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A cause of excessive daytime sleepiness. The upper airway resistance syndrome.
Subjects with isolated complaints of chronic daytime sleepiness are usually classified as "idiopathic hypersomniacs" and treated symptomatically. A group of these subjects was investigated duringExpand
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"Stress-responsive" mitogen-activated protein kinases (c-Jun N-terminal kinases and p38 mitogen-activated protein kinases) in the myocardium.
The best-characterized subfamilies of the mitogen-activated protein kinase (MAPK) superfamily are the extracellularly responsive kinases (ERKs) and the two “stress-responsive” MAPK subfamilies,Expand
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The p38‐MAPK inhibitor, SB203580, inhibits cardiac stress‐activated protein kinases/c‐Jun N‐terminal kinases (SAPKs/JNKs)
SB203580 is a recognised inhibitor of p38‐MAPKs. Here, we investigated the effects of SB203580 on cardiac SAPKs/JNKs. The IC50 for inhibition of p38‐MAPK stimulation of MAPKAPK2 was approximatelyExpand
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Glycogen synthase kinase 3 (GSK3) in the heart: a point of integration in hypertrophic signalling and a therapeutic target? A critical analysis
Glycogen synthase kinase 3 (GSK3, of which there are two isoforms, GSK3α and GSK3β) was originally characterized in the context of regulation of glycogen metabolism, though it is now known toExpand
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Differential activation of protein kinase C isoforms by endothelin-1 and phenylephrine and subsequent stimulation of p42 and p44 mitogen-activated protein kinases in ventricular myocytes cultured
The translocation of protein kinase C (PKC) isoforms PKC-alpha, PKC-delta, PKC-epsilon, and PKC-zeta from soluble to particulate fractions was studied in ventricular cardiomyocytes cultured fromExpand
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Regulation of bcl-2 family proteins during development and in response to oxidative stress in cardiac myocytes: association with changes in mitochondrial membrane potential.
Cardiac myocyte apoptosis is potentially important in many cardiac disorders. In other cells, Bcl-2 family proteins and mitochondrial dysfunction are probably key regulators of the apoptoticExpand
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Small guanine nucleotide-binding proteins and myocardial hypertrophy.
The small (21 kDa) guanine nucleotide-binding protein (small G protein) superfamily comprises 5 subfamilies (Ras, Rho, ADP ribosylation factors [ARFs], Rab, and Ran) that act as molecular switches toExpand
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Stimulation of “Stress-regulated” Mitogen-activated Protein Kinases (Stress-activated Protein Kinases/c-Jun N-terminal Kinases and p38-Mitogen-activated Protein Kinases) in Perfused Rat Hearts by
“Stress-regulated” mitogen-activated protein kinases (SR-MAPKs) comprise the stress-activated protein kinases (SAPKs)/c-Jun N-terminal kinases (JNKs) and the p38-MAPKs. In the perfused heart,Expand
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Cellular mechanisms of cardiac hypertrophy
Hypertrophy of myocytes in the heart ventricles is an important adaptation that in vivo occurs in response to a requirement for increased contractile power. It involves changes at the level of geneExpand
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Stimulation of the p38 Mitogen-activated Protein Kinase Pathway in Neonatal Rat Ventricular Myocytes by the G Protein–coupled Receptor Agonists, Endothelin-1 and Phenylephrine: A Role in Cardiac
We examined the activation of the p38 mitogen-activated protein kinase (p38-MAPK) pathway by the G protein–coupled receptor agonists, endothelin-1 and phenylephrine in primary cultures of cardiacExpand
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