5 results match your criteria: "St Joseph's Hospital and Medical Center (SJHMC)[Affiliation]"
Remote Ischemic Post-Conditioning (RIC) Mediates Anti-Inflammatory Signaling via Myeloid AMPKα1 in Murine Traumatic Optic Neuropathy (TON).
Int J Mol Sci
December 2024
Department of Translational Neuroscience, Barrow Neurological Institute, St Joseph's Hospital and Medical Center (SJHMC), Phoenix, AZ 85013, USA.
Traumatic optic neuropathy (TON) has been regarded a vision-threatening condition caused by either ocular or blunt/penetrating head trauma, which is characterized by direct or indirect TON. Injury happens during sports, vehicle accidents and mainly in military war and combat exposure. Earlier, we have demonstrated that remote ischemic post-conditioning (RIC) therapy is protective in TON, and here we report that AMPKα1 activation is crucial.
View Article and Find Full Text PDFStroke in critically ill patients with respiratory failure due to COVID-19: Disparities between low-middle and high-income countries.
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.
Article Synopsis
- A study was conducted to compare stroke incidences and mortality rates in critically ill COVID-19 patients from low-and middle-income countries (LMICs) and high-income countries (HICs).
- The results showed that stroke incidence was significantly higher in LMICs (35.7 per 1000 admitted-days) compared to HICs (17.6 per 1000 admitted-days), with patients from LMICs also facing higher mortality rates (43.6% vs. 29.2%).
- The findings highlight the need for better stroke diagnosis and healthcare resource allocation in LMICs, as both higher income status and the presence of stroke are associated with increased risk of death
Complement C3a receptor-mediated vascular dysfunction: a complex interplay between aging and neurodegeneration.
J Clin Invest
January 2021
Department of Neurosurgery, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center (SJHMC), Dignity Health, Phoenix, Arizona, USA.
Article Synopsis
- Vascular dysfunction and compromised blood-brain barrier (BBB) integrity are linked to aging and diseases, particularly through the complement C3a/C3a receptor (C3a/C3aR) axis.
- Propson et al. examined how C3aR signaling in endothelial cells affects neurovascular inflammation and BBB permeability in mouse models of aging and neurodegeneration.
- Their findings suggest that blocking C3aR could mitigate age-related microglial reactivity and BBB damage, pointing to complement inhibitors as a potential treatment for vascular issues in the brain.
Acetyl-11-keto-β-boswellic acid (AKBA) Attenuates Oxidative Stress, Inflammation, Complement Activation and Cell Death in Brain Endothelial Cells Following OGD/Reperfusion.
Neuromolecular 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 PDFThe Role of Complement C3a Receptor in Stroke.
Neuromolecular 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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