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During most of 2020, the COVID-19 pandemic gave rise to considerable and growing numbers of hospitalizations across most of the U.S. Typical COVID-19 hospitalization data, including length of stay, intensive care unit (ICU) use, mechanical ventilation (Vent), and in-hospital mortality provide clearly interpretable health care endpoints that can be compared across population strata. They capture the resources consumed for the care of COVID-19 patients, and analysis of these endpoints can be used for resource planning at the local level. Yet, hospitalization data embody novel features that require careful statistical treatment to be useful in this context. Specifically, statistical models must meet three goals: (i) They should mesh with and inform mathematical epidemiologic or agent-based models of the COVID-19 experience in the population. (ii) They need to handle administrative censoring of hospitalization experience when data are extracted and downloaded for a given patient before that patients hospitalization experience has terminated. And, (iii) models need to handle risks for competing events, the occurrence of one blocking the possibility of the other(s). For example, live discharge from the hospital "competes with" (i.e., blocks) in-hospital mortality. We have adapted approaches from the survival analysis literature to address these challenges in order to better understand and quantify the population experience in hospital with respect to length of stay, ICU, Vent use and so on. Using hospitalization data from a large U.S. metropolitan region, in this report, we show how standard techniques from survival analysis can be brought to bear to address these challenges and yield interpretable results. In the breakout/discussion, we will discuss formulation, estimation and inference, and interpretation of competing risks models.
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Introducción: El gen NOS1AP codifica para la proteína adaptadora de óxido nítrico sintasa neuronal 1, que posiblemente está implicada en la etiopatogénesis de la esquizofrenia. Objetivos: Determinar si existe asociación de variantes en el gen NOS1AP con esquizofrenia y si estas variantes tienen relación con las dimensiones clínicas del trastorno en población colombiana. Metodología: Es un estudio de casos y controles, con 255 sujetos por grupo. Se tipificaron marcadores dentro del gen NOS1AP y otros informativos de origen genético, con el fin de ajustar por estratificación de la población. Se hizo un análisis factorial de componentes principales de cada uno de los ítems de las escalas de evaluación de síntomas negativos (SANS) y de síntomas positivos (SAPS) para determinar las dimensiones clínicas. Posteriormente, se evaluó la asociación de las variantes genéticas con la esquizofrenia y con cada una de las dimensiones. Resultados: Se encontró asociación entre el genotipo C/C del marcador rs945713 con esquizofrenia (OR = 1,79, IC95%: 1,13-2,84). El genotipo C/C de rs945713 se asoció con puntuaciones más altas en la dimensión aplanamiento afectivo y alogia y el genotipo A/A del marcador rs4657181 se relacionó con puntuaciones más bajas en esa misma dimensión. Conclusiones: Se encontró asociación significativa de marcadores dentro de NOS1AP con esquizofrenia y la dimensión clínica aplanamiento afectivo y alogia. Estos resultados son consistentes con estudios previos y apoyan la posibilidad de que NOS1AP influya en la susceptibilidad a esquizofrenia y que sea un modificador de sus características clínicas
Introduction: The nitric oxide synthase 1 adaptor protein (NOS1AP) gene is possibly implicated in schizophrenia etiopathogenesis. Objective: To determine the association of NOS1AP gene variants with schizophrenia and the relationship of variants with the clinical dimensions of the disorder in the Colombian population. Methodology: It is a case-control study with 255 subjects per group. Markers within the NOS1AP gene were typified as well as other informative material of genetic origin so as to adjust by population stratification. A factorial analysis of the main components for each item in the Scales for Evaluating Negative Symptoms (SENS) together with the Scales for Evaluating Positive Symptoms (SEPS) to determine clinical dimensions. Results: Association between the C/C genotype of the rs945713 marker with schizophrenia (OR = 1.79, 95% CI: 1.13 2.84) was found. The C/C genotype of the rs945713 was related to higher scores in the affective flattening and alogia dimension; and the A/A genotype of the rs4657181 marker was associated to lower scores in the same dimension. Conclusions: Significant associations of markers inside the NOS1AP gene with schizophrenia and the affective flattening and alogia clinical dimension were found. These results are consistent with previous studies and support the possibility that NOS1AP influences schizophrenia susceptibility. Furthermore, NOS1AP might be a modifier of schizophrenia clinical characteristics
Asunto(s)
Genes , Genes/genética , EsquizofreniaRESUMEN
INTRODUCTION: The nitric oxide synthase 1 adaptor protein (NOS1AP) gene is possibly implicated in schizophrenia etiopathogenesis. OBJECTIVE: To determine the association of NOS1AP gene variants with schizophrenia and the relationship of variants with the clinical dimensions of the disorder in the Colombian population. METHODOLOGY: It is a case-control study with 255 subjects per group. Markers within the NOS1AP gene were typified as well as other informative material of genetic origin so as to adjust by population stratification. A factorial analysis of the main components for each item in the Scales for Evaluating Negative Symptoms (SENS) together with the Scales for Evaluating Positive Symptoms (SEPS) to determine clinical dimensions. RESULTS: Association between the C/C genotype of the rs945713 marker with schizophrenia (OR = 1.79, 95% CI: 1.13 - 2.84) was found. The C/C genotype of the rs945713 was related to higher scores in the "affective flattening and alogia" dimension; and the A/A genotype of the rs4657181 marker was associated to lower scores in the same dimension. CONCLUSIONS: Significant associations of markers inside the NOS1AP gene with schizophrenia and the "affective flattening and alogia" clinical dimension were found. These results are consistent with previous studies and support the possibility that NOS1AP influences schizophrenia susceptibility. Furthermore, NOS1AP might be a modifier of schizophrenia clinical characteristics.
