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Torijano-Casalengua M.L.,Medicina de Familia y Comunitaria | Olivera-Canadas G.,Direccion Tecnica de Procesos y Calidad | Maderuelo-Fernandez J.A.,Institute Investigacion Biomedica Of Salamanca Ibsal
Atencion Primaria | Year: 2013

Objetive: To validate a tool to measure patient safety culture in Spanish primary care professionals. Methods: Medical Office Survey on Patient Safety Culture (MOSPSC), from the Agency for Healthcare and Research in Quality (AHRQ). The process has been performed in five steps: original version traslation, conceptual equivalence evaluation, acceptability and viability assessment, content validity and questionnaire test and response analysis and psichometric properties assessment. Setting: Primary care. Subjects: 185 Primary care professionals from different Spanish regions represented the sample test. Main outcome measures: Frecuency, response pattern and discrimination power of each item. Cronbach's alpha coefficient and dimensions obtained through factor analysis. Results: 17, 8% of respondents answered all the items and 28, 7% of them did not answer, or answered the option "Don't know/Does not apply", to one to four items. All the sentences, with only one exception, present discrimination capacity. Cronbach's alpha coefficient results 0,96 and information is sumarized in 15 factors obtaining the same items in 7 of the total 12 factors in the original questionnaire. Conclusions: Traslated, adapted, extended and validated AHRQ questionnaire is, in this setting, a reliable and useful instrument and it must be used for international comparisons.

Risueno A.,Celgene | Roson-Burgo B.,Institute Investigacion Biomedica Of Salamanca Ibsal | Dolnik A.,University of Ulm | Hernandez-Rivas J.M.,Hospital Universitario Of Salamanca Hus | And 2 more authors.
BMC Genomics | Year: 2015

Background: Accurate analysis of whole-gene expression and individual-exon expression is essential to characterize different transcript isoforms and identify alternative splicing events in human genes. One of the omic technologies widely used in many studies on human samples are the exon-specific expression microarray platforms. Results: Since there are not many validated comparative analyses to identify specific splicing events using data derived from these types of platforms, we have developed an algorithm (called ESLiM) to detect significant changes in exon use, and applied it to a reference dataset of 270 human genes that show alternative expression in different tissues. We compared the results with three other methodological approaches and provided the R source code to be applied elsewhere. The genes positively detected by these analyses also provide a verified subset of human genes that present tissue-regulated isoforms. Furthermore, we performed a validation analysis on human patient samples comparing two different subtypes of acute myeloid leukemia (AML) and we experimentally validated the splicing in several selected genes that showed exons with highly significant signal change. Conclusions: The comparative analyses with other methods using a fair set of human genes that show alternative splicing and the validation on clinical samples demonstrate that the proposed novel algorithm is a reliable tool for detecting differential splicing in exon-level expression data. © 2014 Risueño et al.; licensee BioMed Central Ltd.

Munoz-Felix J.M.,University of Salamanca | Munoz-Felix J.M.,Institute Investigacion Biomedica Of Salamanca Ibsal | Lopez-Novoa J.M.,University of Salamanca | Lopez-Novoa J.M.,Institute Investigacion Biomedica Of Salamanca Ibsal | And 3 more authors.
Kidney International | Year: 2014

Tubulointerstitial fibrosis is characterized by an accumulation of extracellular matrix in the renal interstitium, myofibroblast activation, cell infiltration, and tubular cell apoptosis, leading to chronic renal failure. Activin receptor-like kinase 1 (ALK1) is a transforming growth factor-β1 type I receptor with a pivotal role in endothelial proliferation and migration, but its role in the development of renal fibrosis is unknown. To assess this we used the unilateral ureteral obstruction model of tubulointerstitial fibrosis in ALK1 haploinsufficient (ALK1 +/-) and wild-type mice. After 15 days, there was an increase in extracellular matrix protein expression in the obstructed kidneys from both ALK1 +/+ and ALK1 +/- mice, but obstructed kidneys from ALK1 +/- mice showed significantly higher expression of type I collagen than those from wild-type mice. Ureteral obstruction increased kidney myofibroblasts markers (α-smooth muscle actin and S100A4), without differences between mouse genotypes. ALK1 expression was increased after ureteral obstruction, and this increased expression was located in myofibroblasts. Moreover, cultured renal fibroblasts from ALK1 +/- mice expressed more collagen type I and fibronectin than fibroblasts derived from wild-type mice. Thus, ALK1 modulates obstruction-induced renal fibrosis by increased extracellular matrix synthesis in myofibroblasts, but without differences in myofibroblast number. © 2013 International Society of Nephrology.

Munoz-Felix J.M.,University of Salamanca | Munoz-Felix J.M.,Institute Investigacion Biomedica Of Salamanca Ibsal | Gonzalez-Nunez M.,University of Salamanca | Gonzalez-Nunez M.,Institute Investigacion Biomedica Of Salamanca Ibsal | And 5 more authors.
Pharmacology and Therapeutics | Year: 2015

The understanding of renal fibrosis in chronic kidney disease (CKD) remains as a challenge. More than 10% of the population of developed countries suffer from CKD. Proliferation and activation of myofibroblasts and accumulation of extracellular matrix proteins are the main features of kidney fibrosis, a process in which a large number of cytokines are involved. Targeting cytokines responsible for kidney fibrosis development might be an important strategy to face the problem of CKD. The increasing knowledge of the signaling pathway network of the transforming growth factor beta (TGF-β) superfamily members, such as the profibrotic cytokine TGF-β1 or the bone morphogenetic proteins (BMPs), and their involvement in the regulation of kidney fibrosis, has stimulated numerous research teams to look for potential strategies to inhibit profibrotic cytokines or to enhance the anti-fibrotic actions of other cytokines. The consequence of all these studies is a better understanding of all these canonical (Smad-mediated) and non-canonical signaling pathways. In addition, the different receptors involved for signaling of each cytokine, the different combinations of type I-type II receptors, and the presence and function of co-receptors that can influence the biological response have been also described. However, are these studies leading to suitable strategies to block the appearance and progression of kidney fibrosis? In this review, we offer a critical perspective analyzing the achievements using the most important strategies developed up till now: TGF-β antibodies, chemical inhibitors of TGF-β receptors, miRNAs and signaling pathways and BMP agonists with a potential role as therapeutic molecules against kidney fibrosis. © 2015 Elsevier Inc. All rights reserved.

Sancho-Martinez S.M.,Institute Investigacion Biomedica Of Salamanca Ibsal | Sancho-Martinez S.M.,University of Salamanca | Sancho-Martinez S.M.,Instituto Reina Sofia Of Investigacion Nefrologica | Prieto-Garcia L.,Institute Investigacion Biomedica Of Salamanca Ibsal | And 11 more authors.
Pharmacology and Therapeutics | Year: 2012

Cisplatin is a chemotherapeutic drug widely used against a variety of cancers. Its clinical utility is severely limited by its toxicity, which mainly affects, but is not limited to, the inner ear and renal tubules. Cisplatin toxicity is determined by target tissue and cell accumulation, subcellular handling and trafficking through diverse subcellular structures, and interaction with macromolecules. Cisplatin accumulates and stresses different organelles from which delay signaling is activated, including mitochondria, lysosomes, the endoplasmic reticulum, the nucleus, the cell membrane and cytoskeleton, and can also be found in the cytosol. This article critically summarizes the available information in order to establish the connection among its known subcellular effects in a hierarchical and integrative framework. Cisplatin causes different types of cell death in a concentration-dependent manner. Knowledge of the events and signaling leading to the different phenotypes is also intertwined within the model, within the scope of the potential utility of this information in the improvement of the pharmacotoxicological profile of this drug. Perspectives for the key aspects that need to be addressed by future investigation are also outlined. © 2012 Elsevier Inc.

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