J
John M. Land
Researcher at UCL Institute of Neurology
Publications - 103
Citations - 8479
John M. Land is an academic researcher from UCL Institute of Neurology. The author has contributed to research in topics: Nitric oxide & Mitochondrial respiratory chain. The author has an hindex of 41, co-authored 103 publications receiving 7975 citations. Previous affiliations of John M. Land include University College Hospital & John Radcliffe Hospital.
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Journal ArticleDOI
Association between mitochondrial dysfunction and severity and outcome of septic shock
David Brealey,M. P. Brand,Iain P. Hargreaves,Simon J.R. Heales,John M. Land,Ryszard T. Smolenski,Nathan Davies,Chris E. Cooper,Mervyn Singer +8 more
TL;DR: In septic patients, an association between nitric oxide overproduction, antioxidant depletion, mitochondrial dysfunction, and decreased ATP concentrations that relate to organ failure and eventual outcome is found.
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Nitric oxide-mediated mitochondrial damage in the brain: mechanisms and implications for neurodegenerative diseases
Juan P. Bolaños,Angeles Almeida,VC Stewart,Stephan Peuchen,John M. Land,John B. Clark,Simon J.R. Heales +6 more
TL;DR: It is concluded that neurotoxicity elicited by excessive •NO production may be mediated by mitochondrial dysfunction leading to an energy deficiency state.
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Effect of peroxynitrite on the mitochondrial respiratory chain: differential susceptibility of neurones and astrocytes in primary culture.
TL;DR: It is concluded that the acute exposure of ONOO− selectively damages neurones, whereas astrocytes remain unaffected, and intracellular glutathione appears to be an important factor for ameliorating ONOO‐‐mediated mitochondrial damage.
Journal ArticleDOI
Nitric oxide, mitochondria and neurological disease.
TL;DR: The evidence available for NO/ONOO--mediated mitochondrial damage in various neurological disorders is considered and potential therapeutic strategies are proposed.
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Beta-amyloid inhibits integrated mitochondrial respiration and key enzyme activities.
TL;DR: It is concluded that β‐amyloid can directly disrupt mitochondrial function, inhibits key enzymes and may contribute to the deficiency of energy metabolism seen in Alzheimer's disease.