<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Delfino, Riccarda</style></author><author><style face="normal" font="default" size="100%">Biasotto, Matteo</style></author><author><style face="normal" font="default" size="100%">Candido, Riccardo</style></author><author><style face="normal" font="default" size="100%">Altissimo, Matteo</style></author><author><style face="normal" font="default" size="100%">Stebel, Marco</style></author><author><style face="normal" font="default" size="100%">Salomè, Murielle</style></author><author><style face="normal" font="default" size="100%">van Elteren, Johannes T</style></author><author><style face="normal" font="default" size="100%">Vogel Mikuš, Katarina</style></author><author><style face="normal" font="default" size="100%">Zennaro, Cristina</style></author><author><style face="normal" font="default" size="100%">Šala, Martin</style></author><author><style face="normal" font="default" size="100%">Addobbati, Riccardo</style></author><author><style face="normal" font="default" size="100%">Tromba, Giuliana</style></author><author><style face="normal" font="default" size="100%">Pascolo, Lorella</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Gadolinium tissue deposition in the periodontal ligament of mice with reduced renal function exposed to Gd-based contrast agents.</style></title><secondary-title><style face="normal" font="default" size="100%">Toxicol Lett</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Toxicol. Lett.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Contrast Media</style></keyword><keyword><style  face="normal" font="default" size="100%">Disease Models, Animal</style></keyword><keyword><style  face="normal" font="default" size="100%">Dose-Response Relationship, Drug</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Gadolinium</style></keyword><keyword><style  face="normal" font="default" size="100%">Gadolinium DTPA</style></keyword><keyword><style  face="normal" font="default" size="100%">Magnetic Resonance Imaging</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice</style></keyword><keyword><style  face="normal" font="default" size="100%">Nephrogenic Fibrosing Dermopathy</style></keyword><keyword><style  face="normal" font="default" size="100%">Periodontal Ligament</style></keyword><keyword><style  face="normal" font="default" size="100%">Renal Insufficiency</style></keyword><keyword><style  face="normal" font="default" size="100%">Tissue Distribution</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2019</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2019 Feb</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">301</style></volume><pages><style face="normal" font="default" size="100%">157-167</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Gadolinium deposition in tissue is linked to nephrogenic systemic fibrosis (NSF): a rare disorder occurring in patients with severe chronic kidney disease and associated with administration of Gd-based contrast agents (GBCAs) for Magnetic Resonance Imaging (MRI). It is suggested that the GBCAs prolonged permanence in blood in these patients may result in a Gd precipitation in peripheral or central organs, where it initiates a fibrotic process. In this study we investigated new sites of retention/precipitation of Gd in a mouse model of renal disease (5/6 nephrectomy) receiving two doses (closely after each other) of a linear GBCA. Two commercial GBCAs (Omniscan® and Magnevist®) were administered at doses slightly higher than those used in clinical practice (0.7 mmol/kg body weight, each). The animals were sacrificed one month after the last administration and the explanted organs (kidney, liver, femur, dorsal skin, teeth) were analysed by X-ray fluorescence (XRF) at two synchrotron facilities. The XRF analysis with a millimetre-sized beam at the SYRMEP beamline (Elettra, Italy) produced no detectable levels of Gd in the examined tissues, with the notable exception of the incisors of the nephrectomised mice. The XRF analyses at sub-micron resolution performed at ID21 (ESRF, France) allowed to clearly localize Gd in the periodontal ligaments of teeth both from Omniscan® and Magnevist® treated nephrectomised mice. The latter results were further confirmed by laser ablation inductively coupled plasma mass spectrometry (LA-ICP-MS). The study prompts that prolonged permanence of GBCAs in blood may result in Gd retention in this particular muscular tissue, opening possibilities for diagnostic applications at this level when investigating Gd-related toxicities.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/30476537?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Bellazzo, Arianna</style></author><author><style face="normal" font="default" size="100%">Di Minin, Giulio</style></author><author><style face="normal" font="default" size="100%">Valentino, Elena</style></author><author><style face="normal" font="default" size="100%">Sicari, Daria</style></author><author><style face="normal" font="default" size="100%">Torre, Denis</style></author><author><style face="normal" font="default" size="100%">Marchionni, Luigi</style></author><author><style face="normal" font="default" size="100%">Serpi, Federica</style></author><author><style face="normal" font="default" size="100%">Stadler, Michael B</style></author><author><style face="normal" font="default" size="100%">Taverna, Daniela</style></author><author><style face="normal" font="default" size="100%">Zuccolotto, Gaia</style></author><author><style face="normal" font="default" size="100%">Montagner, Isabella Monia</style></author><author><style face="normal" font="default" size="100%">Rosato, Antonio</style></author><author><style face="normal" font="default" size="100%">Tonon, Federica</style></author><author><style face="normal" font="default" size="100%">Zennaro, Cristina</style></author><author><style face="normal" font="default" size="100%">Agostinis, Chiara</style></author><author><style face="normal" font="default" size="100%">Bulla, Roberta</style></author><author><style face="normal" font="default" size="100%">Mano, Miguel</style></author><author><style face="normal" font="default" size="100%">Del Sal, Giannino</style></author><author><style face="normal" font="default" size="100%">Collavin, Licio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Cell-autonomous and cell non-autonomous downregulation of tumor suppressor DAB2IP by microRNA-149-3p promotes aggressiveness of cancer cells.</style></title><secondary-title><style face="normal" font="default" size="100%">Cell Death Differ</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Cell Death Differ.</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2018</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2018 Jul</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">25</style></volume><pages><style face="normal" font="default" size="100%">1224-1238</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;The tumor suppressor DAB2IP contributes to modulate the network of information established between cancer cells and tumor microenvironment. Epigenetic and post-transcriptional inactivation of this protein is commonly observed in multiple human malignancies, and can potentially favor progression of tumors driven by a variety of genetic mutations. Performing a high-throughput screening of a large collection of human microRNA mimics, we identified miR-149-3p as a negative post-transcriptional modulator of DAB2IP. By efficiently downregulating DAB2IP, this miRNA enhances cancer cell motility and invasiveness, facilitating activation of NF-kB signaling and promoting expression of pro-inflammatory and pro-angiogenic factors. In addition, we found that miR-149-3p secreted by prostate cancer cells induces DAB2IP downregulation in recipient vascular endothelial cells, stimulating their proliferation and motility, thus potentially remodeling the tumor microenvironment. Finally, we found that inhibition of endogenous miR-149-3p restores DAB2IP activity and efficiently reduces tumor growth and dissemination of malignant cells. These observations suggest that miR-149-3p can promote cancer progression via coordinated inhibition of DAB2IP in tumor cells and in stromal cells.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">7</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/29568059?dopt=Abstract</style></custom1></record></records></xml>