Zobrazeno 1 - 10
of 12
pro vyhledávání: '"Andrew Willeford"'
Publikováno v:
JACCP: JOURNAL OF THE AMERICAN COLLEGE OF CLINICAL PHARMACY. 4:1392-1400
Publikováno v:
Ann Pharmacother
Background Use of direct oral anticoagulants (DOACs) for the treatment of left ventricular (LV) thrombus has gained considerable interest. Objective We aimed to evaluate if DOACs are effective in the treatment of LV thrombus compared with warfarin. M
Publikováno v:
The Journal of emergency medicine. 59(2)
Background Methohexital is a short-acting barbiturate used for procedural sedation in the emergency department (ED). As with other sedatives, adverse effects with methohexital include excess sedation and hypotension, but this agent can also lower the
Autor:
Robert S. Ross, Yoshitake Cho, Shigeki Miyamoto, Andrew Willeford, Joan Heller Brown, Cameron S. Brand, Takeshi Suetomi
Publikováno v:
Circulation. 138:2530-2544
Background: Inflammation is associated with cardiac remodeling and heart failure, but how it is initiated in response to nonischemic interventions in the absence of cell death is not known. We tested the hypothesis that activation of Ca 2+ /calmoduli
Publikováno v:
The FASEB Journal. 34:1-1
Autor:
Shigeki Miyamoto, Hal M. Hoffman, Andrew Willeford, Audrey Nickle, Joan Heller Brown, Takeshi Suetomi
Publikováno v:
Willeford, A; Suetomi, T; Nickle, A; Hoffman, HM; Miyamoto, S; & Heller Brown, J. (2018). CaMKIIδ-mediated inflammatory gene expression and inflammasome activation in cardiomyocytes initiate inflammation and induce fibrosis. JCI Insight, 3(12). doi: 10.1172/jci.insight.97054. UC San Diego: Retrieved from: http://www.escholarship.org/uc/item/39g1c6h8
JCI insight, vol 3, iss 12
JCI insight, vol 3, iss 12
Inflammation accompanies heart failure and is a mediator of cardiac fibrosis. CaMKIIδ plays an essential role in adverse remodeling and decompensation to heart failure. We postulated that inflammation is the mechanism by which CaMKIIδ contributes t
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::27d73cda213162c9acd726be6dd1e70c
http://www.escholarship.org/uc/item/39g1c6h8
http://www.escholarship.org/uc/item/39g1c6h8
Publikováno v:
The FASEB Journal. 32
Autor:
Prabhleen Singh, Andrew Willeford, Mark Hepokoski, Joan Heller Brown, Laura E. Crotty Alexander, Jiang Tian, Zachary Yong, Ashley Du, John Shin, Christopher A. Drummond, A. Moshensky, Christian Javier, Denzil P. Mathew, Jasmine Lee, Kevin Vega, Ellen C. Breen, Soumita Das
Publikováno v:
American journal of physiology. Regulatory, integrative and comparative physiology, vol 314, iss 6
Am J Physiol Regul Integr Comp Physiol
Alexander, LEC; Drummond, CA; Hepokoski, M; Mathew, D; Moshensky, A; Willeford, A; et al.(2018). Chronic inhalation of e-cigarette vapor containing nicotine disrupts airway barrier function and induces systemic inflammation and multiorgan fibrosis in mice. AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY, 314(6), R834-R847. doi: 10.1152/ajpregu.00270.2017. UC San Diego: Retrieved from: http://www.escholarship.org/uc/item/3cj3r0h3
Am J Physiol Regul Integr Comp Physiol
Alexander, LEC; Drummond, CA; Hepokoski, M; Mathew, D; Moshensky, A; Willeford, A; et al.(2018). Chronic inhalation of e-cigarette vapor containing nicotine disrupts airway barrier function and induces systemic inflammation and multiorgan fibrosis in mice. AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY, 314(6), R834-R847. doi: 10.1152/ajpregu.00270.2017. UC San Diego: Retrieved from: http://www.escholarship.org/uc/item/3cj3r0h3
Electronic (e)-cigarettes theoretically may be safer than conventional tobacco. However, our prior studies demonstrated direct adverse effects of e-cigarette vapor (EV) on airway cells, including decreased viability and function. We hypothesize that
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6078c6dc4010ca8feacc1dfa1616bb1f
https://europepmc.org/articles/PMC6032308/
https://europepmc.org/articles/PMC6032308/
Autor:
Haiyun Ling, Charles B.B. Gray, Jonathan L. Respress, Andrew Willeford, Donald M. Bers, Michael Grimm, Laetitia Pereira, Jeffrey R. Erickson, Satyam Sarma, Joan Heller Brown, Xander H.T. Wehrens
Publikováno v:
Journal of Molecular and Cellular Cardiology. 85:282-291
Chronic activation of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) has been implicated in the deleterious effects of β-adrenergic receptor (β-AR) signaling on the heart, in part, by enhancing RyR2-mediated sarcoplasmic reticulum (SR) Ca(2
Publikováno v:
Circulation Research. 121
Background: There is evidence that inflammation is associated with pressure overload induced cardiac remodeling and heart failure, as well as evidence for a role of CaMKII in remodeling and heart failure development. Whether CaMKII mediates inflammat