<?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%">Sánchez-Tena, Susana</style></author><author><style face="normal" font="default" size="100%">Lizarraga, Daneida</style></author><author><style face="normal" font="default" size="100%">Miranda, Anibal</style></author><author><style face="normal" font="default" size="100%">Vinardell, Maria P</style></author><author><style face="normal" font="default" size="100%">Garcia-Garcia, Francisco</style></author><author><style face="normal" font="default" size="100%">Dopazo, Joaquin</style></author><author><style face="normal" font="default" size="100%">Torres, Josep L</style></author><author><style face="normal" font="default" size="100%">Saura-Calixto, Fulgencio</style></author><author><style face="normal" font="default" size="100%">Capellà, Gabriel</style></author><author><style face="normal" font="default" size="100%">Cascante, Marta</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Grape antioxidant dietary fiber inhibits intestinal polyposis in ApcMin/+ mice: relation to cell cycle and immune response.</style></title><secondary-title><style face="normal" font="default" size="100%">Carcinogenesis</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Carcinogenesis</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Antioxidants</style></keyword><keyword><style  face="normal" font="default" size="100%">Body Weight</style></keyword><keyword><style  face="normal" font="default" size="100%">Carcinogenesis</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Cycle</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Cycle Checkpoints</style></keyword><keyword><style  face="normal" font="default" size="100%">Colorectal Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">Dietary Fiber</style></keyword><keyword><style  face="normal" font="default" size="100%">Dietary Supplements</style></keyword><keyword><style  face="normal" font="default" size="100%">Down-Regulation</style></keyword><keyword><style  face="normal" font="default" size="100%">G1 Phase</style></keyword><keyword><style  face="normal" font="default" size="100%">Inflammation</style></keyword><keyword><style  face="normal" font="default" size="100%">Intestinal Polyposis</style></keyword><keyword><style  face="normal" font="default" size="100%">Intestinal Polyps</style></keyword><keyword><style  face="normal" font="default" size="100%">Intestine, Small</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice</style></keyword><keyword><style  face="normal" font="default" size="100%">Transcriptome</style></keyword><keyword><style  face="normal" font="default" size="100%">Vitis</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2013</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2013 Aug</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">34</style></volume><pages><style face="normal" font="default" size="100%">1881-8</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Epidemiological and experimental studies suggest that fiber and phenolic compounds might have a protective effect on the development of colon cancer in humans. Accordingly, we assessed the chemopreventive efficacy and associated mechanisms of action of a lyophilized red grape pomace containing proanthocyanidin (PA)-rich dietary fiber [grape antioxidant dietary fiber (GADF)] on spontaneous intestinal tumorigenesis in the Apc(Min/+) mouse model. Mice were fed a standard diet (control group) or a 1% (w/w) GADF-supplemented diet (GADF group) for 6 weeks. GADF supplementation greatly reduced intestinal tumorigenesis, significantly decreasing the total number of polyps by 76%. Moreover, size distribution analysis showed a considerable reduction in all polyp size categories [diameter &lt;1mm (65%), 1-2mm (67%) and &gt;2mm (87%)]. In terms of polyp formation in the proximal, middle and distal portions of the small intestine, a decrease of 76, 81 and 73% was observed, respectively. Putative molecular mechanisms underlying the inhibition of intestinal tumorigenesis were investigated by comparison of microarray expression profiles of GADF-treated and non-treated mice. We observed that the effects of GADF are mainly associated with the induction of a G1 cell cycle arrest and the downregulation of genes related to the immune response and inflammation. Our findings show for the first time the efficacy and associated mechanisms of action of GADF against intestinal tumorigenesis in Apc(Min/+) mice, suggesting its potential for the prevention of colorectal cancer. &lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">8</style></issue><custom1><style face="normal" font="default" size="100%">https://www.ncbi.nlm.nih.gov/pubmed/23615403?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%">Vivas, Yurena</style></author><author><style face="normal" font="default" size="100%">Martinez-Garcia, Cristina</style></author><author><style face="normal" font="default" size="100%">Izquierdo, Adriana</style></author><author><style face="normal" font="default" size="100%">Garcia-Garcia, Francisco</style></author><author><style face="normal" font="default" size="100%">Callejas, Sergio</style></author><author><style face="normal" font="default" size="100%">Velasco, Ismael</style></author><author><style face="normal" font="default" size="100%">Campbell, Mark</style></author><author><style face="normal" font="default" size="100%">Ros, Manuel</style></author><author><style face="normal" font="default" size="100%">Dopazo, Ana</style></author><author><style face="normal" font="default" size="100%">Dopazo, Joaquin</style></author><author><style face="normal" font="default" size="100%">Vidal-Puig, Antonio</style></author><author><style face="normal" font="default" size="100%">Medina-Gomez, Gema</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Early peroxisome proliferator-activated receptor gamma regulated genes involved in expansion of pancreatic beta cell mass.</style></title><secondary-title><style face="normal" font="default" size="100%">BMC Med Genomics</style></secondary-title><alt-title><style face="normal" font="default" size="100%">BMC Med Genomics</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Proliferation</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Survival</style></keyword><keyword><style  face="normal" font="default" size="100%">Cholesterol</style></keyword><keyword><style  face="normal" font="default" size="100%">Down-Regulation</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Regulation</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Knockout Techniques</style></keyword><keyword><style  face="normal" font="default" size="100%">Insulin Resistance</style></keyword><keyword><style  face="normal" font="default" size="100%">Insulin-Secreting Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice</style></keyword><keyword><style  face="normal" font="default" size="100%">obesity</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxidation-Reduction</style></keyword><keyword><style  face="normal" font="default" size="100%">Phosphorylation</style></keyword><keyword><style  face="normal" font="default" size="100%">PPAR gamma</style></keyword><keyword><style  face="normal" font="default" size="100%">Signal Transduction</style></keyword><keyword><style  face="normal" font="default" size="100%">Transcription, Genetic</style></keyword><keyword><style  face="normal" font="default" size="100%">Transforming Growth Factor beta</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2011</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2011 Dec 30</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">4</style></volume><pages><style face="normal" font="default" size="100%">86</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;BACKGROUND: &lt;/b&gt;The progression towards type 2 diabetes depends on the allostatic response of pancreatic beta cells to synthesise and secrete enough insulin to compensate for insulin resistance. The endocrine pancreas is a plastic tissue able to expand or regress in response to the requirements imposed by physiological and pathophysiological states associated to insulin resistance such as pregnancy, obesity or ageing, but the mechanisms mediating beta cell mass expansion in these scenarios are not well defined. We have recently shown that ob/ob mice with genetic ablation of PPARγ2, a mouse model known as the POKO mouse failed to expand its beta cell mass. This phenotype contrasted with the appropriate expansion of the beta cell mass observed in their obese littermate ob/ob mice. Thus, comparison of these models islets particularly at early ages could provide some new insights on early PPARγ dependent transcriptional responses involved in the process of beta cell mass expansion&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Here we have investigated PPARγ dependent transcriptional responses occurring during the early stages of beta cell adaptation to insulin resistance in wild type, ob/ob, PPARγ2 KO and POKO mice. We have identified genes known to regulate both the rate of proliferation and the survival signals of beta cells. Moreover we have also identified new pathways induced in ob/ob islets that remained unchanged in POKO islets, suggesting an important role for PPARγ in maintenance/activation of mechanisms essential for the continued function of the beta cell.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Our data suggest that the expansion of beta cell mass observed in ob/ob islets is associated with the activation of an immune response that fails to occur in POKO islets. We have also indentified other PPARγ dependent differentially regulated pathways including cholesterol biosynthesis, apoptosis through TGF-β signaling and decreased oxidative phosphorylation.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">https://www.ncbi.nlm.nih.gov/pubmed/22208362?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%">Prado-Lopez, Sonia</style></author><author><style face="normal" font="default" size="100%">Conesa, Ana</style></author><author><style face="normal" font="default" size="100%">Armiñán, Ana</style></author><author><style face="normal" font="default" size="100%">Martínez-Losa, Magdalena</style></author><author><style face="normal" font="default" size="100%">Escobedo-Lucea, Carmen</style></author><author><style face="normal" font="default" size="100%">Gandia, Carolina</style></author><author><style face="normal" font="default" size="100%">Tarazona, Sonia</style></author><author><style face="normal" font="default" size="100%">Melguizo, Dario</style></author><author><style face="normal" font="default" size="100%">Blesa, David</style></author><author><style face="normal" font="default" size="100%">Montaner, David</style></author><author><style face="normal" font="default" size="100%">Sanz-González, Silvia</style></author><author><style face="normal" font="default" size="100%">Sepúlveda, Pilar</style></author><author><style face="normal" font="default" size="100%">Götz, Stefan</style></author><author><style face="normal" font="default" size="100%">O'Connor, José Enrique</style></author><author><style face="normal" font="default" size="100%">Moreno, Ruben</style></author><author><style face="normal" font="default" size="100%">Dopazo, Joaquin</style></author><author><style face="normal" font="default" size="100%">Burks, Deborah J</style></author><author><style face="normal" font="default" size="100%">Stojkovic, Miodrag</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Hypoxia promotes efficient differentiation of human embryonic stem cells to functional endothelium.</style></title><secondary-title><style face="normal" font="default" size="100%">Stem Cells</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Stem Cells</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Angiopoietin-1</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">biomarkers</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Culture Techniques</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Differentiation</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Hypoxia</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Transplantation</style></keyword><keyword><style  face="normal" font="default" size="100%">Cells, Cultured</style></keyword><keyword><style  face="normal" font="default" size="100%">Down-Regulation</style></keyword><keyword><style  face="normal" font="default" size="100%">Embryonic Stem Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Endothelial Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Profiling</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Regulation</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Myocardial Infarction</style></keyword><keyword><style  face="normal" font="default" size="100%">Neovascularization, Physiologic</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxygen</style></keyword><keyword><style  face="normal" font="default" size="100%">Pluripotent Stem Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Rats</style></keyword><keyword><style  face="normal" font="default" size="100%">Rats, Nude</style></keyword><keyword><style  face="normal" font="default" size="100%">Vascular Endothelial Growth Factor A</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2010</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2010 Mar 31</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">28</style></volume><pages><style face="normal" font="default" size="100%">407-18</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Early development of mammalian embryos occurs in an environment of relative hypoxia. Nevertheless, human embryonic stem cells (hESC), which are derived from the inner cell mass of blastocyst, are routinely cultured under the same atmospheric conditions (21% O(2)) as somatic cells. We hypothesized that O(2) levels modulate gene expression and differentiation potential of hESC, and thus, we performed gene profiling of hESC maintained under normoxic or hypoxic (1% or 5% O(2)) conditions. Our analysis revealed that hypoxia downregulates expression of pluripotency markers in hESC but increases significantly the expression of genes associated with angio- and vasculogenesis including vascular endothelial growth factor and angiopoitein-like proteins. Consequently, we were able to efficiently differentiate hESC to functional endothelial cells (EC) by varying O(2) levels; after 24 hours at 5% O(2), more than 50% of cells were CD34+. Transplantation of resulting endothelial-like cells improved both systolic function and fractional shortening in a rodent model of myocardial infarction. Moreover, analysis of the infarcted zone revealed that transplanted EC reduced the area of fibrous scar tissue by 50%. Thus, use of hypoxic conditions to specify the endothelial lineage suggests a novel strategy for cellular therapies aimed at repair of damaged vasculature in pathologies such as cerebral ischemia and myocardial infarction.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">3</style></issue><custom1><style face="normal" font="default" size="100%">https://www.ncbi.nlm.nih.gov/pubmed/20049902?dopt=Abstract</style></custom1></record></records></xml>