Zobrazeno 1 - 10
of 57
pro vyhledávání: '"Rayna J. Gonzales"'
Autor:
Daniel R, Griffiths, L Matthew, Law, Conor, Young, Alberto, Fuentes, Seth, Truran, Nina, Karamanova, Laura C, Bell, Gregory, Turner, Hannah, Emerson, Diego, Mastroeni, Rayna J, Gonzales, Peter D, Reaven, C Chad, Quarles, Raymond Q, Migrino, Jonathan, Lifshitz
Publikováno v:
Journal of Neurotrauma. 39:1429-1441
Severe traumatic brain injury (TBI) results in cognitive dysfunction in part due to vascular perturbations. In contrast, the long-term vasculo-cognitive pathophysiology of mild TBI (mTBI) remains unknown. We evaluated mTBI effects on chronic cognitiv
Autor:
Samuel X. Shi, Yu-Jing Li, Trevor S. Wendt, Kaibin Shi, Weina Jin, Qiang Liu, Rayna J. Gonzales
Sphingosine-1-phosphate receptor 1 (S1PR1) is highly expressed in endothelial cells and receptor activation plays an important role in mediating endothelial function and health, thus showing promise as a pharmacologic target for acute ischemic stroke
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::91581f645449f46abdc4d9499ee57651
https://doi.org/10.1101/2023.03.27.534410
https://doi.org/10.1101/2023.03.27.534410
Publikováno v:
American Journal of Physiology-Cell Physiology. 320:C1055-C1073
Vascular smooth muscle (VSM) cell phenotypic expression and autophagic state are dynamic responses to stress. Vascular pathologies, such as hypoxemia and ischemic injury, induce a synthetic VSM phenotype and autophagic flux resulting in a loss of vas
Publikováno v:
The FASEB Journal. 36
Autor:
Trevor S. Wendt, Rayna J. Gonzales
Publikováno v:
The FASEB Journal. 36
Autor:
Trevor S. Wendt, Rayna J. Gonzales
Publikováno v:
The FASEB Journal. 36
Publikováno v:
The FASEB Journal. 35
Publikováno v:
The FASEB Journal. 35
Publikováno v:
The FASEB Journal. 35
Publikováno v:
American journal of physiology. Cell physiology. 320(6)
Vascular smooth muscle (VSM) cell phenotypic expression and autophagic state are dynamic responses to stress. Vascular pathologies, such as hypoxemia and ischemic injury, induce a synthetic VSM phenotype and autophagic flux resulting in a loss of vas