<?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%">Hillung, Julia</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%">Cuevas, José M</style></author><author><style face="normal" font="default" size="100%">Elena, Santiago F</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">The transcriptomics of an experimentally evolved plant-virus interaction.</style></title><secondary-title><style face="normal" font="default" size="100%">Sci Rep</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Sci Rep</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Arabidopsis</style></keyword><keyword><style  face="normal" font="default" size="100%">Ecotype</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Profiling</style></keyword><keyword><style  face="normal" font="default" size="100%">Host-Pathogen Interactions</style></keyword><keyword><style  face="normal" font="default" size="100%">Potyvirus</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 04 26</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">6</style></volume><pages><style face="normal" font="default" size="100%">24901</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Models of plant-virus interaction assume that the ability of a virus to infect a host genotype depends on the matching between virulence and resistance genes. Recently, we evolved tobacco etch potyvirus (TEV) lineages on different ecotypes of Arabidopsis thaliana, and found that some ecotypes selected for specialist viruses whereas others selected for generalists. Here we sought to evaluate the transcriptomic basis of such relationships. We have characterized the transcriptomic responses of five ecotypes infected with the ancestral and evolved viruses. Genes and functional categories differentially expressed by plants infected with local TEV isolates were identified, showing heterogeneous responses among ecotypes, although significant parallelism existed among lineages evolved in the same ecotype. Although genes involved in immune responses were altered upon infection, other functional groups were also pervasively over-represented, suggesting that plant resistance genes were not the only drivers of viral adaptation. Finally, the transcriptomic consequences of infection with the generalist and specialist lineages were compared. Whilst the generalist induced very similar perturbations in the transcriptomes of the different ecotypes, the perturbations induced by the specialist were divergent. Plant defense mechanisms were activated when the infecting virus was specialist but they were down-regulated when infecting with generalist.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">https://www.ncbi.nlm.nih.gov/pubmed/27113435?dopt=Abstract</style></custom1></record></records></xml>