2 research outputs found
Multidimensional scale for affective disorders-MSAD: psychometric indicators generation and regulations scale clinical use
En este trabajo se desarrolló un estudio instrumental correspondiente a la tercera fase del proceso de estandarización de la Escala Multidimensional de Trastornos Afectivos-EMTA. Su propósito fue la generación de indicadores psicométricos y escalas normativas de uso clínico a partir de una muestra de 60 sujetos con diagnóstico de trastornos del estado de ánimo, elegidos por un muestreo no probabilístico, por criterio de expertos. Se administraron tres instrumentos psicométricos: EMTA (Subescala de manía α=.87 - Subescala de Depresión α=.958), el Inventario de Depresión de Beck - II (α=.901) y el Inventario Chino de Polaridad (α=.901 y α=.826). Los resultados indicaron que los ítems se ajustan satisfactoriamente a los parámetros de los Modelo Lineal (TCT) y el modelo de crédito parcial de Rasch, evidenciando un ajuste monotónico creciente de los reactivos, con lo cual se corrobora el cumplimiento del principio de la invarianza en la medición del rasgo latenteIn this assignment it development an instrumental study corresponding to the third phase of EMTA standardization. The main was to generate psychometric indicators and regulations scales of clinic use from a 60 subject sample with mood disorder diagnostic selected by a non- probability sampling per expert judges. Three psychometric instruments was administer: EMTA (Mania Subscale α=.87 - Depression Subscale α=.958), Beck Depression Inventory - II (α=.901) and Chinese Polarity Inventory (α=.901 y α=.826). The results indicated items adjust succesfully to Lineal Models parameters and Rasch partial credit model, showing an increasing monotonic adjustment of reagents which bear out fulfillment the principle of invariance in the latent trait measurin
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Single-cell multi-omics analysis of the immune response in COVID-19
Funder: Lister Institute of Preventive Medicine; doi: https://doi.org/10.13039/501100001255Funder: University College London, Birkbeck MRC Doctoral Training ProgrammeFunder: The Jikei University School of MedicineFunder: Action Medical Research (GN2779)Funder: NIHR Clinical Lectureship (CL-2017-01-004)Funder: NIHR (ACF-2018-01-004) and the BMA FoundationFunder: Chan Zuckerberg Initiative (grant 2017-174169) and from Wellcome (WT211276/Z/18/Z and Sanger core grant WT206194)Funder: UKRI Innovation/Rutherford Fund Fellowship allocated by the MRC and the UK Regenerative Medicine Platform (MR/5005579/1 to M.Z.N.). M.Z.N. and K.B.M. have been funded by the Rosetrees Trust (M944)Funder: Barbour FoundationFunder: ERC Consolidator and EU MRG-Grammar awardsFunder: Versus Arthritis Cure Challenge Research Grant (21777), and an NIHR Research Professorship (RP-2017-08-ST2-002)Funder: European Molecular Biology Laboratory (EMBL)Abstract: Analysis of human blood immune cells provides insights into the coordinated response to viral infections such as severe acute respiratory syndrome coronavirus 2, which causes coronavirus disease 2019 (COVID-19). We performed single-cell transcriptome, surface proteome and T and B lymphocyte antigen receptor analyses of over 780,000 peripheral blood mononuclear cells from a cross-sectional cohort of 130 patients with varying severities of COVID-19. We identified expansion of nonclassical monocytes expressing complement transcripts (CD16+C1QA/B/C+) that sequester platelets and were predicted to replenish the alveolar macrophage pool in COVID-19. Early, uncommitted CD34+ hematopoietic stem/progenitor cells were primed toward megakaryopoiesis, accompanied by expanded megakaryocyte-committed progenitors and increased platelet activation. Clonally expanded CD8+ T cells and an increased ratio of CD8+ effector T cells to effector memory T cells characterized severe disease, while circulating follicular helper T cells accompanied mild disease. We observed a relative loss of IgA2 in symptomatic disease despite an overall expansion of plasmablasts and plasma cells. Our study highlights the coordinated immune response that contributes to COVID-19 pathogenesis and reveals discrete cellular components that can be targeted for therapy