18 research outputs found

    Analysis of additive manufacturing technology applied to valve housings for mobile machinery

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    Treball desenvolupat en el marc del programa "European Project Semester".L’ European Project Semester va començar l’1 de març de 2018, amb una visita a la empresa, per la qual hem estat treballant aquests quatre mesos, els meus tres companys internacionals i jo. L’empresa és anomenada Buchholz Hydraulik i la seva funció és proveir vàlvules de control hidràulic per a sistemes hidràulics. El projecte es basa amb la factibilitat de canviar la producció actual de la empresa, producció basada amb màquines de control numèric, per a una producció additiva. L’empresa ens va donar una sèrie de requeriments, els qual havíem de complir amb aquesta nova tecnologia, les impressores 3D. A partir d’aquests requeriments el projecte recopila una àmplia recerca sobre diferents possibles proveïdors per a la empresa, amb dels quals es va obtenir un únic proveïdor a partir del “Scoring Model”. Un cop ja es va obtenir el proveïdor i per tant, la impressora i els possibles materials, es va passar a contrastar-los suggerint finalment els que millors s’adapten al requeriments. A partir d’aquí, va venir el moment d’adaptar l’actual disseny de la empresa a la producció additiva, amb la qual vam obtenir completa llibertat a la hora de dissenyar. Finalment, un anàlisis dels costos amb aquesta nova producció es presentat al final i una conclusió dels resultats obtinguts.Outgoin

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

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    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

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    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

    Análisis de tecnología de fabricación aditiva aplicada a carcasas de válvulas para maquinaria móvil

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    [ES] Proyecto realizado para la empresa Buchholz Hydraulik GMBH, dentro del European Project Semester en la Facchochschule en Kiel. El proyecto consiste en la investigación y análisis de las diferentes tecnologías de adición de material (tecnologías 3D), para ver la viabilidad a la hora de sustituir el proceso de fabricación actual de los cuerpos de válvulas de control "valve housing" (actualmente la empresa hace uso de maquinas de control numérico). El proyecto consiste en comparar ambas tecnologías tanto en especificaciones mecánicas de los materiales ofrecidos hoy en día en las impresoras 3D, los cuales deben adaptarse a las condiciones de la empresa y los materiales que utilizan actualmente, así como una comparación económica, englobando diferencias en los tiempos de fabricación y costes.Lara Domínguez, A.; Cladera Escalas, A.; Beguin, N.; Yasin, T. (2018). Analysis of additive manufacturing technology applied to valve housings for mobile machinery. Universitat Politècnica de València. http://hdl.handle.net/10251/142731TFG

    Mapping the human genetic architecture of COVID-19

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    The genetic make-up of an individual contributes to the susceptibility and response to viral infection. Although environmental, clinical and social factors have a role in the chance of exposure to SARS-CoV-2 and the severity of COVID-191,2, host genetics may also be important. Identifying host-specific genetic factors may reveal biological mechanisms of therapeutic relevance and clarify causal relationships of modifiable environmental risk factors for SARS-CoV-2 infection and outcomes. We formed a global network of researchers to investigate the role of human genetics in SARS-CoV-2 infection and COVID-19 severity. Here we describe the results of three genome-wide association meta-analyses that consist of up to 49,562 patients with COVID-19 from 46 studies across 19 countries. We report 13 genome-wide significant loci that are associated with SARS-CoV-2 infection or severe manifestations of COVID-19. Several of these loci correspond to previously documented associations to lung or autoimmune and inflammatory diseases3–7. They also represent potentially actionable mechanisms in response to infection. Mendelian randomization analyses support a causal role for smoking and body-mass index for severe COVID-19 although not for type II diabetes. The identification of novel host genetic factors associated with COVID-19 was made possible by the community of human genetics researchers coming together to prioritize the sharing of data, results, resources and analytical frameworks. This working model of international collaboration underscores what is possible for future genetic discoveries in emerging pandemics, or indeed for any complex human disease
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