about
Heat-shock response increases lung injury caused by Pseudomonas aeruginosa via an interleukin-10-dependent mechanism in mice.Transforming growth factor beta1 inhibits cystic fibrosis transmembrane conductance regulator-dependent cAMP-stimulated alveolar epithelial fluid transport via a phosphatidylinositol 3-kinase-dependent mechanismBi-specific molecule against EGFR and death receptors simultaneously targets proliferation and death pathways in tumorsHMGB1 accelerates alveolar epithelial repair via an IL-1β- and αvβ6 integrin-dependent activation of TGF-β1Role of small GTPases and alphavbeta5 integrin in Pseudomonas aeruginosa-induced increase in lung endothelial permeabilityA novel caspase 8 selective small molecule potentiates TRAIL-induced cell death.Fractional killing arises from cell-to-cell variability in overcoming a caspase activity thresholdThe lectin-like domain of tumor necrosis factor improves lung function after rat lung transplantation--potential role for a reduction in reactive oxygen species generation.Interleukin-1beta causes acute lung injury via alphavbeta5 and alphavbeta6 integrin-dependent mechanisms.Extracellular heat shock protein 72 is a marker of the stress protein response in acute lung injury.Critical role of the small GTPase RhoA in the development of pulmonary edema induced by Pseudomonas aeruginosa in mice.Activation of the stress protein response inhibits the STAT1 signalling pathway and iNOS function in alveolar macrophages: role of Hsp90 and Hsp70.Serotonin decreases alveolar epithelial fluid transport via a direct inhibition of the epithelial sodium channel.Sensitization of mesothelioma cells to tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis by heat stress via the inhibition of the 3-phosphoinositide-dependent kinase 1/Akt pathway.HO-1 induction restores c-AMP-dependent lung epithelial fluid transport following severe hemorrhage in rats.PAI-1 is an essential component of the pulmonary host response during Pseudomonas aeruginosa pneumonia in miceInterleukin-1beta decreases expression of the epithelial sodium channel alpha-subunit in alveolar epithelial cells via a p38 MAPK-dependent signaling pathway.Mammalian osmolytes and S-nitrosoglutathione promote Delta F508 cystic fibrosis transmembrane conductance regulator (CFTR) protein maturation and function.Transforming growth factor-beta1 decreases expression of the epithelial sodium channel alphaENaC and alveolar epithelial vectorial sodium and fluid transport via an ERK1/2-dependent mechanism.Sevoflurane but not propofol increases interstitial glycolysis metabolites availability during tourniquet-induced ischaemia-reperfusion.Synergistic Inhibition of β2-adrenergic Receptor-mediated Alveolar Epithelial Fluid Transport by Interleukin-8 and Transforming Growth Factor-β.[Intraclonal heterogeneity in tumors and its impact on precision medicine].
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description
hulumtues
@sq
researcher
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wetenschapper
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հետազոտող
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name
Jérémie Roux
@ast
Jérémie Roux
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Jérémie Roux
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Jérémie Roux
@nl
Jérémie Roux
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type
label
Jérémie Roux
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Jérémie Roux
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Jérémie Roux
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Jérémie Roux
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Jérémie Roux
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prefLabel
Jérémie Roux
@ast
Jérémie Roux
@en
Jérémie Roux
@es
Jérémie Roux
@nl
Jérémie Roux
@sl
P108
P106
P1153
7202424346
P21
P31
P496
0000-0001-5712-8660