Výsledky vyhledávání - "Christine L. Rothnie"

Toll-like receptor 4 mediates ischemia/reperfusion injury of the heart

Autor: Christine L. Rothnie, Edward D. Verrier, Hiroo Takayama, Denise J. Spring, Craig R. Hampton, Akira Shimamoto, Timothy H. Pohlman, Masaki Yada, Albert J. Chong

Publikováno v: The Journal of Thoracic and Cardiovascular Surgery. 128(2):170-179

BackgroundRestoration of blood flow to the ischemic heart may paradoxically exacerbate tissue injury (ischemia/reperfusion injury). Toll-like receptor 4, expressed on several cell types, including cardiomyocytes, is a mediator of the host inflammator

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::361f4e0a4902ee2b85cad78f347b789a

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Regulation and actions of activin A and follistatin in myocardial ischaemia-reperfusion injury

Autor: David James Phillips, Kylie Venardos, Denise J. Spring, Julian A. Smith, Mark P. Hedger, Christine L. Rothnie, David M. Kaye, Yi Chen, Edward D. Verrier

Publikováno v: Cytokine. 69(2)

Activin A, a member of the transforming growth factor-β superfamily, is stimulated early in inflammation via the Toll-like receptor (TLR) 4 signalling pathway, which is also activated in myocardial ischaemia-reperfusion. Neutralising activin A by tr

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::58593814b85e166371fb87232f417d6f
https://pubmed.ncbi.nlm.nih.gov/25052838

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ANTIBODY TO CD18 REDUCES NEUTROPHIL AND T LYMPHOCYTE INFILTRATION AND VASCULAR CELL ADHESION MOLECULE-1 EXPRESSION IN CARDIAC REJECTION1

Autor: John T. Weyhrich, Robert Thomas, Hiroji Akimoto, Margaret D. Allen, Christine L. Rothnie, Thomas O. McDonald

Publikováno v: Transplantation. 61:1610-1617

Most antirejection therapies target immune activation but may not reduce leukocyte infiltration into the graft. The leukocyte integrin CD18 has been shown to be important for leukocyte migration in vitro. We postulated that antibody blockade of CD18

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_________::703cdfd59847a0ec3e8257f7c8450a28
https://doi.org/10.1097/00007890-199606150-00011

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Inhibition of Toll-like receptor 4 with eritoran attenuates myocardial ischemia-reperfusion injury

Autor: Masaki Yada, Matthew L. Agnew, Hideto Shimpo, Craig R. Hampton, Akira Shimamoto, Albert J. Chong, Edward D. Verrier, Christine L. Rothnie, Timothy H. Pohlman, Hiroo Takayama, Shin Shomura, Ani J. Fleisig, Denise J. Spring

Publikováno v: Circulation. 114

Background— We previously reported that the functional mutation of Toll-like receptor 4 (TLR4) in C3H/HeJ mice subjected to myocardial ischemia-reperfusion (MI/R) injury resulted in an attenuation of myocardial infarction size. To investigate the l

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c65337653815eb4143f30454a1bcca95
https://pubmed.ncbi.nlm.nih.gov/16820585

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HSP70.1 and -70.3 are required for late-phase protection induced by ischemic preconditioning of mouse hearts

Autor: Jeaneatte Griscavage-Ennis, Albert J. Chong, Craig R. Hampton, Edward D. Verrier, Akira Shimamoto, David J. Dix, Timothy H. Pohlman, Christine L. Rothnie

Publikováno v: American journal of physiology. Heart and circulatory physiology. 285(2)

We investigated the role of inducible heat shock proteins 70.1 and 70.3 (HSP70.1 and HSP70.3, respectively) in myocardial ischemic preconditioning (IP) in mice. Wild-type (WT) mice and HSP70.1- and HSP70.3-null [HSP70.1/3(–/–)] mice were subjecte

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3f5b2bee25608aa94691d6be3adfc4e5
https://pubmed.ncbi.nlm.nih.gov/12714332

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Left ventricular dysfunction during extracorporeal membrane oxygenation in a hypoxemic swine model

Autor: Irving Shen, P. Pearl O'Rourke, Edward D. Verrier, Arnold M Benak, Fiona H Levy, Christine L. Rothnie, Brian W. Duncan

Publikováno v: The Annals of thoracic surgery. 71(3)

Perfusion of the coronary circulation with hypoxemic blood from the left ventricle has been postulated to cause myocardial dysfunction during venoarterial extracorporeal membrane oxygenation for respiratory support.We investigated this hypothesis in

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::707d4553c34f191bb2497473aa064fa4
https://pubmed.ncbi.nlm.nih.gov/11269466

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