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1.
Clin Infect Dis ; 71(16): 2089-2098, 2020 11 19.
Artículo en Inglés | MEDLINE | ID: mdl-32361738

RESUMEN

BACKGROUND: With evidence of sustained transmission in more than 190 countries, coronavirus disease 2019 (COVID-19) has been declared a global pandemic. Data are urgently needed about risk factors associated with clinical outcomes. METHODS: A retrospective review of 323 hospitalized patients with COVID-19 in Wuhan was conducted. Patients were classified into 3 disease severity groups (nonsevere, severe, and critical), based on initial clinical presentation. Clinical outcomes were designated as favorable and unfavorable, based on disease progression and response to treatments. Logistic regression models were performed to identify risk factors associated with clinical outcomes, and log-rank test was conducted for the association with clinical progression. RESULTS: Current standard treatments did not show significant improvement in patient outcomes. By univariate logistic regression analysis, 27 risk factors were significantly associated with clinical outcomes. Multivariate regression indicated age >65 years (P < .001), smoking (P = .001), critical disease status (P = .002), diabetes (P = .025), high hypersensitive troponin I (>0.04 pg/mL, P = .02), leukocytosis (>10 × 109/L, P < .001), and neutrophilia (>75 × 109/L, P < .001) predicted unfavorable clinical outcomes. In contrast, the administration of hypnotics was significantly associated with favorable outcomes (P < .001), which was confirmed by survival analysis. CONCLUSIONS: Hypnotics may be an effective ancillary treatment for COVID-19. We also found novel risk factors, such as higher hypersensitive troponin I, predicted poor clinical outcomes. Overall, our study provides useful data to guide early clinical decision making to reduce mortality and improve clinical outcomes of COVID-19.


Asunto(s)
COVID-19/epidemiología , Coronavirus/patogenicidad , Hospitalización/estadística & datos numéricos , Adulto , Anciano , Anciano de 80 o más Años , Distribución de Chi-Cuadrado , China/epidemiología , Femenino , Humanos , Hipnóticos y Sedantes/uso terapéutico , Masculino , Persona de Mediana Edad , Obesidad/complicaciones , Obesidad/epidemiología , Estudios Retrospectivos , Factores de Riesgo , Adulto Joven
2.
Med Sci Monit ; 24: 1-10, 2018 Jan 01.
Artículo en Inglés | MEDLINE | ID: mdl-29290631

RESUMEN

BACKGROUND Idiopathic pulmonary fibrosis (IPF) can severely damage lung function, which may result in death. Emodin is a major ingredient of rhubarb and has been proven to protect against lung disruptions. Our study focused on the potential medicinal effect of emodin against IPF. MATERIAL AND METHODS The experiment subjects were fully-grown male Sprague-Dawley rats with average weight of 180-220 kg. Histological analyses, Western blotting analysis, quantitative real-time PCR, and statistical analysis were used in the study. RESULTS We found that emodin significantly reduced lung structural distortion, collagen overproduction, massive inflammatory cells infiltration, proinflammatory cytokines expansion, and injuries caused by administration of bleomycin (BLM). Additionally, emodin suppressed the accumulation of p-IκBα and NF-κB, while stimulating the Nrf2-antioxidant signaling process in damaged lungs. Emodin inhibited epithelial-mesenchymal transition (EMT) induced by BLM in the lungs. Moreover, emodin suppressed the TGF-ß1 expression and the downstream signal molecules p-Smad-2 and p-Smad-3, which are reinforced by BLM. Emodin can also reverse EMT-like shifts induced by recombinant TGF-ß1 in alveolar epithelial cultured cells. CONCLUSIONS The effect of emodin in fibrotic lung injury is closely related to its favorable properties of anti-inflammation and anti-oxidation.


Asunto(s)
Emodina/farmacología , Fibrosis Pulmonar Idiopática/tratamiento farmacológico , Células A549/efectos de los fármacos , Animales , Antiinflamatorios/uso terapéutico , Antioxidantes/farmacología , Bleomicina , Técnicas de Cultivo de Célula , Citocinas/metabolismo , Modelos Animales de Enfermedad , Humanos , Fibrosis Pulmonar Idiopática/fisiopatología , Inflamación/patología , Pulmón/patología , Masculino , Factor 2 Relacionado con NF-E2/efectos de los fármacos , Inhibidor NF-kappaB alfa/efectos de los fármacos , FN-kappa B/efectos de los fármacos , Estrés Oxidativo/efectos de los fármacos , Fibrosis Pulmonar/tratamiento farmacológico , Ratas , Ratas Sprague-Dawley , Transducción de Señal/efectos de los fármacos , Proteínas Smad/efectos de los fármacos
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