24 resultados para causation

em BORIS: Bern Open Repository and Information System - Berna - Suiça


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Due to its scope and depth, Moore’s Causation and Responsibility is probably the most important publication in the philosophy of law since the publication of Hart’s and Honoré’s Causation in the Law in 1959. This volume offers, for the first time, a detailed exchange between legal and philosophical scholars over Moore’s most recent work. In particular, it pioneers the dialogue between English-speaking and German philosophy of law on a broad range of pressing foundational questions concerning causation in the law. It thereby fulfills the need for a comprehensive, international and critical discussion of Moore’s influential arguments. The 15 contributors to the proposed volume span the whole interdisciplinary field from law and morals to metaphysics, and the authors include distinguished criminal and tort lawyers, as well as prominent theoretical and practical philosophers from four nations. In addition, young researchers take brand-new approaches in the field. The collection is essential reading for anyone interested in legal and moral theory.

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The paper analyzes Karl Popper’s and John Eccles’ account of mind-matter interaction and compares their use of the concept of downward causation with other more recent accounts of it, especially those of Nancey Murphy and George Ellis. The argument includes John Polkinghorne’s take on Divine action, as it provides an interesting version of downward mind/matter-interaction. It will be argued that while downward causation is a speculative concept, it nevertheless remains the best approximation to a scientific perspective on mind/matter interaction that we can obtain. As a result, Popper’s and Eccles’ account seems to be more interesting in these regards than usually assumed, and should not continue to be overlooked in the debate.

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Autophagy is a conserved proteolytic mechanism that degrades cytoplasmic material including cell organelles. Although the importance of autophagy for cell homeostasis and survival has long been appreciated, our understanding of how autophagy is regulated at a molecular level just recently evolved. The importance of autophagy for the quality control of proteins is underscored by the fact that many neurodegenerative and myodegenerative diseases are characterized by an increased but still insufficient autophagic activity. Similarly, if the cellular stress, leading to deoxyribonucleic acid (DNA) damage, mitochondrial damage and/or damaged proteins, does not result in sufficient autophagic repair mechanisms, cells seem to be prone to transform into tumour cells. Therefore, autophagy has multiple roles to play in the causation and prevention of human diseases.

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Simple descriptive population data are potentially helpful in understanding how bullous pemphigoid (BP) originates and evolves over time. Before embarking with etiological correlations, artifacts and biases should be ruled out. Ideally, epidemiological data should be complemented by immunological and genetic analyses aimed at providing better insight into the causation and prognosis of BP.

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The paper aims at explaining the adoption of policy programs. We use the garbage can model of organizational choice as our theoretical framework and complement it with the institutional setting of administrative decision-making in order to understand the complex causation of policy program adoption. Institutions distribute decision power by rules and routines and coin actor identities and their interpretations of situations. We therefore expect institutions to play a role when a policy window opens. We explore the configurative explanations for program adoption in a systematic comparison of the adoption of new alcohol policy programs in the Swiss cantons employing Qualitative Comparative Analysis. The most important conditions are the organizational elements of the administrative structure decisive for the coupling of the streams. The results imply that classic bureaucratic structures are better suited to put policies into practice than limited government.

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BACKGROUND: In industrialized countries vaccination coverage remains suboptimal, partly because of perception of an increased risk of asthma. Epidemiologic studies of the association between childhood vaccinations and asthma have provided conflicting results, possibly for methodologic reasons such as unreliable vaccination data, biased reporting, and reverse causation. A recent review stressed the need for additional, adequately controlled large-scale studies. OBJECTIVE: Our goal was to determine if routine childhood vaccination against pertussis was associated with subsequent development of childhood wheezing disorders and asthma in a large population-based cohort study. METHODS: In 6811 children from the general population born between 1993 and 1997 in Leicestershire, United Kingdom, respiratory symptom data from repeated questionnaire surveys up to 2003 were linked to independently collected vaccination data from the National Health Service database. We compared incident wheeze and asthma between children of different vaccination status (complete, partial, and no vaccination against pertussis) by computing hazard ratios. Analyses were based on 6048 children, 23 201 person-years of follow-up, and 2426 cases of new-onset wheeze. RESULTS: There was no evidence for an increased risk of wheeze or asthma in children vaccinated against pertussis compared with nonvaccinated children. Adjusted hazard ratios comparing fully and partially vaccinated with nonvaccinated children were close to one for both incident wheeze and asthma. CONCLUSION: This study provides no evidence of an association between vaccination against pertussis in infancy and an increased risk of later wheeze or asthma and does not support claims that vaccination against pertussis might significantly increase the risk of childhood asthma.