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1.
Nan Fang Yi Ke Da Xue Xue Bao ; 40(11): 1537-1542, 2020 Nov 30.
Artigo em Chinês | MEDLINE | ID: mdl-33243750

RESUMO

OBJECTIVE: To determine the impact of hypertension on the outcomes of patients with COVID-19. METHODS: This matched cohort study was conducted among a total 442 patients with COVID-19 admitted in Honghu People's Hospital and First Affiliated Hospital of Nanchang University between January 1 to March 18, 2020, including 61 patients with hypertension and 381 normotensive patients. To minimize the effects of the confounding factors including age, gender and other comorbidities, we excluded patients with comorbidities other than hypertension, and matched the patients with and without hypertension for age and gender at a 1:1 ratio. We analyzed the clinical characteristics, laboratory findings and clinical outcomes of in 32 matched pairs of patients with and without hypertension. RESULTS: Compared with the normotensive patients, COVID-19 patients with hypertension were more likely to develop bacterial infections (P=0.002) and had higher neutrophil counts (P=0.007), neutrophil/lymphocyte ratio (P=0.045), and lactate dehydrogenase levels (P=0.035). A greater proportion of patients had bilateral patchy opacities on chest CT (P=0.012) in the hypertension group than in the normotensive group. COVID-19 patients with hypertension group were more likely to receive antibiotics (P=0.035) and corticosteroid therapies (P=0.035). CONCLUSIONS: Hypertension increases the risk of bacterial infection in patients with COVID-19. Hypertensive patients with COVID-19 have higher neutrophil counts and neutrophil/ lymphocyte ratios and are more likely to require treatment with antibiotics. Hypertensive patients with COVID-19 should therefore take cautions to avoid bacterial infections.


Assuntos
COVID-19 , Hipertensão , SARS-CoV-2 , China , Estudos de Coortes , Humanos , Hipertensão/epidemiologia , Estudos Retrospectivos
2.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-880765

RESUMO

OBJECTIVE@#To screen the key genes related to the prognosis of lung adenocarcinoma through big data analysis and explore their clinical value and potential mechanism.@*METHODS@#We analyzed GSE18842, GSE27262, and GSE33532 gene expression profile data obtained from the Gene Expression Omnibus (GEO). Bioinformatics methods were used to screen the differentially expressed genes in lung adenocarcinoma tissues and KEGG and GO enrichment analysis was performed, followed by PPI interaction network analysis, module analysis, differential expression analysis, and prognosis analysis. The expressions of MAD2L1 and TTK by immunohistochemistry were verified in 35 non-small cell lung cancer specimens and paired adjacent tissues.@*RESULTS@#We identified a total of 256 genes that showed significant differential expressions in lung adenocarcinoma, including 66 up-regulated and 190 down-regulated genes. Thirty-two up-regulated core genes were screened by functional analysis, and among them 29 were shown to significantly correlate with a poor prognosis of patients with lung adenocarcinoma. All the 29 genes were highly expressed in lung adenocarcinoma tissues compared with normal lung tissues and were mainly enriched in cell cycle pathways. Seven of these key genes were closely related to the spindle assembly checkpoint (SAC) complex and responsible for regulating cell behavior in G2/M phase. We selected SAC-related proteins TTK and MAD2L1 to test their expressions in clinical tumor samples, and detected their overexpression in lung adenocarcinoma tissues as compared with the adjacent tissues.@*CONCLUSIONS@#Seven SAC complex-related genes, including TTK and MAD2L1, are overexpressed in lung adenocarcinoma tissues with close correlation with the prognosis of the patients.


Assuntos
Humanos , Adenocarcinoma de Pulmão/genética , Big Data , Proteínas de Ciclo Celular/genética , Biologia Computacional , Perfilação da Expressão Gênica , Regulação Neoplásica da Expressão Gênica , Neoplasias Pulmonares/genética , Pontos de Checagem da Fase M do Ciclo Celular , Proteínas Mad2/genética , Proteínas Serina-Treonina Quinases/genética , Proteínas Tirosina Quinases/genética
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