Journal of internal medicine
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Our understanding of the development of congenital heart disease (CHD) across the lifespan has evolved. These include the evidence for the change in demographics of CHD, the observations that lifelong complications of CHD result in CHD as a lifespan disease, and the concept of long windows of exposure to risk that start in foetal life and magnify the expression of risk in adulthood. These observations set the stage for trajectories as an emerging construct to target health-service interventions. ⋯ For researchers, life-course epidemiology offers a framework that will help increase the relevance of clinical enquiry and improve study design and analyses. A health-service policy framework is proposed for a growing number of conditions that start in the before birth and extend as long as contemporary survival now permits. Ultimately, the goal is the precision delivery of health services that enables lifelong health management, organization of developmental health services, and integration of vertical and horizontal health-service delivery.
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The prognosis of patients with congenital heart defects has improved significantly: more and more patients reach adulthood and old age. At the same time, the possibility of cardiovascular morbidity increases. The conventional risk factors for coronary artery disease are at least as high or even higher in patients than in the general population. ⋯ Fontan), the incidence of CAD might be lower, but it usually returns to the average level or higher after correction of the defect. Coronary artery disease is one of the most important reasons for mortality also in ACHD patients, and the consequences of a coronary event might be more fateful in a patient with a corrected congenital heart defect than in her/his peer. There should be a paradigm shift from operative mortality and short-term outcome to long-term morbidity and prevention of cardiovascular disease - a task that often has been forgotten during follow-up visits.
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One of the most frequent causes of cardiac embolism in cryptogenic stroke is a paradoxical embolus, which originate from systemic venous source though an unidentified patent foramen ovale (PFO). PFO is a common finding in the general population with a prevalence of 25% to 30%. Transcatheter PFO device closure is known to be feasible and safety treatment for such patients. ⋯ Based on these data, PFO device closure is recommended to carefully select cryptogenic stroke patients aged from 18 to 65 years, with a high probability of a causal role of the PFO in stroke events. However, it is still uncertain whether PFO closure is superior to oral anticoagulants therapy in these patients. Therefore, further prospective randomized trials are needed to address the efficacy of PFO device closure to oral anticoagulants therapy.
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The disproportionate obesity in African American (AA) women has a physiologic basis and can be explained by the interactive effects of insulin secretion, insulin clearance, insulin sensitivity and the glycaemic load of the diet. This review will present data supporting a physiologic basis for obesity propensity in obesity-prone AA women that resides in their unique metabolic/endocrine phenotype: high beta-cell responsiveness, low hepatic insulin extraction and relatively high insulin sensitivity, which together result in a high exposure of tissues and organs to insulin. When combined with a high-glycaemic (HG) diet (that stimulates insulin secretion), this underlying propensity to obesity becomes manifest, as ingested calories are diverted from energy production to storage. ⋯ Greater bioenergetic efficiency has been reported in AA and, via resultant oxidative damage, could plausibly contribute to insulin resistance. In summary, it is proposed here that a subset of AA women are predisposed to obesity due to a specific metabolic/endocrine phenotype. However, greater diabetes risk in AA has an independent aetiology based on impaired lipid storage and mitochondrial efficiency/oxidative stress.
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Review
Male reproductive health and intergenerational metabolic responses from a small RNA perspective.
The world has recently experienced a decline in male reproductive (e.g. sperm counts and motility) and metabolic (e.g. obesity and diabetes) health. Accumulated evidence from animal models also shows that the metabolic health of the father may influence the metabolic health in his offspring. Vectors for such paternal intergenerational metabolic responses (IGMRs) involve small noncoding RNAs (sncRNAs) that often increase in spermatozoa during the last days of maturation in the epididymis. ⋯ Together, this suggests that there are overlapping aetiologies between the male metabolic syndrome, male factor infertility and intergenerational responses. In this review, we present a theoretical framework for an overlap of these aetiologies by exploring the advances in our understanding of the roles of sncRNA in spermatogenesis and offspring development. A special focus will lie on novel findings about tRNA-derived small RNA (tsRNA), rRNA-derived small RNA (rsRNA) and small mitochondrial RNA (mitoRNA), and their emerging roles in intergenerational metabolic and reproductive health.