Brandon Quaid, Texas A&M University Rate Professors

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Texas A&M University-Texarkana
Instructor of Biology
Brandon worked at Texas A&M University-Texarkana as a Instructor of Biology
UT Health Northeast
Research Associate
Brandon worked at UT Health Northeast as a Research Associate

Texas A&M University-Texarkana
Bachelor of Science (BS)
Biology, General
Texas A&M University-Texarkana
Instructor of Biology
UTHSCT/SFA
Master of Science (MS)
Biotechnology
Researched the development of a novel murine model of empyema

Plasminogen Activator Inhibitor-1 Deficiency Augments Visceral Mesothelial Organization, Intrapleural Coagulation, and Lung Restriction in Mice with Carbon Black/Bleomycin-Induced Pleural Injury
American Journal of Respiratory Cell and Molecular Biology Volume 50 Number 2
Local derangements of fibrin turnover and plasminogen activator inhibitor (PAI)-1 have been implicated in the pathogenesis of pleural injury. However, their role in the control of pleural organization has been unclear. We found that a C57Bl/6j mouse model of carbon black/bleomycin (CBB) injury demonstrates pleural organization resulting in pleural rind formation (14 d). In transgenic mice overexpressing human PAI-1, intrapleural fibrin deposition was increased, but visceral pleural thickness, lung volumes, and compliance were comparable to wild type. CBB injury in PAI-12/2 mice significantly increased visceral pleural thickness (P , 0.001), elastance (P , 0.05), and total lung resistance (P , 0.05), while decreasing lung compliance (P , 0.01) and lung volumes (P , 0.05). Collagen, a-smooth muscle actin, and tissue factor were increased in the thickened visceral pleura of PAI-12/2 mice. Colocalization of a-smooth muscle actin and calretinin within pleural mesothelial cells was increased in CBB-injured PAI-12/2 mice. Thrombin, factor Xa, plasmin, and urokinase induced mesothelial–mesenchymal transition, tissue factor expression, and activity in primary human

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Brandon Quaid