988 resultados para Public image of science
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This paper analyses the effects of public funding of higher education on the welfare of the different agents. It takes into account the hierarchical nature of the educational system and also the fact that parents always have the possibility to complement basic public education with private expenditures in individual tutoring. It is obtained that although public funding implies a larger access to higher education it is always the case that some of the agents that gain access lose in welfare terms. Moreover, it is shown that the marginal agent to access university would always prefer a pure private funding system. Thus, when studying the effects of public funding of higher education, we can not identify gaining access to University with an increase in welfare. Finally, I consider a funding system where only those that send their o¤spring to university support the funding of higher education.
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A Work Project, presented as part of the requirements for the Award of a Masters Degree in Management from the NOVA – School of Business and Economics
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Tese apresentada para cumprimento dos requisitos necessários à obtenção do grau de Doutor em Geografia e Planeamento Territorial - Especialidade: Geografia Humana
Staging the Scientist: The Representation of Science and its Processes in American and British Drama
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Dissertação apresentada para cumprimento dos requisitos necessários à obtenção do grau de Mestre em Estudos Ingleses e Norte Americanos
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In museum studies and history of art, what happens behind the scenes of museums stays relatively unseen and unspoken about. In the arts, generally speaking, what is dismissed as irrelevant (e.g. the realm of practices) is deliberately detached from what is thought to really matter; theory, discourse, content and meaning. Up till recently, backstage activities such as conservation practices are merely discussed among specialists and museum professionals. Only the outcomes of these discussions are sometimes – if at all – explicitly communicated to a larger public. Studies into the practices of contemporary art conservation however show that practices behind the scenes play an important role in the perpetuation of these artworks. What happens behind the scenes in terms of conservation has, in several ways, important effects on the ongoing life of these artworks in a museum context. Conservation practices, I argue, should therefore become a necessary part of museum studies and history of art. How can the working practices of conservators become more visible and transparent to a diversity of audiences, including researchers? And what does this mean in terms of research methodology?
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Este relatório segue a metodologia utilizada no estudo da produção científica da Universidade do Minho do quinquénio 2008-2012. No estudo da produção de 2009-2013, para além da análise dos dados indexados na Web of Science, optou-se por acrescentar a análise dos dados indexados na Scopus, procedendo-se à comparação dos resultados entre ambas as bases de dados sempre que adequado e possível.
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Rational manipulation of mRNA folding free energy allows rheostat control of pneumolysin production by Streptococcus pneumoniae
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Rare germline mutations in TP53 (17p13.1) cause a highly penetrant predisposition to a specific spectrum of early cancers, defining the Li-Fraumeni Syndrome (LFS). A germline mutation at codon 337 (p.Arg337His, c1010G>A) is found in about 0.3% of the population of Southern Brazil. This mutation is associated with partially penetrant LFS traits and is found in the germline of patients with early cancers of the LFS spectrum unselected for familial his- tory. To characterize the extended haplotypes carrying the mutation, we have genotyped 9 short tandem repeats on chromosome 17p in 12 trios of Brazilian p.Arg337His carriers. Results confirm that all share a common ancestor haplotype of Caucasian/Portuguese-Ibe- ric origin, distant in about 72–84 generations (2000 years assuming a 25 years intergenera- tional distance) and thus pre-dating European migration to Brazil. So far, the founder p. Arg337His haplotype has not been detected outside Brazil, with the exception of two resi- dents of Portugal, one of them of Brazilian origin. On the other hand, increased meiotic recombination in p.Arg337His carriers may account for higher than expected haplotype diversity. Further studies comparing haplotypes in populations of Brazil and of other areas of Portuguese migration are needed to understand the historical context of this mutation in Brazil.
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Activation of the dorsomedial nucleus of the hypothalamus (DMH) by galanin (GAL) induces behavioural hyperalgesia. Since DMH neurones do not project directly to the spinal cord, we hypothesized that the medullary dorsal reticular nucleus (DRt), a pronociceptive region projecting to the spinal dorsal horn (SDH) and/or the serotoninergic raphe-spinal pathway acting on the spinal 5-HT3 receptor (5HT3R) could relay descending nociceptive facilitation induced by GAL in the DMH. Heat-evoked paw-withdrawal latency (PWL) and activity of SDH neurones were assessed in monoarthritic (ARTH) and control (SHAM) animals after pharmacological manipulations of the DMH, DRt and spinal cord. The results showed that GAL in the DMH and glutamate in the DRt lead to behavioural hyperalgesia in both SHAM and ARTH animals, which is accompanied particularly by an increase in heat-evoked responses of wide-dynamic range neurons, a group of nociceptive SDH neurones. Facilitation of pain behaviour induced by GAL in the DMH was reversed by lidocaine in the DRt and by ondansetron, a 5HT3R antagonist, in the spinal cord. However, the hyperalgesia induced by glutamate in the DRt was not blocked by spinal ondansetron. In addition, in ARTH but not SHAM animals PWL was increased after lidocaine in the DRt and ondansetron in the spinal cord. Our data demonstrate that GAL in the DMH activates two independent descending facilitatory pathways: (i) one relays in the DRt and (ii) the other one involves 5-HT neurones acting on spinal 5HT3Rs. In experimental ARTH, the tonic pain-facilitatory action is increased in both of these descending pathways.
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Spinocerebellar ataxia type 3 (SCA3), also known as Machado-Joseph disease (MJD), is an untreatable autosomal dominant neurodegenerative disease, and the most common such inherited ataxia worldwide. The mutation in SCA3 is the expansion of a polymorphic CAG tri-nucleotide repeat sequence in the C-terminal coding region of the ATXN3 gene at chromosomal locus 14q32.1. The mutant ATXN3 protein encoding expanded glutamine (polyQ) sequences interacts with multiple proteins in vivo, and is deposited as aggregates in the SCA3 brain. A large body of literature suggests that the loss of function of the native ATNX3-interacting proteins that are deposited in the polyQ aggregates contributes to cellular toxicity, systemic neurodegeneration and the pathogenic mechanism in SCA3. Nonetheless, a significant understanding of the disease etiology of SCA3, the molecular mechanism by which the polyQ expansions in the mutant ATXN3 induce neurodegeneration in SCA3 has remained elusive. In the present study, we show that the essential DNA strand break repair enzyme PNKP (polynucleotide kinase 3'-phosphatase) interacts with, and is inactivated by, the mutant ATXN3, resulting in inefficient DNA repair, persistent accumulation of DNA damage/strand breaks, and subsequent chronic activation of the DNA damage-response ataxia telangiectasia-mutated (ATM) signaling pathway in SCA3. We report that persistent accumulation of DNA damage/strand breaks and chronic activation of the serine/threonine kinase ATM and the downstream p53 and protein kinase C-d pro-apoptotic pathways trigger neuronal dysfunction and eventually neuronal death in SCA3. Either PNKP overexpression or pharmacological inhibition of ATM dramatically blocked mutant ATXN3-mediated cell death. Discovery of the mechanism by which mutant ATXN3 induces DNA damage and amplifies the pro-death signaling pathways provides a molecular basis for neurodegeneration due to PNKP inactivation in SCA3, and for the first time offers a possible approach to treatment.
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DNA strand-breaks (SBs) with non-ligatable ends are generated by ionizing radiation, oxidative stress, various chemotherapeutic agents, and also as base excision repair (BER) intermediates. Several neurological diseases have already been identified as being due to a deficiency in DNA end-processing activities. Two common dirty ends, 3'-P and 5'-OH, are processed by mammalian polynucleotide kinase 3'-phosphatase (PNKP), a bifunctional enzyme with 3'-phosphatase and 5'-kinase activities. We have made the unexpected observation that PNKP stably associates with Ataxin-3 (ATXN3), a polyglutamine repeat-containing protein mutated in spinocerebellar ataxia type 3 (SCA3), also known as Machado-Joseph Disease (MJD). This disease is one of the most common dominantly inherited ataxias worldwide; the defect in SCA3 is due to CAG repeat expansion (from the normal 14-41 to 55-82 repeats) in the ATXN3 coding region. However, how the expanded form gains its toxic function is still not clearly understood. Here we report that purified wild-type (WT) ATXN3 stimulates, and by contrast the mutant form specifically inhibits, PNKP's 3' phosphatase activity in vitro. ATXN3-deficient cells also show decreased PNKP activity. Furthermore, transgenic mice conditionally expressing the pathological form of human ATXN3 also showed decreased 3'-phosphatase activity of PNKP, mostly in the deep cerebellar nuclei, one of the most affected regions in MJD patients' brain. Finally, long amplicon quantitative PCR analysis of human MJD patients' brain samples showed a significant accumulation of DNA strand breaks. Our results thus indicate that the accumulation of DNA strand breaks due to functional deficiency of PNKP is etiologically linked to the pathogenesis of SCA3/MJD.
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Here we focus on factor analysis from a best practices point of view, by investigating the factor structure of neuropsychological tests and using the results obtained to illustrate on choosing a reasonable solution. The sample (n=1051 individuals) was randomly divided into two groups: one for exploratory factor analysis (EFA) and principal component analysis (PCA), to investigate the number of factors underlying the neurocognitive variables; the second to test the "best fit" model via confirmatory factor analysis (CFA). For the exploratory step, three extraction (maximum likelihood, principal axis factoring and principal components) and two rotation (orthogonal and oblique) methods were used. The analysis methodology allowed exploring how different cognitive/psychological tests correlated/discriminated between dimensions, indicating that to capture latent structures in similar sample sizes and measures, with approximately normal data distribution, reflective models with oblimin rotation might prove the most adequate.
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El presente trabajo aborda el estudio multidisciplinario de las ideas acerca de la física y la ciencia en general en Córdoba en el siglo XVIII a través de Physica Particularis de Elías del Carmen Pereira (1786), texto manuscrito en lengua latina inédito y recuperado luego de dos siglos de desaparición. El trabajo comprende su transcripción paleográfica, versión española y estudio centrado en la asimilación del paradigma de la ciencia moderna y su enseñanza en la universidad. Se atenderá especialmente a los conceptos que permiten ver en este texto un grado notable de actualización y conocimiento de las ideas de científicos contemporáneos como Nollet y Newton.
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pt.1-2 (1830-1832)
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Background: Previous studies indicate that compared with physical examination, Doppler echocardiography identifies a larger number of cases of rheumatic heart disease in apparently healthy individuals. Objectives: To determine the prevalence of rheumatic heart disease among students in a public school of Belo Horizonte by clinical evaluation and Doppler echocardiography. Methods: This was a cross-sectional study conducted with 267 randomly selected school students aged between 6 and 16 years. students underwent anamnesis and physical examination with the purpose of establishing criteria for the diagnosis of rheumatic fever. They were all subjected to Doppler echocardiography using a portable machine. Those who exhibited nonphysiological mitral regurgitation (MR) and/or aortic regurgitation (AR) were referred to the Doppler echocardiography laboratory of the Hospital das Clínicas of the Universidade Federal of Minas Gerais (HC-UFMG) to undergo a second Doppler echocardiography examination. According to the findings, the cases of rheumatic heart disease were classified as definitive, probable, or possible. Results: Of the 267 students, 1 (0.37%) had a clinical history compatible with the diagnosis of acute rheumatic fever (ARF) and portable Doppler echocardiography indicated nonphysiological MR and/or AR in 25 (9.4%). Of these, 16 (6%) underwent Doppler echocardiography at HC-UFMG. The results showed definitive rheumatic heart disease in 1 student, probable rheumatic heart disease in 3 students, and possible rheumatic heart disease in 1 student. Conclusion: In the population under study, the prevalence of cases compatible with rheumatic involvement was 5 times higher on Doppler echocardiography (18.7/1000; 95% CI 6.9/1000-41.0/1000) than on clinical evaluation (3.7/1000-95% CI).