Zobrazeno 1 - 10
of 19
pro vyhledávání: '"David J, Greensmith"'
Autor:
Jenna Scotcher, Oleksandra Prysyazhna, Andrii Boguslavskyi, Kornel Kistamas, Natasha Hadgraft, Eva D. Martin, Jenny Worthington, Olena Rudyk, Pedro Rodriguez Cutillas, Friederike Cuello, Michael J. Shattock, Michael S. Marber, Maria R. Conte, Adam Greenstein, David J. Greensmith, Luigi Venetucci, John F. Timms, Philip Eaton
Publikováno v:
Nature Communications, Vol 7, Iss 1, Pp 1-11 (2016)
The stroke volume of the heart increases in response to an increase in the blood volume filling the heart. Here the authors reveal that this coordinated process is mediated in part by oxidative activation of the protein kinase G Iα, which phosphoryl
Externí odkaz:
https://doaj.org/article/03ace94ba067478fa8463d2ab1ace41b
Autor:
Javier Palacios, Adrián Paredes, Fredi Cifuentes, Marcelo A. Catalán, Angel Luis García-Villalón, Jorge Borquez, Mario J. Simirgiotis, Matthew Jones, Amy Foster, David J. Greensmith
Publikováno v:
Journal of Ethnopharmacology. 300:115747
The plant Senecio nutans SCh. Bip. is used by Andean communities to treat altitude sickness. Recent evidence suggests it may produce vasodilation and negative cardiac inotropy, though the cellular mechanisms have not been elucidated.To determinate th
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f49537eb89906343282b58b38397acc3
https://doi.org/10.1016/j.jep.2022.115747
https://doi.org/10.1016/j.jep.2022.115747
Autor:
David J. Greensmith, Natasha Hadgraft
Publikováno v:
Basic Science.
Cytokines including tumour necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β) are known to mediate systolic and diastolic myocardial dysfunction in inflammatory disease such as sepsis. To provide a cellular basis, we separately studied th
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::5448fa91f449d8d1319816e230855d5e
https://doi.org/10.1136/heartjnl-2018-bcs.135
https://doi.org/10.1136/heartjnl-2018-bcs.135
Autor:
Rajiv, Sankaranarayanan, Kornél, Kistamás, David J, Greensmith, Luigi A, Venetucci, David A, Eisner
Publikováno v:
The Journal of Physiology
Key points For the heart to function as a pump, intracellular calcium concentration ([Ca2+]i) must increase during systole to activate contraction and then fall, during diastole, to allow the myofilaments to relax and the heart to refill with blood.T
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=pmid________::d7a18218d2f9a471207705521f71f9de
https://pubmed.ncbi.nlm.nih.gov/28617952
https://pubmed.ncbi.nlm.nih.gov/28617952
Autor:
Margaux A. Horn, David J. Greensmith, Helen K. Graham, Jessica D. Clarke, Mark C.S. Hall, Katharine M. Dibb, Sarah J. Briston, Andrew W. Trafford, Mark A. Richards
Publikováno v:
Journal of Molecular and Cellular Cardiology. 53:82-90
The incidence of heart failure (HF) increases with age. This study sought to determine whether aging exacerbates structural and functional remodeling of the myocardium in HF. HF was induced in young (~18months) and aged sheep (>8years) by right ventr
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9300c27d0a0f81ed00924dfe57f9aeef
https://doi.org/10.1016/j.yjmcc.2012.03.011
https://doi.org/10.1016/j.yjmcc.2012.03.011
Autor:
Sarah J. Briston, Andrew W. Trafford, Mark A. Richards, Jessica D. Clarke, David A. Eisner, Jessica L. Caldwell, Margaux A. Horn, Katharine M. Dibb, Mark C.S. Hall, Helen K. Graham, David J. Greensmith
Publikováno v:
The Journal of Physiology. 589:1367-1382
Reduced inotropic responsiveness is characteristic of heart failure (HF). This study determined the cellular Ca2+ homeostatic and molecular mechanisms causing the blunted β-adrenergic (β-AR) response in HF.We induced HF by tachypacing in sheep; int
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::19b72623b7afadf7ad6032d87907c808
https://doi.org/10.1113/jphysiol.2010.203984
https://doi.org/10.1113/jphysiol.2010.203984
Publikováno v:
Cell Calcium. 48:341-351
Elevations in reactive oxygen species are implicated in many disease states and cause systolic and diastolic myocardial dysfunction. To understand the underlying cellular dysfunction, we characterised the effects of H₂O₂ on [Ca(2+)](i) handling a
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ef422fb77d1407ec74d3d99531fe2111
https://doi.org/10.1016/j.ceca.2010.10.007
https://doi.org/10.1016/j.ceca.2010.10.007
Publikováno v:
The Journal of Physiology
Key points Ca leak from the sarcoplasmic reticulum through the ryanodine receptor (RyR) reduces the amplitude of the Ca transient and slows its rate of decay.In the presence of β‐adrenergic stimulation, RyR‐mediated Ca leak produces a biphasic d
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=pmid________::4c6798aaed5942cd54b5f758f8f5562c
https://pubmed.ncbi.nlm.nih.gov/26537441
https://pubmed.ncbi.nlm.nih.gov/26537441
Publikováno v:
Heart. 103:A122.1-A122
In a recent study, 2,5-Di-(tert-butyl)−1,4-benzohydroquinone (TBQ) produced a concentration dependent and fully reversible inhibition of the sarcoplasmic reticulum Ca 2+ ATPase (SERCA) in rat ventricular myocytes 1 . While TBQ is a potentially usef
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::27b562044857321bdf17fea6eaeeab6e
https://doi.org/10.1136/heartjnl-2017-311726.173
https://doi.org/10.1136/heartjnl-2017-311726.173
Autor:
Angela Vincent, David J. Greensmith, Martin Leuwer, Victoria Thompson, Maria Isabella Leite, Anoop Kuttikat, Andreas Goebel, Christian Maihöfner, Nicolas Shenker, Eric Dubuis, Franz Blaes
Publikováno v:
Pain. 155(11)
Complex regional pain syndrome (CRPS) is a limb-confined posttraumatic pain syndrome with sympathetic features. The cause is unknown, but the results of a randomized crossover trial on low-dose intravenous immunoglobulins (IVIG) treatment point to a
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::7cd246cc3fb30c84bea32fcb8d7c852a
https://pubmed.ncbi.nlm.nih.gov/25250722
https://pubmed.ncbi.nlm.nih.gov/25250722