DataSheet_1_Association between circulating resistin levels and thyroid dysfunction: A systematic review and meta-analysis.xlsx

BackgroundAs a product of adipose tissue, resistin exceeds other adipokines in its role in regulating appetite, energy expenditure, insulin sensitivity, inflammation, and immunity, similar to thyroid hormones. This study aimed to evaluate the association between resistin levels and thyroid dysfunction and to explore variations in circulating resistin levels before and after treatment for thyroid dysfunction.MethodsThis study was conducted according to the Preferred Reporting Items for Systematic Review and Meta-Analysis statement. A comprehensive search of PubMed, Embase, and Cochrane databases was conducted until June 15, 2022, with no start date restriction, according to the preregistered protocol (PROSPERO-CRD42022336617). RevMan version 5.4 and R software package version 4.2.0 were used for statistical analyses.ResultsFourteen studies with 1716 participants were included in this study. The findings of the meta-analysis confirmed that the resistin levels of patients with thyroid dysfunction were significantly higher than those of the euthyroid function control group (mean difference [MD] = 2.11, 95% confidence interval [CI] = 1.11–3.11, P ConclusionsOur meta-analysis demonstrates that resistin levels are significantly higher in patients with thyroid dysfunction, and the resistin levels after treatment in patients with thyroid dysfunction are significantly lower than those before treatment. Correlation analysis shows a positive correlation between resistin levels and FT3 levels in patients with thyroid dysfunction.Systematic review registrationhttps://www.crd.york.ac.uk/PROSPERO/, identifier CRD42022336617.</p

Table_1_Association between circulating resistin levels and thyroid dysfunction: A systematic review and meta-analysis.xlsx

BackgroundAs a product of adipose tissue, resistin exceeds other adipokines in its role in regulating appetite, energy expenditure, insulin sensitivity, inflammation, and immunity, similar to thyroid hormones. This study aimed to evaluate the association between resistin levels and thyroid dysfunction and to explore variations in circulating resistin levels before and after treatment for thyroid dysfunction.MethodsThis study was conducted according to the Preferred Reporting Items for Systematic Review and Meta-Analysis statement. A comprehensive search of PubMed, Embase, and Cochrane databases was conducted until June 15, 2022, with no start date restriction, according to the preregistered protocol (PROSPERO-CRD42022336617). RevMan version 5.4 and R software package version 4.2.0 were used for statistical analyses.ResultsFourteen studies with 1716 participants were included in this study. The findings of the meta-analysis confirmed that the resistin levels of patients with thyroid dysfunction were significantly higher than those of the euthyroid function control group (mean difference [MD] = 2.11, 95% confidence interval [CI] = 1.11–3.11, P ConclusionsOur meta-analysis demonstrates that resistin levels are significantly higher in patients with thyroid dysfunction, and the resistin levels after treatment in patients with thyroid dysfunction are significantly lower than those before treatment. Correlation analysis shows a positive correlation between resistin levels and FT3 levels in patients with thyroid dysfunction.Systematic review registrationhttps://www.crd.york.ac.uk/PROSPERO/, identifier CRD42022336617.</p

Baicalin suppresses <i>P. gingivalis</i> LPS-induced nuclear translocation of p65.

<p><b>A.</b> The representative experiment was performed by pooling nuclear protein extracts equally from three independent experiments. 2 µg aliquots were added to each well. The assay was carried out according to the manufacturer’s instruction. <b>B.</b> The intensity analysis of the luminescent signals. Cells treated with culture media alone served as the blank control group, and those treated with <i>P. gingivalis</i> (<i>P.g.</i>) LPS (10 µg/ml) alone represented the positive control group. Cells treated with <i>P.g.</i> LPS at 10 µg/ml and 0.08% DMSO served as the vehicle control group. Data from three independent experiments were depicted as relative fold change as compared with the blank control groups (set as 1). *<i>p</i><0.05 and **<i>p</i><0.01 as compared with the respective positive control group (LPS) at each time point. BI: baicalin.</p

The fold change in the expression of genes in baicalin/<i>P. gingivalis</i> LPS-treated cells (test) with reference to the <i>P. gingivalis</i> LPS-treated cells (control).

<p>The genes downregulated over four folds are highlighted in bold, and those up or downregulated two to four folds are highlighted in italics.</p

Table1_An immune and epithelial–mesenchymal transition-related risk model and immunotherapy strategy for grade II and III gliomas.DOCX

Grade II and III gliomas are heterogeneous and aggressive diseases. More efficient prognosis models and treatment methods are needed. This study aims to construct a new risk model and propose a new strategy for grade II and III gliomas. The data were downloaded from The Cancer Genome Atlas (TCGA), the Gene Expression Omnibus (GEO), gene set enrichment analysis (GSEA), and the EMTome website for analysis. The Human Cell Landscape website and the Genomics of Drug Sensitivity in Cancer website were used for single-cell analysis and drug susceptibility analysis. Gene set enrichment analysis, gene function enrichment analysis, univariate and multivariate Cox regression analyses, Pearson’s correlation analysis, log-rank test, Kaplan–Meier survival analysis, and ROC analysis were performed. We constructed an immune-related prognostic model associated with the isocitrate dehydrogenase 1 (IDH1) mutation status. By analyzing the immune microenvironment of patients with different risk scores, we found that high-risk patients were more likely to have an inflammatory immune microenvironment and a higher programmed death ligand-1 (PD-L1) expression level. Epithelial–mesenchymal transition (EMT)-related gene sets were significantly enriched in the high-risk group, and the epithelial–mesenchymal transition phenotype was associated with a decrease in CD8+ T cells and an increase in M2 macrophages. Transforming growth factor-β (TGF-β) signaling was the most important signaling in inducing epithelial–mesenchymal transition, and TGFB1/TGFBR1 was correlated with an increase in CD8+ T cytopenia and M2 macrophages. Survival analysis showed that simultaneous low expression of TGFBR1 and PD-L1 had better survival results. Through single-cell analysis, we found that TGFB1 is closely related to microglia and macrophages, especially M2 macrophages. Finally, we discussed the sensitivity of TGFB1 inhibitors in gliomas using cell line susceptibility data. These results demonstrated a potential immunotherapy strategy in combination with the TGFB1/TGFBR1 inhibitor and PD-1/PD-L1 inhibitor for grade II and III gliomas.</p

Image1_An immune and epithelial–mesenchymal transition-related risk model and immunotherapy strategy for grade II and III gliomas.JPEG

Grade II and III gliomas are heterogeneous and aggressive diseases. More efficient prognosis models and treatment methods are needed. This study aims to construct a new risk model and propose a new strategy for grade II and III gliomas. The data were downloaded from The Cancer Genome Atlas (TCGA), the Gene Expression Omnibus (GEO), gene set enrichment analysis (GSEA), and the EMTome website for analysis. The Human Cell Landscape website and the Genomics of Drug Sensitivity in Cancer website were used for single-cell analysis and drug susceptibility analysis. Gene set enrichment analysis, gene function enrichment analysis, univariate and multivariate Cox regression analyses, Pearson’s correlation analysis, log-rank test, Kaplan–Meier survival analysis, and ROC analysis were performed. We constructed an immune-related prognostic model associated with the isocitrate dehydrogenase 1 (IDH1) mutation status. By analyzing the immune microenvironment of patients with different risk scores, we found that high-risk patients were more likely to have an inflammatory immune microenvironment and a higher programmed death ligand-1 (PD-L1) expression level. Epithelial–mesenchymal transition (EMT)-related gene sets were significantly enriched in the high-risk group, and the epithelial–mesenchymal transition phenotype was associated with a decrease in CD8+ T cells and an increase in M2 macrophages. Transforming growth factor-β (TGF-β) signaling was the most important signaling in inducing epithelial–mesenchymal transition, and TGFB1/TGFBR1 was correlated with an increase in CD8+ T cytopenia and M2 macrophages. Survival analysis showed that simultaneous low expression of TGFBR1 and PD-L1 had better survival results. Through single-cell analysis, we found that TGFB1 is closely related to microglia and macrophages, especially M2 macrophages. Finally, we discussed the sensitivity of TGFB1 inhibitors in gliomas using cell line susceptibility data. These results demonstrated a potential immunotherapy strategy in combination with the TGFB1/TGFBR1 inhibitor and PD-1/PD-L1 inhibitor for grade II and III gliomas.</p

Baicalin significantly downregulates <i>P. gingivalis</i> LPS-upregulated IL-8 expression.

<p><b>A</b>. Baicalin (BI) at 80 µM significantly downregulated <i>P. gingivalis</i> (<i>P.g.</i>) LPS-upregulated IL-8 mRNA expression. <b>B</b>. Baicalin at 80 µM significantly downregulated <i>P.g.</i> LPS-upregulated IL-8 protein expression. Cells treated with culture media alone served as the blank control group, and those treated with <i>P.g.</i> LPS (10 µg/ml) alone represented the positive control group. Cells treated with 0.08% DMSO and <i>P.g.</i> LPS at 10 µg/ml served as the vehicle control group. Data of three independent experiments were depicted as relative fold change as compared to the blank control group (set as 1) (<b>A</b>), or presented as protein concentration (<b>B</b>). *<i>p</i><0.01 as compared with the positive control group (<i>P.g.</i> LPS).</p

Summary of Illumina paired-end sequencing and assembly for <i>H</i>. <i>erectus</i> and <i>H</i>. <i>mohnikei</i>.

<p>Summary of Illumina paired-end sequencing and assembly for <i>H</i>. <i>erectus</i> and <i>H</i>. <i>mohnikei</i>.</p

Controlled Synthesis of Mesoporous MnO/C Networks by Microwave Irradiation and Their Enhanced Lithium-Storage Properties

A rapid and controllable route is developed for the synthesis of MnO nanoparticles that are encapsulated uniformly in three-dimensional (3D) mesoporous interconnected carbon networks (MnO-MICN) through an efficient microwave-polyol process, combined with a subsequent thermal treatment. The dependence of sodium citrate on the morphology of the Mn-based precursors was investigated systematically. Results show that the unique mesoporous interconnected carbon network (MICN) can not only buffer the large volume expansion of MnO during the electrochemical cycling, but also improve the electrode/electrolyte contact area, favoring the fast Li-ion transport and high specific capacity, superior cyclability, and excellent rate capability. When evaluated as an anode material for lithium-ion batteries, the as-formed 3D MnO-MICN nanocomposite exhibits a highly reversible capacity of 1224 mA h g^–1, with a Coulombic efficiency of ∼99% at a current density of 200 mA g^–1 over 200 cycles

Length distribution of all contigs, unigenes and CDSs for <i>H</i>. <i>erectus</i> and <i>H</i>. <i>mohnikei</i> (Unit: bp).

<p>Length distribution of all contigs, unigenes and CDSs for <i>H</i>. <i>erectus</i> and <i>H</i>. <i>mohnikei</i> (Unit: bp).</p