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Barbara Casadei
Researcher at University of Oxford
Publications - 274
Citations - 23925
Barbara Casadei is an academic researcher from University of Oxford. The author has contributed to research in topics: Atrial fibrillation & Medicine. The author has an hindex of 60, co-authored 242 publications receiving 19620 citations. Previous affiliations of Barbara Casadei include Newman University & King's College London.
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Cardiac Nitric Oxide Synthase 1 Regulates Basal and β-Adrenergic Contractility in Murine Ventricular Myocytes
TL;DR: Findings indicate that cardiac NOS1-derived NO plays a significant role in the autocrine regulation of myocardial contractility and the inotropic response to &bgr;-adrenergic stimulation in murine ventricular myocytes.
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Identification of higher brain centres that may encode the cardiorespiratory response to exercise in humans.
Judith Thornton,Abe Guz,Kevin Murphy,Alison R. Griffith,David L. Pedersen,Attila Kardos,Alexander P. Leff,Lewis Adams,Barbara Casadei,David J. Paterson +9 more
TL;DR: The neuroanatomical areas activated suggest that a significant component of the respiratory response to ‘exercise’, in the absence of both movement feedback and an increase in CO2 production, can be generated by what appears to be a behavioural response.
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nNOS Gene Deletion Exacerbates Pathological Left Ventricular Remodeling and Functional Deterioration After Myocardial Infarction
TL;DR: In this article, the authors investigated the role of the neuronal isoform of nitric oxide synthase (nNOS) in the regulation of basal and β-adrenergic inotropy in normal and chronically infarcted hearts.
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Nitric oxide synthases in heart failure.
TL;DR: Improvements in the clinical translation of potent modulators of NOS function/dysfunction may ultimately provide a powerful new treatment for many hearts diseases that are fueled by nitroso-redox imbalance.
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Neuronal nitric oxide synthase and human vascular regulation.
TL;DR: The studies reveal that SMTC causes a reduction in basal blood flow in the normal human forearm and coronary circulations, without affecting the eNOS-mediated vasodilatation elicited by acetylcholine, substance P, or increased shear stress, suggesting that eN OS and nNOS have distinct roles in the physiologic local regulation of human microvascular tone in vivo.