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1.
Acta Clin Belg ; 75(5): 348-356, 2020 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-32723027

RESUMO

OBJECTIVES: To recognise clinical features of COVID-19 pneumonia and its differences from influenza pneumonia. METHODS: 246 patients were enrolled into COVID-19 cohort and 120 patients into influenza cohort. All data were collected and analysed retrospectively. The variables under focus included demographic, epidemiological, clinical, laboratory and imaging characteristics of COVID-19 pneumonia and comparison were made with influenza pneumonia. RESULTS: The COVID-19 cohort included 53.25% female and 46.75% male. Their main symptom was fever; while 28.05% of patients had only initially fever; 21.54% of them remained feverless. After excluding prior kidney diseases, some patients showed abnormal urinalysis (32.11%), elevated blood creatinine (15.04%) and blood urea nitrogen (19.11%). Typical CT features included ground glass opacity, consolidation and band opacity, which could present as characteristic 'bat wing sign'. Our data showed that male, aged 65 or above, smoking, with comorbidities including diabetes, cardiovascular and kidney diseases, would experience more severe COVID-19 pneumonia. In comparison, COVID-19 cohort showed significantly higher incidence of clustering; the influenza cohort showed higher rate of fever. Both cohorts showed reduced lymphocyte numbers; however, 6 influenza patients showed lymphocytes increased, which was statistical significant compared with COVID-19 cohort. Also, influenza cohort displayed higher white blood cell counts and PCT values. CONCLUSION: There is no significant gender difference in the incidence of COVID-19 pneumonia. It predominantly affects the lung as well as the kidney. Age, smoking and comorbidities could contribute to disease severity. Although COVID-19 is more infectious, the rate of secondary bacterial infection is lower than influenza.


Assuntos
Betacoronavirus , Infecções por Coronavirus/diagnóstico , Influenza Humana/diagnóstico , Pneumonia Viral/diagnóstico , Pneumonia Viral/virologia , Adolescente , Adulto , Idoso , COVID-19 , Infecções por Coronavirus/complicações , Diagnóstico Diferencial , Feminino , Humanos , Influenza Humana/complicações , Masculino , Pessoa de Meia-Idade , Pandemias , Pneumonia Viral/complicações , Estudos Retrospectivos , SARS-CoV-2 , Avaliação de Sintomas , Tomografia Computadorizada por Raios X , Adulto Jovem
2.
Oncotarget ; 8(31): 50911-50920, 2017 Aug 01.
Artigo em Inglês | MEDLINE | ID: mdl-28881615

RESUMO

The association of perfluorodecanoicacid (PFDA) with tumor promotion and associated effects is not clear. Given that PDFA is mostly consumed with food and drinking water, we evaluated the effects of PFDA on a gastric cell line. When added to cell cultures, PFDA significantly increased growth rate and colony forming ability compared with control treatment. We found that suppression of cell senescence, but not apoptosis or autophagy was associated with PFDA-induced promotion of cell amount. To determine the molecular mechanism that was involved, DNA microarray assays was used to analyze changes in gene expression in response to PFDA treatment. Data analysis demonstrated that the vascular endothelial growth factor signaling pathway had the lowest p-value, with sPLA2-IIA (pla2g2a) exhibits the most altered expression pattern within the pathway. Moreover, sPLA2-IIA and its transcription factor TCF4, known as a direct target and a binding partner of Wnt/ß-catenin signaling in gastric cells respectively, were the third and second most varied genes globally. Cells transfected with expression plasmids pENTER-tcf4 and pENTER-pla2g2a show reduced cell proliferation by more than 60% and 30% respectively. Knockdown with sPLA2-IIA siRNA provided additional evidence that sPLA2-IIA was a mediator of PFDA-induced cell senescence suppression. The results suggest for the first time that PFDA induced suppression of cell senescence through inhibition of sPLA2-IIA protein expression and might increased the proliferative capacity of an existing tumor.

3.
Oncol Rep ; 38(2): 1287-1294, 2017 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-28677753

RESUMO

Papillary thyroid carcinoma is the most common thyroid cancer and the incidence is increasing. Aberrant activation of the WNT/ß­catenin pathway plays an important role in carcinogenesis. In the present study, microarray analysis was employed to compare tissues from papillary thyroid cancer and adjacent normal tissues to determine candidate genes facilitating tumor invasion. The result demonstrated that genes involved in WNT/ß­catenin signaling pathway were activated in papillary thyroid cancer, WNT10A expression was found to be upregulated >4-fold. The variations in gene expression were verified in tissues obtained from other papillary thyroid cancer patients. Molecular mechanism exploration in thyroid cells showed that enhanced WNT10A/ß­catenin signaling pathway activation promoted cell proliferation and migration. The promotion was validated by RNA interference of WNT10A and LEF1 expression. Moreover, results from flow cytometry demonstrated that WNT/ß­catenin signaling pathway activation reduced the percentage of late apoptotic thyroid cells. Conclusively, the results suggest for the first time that WNT10A/ß­catenin signaling pathway plays a crucial role in human papillary thyroid cancer.


Assuntos
Biomarcadores Tumorais/metabolismo , Carcinoma Papilar/patologia , Transformação Celular Neoplásica/patologia , Fator 1 de Ligação ao Facilitador Linfoide/metabolismo , Neoplasias da Glândula Tireoide/patologia , Proteínas Wnt/metabolismo , beta Catenina/metabolismo , Apoptose , Biomarcadores Tumorais/genética , Carcinoma Papilar/genética , Carcinoma Papilar/metabolismo , Estudos de Casos e Controles , Proliferação de Células , Transformação Celular Neoplásica/genética , Transformação Celular Neoplásica/metabolismo , Seguimentos , Regulação Neoplásica da Expressão Gênica , Humanos , Fator 1 de Ligação ao Facilitador Linfoide/genética , Prognóstico , Neoplasias da Glândula Tireoide/genética , Neoplasias da Glândula Tireoide/metabolismo , Células Tumorais Cultivadas , Proteínas Wnt/genética , beta Catenina/genética
4.
Exp Ther Med ; 13(6): 2793-2800, 2017 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-28587343

RESUMO

Atrophic gastritis is considered to be an antecedent to intestinal metaplasia and gastric cancer. A previous study identified that Helicobacter pylori was absent at the severe atrophic gastritis stage, and alterations in the gastric microbial composition resembled those in gastric cancer. To explore the role of the bacteria absence of H. pylori in gastric carcinogenesis, in the current study, we compared the microbiota of clinically collected H. pylori-free gastric fluids from 30 patients with non-atrophic gastritis (N) and 22 patients with severe atrophic gastritis (S). We estimated the bacterial loads in the N and S groups by colony counting in culture agar as well as by measuring the concentration of the extracted DNA. The results showed a significant increase in bacterial load in patients with atrophic gastritis in comparison to non-atrophic gastritis. Then, we analyzed the microbial communities of the gastric fluids from all 52 patients using high-throughput sequencing of 16S rRNA amplicons. The Chao 1, Shannon and Simpson diversity indexes demonstrated that the bacterial richness and diversity were not significantly different between the N and S groups. Moreover, principal component analysis illustrated that the microbiomes from the S group were more scattered. Microbiota composition analysis showed that the entire dataset was clustered into 27 phyla, 61 classes, 106 orders, 177 families, 292 genera and 121 species. At the genus level, only the abundance of Prevotella was significantly different between the N and S groups. Further analysis showed that all the higher taxonomic categories were significantly different between the N and S groups. To assess the effects of the metabolic products of Prevotella spp. on gastric cell physiology, we treated the human gastric epithelial cell line AGS with acetic acid and monitored nitric oxide (NO) production. The results showed that acetic acid at low concentrations (0.5 and 5 µM) significantly inhibited AGS cells to secrete NO compared to phosphate buffer saline-treated control cells. These results suggest that the microbiota in non-atrophic gastritis may influence gastric epithelial cell physiology.

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