<?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%">León, Carlos</style></author><author><style face="normal" font="default" size="100%">Garcia-Garcia, Francisco</style></author><author><style face="normal" font="default" size="100%">Llames, Sara</style></author><author><style face="normal" font="default" size="100%">García-Pérez, Eva</style></author><author><style face="normal" font="default" size="100%">Carretero, Marta</style></author><author><style face="normal" font="default" size="100%">Arriba, María Del Carmen</style></author><author><style face="normal" font="default" size="100%">Dopazo, Joaquin</style></author><author><style face="normal" font="default" size="100%">Del Rio, Marcela</style></author><author><style face="normal" font="default" size="100%">Escamez, Maria José</style></author><author><style face="normal" font="default" size="100%">Martínez-Santamaría, Lucía</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Transcriptomic Analysis of a Diabetic Skin-Humanized Mouse Model Dissects Molecular Pathways Underlying the Delayed Wound Healing Response.</style></title><secondary-title><style face="normal" font="default" size="100%">Genes (Basel)</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Genes (Basel)</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Diabetes Mellitus, Experimental</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%">Gene ontology</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Metabolic Networks and Pathways</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice, Nude</style></keyword><keyword><style  face="normal" font="default" size="100%">Microarray Analysis</style></keyword><keyword><style  face="normal" font="default" size="100%">Molecular Sequence Annotation</style></keyword><keyword><style  face="normal" font="default" size="100%">Principal Component Analysis</style></keyword><keyword><style  face="normal" font="default" size="100%">Signal Transduction</style></keyword><keyword><style  face="normal" font="default" size="100%">Skin</style></keyword><keyword><style  face="normal" font="default" size="100%">Skin Transplantation</style></keyword><keyword><style  face="normal" font="default" size="100%">Skin Ulcer</style></keyword><keyword><style  face="normal" font="default" size="100%">Streptozocin</style></keyword><keyword><style  face="normal" font="default" size="100%">Tissue Engineering</style></keyword><keyword><style  face="normal" font="default" size="100%">Transcriptome</style></keyword><keyword><style  face="normal" font="default" size="100%">Transplantation, Heterologous</style></keyword><keyword><style  face="normal" font="default" size="100%">Wound Healing</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2020</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2020 12 31</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">12</style></volume><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Defective healing leading to cutaneous ulcer formation is one of the most feared complications of diabetes due to its consequences on patients' quality of life and on the healthcare system. A more in-depth analysis of the underlying molecular pathophysiology is required to develop effective healing-promoting therapies for those patients. Major architectural and functional differences with human epidermis limit extrapolation of results coming from rodents and other small mammal-healing models. Therefore, the search for reliable humanized models has become mandatory. Previously, we developed a diabetes-induced delayed humanized wound healing model that faithfully recapitulated the major histological features of such skin repair-deficient condition. Herein, we present the results of a transcriptomic and functional enrichment analysis followed by a mechanistic analysis performed in such humanized wound healing model. The deregulation of genes implicated in functions such as angiogenesis, apoptosis, and inflammatory signaling processes were evidenced, confirming published data in diabetic patients that in fact might also underlie some of the histological features previously reported in the delayed skin-humanized healing model. Altogether, these molecular findings support the utility of such preclinical model as a valuable tool to gain insight into the molecular basis of the delayed diabetic healing with potential impact in the translational medicine field.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">https://www.ncbi.nlm.nih.gov/pubmed/33396192?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%">Garcia-Garcia, Francisco</style></author><author><style face="normal" font="default" size="100%">Panadero, Joaquin</style></author><author><style face="normal" font="default" size="100%">Dopazo, Joaquin</style></author><author><style face="normal" font="default" size="100%">Montaner, David</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Integrated gene set analysis for microRNA studies.</style></title><secondary-title><style face="normal" font="default" size="100%">Bioinformatics</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Bioinformatics</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Computational Biology</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Profiling</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene ontology</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Regulatory Networks</style></keyword><keyword><style  face="normal" font="default" size="100%">High-Throughput Nucleotide Sequencing</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">MicroRNAs</style></keyword><keyword><style  face="normal" font="default" size="100%">Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">Reproducibility of Results</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016 Sep 15</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">32</style></volume><pages><style face="normal" font="default" size="100%">2809-16</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;MOTIVATION: &lt;/b&gt;Functional interpretation of miRNA expression data is currently done in a three step procedure: select differentially expressed miRNAs, find their target genes, and carry out gene set overrepresentation analysis Nevertheless, major limitations of this approach have already been described at the gene level, while some newer arise in the miRNA scenario.Here, we propose an enhanced methodology that builds on the well-established gene set analysis paradigm. Evidence for differential expression at the miRNA level is transferred to a gene differential inhibition score which is easily interpretable in terms of gene sets or pathways. Such transferred indexes account for the additive effect of several miRNAs targeting the same gene, and also incorporate cancellation effects between cases and controls. Together, these two desirable characteristics allow for more accurate modeling of regulatory processes.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;We analyze high-throughput sequencing data from 20 different cancer types and provide exhaustive reports of gene and Gene Ontology-term deregulation by miRNA action.&lt;/p&gt;&lt;p&gt;&lt;b&gt;AVAILABILITY AND IMPLEMENTATION: &lt;/b&gt;The proposed methodology was implemented in the Bioconductor library mdgsa http://bioconductor.org/packages/mdgsa For the purpose of reproducibility all of the scripts are available at https://github.com/dmontaner-papers/gsa4mirna&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONTACT: &lt;/b&gt;: david.montaner@gmail.com&lt;/p&gt;&lt;p&gt;&lt;b&gt;SUPPLEMENTARY INFORMATION: &lt;/b&gt;Supplementary data are available at Bioinformatics online.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">18</style></issue><custom1><style face="normal" font="default" size="100%">https://www.ncbi.nlm.nih.gov/pubmed/27324197?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%">Moschen, Sebastián</style></author><author><style face="normal" font="default" size="100%">Bengoa Luoni, Sofía</style></author><author><style face="normal" font="default" size="100%">Di Rienzo, Julio A</style></author><author><style face="normal" font="default" size="100%">Caro, María Del Pilar</style></author><author><style face="normal" font="default" size="100%">Tohge, Takayuki</style></author><author><style face="normal" font="default" size="100%">Watanabe, Mutsumi</style></author><author><style face="normal" font="default" size="100%">Hollmann, Julien</style></author><author><style face="normal" font="default" size="100%">Gonzalez, Sergio</style></author><author><style face="normal" font="default" size="100%">Rivarola, Máximo</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%">Hopp, Horacio Esteban</style></author><author><style face="normal" font="default" size="100%">Hoefgen, Rainer</style></author><author><style face="normal" font="default" size="100%">Fernie, Alisdair R</style></author><author><style face="normal" font="default" size="100%">Paniego, Norma</style></author><author><style face="normal" font="default" size="100%">Fernandez, Paula</style></author><author><style face="normal" font="default" size="100%">Heinz, Ruth A</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Integrating transcriptomic and metabolomic analysis to understand natural leaf senescence in sunflower.</style></title><secondary-title><style face="normal" font="default" size="100%">Plant Biotechnol J</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Plant Biotechnol J</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Gas Chromatography-Mass Spectrometry</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, Plant</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene ontology</style></keyword><keyword><style  face="normal" font="default" size="100%">Genes, Plant</style></keyword><keyword><style  face="normal" font="default" size="100%">Helianthus</style></keyword><keyword><style  face="normal" font="default" size="100%">Ions</style></keyword><keyword><style  face="normal" font="default" size="100%">metabolomics</style></keyword><keyword><style  face="normal" font="default" size="100%">Oligonucleotide Array Sequence Analysis</style></keyword><keyword><style  face="normal" font="default" size="100%">Plant Leaves</style></keyword><keyword><style  face="normal" font="default" size="100%">Principal Component Analysis</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA, Messenger</style></keyword><keyword><style  face="normal" font="default" size="100%">Transcription Factors</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016 Feb</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">14</style></volume><pages><style face="normal" font="default" size="100%">719-34</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Leaf senescence is a complex process, which has dramatic consequences on crop yield. In sunflower, gap between potential and actual yields reveals the economic impact of senescence. Indeed, sunflower plants are incapable of maintaining their green leaf area over sustained periods. This study characterizes the leaf senescence process in sunflower through a systems biology approach integrating transcriptomic and metabolomic analyses: plants being grown under both glasshouse and field conditions. Our results revealed a correspondence between profile changes detected at the molecular, biochemical and physiological level throughout the progression of leaf senescence measured at different plant developmental stages. Early metabolic changes were detected prior to anthesis and before the onset of the first senescence symptoms, with more pronounced changes observed when physiological and molecular variables were assessed under field conditions. During leaf development, photosynthetic activity and cell growth processes decreased, whereas sucrose, fatty acid, nucleotide and amino acid metabolisms increased. Pathways related to nutrient recycling processes were also up-regulated. Members of the NAC, AP2-EREBP, HB, bZIP and MYB transcription factor families showed high expression levels, and their expression level was highly correlated, suggesting their involvement in sunflower senescence. The results of this study thus contribute to the elucidation of the molecular mechanisms involved in the onset and progression of leaf senescence in sunflower leaves as well as to the identification of candidate genes involved in this process. &lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">2</style></issue><custom1><style face="normal" font="default" size="100%">https://www.ncbi.nlm.nih.gov/pubmed/26132509?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%">Alvarez-Mora, M I</style></author><author><style face="normal" font="default" size="100%">Rodriguez-Revenga, L</style></author><author><style face="normal" font="default" size="100%">Madrigal, I</style></author><author><style face="normal" font="default" size="100%">García-García, F</style></author><author><style face="normal" font="default" size="100%">Duran, M</style></author><author><style face="normal" font="default" size="100%">Dopazo, J</style></author><author><style face="normal" font="default" size="100%">Estivill, X</style></author><author><style face="normal" font="default" size="100%">Milà, M</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Deregulation of key signaling pathways involved in oocyte maturation in FMR1 premutation carriers with Fragile X-associated primary ovarian insufficiency.</style></title><secondary-title><style face="normal" font="default" size="100%">Gene</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Gene</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Fragile X Mental Retardation Protein</style></keyword><keyword><style  face="normal" font="default" size="100%">Fragile X Syndrome</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, Developmental</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene ontology</style></keyword><keyword><style  face="normal" font="default" size="100%">Genome-Wide Association Study</style></keyword><keyword><style  face="normal" font="default" size="100%">Heterozygote</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Models, Genetic</style></keyword><keyword><style  face="normal" font="default" size="100%">mutation</style></keyword><keyword><style  face="normal" font="default" size="100%">Oligonucleotide Array Sequence Analysis</style></keyword><keyword><style  face="normal" font="default" size="100%">Oocytes</style></keyword><keyword><style  face="normal" font="default" size="100%">Primary Ovarian Insufficiency</style></keyword><keyword><style  face="normal" font="default" size="100%">Signal Transduction</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2015 Oct 15</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">571</style></volume><pages><style face="normal" font="default" size="100%">52-7</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;FMR1 premutation female carriers are at risk for Fragile X-associated primary ovarian insufficiency (FXPOI). Insights from knock-in mouse model have recently demonstrated that FXPOI is due to an increased rate of follicle depletion or an impaired development of the growing follicles. Molecular mechanisms responsible for this reduced viability are still unknown. In an attempt to provide new data on the mechanisms that lead to FXPOI, we report the first investigation involving transcription profiling of total blood from FMR1 premutation female carriers with and without FXPOI. A total of 16 unrelated female individuals (6 FMR1 premutated females with FXPOI; 6 FMR1 premutated females without FXPOI; and 4 no-FXPOI females) were studied by whole human genome oligonucleotide microarray (Agilent Technologies). Fold change analysis did not show any genes with significant differential gene expression. However, functional profiling by gene set analysis showed large number of statistically significant deregulated GO annotations as well as numerous KEGG pathways in FXPOI females. These results suggest that the impairment of fertility in these females might be due to a generalized deregulation of key signaling pathways involved in oocyte maturation. In particular, the vasoendotelial growth factor signaling, the inositol phosphate metabolism, the cell cycle, and the MAPK signaling pathways were found to be down-regulated in FXPOI females. Furthermore, a high statistical enrichment of biological processes involved in cell death and survival were found deregulated among FXPOI females. Our results provide new strategic approaches to further investigate the molecular mechanisms and potential therapeutic targets for FXPOI not focused in a single gene but rather in the set of genes involved in these pathways. &lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">https://www.ncbi.nlm.nih.gov/pubmed/26095811?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%">Larriba, Eduardo</style></author><author><style face="normal" font="default" size="100%">Jaime, María D L A</style></author><author><style face="normal" font="default" size="100%">Carbonell-Caballero, José</style></author><author><style face="normal" font="default" size="100%">Conesa, Ana</style></author><author><style face="normal" font="default" size="100%">Dopazo, Joaquin</style></author><author><style face="normal" font="default" size="100%">Nislow, Corey</style></author><author><style face="normal" font="default" size="100%">Martín-Nieto, José</style></author><author><style face="normal" font="default" size="100%">Lopez-Llorca, Luis Vicente</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Sequencing and functional analysis of the genome of a nematode egg-parasitic fungus, Pochonia chlamydosporia.</style></title><secondary-title><style face="normal" font="default" size="100%">Fungal Genet Biol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Fungal Genet Biol</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Ascomycota</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Regulation, Fungal</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene ontology</style></keyword><keyword><style  face="normal" font="default" size="100%">Genome, Fungal</style></keyword><keyword><style  face="normal" font="default" size="100%">Hordeum</style></keyword><keyword><style  face="normal" font="default" size="100%">Host-Pathogen Interactions</style></keyword><keyword><style  face="normal" font="default" size="100%">Nematoda</style></keyword><keyword><style  face="normal" font="default" size="100%">Ovum</style></keyword><keyword><style  face="normal" font="default" size="100%">Phylogeny</style></keyword><keyword><style  face="normal" font="default" size="100%">Plant Roots</style></keyword><keyword><style  face="normal" font="default" size="100%">Sequence Analysis, DNA</style></keyword><keyword><style  face="normal" font="default" size="100%">Signal Transduction</style></keyword><keyword><style  face="normal" font="default" size="100%">Transcriptome</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2014 Apr</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">65</style></volume><pages><style face="normal" font="default" size="100%">69-80</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Pochonia chlamydosporia is a worldwide-distributed soil fungus with a great capacity to infect and destroy the eggs and kill females of plant-parasitic nematodes. Additionally, it has the ability to colonize endophytically roots of economically-important crop plants, thereby promoting their growth and eliciting plant defenses. This multitrophic behavior makes P. chlamydosporia a potentially useful tool for sustainable agriculture approaches. We sequenced and assembled ∼41 Mb of P. chlamydosporia genomic DNA and predicted 12,122 gene models, of which many were homologous to genes of fungal pathogens of invertebrates and fungal plant pathogens. Predicted genes (65%) were functionally annotated according to Gene Ontology, and 16% of them found to share homology with genes in the Pathogen Host Interactions (PHI) database. The genome of this fungus is highly enriched in genes encoding hydrolytic enzymes, such as proteases, glycoside hydrolases and carbohydrate esterases. We used RNA-Seq technology in order to identify the genes expressed during endophytic behavior of P. chlamydosporia when colonizing barley roots. Functional annotation of these genes showed that hydrolytic enzymes and transporters are expressed during endophytism. This structural and functional analysis of the P. chlamydosporia genome provides a starting point for understanding the molecular mechanisms involved in the multitrophic lifestyle of this fungus. The genomic information provided here should also prove useful for enhancing the capabilities of this fungus as a biocontrol agent of plant-parasitic nematodes and as a plant growth-promoting organism.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">https://www.ncbi.nlm.nih.gov/pubmed/24530791?dopt=Abstract</style></custom1></record></records></xml>