Zobrazeno 1 - 10
of 10
pro vyhledávání: '"Hans J. De Haas"'
Autor:
Hans J. de Haas, Jagat Narula
Publikováno v:
Journal of Nuclear Cardiology, 25(4), 1124-1127. SPRINGER
Autor:
Martin Picard, Jeremy Leipzig, Meagan J. McManus, Hans J. De Haas, Atif Towheed, Marc Vermulst, Jagat Narula, Alessia Angelin, Prasanth Potluri, Partho P. Sengupta, Ryan M. Morrow, Douglas C. Wallace, Brett A. Kauffman, Hsiao-Wen Chen
Nuclear-encoded mutations causing metabolic and degenerative diseases have highly variable expressivity. Patients sharing the homozygous mutation (c.523delC) in the adenine nucleotide translocator 1 gene (SLC25A4, ANT1) develop cardiomyopathy that va
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::bd64df0a0f06a407b6f4b02cb3a331ee
https://europepmc.org/articles/PMC6717513/
https://europepmc.org/articles/PMC6717513/
Autor:
Hans J. de Haas, Atsuko Tahara, Jun Zhou, Dilbahar Mohar, H. William Strauss, Takayoshi Yamaki, Nobuhiro Tahara, Tiziano Scarabelli, Hendrikus H. Boersma, Annapoorna Kini, Neena B. Haider, Artiom Petrov, Jagat Narula, Yasuchika Takeishi
Publikováno v:
Journal of Nuclear Cardiology, 25(1), 94-100. SPRINGER
BACKGROUND: Preclinical studies indicate that minocycline protects against myocardial ischemia/reperfusion injury. In these studies, minocycline was administered before ischemia, which can rarely occur in clinical practice. The current study aimed to
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e2ce1c49b83e2c86256f659492538122
https://research.rug.nl/en/publications/8158e91d-1f23-4611-9194-f5d9e2486600
https://research.rug.nl/en/publications/8158e91d-1f23-4611-9194-f5d9e2486600
Autor:
Takayoshi, Yamaki, Hans J, de Haas, Nobuhiro, Tahara, Artiom, Petrov, Dilbahar, Mohar, Nezam, Haider, Jun, Zhou, Atsuko, Tahara, Yasuchika, Takeishi, Hendrikus H, Boersma, Tiziano, Scarabelli, Annapoorna, Kini, H William, Strauss, Jagat, Narula
Publikováno v:
Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology. 25(1)
Preclinical studies indicate that minocycline protects against myocardial ischemia/reperfusion injury. In these studies, minocycline was administered before ischemia, which can rarely occur in clinical practice. The current study aimed to evaluate ca
Autor:
Valentin Fuster, Zahi A. Fayad, Hans J. de Haas, Lisa Changchien, Puneet Dabas, Cheuk Y. Tang, Georg Goliasch, Jagat Narula, Joseph I. Friedman, Victoria X. Wang
Publikováno v:
JACC: Cardiovascular Imaging. 7(10):1039-1053
Reviews of imaging studies assessing the brain effects of vascular risk factors typically include a substantial number of studies with subjects with a history of symptomatic cardiovascular or cerebrovascular disease and/or events, limiting our abilit
Publikováno v:
Circulation Research; Vol 114
Circulation Research
Circulation Research
In almost all cardiac diseases, an increase in extracellular matrix (ECM) deposition or fibrosis occurs, mostly consisting of collagen I. Whereas replacement fibrosis follows cardiomyocyte loss in myocardial infarction, reactive fibrosis is triggered
Autor:
Nobuhiro Tahara, Tsutomu Imaizumi, Ahmed Tawakol, Cristian Constantinescu, Zahi A. Fayad, Neena B. Haider, Masataka Nakano, Jun Zhou, Hans J. de Haas, Aloke V. Finn, Jagat Narula, Valentin Fuster, Artiom Petrov, Atsuko Tahara, Jogeshwar Mukherjee, Hendrikus H. Boersma, Renu Virmani, Lisardo Boscá
Publikováno v:
Nature Medicine, 20(2), 215-219. Nature Publishing Group
Digital.CSIC. Repositorio Institucional del CSIC
instname
Digital.CSIC. Repositorio Institucional del CSIC
instname
et al.
Progressive inflammation in atherosclerotic plaques is associated with increasing risk of plaque rupture. Molecular imaging of activated macrophages with 2-deoxy-2-[ 18 F]fluoro-D-glucose ([ 18 F]FDG) has been proposed for identification
Progressive inflammation in atherosclerotic plaques is associated with increasing risk of plaque rupture. Molecular imaging of activated macrophages with 2-deoxy-2-[ 18 F]fluoro-D-glucose ([ 18 F]FDG) has been proposed for identification
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e792bff13b9c95dfee2e08eb4cd9b5ad
https://research.rug.nl/en/publications/d6296f26-671e-4578-ab2c-77224685d6e2
https://research.rug.nl/en/publications/d6296f26-671e-4578-ab2c-77224685d6e2
Autor:
Jagat Narula, Jun Zhou, Navneet Narula, Tsutomu Imaizumi, Riemer H. J. A. Slart, Raghu Pandurangi, Nobuhiro Tahara, Chris P. M. Reutelingsperger, Tiziano M. Scarabelli, Hans J. de Haas, Annapoorna Kini, Mary Dyszlewski, Takayoshi Yamaki, H. Reinier Zandbergen, Valentin Fuster, Artiom Petrov
Publikováno v:
Scientific Reports
Scientific Reports, 4:6826. Nature Publishing Group
Repisalud
Instituto de Salud Carlos III (ISCIII)
Scientific Reports, 4:6826. Nature Publishing Group
Repisalud
Instituto de Salud Carlos III (ISCIII)
Acute insult to the myocardium is associated with substantial loss of cardiomyocytes during the process of myocardial infarction. In this setting, apoptosis (programmed cell death) and necrosis may operate on a continuum. Because the latter is charac
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6f6811c8e9602bb6a8abe9fece613f5e
https://hdl.handle.net/20.500.12105/5538
https://hdl.handle.net/20.500.12105/5538
The impact of pressure overload on coronary vascular changes following myocardial infarction in rats
Autor:
Jagat Narula, Lifan Liang, Jiqiu Chen, Elisa Yaniz-Galende, Roger J. Hajjar, Hans J. de Haas, Artiom Petrov
This study investigates the impact of pressure overload on vascular changes after myocardial infarction (MI) in rats. To evaluate the effect of pressure overload, MI was induced in three groups: 1) left coronary artery ligation for 1 mo (MI-1m), 2) i
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a72fa4c05f3d577684f3e1e85f83a08d
https://europepmc.org/articles/PMC3602756/
https://europepmc.org/articles/PMC3602756/
Publikováno v:
Journal of Nuclear Medicine, 52(9), 1337-1338. SOC NUCLEAR MEDICINE INC
See page [1433][1] Inflammation and hemostasis are key processes in the pathogenesis of atherosclerotic cardiovascular disease ([1][2],[2][3]). Vascular inflammation in response to lipid depositions causes formation of atherosclerotic plaques ([1][2]