4 results match your criteria: "St. Joseph's Hospital and Medical Center (SJHMC)[Affiliation]"
Heart Lung
October 2024
Division of Neuroscience Critical Care, Departments of Neurology, Neurosurgery, and Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
J Clin Invest
January 2021
Department of Neurosurgery, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center (SJHMC), Dignity Health, Phoenix, Arizona, USA.
Vascular dysfunction resulting in compromised blood-brain barrier (BBB) integrity is evident in aging and disease. Although the complement C3a/C3a receptor (C3a/C3aR) axis influences normal brain aging and disease progression, the mechanisms governing endothelial C3aR-mediated neurovascular inflammation and BBB permeability remain unexplored. In this issue of the JCI, Propson et al.
View Article and Find Full Text PDFNeuromolecular Med
December 2019
Department of Neurosurgery, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center (SJHMC), Dignity Health, 350 W Thomas Rd, Phoenix, AZ, 85013, USA.
Brain endothelial cells play an important role in maintaining blood flow homeostasis in the brain. Cerebral ischemia is a major cause of endothelial dysfunction which can disrupt the blood-brain barrier (BBB). Oxygen-glucose deprivation (OGD)/reperfusion promote cell death and BBB breakdown in brain endothelial cells.
View Article and Find Full Text PDFNeuromolecular Med
December 2019
Department of Neurosurgery, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center (SJHMC), Dignity Health, 350 W Thomas Rd, Phoenix, AZ, 85013, USA.
The complement system is a key regulator of the innate immune response against diseased tissue that functions across multiple organ systems. Dysregulation of complement contributes to the pathogenesis of a number of neurological diseases including stroke. The C3a anaphylatoxin, via its cognate C3a receptor (C3aR), mediates inflammation by promoting breakdown of the blood-brain barrier and the massive infiltration of leukocytes into ischemic brain in experimental stroke models.
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