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Journal: eBioMedicine
Article Title: Autoantibodies against type I interferons in patients with zoonotic H7N9 influenza: an observational case–control study
doi: 10.1016/j.ebiom.2026.106387
Figure Lengend Snippet: Autoantibodies binding to IFNα 2 , IFNβ 1b and IFNω in patients with H7N9 infection and healthy controls. (A) Age and sex distribution of the three study groups. For each age group, the number of individuals positive for autoantibodies neutralising at least one tested IFN-I (IFNα 2 , IFNβ 1b , IFNω) at low concentrations is indicated in red. M, male; F, female; nAb+, positive for IFN-I-neutralising autoantibodies. (B) Detection of IgG autoantibodies binding to IFNα 2 , IFNβ 1b or IFNω in serum samples by multiplex bead-based assay. Samples with a Z-score >7 were considered positive for IFN-I-binding autoantibodies. Measurements were performed without technical replicates because of limited sample availability. (C) Prevalence of IFN-I-binding autoantibodies by IFN type and study group. IFNα 2 ± IFNβ 1b ± IFNω, positive for autoantibodies binding to at least one of the tested IFN-I; IFNα 2 + IFNω, positive for autoantibodies binding to both IFNα 2 and IFNω.
Article Snippet: Serum was diluted 1:50 in DMEM supplemented with 10% FCS and penicillin/streptomycin, and pre-incubated for 1 h at room temperature with one of the following IFN concentrations: (i) IFNα 2 (Novus Biologicals, NBP2-34971) at 10 ng/ml or 0.5 ng/ml; (ii)
Techniques: Binding Assay, Infection, Multiplex Assay, Bead-based Assay
Journal: eBioMedicine
Article Title: Autoantibodies against type I interferons in patients with zoonotic H7N9 influenza: an observational case–control study
doi: 10.1016/j.ebiom.2026.106387
Figure Lengend Snippet: Autoantibodies neutralising IFN-I in patients with H7N9 infection and healthy controls. (A) Luciferase-based reporter assay to assess the capacity of autoantibody positive sera to neutralise IFNα 2 (10 or 0.5 ng/ml), IFNβ 1b (1 or 0.25 ng/ml) or IFNω (10 or 0.2 ng/ml). Each sample was tested in biological duplicates and the mean values are shown. Samples were classified as neutralising if the mean of the relative luciferase activities was below 25% (dotted line) of the mean of the negative pool (four autoantibody-negative control sera). All sera positive for IFN-I-binding autoantibodies were tested; numbers are indicated above the graphs. Lines connect measurements of neutralising activity from the same serum sample at low and high IFN concentrations. (B) Prevalence of autoantibodies neutralising low IFN concentrations (IFNα 2 : 0.5 ng/ml, IFNβ 1b : 0.25 ng/ml; IFNω: 0.2 ng/ml) by IFN type and study group. IFNα 2 ± IFNβ 1b ± IFNω, positive for autoantibodies neutralising at least one tested IFN-I; IFNα 2 + IFNω, positive for autoantibodies neutralising both IFNα 2 and IFNω. (C) Area-proportional Venn diagrams illustrating the absolute numbers of samples with autoantibodies neutralising high and low concentrations of IFNα 2 (10 or 0.5 ng/ml), IFNβ 1b (1 or 0.25 ng/ml) or IFNω (10 or 0.2 ng/ml). Venn diagrams were created with BioVenn ( https://www.biovenn.nl/index.php ).
Article Snippet: Serum was diluted 1:50 in DMEM supplemented with 10% FCS and penicillin/streptomycin, and pre-incubated for 1 h at room temperature with one of the following IFN concentrations: (i) IFNα 2 (Novus Biologicals, NBP2-34971) at 10 ng/ml or 0.5 ng/ml; (ii)
Techniques: Infection, Luciferase, Reporter Assay, Negative Control, Binding Assay, Activity Assay
Journal: eBioMedicine
Article Title: Autoantibodies against type I interferons in patients with zoonotic H7N9 influenza: an observational case–control study
doi: 10.1016/j.ebiom.2026.106387
Figure Lengend Snippet: Association between the presence of IFN-I-neutralising autoantibodies and H7N9 infection. (A) The association between age, sex and IFN-I-neutralising autoantibodies in patients with H7N9 infection or in the two control groups combined (poultry workers + close contacts) was assessed using Firth's penalised logistic regression. Predicted probabilities for the presence of autoantibodies with 95% confidence intervals (CIs, shaded areas around the curve) are shown across participant age for men and women. To visualise the modelled probabilities in relation to the underlying data, we overlaid sex-specific age density distributions beneath the predicted probability curves. (B) Odds ratios (OR) with 95% CIs for the presence of autoantibodies neutralising low IFN concentrations in patients compared to healthy controls, adjusted for age and sex, determined by Firth’s penalised logistic regression models. See also for the results of the logistic regression analyses and for unadjusted estimates. IFNα 2 ± IFNω ± IFNβ 1b , positive for autoantibodies neutralising at least one of the tested IFN-I; IFNα 2 ± IFNω, positive for autoantibodies neutralising IFNα 2 and/or IFNω; ∗∗∗∗, p < 0.0001 (Firth’s penalised logistic regression).
Article Snippet: Serum was diluted 1:50 in DMEM supplemented with 10% FCS and penicillin/streptomycin, and pre-incubated for 1 h at room temperature with one of the following IFN concentrations: (i) IFNα 2 (Novus Biologicals, NBP2-34971) at 10 ng/ml or 0.5 ng/ml; (ii)
Techniques: Infection, Control
Journal: eBioMedicine
Article Title: Autoantibodies against type I interferons in patients with zoonotic H7N9 influenza: an observational case–control study
doi: 10.1016/j.ebiom.2026.106387
Figure Lengend Snippet: Neutralising sera block the antiviral effect of IFNα 2 in cell culture infected with IAV. Antiviral activity of IFNα 2 (5 ng/ml) against IAV (PR8-GFP, MOI 1) alone or in the presence of serially diluted IFN-I-neutralising sera (n = 19), autoantibody-negative sera (n = 4), or a monoclonal anti-IFNα 2 antibody in A549 cells. Infection rates (GFP + /DAPI + cells) at 7 h post-infection were normalised to untreated, infected cells. The dotted line indicates the reduction of infected cells after IFN treatment alone. If possible, the mean of two independent experiments is shown. Sufficient material was available for 12 out of 19 samples.
Article Snippet: Serum was diluted 1:50 in DMEM supplemented with 10% FCS and penicillin/streptomycin, and pre-incubated for 1 h at room temperature with one of the following IFN concentrations: (i) IFNα 2 (Novus Biologicals, NBP2-34971) at 10 ng/ml or 0.5 ng/ml; (ii)
Techniques: Blocking Assay, Cell Culture, Infection, Activity Assay
Journal: Bioactive Materials
Article Title: Mesenchymal stromal cells-loaded 3D radially aligned composite scaffold with potentiated paracrine signaling for sequential bone regeneration
doi: 10.1016/j.bioactmat.2026.02.059
Figure Lengend Snippet: Temporal analysis of the BMSC paracrine profile on different scaffolds. (A) Confocal microscopy images from Live/Dead fluorescence staining of BMSCs encapsulated within the PCL/HAp-GelMA/BMSCs scaffold after 1, 3, 5, and 14 d of 3D culture (live cells, green; dead cells, red). (B) The concentrations of key paracrine factors (TGF-β, PGE2, VEGF, HGF, and BMP-2) from BMSCs cultured in different scaffolds, quantified from culture supernatants at day 3 and day 7. (C) Corresponding relative mRNA expression levels of TGFB1, PTGS2, VEGFA, HGF, and BMP-2 in BMSCs at day 3 and day 7, as determined by qPCR analysis. Data are presented as mean ± SD (n = 3) *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001; ns: not significant.
Article Snippet: ELISA kits for PGE2 (Cat. No. E-EL-0034),
Techniques: Confocal Microscopy, Fluorescence, Staining, Cell Culture, Expressing
Journal: Bioactive Materials
Article Title: Precisely regulated physically-crosslinked carriers enable synergetic release of bioactive factors for MSC-mediated cartilage regeneration
doi: 10.1016/j.bioactmat.2026.01.009
Figure Lengend Snippet: In vivo chondrogenesis of hydrogels incorporated with different combinations of PSF and KSF. (a) Alcian blue and Safranin O staining of different combinations after 21-day implantation. G1: 5 % β-sheet PSF +5 % β-sheet KSF; G2: 15 % β-sheet PSF +30 % β-sheet KSF; G3: 30 % β-sheet PSF +40 % β-sheet KSF; G4: 40 % β-sheet PSF +50 % β-sheet KSF. Scale bar = 200 μm. (b–d) Quantitative analysis of IL-1β, IL-6 and TNF-α surrounding defect cartilage 1 week and 3 weeks after operation. (e, f) Macroscopic and MRI observations of rat femoral condyles at week 6 and 12. Red circles and red arrows show the original defect zone under macroscope and MRI respectively. Scale bar = 1 mm. (g) Relative ratio of average optical density (versus G1) that shows the staining intensity of Alcian blue and Safranin O staining. (h) ICRS scoring of macroscopic evaluations. (i) The repaired cartilage using a nanoindentation instrument. Scale bar = 1 cm. (j, k) Reduced modulus and hardness of the regenerated cartilage. ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001; ∗∗∗∗p < 0.0001.
Article Snippet: The suspension was centrifuged at 10,000 rpm for 10 min at 4 °C, and the supernatant was collected, and Elisa assay was performed following the manufacturer's instructions for
Techniques: In Vivo, Staining
Journal: Genes & Diseases
Article Title: Targeting MDK alleviates bone loss via dual regulation of osteogenic differentiation and inflammatory cytokine expression
doi: 10.1016/j.gendis.2025.101931
Figure Lengend Snippet: iMDK alleviates bone loss via dual regulation of bone formation and inflammatory cytokines. (A) Representative micro-CT images of distal femora (top) with three-dimensional reconstruction of the region of interest (bottom), with the blue indicating higher-density bone and the red indicating lower-density bone. (B – D) Statistical quantification of trabecular bone microstructural parameters (BMD, BV/TV, and Tb.Th). Inter-group comparisons were analyzed by one-way ANOVA. (E) Representative images of trabecular bone area in distal femur sections stained with hematoxylin and eosin. Scale bar, 200 μm or 50 μm. (F) Quantitative analysis of the trabecular bone area of the distal femur stained with hematoxylin and eosin. Inter-group comparisons were analyzed by one-way ANOVA. (G) Immunohistochemical staining of OCN in distal femurs. Scale bar, 200 μm or 50 μm. (H) Quantitative analysis of OCN-positive area. Inter-group comparisons were analyzed by one-way ANOVA. (I) Western blotting analysis of inflammatory cytokine expression (IL-6, TNF-α, and IL-1β) in mouse bone tissues. (J) Inflammatory cytokine expression (IL-6, TNF-α, and IL-1β) in mouse serum was detected by ELISA. Inter-group comparisons were analyzed by one-way ANOVA. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001; “ns” indicates non-significant differences.
Article Snippet: We purchased the Mouse P1NP (Procollagen 1 N-Terminal Propeptide) ELISA Kit (Cat#e-el-m0233), Mouse IL-6 ELISA Kit (Cat#e-el-m0044), Mouse TNF-α ELISA Kit (Cat#e-el-m3063), and
Techniques: Micro-CT, Staining, Immunohistochemical staining, Western Blot, Expressing, Enzyme-linked Immunosorbent Assay
Journal: Genes & Diseases
Article Title: Targeting MDK alleviates bone loss via dual regulation of osteogenic differentiation and inflammatory cytokine expression
doi: 10.1016/j.gendis.2025.101931
Figure Lengend Snippet: Recombinant MDK protein triggers the activation of inflammatory cytokines through the NF-κB signaling pathway. (A, B) IL-6, TNFα, and IL-1β expression levels were detected using Western blotting. MC3T3-E1 cells were treated with recombinant MDK protein (600 ng/mL). Osteogenic differentiation was induced for 7 days. Inter-group comparisons were analyzed by a two-tailed unpaired Student's t -test (for normally distributed data with equal variance). (C, D) Western blotting analysis of NF-κB signaling pathway molecules in MC3T3-E1 cells treated with recombinant MDK protein for 7 days during osteoblastic differentiation. Inter-group comparisons were analyzed by two-tailed unpaired Student's t -test (for normally distributed data with equal variance). (E, F) IL-6 and IL-1β expression levels were detected using Western blotting. MC3T3-E1 cells were pretreated with 10 μM BAY 11–7082. Osteogenic differentiation was induced for 7 days. Inter-group comparisons were analyzed by one-way ANOVA. ∗ p < 0.05 and ∗∗ p < 0.01.
Article Snippet: We purchased the Mouse P1NP (Procollagen 1 N-Terminal Propeptide) ELISA Kit (Cat#e-el-m0233), Mouse IL-6 ELISA Kit (Cat#e-el-m0044), Mouse TNF-α ELISA Kit (Cat#e-el-m3063), and
Techniques: Recombinant, Activation Assay, Expressing, Western Blot, Two Tailed Test
Journal: Genes & Diseases
Article Title: Targeting MDK alleviates bone loss via dual regulation of osteogenic differentiation and inflammatory cytokine expression
doi: 10.1016/j.gendis.2025.101931
Figure Lengend Snippet: Schematic representation of MDK alleviating bone loss. MDK is significantly elevated in the serum of postmenopausal osteoporotic women and ovariectomized mice. Due to estrogen deficiency, iMDK alleviates bone loss by promoting bone formation and inhibiting inflammatory factors. Recombinant MDK protein inhibits osteogenic differentiation through the PI3K/AKT signaling pathway and up-regulates inflammatory factors IL-6, TNF-α, and IL-1β via the NF-κB signaling pathway.
Article Snippet: We purchased the Mouse P1NP (Procollagen 1 N-Terminal Propeptide) ELISA Kit (Cat#e-el-m0233), Mouse IL-6 ELISA Kit (Cat#e-el-m0044), Mouse TNF-α ELISA Kit (Cat#e-el-m3063), and
Techniques: Recombinant