6 results match your criteria: "F. Edward Hebert Medical School[Affiliation]"
J Nucl Cardiol
August 2023
Department of Medicine, University of Missouri-Kansas City School of Medicine, Kansas City, KS, USA.
J Nucl Cardiol
April 2021
NYU Langone Health and Bellevue Hospital, NYU School of Medicine, 435 East 30th Street, Science Building, Room 713, New York, NY, 10016, USA.
We advocate an evidence-based discussion for a patient first philosophy when considering "the right test for the right patient." Numerous test options exist for the evaluation of symptoms of possible stable ischemic heart disease. Major guidelines have traditionally focused on functional testing with or without imaging to clarify symptoms, diagnose ischemia, stratify prognosis, and guide management.
View Article and Find Full Text PDFJACC Cardiovasc Imaging
May 2021
National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA.
Arch Pathol Lab Med
December 2015
From the Departments of Preventive Medicine and Biometrics (Dr Henson) and Pathology (Dr Grimley), The Uniformed Services University of the Health Sciences, F. Edward Hebert Medical School, Bethesda, Maryland.
Biochem Biophys Res Commun
December 1988
Department of Pathology, F. Edward Hebert Medical School, USUHS, Bethesda, Maryland 20814.
Lateral diffusion coefficients (D) of two surface differentiation antigens (sIgM and Bp35) were determined on interferon-sensitive (-IFs) or resistant (-IFr) Daudi cells by fluorescence photobleaching, using monospecific FITC-anti-IgM or PE-anti-Leu 16 probes. For untreated Daudi -IFs, mean (D) were 5.8 and 5.
View Article and Find Full Text PDFScanning Microsc
December 1988
F. Edward Hebert Medical School, Bethesda, MD.
Human alpha interferons (IFN-a) cause a reorganization of internal cell membranes into tubuloreticular inclusions (TRI). Morphogenesis and cytochemistry indicate a pre-Golgi intracisternal origin from the endoplasmic reticulum. Clinically, TRI formation in human blood mononuclear cells correlates with systemic IFN-a treatment or with endogenous overproduction of IFN-a in viral or autoimmune diseases (e.
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