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1.
Innovation ; : 42-45, 2021.
Artigo em Inglês | WPRIM | ID: wpr-976426

RESUMO

Purpose@#Behcet’s disease is characterized by repeated acute inflammatory attacks with aphthous ulcers of the oral mucosa, uveitis of the eyes, skin symptoms, and genital ulcers. Although its etiology is still unknown, there is evidence of the involvement of oral bacteria in systemic diseases. Various types of oral bacteria may be involved in the development and progression of Behcet's disease. Therefore, the present study investigated alterations in the oral flora of patients with Behcet’s disease in Mongolia. We collected saliva samples from the Mongolian Behcet's disease (BD) group and healthy control (HC) group, and the oral flora were analyzed using next generation sequencer (NGS).@*Methods@#DNA was extracted from the unstimulated saliva samples from the 47 BD and 48 HC subjects. The DNA was amplified from the V3-V4 region of 16S rRNA using PCR, and the data were acquired using NGS. Based on the obtained data, we analyzed the alpha diversity, beta diversity, and bacterial taxonomy of the salivary flora.</br> Household survey covered 148 people with visual and hearing impairments to assess social service accessibility.@*Results@#Beta diversity differed significantly between the BD and HC flora, but no significant differences were observed in alpha diversity. We found that the proportions of three genera—an S24-7 family unknown species, a mitochondria family unknown species, and Akkermansia species were significantly lower in the BD than in the HC group.@*Conclusion@#The reduced proportions of the S24-7 family and symbiotic Akkermansia species may be key phenomena in the oral flora of patients with BD.

2.
Chinese Journal of Hepatology ; (12): 291-296, 2017.
Artigo em Chinês | WPRIM | ID: wpr-808548

RESUMO

Objective@#To investigate the changes in the composition of intestinal microbiota in mice with acute liver failure and identify characteristic bacteria, and to provide a basis for the diagnosis and treatment of acute liver failure with intestinal microbiota disorders.@*Methods@#A total of 30 specific pathogen-free male BALB/c mice were used in this study, including 25 mice in the model group and 5 mice in the control group. An acute liver failure model was induced by D-galactosamine. Microbial DNA was extracted from intestinal contents in different segments of the lower digestive tract (ileum and colon) and feces and then were amplified using PCR. The regions of 16S V3-V4 were subjected to high-throughput sequencing, followed by bioinformatics analyses, including OTU hierarchical clustering, species annotation, alpha-diversity analysis, and LEfSe (LDA Effect Size) analysis. Comparison of continuous data was made using t-test, while comparison of categorical data was made using χ2 test.@*Results@#A total of 10 mice survived in the two groups, with 80% mortality rate in the model group. The alpha-diversity analysis revealed increased bacterial diversity and abundance in the ileum, increased bacterial diversity and reduced bacterial abundance in the colon, and reduced bacterial diversity and insignificantly changed bacterial abundance in feces in the model group compared with the control group. Based on the optimized classification level, significantly reduced abundance of Clostridiaceae (44.95% ± 19.28% vs 7.51% ± 16.57%, P = 0.011) in the ileum, whereas significantly increased abundance of Rikenellaceae (1.08% ± 1.01% vs 4.18% ± 2.39%, P = 0.028), S24-7 (4.75% ± 4.87% vs 22.77% ± 13.05%, P = 0.020), and F16 (0.24% ± 0.28% vs 2.18% ± 1.61%, P = 0.029) in the colon were found in model group compared with the control group. The LEfSe analysis demonstrated that there were significant differences in Staphylococcaceae and S24-7 between the two groups, and S24-7 could be defined as the characteristic bacteria.@*Conclusion@#Intestinal microbiota disorders, especially the excessive growth of microbes in the ileum, are observed in mice with acute liver failure. Moreover, acute liver failure may be closely associated with the excessive growth of S24-7.

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