984 resultados para Vannozzi, Bonifazio, 1551-1627.


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Propomos neste texto uma nova leitura da Farsa dos Físicos, relacionada com a alimentação gorda do Carnaval e os jejuns da Quaresma, os quatro humores e os rituais do calendário religioso e profano. A Farsa dos Físicos foi certamente representada perante a corte portuguesa na Terça-feira de Entrudo^ dia 9 de Fevereiro do ano bissexto de 1524, ano em que o domingo de Páscoa calhou a um 27 de Março. A. da Rocha Brito^ é de opinião que a farsa data de 1524, opinião essa partilhada por Maximiano Lemos^ e os investigadores Israel Salvator Révah e Augusta Ventura"^. No entanto, Braamcamp Freire defende a data de 1512 enquanto Paul Teyssier não se pronuncia. A farsa foi proibida pelo Index do Vaticano de 3 de Julho de 1551, certamente pelo tema e pelas blasfêmias proferidas pelo clérigo, juntamente com outras seis peças^, mas será publicada na Compilação de todas as obras, editada pela filha e o filho do dramaturgo, em 1562.

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Objectivos: Determinar a prevalência e caracterizar o perfil dos doentes com rinossinusite aguda e crónica, em Portugal Continental. Desenho do estudo: Estudo epidemiológico transversal. Metodos: Aplicação de um questionário a um grupo representativo de 5.116 indivíduos de ambos os sexos, entre os 14 e os 65 anos. Resultados: A prevalência total de rinossinusite foi de 13,7%(11,3% aguda e 2,4% crónica), sendo mais frequente em mulheres, nas faixas etárias dos 30 aos 39 anos e acima dos 60 anos, nas zonas de Lisboa e Vale do Tejo (LVT), Alentejo e Algarve. A prevalência de rinossinusite crónica é maior no Norte (50%), em inquiridos com idade media de 43 anos. A rinossinusite crónica é frequentemente acompanhada de outras patologias e sintomas e motiva mais consultas médicas do que a rinossinusite aguda. Conclusão: A sensibilização para a importância do diagnóstico correcto, ao mesmo tempo que se contraria a tendência da automedicação recorrente de relevância extrema na prevenção e tratamento da rinossinusite.

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Disponível em : http://193.136.113.6/Opac/Pages/Search/Results.aspx?SearchText=UID=8ce70d92-b636-4073-a151-a09f90bc9b5a&DataBase=10449_UNLFCSH

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This paper presents a mobile information system denominated as Vehicle-to-Anything Application (V2Anything App), and explains its conceptual aspects. This application is aimed at giving relevant information to Full Electric Vehicle (FEV) drivers, by supporting the integration of several sources of data in a mobile application, thus contributing to the deployment of the electric mobility process. The V2Anything App provides recommendations to the drivers about the FEV range autonomy, location of battery charging stations, information of the electricity market, and also a route planner taking into account public transportations and car or bike sharing systems. The main contributions of this application are related with the creation of an Information and Communication Technology (ICT) platform, recommender systems, data integration systems, driver profile, and personalized range prediction. Thus, it is possible to deliver relevant information to the FEV drivers related with the electric mobility process, electricity market, public transportation, and the FEV performance.

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Neural stem cells have been proposed as a new and promising treatment modality in various pathologies of the central nervous system, including malignant brain tumors. However, the underlying mechanism by which neural stem cells target tumor areas remains elusive. Monitoring of these cells is currently done by use of various modes of molecular imaging, such as optical imaging, magnetic resonance imaging and positron emission tomography, which is a novel technology for visualizing metabolism and signal transduction to gene expression. In this new context, the microenvironment of (malignant) brain tumors and the blood-brain barrier gains increased interest. The authors of this review give a unique overview of the current molecular-imaging techniques used in different therapeutic experimental brain tumor models in relation to neural stem cells. Such methods for molecular imaging of gene-engineered neural stem/progenitor cells are currently used to trace the location and temporal level of expression of therapeutic and endogenous genes in malignant brain tumors, closing the gap between in vitro and in vivo integrative biology of disease in neural stem cell transplantation.

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OBJECTIVE: To identify the genetic causes underlying autosomal recessive retinitis pigmentosa (arRP) and to describe the associated phenotype. DESIGN: Case series. PARTICIPANTS: Three hundred forty-seven unrelated families affected by arRP and 33 unrelated families affected by retinitis pigmentosa (RP) plus noncongenital and progressive hearing loss, ataxia, or both, respectively. METHODS: A whole exome sequencing (WES) analysis was performed in 2 families segregating arRP. A mutational screening was performed in 378 additional unrelated families for the exon-intron boundaries of the ABHD12 gene. To establish a genotype-phenotype correlation, individuals who were homozygous or compound heterozygotes of mutations in ABHD12 underwent exhaustive clinical examinations by ophthalmologists, neurologists, and otologists. MAIN OUTCOME MEASURES: DNA sequence variants, best-corrected visual acuity, visual field assessments, electroretinogram responses, magnetic resonance imaging, and audiography. RESULTS: After a WES analysis, we identified 4 new mutations (p.Arg107Glufs*8, p.Trp159*, p.Arg186Pro, and p.Thr202Ile) in ABHD12 in 2 families (RP-1292 and W08-1833) previously diagnosed with nonsyndromic arRP, which cosegregated with the disease among the family members. Another homozygous mutation (p.His372Gln) was detected in 1 affected individual (RP-1487) from a cohort of 378 unrelated arRP and syndromic RP patients. After exhaustive clinical examinations by neurologists and otologists, the 4 affected members of the RP-1292 had no polyneuropathy or ataxia, and the sensorineural hearing loss and cataract were attributed to age or the normal course of the RP, whereas the affected members of the families W08-1833 and RP-1487 showed clearly symptoms associated with polyneuropathy, hearing loss, cerebellar ataxia, RP, and early-onset cataract (PHARC) syndrome. CONCLUSIONS: Null mutations in the ABHD12 gene lead to PHARC syndrome, a neurodegenerative disease including polyneuropathy, hearing loss, cerebellar ataxia, RP, and early-onset cataract. Our study allowed us to report 5 new mutations in ABHD12. This is the first time missense mutations have been described for this gene. Furthermore, these findings are expanding the spectrum of phenotypes associated with ABHD12 mutations ranging from PHARC syndrome to a nonsyndromic form of retinal degeneration.