10 research outputs found

    Table_1_Are serum levels of inflammatory markers associated with the severity of symptoms of bipolar disorder?.xls

    No full text
    BackgroundTo explore the relationship between serum levels of inflammatory markers and symptomatic severity of bipolar disorder (BD).Materials and methodsA cross-sectional study was conducted on 126 BD patients with current depressive episode (BDD), 102 BD patients with current mixed or (hypo)manic episode (BDM) and 94 healthy controls (HC). All participants were drug-naïve and had no current active physical illness associated with inflammatory response or history of substance abuse. Fasting serum levels of CRP, leptin (LEP), adiponectin (ADP), visfatin (VIS), TNF-α, IL-2, IL-6, IL-10, IL-17), and monocyte chemoattractant protein-1 (MCP-1) were measured with enzyme-linked immunosorbent assay (ELISA). Symptomatic severity of BD was assessed with HAMD-17 and YMRS. Generalized linear model was used to determine the association between the serum levels of inflammatory markers and symptomatic severity of BD.ResultsThe serum levels of IL-6, IL-10 and IL-17, and the IL-6/IL-10 ratio were significantly lower in mild BDD than in HC. In moderate BDD, the serum levels of MCP, IL-6 and IL-17 were significantly lower than in HC. In severe BDD, the serum level of ADP, MCP-1, IL-10 and IL-17and the IL-17/IL-10 ratio were significantly lower than in HC. The serum levels of TNF-α and the IL-6/IL-10 ratio were significantly higher in mild BDM than in HC. In moderate BDM, the serum level of VIS, IL-2, and IL-17 were significantly higher than in HC, but the IL-6/IL-10 ratio was significantly lower than in control. In severe BDM, the serum levels of IL-6 and IL-17 and the ratios of IL-6/IL-10 and IL-17/IL-10 were significantly lower than in HC, but the neutrophil/lymphocyte ratio was significantly higher than in HC.ConclusionIn BDD, immune-inhibition is persistently predominant, while in mild-to-moderate BDM, immune system is activated but inhibited in severe BDM. The dynamic change of serum inflammatory markers suggests that alteration of peripheral inflammatory markers in BD is state-dependent instead of trait-marked.</p

    Additional file 1 of METTL3-mediated m6A RNA methylation induces the differentiation of lung resident mesenchymal stem cells into myofibroblasts via the miR-21/PTEN pathway

    No full text
    Additional file 1: Figure S1. Construction of METTL3-overexpressing or METTL3-silenced LR-MSCs. A, B The mRNA and protein expression levels of METTL3 in METTL3-overexpressing or METTL3-silenced LR-MSCs compared to controls. β-Actin was used as a reference gene. **P < 0.01. Figure S2. Successful construction of a bleomycin-induced pulmonary fibrosis mouse model. A HE staining of lung tissues from mice with or without bleomycin exposure. B The α-SMA, type I collagen, and vimentin expression levels in lung tissues from mice with or without bleomycin exposure. β-Actin was used as a reference gene. **P < 0.01. Figure S3. Generation of the METTL3-silenced mouse model. A, B The mRNA and protein expression levels of METTL3 in the lung tissue of mice treated with METTL3 knockout adenovirus or control adenovirus. β-Actin was used as a reference gene. **P < 0.01. Figure S4. Local RNA structures of pri-miR-21 with very high confidence in m6A modification potential. Yellow, m6A binding sites. Figure S5. The construction of PTEN-overexpressing or PTEN-silenced LR-MSCs. A, B The mRNA and protein expression levels of PTEN in PTEN-overexpressing or PTEN-silenced LR-MSCs compared to controls. β-Actin was used as a reference gene. **P < 0.01

    Additional file 3 of Macrophage polarization toward M1 phenotype through NF-κB signaling in patients with Behçet’s disease

    No full text
    Additional file 3: Supplemental Figure S1. Representative FACS plot depicts the purity of monocytes, macrophages and naïve T CD4+T cells. Supplemental Figure S2. MFI analysis of BD serum-promoted macrophage polarization. Supplemental Figure S3. BD serum promotes CD86+CD163-CD206- M1-like macrophage polarization. Supplemental Figure S4. BD serum-treated macrophages facilitate Th1 differentiation under Th0 condition. Supplemental Figure S5. MFI analysis of T-bet in BD serum-treated macrophages. Supplemental Figure S6. BD serum-treated macrophages facilitate Th17 differentiation. Supplemental Figure S7. BD serum-treated macrophages produced more CXCL2 and CXCL3. Supplemental Figure S8. NF-κB inhibition attenuated CD86 expression on macrophages stimulated by BD serum. Supplemental Figure S9. Activated JAK/STAT pathway in BD serum-treated macrophages

    Additional file 5: of Metabolomic alterations associated with Behçet’s disease

    No full text
    Comparison of the content of AA and LA in an independent cohort. (A) Identification of AA and LA in serum samples by comparison with reference standards. (B) Calibration curves of AA and LA with rosmarinic acid as the internal standard. (C) Contents of LA and AA in BD and HC samples. (D) Correlation of ESR and CRP with the serum levels of LA and AA in BD. (PDF 253 kb

    Additional file 4: of Metabolomic alterations associated with Behçet’s disease

    No full text
    The ROC curve of PCs, AA, and LA in BD patients. (A) The ROC curve of PCs with area under the curve (AUC) > 0.85 in BD patients. (B) The ROC curve of AA and LA in BD patients. (PDF 18 kb

    Additional file 2: of Metabolomic alterations associated with Behçet’s disease

    No full text
    Verification of PUFAs by MS/MS. Retention time of two n-6 PUFAs, linoleic acid and arachidonic acid were compared with that of the pure chemicals. MS/MS spectra are shown. (PDF 46 kb

    Additional file 1: of Metabolomic alterations associated with Behçet’s disease

    No full text
    Verification of PCs by multiple reaction monitoring. These panels show MS/MS spectra of the indicated ions. Multiple reaction monitoring transitions were monitored for PC signature fragmentation (m/z 184). (PDF 46 kb

    Additional file 3: of Metabolomic alterations associated with Behçet’s disease

    No full text
    Treatment reverses the increased level of oleic acid in serum. (A) Abundance of oleic acid in healthy volunteers, pretreatment BD (Pre-) patients, and post-treatment BD (Post-) patients. ***p < 0.001. (B) Verification of oleic acid by MS/MS. (PDF 59 kb
    corecore