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Full-Text Articles in Medical Physiology
Osteoarthritis, Cerebrovascular Dysfunction And The Common Denominator Of Inflammation: A Narrative Review, B. K. Al-Khazraji, C. T. Appleton, F. Beier, T. B. Birmingham, J. K. Shoemaker
Osteoarthritis, Cerebrovascular Dysfunction And The Common Denominator Of Inflammation: A Narrative Review, B. K. Al-Khazraji, C. T. Appleton, F. Beier, T. B. Birmingham, J. K. Shoemaker
Physiology and Pharmacology Publications
© 2018 The Author(s) Objective: Population-based cohort studies suggest an association between osteoarthritis (OA) and cerebrovascular disease, yet the mechanisms underlying vascular comorbidities in OA remain unclear. The purpose of this narrative review is to discuss the literature examining inflammation in OA with a focus on physiological mechanisms, and whether overlapping mechanisms exist in cerebrovascular dysfunction. Method: A literature search was conducted in PubMed using combinations of search terms: osteoarthritis, cerebrovascular (disease/dysfunction/risk), cardiovascular (disease/dysfunction/risk), aging/ageing, inflammation, inflammatory mediators, cytokine, c-reactive protein, interleukin, advanced glycation end-products, metabolic syndrome, reactive oxidative species, cognitive impairment, (vascular-related) dementia, small cerebral vessel disease, endothelial function, …
Group Ii Innate Lymphoid Cells And Microvascular Dysfunction From Pulmonary Titanium Dioxide Nanoparticle Exposure, Alaeddin Bashir Abukabda, Carroll Rolland Mcbride, Thomas Paul Batchelor, William Travis Goldsmith, Elizabeth Compton Bowdridge, Krista Lee Garner, Sherri Friend, Timothy Robert Nurkiewicz
Group Ii Innate Lymphoid Cells And Microvascular Dysfunction From Pulmonary Titanium Dioxide Nanoparticle Exposure, Alaeddin Bashir Abukabda, Carroll Rolland Mcbride, Thomas Paul Batchelor, William Travis Goldsmith, Elizabeth Compton Bowdridge, Krista Lee Garner, Sherri Friend, Timothy Robert Nurkiewicz
Faculty & Staff Scholarship
Background: The cardiovascular effects of pulmonary exposure to engineered nanomaterials (ENM) are poorly understood, and the reproductive consequences are even less understood. Inflammation remains the most frequently explored mechanism of ENM toxicity. However, the key mediators and steps between lung exposure and uterine health remain to be fully defined. The purpose of this study was to determine the uterine inflammatory and vascular effects of pulmonary exposure to titanium dioxide nanoparticles (nano-TiO2). We hypothesized that pulmonary nano-TiO2 exposure initiates a Th2 inflammatory response mediated by Group II innate lymphoid cells (ILC2), which may be associated with an impairment in uterine microvascular …