Publications by authors named "Sarah Vermij"

Aim Of The Study: The aim of this study is to provide an analysis of the career trajectory of the recipients of a Swiss National MD-PhD grant thirty years after the creation of the Swiss interuniversity MD-PhD programme.

Methods: The study surveyed 277 recipients of a Swiss National MD-PhD grant using an online questionnaire in April 2022. There were twenty questions about participants' demographics, the duration of their MD-PhD training, their career trajectory, current position, research and clinical activity, the impact of the support on the recipients' careers, and their satisfaction with various aspects of the grant.

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Rationale: The cardiac sodium channel Na1.5 has a fundamental role in excitability and conduction. Previous studies have shown that sodium channels cluster together in specific cellular subdomains.

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The cardiac voltage-gated sodium channel Na1.5 conducts the rapid inward sodium current crucial for cardiomyocyte excitability. Loss-of-function mutations in its gene are linked to cardiac arrhythmias such as Brugada Syndrome (BrS).

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Background: Mutations in the gene encoding the cardiac voltage-gated sodium channel Na1.5 cause various cardiac arrhythmias. This variety may arise from different determinants of Na1.

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T-tubules are invaginations of the lateral membrane of striated muscle cells that provide a large surface for ion channels and signaling proteins, thereby supporting excitation-contraction coupling. T-tubules are often remodeled in heart failure. To better understand the electrical behavior of T-tubules of cardiac cells in health and disease, this study addresses two largely unanswered questions regarding their electrical properties: (1) the delay of T-tubular membrane depolarization and (2) the effects of T-tubular sodium current on T-tubular potentials.

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Human variants in plakophilin-2 (PKP2) associate with most cases of familial arrhythmogenic cardiomyopathy (ACM). Recent studies show that PKP2 not only maintains intercellular coupling, but also regulates transcription of genes involved in Ca cycling and cardiac rhythm. ACM penetrance is low and it remains uncertain, which genetic and environmental modifiers are crucial for developing the cardiomyopathy.

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Mice are used universally as model organisms for studying heart physiology, and a plethora of genetically modified mouse models exist to study cardiac disease. Transcriptomic data for whole-heart tissue are available, but not yet for isolated ventricular cardiomyocytes. Our lab therefore collected comprehensive RNA-seq data from wildtype murine ventricular cardiomyocytes as well as from knockout models of the ion channel regulators CASK, dystrophin, and SAP97.

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This review presents an extensively integrated model of the cardiac intercalated disc (ID), a highly orchestrated structure that connects adjacent cardiomyocytes. Classically, three main structures are distinguished: gap junctions (GJs) metabolically and electrically connect cytoplasm of adjacent cardiomyocytes; adherens junctions (AJs) connect the actin cytoskeleton of adjacent cells; and desmosomes function as cell anchors and connect intermediate filaments. Furthermore, ion channels reside in the ID.

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