|1.||Hidalgo, Cecilia: 3 articles (01/2015 - 01/2008)|
|2.||Donoso, Paulina: 3 articles (09/2008 - 12/2003)|
|3.||Sánchez, Gina: 3 articles (09/2008 - 12/2003)|
|4.||Ogawa, Yasuo: 3 articles (03/2007 - 12/2005)|
|5.||Pollock, Neil: 2 articles (01/2015 - 06/2010)|
|6.||Caputo, Carlo: 2 articles (12/2013 - 08/2008)|
|7.||Knollmann, Björn C: 2 articles (04/2013 - 01/2009)|
|8.||Katina, I E: 2 articles (11/2008 - 07/2002)|
|9.||Nasledov, G A: 2 articles (11/2008 - 07/2002)|
|10.||Macho, Pilar: 2 articles (01/2008 - 12/2003)|
12/01/1991 - "This study supports previous work suggesting the ryanodine contracture test as an improvement in the in-vitro diagnosis of MH susceptibility."
03/01/1998 - "In this study, four end-points were investigated: time to initial contracture development (Ot); time to development of a 10-mN contracture (10t); time from addition of ryanodine to when baseline tension exceeds pre-drug tension (0tp); and time for contracture to reach 10 mN above pre-drug baseline tension (10tp). "
08/01/2004 - "Ryanodine induced contractures in all specimens. "
08/01/2004 - "The effects of ryanodine on contracture responses were measured. "
08/01/2003 - "The ryanodine contracture test performed in addition to the IVCT may add clarity into diagnosing a patient as MH-susceptible or not."
09/01/1992 - "Ischemia produced a significant reduction in the number of ryanodine binding sites, while the dissociation constant of the binding reaction was unaffected."
04/01/2001 - "The study also compared [3H] ryanodine binding before ischemia (control group), after 30 min of ischemia (either global ischemia (GI group) or cardioplegic arrest (CA group)), and after 20 min of reperfusion. "
10/01/1992 - "In this study, the effects of regional ischemia on intrinsic SR Ca2+ release channel function were determined by studying the Ca2+ transport and release, and [3H]ryanodine binding properties of whole muscle homogenates and SR-enriched membrane fractions from normal and ischemic myocardium. "
09/12/2003 - "The main results on cardiac muscle were as follows: 1) Ischemia for up to 45 min in normal rat hearts had no obvious effect on the equilibrium ryanodine binding constant (K(d)), while the maximum number of ryanodine binding sites (B(max)) was affected in a time-dependent manner. "
11/02/1998 - "In parallel experiments, sarcoplasmic reticulum Ca2+ release and [3H]-ryanodine binding were determined before the sustained ischemia. "
07/01/2012 - "In PASMC perfused with normal KRBS, acute hypoxia caused a sustained increase in [Ca(2+)](i) that was abolished by ryanodine or XeC. "
09/01/2007 - "The results provide evidence that CCE activated by depletion of both InsP(3) and ryanodine SR Ca(2+) stores in canine PASMCs is dependent on functional InsP(3) receptors, whereas the activation of CCE by hypoxia appears to be independent of functional InsP(3) receptors."
04/01/2003 - "Importantly, ryanodine blunted hypoxic relaxation in control coronary arteries, suggesting that upregulated RyR might play a novel role in altered intracellular Ca(2+) handling during hypoxia."
02/01/2003 - "Ryanodine, a specific inhibitor of SR function, significantly increased force loss in ventricle preparations under anoxia. "
08/01/2001 - "We conclude that hypoxia releases intracellular Ca2+ from ryanodine-sensitive stores by a mechanism intrinsic to pulmonary vascular smooth muscle without the need for Ca2+ influx across the plasmalemma or an endothelial factor. "
|4.||Cardiac Arrhythmias (Arrythmia)
08/01/2009 - "Therapeutics, which are referred to as rycals, are currently being developed to treat cardiac arrhythmia via enhancement of calstabin-ryanodine affinities that causes a stabilization of the RyR. "
12/01/2012 - "It was suggested that defects in CASQ2 cause protein deficiency and impair Ca(2+) uptake to the sarcoplasmic reticulum and Ca(2+)-dependent inhibition of ryanodine channels, leading to diastolic Ca(2+) leak, after-depolarizations, and arrhythmia. "
04/01/2013 - "Flecainide was effective in patients with genotype-negative CPVT, suggesting that spontaneous Ca(2+) release from ryanodine channels plays a role in arrhythmia susceptibility, similar to that in patients with genotype-positive CPVT."
01/01/2012 - "The CaMKII-ryanodine signaling pathway can be used as a new means of treating ventricular arrhythmia."
01/01/2012 - "KN-93 and ryanodine can effectively reduce the occurrence of triggered ventricular arrhythmia in rabbits with LVH. "
02/14/1991 - "These data demonstrate that the Ca2(+)-induced Ca2+ release via the ryanodine-sensitive Ca2+ channel in canine cardiac SR was reduced during endotoxin shock. "
04/01/1998 - "Heat shock or PMA treatment of vector- or HSF1 cDNA-transfected cells to induce HSP-70 also attenuated the NaCN-induced increase in [Ca2+]i, perhaps because of a decrease in Vmax for the uptake of external Ca2+. Removal of external Ca2+ or treatment with inhibitors of Na+/Ca2+ exchangers eliminated the NaCN-induced increase in [Ca2+]i in HSP-70 cDNA-transfected cells, but ryanodine treatment did not. "
08/01/2008 - "We present evidence for the first time that the increase in [Ca(2+)](i) in rat cerebellar Type-1 astrocytes, resulting from moderate hypotonic shock, is mediated by Ca(2+) release from ryanodine-operated Ca(2+)(i) stores, and that the magnitude of the intracellular Ca(2+) signal induced by hypotonicity in the short term (up to 240 s) is small and controlled by the activity of the Na(+)/Ca(2+) exchanger operating in its extrusion mode. "
12/01/2013 - "Experiments using 2-aminoethoxydiphenyl borate, nifedipine, or Mn(2+) quenching, strongly suggest that the increased [Ca(2+)](myo) by ryanodine or hypertonic shock is mediated by potentiated SOCE activation. "
07/01/1992 - "Caffeine, ATP, and AMP-PCP activated while calmodulin, SKF-525A, ruthenium red, and Mg2+ inhibited [3H]ryanodine binding in both groups but the A0.5 (concentration requires for half-maximum activation) and the I50 (concentration requires for half-maximum inhibition) for the above-mentioned activators and inhibitors, respectively, were unaffected during endotoxin shock. "
|1.||Caffeine (No Doz)
|4.||Calcium Channels (Calcium Channel)
|6.||Adenosine Triphosphatases (ATPase)
|9.||Complementary DNA (cDNA)
|1.||Induced Heart Arrest (Cardioplegia)
|4.||Heart Transplantation (Grafting, Heart)