32 research outputs found

    Tecnologias digitais no processo de alfabetização: analisando o uso do laboratório de informática nos anos iniciais

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    Este artigo discute tecnologias digitais na alfabetização, onde os estudantes as utilizam para desenvolver seus conhecimentos. Iniciamos com breves considerações sobre o uso das tecnologias na educação e as implicações na alfabetização. Em seguida, apresentamos resultados de uma pesquisa qualitativa, realizada com 15 professores que atuam nas salas de aula de alfabetização de 1º e 2º anos do Ensino Fundamental e professores de laboratório de informática de seis escolas no Município de Curitiba – PR. O propósito deste estudo foi analisar e investigar o impacto do uso do laboratório de informática no processo de alfabetização dos educandos nos anos iniciais. Este trabalho de pesquisa junto aos professores alfabetizadores permitiu que se elencassem duas categorias de análise preliminar: Uso e Planejamento para o Laboratório de Informática; Contribuições para Aprendizagem e Alfabetização no Laboratório de Informática. As reflexões baseiam-se nos estudos de Almeida (2005; 1998); Kenski (2012), Leite, Colello e Arantes (2010), Lucena (2002), Masetto(2000), Moran (2007), Nóvoa (2010), Pretto (2000), Sancho e Hernandez (2006), Soares (2004; 1998), Valente (1999; 1998). O resultado apontou que os professores alfabetizadores utilizam o laboratório de informática nas práticas educativas e que há saberes e habilidades que os alfabetizandos adquirem fazendo uso deste ambiente como melhora na leitura e na oralidade,reconhecimento de letras, registro de letras, palavras e textos, coordenação motora, atenção, raciocínio e nas suas produções

    The Netherlands Arrhythmogenic Cardiomyopathy Registry: design and status update

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    Background Clinical research on arrhythmogenic cardiomyopathy (ACM) is typically limited by small patient numbers, retrospective study designs, and inconsistent definitions. Aim To create a large national ACM patient cohort with a vast amount of uniformly collected high-quality data that is readily available for future research. Methods This is a multicentre, longitudinal, observational cohort study that includes (1) patients with a definite ACM diagnosis, (2) at-risk relatives of ACM patients, and (3) ACM-associated mutation carriers. At baseline and every follow-up visit, a medical history as well information regarding (non-)invasive tests is collected (e. g. electrocardiograms, Holter recordings, imaging and electrophysiological studies, pathology reports, etc.). Outcome data include (non-)sustained ventricular and atrial arrhythmias, heart failure, and (cardiac) death. Data are collected on a research electronic data capture (REDCap) platform in which every participating centre has its own restricted data access group, thus empowering local studies while facilitating data sharing. Discussion The Netherlands ACM Registry is a national observational cohort study of ACM patients and relatives. Prospective and retrospective data are obtained at multiple time points, enabling both cross-sectional and longitudinal research in a hypothesis-generating approach that extends beyond one specific research question. In so doing, this registry aims to (1) increase the scientific knowledge base on disease mechanisms, genetics, and novel diagnostic and treatment strategies of ACM; and (2) provide education for physicians and patients concerning ACM, e. g. through our website (www.acmregistry.nl) and patient conferences

    Variant location is a novel risk factor for individuals with arrhythmogenic cardiomyopathy due to a desmoplakin (DSP) truncating variant.

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    BACKGROUND: Truncating variants in desmoplakin (DSPtv) are an important cause of arrhythmogenic cardiomyopathy; however the genetic architecture and genotype-specific risk factors are incompletely understood. We evaluated phenotype, risk factors for ventricular arrhythmias, and underlying genetics of DSPtv cardiomyopathy. METHODS: Individuals with DSPtv and any cardiac phenotype, and their gene-positive family members were included from multiple international centers. Clinical data and family history information were collected. Event-free survival from ventricular arrhythmia was assessed. Variant location was compared between cases and controls, and literature review of reported DSPtv performed. RESULTS: There were 98 probands and 72 family members (mean age at diagnosis 43±8 years, 59% women) with a DSPtv, of which 146 were considered clinically affected. Ventricular arrhythmia (sudden cardiac arrest, sustained ventricular tachycardia, appropriate implantable cardioverter defibrillator therapy) occurred in 56 (33%) individuals. DSPtv location and proband status were independent risk factors for ventricular arrhythmia. Further, gene region was important with variants in cases (cohort n=98; Clinvar n=167) more likely to occur in the regions resulting in nonsense mediated decay of both major DSP isoforms, compared with n=124 genome aggregation database control variants (148 [83.6%] versus 29 [16.4%]; P<0.0001). CONCLUSIONS: In the largest series of individuals with DSPtv, we demonstrate that variant location is a novel risk factor for ventricular arrhythmia, can inform variant interpretation, and provide critical insights to allow for precision-based clinical management

    Physiology-based regularization of the electrocardiographic inverse problem

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    The inverse problem of electrocardiography aims at noninvasively reconstructing electrical activity of the heart from recorded body-surface electrocardiograms. A crucial step is regularization, which deals with ill-posedness of the problem by imposing constraints on the possible solutions. We developed a regularization method that includes electrophysiological input. Body-surface potentials are recorded and a computed tomography scan is performed to obtain the torso–heart geometry. Propagating waveforms originating from several positions at the heart are simulated and used to generate a set of basis vectors representing spatial distributions of potentials on the heart surface. The real heart-surface potentials are then reconstructed from the recorded body-surface potentials by finding a sparse representation in terms of this basis. This method, which we named ‘physiology-based regularization’ (PBR), was compared to traditional Tikhonov regularization and validated using in vivo recordings in dogs. PBR recovered details of heart-surface electrograms that were lost with traditional regularization, attained higher correlation coefficients and led to improved estimation of recovery times. The best results were obtained by including approximate knowledge about the beat origin in the PBR basis

    End-diastolic myofiber stress and ejection strain increase with ventricular volume overload

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    Background Myocardial stress and strain are considered primary mechanical stimuli for hypertrophic remodeling. Their values and significance in the intact beating heart during chronic overload remain poorly characterized. Methods and results Left-ventricular (LV) dimensions (echocardiography) and pressure ( invasive) were simultaneously recorded in anesthetized dogs at sinus rhythm (SR), acute and 1, 2, 6, 12 weeks of atrioventricular block (AVB), leading to structural, electrical and contractile remodeling. Mechanical load of the myocardium was quantified as myofiber stress (sigma(f)), being force along myofiber orientation per cross-sectional area, and natural myofiber strain (e(f)), being change in natural logarithm of myofiber length ( l) divided by its reference length: e(f) = ln( l/l(ref)). Time courses of sigma(f) and e(f) were calculated from LV pressure and dimensions, using a validated mathematical model of cardiac mechanics. End-diastolic sigma(f) increased from 2.0 +/- 0.1 kPa at SR to 3.4 +/- 0.3 kPa at acute AVB, remaining elevated for > 6 weeks. Systolic sigma(f) was not affected by AVB. Ejection strain rose instantly upon AVB, reaching a maximum at 2 weeks: 0.24 +/- 0.02 vs. 0.10 +/- 0.01 at SR. The increase of myofiber stroke work ( sigma(f)-e(f) loop area) from 3.1 +/- 0.3 at SR to 6.0 +/- 0.5 kJ/m(3)/ beat at 1 week AVB was attributed mainly to an increase of strain during ejection. Stroke work and ejection strain remained elevated up to 12 weeks. The rate of LV-mass increase was maximal (2.2 +/- 0.4 g/day) at 1 week AVB. Conclusions Serial mechanical phenotyping is feasible in the intact anesthetized dog with chronic ventricular overload. Our new approach yields values of mechanical load that are comparable to those found in isolated myocardium by others. In chronic AVB, both end-diastolic myofiber stress and ejection strain are increased. Early increases of both parameters coincide with peak hypertrophic growth, suggesting their important role for mechanotransduction. Peak systolic sigma f is likely not important for hypertrophy in this model, since it does not change throughout the experiment
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