16 research outputs found

    Evaluation of the chemical and physical changes induced by KrF laser irradiation of tempera paints

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    A systematic study of the chemical and physical changes induced by exposure to UV (248 nm) excimer laser light of unvarnished tempera paint samples has been undertaken as a part of the research activities included in the European project "Advanced workstation for controlled laser cleaning of artworks". The direct exposure of the paint to the UV laser configures the worst case scenario of laser cleaning, as a thin protective layer of varnish is normally left to minimize the dose of UV radiation that reaches the paint surface. However, in the practice of laser cleaning, there is a need to characterize and quantify the possible effects of direct UV laser irradiation of unvarnished paints. To this purpose, a broad range of techniques have been used including profilometry, colorimetry, optical and vibrational spectroscopic techniques, such as laser-induced fluorescence (LIF), laser-induced breakdown spectroscopy (LIBS), Fourier transform Raman (FTR) and infrared (FTIR), and analytical mass spectrometric techniques, like direct-temperature-resolved mass spectrometry (DTMS) and laser desorption and ionization time of flight mass spectrometry (LDI-TOF). Integration of the results obtained by these techniques allowed the investigation of the nature and degree of change of the irradiated paint systems. These were observed to strongly depend on the type of paint system. © 2003 Éditions scientifiques et médicales Elsevier SAS. All rights reserved

    Water intake, hydration status and 2-year changes in cognitive performance: a prospective cohort study

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    BackgroundWater intake and hydration status have been suggested to impact cognition; however, longitudinal evidence is limited and often inconsistent. This study aimed to longitudinally assess the association between hydration status and water intake based on current recommendations, with changes in cognition in an older Spanish population at high cardiovascular disease risk.MethodsA prospective analysis was conducted of a cohort of 1957 adults (aged 55-75) with overweight/obesity (BMI between >= 27 and = 300 mmol/L (dehydrated). Water intake was assessed as total drinking water intake and total water intake from food and beverages and according to EFSA recommendations. Global cognitive function was determined as a composite z-score summarizing individual participant results from all neuropsychological tests. Multivariable linear regression models were fitted to assess the associations between baseline hydration status and fluid intake, continuously and categorically, with 2-year changes in cognitive performance.ResultsThe mean baseline daily total water intake was 2871 +/- 676 mL/day (2889 +/- 677 mL/day in men; 2854 +/- 674 mL/day in women), and 80.2% of participants met the ESFA reference values for an adequate intake. Serum osmolarity (mean 298 +/- 24 mmol/L, range 263 to 347 mmol/L) indicated that 56% of participants were physiologically dehydrated. Lower physiological hydration status (i.e., greater serum osmolarity) was associated with a greater decline in global cognitive function z-score over a 2-year period (beta: - 0.010; 95% CI - 0.017 to - 0.004, p-value = 0.002). No significant associations were observed between water intake from beverages and/or foods with 2-year changes in global cognitive function.ConclusionsReduced physiological hydration status was associated with greater reductions in global cognitive function over a 2-year period in older adults with metabolic syndrome and overweight or obesity. Future research assessing the impact of hydration on cognitive performance over a longer duration is needed

    A Novel Circulating MicroRNA for the Detection of Acute Myocarditis.

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    The diagnosis of acute myocarditis typically requires either endomyocardial biopsy (which is invasive) or cardiovascular magnetic resonance imaging (which is not universally available). Additional approaches to diagnosis are desirable. We sought to identify a novel microRNA for the diagnosis of acute myocarditis. To identify a microRNA specific for myocarditis, we performed microRNA microarray analyses and quantitative polymerase-chain-reaction (qPCR) assays in sorted CD4+ T cells and type 17 helper T (Th17) cells after inducing experimental autoimmune myocarditis or myocardial infarction in mice. We also performed qPCR in samples from coxsackievirus-induced myocarditis in mice. We then identified the human homologue for this microRNA and compared its expression in plasma obtained from patients with acute myocarditis with the expression in various controls. We confirmed that Th17 cells, which are characterized by the production of interleukin-17, are a characteristic feature of myocardial injury in the acute phase of myocarditis. The microRNA mmu-miR-721 was synthesized by Th17 cells and was present in the plasma of mice with acute autoimmune or viral myocarditis but not in those with acute myocardial infarction. The human homologue, designated hsa-miR-Chr8:96, was identified in four independent cohorts of patients with myocarditis. The area under the receiver-operating-characteristic curve for this novel microRNA for distinguishing patients with acute myocarditis from those with myocardial infarction was 0.927 (95% confidence interval, 0.879 to 0.975). The microRNA retained its diagnostic value in models after adjustment for age, sex, ejection fraction, and serum troponin level. After identifying a novel microRNA in mice and humans with myocarditis, we found that the human homologue (hsa-miR-Chr8:96) could be used to distinguish patients with myocarditis from those with myocardial infarction. (Funded by the Spanish Ministry of Science and Innovation and others.).Supported by a grant (PI19/00545, to Dr. Martín) from the Ministry of Science and Innovation through the Carlos III Institute of Health–Fondo de Investigación Sanitaria; by a grant from the Biomedical Research Networking Center on Cardiovascular Diseases (to Drs. Martín, Sánchez-Madrid, and Ibáñez); by grants (S2017/BMD-3671-INFLAMUNE-CM, to Drs. Martín and Sánchez-Madrid; and S2017/BMD-3867-RENIM-CM, to Dr. Ibáñez) from Comunidad de Madrid; by a grant (20152330 31, to Drs. Martín, Sánchez-Madrid, and Alfonso) from Fundació La Marató de TV3; by grants (ERC-2011-AdG 294340-GENTRIS, to Dr. Sánchez-Madrid; and ERC-2018-CoG 819775-MATRIX, to Dr. Ibáñez) from the European Research Council; by grants (SAF2017-82886R, to Dr. Sánchez-Madrid; RETOS2019-107332RB-I00, to Dr. Ibáñez; and SAF2017-90604-REDT-NurCaMeIn and RTI2018-095928-BI00, to Dr. Ricote) from the Ministry of Science and Innovation; by Fondo Europeo de Desarrollo Regional (FEDER); and by a 2016 Leonardo Grant for Researchers and Cultural Creators from the BBVA Foundation to Dr. Martín. The National Center for Cardiovascular Research (CNIC) is supported by the Carlos III Institute of Health, the Ministry of Science and Innovation, the Pro CNIC Foundation, and by a Severo Ochoa Center of Excellence grant (SEV-2015-0505). Mr. Blanco-Domínguez is supported by a grant (FPU16/02780) from the Formación de Profesorado Universitario program of the Spanish Ministry of Education, Culture, and Sports. Ms. Linillos-Pradillo is supported by a fellowship (PEJD-2016/BMD-2789) from Fondo de Garantía de Empleo Juvenil de Comunidad de Madrid. Dr. Relaño is supported by a grant (BES-2015-072625) from Contratos Predoctorales Severo Ochoa para la Formación de Doctores of the Ministry of Economy and Competitiveness. Dr. Alonso-Herranz is supported by a fellowship from La Caixa–CNIC. Dr. Caforio is supported by Budget Integrato per la Ricerca dei Dipartimenti BIRD-2019 from Università di Padova. Dr. Das is supported by grants (UG3 TR002878 and R35 HL150807) from the National Institutes of Health and the American Heart Association through its Strategically Focused Research Networks.S

    Retinoid X receptors in macrophage biology

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    Retinoid X receptors (RXRs) form a distinct and unique subclass within the nuclear receptor (NR) superfamily of ligand-dependent transcription factors. RXRs regulate a plethora of genetic programs, including cell differentiation, the immune response, and lipid and glucose metabolism. Recent advances reveal that RXRs are important regulators of macrophages, key players in inflammatory and metabolic disorders. This review outlines the versatility of RXR action in the control of macrophage gene transcription through its heterodimerization with other NRs or through RXR homodimerization. We also highlight the potential of RXR-controlled transcriptional programs as targets for the treatment of pathologies associated with altered macrophage function, such as atherosclerosis, insulin resistance, autoimmunity, and neurodegeneration.Work performed in the laboratory of the authors was funded by awards from the Spanish Ministry of Economy and Competitiveness (SAF201231483) to M.R., a European Foundation for the Study of Diabetes–Lilly Fellowship Program to T.R., and a Spanish Ministry of Science, and Innovation (FPU, AP2008-00508) grant to M.C. The CNIC is supported by the Spanish Ministry of Economy and Competitiveness and the Pro-CNIC Foundation.S

    Gas phase detection of chemical warfare agents CWAs with portable Raman

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    The development of SERS substrates for chemical detection of specific analytes requires appropriate selection of plasmonic metal and the surface where it is deposited. Here we deposited Ag nanoplates on three substrates: i) conventional SiO2/Si wafer, ii) stainless steel mesh and iii) graphite foils. The SERS enhancement of the signal was studied for Rhodamine 6 G (R6 G) as common liquid phase probe molecule. We conducted a comprehensive study with λ = 532, 633 and 785 nm on all the substrates. The best substrate was investigated, at the optimum laser 785 nm, for gas phase detection of dimethyl methyl phosphonate (DMMP), simulant of the G-series nerve agents, at a concentration of 2.5 ppmV (14 mg/m3). The spectral fingerprint was clearly observed; with variations on the relative intensities of SERS Raman bands compared to bulk DMMP in liquid phase reflects the DMMP-Ag interactions. These interactions were simulated by Density Functional Theory (DFT) calculations and the simulated spectra matched with the experimental one. Finally, we were detected the characteristics DMMP fingerprint with hand-held portable equipment. These results open the way for the application of SERS technique on real scenarios where robust, light-weight, miniaturized and simple to use and cost-effective tools are required by first responders.Authors are grateful for financial support from the European Union’s Horizon 2020 research and innovation programme under the Marie Sklodowska-Curie grant agreement Nr. 823895; MICINN, Spain (CTQ2013-49068-C2-1-R and CTQ2016-79419-R); Gobierno de Aragón (T57-17R p), Feder 2014-2020 “Construyendo Europa desde Aragón”) and CIBER-BBN (initiative funded by the VI National R&D&i Plan 2008–2011, Iniciativa Ingenio 2010, Consolider Program, CIBER Actions and financed by the Instituto de Salud Carlos III with assistance from the European Regional Development Fund), Spain.Peer reviewe

    CORIOAMNIONITIS HISTOLÓGICA Y MORBIMORTALIDAD NEONATAL: APROXIMACIÓN AL SÍNDROME DE RESPUESTA INFLAMATORIA FETAL

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    Antecedentes: El síndrome de respuesta inflamatoria fetal (SRIF) es una entidad relacionada con la presencia de inflamación intrauterina y suele asociarse a infección intraamniótica. Su consecuencia más grave es la lesión cerebral y posterior desarrollo de parálisis cerebral. Objetivo: Evaluar la relación entre el síndrome de respuesta inflamatoria fetal y el desarrollo de complicaciones neonatales. Método: Estudio descriptivo y retrospectivo, realizado en el Hospital Universitario La Paz de Madrid, buscando una aproximación al SRIF desde la corioamnionitis histológica/funiculitis. El grupo de estudio constituido por 35 gestaciones simples pretérmino recogidas durante el primer semestre de 2008 y en las que la anatomía patológica de la placenta y anexos ovulares demostró la presencia de una corioamnionitis histológica y/o funiculitis. Resultados: Siete casos (20%) presentaban clínica sospechosa de infección intraamniótica, si bien en 28 gestantes (80%) existían factores de riesgo asociados al síndrome de respuesta inflamatoria fetal. Mortalidad perinatal en el grupo estudiado fue de 11,4% (4 casos). Sólo en 2 pacientes (5,7%) se pudo relacionar la muerte con el SRIF. En 28 recién nacidos (80%) se encontró algún tipo de patología, siendo la misma inherente a dicho síndrome en 17 casos (48,6%), destacando sepsis neonatal (40%), leucomalacia periventricular (14,3%) y displasia broncopulmonar (5,7%). Conclusión: Se comprueba el alto riesgo neonatal del SRIF. El conocimiento de esta condición, abre una serie de controversias diagnósticas y terapéuticas que obliga a una reevaluación de los protocolos actuales de manejo de la amenaza de parto pretérmino y la rotura prematura de membranas de pretérmino

    CESÁREA CORPORAL Y MIOMECTOMÍA: INDICACIONES ACTUALES

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    Actualmente, tanto la realización de una cesárea corporal como la práctica de una miomectomía en el transcurso de una cesárea, suponen dos hechos muy infrecuentes. No obstante, en determinados casos, ambos procedimientos pueden ser necesarios. La cesárea corporal es una técnica quirúrgica poco menos que abandonada, si bien aún mantiene algunas indicaciones; y la exéresis de un mioma durante una cesárea está clásicamente contraindicada, salvo en circunstancias muy concretas. Sin embargo, hay que destacar que en los últimos años se está constatando un incremento significativo de ambos procedimientos, siendo las razones muy diversas (aumento de las gestaciones pretérmino que se finalizan por vía abdominal, incremento de la edad materna, mayores tasas de cesáreas, etc.). Se presenta el caso clínico de una gestante con un gran mioma localizado en segmento inferior uterino y en la que fue preciso llevar a cabo una cesárea corporal, seguida de una miomectomía

    Deciphering the Dynamic Transcriptional and Post-transcriptional Networks of Macrophages in the Healthy Heart and after Myocardial Injury

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    Summary: Macrophage plasticity has been studied in vitro, but transcriptional regulation upon injury is poorly understood. We generated a valuable dataset that captures transcriptional changes in the healthy heart and after myocardial injury, revealing a dynamic transcriptional landscape of macrophage activation. Partial deconvolution suggested that post-injury macrophages exhibit overlapping activation of pro-inflammatory and anti-inflammatory programs rather than aligning to canonical M1/M2 programs. Furthermore, simulated dynamics and experimental validation of a regulatory core of the underlying gene-regulatory network revealed a negative-feedback loop that limits initial inflammation via hypoxia-mediated upregulation of Il10. Our results also highlight the prominence of post-transcriptional regulation (miRNAs, mRNA decay, and lincRNAs) in attenuating the myocardial injury-induced inflammatory response. We also identified a cardiac-macrophage-specific gene signature (e.g., Egfr and Lifr) and time-specific markers for macrophage populations (e.g., Lyve1, Cd40, and Mrc1). Altogether, these data provide a core resource for deciphering the transcriptional network in cardiac macrophages in vivo. : Walter et al. generate a whole transcriptome dataset (mRNA, miRNA, and lincRNA) of macrophages in the healthy heart and after myocardial injury. This study reveals that post-injury macrophages simultaneously activate pro- and anti-inflammatory programs. Furthermore, they identified transcriptional and post-transcriptional mechanisms regulating myocardial injury-induced inflammation. Keywords: heart, myocardial injury, IL-10, transcriptome analysis, partial deconvolution, Boolean dynamical model, miRnome, lincRNA

    Macrophages promote endothelial-to-mesenchymal transition via MT1-MMP/ TGFβ1\beta 1 after myocardial infarction

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    Macrophages (M φs\varphi s ) produce factors that participate in cardiac repair and remodeling after myocardial infarction (MI); however, how these factors crosstalk with other cell types mediating repair is not fully understood. Here we demonstrated that cardiac M φ\varphi s increased the expression of Mmp14 (MT1-MMP) 7 days post-MI. We selectively inactivated the Mmp14M m p 14 gene in Mφ\mathrm{M} \varphi s using a genetic strategy (Mmp14ff: Lyz2-Cre). This conditional KO (MAC-Mmp14 KO) resulted in attenuated post-MI cardiac dysfunction, reduced fibrosis, and preserved cardiac capillary network. Mechanistically, we showed that MT1-MMP activates latent TGF β1\beta 1 in M φ\varphi s, leading to paracrine SMAD2-mediated signaling in endothelial cells (ECs) and endothelial-to-mesenchymal transition (EndMT). Post-MI MAC-Mmp14 KO hearts contained fewer cells undergoing EndMT than their wild-type counterparts, and Mmp14-deficient Mφs\mathrm{M} \varphi \mathrm{s} showed a reduced ability to induce EndMT in co-cultures with ECs. Our results indicate the contribution of EndMT to cardiac fibrosis and adverse remodeling post-MI and identify M φ\varphi MT1-MMP as a key regulator of this process

    Running title: Macrophages and post-MI EndMT

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    30 p.-7 fig.-3 tab.-12 fig. supl.Macrophages (Mφs) produce factors that participate in cardiac repair and remodeling after myocardial infarction (MI); however, how these factors crosstalk with other cell types mediating repair is not fully understood. Here, we demonstrated that cardiac Mφs increased expression of Mmp14 (MT1-MMP) 7 days post-MI. We selectively inactivated the Mmp14 gene in Mφs using a genetic strategy (Mmp14f/f:Lyz2-Cre). This conditional KO (MAC-Mmp14 KO) resulted in attenuated post-MI cardiac dysfunction, reduced fibrosis, and preserved cardiac capillary network. Mechanistically, we showed that MT1-MMP activates latent TGFβ1 in Mφs, leading to paracrine SMAD2-mediated signaling in endothelial cells (ECs) and endothelial-to-mesenchymal transition (EndMT). Post-MI MAC-Mmp14 KO hearts contained fewer cells undergoing EndMT than their wild-type counterparts, and Mmp14-deficient Mφs showed a reduced ability to induce EndMT in co-cultures with ECs. Our results indicate the contribution of EndMT to cardiac fibrosis and adverse remodeling post-MI and identify Mφ MT1-MMP as a key regulator of this process.This study was supported by grants from the Spanish Ministry of Science, Innovation and Universities (SAF2017-90604-REDT-NurCaMein, RTI2018-095928-BI00 to M.R.; SAF2017-83229-R to A.G.A.), Comunidad de Madrid (MOIR-B2017/BMD-3684) to M.R, and La Marató de TV3 Foundation to D.G.D, A.G.A., and M.R.Peer reviewe
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