Co-occurrence of colistin-resistance genes mcr-1 and mcr-3 among multidrug-resistant Escherichia coli isolated from cattle, Spain, September 2015

Los genes de resistencia a colistina mcr-3 y mcr-1 se detectaron en un aislado de Escherichia coli de heces de ganado en un matadero español en 2015. Las secuencias de ambos genes se hibridaron a la misma banda de plásmidos de aproximadamente 250 kb, aunque la resistencia a la colistina no fue movilizable . El aislado producía betalactamasas de espectro extendido y pertenecía al serotipo O9: H10 y al tipo de secuencia ST533. Aquí informamos un gen mcr-3 detectado en Europa después de informes anteriores de Asia y los Estados Unidos.Colistin resistance genes mcr-3 and mcr-1 have been detected in an Escherichia coli isolate from cattle faeces in a Spanish slaughterhouse in 2015. The sequences of both genes hybridised to same plasmid band of ca 250 kb, although colistin resistance was non-mobilisable. The isolate was producing extended-spectrum beta-lactamases and belonged to serotype O9:H10 and sequence type ST533. Here we report an mcr-3 gene detected in Europe following earlier reports from Asia and the United States.• Ministerio de Economía, Industria y Competitividad. Proyecto AGL2016- 74882-C3 • Ministerio de Agricultura y Pesca (España) y Comunidad Autónoma de Comunidad Autónoma de Madrid. Ayuda S2013 / ABI-2747 • Junta de Extremadura y Fondo Europeo de Desarrollo Regional. Ayuda GR15075 e IB16073 • Fundación para la Ciencia y la Tecnología (Portugal). Ayudas UID / MAR / 04292/2013 • Fundación Tatiana de Guzmán El Bueno (España). Beca doctoral para María del Rocío Iglesias Parro • Instituto Nacional de Agricultura y Alimentación. Investigación y Tecnología (INIA). Beca doctoral para María del Rocío Iglesias Parro • Ministerio de Economía, Industria y Competitividad. Beca FPI2014-020, para Narciso Martín QuijadapeerReviewe

Dissecting the Shared Genetic Architecture of Suicide Attempt, Psychiatric Disorders, and Known Risk Factors

Background Suicide is a leading cause of death worldwide, and nonfatal suicide attempts, which occur far more frequently, are a major source of disability and social and economic burden. Both have substantial genetic etiology, which is partially shared and partially distinct from that of related psychiatric disorders. Methods We conducted a genome-wide association study (GWAS) of 29,782 suicide attempt (SA) cases and 519,961 controls in the International Suicide Genetics Consortium (ISGC). The GWAS of SA was conditioned on psychiatric disorders using GWAS summary statistics via multitrait-based conditional and joint analysis, to remove genetic effects on SA mediated by psychiatric disorders. We investigated the shared and divergent genetic architectures of SA, psychiatric disorders, and other known risk factors. Results Two loci reached genome-wide significance for SA: the major histocompatibility complex and an intergenic locus on chromosome 7, the latter of which remained associated with SA after conditioning on psychiatric disorders and replicated in an independent cohort from the Million Veteran Program. This locus has been implicated in risk-taking behavior, smoking, and insomnia. SA showed strong genetic correlation with psychiatric disorders, particularly major depression, and also with smoking, pain, risk-taking behavior, sleep disturbances, lower educational attainment, reproductive traits, lower socioeconomic status, and poorer general health. After conditioning on psychiatric disorders, the genetic correlations between SA and psychiatric disorders decreased, whereas those with nonpsychiatric traits remained largely unchanged. Conclusions Our results identify a risk locus that contributes more strongly to SA than other phenotypes and suggest a shared underlying biology between SA and known risk factors that is not mediated by psychiatric disorders.Peer reviewe

Geoeconomic variations in epidemiology, ventilation management, and outcomes in invasively ventilated intensive care unit patients without acute respiratory distress syndrome: a pooled analysis of four observational studies

Background: Geoeconomic variations in epidemiology, the practice of ventilation, and outcome in invasively ventilated intensive care unit (ICU) patients without acute respiratory distress syndrome (ARDS) remain unexplored. In this analysis we aim to address these gaps using individual patient data of four large observational studies. Methods: In this pooled analysis we harmonised individual patient data from the ERICC, LUNG SAFE, PRoVENT, and PRoVENT-iMiC prospective observational studies, which were conducted from June, 2011, to December, 2018, in 534 ICUs in 54 countries. We used the 2016 World Bank classification to define two geoeconomic regions: middle-income countries (MICs) and high-income countries (HICs). ARDS was defined according to the Berlin criteria. Descriptive statistics were used to compare patients in MICs versus HICs. The primary outcome was the use of low tidal volume ventilation (LTVV) for the first 3 days of mechanical ventilation. Secondary outcomes were key ventilation parameters (tidal volume size, positive end-expiratory pressure, fraction of inspired oxygen, peak pressure, plateau pressure, driving pressure, and respiratory rate), patient characteristics, the risk for and actual development of acute respiratory distress syndrome after the first day of ventilation, duration of ventilation, ICU length of stay, and ICU mortality. Findings: Of the 7608 patients included in the original studies, this analysis included 3852 patients without ARDS, of whom 2345 were from MICs and 1507 were from HICs. Patients in MICs were younger, shorter and with a slightly lower body-mass index, more often had diabetes and active cancer, but less often chronic obstructive pulmonary disease and heart failure than patients from HICs. Sequential organ failure assessment scores were similar in MICs and HICs. Use of LTVV in MICs and HICs was comparable (42\ub74% vs 44\ub72%; absolute difference \u20131\ub769 [\u20139\ub758 to 6\ub711] p=0\ub767; data available in 3174 [82%] of 3852 patients). The median applied positive end expiratory pressure was lower in MICs than in HICs (5 [IQR 5\u20138] vs 6 [5\u20138] cm H2O; p=0\ub70011). ICU mortality was higher in MICs than in HICs (30\ub75% vs 19\ub79%; p=0\ub70004; adjusted effect 16\ub741% [95% CI 9\ub752\u201323\ub752]; p<0\ub70001) and was inversely associated with gross domestic product (adjusted odds ratio for a US$10 000 increase per capita 0\ub780 [95% CI 0\ub775\u20130\ub786]; p<0\ub70001). Interpretation: Despite similar disease severity and ventilation management, ICU mortality in patients without ARDS is higher in MICs than in HICs, with a strong association with country-level economic status. Funding: No funding

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

Prognostic value of end-of-induction PET response after first-line immunochemotherapy for follicular lymphoma (GALLIUM): secondary analysis of a randomised, phase 3 trial

International audiencePET investigators from the GALLIUM study (2018). Prognostic value of end-of-induction PET response after first-line immunochemotherapy for follicular lymphoma (GALLIUM): secondary analysis of a randomised, phase 3 trial. The Lancet Oncology

Jornadas Nacionales de Robótica y Bioingeniería 2023: Libro de actas

Las Jornadas de Robótica y Bioingeniería de 2023 tienen lugar en la Escuela Técnica Superior de Ingeniería Industrial de la Universidad Politécnica de IVIadrid, entre los días 14 y 16 de junio de 2023. En este evento propiciado por el Comité Español de Automática (CEA) tiene lugar la celebración conjunta de las XII Jornadas Nacionales de Robótica y el XIV Simposio CEA de Bioingeniería. Las Jornadas Nacionales de Robótica es un evento promovido por el Grupo Temático de Robótica (GTRob) de CEA para dar visibilidad y mostrar las actividades desarrolladas en el ámbito de la investigación y transferencia tecnológica en robótica. Asimismo, el propósito de Simposio de Bioingeniería, que cumple ahora su decimocuarta dicción, es el de proporcionar un espacio de encuentro entre investigadores, desabolladores, personal clínico, alumnos, industriales, profesionales en general e incluso usuarios que realicen su actividad en el ámbito de la bioingeniería. Estos eventos se han celebrado de forma conjunta en la anualidad 2023. Esto ha permitido aunar y congregar un elevado número de participantes tanto de la temática robótica como de bioingeniería (investigadores, profesores, desabolladores y profesionales en general), que ha posibilitado establecer puntos de encuentro, sinergias y colaboraciones entre ambos. El programa de las jornadas aúna comunicaciones científicas de los últimos resultados de investigación obtenidos, por los grupos a nivel español más representativos dentro de la temática de robótica y bioingeniería, así como mesas redondas y conferencias en las que se debatirán los temas de mayor interés en la actualidad. En relación con las comunicaciones científicas presentadas al evento, se ha recibido un total de 46 ponencias, lo que sin duda alguna refleja el alto interés de la comunidad científica en las Jornadas de Robótica y Bioingeniería. Estos trabajos serán expuestos y presentados a lo largo de un total de 10 sesiones, distribuidas durante los diferentes días de las Jornadas. Las temáticas de los trabajos cubren los principales retos científicos relacionados con la robótica y la bioingeniería: robótica aérea, submarina, terrestre, percepción del entorno, manipulación, robótica social, robótica médica, teleoperación, procesamiento de señales biológicos, neurorehabilitación etc. Confiamos, y estamos seguros de ello, que el desarrollo de las jornadas sea completamente productivo no solo para los participantes en las Jornadas que podrán establecer nuevos lazos y relaciones fructíferas entre los diferentes grupos, sino también aquellos investigadores que no hayan podido asistir. Este documento que integra y recoge todas las comunicaciones científicas permitirá un análisis más detallado de cada una de las mismas