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Open Physics
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2014
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vol. 12
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issue 8
541-553
EN
The residual symmetries of the famous modified Korteweg-de Vries (mKdV) equation are researched in this paper. The initial problem on the residual symmetry of the mKdV equation is researched. The residual symmetries for the mKdV equation are proved to be nonlocal and the nonlocal residual symmetries are extended to the local Lie point symmetries by means of enlarging the mKdV equations. One-parameter invariant subgroups and the invariant solutions for the extended system are listed. Eight types of similarity solutions and the reduction equations are demonstrated. It is noted that we researched the twofold residual symmetries by means of taking the mKdV equation as an example. Similarity solutions and the reduction equations are demonstrated for the extended mKdV equations related to the twofold residual symmetries.
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2013
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vol. 60
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issue 3
381-386
EN
The expression of predominant housekeeping genes used in RT-qPCR can vary during development and differentiation. The frequently used housekeeping genes (ACTB, GAPDH, 18S rRNA, EF1α and RPL 13a) were evaluated during an early stage of the osteogenic differentiation of mouse bone marrow-derived mesenchymal stem cells (mMSCs) (under normal conditions or treated with CCG-4986) to identify housekeeping genes whose expression remained constant during osteogenic differentiation. When we used RGS4 mRNA, which was determined as copy number per μg of total RNA, to normalize gene expression, we observed that the relative EF1α expression profile was consistent with RGS4 expression after treatment with CCG-4986. All the relative expression profiles of the EF1α, 18S rRNA, and RPL13a housekeeping genes were consistent with RGS4 profiles determined by measuring mRNA copies under normal osteogenic differentiation conditions. The expression profiles calibrated by ACTB and GAPDH were not consistent with those determined using mRNA copy number in untreated cells or cells treated with CCG-4986 under osteogenic differentiation conditions. Under normal osteogenic differentiation conditions, EF1α, 18S rRNA, and RPL 13a are suitable housekeeping genes for RT-qPCR analysis. However, EF1α is the only suitable gene upon CCG-4986 treatment.
EN
Objective. To explore the effect of dexamethasone (DEX) on monocyte adhesion function and its underlying mechanism. Methods. The effects of DEX and fasudil on adhesion of cultured U937 monocytes to human umbilical vein endothelial cells (HUVEC) following stimulation with phorbol myristate acetate (PMA) were studied; Changes in the Rho-associated coiled-coil protein kinase 1 (ROCK1) protein content and activity were evaluated. Results. DEX and fasudil significantly inhibited U937 cell adhesion rates under PMA stimulation and inhibited ROCK1 activity. Mifepristone (RU-486) and cycloheximide (CHX) did not alter these effects of DEX. Conclusions. DEX interferes with the adhesion function of U937 cells through the inhibition of ROCK1 activity.
EN
Glucocorticoid receptor (GR) is a steroid hormone receptor that has been shown to play important roles in diverse cellular and physiological processes. More and more evidence has revealed that the effects of glucocorticoids are mediated by the glucocorticoid receptor through genomic or nongenomic mechanisms. A growing number of glucocorticoid receptor splice variants have been identified in human tissues, but few are known in rat tissues. In this work, a novel rGR cDNA, called rGRβ, was cloned from Sprague Dawlay (SD) rat liver. Sequence analysis revealed that the rGRβ mRNA was 39 base pairs (bp) shorter than the rGR mRNA reported earlier. The deleted segment is located in exon 1 and encodes 13 repeated glutamine residues. Both the rGR and rGRβ mRNAs were quantitated by Northern blot hybridization using non-homologous glucocorticoid cDNA probes. Results showed that the rGR and rGRβ mRNAs were most abundant in the lung, the least abundant in the heart, and there were more rGR and rGRβ mRNAs in the kidney than in the liver. The identification of rGRβ may contribute to the understanding of the genomic or nongenomic effects of glucocorticoids.
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