Zobrazeno 1 - 4
of 4
pro vyhledávání: '"Esther Bolanis"'
Autor:
Angelia D Lockett, Mary Beth Brown, Nieves Santos-Falcon, Natalia I Rush, Houssam Oueini, Amber J Oberle, Esther Bolanis, Miryam A Fragoso, Daniela N Petrusca, Karina A Serban, Kelly S Schweitzer, Robert G Presson, Michael Campos, Irina Petrache
Publikováno v:
PLoS ONE, Vol 9, Iss 4, p e93979 (2014)
The homeostatic lung protective effects of alpha-1 antitrypsin (A1AT) may require the transport of circulating proteinase inhibitor across an intact lung endothelial barrier. We hypothesized that uninjured pulmonary endothelial cells transport A1AT t
Externí odkaz:
https://doaj.org/article/fc30a692adeb457cafbf28e54ccf3fd5
Autor:
Esther Bolanis, Theodore R. Holman, Raghavendra G. Mirmira, Jerry L. Nadler, Sarah A. Tersey, David J. Maloney
Publikováno v:
Molecular Endocrinology. 29:791-800
The insulin producing islet β-cells have increasingly gained attention for their role in the pathogeneses of virtually all forms of diabetes. Dysfunction, de-differentiation, and/or death of β-cells are pivotal features in the transition from normo
Autor:
Yong Gao, Esther Bolanis, D. Wade Clapp, Shawn K. Ahlfeld, Jian Wang, Emrin Horgusluoglu, Simon J. Conway
Publikováno v:
Birth Defects Research Part A: Clinical and Molecular Teratology. 97:373-385
BACKGROUND Extreme preterm birth exposes the saccular lung to multiple teratogens, which ultimately retard alveolar development. Specifically, therapeutic high level oxygen supplementation adversely affects the premature lungs and results in blunted
Autor:
Natalia I. Rush, Nieves Santos-Falcon, Michael Campos, Houssam Oueini, Esther Bolanis, Amber Oberle, Mary Beth Brown, Kelly S. Schweitzer, Irina Petrache, Angelia D. Lockett, Robert G. Presson, Karina A. Serban, Miryam A. Fragoso, Daniela N. Petrusca
Publikováno v:
PLoS ONE
PLoS ONE, Vol 9, Iss 4, p e93979 (2014)
PLoS ONE, Vol 9, Iss 4, p e93979 (2014)
The homeostatic lung protective effects of alpha-1 antitrypsin (A1AT) may require the transport of circulating proteinase inhibitor across an intact lung endothelial barrier. We hypothesized that uninjured pulmonary endothelial cells transport A1AT t