Research Topics
| James DowneySummaryAffiliation: University of South Alabama Country: USA Publications
Research Grants
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Detail Information
Publications
Cardioprotective PKG-independent NO signaling at reperfusionMichael V Cohen
Department of Physiology, University of South Alabama College of Medicine, Mobile, Alabama 36688, USA
Am J Physiol Heart Circ Physiol 299:H2028-36. 2010..Hence, NO signaling occurs in IPC's mediator pathway downstream of Akt and ERK, and its protection is independent of PKG...- Reducing infarct size in the setting of acute myocardial infarctionJames M Downey
Department of Physiology, University of South Alabama, College of Medicine, Mobile, AL 36688, USA
Prog Cardiovasc Dis 48:363-71. 2006..Before any approach is tested in the clinical arena, however, it should be thoroughly vetted in preclinical settings. Only then can industry maximize the chances that its application in man will have the highest chance of success... - Unraveling the mysteries of classical preconditioningJames M Downey
Department of Physiology, MSB 3074, College of Medicine, University of South Alabama, Mobile, AL 36688, USA
J Mol Cell Cardiol 39:845-8. 2005..In this document, we have been asked to reflect on those four papers and comment on where they have led us... - Why do we still not have cardioprotective drugs?James M Downey
Department of Physiology, College of Medicine, University of South Alabama, Mobile, AL 36688, USA
Circ J 73:1171-7. 2009..Clearly more study is needed to identify which interventions are adversely affected by comorbidities... - Mapping preconditioning's signaling pathways: an engineering approachJames M Downey
Department of Physiology and Medicine, University of South Alabama, Mobile, AL 36688, USA
Ann N Y Acad Sci 1123:187-96. 2008..The proposed signaling maps reveal many points at which drugs can trigger the protected phenotype... - Bradykinin induces mitochondrial ROS generation via NO, cGMP, PKG, and mitoKATP channel opening and leads to cardioprotectionOlaf Oldenburg
Dept. of Physiology, MSB 3074, Univ. of South Alabama, College of Medicine, Mobile, AL 36688, USA
Am J Physiol Heart Circ Physiol 286:H468-76. 2004..control). Hence, BK preconditions through receptor-mediated production of nitric oxide, which activates guanylyl cyclase. The resulting cGMP activates PKG, which opens mitoKATP. Subsequent release of ROS triggers cardioprotection... - Redox signaling at reperfusion is required for protection from ischemic preconditioning but not from a direct PKC activatorYanping Liu
Department of Physiology, MSB 3074, University of South Alabama College of Medicine, Mobile, AL 36688, USA
Basic Res Cardiol 103:54-9. 2008..We conclude that while redox signaling during the first few minutes of reperfusion is an essential component of preconditioning's protective mechanism, this step occurs upstream of PKC activation... - P1075 opens mitochondrial K(ATP) channels and generates reactive oxygen species resulting in cardioprotection of rabbit heartsOlaf Oldenburg
Department of Physiology, University of South Alabama, College of Medicine, Mobile, AL 36688, USA
J Mol Cell Cardiol 35:1035-42. 2003..7 +/- 9.5% and 27.7 +/- 4.6% infarction, respectively; P = n.s. vs. untreated hearts). These data provide strong evidence that P1075 does open mitoK(ATP) channels and protects the ischemic rabbit heart in a mitoK(ATP)-dependent manner... - Mitochondrial ROS generation following acetylcholine-induced EGF receptor transactivation requires metalloproteinase cleavage of proHB-EGFThomas Krieg
Department of Physiology, College of Medicine, University of South Alabama, MSB 3074, Mobile, AL 36688, USA
J Mol Cell Cardiol 36:435-43. 2004.... - ACh and adenosine activate PI3-kinase in rabbit hearts through transactivation of receptor tyrosine kinasesThomas Krieg
Department of Physiology, University of South Alabama, Mobile 36688, USA
Am J Physiol Heart Circ Physiol 283:H2322-30. 2002..Therefore, G(i) protein-coupled receptors can activate PI3-kinase/Akt through transactivation of receptor tyrosine kinases in an Src tyrosine kinase-dependent manner... - The relative order of mK(ATP) channels, free radicals and p38 MAPK in preconditioning's protective pathway in rat heartYuankun Yue
Department of Cell Biology and Neuroscience, MSB 2342, University of South Alabama, College of Medicine, Mobile 36688, USA
Cardiovasc Res 55:681-9. 2002..CONCLUSIONS: These results indicate that mK(ATP) opening occurs upstream of mitochondrial ROS generation in the protective pathway. Furthermore, protection afforded by anisomycin was p38 MAPK- and ROS-dependent... - Localizing extracellular signal-regulated kinase (ERK) in pharmacological preconditioning's trigger pathwaySebastian Philipp
Department of Physiology, MSB 3074, University of South Alabama College of Medicine, Mobile, 36688, USA
Basic Res Cardiol 101:159-67. 2006..In isolated hearts, ACh caused phosphorylation of both Akt and ERK. U0126 blocked phosphorylation of ERK but not of Akt. The PI3-K inhibitor wortmannin blocked both. Together these data indicate that ERK is located between Akt and NOS... - Postconditioning protects rabbit hearts through a protein kinase C-adenosine A2b receptor cascadeSebastian Philipp
Department of Physiology, University of South Alabama, College of Medicine, Mobile, AL 36688, United States
Cardiovasc Res 70:308-14. 2006..It is still unclear why PKC activation is required to make the heart's adenosine become protective... - Acetylcholine leads to free radical production dependent on K(ATP) channels, G(i) proteins, phosphatidylinositol 3-kinase and tyrosine kinaseOlaf Oldenburg
Department of Physiology, MSB 3024, College of Medicine, University of South Alabama, Mobile 36688, USA
Cardiovasc Res 55:544-52. 2002.... - Protein kinase C protects preconditioned rabbit hearts by increasing sensitivity of adenosine A2b-dependent signaling during early reperfusionAtsushi Kuno
Department of Physiology, MSB 3074, University of South Alabama, College of Medicine, Mobile, AL 36688, USA
J Mol Cell Cardiol 43:262-71. 2007..We propose that the key protective event in IPC occurs when PKC increases the heart's sensitivity to adenosine so that endogenous adenosine can activate A(2b)-dependent signaling... - Infarct limitation by a protein kinase G activator at reperfusion in rabbit hearts is dependent on sensitizing the heart to A2b agonists by protein kinase CAtsushi Kuno
Department of Physiology, University of South Alabama, College of Medicine, Mobile, AL 36688, USA
Am J Physiol Heart Circ Physiol 295:H1288-H1295. 2008..Activated PKC then augments sensitivity of normally low-affinity cardiac adenosine A2b receptors so endogenous adenosine can protect by activating Akt and ERK... - Acetylcholine but not adenosine triggers preconditioning through PI3-kinase and a tyrosine kinaseQining Qin
Department of Physiology, University of South Alabama, Mobile 36688, USA
Am J Physiol Heart Circ Physiol 284:H727-34. 2003..Neither PI3-kinase nor Src kinase is a mediator of the protection of ACh... - Mechanism of cardioprotection by early ischemic preconditioningXiulan Yang
Department of Physiology, College of Medicine, University of South Alabama, MSB 3074, Mobile, AL 36688, USA
Cardiovasc Drugs Ther 24:225-34. 2010..Herein we review the evidence for the above mechanisms and their functional details... - Multiple, brief coronary occlusions during early reperfusion protect rabbit hearts by targeting cell signaling pathwaysXi-Ming Yang
Department of Physiology, University of South Alabama, College of Medicine, Mobile 36688, USA
J Am Coll Cardiol 44:1103-10. 2004..These observations suggest that a similar approach could be applied in the cardiac catheterization laboratory to protect reperfused myocardium after primary angioplasty in patients with acute myocardial infarction... - Timing and duration of administration are crucial for antiinfarct effect of AMP 579 infused at reperfusion in rabbit heartZhelong Xu
Departments of Physiology, University of South Alabama, College of Medicine, Mobile, AL 36688, USA
Heart Dis 5:368-71. 2003..Importantly, because AMP 579 can protect when administered up to the time of reperfusion, it likely prevents a reperfusion injury, and, therefore, has impressive clinical potential... - Protection from AMP 579 can be added to that from either cariporide or ischemic preconditioning in ischemic rabbit heartZhelong Xu
Deparment of Physiology, University of South Alabama, College of Medicine, Mobile, AL 36688, USA
J Cardiovasc Pharmacol 40:510-8. 2002..The combination of AMP 579 + cariporide was particularly efficacious and could be useful in the surgical setting... - AMP579 is revealed to be a potent A2b-adenosine receptor agonist in human 293 cells and rabbit heartsYanping Liu
Department of Physiology, University of South Alabama Collegeof Medicine, MSB 3074, Mobile, AL 36688, USA
Basic Res Cardiol 105:129-37. 2010..2 +/- 3.1% infarction) which is consistent with an A2b mechanism. We conclude that AMP579 is a non-selective, but potent A2b-AR agonist, and that its protection against infarction is through that receptor... - Desferoxamine and ethyl-3,4-dihydroxybenzoate protect myocardium by activating NOS and generating mitochondrial ROSSebastian Philipp
Dept. of Physiology, Univ. of South Alabama College of Medicine, Mobile, AL 36688, USA
Am J Physiol Heart Circ Physiol 290:H450-7. 2006..Hence, DFO and EDHB stimulate NO-dependent activation of PKG to open mitoK(ATP) channels and produce ROS, which act as second messengers to trigger entrance into the preconditioned state... - Redox signaling triggers protection during the reperfusion rather than the ischemic phase of preconditioningTurhan Dost
Dept of Physiology, MSB 3074, University of South Alabama, College of Medicine, Mobile, AL, 36688, USA
Basic Res Cardiol 103:378-84. 2008..5 +/- 9.0%). Hence redox signaling occurs during the reperfusion phase of IPC, and the critical component in that reperfusion phase appears to be molecular oxygen... - Preconditioning one myocardial region does not neccessarily precondition the whole rabbit heartAtsushi Nakano
Department of Physiology, University of South Alabama, College of Medicine, Mobile 36688, USA
Basic Res Cardiol 97:35-9. 2002..Because remote PC could not be demonstrated in rabbits, this phenomenon may be species or protocol-specific, and should not be assumed to occur in man... - Atrial natriuretic peptide administered just prior to reperfusion limits infarction in rabbit heartsXi-Ming Yang
Department of Physiology, University of South Alabama College of Medicine, MSB 3050, Mobile, AL 36688, USA
Basic Res Cardiol 101:311-8. 2006..ANP administered just prior to reperfusion protects hearts against infarction, likely by activation of PKG, opening of mKATP, and stimulation of downstream kinases... - Nicorandil opens mitochondrial K(ATP) channels not only directly but also through a NO-PKG-dependent pathwayAtsushi Kuno
Dept of Physiology, MSB 3070, College of Medicine University of South Alabama, Mobile, AL 36688, USA
Basic Res Cardiol 102:73-9. 2007..These results indicate that nicorandil, in addition to its direct effect on the channels, opens mitoK(ATP) channels indirectly via a NO-PKG signaling pathway... - Signaling pathways in ischemic preconditioningJames M Downey
Department of Physiology, College of Medicine, University of South Alabama, Mobile, AL 36688, USA
Heart Fail Rev 12:181-8. 2007..The reperfused heart requires the support of the protective signals for only about an hour after which the ischemic injury is repaired and the signals are no longer needed... - Endogenous adenosine protects preconditioned heart during early minutes of reperfusion by activating AktNataliya V Solenkova
Dept. of Physiology, Univ. of South Alabama, College of Medicine, Mobile, AL 36688, USA
Am J Physiol Heart Circ Physiol 290:H441-9. 2006..Although PI3K activity must continue long into the reperfusion phase, adenosine receptor occupancy is no longer needed by 30 min of reperfusion, and ERK activity is only required in the first few minutes of reperfusion... - Mitochondrial K(ATP) channels: role in cardioprotectionOlaf Oldenburg
Department of Physiology, MSB 3024, University of South Alabama, College of Medicine, Mobile 36688, USA
Cardiovasc Res 55:429-37. 2002..Thus the mK(ATP) probably serves a dual role as both a trigger and a mediator. Possible end-effectors of preconditioning's protection are discussed including the mK(ATP) itself... - Exogenous NO triggers preconditioning via a cGMP- and mitoKATP-dependent mechanismQining Qin
Department of Physiology, College of Medicine, University of South Alabama, Mobile, AL 36688, USA
Am J Physiol Heart Circ Physiol 287:H712-8. 2004.... - Acidosis, oxygen, and interference with mitochondrial permeability transition pore formation in the early minutes of reperfusion are critical to postconditioning's successMichael V Cohen
Dept of Physiology, University of South Alabama, College of Medicine, Mobile, AL 36688, USA
Basic Res Cardiol 103:464-71. 2008..The low pH, on the other hand, is equally necessary and seems to suppress MPTP directly rather than through upstream signaling... - Acetylcholine-induced production of reactive oxygen species in adult rabbit ventricular myocytes is dependent on phosphatidylinositol 3- and Src-kinase activation and mitochondrial K(ATP) channel openingOlaf Oldenburg
Department of Physiology, MSB 1201, University of South Alabama, College of Medicine, Mobile, AL 36688, USA
J Mol Cell Cardiol 35:653-60. 2003.... - Adenosine: trigger and mediator of cardioprotectionMichael V Cohen
Division of Physiology, College of Medicine, University of South Alabama, Mobile, AL 36688, USA
Basic Res Cardiol 103:203-15. 2008..The same A(2B) receptors are critical for postconditioning's protection. Thus adenosine is both an important trigger and a mediator of cardioprotection... - The pH hypothesis of postconditioning: staccato reperfusion reintroduces oxygen and perpetuates myocardial acidosisMichael V Cohen
Department of Physiology, MSB 3050, University of South Alabama, College of Medicine, Mobile, AL 36688, USA
Circulation 115:1895-903. 2007..Acidosis also suppresses MPTP formation. We tested whether postconditioning protects by maintaining acidosis during early reoxygenation... - Preconditioning-mimetics bradykinin and DADLE activate PI3-kinase through divergent pathwaysMichael V Cohen
Department of Physiology, University of South Alabama, College of Medicine, Mobile, AL 36688, USA
J Mol Cell Cardiol 42:842-51. 2007..Hence bradykinin, unlike acetylcholine or opioid, does not transactivate EGFR, although all 3 agonists do signal through Src and PI3-K... - Modulation of receptor sensitivity: possible therapeutic target?Michel V Cohen
Department of Physiology, University of South Alabama, College of Medicine, Mobile, AL 36688, USA
Br J Pharmacol 156:899-900. 2009.... - Peptide blockers of PKG inhibit ROS generation by acetylcholine and bradykinin in cardiomyocytes but fail to block protection in the whole heartThomas Krieg
Dept of Physiology, MSB 3050, University of South Alabama College of Medicine, Mobile, AL 36688, USA
Am J Physiol Heart Circ Physiol 288:H1976-81. 2005..Although the peptides may be inappropriate for a whole heart model, they are likely to become important tool drugs for elucidation of signal transduction pathways in cell preparations... - Attenuation of infarction in cynomolgus monkeys: preconditioning and postconditioningXi Ming Yang
Department of Physiology, MSB 3050, College of Medicine, University of South Alabama, Mobile, AL 36688, USA
Basic Res Cardiol 105:119-28. 2010..We conclude that ischemic preconditioning is extremely protective in cynomolgus hearts despite their sparse collateralization but, surprisingly, the protocol of IPOC used in this study offers less protection... - Acetylcholine and bradykinin trigger preconditioning in the heart through a pathway that includes Akt and NOSThomas Krieg
Dept. of Physiology, MSB 3074, Univ. of South Alabama, College of Medicine, Mobile, AL 36688, USA
Am J Physiol Heart Circ Physiol 287:H2606-11. 2004..L-NIO also blocked the anti-infarct effect of ACh (550 microM) in isolated rabbit hearts exposed to 30 min of regional ischemia. We conclude that both bradykinin and ACh trigger ROS generation by sequentially activating Akt and NOS... - Mechanisms of acetylcholine- and bradykinin-induced preconditioningStuart D Critz
Department of Cell Biology and Neuroscience, MSB 2342, University of South Alabama College of Medicine, Mobile, AL 36688, United States
Vascul Pharmacol 42:201-9. 2005..Understanding the cellular basis of protection by ACh and BK is a critical step towards developing pharmacological agents that will prevent infarction during ischemia resulting from coronary occlusion or heart attack... - NECA and bradykinin at reperfusion reduce infarction in rabbit hearts by signaling through PI3K, ERK, and NOXi-Ming Yang
Department of Physiology, College of Medicine, University of South Alabama, MSB 3074, Mobile, AL 36688, USA
J Mol Cell Cardiol 36:411-21. 2004..Curiously, however, ACh, unlike bradykinin, was not protective when administered at reperfusion. Hence, both NECA and bradykinin administered at reperfusion protect through a common signaling pathway that includes PI3K, NO, and ERK... - Ischemic postconditioning: from receptor to end-effectorMichael V Cohen
Department of Physiology, College of Medicine, University of South Alabama, Mobile, AL 36688, USA
Antioxid Redox Signal 14:821-31. 2011..Interference with MPTP may be the final step that determines cell salvage... - Postconditioning's protection is not dependent on circulating blood factors or cells but involves adenosine receptors and requires PI3-kinase and guanylyl cyclase activationXi-Ming Yang
Dept. of Physiology, MSB 3050 University of South Alabama, College of Medicine, Mobile (AL) 36688, USA
Basic Res Cardiol 100:57-63. 2005..These signaling steps have also been identified in preconditioning and during pharmacologic cardioprotection and suggest commonality of a protective mechanism... - Nitric oxide is a preconditioning mimetic and cardioprotectant and is the basis of many available infarct-sparing strategiesMichael V Cohen
Department of Physiology, University of South Alabama, College of Medicine, Mobile, AL 36688, United States
Cardiovasc Res 70:231-9. 2006..Activation of NOS or production of NO can be done pharmacologically with exogenous agents to trigger this cascade. Many of these strategies are already available and safe... - A(2b) adenosine receptors can change their spotsMichael V Cohen
Department of Physiology, University of South Alabama, Mobile, 36688, USA
Br J Pharmacol 159:1595-7. 2010..This plasticity and versatility of A(2b) adenosine receptors position them as potential triggers of signalling in multiple signalling cascades in many physiological responses, making this a most interesting receptor indeed... - Activation of Akt is essential for acetylcholine to trigger generation of oxygen free radicalsThomas Krieg
Department of Physiology, University of South Alabama, Mobile, AL 36688, USA
Cardiovasc Res 58:196-202. 2003..The experiments reveal that Akt is positioned between the receptor and the K(ATP) channel in this model... - Opening of ATP-sensitive potassium channels causes generation of free radicals in vascular smooth muscle cellsMaike Krenz
Department of Physiology, MSB 3024, University of South Alabama, College of Medicine, Mobile, AL 36688, USA
Basic Res Cardiol 97:365-73. 2002..Furthermore, a potassium-selective ionophore can mimic the effect of putative mitochondrial KATP channel openers. We conclude that potassium movement through KATP directly leads to ROS production by the mitochondria... - CGX-1051, a peptide from Conus snail venom, attenuates infarction in rabbit hearts when administered at reperfusionShi Jun Zhang
Department of Physiology, University of South Alabama, College of Medicine, Mobile, Alabama 36688, USA
J Cardiovasc Pharmacol 42:764-71. 2003..CGX-1051 caused no hemodynamic alterations at any dose tested. We conclude that CGX-1051 has a powerful anti-infarct effect when given just before reperfusion... - Dose-response relationships of the protective and antiprotective effects of acute ethanol exposure in isolated rabbit heartsMaike Krenz
Department of Physiology, University of South Alabama, College of Medicine, Mobile, Alabama 36688, USA
Heart Dis 4:276-81. 2002..Since it might be impossible to find a dose of ethanol that would be protective if administered shortly before ischemia, ethanol should be removed before that ischemia to protect myocardium... - Total liquid ventilation provides ultra-fast cardioprotective coolingRenaud Tissier
Department of Physiology, University of South Alabama, College of Medicine, Mobile, Alabama 36688, USA
J Am Coll Cardiol 49:601-5. 2007..We tested whether total liquid ventilation (TLV) can be used to rapidly cool and protect the infarcting heart... - Mitochondrial K(ATP) channels in preconditioningOlaf Oldenburg
Department of Physiology, College of Medicine, University of South Alabama, MSB 3074, Mobile, AL 36688, USA
J Mol Cell Cardiol 35:569-75. 2003 - Mitochondria and their role in preconditioning's trigger phaseThomas Krieg
Department of Physiology, MSB 3024, University of South Alabama College of Medicine, Mobile, AL 36688, USA
Basic Res Cardiol 98:228-34. 2003 - Xanthine oxidase contributes to preconditioning's preservation of left ventricular developed pressure in isolated rat heart: developed pressure may not be an appropriate end-point for studies of preconditioningRicardo J Gelpi
Department of Pathology, Faculty of Medicine, University of Buenos Aires, Argentina
Basic Res Cardiol 97:40-6. 2002..Therefore, post-ischemic developed pressure in the rat is significantly affected by purine-dependent stunning, and, hence, may be an unreliable marker of tissue salvage and also a poor index of what might be cardioprotective in man... - Free radicals in the heart: friend or foe?James M Downey
Expert Rev Cardiovasc Ther 6:589-91. 2008 - Spotlight on preconditioningDerek M Yellon
Cardiovasc Res 55:425-8. 2002 - The protective and anti-protective effects of ethanol in a myocardial infarct modelMaike Krenz
Department of Molecular and Cardiovascular Biology, The University of Cincinnati, Cincinnati, Ohio 45229, USA
Ann N Y Acad Sci 957:103-14. 2002..Ethanol can only exert its protective effect if it is removed before the onset of ischemia. If still present during ischemia, ethanol has the opposite effect, and inhibits preconditioning by an as yet unidentified mechanism... - cGMP signalling in pre- and post-conditioning: the role of mitochondriaAlexandre D T Costa
Department of Biology, Portland State University, PO Box 751, Portland, OR 97201, USA
Cardiovasc Res 77:344-52. 2008..The resulting ROS then activate a second PKC pool which, through another signal transduction pathway termed the mediator pathway, causes inhibition of MPT and reduction in cell death... - Protein kinase G transmits the cardioprotective signal from cytosol to mitochondriaAlexandre D T Costa
Department of Biology, Portland State University, Portland, Ore, USA
Circ Res 97:329-36. 2005..We conclude PKG is the terminal cytosolic component of the trigger pathway; it transmits the cardioprotective signal from cytosol to inner mitochondrial membrane by a pathway that includes PKC-epsilon... - Cardioprotection with adenosine A2 receptor activation at reperfusionZhelong Xu
Department of Anesthesiology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
J Cardiovasc Pharmacol 46:794-802. 2005.... - A really radical observation--a comment on Penna et al. in Basic Res Cardiol (2006) 101:180-189James M Downey
Basic Res Cardiol 101:190-1. 2006 - AMISTAD trials: possible reasons for lack of successMichael V Cohen
J Am Coll Cardiol 47:1236; author reply 1236-7. 2006 - Preconditioning the myocardium: from cellular physiology to clinical cardiologyDerek M Yellon
The Hatter Institute for Cardiovascular Studies, Centre for Cardiology, University College London Hospital and Medical School, Grafton Way, London, UK
Physiol Rev 83:1113-51. 2003.... - We think we see a pattern emerging hereJames M Downey
Circulation 111:120-1. 2005 - Making the heart resistant to infarction: how can we further decrease infarct size?Renaud Tissier
INSERM, Unite 841, Creteil, F 94000 France
Front Biosci 13:284-301. 2008..g., calcium overload and free radical attack), (2) those based on activation of the RISK pathway including postconditioning, and (3) myocardial cooling... - Protection from post-conditioning depends on the number of short ischemic insults in anesthetized pigsEfstathios K Iliodromitis
Second University Department of Cardiology, Medical School, Attikon General Hospital, University of Athens, Athens, Greece
Basic Res Cardiol 101:502-7. 2006..Post-conditioning may protect by inhibiting mitochondrial permeability transition pore formation by keeping the heart acidotic as it is reoxygenated. If true, then it would be difficult to employ too many occlusion cycles... - Bypassing big pharmaJames M Downey
Circulation 116:1344-5. 2007
Research Grants
- PHYSICAL FACTORS AND CORONARY FLOWJames Downey; Fiscal Year: 2002..I will test whether the presence of PC's protected state is due to translocation of a PKC isoform to a specific intracellular site. Finally, I propose to examine the role of c-jun kinase (JNK) in the PC heart. ..
- Aging Heart and Vessels (International Conference)James Downey; Fiscal Year: 2004..7. To give governments a summary of new research findings and potential for the future that may contribute to health planning and problem solving from community to nation level. 8. To publish the proceedings as a public record. ..
- PHYSICAL FACTORS AND CORONARY FLOWJames Downey; Fiscal Year: 2006..The 6th aim will test whether ROS from high levels of xanthine oxidase in rat heart can lead to non-receptor triggering of preconditioning in that species. ..
- PHYSICAL FACTORS AND CORONARY FLOWJames Downey; Fiscal Year: 1980..These experiments will better define the nature of the salvageable tissue following coronary occlusion...
- PHYSICAL FACTORS AND CORONARY FLOWJames Downey; Fiscal Year: 1993..Finally we will test whether Gi proteins are involved in this response. The overall aim is to identify a compound which would be capable of maintaining a patient's heart in a preconditioned state indefinitely...
- PHYSICAL FACTORS AND CORONARY FLOWJames M Downey; Fiscal Year: 2010..Understanding its mechanism should help us devise ways to duplicate preconditioning's protection in the coronary patient. ..