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Sökning: WFRF:(Bodin Inger)

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1.
  • Peng, Zhuochun, et al. (författare)
  • Operator Dependent Choice of Prostate Cancer Biopsy Has Limited Impact on a Gene Signature Analysis for the Highly Expressed Genes IGFBP3 and F3 in Prostate Cancer Epithelial Cells
  • 2014
  • Ingår i: PLOS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 9:10, s. e109610-
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Predicting the prognosis of prostate cancer disease through gene expression analysis is receiving increasing interest. In many cases, such analyses are based on formalin-fixed, paraffin embedded (FFPE) core needle biopsy material on which Gleason grading for diagnosis has been conducted. Since each patient typically has multiple biopsy samples, and since Gleason grading is an operator dependent procedure known to be difficult, the impact of the operator's choice of biopsy was evaluated. Methods: Multiple biopsy samples from 43 patients were evaluated using a previously reported gene signature of IGFBP3, F3 and VGLL3 with potential prognostic value in estimating overall survival at diagnosis of prostate cancer. A four multiplex one-step qRT-PCR test kit, designed and optimized for measuring the signature in FFPE core needle biopsy samples was used. Concordance of gene expression levels between primary and secondary Gleason tumor patterns, as well as benign tissue specimens, was analyzed. Results: The gene expression levels of IGFBP3 and F3 in prostate cancer epithelial cell-containing tissue representing the primary and secondary Gleason patterns were high and consistent, while the low expressed VGLL3 showed more variation in its expression levels. Conclusion: The assessment of IGFBP3 and F3 gene expression levels in prostate cancer tissue is independent of Gleason patterns, meaning that the impact of operator's choice of biopsy is low.
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  • Sheikine, Yuri, et al. (författare)
  • Activation of VPAC(1) receptors aggravates early atherosclerosis in hypercholesterolemic apolipoprotein E-deficient mice
  • 2010
  • Ingår i: Biochemical and Biophysical Research Communications - BBRC. - : Elsevier Science B.V., Amsterdam. - 0006-291X .- 1090-2104. ; 402:3, s. 471-476
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective Vasoactive intestinal peptide (VIP) is a 28-amino acid peptide widely expressed in the body and binding three types of receptors VPAC(1)-R, VPAC(2)-R and PAC(1)-R Based on beneficial effects of VIP and VPAC(1)-R agonists in mouse models of several chronic inflammatory disorders, we hypothesized that activation of VIP receptors would prevent atherosclerosis development in apolipoprotein E-deficient mice Methods and results Contrary to our hypothesis, administration of a VPAC(1)-R agonist. (Ala(11 22,28))-VIP aggravated atherosclerotic lesion development in the aortic root of these mice compared to control mice This was accompanied by a significant Increase in the expression of MHC class II protein I-A(b), and suggests enhanced inflammatory activity in the vessel wall The amount of macrophage-specific CD68 staining as well as serum cholesterol and triglyceride levels did not change as a result of the (Ala(11 22,28))-VIP treatment, i e the treatment resulted in significant changes in lipid accumulation in the lesions without changing the number of macrophages or systemic lipid levels Interestingly, administration of VIP did not alter the course of the disease. Conclusion: Despite beneficial effects in murine models of several inflammatory disorders, VPAC(1)-R activation aggravates atherosclerotic lesion formation in apolipoprotein E-deficient mice through enhanced inflammatory activity in the vessel wall
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