about
Oxygen-sensing pathways and the development of mammalian gas exchange.Hochachka's "Hypoxia Defense Strategies" and the development of the pathway for oxygen.Redox regulation of lung development and perinatal lung epithelial function.Inhibition of cellular and systemic inflammation cues in human bronchial epithelial cells by melanocortin-related peptides: mechanism of KPV action and a role for MC3R agonistsAbsence of the Birt-Hogg-Dubé gene product is associated with increased hypoxia-inducible factor transcriptional activity and a loss of metabolic flexibilityUnifying theory of hypoxia tolerance: molecular/metabolic defense and rescue mechanisms for surviving oxygen lack.Thymulin evokes IL-6-C/EBPbeta regenerative repair and TNF-alpha silencing during endotoxin exposure in fetal lung explants.Hypoxia-inducible factor 1alpha is regulated by the mammalian target of rapamycin (mTOR) via an mTOR signaling motif.iNOS initiates and sustains metabolic arrest in hypoxic lung adenocarcinoma cells: mechanism of cell survival in solid tumor core.Hypoxic activation of an amiloride-sensitive cation conductance in alveolar epithelial cells.Alpha-melanocyte-related tripeptide, Lys-d-Pro-Val, ameliorates endotoxin-induced nuclear factor kappaB translocation and activation: evidence for involvement of an interleukin-1beta193-195 receptor antagonism in the alveolar epitheliumControl of HIF-1{alpha} and vascular signaling in fetal lung involves cross talk between mTORC1 and the FGF-10/FGFR2b/Spry2 airway branching periodicity clock.Cardioprotective SUR2A promotes stem cell properties of cardiomyocytes.Nuclear factor-kappab blockade attenuates but does not abrogate lipopolysaccharide-dependent tumor necrosis factor-alpha biosynthesis in alveolar epithelial cells.Amiloride blockades lipopolysaccharide-induced proinflammatory cytokine biosynthesis in an IkappaB-alpha/NF-kappaB-dependent mechanism. Evidence for the amplification of an antiinflammatory pathway in the alveolar epithelium.Immunopharmacological potential of selective phosphodiesterase inhibition. I. Differential regulation of lipopolysaccharide-mediated proinflammatory cytokine (interleukin-6 and tumor necrosis factor-alpha) biosynthesis in alveolar epithelial cells.Immunopharmacological potential of selective phosphodiesterase inhibition. II. Evidence for the involvement of an inhibitory-kappaB/nuclear factor-kappaB-sensitive pathway in alveolar epithelial cells.Redox signaling-mediated regulation of lipopolysaccharide-induced proinflammatory cytokine biosynthesis in alveolar epithelial cells.O2 can raise fetal pneumocyte Na+ conductance without affecting ENaC mRNA abundance.A regulated apical Na(+) conductance in dexamethasone-treated H441 airway epithelial cells.Scaling effects on hypoxia tolerance in the Amazon fish Astronotus ocellatus (Perciformes: Cichlidae): contribution of tissue enzyme levels.Antioxidant/pro-oxidant equilibrium regulates HIF-1alpha and NF-kappa B redox sensitivity. Evidence for inhibition by glutathione oxidation in alveolar epithelial cells.The ex vivo differential expression of apoptosis signaling cofactors in the developing perinatal lung: essential role of oxygenation during the transition from placental to pulmonary-based respirationThe differential expression of apoptosis factors in the alveolar epithelium is redox sensitive and requires NF-kappaB (RelA)-selective targetingImmunomodulatory potential of thymulin-Zn(2+) in the alveolar epithelium: amelioration of endotoxin-induced cytokine release and partial amplification of a cytoprotective IL-10-sensitive pathwayA non-hypoxic, ROS-sensitive pathway mediates TNF-alpha-dependent regulation of HIF-1alpha
P50
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P50
description
hulumtues
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researcher
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հետազոտող
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name
Stephen C. Land
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Stephen C. Land
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Stephen C. Land
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Stephen C. Land
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Stephen C. Land
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type
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Stephen C. Land
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Stephen C. Land
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Stephen C. Land
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Stephen C. Land
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Stephen C. Land
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Stephen C. Land
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Stephen C. Land
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Stephen C. Land
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Stephen C. Land
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Stephen C. Land
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P106
P1153
7005545759
P21
P31
P496
0000-0001-9216-5969