Zobrazeno 1 - 10
of 19
pro vyhledávání: '"Joseph C. Hockenberry"'
Publikováno v:
BMC Anesthesiology, Vol 22, Iss 1, Pp 1-6 (2022)
Abstract Background Hypotension that is resistant to phenylephrine is a complication that occurs in anesthetized patients treated with angiotensin converting enzyme (ACE) inhibitors. We tested the hypothesis that Ang 1–7 and the endothelial Mas rec
Externí odkaz:
https://doaj.org/article/b61412f3162d48e48ffdf5f5117c8ff6
Publikováno v:
Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, Vol 8, Iss 17 (2019)
Background Elevated levels of ceramide, a sphingolipid known to cause a transition from nitric oxide (NO)– to hydrogen peroxide–dependent flow‐induced dilation (FID) in human arterioles, correlate with adverse cardiac events. However, elevation
Externí odkaz:
https://doaj.org/article/42ccd2f7aba3410a8d6529bb53450bdc
Autor:
Dawid S. Chabowski, William E. Hughes, Joseph C. Hockenberry, John LoGiudice, Andreas M. Beyer, David D. Gutterman
Publikováno v:
The Journal of physiologyReferences.
Microvascular dysfunction predicts adverse cardiovascular events despite absence of large vessel disease. A shift in the mediator of flow-mediated dilatation (FMD) from nitric oxide (NO) to mitochondrial-derived hydrogen peroxide (H
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f9a178128cd6abc6cbe6c48a268c58a0
https://pubmed.ncbi.nlm.nih.gov/36575638
https://pubmed.ncbi.nlm.nih.gov/36575638
Autor:
Joseph C. Hockenberry, Dawid S. Chabowski, Jessica L. Fetterman, Andreas M. Beyer, William E. Hughes, David D. Gutterman, Karima Ait-Aissa
Publikováno v:
Arterioscler Thromb Vasc Biol
Objective: Coronary artery disease (CAD) is associated with a compensatory switch in mechanism of flow-mediated dilation (FMD) from nitric oxide (NO) to H 2 O 2 . The underlying mechanism responsible for the pathological shift is not well understood,
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::2e011b45c58c017cd39af93e153e6fb3
https://doi.org/10.1161/atvbaha.120.314944
https://doi.org/10.1161/atvbaha.120.314944
Autor:
Joseph C. Hockenberry, Dawid S. Chabowski, Andreas M. Beyer, Karima Ait-Aissa, Paul J. Pearson, David D. Gutterman, Andrew O. Kadlec
Publikováno v:
British Journal of Pharmacology. 175:4266-4280
Background and purpose NO produces arteriolar flow-induced dilation (FID) in healthy subjects but is replaced by mitochondria-derived hydrogen peroxide (mtH2 O2 ) in patients with coronary artery disease (CAD). Lysophosphatidic acid (LPA) is elevated
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::38b7b74e55c817520bf4500ff9228080
https://doi.org/10.1111/bph.14492
https://doi.org/10.1111/bph.14492
Autor:
David D. Gutterman, Andreas M. Beyer, Joseph C. Hockenberry, Karima Ait-Aissa, Andrew O. Kadlec
Publikováno v:
American Journal of Physiology-Heart and Circulatory Physiology. 314:H1053-H1060
A rise in reactive oxygen species (ROS) may contribute to cardiovascular disease by reducing nitric oxide (NO) levels, leading to loss of NO’s vasodilator and anti-inflammatory effects. Although primarily studied in larger conduit arteries, excess
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1b6b9273e70476bfc091a3f70ea6ebb7
https://doi.org/10.1152/ajpheart.00472.2017
https://doi.org/10.1152/ajpheart.00472.2017
Autor:
Mary F. Otterson, Andreas M. Beyer, Joseph C. Hockenberry, Karima Ait-Aissa, Julie K. Freed, Matthew J. Durand, Dawid S. Chabowski, Andrew O. Kadlec, David D. Gutterman
Publikováno v:
Hypertension. 70:166-173
Blood flow through healthy human vessels releases NO to produce vasodilation, whereas in patients with coronary artery disease (CAD), the mediator of dilation transitions to mitochondria-derived hydrogen peroxide ( mt H 2 O 2 ). Excessive mt H 2 O 2
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::df781f95bbac233eac36914e3fa0a5f9
https://doi.org/10.1161/hypertensionaha.117.09289
https://doi.org/10.1161/hypertensionaha.117.09289
Publikováno v:
Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
Background Elevated levels of ceramide, a sphingolipid known to cause a transition from nitric oxide (NO)– to hydrogen peroxide–dependent flow‐induced dilation ( FID ) in human arterioles, correlate with adverse cardiac events. However, elevati
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f841f146a3c9865fd50ac4c0078f5e71
https://doi.org/10.1161/jaha.119.013153
https://doi.org/10.1161/jaha.119.013153
Autor:
Julie K. Freed, Matthew J. Durand, Paula D. Green, Andreas M. Beyer, Karima Ait-Aissa, Janine H. Santos, Esther Priel, David D. Gutterman, Chris K. Rokkas, Refael Peleg, Mario Gasparri, R. Garret Morgan, Joseph C. Hockenberry, Michael Riedel, Anthony J. Donato
Publikováno v:
Circulation Research
Supplemental Digital Content is available in the text.
Rationale: Telomerase is a nuclear regulator of telomere elongation with recent reports suggesting a role in regulation of mitochondrial reactive oxygen species. Flow-mediated dilation in pa
Rationale: Telomerase is a nuclear regulator of telomere elongation with recent reports suggesting a role in regulation of mitochondrial reactive oxygen species. Flow-mediated dilation in pa
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::bfc99d7c772cbaa13bf445c0c86c5e4c
http://europepmc.org/articles/PMC4772813
http://europepmc.org/articles/PMC4772813
Autor:
Dawid S. Chabowski, Jasmine M. Linn, Andreas M. Beyer, Andrew O. Kadlec, Karima Ait-Aissa, Joseph C. Hockenberry, David D. Gutterman
Publikováno v:
Circulation Research. 123
Vascular endothelial dysfunction is an early event in the development of atherosclerosis. Flow-mediated dilation (FMD) can be used to identify such endothelial dysfunction which is characterized by a decrease of nitric oxide (NO). Indeed, in subjects
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::d27c31ad3349e47d7ba8a690a0062df3
https://doi.org/10.1161/res.123.suppl_1.247
https://doi.org/10.1161/res.123.suppl_1.247