|1.||Jacobson, Kenneth A: 6 articles (04/2015 - 01/2006)|
|2.||Madi, Lea: 6 articles (01/2013 - 06/2002)|
|3.||Fishman, Pnina: 6 articles (10/2007 - 06/2002)|
|4.||Bar-Yehuda, Sara: 6 articles (10/2007 - 06/2002)|
|5.||Salvemini, Daniela: 4 articles (04/2015 - 05/2012)|
|6.||Ochaion, Avivit: 4 articles (10/2007 - 05/2003)|
|7.||Tosh, Dilip K: 3 articles (04/2015 - 01/2009)|
|8.||Doyle, Timothy: 3 articles (04/2015 - 12/2014)|
|9.||Janes, Kali: 3 articles (02/2015 - 05/2012)|
|10.||Panjehpour, Mojtaba: 3 articles (11/2014 - 08/2004)|
02/19/1999 - "We have previously shown that chronic administration of the selective A3 receptor agonist N6-(3-iodobenzyl)-5'-N-methylcarboxoamidoadenosine (IB-MECA) leads to a significant improvement of postocclusive cerebral blood flow, and protects against neuronal damage and mortality induced by severe forebrain ischemia in gerbils. "
12/01/2004 - "In a spontaneously breathing cat model, in which the left lower lobe of the lung was isolated and subjected to 2 h of ischemia and 3 h of reperfusion, we tested the effect of IB-MECA, a selective A3AR agonist, on lung apoptosis and injury. "
02/01/2003 - "Higher doses of IB-MECA were lethal in C57 mice subjected to renal ischemia. "
02/01/1997 - "Replacing global ischemia with 5 min perfusion of the rabbit A3-selective agonist, IB-MECA (A3 Ki: 2 nM; A1 Ki: 30 nM) elicited a concentration-dependent reduction in infarct size; 50 nM IB-MECA reduced IA/AAR to 24 +/- 4%. "
11/01/2006 - "More importantly, IB-MECA can also protect the heart even when administered at the onset of reperfusion after ischemia, indicating a strong likelihood that the drug may be useful for the treatment of patients with acute myocardial infarction. "
03/16/2001 - "We investigated whether activation of A(1) or A(3) adenosine receptors (ARs) induces late preconditioning (PC) against infarction in conscious rabbits using the selective AR agonists 2-chloro-N(6)-cyclopentyladenosine (CCPA) and N(6)-3-iodobenzyladenosine-5'-N-methylcarboxamide (IB-MECA). "
08/01/2001 - "Recent studies have demonstrated that the adenosine A1 receptor agonist 2-chloro-N6-cyclopentyladenosine (CCPA) and the adenosine A3 receptor agonist N6-(3-iodobenzyl)adenosine-5'-N-methyluronamide (IB-MECA) produce a delayed phase of protection against infarction similar to the late phase of ischemic preconditioning (PC). "
06/01/1997 - "To examine the cardioprotective role of A3 adenosine receptors during myocardial ischemia/reperfusion injury, we tested the effect of N6-(3-iodobenzyl)adenosine-5'-N-methyluronamide (IB-MECA), a potent and selective A3 adenosine receptor agonist, in models of myocardial stunning and infarction in chronically instrumented conscious rabbits. "
07/01/2006 - "IB-MECA enhanced phosphorylation of GSK-3beta (Ser9) upon reperfusion, and the GSK-3 inhibitor 3-(2,4-dichlorophenyl)-4-(1-methyl-1H-indol-3-yl)-1H-pyrrole-2,5-dione (SB216763) (3 microM) mimicked the protective effect of IB-MECA by attenuating both infarction and the loss of DeltaPsim. "
06/01/1997 - "These results demonstrate that in conscious rabbits the A3 adenosine receptor agonist IB-MECA confers a powerful protection against both reversible (stunning) and irreversible (infarction) injury during acute myocardial ischemia and reperfusion by a protein kinase C-mediated pathway, suggesting that selective activation of A3 receptors is an effective means of protecting the ischemic myocardium without hemodynamic changes."
|3.||Myocardial Stunning (Stunned Myocardium)
06/01/1997 - "In phase I, IB-MECA markedly improved the recovery of wall thickening after the six occlusion/reperfusion cycles, and this effect was sustained throughout the 5-hour observation period; the total deficit of wall thickening (a measure of the overall severity of myocardial stunning) was reduced by 68% (control, 129 +/- 16 arbitrary units, n = 7; IB-MECA, 41 +/- 6 arbitrary units, n = 6; P < .01). "
09/01/2001 - "The goal of this study was to determine whether the protective effects of the A3AR agonist N6-(3-iodobenzyl)adenosine-5'-N-methylcarboxamide (IB-MECA) against myocardial stunning are mediated by the A1AR. "
09/23/2003 - "This myocardial stunning was unaffected by IB-MECA (3 x 10(-7) M) added 10 min into hypoxia. "
09/01/2001 - "Protection of IB-MECA against myocardial stunning in conscious rabbits is not mediated by the A1 adenosine receptor."
09/23/2003 - "Protection from myocardial stunning by ischaemia and hypoxia with the adenosine A3 receptor agonist, IB-MECA."
11/01/2004 - "In the feline lung, the A3AR agonist IB-MECA confers a powerful protection against IR lung injury. "
12/01/2004 - "In summary, even when given after the onset of ischemia, the A3AR agonist IB-MECA conferred a powerful protection against reperfusion lung injury, which was associated with decreased apoptosis. "
01/01/2006 - "Also, MRS3558 was found to be more potent than IB-MECA in attenuating reperfusion lung injury. "
07/01/2003 - "IB-MECA caused postischemic reduction in necrosis and improvement in ventricular function, which was abolished by CHE. "
03/01/2002 - "IB-MECA caused post-ischemic reduction in necrosis and improvement in myocardial performance which was abolished by A(3)AR antagonist, MRS1191. "
04/01/2001 - "Tissue necrosis was significantly reduced in the presence of R-PIA or IB-MECA. "
|1.||Adenosine A3 Receptor
|2.||Adenosine A1 Receptor
|3.||Purinergic P1 Receptors (Adenosine Receptor)
|5.||Staphylococcal Protein A (A, Protein)
|9.||2- chloro- N(6)- (3- iodobenzyl)- 5'- N- methylcarboxamidoadenosine (Cl-IB-MECA)
|1.||Drug Therapy (Chemotherapy)