39 research outputs found

    Effect of the mutations on the formation of the initial non-covalent complex as assayed by the gel mobility shift assay using a 5′ end-labeled oligonucleotide

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    <p><b>Copyright information:</b></p><p>Taken from "Experimental and computational investigations of Ser10 and Lys13 in the binding and cleavage of DNA substrates by DNA topoisomerase I"</p><p>Nucleic Acids Research 2006;34(6):1785-1797.</p><p>Published online 31 Mar 2006</p><p>PMCID:PMC1421505.</p><p>© The Author 2006. Published by Oxford University Press. All rights reserved</p

    Reduction in cellular infiltration and inflammatory markers in UUO kidneys exposed to telmisartan or PXS64.

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    <p>Untreated UUO kidneys showed increased F4/80, CD68 and CD45 positively stained cells as compared to the sham operated control animals. PXS64 significantly reduced F4/80 and CD45 positive stained cells (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0116888#pone.0116888.g006" target="_blank">Fig. 6C and E</a>) with a trend to a reduction in CD68 cells, although this was not statistically significant (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0116888#pone.0116888.g006" target="_blank">Fig. 6D</a>). Telmisartan treated kidneys showed a reduction in F4/80 positive cells but no difference in CD45 or CD68 stained cells, suggesting a differential action of PXS64 and telmisartan in modifying cellular infiltration. Results are presented as mean showed (n = 8, *P < 0.05 vs. UUO, ** P < 0.01 vs. UUO). Magnification x 400.</p

    KCa3.1 blocker TRAM34 suppressed the overexpression of TGF-β1 in mice with established diabetic nephropathy.

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    <p><b>A</b>. Immunohistochemical analysis showed increased TGF-β1 expression in mice with diabetic nephropathy mice compared to control mice, which was suppressed by TRAM34 <b>B</b>. The quantitation of TGF-β1 expression in mice kidneys. <b>C</b>. Quantitative RT-PCR showed increased mRNA expression of TGF-β1 mice with diabetic nephropathy compared to control mice but reduced with TRAM34 treatment. Results are presented as mean ± SEM. *<i>P</i><0.05, **<i>P</i><0.01. Original magnification: × 400. N = 5–8.</p

    PXS64 reduced extracellular matrix mRNA and protein expressions in the UUO.

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    <p>Real time PCR showing increased fibronectin and collagen IV mRNA levels in UUO mice vs. sham and reduced levels by telmisartan and PXS64 (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0116888#pone.0116888.g005" target="_blank">Fig. 5A and B</a>). Western blot and Hydroxy-proline showing fibronectin protein expression and collagen release in the UUO kidney, telmisartan and PXS64 treated mice (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0116888#pone.0116888.g005" target="_blank">Fig. 5C and Fig. 5D</a> respectively). Western blot shows three lanes of each group representing three independent experiments of sham, UUO control, UUO+telmisartan and UUO+PXS64. Immunostaining of kidney tissue showing fibronectin and collagen IV protein expression in UUO mice in the absence and presence of telimisartan or PXS64 (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0116888#pone.0116888.g005" target="_blank">Fig. 5E and 5F</a>). Isotype specific IgG1 was used to confirm specificity of the staining (data not shown). (n = 8, *P < 0.05, ** P < 0.01).</p

    KCa3.1 blocker TRAM34 inhibited the phosphorylation of Smad2/3 in mice with established diabetic nephropathy.

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    <p><b>A</b>. Immunohistochemical analysis showed increased phosphorylation of Smad2/3 in mice with diabetic nephropathy compared to control which was reversed by treatment with TRAM34. <b>B</b>. The quantitation of pSmad2/3+ cells in mice kidneys. Results are presented as mean ± SEM. **<i>P</i><0.01. Original magnification: × 400. N = 5–8.</p

    PXS64 inhibited TGF-β1-induced fibrotic and inflammatory markers in HK2 cells.

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    <p>HK2 cells exposed to 100ng/ml latent TGF-β1 showed a significant increase in fibronectin and collagen IV mRNA (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0116888#pone.0116888.g002" target="_blank">Fig. 2A and B</a>) and protein (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0116888#pone.0116888.g002" target="_blank">Fig. 2D and E</a>) expression, which were suppressed when co-exposed to PXS-64. These cells had increased mRNA expression of MCP-1 (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0116888#pone.0116888.g002" target="_blank">Fig. 2C</a>), which was translated to increased secretory MCP-1 in the supernatant (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0116888#pone.0116888.g002" target="_blank">Fig. 2F</a>). There were no difference mRNA and protein expression of the fibrotic and inflammatory markers s in HK2 cells under basal conditions or when cells were exposed to PXS64 alone (*<i>P</i> < 0.05, ** p<0.01 vs. appropriate control) Results are expressed as mean ± SEM, n = 4</p
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