7 results match your criteria: "3710 SW US Veterans' Hospital Rd[Affiliation]"
Immunol Cell Biol
January 2021
VA Portland Health Care System, Research and Development Service, 3710 SW US Veterans' Hospital Rd, Portland, OR, 97239, USA.
Multiple sclerosis (MS) is a disabling neuroinflammatory disease. Its etiology is unknown, but both oxidative stress and inflammation appear to be involved in disease pathology. Macrophages are the predominant cell type in acute inflammatory brain lesions in MS.
View Article and Find Full Text PDFMol Neurobiol
July 2018
VA Portland Health Care System, Research and Development Service, Mail Code R&D8, 3710 SW US Veterans' Hospital Rd, Portland, OR, 97239, USA.
Lipoic acid (LA) exhibits antioxidant and anti-inflammatory properties; supplementation reduces disease severity and T lymphocyte migration into the central nervous system in a murine model of multiple sclerosis (MS), and administration in secondary progressive MS (SPMS) subjects reduces brain atrophy compared to placebo. The mechanism of action (MOA) of LA's efficacy in suppression of MS pathology is incompletely understood. LA stimulates production of the immunomodulator cyclic AMP (cAMP) in vitro.
View Article and Find Full Text PDFBMC Res Notes
November 2017
VA Portland Health Care System, Research and Development Service, 3710 SW US Veterans' Hospital Rd., Mail Code R&D8, Portland, OR, 97239, USA.
Objective: Dimethyl fumarate (DMF) is an anti-inflammatory and antioxidant drug used to treat multiple sclerosis, but its mechanism(s) of action are not fully understood. In central nervous system (CNS) cells, DMF activates nuclear factor E2-related factor 2 (Nrf2), perhaps ameliorating oxidative stress-induced damage. However, it is not known whether DMF also activates Nrf2 in peripheral immune cells, which are known to participate in CNS demyelination.
View Article and Find Full Text PDFJ Syst Integr Neurosci
May 2017
VA Portland Health Care System, Research and Development Service, 3710 SW US Veterans' Hospital Rd. Portland, OR 97239, USA.
Objective And Design: The etiology of multiple sclerosis (MS) is unknown, but blood derived monocytes/macrophages are believed to be involved in the pathogenesis through phagocytosis of myelin and production of inflammatory mediators. The objective of this study is to examine inflammatory cytokines that are present at elevated levels in active MS lesions to determine whether there are differences between classically stimulated monocytes isolated from healthy control (HC) and relapsing-remitting MS (RRMS) subjects taking disease modifying drugs (DMDs), including dimethyl fumarate (DMF).
Subjects: Thirty-nine veterans of the US Armed Forces were enrolled, 21 health controls (HC), and 18 with relapsing-remitting MS (RRMS), all taking DMDs.
Biochem Biophys Res Commun
June 2016
VA Portland Health Care System, Research and Development Service, 3710 SW US Veterans' Hospital Rd., Portland, OR 97239, USA; Department of Neurology, Oregon Health & Sciences University, 3181 SW Sam Jackson Park Rd., Portland, OR 97239, USA. Electronic address:
Dimethyl fumarate (DMF) was recently approved by the FDA for the treatment of relapsing remitting MS. The pathology of MS is a result of both immune dysregulation and oxidative stress induced damage, and DMF is believed to have therapeutic effects on both of these processes. However, the mechanisms of action of DMF are not fully understood.
View Article and Find Full Text PDFCytoskeleton (Hoboken)
January 2012
VA Medical Center, 3710 SW US Veterans' Hospital Rd., Portland, Oregon 97239, USA.
Protein kinase A (PKA) signaling is targeted by interactions with A-kinase anchoring proteins (AKAPs) via a dimerization/docking domain on the regulatory (R) subunit of PKA. Four other mammalian proteins [AKAP-associated sperm protein (ASP), ropporin (ROPN1), sperm protein 17 (SP17) and calcium binding tyrosine-(Y)-phosphorylation regulated protein (CABYR)] share this highly conserved RII dimerization/docking (R2D2) domain. ASP and ROPN1 are 41% identical in sequence, interact with a variety of AKAPs in a manner similar to PKA, and are expressed in ciliated and flagellated human cells.
View Article and Find Full Text PDFJ Neuroimmunol
February 2011
Neuroimmunology Research, Veterans Affairs Medical Center, 3710 SW US Veterans' Hospital Rd., Portland, OR 97239, United States.
A human recombinant T cell receptor ligand (RTL1000) consisting of DR2 α1 and β1 domains linked covalently to MOG-35-55 peptide can reverse clinical and histological signs of experimental autoimmune encephalomyelitis (EAE), and was evaluated for safety in a Phase 1 randomized, placebo-controlled, escalating dose study in 34 subjects with multiple sclerosis (MS). RTL1000 was safe and well tolerated at a dose of ≤60 mg that is well within the effective dose range for EAE and did not cause worsening of MS disease at doses ≤200 mg. RTL1000 represents a novel approach for the treatment of MS that promises potent immunoregulation and CNS repair without global immunosuppression.
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