<?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%">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><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%">Reumers, Joke</style></author><author><style face="normal" font="default" size="100%">Conde, Lucia</style></author><author><style face="normal" font="default" size="100%">Medina, Ignacio</style></author><author><style face="normal" font="default" size="100%">Maurer-Stroh, Sebastian</style></author><author><style face="normal" font="default" size="100%">Van Durme, Joost</style></author><author><style face="normal" font="default" size="100%">Dopazo, Joaquin</style></author><author><style face="normal" font="default" size="100%">Rousseau, Frederic</style></author><author><style face="normal" font="default" size="100%">Schymkowitz, Joost</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Joint annotation of coding and non-coding single nucleotide polymorphisms and mutations in the SNPeffect and PupaSuite databases.</style></title><secondary-title><style face="normal" font="default" size="100%">Nucleic Acids Res</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Nucleic Acids Res</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Amino Acid Substitution</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Databases, Genetic</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Diseases, Inborn</style></keyword><keyword><style  face="normal" font="default" size="100%">HSP70 Heat-Shock Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Internet</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice</style></keyword><keyword><style  face="normal" font="default" size="100%">MicroRNAs</style></keyword><keyword><style  face="normal" font="default" size="100%">mutation</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Single Nucleotide</style></keyword><keyword><style  face="normal" font="default" size="100%">Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Rats</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA Splice Sites</style></keyword><keyword><style  face="normal" font="default" size="100%">Transcription Factors</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2008</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2008 Jan</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">36</style></volume><pages><style face="normal" font="default" size="100%">D825-9</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Single nucleotide polymorphisms (SNPs) are, together with copy number variation, the primary source of variation in the human genome. SNPs are associated with altered response to drug treatment, susceptibility to disease and other phenotypic variation. Furthermore, during genetic screens for disease-associated mutations in groups of patients and control individuals, the distinction between disease causing mutation and polymorphism is often unclear. Annotation of the functional and structural implications of single nucleotide changes thus provides valuable information to interpret and guide experiments. The SNPeffect and PupaSuite databases are now synchronized to deliver annotations for both non-coding and coding SNP, as well as annotations for the SwissProt set of human disease mutations. In addition, SNPeffect now contains predictions of Tango2: an improved aggregation detector, and Waltz: a novel predictor of amyloid-forming sequences, as well as improved predictors for regions that are recognized by the Hsp70 family of chaperones. The new PupaSuite version incorporates predictions for SNPs in silencers and miRNAs including their targets, as well as additional methods for predicting SNPs in TFBSs and splice sites. Also predictions for mouse and rat genomes have been added. In addition, a PupaSuite web service has been developed to enable data access, programmatically. The combined database holds annotations for 4,965,073 regulatory as well as 133,505 coding human SNPs and 14,935 disease mutations, and phenotypic descriptions of 43,797 human proteins and is accessible via http://snpeffect.vib.be and http://pupasuite.bioinfo.cipf.es/.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">Database issue</style></issue><custom1><style face="normal" font="default" size="100%">https://www.ncbi.nlm.nih.gov/pubmed/18086700?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%">Saar, Kathrin</style></author><author><style face="normal" font="default" size="100%">Beck, Alfred</style></author><author><style face="normal" font="default" size="100%">Bihoreau, Marie-Thérèse</style></author><author><style face="normal" font="default" size="100%">Birney, Ewan</style></author><author><style face="normal" font="default" size="100%">Brocklebank, Denise</style></author><author><style face="normal" font="default" size="100%">Chen, Yuan</style></author><author><style face="normal" font="default" size="100%">Cuppen, Edwin</style></author><author><style face="normal" font="default" size="100%">Demonchy, Stephanie</style></author><author><style face="normal" font="default" size="100%">Dopazo, Joaquin</style></author><author><style face="normal" font="default" size="100%">Flicek, Paul</style></author><author><style face="normal" font="default" size="100%">Foglio, Mario</style></author><author><style face="normal" font="default" size="100%">Fujiyama, Asao</style></author><author><style face="normal" font="default" size="100%">Gut, Ivo G</style></author><author><style face="normal" font="default" size="100%">Gauguier, Dominique</style></author><author><style face="normal" font="default" size="100%">Guigó, Roderic</style></author><author><style face="normal" font="default" size="100%">Guryev, Victor</style></author><author><style face="normal" font="default" size="100%">Heinig, Matthias</style></author><author><style face="normal" font="default" size="100%">Hummel, Oliver</style></author><author><style face="normal" font="default" size="100%">Jahn, Niels</style></author><author><style face="normal" font="default" size="100%">Klages, Sven</style></author><author><style face="normal" font="default" size="100%">Kren, Vladimir</style></author><author><style face="normal" font="default" size="100%">Kube, Michael</style></author><author><style face="normal" font="default" size="100%">Kuhl, Heiner</style></author><author><style face="normal" font="default" size="100%">Kuramoto, Takashi</style></author><author><style face="normal" font="default" size="100%">Kuroki, Yoko</style></author><author><style face="normal" font="default" size="100%">Lechner, Doris</style></author><author><style face="normal" font="default" size="100%">Lee, Young-Ae</style></author><author><style face="normal" font="default" size="100%">Lopez-Bigas, Nuria</style></author><author><style face="normal" font="default" size="100%">Lathrop, G Mark</style></author><author><style face="normal" font="default" size="100%">Mashimo, Tomoji</style></author><author><style face="normal" font="default" size="100%">Medina, Ignacio</style></author><author><style face="normal" font="default" size="100%">Mott, Richard</style></author><author><style face="normal" font="default" size="100%">Patone, Giannino</style></author><author><style face="normal" font="default" size="100%">Perrier-Cornet, Jeanne-Antide</style></author><author><style face="normal" font="default" size="100%">Platzer, Matthias</style></author><author><style face="normal" font="default" size="100%">Pravenec, Michal</style></author><author><style face="normal" font="default" size="100%">Reinhardt, Richard</style></author><author><style face="normal" font="default" size="100%">Sakaki, Yoshiyuki</style></author><author><style face="normal" font="default" size="100%">Schilhabel, Markus</style></author><author><style face="normal" font="default" size="100%">Schulz, Herbert</style></author><author><style face="normal" font="default" size="100%">Serikawa, Tadao</style></author><author><style face="normal" font="default" size="100%">Shikhagaie, Medya</style></author><author><style face="normal" font="default" size="100%">Tatsumoto, Shouji</style></author><author><style face="normal" font="default" size="100%">Taudien, Stefan</style></author><author><style face="normal" font="default" size="100%">Toyoda, Atsushi</style></author><author><style face="normal" font="default" size="100%">Voigt, Birger</style></author><author><style face="normal" font="default" size="100%">Zelenika, Diana</style></author><author><style face="normal" font="default" size="100%">Zimdahl, Heike</style></author><author><style face="normal" font="default" size="100%">Hubner, Norbert</style></author></authors><translated-authors><author><style face="normal" font="default" size="100%">STAR Consortium</style></author></translated-authors></contributors><titles><title><style face="normal" font="default" size="100%">SNP and haplotype mapping for genetic analysis in the rat.</style></title><secondary-title><style face="normal" font="default" size="100%">Nat Genet</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Nat Genet</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Chromosome Mapping</style></keyword><keyword><style  face="normal" font="default" size="100%">Databases, Genetic</style></keyword><keyword><style  face="normal" font="default" size="100%">Genome</style></keyword><keyword><style  face="normal" font="default" size="100%">Haplotypes</style></keyword><keyword><style  face="normal" font="default" size="100%">Linkage Disequilibrium</style></keyword><keyword><style  face="normal" font="default" size="100%">Phylogeny</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Single Nucleotide</style></keyword><keyword><style  face="normal" font="default" size="100%">Quantitative Trait Loci</style></keyword><keyword><style  face="normal" font="default" size="100%">Rats</style></keyword><keyword><style  face="normal" font="default" size="100%">Rats, Inbred Strains</style></keyword><keyword><style  face="normal" font="default" size="100%">Recombination, Genetic</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2008</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2008 May</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">40</style></volume><pages><style face="normal" font="default" size="100%">560-6</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 laboratory rat is one of the most extensively studied model organisms. Inbred laboratory rat strains originated from limited Rattus norvegicus founder populations, and the inherited genetic variation provides an excellent resource for the correlation of genotype to phenotype. Here, we report a survey of genetic variation based on almost 3 million newly identified SNPs. We obtained accurate and complete genotypes for a subset of 20,238 SNPs across 167 distinct inbred rat strains, two rat recombinant inbred panels and an F2 intercross. Using 81% of these SNPs, we constructed high-density genetic maps, creating a large dataset of fully characterized SNPs for disease gene mapping. Our data characterize the population structure and illustrate the degree of linkage disequilibrium. We provide a detailed SNP map and demonstrate its utility for mapping of quantitative trait loci. This community resource is openly available and augments the genetic tools for this workhorse of physiological studies.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">5</style></issue><custom1><style face="normal" font="default" size="100%">https://www.ncbi.nlm.nih.gov/pubmed/18443594?dopt=Abstract</style></custom1></record></records></xml>