931 resultados para Mortality due to Ill defined causes
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Excavation works in urban areas require a preliminary risk damage assessment. In historical cities, the prediction of building response to settlements is necessary to reduce the risk of damage of the architectural heritage. The current method used to predict the building damage due to ground deformations is the Limiting Tensile Strain Method (LTSM). This method is based on an uncoupled soil-structure analysis, in which the building is modelled as an elastic beam subject to imposed greenfield settlements and the induced tensile strains are compared with a limit value for the material. This approach neglects many factors which play an important rule in the response of the structure to tunneling induced settlements. In this paper, the possibility to apply a settlement risk assessment derived from the seismic vulnerability approach is considered. The parameters that influence the structural response to settlements can be defined through numerical coupled analyses which take into account the nonlinear behaviour of masonry and the soil-structure interaction.
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Secretory leucoprotease inhibitor (SLPI) is a neutrophil serine protease inhibitor constitutively expressed at many mucosal surfaces, including that of the lung. Originally identified as a serine protease inhibitor, it is now evident that SLPI also has antimicrobial and anti-inflammatory functions, and therefore plays an important role in host defense. Previous work has shown that some host defense proteins such as SLPI and elafin are susceptible to proteolytic degradation. Consequently, we investigated the status of SLPI in the cystic fibrosis (CF) lung. A major factor that contributes to the high mortality rate among CF patients is Pseudomonas aeruginosa infection. In this study, we report that P. aeruginosa-positive CF bronchoalveolar lavage fluid, which contains lower SLPI levels and higher neutrophil elastase (NE) activity compared with P. aeruginosa-negative samples, was particularly effective at cleaving recombinant human SLPI. Additionally, we found that only NE inhibitors were able to prevent SLPI cleavage, thereby implicating NE in this process. NE in excess was found to cleave recombinant SLPI at two novel sites in the NH(2)-terminal region and abrogate its ability to bind LPS and NF-kappaB consensus binding sites but not its ability to inhibit activity of the serine protease cathepsin G. In conclusion, this study provides evidence that SLPI is cleaved and inactivated by NE present in P. aeruginosa-positive CF lung secretions and that P. aeruginosa infection contributes to inactivation of the host defense screen in the CF lung.
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Aims: The aim of the study was to assess whether alcohol-related mortality data in the UK should be extended to include contributory as well as underlying cause of death. Methods: A total of 101,320 deaths registered in Northern Ireland between 2001 and 2007 were analysed to determine the quantity and characteristics of those with an underlying or contributory alcohol-related cause of death. Results: Alcohol was found to be an underlying cause of death in 1690 cases (1.7% of deaths) and a contributory cause in a further 1105 cases. Analyses show that the addition of alcohol-related contributory causes of deaths would increase the male-female ratio, result in steeper socio-economic gradients and amplify the apparent rate of increase of alcohol-related deaths. The significant contribution of alcohol to external causes of death, such as accidents and suicide, is also more evident. Conclusions: Using only underlying cause of death undoubtedly underestimates the burden of alcohol-related harm and may provide an inaccurate picture of those most likely to suffer from an alcohol-related death, especially among younger men.
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Langer's axillary arch is a recognized muscular anomaly characterized by an accessory muscular band crossing the axilla that rarely causes symptoms. We describe a patient who presented with an upper limb deep vein thrombosis caused by this aberrant muscle, which we believe is the first reported case. Axillary surgery with division of the aberrant muscle relieved upper limb venous obstruction in this patient. (J Vase Surg 2012;55:234-6.)
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Light of wavelength 632.8 nm and p-polarization is incident on a prism-air gap (varied from 0.7 to 7 mum)-Al-GaAs arrangement. Both the photosignal generated by the Schottky diode and the reflectance are measured as a function of the internal angle of incidence in the prism. There is significant, well-defined enhancement of the photosignal, up to a factor of approximately 7.5, associated with two different types of enhanced absorption modes. For air gaps <1.5 mum there is photosignal enhancement due to an enhanced absorption feature (reflectance dip) that occurs at an angle of incidence just above critical angle in the prism; this feature corresponds to the excitation of a surface plasmon polariton at the Al-air interface. For air gaps > 1 mum there are between one and ten photoresponse peaks at input angles less than the critical angle. The corresponding enhanced absorption features are due to leaky guided wave modes set up in the air gap.
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Background and Purpose-The aim was to investigate prospectively the all-cause mortality risk up to and after coronary heart disease (CHD) and stroke events in European middle-aged men.
Methods-The study population comprised 10 424 men 50 to 59 years of age recruited between 1991 and 1994 in France (N=7855) and Northern Ireland (N=2747) within the Prospective Epidemiological Study of Myocardial Infarction. Incident CHD and stroke events and deaths from all causes were prospectively registered during the 10-year follow-up. In Cox's proportional hazards regression analysis, CHD and stroke events during follow-up were used as time-dependent covariates.
Results-A total of 769 CHD and 132 stroke events were adjudicated, and 569 deaths up to and 66 after CHD or stroke occurred during follow-up. After adjustment for study country and cardiovascular risk factors, the hazard ratios of all-cause mortality were 1.58 (95% confidence interval 1.18-2.12) after CHD and 3.13 (95% confidence interval 1.98-4.92) after stroke.
Conclusions-These findings support continuous efforts to promote both primary and secondary prevention of cardiovascular disease.
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The high dependence of Portugal from foreign energy sources (mainly fossil fuels), together with the international commitments assumed by Portugal and the national strategy in terms of energy policy, as well as resources sustainability and climate change issues, inevitably force Portugal to invest in its energetic self-sufficiency. The 20/20/20 Strategy defined by the European Union defines that in 2020 60% of the total electricity consumption must come from renewable energy sources. Wind energy is currently a major source of electricity generation in Portugal, producing about 23% of the national total electricity consumption in 2013. The National Energy Strategy 2020 (ENE2020), which aims to ensure the national compliance of the European Strategy 20/20/20, states that about half of this 60% target will be provided by wind energy. This work aims to implement and optimise a numerical weather prediction model in the simulation and modelling of the wind energy resource in Portugal, both in offshore and onshore areas. The numerical model optimisation consisted in the determination of which initial and boundary conditions and planetary boundary layer physical parameterizations options provide wind power flux (or energy density), wind speed and direction simulations closest to in situ measured wind data. Specifically for offshore areas, it is also intended to evaluate if the numerical model, once optimised, is able to produce power flux, wind speed and direction simulations more consistent with in situ measured data than wind measurements collected by satellites. This work also aims to study and analyse possible impacts that anthropogenic climate changes may have on the future wind energetic resource in Europe. The results show that the ECMWF reanalysis ERA-Interim are those that, among all the forcing databases currently available to drive numerical weather prediction models, allow wind power flux, wind speed and direction simulations more consistent with in situ wind measurements. It was also found that the Pleim-Xiu and ACM2 planetary boundary layer parameterizations are the ones that showed the best performance in terms of wind power flux, wind speed and direction simulations. This model optimisation allowed a significant reduction of the wind power flux, wind speed and direction simulations errors and, specifically for offshore areas, wind power flux, wind speed and direction simulations more consistent with in situ wind measurements than data obtained from satellites, which is a very valuable and interesting achievement. This work also revealed that future anthropogenic climate changes can negatively impact future European wind energy resource, due to tendencies towards a reduction in future wind speeds especially by the end of the current century and under stronger radiative forcing conditions.
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Tese de doutoramento, Ciências do Mar, da Terra e do Ambiente, Faculdade de Ciências e Tecnologia, Universidade do Algarve, 2015
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It is known that the fibrous structure of muscle causes light scattering. This phenomenon occurs due to the refractive index discontinuities located between muscle fibers and interstitial fluid. To study the possibility of reducing light scattering inside muscle, we consider its spectral transmittance evolution during an immersion treatment with an optical clearing solution containing ethanol, glycerol, and distilled water. Our methodology consists of registering spectral transmittance of muscle samples while immersed in that solution. With the spectral data collected, we represent the transmittance evolution for some wavelengths during the treatment applied. Additionally, we study the variations that the treatment has caused on the samples regarding tissue refractive index and mass. By analyzing microscopic photographs of tissue cross section, we can also verify changes in the internal arrangement of muscle fibers caused by the immersion treatment. Due to a mathematical model that we develop, we can explain the variations observed in the studied parameters and estimate the amount of optical clearing agent that has diffused into the tissue samples during the immersion treatment. At the end of the study, we observe and explain the improvement in tissue spectral transmittance, which is approximately 65% after 20 min.
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L’hypothyroïdie congénitale par dysgénésie thyroïdienne (HCDT) est la condition endocrinienne néonatale la plus fréquemment rencontrée, avec une incidence d’un cas sur 4000 naissances vivantes. L’HCDT comprend toutes les anomalies du développement de la thyroïde. Parmi ces anomalies, le diagnostic le plus fréquent est l’ectopie thyroïdienne (~ 50% des cas). L’HCDT est fréquemment associée à un déficit sévère en hormones thyroïdiennes (hypothyroïdisme) pouvant conduire à un retard mental sévère si non traitée. Le programme de dépistage néonatal assure un diagnostic et un traitement précoce par hormones thyroïdiennes. Cependant, même avec un traitement précoce (en moyenne à 9 jours de vie), un retard de développement est toujours observé, surtout dans les cas les plus sévères (c.-à-d., perte de 10 points de QI). Bien que des cas familiaux soient rapportés (2% des cas), l’HCTD est essentiellement considérée comme une entité sporadique. De plus, plus de 92% des jumeaux monozygotiques sont discordants pour les dysgénésies thyroïdiennes et une prédominance féminine est rapportée (spécialement dans le cas d’ectopies thyroïdiennes), ces deux observations étant clairement incompatible avec un mode de transmission héréditaire mendélien. Il est donc cohérent de constater que des mutations germinales dans les facteurs de transcription thyroïdiens connus (NKX2.1, PAX8, FOXE1, and NKX2.5) ont été identifiées dans seulement 3% des cas sporadiques testés et furent, de plus, exclues lors d’analyse d’association dans certaines familles multiplex. Collectivement, ces données suggèrent que des mécanismes non mendéliens sont à l’origine de la majorité des cas de dysgénésie thyroïdienne. Parmi ces mécanismes, nous devons considérer des modifications épigénétiques, des mutations somatiques précoces (au stade du bourgeon thyroïdien lors des premiers stades de l’embryogenèse) ou des défauts développementaux stochastiques (c.-à-d., accumulation aléatoire de mutations germinales ou somatiques). Voilà pourquoi nous proposons un modèle «2 hits » combinant des mutations (épi)génétiques germinales et somatiques; ce modèle étant compatible avec le manque de transmission familial observé dans la majorité des cas d’HCDT. Dans cette thèse, nous avons déterminé si des variations somatiques (épi)génétiques sont associées à l’HCTD via une approche génomique et une approche gène candidat. Notre approche génomique a révélé que les thyroïdes ectopiques ont un profil d’expression différent des thyroïdes eutopiques (contrôles) et que ce profil d’expression est enrichi en gènes de la voie de signalisation Wnt. La voie des Wnt est cruciale pour la migration cellulaire et pour le développement de plusieurs organes dérivés de l’endoderme (p.ex. le pancréas). De plus, le rôle de la voie des Wnt dans la morphogénèse thyroïdienne est supporté par de récentes études sur le poisson-zèbre qui montrent des anomalies du développement thyroïdien lors de la perturbation de la voie des Wnt durant différentes étapes de l’organogénèse. Par conséquent, l’implication de la voie des Wnt dans l’étiologie de la dysgénésie thyroïdienne est biologiquement plausible. Une trouvaille inattendue de notre approche génomique fut de constater que la calcitonine était exprimée autant dans les thyroïdes ectopiques que dans les thyroïdes eutopiques (contrôles). Cette trouvaille remet en doute un dogme de l’embryologie de la thyroïde voulant que les cellules sécrétant la calcitonine (cellules C) proviennent exclusivement d’une structure extrathyroïdienne (les corps ultimobranchiaux) fusionnant seulement avec la thyroïde en fin de développement, lorsque la thyroïde a atteint son emplacement anatomique définitif. Notre approche gène candidat ne démontra aucune différence épigénétique (c.-à-d. de profil de méthylation) entre thyroïdes ectopiques et eutopiques, mais elle révéla la présence d’une région différentiellement méthylée (RDM) entre thyroïdes et leucocytes dans le promoteur de FOXE1. Le rôle crucial de FOXE1 dans la migration thyroïdienne lors du développement est connu et démontré dans le modèle murin. Nous avons démontré in vivo et in vitro que le statut de méthylation de cette RDM est corrélé avec l’expression de FOXE1 dans les tissus non tumoraux (c.-à-d., thyroïdes et leucocytes). Fort de ces résultats et sachant que les RDMs sont de potentiels points chauds de variations (épi)génétiques, nous avons lancé une étude cas-contrôles afin de déterminer si des variants génétiques rares localisés dans cette RDM sont associés à la dysgénésie thyroïdienne. Tous ces résultats générés lors de mes études doctorales ont dévoilé de nouveaux mécanismes pouvant expliquer la pathogenèse de la dysgénésie thyroïdienne, condition dont l’étiologie reste toujours une énigme. Ces résultats ouvrent aussi plusieurs champs de recherche prometteurs et vont aider à mieux comprendre tant les causes des dysgénésies thyroïdiennes que le développement embryonnaire normal de la thyroïde chez l’homme.
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Birds are vulnerable to collisions with human-made fixed structures. Despite ongoing development and increases in infrastructure, we have few estimates of the magnitude of collision mortality. We reviewed the existing literature on avian mortality associated with transmission lines and derived an initial estimate for Canada. Estimating mortality from collisions with power lines is challenging due to the lack of studies, especially from sites within Canada, and due to uncertainty about the magnitude of detection biases. Detection of bird collisions with transmission lines varies due to habitat type, species size, and scavenging rates. In addition, birds can be crippled by the impact and subsequently die, although crippling rates are poorly known and rarely incorporated into estimates. We used existing data to derive a range of estimates of avian mortality associated with collisions with transmission lines in Canada by incorporating detection, scavenging, and crippling biases. There are 231,966 km of transmission lines across Canada, mostly in the boreal forest. Mortality estimates ranged from 1 million to 229.5 million birds per year, depending on the bias corrections applied. We consider our most realistic estimate, taking into account variation in risk across Canada, to range from 2.5 million to 25.6 million birds killed per year. Data from multiple studies across Canada and the northern U.S. indicate that the most vulnerable bird groups are (1) waterfowl, (2) grebes, (3) shorebirds, and (4) cranes, which is consistent with other studies. Populations of several groups that are vulnerable to collisions are increasing across Canada (e.g., waterfowl, raptors), which suggests that collision mortality, at current levels, is not limiting population growth. However, there may be impacts on other declining species, such as shorebirds and some species at risk, including Alberta’s Trumpeter Swans (Cygnus buccinator) and western Canada’s endangered Whooping Cranes (Grus americana). Collisions may be more common during migration, which underscores the need to understand impacts across the annual cycle. We emphasize that these estimates are preliminary, especially considering the absence of Canadian studies.
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In both the observational record and atmosphere-ocean general circulation model (AOGCM) simulations of the last ∼∼ 150 years, short-lived negative radiative forcing due to volcanic aerosol, following explosive eruptions, causes sudden global-mean cooling of up to ∼∼ 0.3 K. This is about five times smaller than expected from the transient climate response parameter (TCRP, K of global-mean surface air temperature change per W m−2 of radiative forcing increase) evaluated under atmospheric CO2 concentration increasing at 1 % yr−1. Using the step model (Good et al. in Geophys Res Lett 38:L01703, 2011. doi:10.1029/2010GL045208), we confirm the previous finding (Held et al. in J Clim 23:2418–2427, 2010. doi:10.1175/2009JCLI3466.1) that the main reason for the discrepancy is the damping of the response to short-lived forcing by the thermal inertia of the upper ocean. Although the step model includes this effect, it still overestimates the volcanic cooling simulated by AOGCMs by about 60 %. We show that this remaining discrepancy can be explained by the magnitude of the volcanic forcing, which may be smaller in AOGCMs (by 30 % for the HadCM3 AOGCM) than in off-line calculations that do not account for rapid cloud adjustment, and the climate sensitivity parameter, which may be smaller than for increasing CO2 (40 % smaller than for 4 × CO2 in HadCM3).
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Evolutionary change in New World Monkey (NWM) skulls occurred primarily along the line of least resistance defined by size (including allometric) variation (g(max)). Although the direction of evolution was aligned with this axis, it was not clear whether this macroevolutionary pattern results from the conservation of within population genetic covariance patterns (long-term constraint) or long-term selection along a size dimension, or whether both, constraints and selection, were inextricably involved. Furthermore, G-matrix stability can also be a consequence of selection, which implies that both, constraints embodied in g(max) and evolutionary changes observed on the trait averages, would be influenced by selection Here, we describe a combination of approaches that allows one to test whether any particular instance of size evolution is a correlated by-product due to constraints (g(max)) or is due to direct selection on size and apply it to NWM lineages as a case study. The approach is based on comparing the direction and amount of evolutionary change produced by two different simulated sets of net-selection gradients (beta), a size (isometric and allometric size) and a nonsize set. Using this approach it is possible to distinguish between the two hypotheses (indirect size evolution due to constraints or direct selection on size), because although both may produce an evolutionary response aligned with g(max), the amount of change produced by random selection operating through the variance/covariance patterns (constraints hypothesis) will be much smaller than that produced by selection on size (selection hypothesis). Furthermore, the alignment of simulated evolutionary changes with g(max) when selection is not on size is not as tight as when selection is actually on size, allowing a statistical test of whether a particular observed case of evolution along the line of least resistance is the result of selection along it or not. Also, with matrix diagonalization (principal components [PC]) it is possible to calculate directly the net-selection gradient on size alone (first PC [PC1]) by dividing the amount of phenotypic difference between any two populations by the amount of variation in PC1, which allows one to benchmark whether selection was on size or not
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Supernumerary marker chromosomes (sSMC) may or may not be associated with an abnormal phenotype, depending on the presence of euchromatin, on their chromosomal origin and whether they are inherited. Over 80% of sSMCs are derived from acrocentric chromosomes and half of them include the short arm of chromosome 15. Generally, they appear as bisatellited isodicentric marker chromosomes, most of them are symmetric. These chromosomes are normally originated de novo and are associated with mild to severe intellectual disability but not with physical abnormalities. We report on a patient with an SMC studied using classical and molecular cytogenetic procedures (G and C banding, NOR staining, painting and centromeric fluorescent in situ hybridization (FISH), BAC-FISH, and SKY). The MLPA technique and DNA polymorphic markers were used in order to identify its parental origin. The marker chromosome, monosatellited and monocentric, was found to be derived from a maternal chromosome 15 and was defined as 15pter-q21.2. This is the report of the largest de novo monosatellited 15q marker chromosome ever published presenting detailed cytogenetic and clinical data. It was associated with a phenotype including cardiac defect, absence of septum pellucidum, and dysplasia of the corpus callosum. (C) 2010 Wiley-Liss, Inc.
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)