Annals of medicine
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Comparative Study
Effects of weight loss on visceral and abdominal subcutaneous adipose tissue blood-flow and insulin-mediated glucose uptake in healthy obese subjects.
Rapid weight loss with very-low-calorie diet (VLCD) is known to improve insulin sensitivity and decrease adipose tissue masses. The aim was to investigate the effects of VLCD on adipose tissue regional glucose uptake (rGU) and perfusion and their association with adipokines. ⋯ Abdominal adipose tissue perfusion and rGU are not related in obesity. Rapid weight loss decreases perfusion through adipose tissue depots but has no influence on rGU demonstrating the 'sink' role of adipose tissue.
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Atrial fibrillation (AF) is associated with an increased risk of mortality and morbidity from stroke and thromboembolism. Endothelial damage or dysfunction may contribute to this increased risk of thromboembolism via the mediation of a prothrombotic or hypercoagulable state. However, the precise pathophysiological mechanism(s) relating endothelial (dys)function to AF and thromboembolism are yet to be fully elucidated. This review article aims to provide a comprehensive overview of endothelial (dys)function and AF, as well as the merits and limitations of the different methods used to assess endothelial function in AF.
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Mast cells (MCs) are perivascularly located resident cells of hematopoietic origin, recognized as effectors in inflammation and immunity. Their subendothelial location at the boundary between the intravascular and extravascular milieus, and their ability to rapidly respond to blood- and tissue-borne stimuli via release of potent vasodilatatory, proteolytic, fibrinolytic, and proinflammatory mediators, render MCs with a unique status to act in the first-line defense in various pathologies. We review experimental evidence suggesting a role for MCs in the pathophysiology of brain ischemia and hemorrhage. ⋯ MCs were reported to play a role in the tissue plasminogen activator-mediated cerebral hemorrhages after experimental ischemic stroke, and to be involved in the expansion of hematoma and edema following intracerebral hemorrhage. Importantly, the MC-stabilizing drug cromoglycate inhibited MC-mediated adverse effects on brain pathology and improved survival of experimental animals. This brings us to a position to consider MC stabilization as a novel initial adjuvant therapy in the prevention of brain injuries in hypoxia-ischemia in new-borns, as well as in ischemic stroke and intracerebral hemorrhage in adults.
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Long QT syndrome (LQTS) is an inherited arrhythmia disorder with an estimated prevalence of 0.01%-0.05%. In Finland, four founder mutations constitute up to 70% of the known genetic spectrum of LQTS. In the present survey, we sought to estimate the actual prevalence of the founder mutations and to determine their effect sizes in the general Finnish population. ⋯ In Finland 1 individual out of 250 carries a LQTS founder mutation, which is the highest documented prevalence of LQTS mutations that lead to a marked QT prolongation.
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The multiligand receptor RAGE (receptor for advanced glycation end-products) is emerging as a central mediator in the immune/inflammatory response. Epidemiological evidence accruing in the human suggests upregulation of RAGE's ligands (AGEs, S100/calgranulins, high mobility group box-1 (HMGB1), and amyloid beta-peptide and beta-sheet fibrils) and the receptor itself at sites of inflammation and in chronic diseases such as diabetes and neurodegeneration. ⋯ Lastly, we consider findings from animal model studies suggesting that although tissue-damaging effects ensue from recruitment of the ligand-RAGE interaction, in distinct settings, adaptive and repair/regeneration outcomes appear to override detrimental effects of RAGE. As RAGE blockade moves further into clinical development, clarifying the biology of RAGE garners ever-increasing importance.