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- Leung, K C, et al.
(författare)
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Estrogen inhibits GH signaling by suppressing GH-induced JAK2 phosphorylation, an effect mediated by SOCS-2.
- 2003
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Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 0027-8424. ; 100:3, s. 1016-21
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Tidskriftsartikel (refereegranskat)abstract
- Oral estrogen administration attenuates the metabolic action of growth hormone (GH) in humans. To investigate the mechanism involved, we studied the effects of estrogen on GH signaling through Janus kinase (JAK)2 and the signal transducers and activators of transcription (STATs) in HEK293 cells stably expressing the GH receptor (293GHR), HuH7 (hepatoma) and T-47D (breast cancer) cells. 293GHR cells were transiently transfected with an estrogen receptor-alpha expression plasmid and luciferase reporters with binding elements for STAT3 and STAT5 or the beta-casein promoter. GH stimulated the reporter activities by four- to sixfold. Cotreatment with 17beta-estradiol (E(2)) resulted in a dose-dependent reduction in the response of all three reporters to GH to a maximum of 49-66% of control at 100 nM (P < 0.05). No reduction was seen when E(2) was added 1-2 h after GH treatment. Similar inhibitory effects were observed in HuH7 and T-47D cells. E(2) suppressed GH-induced JAK2 phosphorylation, an effect attenuated by actinomycin D, suggesting a requirement for gene expression. Next, we investigated the role of the suppressors of cytokine signaling (SOCS) in E(2) inhibition. E(2) increased the mRNA abundance of SOCS-2 but not SOCS-1 and SOCS-3 in HEK293 cells. The inhibitory effect of E(2) was absent in cells lacking SOCS-2 but not in those lacking SOCS-1 and SOCS-3. In conclusion, estrogen inhibits GH signaling, an action mediated by SOCS-2. This paper provides evidence for regulatory interaction between a sex steroid and the GHJAKSTAT pathway, in which SOCS-2 plays a central mechanistic role.
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- Tarnawski, V.R., et al.
(författare)
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Inter-particle contact heat transfer in soil systems at moderate temperatures
- 2002
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Ingår i: International Journal of Energy Research. - : Hindawi Limited. - 0363-907X .- 1099-114X. ; 26:15, s. 1345-1358
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Tidskriftsartikel (refereegranskat)abstract
- An inter-particle contact heat transfer model for evaluating soil thermal conductivity is analysed with respect to soils, representing different textural classes, exposed to moderate temperatures ranging from 15 to 30°C. This model is a combination of a self-consistent approximation model, enhanced with an inter-particle contact heat transfer correction coefficient. For dry and saturated soils, this coefficient is defined as a ratio of a soil harmonic mean thermal conductivity of solid and fluid (air or water) phases, to the average thermal conductivity of soil solid grains. For unsaturated soils, we assume a linear interpolation of the correction coefficient between absolutely dry and saturated states, with a Kersten function (Ke) as a proportional factor. The strongest impact of the correction coefficient (maximum reduction of heat transfer) is observed for coarse soils below a critical value of saturation degree (Sr-cr-corresponds to Ke ? 0) followed by medium and fine soils. For Sr > Srcr, the reduction of heat transfer gradually diminishes as Sr approaches 1 (i.e. saturated state). Soil texture, soil specific surface area, porosity and mineralogical composition (particularly quartz content) are important factors influencing the heat transfer correction coefficient. Their influence appears to be more substantial at the lower half of the wetness range (Sr < 0.5). Simulation results from the new enhanced model closely follow experimental data. © 2002 John Wiley and Sons, Ltd.
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