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James Clark

Researcher at King's College London

Publications -  172
Citations -  8486

James Clark is an academic researcher from King's College London. The author has contributed to research in topics: Kinase & Ischemia. The author has an hindex of 41, co-authored 163 publications receiving 7745 citations. Previous affiliations of James Clark include Imperial College London & St Thomas' Hospital.

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Carbon Monoxide-Releasing Molecules Characterization of Biochemical and Vascular Activities

TL;DR: It is reported that a series of transition metal carbonyls, termed here carbon monoxide-releasing molecules (CO-RMs), liberate CO to elicit direct biological activities and caused sustained vasodilation in precontracted rat aortic rings, attenuated coronary vasoconstriction in hearts ex vivo, and significantly reduced acute hypertension in vivo.
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Cardioprotective Actions by a Water-Soluble Carbon Monoxide–Releasing Molecule

TL;DR: It is found that tricarbonylchloro(glycinato)ruthenium(II) (CORM‐3) is stable in water at acidic pH but in physiological buffers rapidly liberates CO in solution, corroborate the notion that transition metal carbonyls could be used as carriers to deliver CO and highlight the bioactivity and potential therapeutic features of CO‐RMs in the mitigation of cardiac dysfunction.
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Heme oxygenase-1-derived bilirubin ameliorates postischemic myocardial dysfunction.

TL;DR: Exogenously administered bilirubin at concentrations as low as 100 nanomolar significantly restored myocardial function and minimized both infarct size and mitochondrial damage on reperfusion, providing strong evidence for a primary role of HO-1-derived bilirUBin in cardioprotection against reperfusions injury.
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Dynamics of haem oxygenase-1 expression and bilirubin production in cellular protection against oxidative stress.

TL;DR: It is found that hemin-mediated increase in HO-1 protein expression and haem oxygenase activity is associated with augmented bilirubin levels, providing direct evidence that bilirubs generated after up-regulation of the HO- 1 pathway is cytoprotective against oxidative stress.
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Thiol Compounds Interact with Nitric Oxide in Regulating Heme Oxygenase-1 Induction in Endothelial Cells INVOLVEMENT OF SUPEROXIDE AND PEROXYNITRITE ANIONS

TL;DR: The existence of a dynamic equilibrium among free NO, O·̄2, and endogenous glutathione, which might constitute an interactive signaling mechanism modulating stress and adaptive responses in tissues is suggested.