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  • 1
    Language: English
    In: Histochemistry and Cell Biology, 2011, Vol.135(5), pp.427-441
    Description: Aortic valve stenosis (AVS) and coronary artery disease (CAD) are accompanied by changes in the cardiac extra cellular matrix (cECM) including the re-expression of oncofetal fibronectin (Fn) and tenascin-C (Tn-C) variants. Human antibodies against these variants are usable for targeted therapy. Aim of the study was the comparative analysis of cECM remodelling in tissue samples from right atrial auricle (RAA) and left ventricular septum (LVS). RAA and LVS specimens from 30 patients (17 × AVS; 13 × AVS+CAD) were analysed with respect to histological changes and ECM remodelling using PCR based ECM gene expression profiling. Re-expression of ED-A + Fn and A1 + Tn-C was investigated on the mRNA and on the protein level. For immunofluorescence, human recombinant small immunoprotein (SIP) format antibodies were used. There was a positive correlation of the grade of histological changes in RAA and corresponding LVS samples ( r  = 0.695). ECM gene expression levels were higher in LVS compared to RAA. For 24 genes, a corresponding relevant (〉2.5-fold) up- or down-regulation in RAA and LVS occurred. Using SIP antibodies, a positive correlation of protein deposition levels in RAA and corresponding LVS ( r  = 0.818) could be shown for ED-A + Fn. Cardiac tissue remodelling is likely a process involving the entire heart reflected by intra-individually comparable histology and cECM changes in RAA and LVS samples. ED-A + Fn might be an excellent target for an antibody-mediated delivery of diagnostic or therapeutic agents. The RAA is a valuable and representative tool to evaluate cardiac remodelling and to plan individualized therapy.
    Keywords: Extra cellular matrix remodelling ; ED-A fibronectin ; A1 tenascin-C ; Aortic valve stenosis ; Coronary artery disease ; Targeted therapy
    ISSN: 0948-6143
    E-ISSN: 1432-119X
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  • 2
    In: Medical Physics, November 2013, Vol.40(11), pp.n/a-n/a
    Description: Purpose: Proton radiotherapy is rapidly becoming a standard treatment option for cancer. However, even though experimental data show an increase of the relative biological effectiveness (RBE) with depth, particularly at the distal end of the treatment field, a generic RBE of 1.1 is currently used in proton radiotherapy. This discrepancy might affect the effective penetration depth of the proton beam and thus the dose to the surrounding tissue and organs at risk. The purpose of this study was thus to analyze the impact of a tissue and dose dependent RBE of protons on the effective range of the proton beam in comparison to the range based on a generic RBE of 1.1.Methods: Factors influencing the biologically effective proton range were systematically analyzed by means of treatment planning studies using the Local Effect Model (LEM IV) and the treatment planning software TRiP98. Special emphasis was put on the comparison of passive and active range modulation techniques.Results: Beam energy, tissue type, and dose level significantly affected the biological extension of the treatment field at the distal edge. Up to 4 mm increased penetration depth as compared to the depth based on a constant RBE of 1.1. The extension of the biologically effective range strongly depends on the initial proton energy used for the most distal layer of the field and correlates with the width of the distal penumbra. Thus, the range extension, in general, was more pronounced for passive as compared to active range modulation systems, whereas the maximum RBE was higher for active systems.Conclusions: The analysis showed that the physical characteristics of the proton beam in terms of the width of the distal penumbra have a great impact on the RBE gradient and thus also the biologically effective penetration depth of the beam.
    Keywords: Therapeutic Applications ; Including Brachytherapy ; Cancer ; Treatment Planning ; Cancer ; Radiation Therapy ; Proton Radiotherapy ; Biologically Effective Range ; Rbe ; Lem ; Treatment Planning ; Distal Penumbra ; Radiation Therapy ; Scintigraphy ; Protons ; Dosimetry ; Tissues ; Environmental Impacts ; Medical Treatment Planning ; Cancer ; Photons ; Radiation Therapy ; Tissue Characterization ; Anatomy
    ISSN: 0094-2405
    E-ISSN: 2473-4209
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  • 3
    Language: English
    In: Histochemistry and Cell Biology, 2010, Vol.134(5), pp.503-517
    Description: Chronic cardiac rejection is represented by cardiac allograft vasculopathy (CAV) and cardiac interstitial fibrosis (CIF) known to cause severe complications. These processes are accompanied by remarkable changes in the cardiac extra cellular matrix (cECM). The aim of our study was to analyse the cECM remodelling in chronic rejection and to elucidate a potential role of ED-A domain containing fibronectin (ED-A + Fn), alpha smooth muscle actin (ASMA) and B domain containing tenascin-C (B + Tn-C). A model of chronic rejection after heterotopic rat heart transplantation was used. Allografts, recipient and control hearts were subjected to histological assessment of rejection grade, to real-time PCR based analysis of 84 genes of ECM and adhesion molecules and to immunofluorescence labelling procedures, including ED-A + Fn, ASMA and B + Tn-C antibodies. Histological analysis revealed different grades of chronic rejection. By gene expression analysis, a relevant up-regulation of the majority of ECM genes in association with chronic rejection could be shown. For 8 genes, there was a relevant up-regulation in allografts as well as in the corresponding recipient hearts. Association of ASMA positive cells with the grade of chronic rejection could be proven. In CAV and also in CIF there were extensive co-depositions of ED-A + Fn, ASMA and B + Tn-C. In conclusion, chronic cardiac allograft rejection is associated with a cECM remodelling. ASMA protein deposition in CAV, and CIF is a valuable marker to detect chronic rejection. Interactions of VSMCs and Fibro-/Myofibroblasts with ED-A + Fn and B + Tn-C might functionally contribute to the development of chronic cardiac rejection.
    Keywords: Chronic cardiac rejection ; Extra cellular matrix ; ED-A fibronectin ; Alpha smooth muscle actin ; B tenascin-C ; Cardiac allograft vasculopathy ; Cardiac interstitial fibrosis
    ISSN: 0948-6143
    E-ISSN: 1432-119X
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