Status epilepticus: Updates on mechanisms and treatments
Abstract Status epilepticus (SE) consists of prolonged, self‐sustaining seizures and is a common neurological emergency that causes respiratory compromise and neuronal injury. Without prompt treatment, the seizures can become resistant to benzodiazepines, leading to the progressive evolution of established, refractory, and super‐refractory SE.
Suchitra Joshi, Jaideep Kapur
wiley +1 more source
Novel perspectives in redox biology and pathophysiology of failing myocytes: modulation of the intramyocardial redox milieu for therapeutic interventions - A review article from the Working Group of Cardiac Cell Biology, Italian Society of Cardiology [PDF]
The prevalence of heart failure (HF) is still increasing worldwide, with enormous human, social, and economic costs, in spite of huge efforts in understanding pathogeneticmechanisms and in developing effective therapies that have transformed this ...
Angelini, Annalisa +8 more
core +5 more sources
Studies of the human m2 (hm2) muscarinic cholinergic receptors (mAChR) have been performed to provide further insights into the potential regulation of these receptors by isoforms of the beta-adrenergic receptor kinase (beta ARK). The hm2 mAChR and the isoforms beta ARK1 and beta ARK2 were individually expressed in, and purified from, insect Sf9 cells ...
R M, Richardson +3 more
openaire +2 more sources
Inhibition of beta-adrenergic receptor kinase prevents rapid homologous desensitization of beta 2-adrenergic receptors. [PDF]
Homologous (agonist-specific) desensitization of beta-adrenergic receptors (beta ARs) is accompanied by and appears to require phosphorylation of the receptors. We have recently described a novel protein kinase, beta AR kinase, which phosphorylates beta ARs in vitro in an agonist-dependent manner.
Lohse, MJ +3 more
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GRK6 regulates the hemostatic response to injury through its rate-limiting effects on GPCR signaling in platelets. [PDF]
G protein-coupled receptors (GPCRs) mediate the majority of platelet activation in response to agonists. However, questions remain regarding the mechanisms that provide negative feedback toward activated GPCRs to limit platelet activation and thrombus ...
Benovic, Jeffrey +13 more
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GRK et arrestines : la piste thérapeutique ? [PDF]
La phosphorylation d’un récepteur couplé aux protéines G (RCPG) par une kinase spécifique, nommée GRK (G protein-coupled receptor kinase), est une première étape qui participe, avec l’action des arrestines, à l’arrêt de la transmission du signal, au ...
Kraimps, Jean-Louis +2 more
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We tested the hypothesis that angiotensin II type 1 receptor blocker (ARB) may improve beta-adrenergic receptor (AR) coupling in heart failure (HF) after myocardial infarction (MI).Beta-AR desensitization is one of the mechanisms underlying the transition from compensated to decompensated HF.
Takahashi, Toshiyuki +7 more
openaire +2 more sources
Altered expression of beta-adrenergic receptor kinase and beta 1-adrenergic receptors in the failing human heart. [PDF]
BACKGROUND In chronic heart failure, the positive inotropic effects of beta-adrenergic receptor agonists are greatly reduced, in part as a result of two alterations of the cardiac beta-adrenergic receptors: loss of their function (receptor uncoupling) and reduction of their number (downregulation).
M, Ungerer +4 more
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ABSTRACT Metabolic dysfunction‐associated steatotic liver disease (MASLD) has emerged as the most prevalent chronic liver disease worldwide, closely linked to the global rising incidence of obesity and metabolic syndrome. This review synthesizes current evidence on the pathogenesis, gut–liver axis, and multidisciplinary management of MASLD within the ...
Beom Kyung Kim
wiley +1 more source
The Camerino symposium series (1978–2013): a privileged observatory of receptorology development [PDF]
The organizers of the Camerino Receptor Symposia survey the development of receptorology. They trace the course from the first Symposium in 1978, which laid the foundation for Pirenzepine, the first selective muscarinic antagonist, to the 2010 Symposium,
Mario Giannella, Piero Angeli
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