La pintura de José Cusachs en el Museo Histórico Militar de Valencia a través de su estudio y conservación

[ES] El presente artículo tiene como objeto dar a conocer distintas obras sobre lienzo de uno de los más destacados pintores de la segunda mitad del siglo XIX: José Cusachs y Cusachs (1851-1908), dos de gran formato, Muerte del teniente Rochera en Vic, de 1897 y La toma del fuerte del Collado de Alpuente firmada y fechada en 1900, y dos retratos de dos Capitanes de artillería, Don Juan Resino y Represa y Don Eduardo Temprado y Pérez, datados ambos en 1898. Esta compilación de obras estará expuesta en una sala dedicada a José Cusachs en el Museo Histórico Militar, sede del Acuartelamiento San Juan de Ribera desde 1898, situado en Valencia. Las obras de gran formato representan dos escenas militares y de batalla con un detallado programa iconográfico: La muerte del teniente Rochera en Vic, documenta el fallecimiento del teniente en la tercera guerra carlista. En La toma del fuerte del Collado de Alpuente se recrea la batalla de la conquista del castillo del Poyo. Las obras presentaban diferentes estados de conservación, apreciándose básicamente suciedad superficial, amarilleamiento de barniz y descohesiones puntuales alrededor de zonas con pérdidas ya tratadas en intervenciones anteriores. Gotor Frías, G.; León Zafra, V.; Robles De La Cruz, C.; Alfonso Buigues, M. (2023). La pintura de José Cusachs en el Museo Histórico Militar de Valencia a través de su estudio y conservación. Editorial Universitat Politècnica de València. 337-344. https://doi.org/10.4995/Icomos2022.2022.1540133734

Implementation tells us more beyond pooled estimates: Secondary analysis of a multicountry mhealth trial to reduce blood pressure

Background: The uptake of an intervention aimed at improving health-related lifestyles may be influenced by the participant’s stage of readiness to change behaviors. Objective: We conducted secondary analysis of the Grupo de Investigación en Salud Móvil en América Latina (GISMAL) trial according to levels of uptake of intervention (dose-response) to explore outcomes by country, in order to verify the consistency of the trial’s pooled results, and by each participant’s stage of readiness to change a given lifestyle at baseline. The rationale for this secondary analysis is motivated by the original design of the GISMAL study that was independently powered for the primary outcome—blood pressure—for each country. Methods: We conducted a secondary analysis of a mobile health (mHealth) multicountry trial conducted in Argentina, Guatemala, and Peru. The intervention consisted of monthly motivational phone calls by a trained nutritionist and weekly tailored text messages (short message service), over a 12-month period, aimed to enact change on 4 health-related behaviors: salt added to foods when cooking, consumption of high-fat and high-sugar foods, consumption of fruits or vegetables, and practice of physical activity. Results were stratified by country and by participants’ stage of readiness to change (precontemplation or contemplation; preparation or action; or maintenance) at baseline. Exposure (intervention uptake) was the level of intervention (<50%, 50%-74%, and ≥75%) received by the participant in terms of phone calls. Linear regressions were performed to model the outcomes of interest, presented as standardized mean values of the following: blood pressure, body weight, body mass index, waist circumference, physical activity, and the 4 health-related behaviors. Results: For each outcome of interest, considering the intervention uptake, the magnitude and direction of the intervention effect differed by country and by participants’ stage of readiness to change at baseline. Among those in the high intervention uptake category, reductions in systolic blood pressure were only achieved in Peru, whereas fruit and vegetable consumption also showed reductions among those who were at the maintenance stage at baseline in Argentina and Guatemala. Conclusions: Designing interventions oriented toward improving health-related lifestyle behaviors may benefit from recognizing baseline readiness to change and issues in implementation uptake.Fil: Carrillo-Larco, Rodrigo M.. Universidad Peruana Cayetano Heredia; Perú. Imperial College London; Reino UnidoFil: Jiwani, Safia S.. Universidad Peruana Cayetano Heredia; PerúFil: Diez Canseco, Francisco. Universidad Peruana Cayetano Heredia; PerúFil: Kanter, Rebecca. Institute of Nutrition of Central America and Panama; Guatemala. Universidad de Chile; ChileFil: Beratarrechea, Andrea Gabriela. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Institute for Clinical Effectiveness and Health Policy; ArgentinaFil: Irazola, Vilma. Institute for Clinical Effectiveness and Health Policy; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Ramirez Zea, Manuel. Institute of Nutrition of Central America and Panama; GuatemalaFil: Rubinstein, Adolfo Luis. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Centro de Investigaciones en Epidemiología y Salud Pública. Instituto de Efectividad Clínica y Sanitaria. Centro de Investigaciones en Epidemiología y Salud Pública; ArgentinaFil: Martinez, Homero. Nutrition International; Canadá. Hospital Infantil de Mexico Federico Gomez; MéxicoFil: Miranda, J. Jaime. Cronicas Centro de Excelencia En Enfermedades Crónicas; Perú. Universidad Peruana Cayetano Heredia; PerúFil: Alasino, Adrían. Funprecal; ArgentinaFil: Budiel Moscoso, Berneth Nuris. Universidad Peruana Cayetano Heredia; PerúFil: Carrara, Carolina. Instituto Universitario del Hospital Italiano de Buenos Aires; ArgentinaFil: Espinoza Surichaqui, Jackelyn. Universidad Peruana Cayetano Heredia; PerúFil: Giardini, Gimena. Instituto Universitario del Hospital Italiano de Buenos Aires; ArgentinaFil: Guevara, Jesica. Institute of Nutrition of Central America And Panama Guatemala; GuatemalaFil: Morales Juárez, Analí. Institute of Nutrition of Central America And Panama Guatemala; GuatemalaFil: Lázaro Cuesta, Lorena. Funprecal; ArgentinaFil: Lewitan, Dalia. Institute For Clinical Effectiveness And Health Policy; ArgentinaFil: Palomares Estrada, Lita. Universidad Peruana Cayetano Heredia; PerúFil: Martínez Ramírez, Carla. Universidad Peruana Cayetano Heredia; PerúFil: de la Cruz, Gloria Robles. Universidad Peruana Cayetano Heredia; PerúFil: Salguero, Julissa. Institute Of Nutrition Of Central America And Panama Guatemala; GuatemalaFil: Saravia Drago, Juan Carlos. Universidad Peruana Cayetano Heredia; PerúFil: Urtasún, María. Institute For Clinical Effectiveness And Health Policy; ArgentinaFil: Zavala Loayza, José Alfredo. Universidad Peruana Cayetano Heredia; Per

Clonal chromosomal mosaicism and loss of chromosome Y in elderly men increase vulnerability for SARS-CoV-2

The pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2, COVID-19) had an estimated overall case fatality ratio of 1.38% (pre-vaccination), being 53% higher in males and increasing exponentially with age. Among 9578 individuals diagnosed with COVID-19 in the SCOURGE study, we found 133 cases (1.42%) with detectable clonal mosaicism for chromosome alterations (mCA) and 226 males (5.08%) with acquired loss of chromosome Y (LOY). Individuals with clonal mosaic events (mCA and/or LOY) showed a 54% increase in the risk of COVID-19 lethality. LOY is associated with transcriptomic biomarkers of immune dysfunction, pro-coagulation activity and cardiovascular risk. Interferon-induced genes involved in the initial immune response to SARS-CoV-2 are also down-regulated in LOY. Thus, mCA and LOY underlie at least part of the sex-biased severity and mortality of COVID-19 in aging patients. Given its potential therapeutic and prognostic relevance, evaluation of clonal mosaicism should be implemented as biomarker of COVID-19 severity in elderly people. Among 9578 individuals diagnosed with COVID-19 in the SCOURGE study, individuals with clonal mosaic events (clonal mosaicism for chromosome alterations and/or loss of chromosome Y) showed an increased risk of COVID-19 lethality

Gestión del conocimiento: perspectiva multidisciplinaria. Volumen 13

El libro “Gestión del Conocimiento. Perspectiva Multidisciplinaria”, Volumen 13 de la Colección Unión Global, es resultado de investigaciones. Los capítulos del libro, son resultados de investigaciones desarrolladas por sus autores. El libro es una publicación internacional, seriada, continua, arbitrada, de acceso abierto a todas las áreas del conocimiento, orientada a contribuir con procesos de gestión del conocimiento científico, tecnológico y humanístico. Con esta colección, se aspira contribuir con el cultivo, la comprensión, la recopilación y la apropiación social del conocimiento en cuanto a patrimonio intangible de la humanidad, con el propósito de hacer aportes con la transformación de las relaciones socioculturales que sustentan la construcción social de los saberes y su reconocimiento como bien público. El libro “Gestión del Conocimiento. Perspectiva Multidisciplinaria”, Volumen 13, de la Colección Unión Global, es resultado de investigaciones. Los capítulos del libro, son resultados de investigaciones desarrolladas por sus autores. El libro cuenta con el apoyo de los grupos de investigación: Universidad Sur del Lago “Jesús María Semprúm” (UNESUR) - Zulia – Venezuela; Universidad Politécnica Territorial de Falcón Alonso Gamero (UPTFAG) - Falcón – Venezuela; Universidad Politécnica Territorial de Mérida Kléber Ramírez (UPTM) - Mérida - Venezuela; Universidad Guanajuato (UG) - Campus Celaya - Salvatierra - Cuerpo Académico de Biodesarrollo y Bioeconomía en las Organizaciones y Políticas Públicas (CABBOPP) - Guanajuato – México; Centro de Altos Estudios de Venezuela (CEALEVE) - Zulia – Venezuela, Centro Integral de Formación Educativa Especializada del Sur (CIFE - SUR) - Zulia – Venezuela; Centro de Investigaciones Internacionales SAS (CEDINTER) - Antioquia – Colombia y diferentes grupos de investigación del ámbito nacional e internacional que hoy se unen para estrechar vínculos investigativos, para que sus aportes científicos formen parte de los libros que se publiquen en formatos digital e impreso

Robust estimation of bacterial cell count from optical density

Optical density (OD) is widely used to estimate the density of cells in liquid culture, but cannot be compared between instruments without a standardized calibration protocol and is challenging to relate to actual cell count. We address this with an interlaboratory study comparing three simple, low-cost, and highly accessible OD calibration protocols across 244 laboratories, applied to eight strains of constitutive GFP-expressing E. coli. Based on our results, we recommend calibrating OD to estimated cell count using serial dilution of silica microspheres, which produces highly precise calibration (95.5% of residuals &lt;1.2-fold), is easily assessed for quality control, also assesses instrument effective linear range, and can be combined with fluorescence calibration to obtain units of Molecules of Equivalent Fluorescein (MEFL) per cell, allowing direct comparison and data fusion with flow cytometry measurements: in our study, fluorescence per cell measurements showed only a 1.07-fold mean difference between plate reader and flow cytometry data

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease