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In patients with left ventricular (LV) dysfunction, the risk of death or heart failure hospitalizations (HFHs) increases with worsening ejection fraction (EF). Whether the relative contribution of atrial fibrillation (AF) to outcomes is more pronounced in patients with worse EF is not confirmed. The present study aimed to investigate the relative influence of AF on the outcome of cardiomyopathy patients by severity of LV dysfunction. In this observational study, data from 18,003 patients with EF ≤50% seen at a large academic institution between 2011 and 2017 were analyzed. Patients were stratified by EF quartiles (EF<25%, 25%≤EF<35%, 35%≤EF<40%, and EF≥40%, for quartiles 1, 2, 3, and 4, respectively). and followed to the end point of death or HFH. Outcomes of AF versus non-AF patients were compared within each EF quartile. During a median follow-up of 3.35 years, 8,037 patients (45%) died and 7,271 (40%) had at least 1 HFH. Rates of HFH and all-cause mortality increased as EF decreased. The hazard ratios (HRs) of death or HFH for AF versus non-AF patients increased steadily with increasing EF (HR of 1.22, 1.27, 1.45, 1.50 for quartiles 1, 2, 3, and 4, respectively, p = 0.045) driven primarily by the risk of HFH (HR of 1.26, 1.45, 1.59, 1.69 for quartiles 1, 2, 3, and 4, respectively, p = 0.045). In conclusion, in patients with LV dysfunction, the detrimental influence of AF on the risk of HFH is more pronounced in those with more preserved EF. Mitigation strategies for AF with the goal of decreasing HFH may be more impactful in patients with more preserved LV function.
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http://dx.doi.org/10.1016/j.amjcard.2023.04.033 | DOI Listing |
Mol Cell Biol
September 2025
Laboratory of Biochemistry, Faculty of Pharmaceutical Sciences, Hokkaido University, Sapporo, Japan.
Mammalian cell membranes contain ether lipids, which include an alkyl chain derived from a fatty alcohol that is produced by fatty acyl-CoA reductases (FARs). There are two mammalian FAR genes, and , and mutations in cause the peroxisomal fatty acyl-CoA reductase 1 disorder (PFCRD), which is accompanied by various symptoms, including neurological disorders. To date, the contributions of and to brain ether lipid production and the molecular mechanism of PFCRD have remained unknown.
View Article and Find Full Text PDFDev Psychobiol
September 2025
Department of Psychiatry, University of Illinois Chicago, Chicago, Illinois, USA.
Depressed mothers often experience parenting difficulties, which can persist after their symptoms have remitted. However, not all depressed mothers show parenting struggles, suggesting that there could be unidentified characteristics that increase risk. Specifically, neurobiological models emphasize that reward system deficits contribute to maladaptive parenting and depression, but no studies have evaluated how they could conjointly lead to parenting challenges.
View Article and Find Full Text PDFGenetics
September 2025
Department of Biology, McGill University, 3649 Sir William Osler, Montreal, Quebec, Canada H3G 0B1.
The E2F family of transcription factors are key regulators of the cell cycle in all metazoans. While they are primarily known for their role in cell cycle progression, E2Fs also play broader roles in cellular physiology, including the maintenance of exocrine tissue homeostasis. However, the underlying mechanisms that render exocrine cells particularly sensitive to E2F deregulation remain poorly understood.
View Article and Find Full Text PDFJ Anim Ecol
September 2025
Biodiversity Research Center, Academia Sinica, Taipei, Taiwan.
Migration is widespread among animals but varies in its manifestation with differences in direction, distance and obligatory nature. Understanding the evolution of migration requires insight into not only the development of this behaviour but also the loss of it. Partial migration, where some individuals within a population migrate while others stay, provides a unique opportunity to identify the proximate factors determining migratory/resident behaviours.
View Article and Find Full Text PDFActa Neuropathol Commun
September 2025
Department of Biomedical and Clinical Sciences and Department of Clinical Pathology, Linköping University, 58185, Linköping, Sweden.
Disruptions in synaptic transmission and plasticity are early hallmarks of Alzheimer's disease (AD). Endosomal trafficking, mediated by the retromer complex, is essential for intracellular protein sorting, including the regulation of amyloid precursor protein (APP) processing. The VPS35 subunit, a key cargo-recognition component of the retromer, has been implicated in neurodegenerative diseases, with mutations such as L625P linked to early-onset AD.
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