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1.
BMC Neurol ; 22(1): 139, 2022 Apr 12.
Artículo en Inglés | MEDLINE | ID: covidwho-2268723

RESUMEN

BACKGROUND: Glioblastoma multiforme (GBM) is the most common aggressive malignant brain tumor. However, the molecular mechanism of glioblastoma formation is still poorly understood. To identify candidate genes that may be connected to glioma growth and development, weighted gene co-expression network analysis (WGCNA) was performed to construct a gene co-expression network between gene sets and clinical characteristics. We also explored the function of the key candidate gene. METHODS: Two GBM datasets were selected from GEO Datasets. The R language was used to identify differentially expressed genes. WGCNA was performed to construct a gene co-expression network in the GEO glioblastoma samples. A custom Venn diagram website was used to find the intersecting genes. The GEPIA website was applied for survival analysis to determine the significant gene, FUBP3. OS, DSS, and PFI analyses, based on the UCSC Cancer Genomics Browser, were performed to verify the significance of FUBP3. Immunohistochemistry was performed to evaluate the expression of FUBP3 in glioblastoma and adjacent normal tissue. KEGG and GO enrichment analyses were used to reveal possible functions of FUBP3. Microenvironment analysis was used to explore the relationship between FUBP3 and immune infiltration. Immunohistochemistry was performed to verify the results of the microenvironment analysis. RESULTS: GSE70231 and GSE108474 were selected from GEO Datasets, then 715 and 694 differentially expressed genes (DEGs) from GSE70231 and GSE108474, respectively, were identified. We then performed weighted gene co-expression network analysis (WGCNA) and identified the most downregulated gene modules of GSE70231 and GSE108474, and 659 and 3915 module genes from GSE70231 and GSE108474, respectively, were selected. Five intersection genes (FUBP3, DAD1, CLIC1, ABR, and DNM1) were calculated by Venn diagram. FUBP3 was then identified as the only significant gene by survival analysis using the GEPIA website. OS, DSS, and PFI analyses verified the significance of FUBP3. Immunohistochemical analysis revealed FUBP3 expression in GBM and adjacent normal tissue. KEGG and GO analyses uncovered the possible function of FUBP3 in GBM. Tumor microenvironment analysis showed that FUBP3 may be connected to immune infiltration, and immunohistochemistry identified a positive correlation between immune cells (CD4 + T cells, CD8 + T cells, and macrophages) and FUBP3. CONCLUSION: FUBP3 is associated with immune surveillance in GBM, indicating that it has a great impact on GBM development and progression. Therefore, interventions involving FUBP3 and its regulatory pathway may be a new approach for GBM treatment.


Asunto(s)
Glioblastoma , Biomarcadores de Tumor , Canales de Cloruro/genética , Biología Computacional/métodos , Proteínas de Unión al ADN/genética , Perfilación de la Expresión Génica/métodos , Regulación Neoplásica de la Expresión Génica/genética , Glioblastoma/patología , Humanos , Pronóstico , Factores de Transcripción/genética , Microambiente Tumoral
2.
Math Biosci Eng ; 19(12): 12247-12259, 2022 08 22.
Artículo en Inglés | MEDLINE | ID: covidwho-2071967

RESUMEN

The purpose of this paper is to give some sufficient conditions for the existence of periodic oscillation of a class of in-host MERS-Cov infection model with cytotoxic T lymphocyte (CTL) immune response. A new technique is developed to obtain a lower bound of the state variable characterizing CTL immune response in the model. Our results expand on some previous works.


Asunto(s)
Coronavirus del Síndrome Respiratorio de Oriente Medio , Linfocitos T Citotóxicos , Inmunidad
3.
Mathematics ; 10(6):975, 2022.
Artículo en Inglés | ProQuest Central | ID: covidwho-1760760

RESUMEN

In this paper, we study the global dynamics of a delayed virus dynamics model with apoptosis and both virus-to-cell and cell-to-cell infections. When the basic reproduction number R0>1, we obtain the uniform persistence of the model, and give some explicit expressions of the ultimate upper and lower bounds of any positive solution of the model. In addition, by constructing the appropriate Lyapunov functionals, we obtain some sufficient conditions for the global attractivity of the disease-free equilibrium and the chronic infection equilibrium of the model. Our results extend existing related works.

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