Zobrazeno 1 - 10
of 16
pro vyhledávání: '"Robert J. Boock"'
Publikováno v:
Journal of Neurosurgery. 93:99-107
Object. Thrombolytic treatments for ischemic stroke can restore circulation, but reperfusion injury, mediated by oxygen free radicals, can limit their utility. The authors hypothesized that, during reperfusion, nitric oxide (NO) provides cytoprotecti
Autor:
Ryszard M. Pluta, Robert J. Boock, Judith Harvey-White, Edward H. Oldfield, B. Gregory Thompson, John K. B. Afshar
Publikováno v:
Journal of Neurosurgery. 92:121-126
Object. The reduction in the level of nitric oxide (NO) is a purported mechanism of delayed vasospasm after subarachnoid hemorrhage (SAH). Evidence in support of a causative role for NO includes the disappearance of nitric oxide synthase (NOS) from t
Autor:
Robert J. Boock, George A. Mashour
Publikováno v:
Brain Research. 842:233-238
Nitric oxide (NO) is an important vasodilator with various activities in the cerebral vasculature. Although the response of NO levels to shear stress has been investigated in various models using systemic endothelium, no study has evaluated human cer
Publikováno v:
Journal of Neurosurgery. 88:557-561
Hemoglobin released from hemolysed erythrocytes has been postulated to be responsible for delayed cerebral vasospasm after subarachnoid hemorrhage (SAH). However, the evidence is indirect and the mechanisms of action are unclear. Cerebrovascular tone
Autor:
Kathleen A. Clouse, Robert J. Boock, Mima Bacic, Hannelore Ehrenreich, Ryszard M. Pluta, John K. B. Afshar, Edward H. Oldfield
Publikováno v:
Journal of Neurosurgery. 87:287-293
✓ Despite years of research, delayed cerebral vasospasm remains a serious complication of subarachnoid hemorrhage (SAH). Recently, it has been proposed that endothelin-1 (ET-1) mediates vasospasm. The authors examined this hypothesis in a series of
Autor:
Thomas A. Peyser, Robert J. Boock, Elaine Watkins, David Price, David R. Liljenquist, Mark P. Christiansen, Timothy L. Bailey, Katherine Nakamura
Publikováno v:
Diabetes technologytherapeutics. 15(10)
Use of continuous glucose monitoring (CGM) systems can improve glycemic control, but widespread adoption of CGM utilization has been limited, in part because of real and perceived problems with accuracy and reliability. This study compared accuracy a
Autor:
Jean, Raymond, Annick, Metcalfe, Anne-Cecile, Desfaits, Edith, Ribourtout, Igor, Salazkin, Kevin, Gilmartin, Gill, Embry, Robert J, Boock
Publikováno v:
AJNR Am J Neuroradiol
BACKGROUND AND PURPOSE: Coil embolization is safe and effective but may be followed by aneurysm recurrence. Our purpose was to explore the use of alginate as a new embolic agent that could deliver growth factors and improve results of endovascular tr
Autor:
B. Iuliano, Robert J. Boock, Edward H. Oldfield, John K. B. Afshar, Ryszard M. Pluta, B. G. Thompson
Publikováno v:
Cerebral Vasospasm ISBN: 9783211836507
Delayed release of hemoglobin from the subarachnoid clot in the vicinity of conductive arteries leads to cerebral vasospasm after SAH. The mechanism of vasospasm however remains unclear. The one thousand times higher affinity of ferrous heme for nitr
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::2f5b324319db9737d079892e1bfd4555
https://doi.org/10.1007/978-3-7091-6232-3_15
https://doi.org/10.1007/978-3-7091-6232-3_15
Publikováno v:
Journal of neurosurgery. 88(2)
Object. Oxyhemoglobin (HbO2) causes vasospasm after subarachnoid hemorrhage (SAH). The most likely spasmogenic component of HbO2 is iron. Various iron chelators, such as deferoxamine, have prevented vasospasm in vivo with limited success. However, on
Publikováno v:
Journal of neurosurgery. 87(5)
✓ Decreased endothelium-derived relaxing factor, nitric oxide (NO), in the arterial wall has been hypothesized to be a potential cause of cerebral vasospasm following subarachnoid hemorrhage (SAH). The authors sought to determine whether intracarot