Zobrazeno 1 - 5
of 5
pro vyhledávání: '"Nicholas A. Floreani"'
Autor:
Scott M. Turner, Lindsay S. Roberts, Marc K. Hellerstein, Nicholas A. Floreani, John C. Price, William E. Holmes, Mahalakshmi Shankaran, Cyrus F. Khambatta, Kelvin W. Li, Matthew D. Bruss, Marcy Dalidd
Publikováno v:
Molecular & Cellular Proteomics : MCP
Calorie restriction (CR) promotes longevity. A prevalent mechanistic hypothesis explaining this effect suggests that protein degradation, including mitochondrial autophagy, is increased with CR, removing damaged proteins and improving cellular fitnes
Publikováno v:
Free Radical Biology and Medicine. 51:1601-1609
Oxidative damage of the endothelium disrupts the integrity of the blood-brain barrier (BBB). We have shown before that alcohol exposure increases the levels of reactive oxygen species (ROS; superoxide and hydroxyl radical) and nitric oxide (NO) in br
Autor:
Nicholas A. Floreani, James Haorah, Yuri Persidsky, Travis J. Rump, P. M. Abdul Muneer, Michael R. Brodie, Brenda Morsey, Saleena Alikunju
Publikováno v:
Journal of Neuroimmune Pharmacology. 5:533-545
Secretion of pro-inflammatory molecules by astrocytes after alcohol treatment was shown to be associated with neuroinflammation. We hypothesized that activation of cytosolic phospholipase A2 (cPLA2) and cyclooxygenase (COX-2) by ethanol in astrocytes
Autor:
Nicholas A. Floreani, William E. Holmes, John C. Price, Kelvin Li, Scott M. Turner, Marc K. Hellerstein, Richard A. Neese
Publikováno v:
Analytical biochemistry. 420(1)
Dysfunction of protein turnover is a feature of many human diseases, and proteins are substrates in important biological processes. Currently, no method exists for the measurement of global protein turnover (i.e., proteome dynamics) that can be appli
Autor:
Brenda Morsey, James Haorah, Yuri Persidsky, Nicholas A. Floreani, Servio H. Ramirez, Santhi Gorantla
Publikováno v:
Free radical biologymedicine. 45(11)
Neuro-cognitive deficits, neuronal injury, and neurodegeneration are well documented in alcoholics, yet the underlying mechanisms remain elusive. Oxidative damage of mitochondria and cellular proteins intertwines with the progression of neuroinflamma