Results 131 to 140 of about 17,482 (208)

Human‐derived cardiac‐neural microtissues reveal catecholaminergic polymorphic ventricular tachycardia is also a disease of the sympathetic neuron

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend Schematic diagram illustrating the proposed pathway in which regulatory defects might occur in sympathetic neurons derived from hiPSC in catecholaminergic polymorphic ventricular tachycardia (CPVT). Specifically, enhanced calcium transients appeared to derive from three sources: enhanced membrane excitability (due to loss of ...
Ni Li   +19 more
wiley   +1 more source

Dysregulation of CD39/Ectonucleoside Triphosphate Diphosphohydrolase 1 Causes Urinary Bladder Dysfunction with Abnormal Smooth Muscle Contractility

open access: yesThe FASEB Journal, Volume 40, Issue 7, 15 April 2026.
Abnormal extracellular ATP levels cause lower urinary tract symptoms (LUTS). Here, we demonstrate that overexpression of ENTPD1 (CD39TG)—an ATP/ADP converting enzyme—reduces voiding frequency while increasing void volume. Conversely, ENTPD1 deficiency results in frequent, small‐volume voiding.
Zhaobo Luo   +7 more
wiley   +1 more source

Neuromuscular Blocking Agents

open access: yesJournal of Pharmacy and Pharmacology, 1961
Fiona MacLeod Carey   +3 more
openaire   +1 more source

Synthesis of p‐Coumarates With Potential Anti‐Alzheimer's Action: Enzyme Inhibition and In Silico Studies

open access: yesChemistry &Biodiversity, Volume 23, Issue 4, April 2026.
ABSTRACT Alzheimer's disease (AD) is a fatal neurodegenerative disorder that affects cognition, memory, and behavior. Such a disease is considered the most common cause of dementia and affects a large portion of the elderly population worldwide. Currently, cholinesterase inhibitors are used to reduce the symptoms and rate of progression of this disease.
Susiany Pereira Lopes   +6 more
wiley   +1 more source

Deficient Cardiolipin Remodelling Alters Muscle Fibre Composition and Neuromuscular Connectivity in Barth Syndrome

open access: yesJournal of Cachexia, Sarcopenia and Muscle, Volume 17, Issue 2, April 2026.
ABSTRACT Background Barth syndrome (BTHS) is a rare X‐linked mitochondrial disorder caused by mutations in the TAFAZZIN gene, which disrupts cardiolipin (CL) remodelling and mitochondrial function. While cardiac manifestations of BTHS are well characterized in male patients, the mechanisms underlying skeletal muscle weakness and fatigability are poorly
Catalina Matias   +7 more
wiley   +1 more source

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