In most people with epilepsy, the condition is readily controlled, but 20-30% develop chronic epilepsy. An estimated 80,000 patients with epilepsy require ongoing specialist care in the United Kingdom. Nutrition may be a factor in the development of chronic epilepsy. Modern Western diets are thought to produce a low-grade chronic metabolic acidosis. The hydrogen ion, H+, is a potent modulator of NMDA-activated currents, and in cultured neurons, increased external [H+] strongly suppresses these currents. The effect of chronic metabolic acidosis in vivo has not been fully studied. It is possible that low-grade chronic metabolic acidosis chronically inhibits the NMDA-activated currents, and this may lead to upregulation of the NMDA receptor. This would result in a greater hyperexcitable state and may contribute to the development of chronic epilepsy.
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http://dx.doi.org/10.1016/j.yebeh.2005.11.012 | DOI Listing |
Fish Physiol Biochem
January 2025
Department of Biology, Ecology and Earth Science, University of Calabria, Rende, Italy.
Under low O, the heart of Carassius auratus (goldfish) shows an enhanced hemodynamics. This is observed in ex vivo cardiac preparations from animals acclimated to both normoxia and short-term (4 days) moderate hypoxia and perfused for 90 min with a hypoxic medium. Under short-term hypoxia, this is associated with a higher ventricular muscularity and an expanded mitochondrial compartment.
View Article and Find Full Text PDFBiol Trace Elem Res
January 2025
Laboratory for Toxicology and Micronutrient Metabolism, Chemical Pathology Department, College of Medicine, University of Ibadan, Ibadan, Nigeria.
Auto-mechanics who often work without safety measures are vulnerable to the harmful effects of toxic metals like lead (Pb) and cadmium (Cd). These toxic metals exert their deleterious effect by interacting with the micronutrients at their primary site of action. This study aimed to investigate the effects of toxic metal exposure on serum micronutrient levels of auto-mechanics in Nigeria.
View Article and Find Full Text PDFClin Exp Med
January 2025
Department of Medical Genetics, School of Medicine, Tehran University of Medical Sciences (TUMS), Tehran, Iran.
Cellular senescence is understood to be a biological process that is defined as irreversible growth arrest and was originally recognized as a tumor-suppressive mechanism that prevents further propagation of damaged cells. More recently, cellular senescence has been shown to have a dual role in prevention and tumor promotion. Senescent cells carry a senescence-associated secretory phenotype (SASP), which is altered by secretory factors including pro-inflammatory cytokines, chemokines, and other proteases, leading to the alteration of the tissue microenvironment.
View Article and Find Full Text PDFUrol Oncol
January 2025
The James Buchanan Brady Urological Institute and Department of Urology, Johns Hopkins University School of Medicine, Baltimore, MD; Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD. Electronic address:
Purpose: To investigate the association of diabetes mellitus and metformin use with metabolic acidosis risk after radical cystectomy (RC) and urinary diversion for bladder cancer.
Materials And Methods: This retrospective cohort study used TriNetX Research Network data. Patients undergoing RC with continent diversion or ileal conduit for bladder cancer were identified using International Classification of Diseases, 10th Revision (ICD-10) and ICD-10 Procedure Coding System (ICD-10-PCS) codes.
Kidney Int
February 2025
Department of Nephrology, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Institute for the Advanced Study of Human Biology, Kyoto University, Kyoto, Japan. Electronic address:
Previous reports have suggested that both the endoplasmic reticulum (ER) stress and cyclic guanosine monophosphate-adenosine monophosphate synthase-stimulator of interferon genes pathways contribute to the progression of chronic kidney disease; however, the relationship between these 2 pathways in kidney injury has not been fully elucidated. Andrade-Silva et al. revealed that the cyclic guanosine monophosphate-adenosine monophosphate synthase-stimulator of interferon genes pathway can enhance ER stress through the protein kinase R-like ER kinase (PERK)-mediated signaling cascade in kidney tubular epithelial cells and sequentially augment fibrosis during kidney injury.
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