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1.
Disaster Med Public Health Prep ; 15(5): e33-e42, 2021 10.
Artículo en Inglés | MEDLINE | ID: mdl-32713377

RESUMEN

OBJECTIVES: An unprecedented wave of patients with acute respiratory failure due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) disease 2019 (COVID-19) hit emergency departments (EDs) in Lombardy, starting in the second half of February 2020. This study describes the direct and indirect impacts of the SARS-CoV-2 outbreak on an urban major-hospital ED. METHODS: Data regarding all patients diagnosed with COVID-19 presenting from February 1 to March 31, 2020, were prospectively collected, while data regarding non-COVID patients presenting within the same period in 2019 were retrospectively retrieved. RESULTS: ED attendance dropped by 37% in 2020. Two-thirds of this reduction occurred early after the identification of the first autochthonous COVID-19 case in Lombardy, before lockdown measures were enforced. Hospital admissions of non-COVID patients fell by 26%. During the peak of COVID-19 attendance, the ED faced an extraordinary increase in: patients needing oxygen (+239%) or noninvasive ventilation (+725%), transfers to the intensive care unit (+57%), and in-hospital mortality (+309%), compared with the same period in 2019. CONCLUSIONS: The COVID-19 outbreak determined an unprecedented upsurge in respiratory failure cases and mortality. Fear of contagion triggered a spontaneous, marked reduction of ED attendance, and, presumably, some as yet unknown quantity of missed or delayed diagnoses for conditions other than COVID-19.


Asunto(s)
COVID-19 , SARS-CoV-2 , Control de Enfermedades Transmisibles , Servicio de Urgencia en Hospital , Miedo , Humanos , Estudios Retrospectivos
2.
J Nephrol ; 16(4): 609-15, 2003.
Artículo en Inglés | MEDLINE | ID: mdl-14696769

RESUMEN

Although everybody agrees that each individual's blood pressure variance is under substantial genetic control, its quantitative estimates vary from 35 to 70%, according to the different experimental designs. The problem is that, in spite of such substantial contribution, the discovery of the "genes that cause hypertension" has been quite discouraging. This is indeed caused by the multifactorial nature of the disease and no improvement is to be expected without dissecting hypertension in its major pathogenetic pathways. As a paradigm of such a dissection, we present the data on adducin system, that proved to be relevant for a common form of salt sensitive in humans and the genetic hypertension of MHS rats.


Asunto(s)
Proteínas de Unión a Calmodulina/genética , Hipertensión/genética , Animales , Proteínas de Unión a Calmodulina/análisis , Modelos Animales de Enfermedad , Marcadores Genéticos/genética , Predisposición Genética a la Enfermedad , Humanos , Hipertensión/diagnóstico , Hipertensión/epidemiología , Incidencia , Pronóstico , Ratas , Ratas Endogámicas SHR , Medición de Riesgo , Sensibilidad y Especificidad
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