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Wilson's disease in two siblings from Ecuador: Two case reports.
World J Clin Cases
January 2025
Department of Radiology, Hospital de Especialidades Eugenio Espejo, Quito 170136, Pichincha, Ecuador.
Background: Wilson's disease (WD) is a rare metabolic disorder of copper accumulation in organs such as liver, brain, and cornea. Diagnoses and treatments are challenging in settings, where advanced diagnostic tests are unavailable, copper chelating agents are frequently scarce, healthcare professionals lack disease awareness, and medical follow-ups are limited. Prompt diagnoses and treatments help prevent complications, improve patients' quality of life, and ensure a normal life expectancy.
View Article and Find Full Text PDFPosttranslational modifications in cardiac metabolic remodeling mediated by metabolites: Implications for disease pathology and therapeutic potential.
Metabolism
January 2025
Department of Burns and Cutaneous Surgery, Xijing Hospital, Fourth Military Medical University, Chang-Le Xi Street #127, Xi' an 710032, China. Electronic address:
The nonenergy-producing or biomass-accumulating functions of metabolism are attracting increasing attention, as metabolic changes are gaining importance as discrete signaling pathways in modulating enzyme activity and gene expression. Substantial evidence suggests that myocardial metabolic remodeling occurring during diabetic cardiomyopathy, heart failure, and cardiac pathological stress (e.g.
View Article and Find Full Text PDFA High-Fat Diet Induces Epigenetic 1-Carbon Metabolism, Homocystinuria, and Renal-Dependent HFpEF.
Nutrients
January 2025
Department of Physiology, University of Louisville School of Medicine, Louisville, KY 40202, USA.
Background/objectives: Chronic gut dysbiosis due to a high-fat diet (HFD) instigates cardiac remodeling and heart failure with preserved ejection fraction (HFpEF), in particular, kidney/volume-dependent HFpEF. Studies report that although mitochondrial ATP citrate lyase (ACLY) supports cardiac function, it decreases more in human HFpEF than HFrEF. Interestingly, ACLY synthesizes lipids and creates hyperlipidemia.
View Article and Find Full Text PDFAssociations of Serum Cystatin C, DNAm Cystatin C, Renal Function, and Mortality in U.S. Adults.
Life (Basel)
December 2024
School of Medicine, College of Medicine, Fu Jen Catholic University, New Taipei City 242, Taiwan.
Serum cystatin C is a well-established marker of renal function and a valuable predictor of health risks and mortality. DNA methylation-predicted cystatin C (DNAmCystatinC), an advanced epigenetic biomarker, serves as a proxy for serum cystatin C levels. However, the relationships between serum cystatin C, DNAmCystatinC, renal function, and mortality outcomes have not been previously examined.
View Article and Find Full Text PDFAntisocial personality disorder:Failure to balance excitation/inhibition?
Neuropharmacology
January 2025
Division of Molecular Psychiatry, Center of Mental Health, University Hospital Würzburg, Würzburg, Germany; Department of Psychiatry, Psychosomatics and Psychotherapy, Center of Mental Health, University Hospital Würzburg, Würzburg, Germany.
While healthy brain function relies on a dynamic but tightly regulated interaction between excitation (E) and inhibition (I), a spectrum of social cognition disorders, including antisocial behavior and antisocial personality disorder (ASPD), frequently ensuing from irregular neurodevelopment, may be associated with E/I imbalance and concomitant alterations in neural connectivity. Technological advances in the evaluation of structural and functional E/I balance proxies in clinical settings and in human cell culture models provide a general basis for identification of biomarkers providing a powerful concept for prevention and intervention across different dimensions of mental health and disease. In this perspective we outline a framework for research to characterize neurodevelopmental pathways to antisocial behavior and ASPD driven by (epi)genetic factors across life, and to identify molecular targets for preventing the detrimental effects of cognitive dysfunction and maladaptive social behavior, considering psychosocial experience; to validate signatures of E/I imbalance and altered myelination proxies as biomarkers of pathogenic neural circuitry mechanisms to determine etiological processes in the transition from mental health to antisocial behavior and ASPD and in the switch from prevention to treatment; to develop a neurobiologically-grounded integrative model of antisocial behavior and ASPD resultant of disrupted E/I balance, allowing to establish objective diagnoses and monitoring tools, to personalize prevention and therapeutic decisions, to predict treatment response, and thus counteract relapse; and finally, to promote transformation of dimensional disorder taxonomy and to enhance societal awareness and reception of the neurobiological basis of antisocial behavior and ASPD.
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