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Juan J. Garrido

Researcher at University of Córdoba (Spain)

Publications -  23
Citations -  832

Juan J. Garrido is an academic researcher from University of Córdoba (Spain). The author has contributed to research in topics: Intestinal mucosa & Ileum. The author has an hindex of 15, co-authored 23 publications receiving 751 citations. Previous affiliations of Juan J. Garrido include Institut national de la recherche agronomique.

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Biological pathway analysis by ArrayUnlock and Ingenuity Pathway Analysis

TL;DR: Two pathways analysis tools, ArrayUnlock and Ingenuity Pathways Analysis (IPA) are described to deal with the post-analyses of microarray data, in the context of the EADGENE and SABRE post-analysis workshop.
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Quantitative analysis of the immune response upon Salmonella typhimurium infection along the porcine intestinal gut.

TL;DR: Regional differences in gene expression profiles along the porcine intestinal gut as well as regional differences in the inflammatory response to S. typhimurium infection are revealed.
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Innate immune activation of swine intestinal epithelial cell lines (IPEC-J2 and IPI-2I) in response to LPS from Salmonella typhimurium.

TL;DR: Differences in the gene expression between both cell lines IPEC-J2 and IPI-2I as response to LPS from S. typhimurium during the activation time may suggest an in vivo variability in the innate immune response against pathogens in different regions of the host's gut.
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Distinct Tissue Distribution in Pigs of Tenascin-X and Tenascin-C Transcripts

TL;DR: Within a given tissue, the level of tenascin-X and tenASCin-C transcripts varied greatly, indicating independent tenascine-X-C transcription regulation mechanisms; this was particularly obvious in adult and fetal nerves but also in the dermis, skin, heart, uterus, placentae and aorta, where tenascIn-X RNA molecules were much more abundant.
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Live attenuated African swine fever viruses as ideal tools to dissect the mechanisms involved in viral pathogenesis and immune protection

TL;DR: Compared the course of the in vivo infection caused by two homologous ASFV strains: the virulent E75 and the cell cultured adapted strain E75CV1, obtained from adapting E75 to grow in the CV1 cell-line, the kinetics of both viruses not only differed on the clinical signs that they caused and in the virus loads found, but also in the immunological pathways activated throughout the infections.