Zobrazeno 1 - 5
of 5
pro vyhledávání: '"Elika Shabrokh"'
Autor:
Josh Pittman, Madlyn I. Frisard, Ryan P. McMillan, Elika Shabrokh, John Kavanaugh, Matthew W. Hulver
Publikováno v:
Open Journal of Molecular and Integrative Physiology. :11-19
Mitochondrial dysfunction is implicated in Alzheimer’s disease (AD) and disruption of mitochondrial dynamic pathways has been documented in brains from patients diagnosed with AD; although it is unclear whether other tissues are also affected. Much
Autor:
Morgan S. White, Mark A. Helvie, Randy J. Seeley, Oliver A. Varban, Rafael Alvarez, Natalie Rizk, Elika Shabrokh, Chuan Zhou, Heang Ping Chan
Publikováno v:
Surgery for Obesity and Related Diseases. 13:S155-S156
Autor:
Yaru Wu, Randall L. Mynatt, Angela S. Anderson, Joseph R. Stevens, Gabrielle Fundaro, Madlyn I. Frisard, Mostafa M. Ali, Mordecai M. Harvey, Kevin A. Voelker, Nabil E. Boutagy, John Kavanaugh, Elika Shabrokh, Matthew W. Hulver, Ryan P. McMillan
Toll-like receptor-4 (TLR-4) is elevated in skeletal muscle of obese humans, and data from our laboratory have shown that activation of TLR-4 in skeletal muscle via LPS results in decreased fatty acid oxidation (FAO). The purpose of this study was to
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::348464737374ae39563e34d46b392304
https://europepmc.org/articles/PMC4525328/
https://europepmc.org/articles/PMC4525328/
Autor:
Matthew W. Hulver, Yaru Wu, Ryan P. McMillan, Elika Shabrokh, Madlyn I. Frisard, John Kavanaugh
Publikováno v:
Annals of Clinical and Laboratory Research. 3
Background: Sporadic Inclusion body myositis (sIBM) is an idiopathic inflammatory myopathy that involves inflammation and damage to skeletal muscle tissue. Studies in humans demonstrate altered mitochondrial morphology in skeletal muscle from patient
Publikováno v:
The FASEB Journal. 25
Spontaneous inclusion body myositis (sIBM) is an inflammatory myopathy characterized by progressive muscle weakness, resulting in loss of function and mobility. Skeletal muscle from patients with sIBM display mitochondrial abnormalities including DNA