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1                                              Osm deletion recapitulated the effects of pioglitazone o
2                                              Osm expression is significantly increased in adipose tis
3 ed to growth in complete medium at 0.14-1.02 Osm, the mean diffusion coefficient <D(peri)> increases
4 ons of cells grown in minimal medium at 0.03 Osm reduce cytoplasmic and cell water to approximately 2
5 f growth, from approximately 3.1 atm at 0.03 Osm to approximately 1.5 at 0.1 Osm and to less than 0.5
6  atm at 0.03 Osm to approximately 1.5 at 0.1 Osm and to less than 0.5 atm above 0.5 Osm.
7     At moderate growth osmolalities (up to 1 Osm), we conclude that GB is an efficient osmoprotectant
8 nge of high external osmolalities (1.02-2.17 Osm) in MOPS-buffered minimal medium (MBM) containing 1
9 t 0.1 Osm and to less than 0.5 atm above 0.5 Osm.
10  ANG II (150 ng) and/or hypertonic NaCl (1.5 Osm/L, 100 mul) through the internal carotid artery sign
11                                         By 5 Osm, the TAATTC "star" sequence complex has lost almost
12 ghly hydrated bulk soil is low (less than 50 Osm/kg); thus the ability to adapt to elevated osmolalit
13 lly modulated during high-fat diet (HFD) and Osm-/- mice displayed early-onset glucose intolerance, i
14 d suspected NFATc1 targets, such as Spp1 and Osm, we have revealed the early upregulation of a number
15 henocopied glucose intolerance of whole-body Osm-/- mice fed a HFD and recapitulated liver damage wit
16     Tumour cells implanted in Osm-deficient (Osm(-/-)) mice display an epithelial-dominated morpholog
17 c mice, pioglitazone treatment downregulated Osm, p66Shc, and Cxcl12 in the hematopoietic BM, restore
18 tor and that lung basophils are enriched for Osm transcripts.
19                                           In Osm(-/-) mice, by micro-computed tomography and histolog
20                    Tumour cells implanted in Osm-deficient (Osm(-/-)) mice display an epithelial-domi
21 , we observed reduced activation of Stat3 in Osm(-/-) mice.
22 interleukin-3 of the genes for oncostatin M (Osm) and the cytokine-inducible, SH2 domain-containing g
23  the neuroprotective molecule, Oncostatin M (Osm), through a Card9-independent pathway, mediated by t
24 MR(FKO) mice exhibit increased expression of Osm, the T cell markers Cd4 and Cd8, and the macrophage
25 s p66Shc independent, and double knockout of Osm and p66Shc completely rescued HSPC mobilization.
26     Moreover, the tumour microenvironment of Osm(-/-) animals exhibit increased abundance of a smooth
27                        The overexpression of Osm resulting from myelopoiesis prevented HSPC mobilizat
28  switched macrophages from M1 to M2, reduced Osm expression, and prevented transcellular induction of
29       Ubiquitous or hematopoietic restricted Osm deletion phenocopied p66Shc deletion in preventing d
30 that GFI1/LSD1 complexes occupy sites at the Osm promoter and an intragenic region of the Tnfa gene a
31                Furthermore, we find that the Osm receptor (OsmR) functioned specifically in astrocyte
32                     Additional studies using Osm-deficient murine macrophages demonstrated that macro