Zobrazeno 1 - 10
of 63
pro vyhledávání: '"Phillip F. Pratt"'
Autor:
Sue C. Kehl, Phillip F. Pratt, Steven M. Callister, Angela M. Thomm, Dean A. Jobe, Konstance K. Knox, Ziyan Yin, Soyoung Kim
Publikováno v:
Open Forum Infectious Diseases
Background Powassan virus (POWV) is the North American member of the tick-borne encephalitis complex of viruses. The potential for concurrent transmission with other tick-borne pathogens, particularly the Lyme disease agent Borrelia burgdorferi, is u
Publikováno v:
Fertility and Sterility. 112:e334
Autor:
David C. Warltier, Ines Baotic, Maria Muravyeva, Martin Bienengraeber, Anna K. Brzezinska, Thorsten M. Leucker, Judy R. Kersten, Dorothee Weihrauch, Phillip F. Pratt
Publikováno v:
Journal of Molecular and Cellular Cardiology. 51:803-811
Endothelial cells (EC) serve a paracrine function to enhance signaling in cardiomyocytes (CM), and conversely, CM secrete factors that impact EC function. Understanding how EC interact with CM may be critically important in the context of ischemia-re
Autor:
Jianhai Du, Zhi-Dong Ge, David C. Warltier, Anna K. Brzezinska, Thorsten M. Leucker, Nikolina Vladic, Phillip F. Pratt, Yang Shi, Judy R. Kersten
Publikováno v:
American Journal of Physiology-Heart and Circulatory Physiology. 301:H2130-H2139
Cardioprotection by ischemic preconditioning (IPC) is impaired during hyperglycemia, but the mechanisms underlying this phenomenon are poorly understood. This study investigated the role of hyperglycemia to adversely modulate tetrahydrobiopterin (BH4
Publikováno v:
American Journal of Physiology-Heart and Circulatory Physiology. 300:H109-H117
The extracellular K+ concentration ([K+]o) has been proposed to link cardiac metabolism with coronary perfusion and arrhythmogenesis, particularly during ischemia. Several animal studies have also supported K+ as an EDHF that activates Na+-K+-ATPase
Autor:
David C. Warltier, Danijel Pravdic, Yasushi Mio, Filip Sedlic, Phillip F. Pratt, Zeljko J. Bosnjak, Martin Bienengraeber
Publikováno v:
British Journal of Pharmacology. 160:220-232
Background and purpose: The volatile anaesthetic isoflurane protects the heart from ischaemia and reperfusion (I/R) injury when applied at the onset of reperfusion [anaesthetic postconditioning (APoC)]. However, the mechanism of APoC-mediated protect
Autor:
Zhi-Dong Ge, David C. Warltier, Garrett J. Gross, John A. Auchampach, Martin Bienengraeber, Phillip F. Pratt, Judy R. Kersten, Danijel Pravdic
Publikováno v:
Anesthesiology. 112:73-85
Background The role of endothelial nitric oxide synthase (eNOS) in isoflurane postconditioning (IsoPC)-elicited cardioprotection is poorly understood. The authors addressed this issue using eNOS mice. Methods In vivo or Langendorff-perfused mouse hea
Autor:
David C. Warltier, Phillip F. Pratt, Nicole L. Lohr, Agnes Keszler, Neil Hogg, Martin Bienengraber
Publikováno v:
Journal of molecular and cellular cardiology
Nitric oxide is an important messenger in numerous biological processes, such as angiogenesis, hypoxic vasodilation, and cardioprotection. Although nitric oxide synthases (NOS) produce the bulk of NO, there is increasing interest in NOS independent g
Autor:
James E. Melvin, Ossama A. Hatoum, Heike Wulff, Kazuyoshi Toyama, Takashi Saito, David L. Mattson, Philippe Azam, Girija Raman, David R. Harder, Hiroto Miura, David D. Gutterman, Phillip F. Pratt, K. George Chandy, Satarupa Das, Yoshimasa Fujiwara
Publikováno v:
Journal of Clinical Investigation. 118:3025-3037
Atherosclerosis remains a major cause of death in the developed world despite the success of therapies that lower cholesterol and BP. The intermediate-conductance calcium-activated potassium channel KCa3.1 is expressed in multiple cell types implicat
Autor:
John G. Krolikowski, Phillip F. Pratt, David C. Warltier, Dorothee Weihrauch, Julien Amour, Yon Hee Shim, Paul S. Pagel
Publikováno v:
Anesthesia & Analgesia. 107:769-775
Prosurvival signaling kinases inhibit glycogen synthase kinase-3beta (GSK-3beta) activity and stimulate apoptotic protein p53 degradation. Helium produces cardioprotection by activating prosurvival kinases, but whether GSK and p53 inhibition mediate