest that BDNF decrease found in apoE4 HS mice could be involved in the earliest impairment in long-term reference memory observed in behavioural studies. The second aim of this thesis was to study possible involvement of leptin in AD. There is growing evidence that leptin has neuroprotective properties in the Central Nervous System (CNS). Recent evidence has shown that leptin and its receptors are widespread in the CNS and may provide neuronal survival signals. However, there are still numerous questions, regarding the molecular mechanism by which leptin acts, that remain unanswered. Thus, given to the importance of the involvement of leptin in AD, we wanted to clarify the function of leptin in the pathogenesis of AD and to investigate if apoE genotype affect leptin levels through studies in vitro, in mice and in human. Our findings suggest that apoE4 TR mice showed an increase of leptin in the brain. Leptin levels are also increased in the cerebral spinal fluid of AD patients and apoE4 carriers with AD have higher levels of leptin than apoE3 carriers. Moreover, leptin seems to be expressed by reactive glial cells in AD brains. In vitro, ApoE4 together with Amyloid beta increases leptin production by microglia and astrocytes. Taken together, all these findings suggest that leptin replacement might not be a good strategy for AD therapy. Our results show that high leptin levels were found in AD brains. These findings suggest that, as high leptin levels do not promote satiety in obese individuals, it might be possible that they do not promote neuroprotection in AD patients. Therefore, we hypothesized that AD brain could suffer from leptin resistance. Further studies will be critical to determine whether or not the central leptin resistance in SNC could affect its potential neuroprotective effects.

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Women with a disability continue to experience social oppression and domestic violence as a consequence of gender and disability dimensions. Current explanations of domestic violence and disability inadequately explain several features that lead women who have a disability to experience violent situations. This article incorporates both disability and material feminist theory as an alternative explanation to the dominant approaches (psychological and sociological traditions) of conceptualising domestic violence. This paper is informed by a study which was concerned with examining the nature and perceptions of violence against women with a physical impairment. The emerging analytical framework integrating material feminist interpretations and disability theory provided a basis for exploring gender and disability dimensions. Insight was also provided by the women who identified as having a disability in the study and who explained domestic violence in terms of a gendered and disabling experience. The article argues that material feminist interpretations and disability theory, with their emphasis on gender relations, disablism and poverty, should be used as an alternative tool for exploring the nature and consequences of violence against women with a disability.

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This study develops a life-cycle model where investors make investment decisions in a realistic environment. Model results show that personal illiquid projects (housing and children), fixed costs (once-off/per-period participation costs plus variable/fixed transaction costs) and endogenous risky human capital (with permanent, transitory and disastrous shocks) together are able to address both the non-participation puzzle and the age-effects puzzle. Empirical implications of the model are examined using Heckman’s two-step method with the latest five Surveys of Consumer Finance (SCF). Regression results show that liquidity, informational cost and human capital are indeed the major determinants of participation and asset allocation decisions at different stages of an investor’s life.

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The issue of ‘rigour vs. relevance’ in IS research has generated an intense, heated debate for over a decade. It is possible to identify, however, only a limited number of contributions on how to increase the relevance of IS research without compromising its rigour. Based on a lifecycle view of IS research, we propose the notion of ‘reality checks’ in order to review IS research outcomes in the light of actual industry demands. We assume that five barriers impact the efficient transfer of IS research outcomes; they are lack of awareness, lack of understandability, lack of relevance, lack of timeliness, and lack of applicability. In seeking to understand the effect of these barriers on the transfer of mature IS research into practice, we used focus groups. We chose DeLone and McLean’s IS success model as our stimulus because it is one of the more widely researched areas of IS.

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The difficulty of communicating during organizational change has intensified with the prevalence of continuously changing organizations (Buchanan, Claydon & Doyle, 1999). The difficulty faced by managers is compounded by the lack of studies examining organizational communication within a context of organizational change (Eisenberg, Andrews, Murphy, & Laine-Timmerman, 1999; Lewis & Seibold, 1996). Not surprisingly then, is there a paucity of organizational change theory to guide further research and practitioners. This paper addresses the lack of organizational change communication research and contributes to theoretical development of communication during organizational change. A model of change communication during continuous change is presented from the analysis of two longitudinal empirical studies. Central constructs of the model are the monologic change communication, the dialogic change communication and the background talk of change. Further Van de Ven and Poole's (1995) Process Theories of Change are extended to consider the sequencing of the three constructs. The findings suggest that the sequencing of the dominant change communication approaches is informed by an alignment of individual communication competences and organizational change communication expectations.