Journal: Materials Today Bio

Article Title: Injectable deferoxamine-loaded microsphere hydrogels for inhibition of ferroptosis and promotion of third-degree burn wound healing

doi: 10.1016/j.mtbio.2025.101806

Figure Lengend Snippet: Inhibition of ferroptosis by DFO@GM-H hydrogels. (a) Representative fluorescent images of intracellular Fe 2+ accumulation in HSFs exposed to different groups for 24 h. Intracellular Fe 2+ were stained with FerroOrange in red fluorescence. (b) Quantitative analysis of intracellular Fe 2+ accumulation in HSFs. (c) Quantitative analysis of MDA content in HSFs exposed to different groups for 24 h. (d) Protein expression of ACSL4, SLC7A11, GPX4 and GAPDH in HSFs treated with different groups by western blot. (e–g) Quantification of fold-change of ACSL4, SLC7A11 and GPX4 in HSFs by western blot. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001, ns means non-significant (p > 0.05).

Article Snippet: Tissue sections were incubated with primary antibodies overnight at 4 °C, including IL-1β mouse mAb (Proteintech, China, 66737-1-Ig, 1:300), Anti-CD31 rabbit mAb (Abcam, England, ab182981, 1:300), VEGFA rabbit pAb (Proteintech, China, 19003-1-ap, 1:500), ferritin light chain rabbit pAb ((Proteintech, China, 10727-1-AP, 1:500), ACSL4 rabbit mAb (Abcam, England, ab155282, 1:500), SLC7A11 rabbit mAb (Abcam, England, ab307601, 1:500), GPX4 mouse mAb (BOSTER, China, BA3802-1, 1:500).

Techniques: Inhibition, Staining, Fluorescence, Expressing, Western Blot

Journal: Materials Today Bio

Article Title: Injectable deferoxamine-loaded microsphere hydrogels for inhibition of ferroptosis and promotion of third-degree burn wound healing

doi: 10.1016/j.mtbio.2025.101806

Figure Lengend Snippet: Immunofluorescence staining and quantification of ferroptosis at burn wound sites. (a) Representative fluorescent images of intracellular Fe 2+ accumulation in skin tissues on day 8 post-wounding. (b) Representative fluorescent staining images of ACLS4, SLC7A11 and GPX4 in skin tissues on day 29 post-wounding. (c) Quantitative analysis of intracellular Fe 2+ level in skin tissues on day 8 post-wounding. (d–f) Quantitative analysis of ACLS4, SLC7A11 and GPX4 levels of skin tissues on days 29 post-wounding. ∗p < 0.05, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001, ns means non-significant (p > 0.05).

Article Snippet: Tissue sections were incubated with primary antibodies overnight at 4 °C, including IL-1β mouse mAb (Proteintech, China, 66737-1-Ig, 1:300), Anti-CD31 rabbit mAb (Abcam, England, ab182981, 1:300), VEGFA rabbit pAb (Proteintech, China, 19003-1-ap, 1:500), ferritin light chain rabbit pAb ((Proteintech, China, 10727-1-AP, 1:500), ACSL4 rabbit mAb (Abcam, England, ab155282, 1:500), SLC7A11 rabbit mAb (Abcam, England, ab307601, 1:500), GPX4 mouse mAb (BOSTER, China, BA3802-1, 1:500).

Techniques: Immunofluorescence, Staining

Journal: bioRxiv

Article Title: Pulmonary Mitochondrial DNA Release and Activation of the cGAS-STING Pathway in Lethal Stx12 Knockout Mice

doi: 10.1101/2024.10.07.616980

Figure Lengend Snippet: A. KEGG pathway analysis based on differentially upregulated expressed genes in Stx12 −/− mice (-log 10 (padj) > 5.5) from RNA-seq data. B. The number of neutrophil in the blood from Stx12 −/− and the littermate control (WT, Stx12 +/+ mice. C. The relative mRNA level of neutrophil markers (Ly6g, MPO, ELANE, and CSF3R) and key chemokines for neutrophil recruitment and activation (CSF3, C3, CXCL1, CXCL2, CXCL5, and TNF) normalized to β-actin. WT n = 5, HO n = 5 independent samples. D. IL-1β levels in the lung lysate from Stx12 −/− (n = 8) and the littermate control (WT) mice (n = 6) by enzyme-linked immunosorbent assay. E. Relative mRNA levels of IL-6 from lung of Stx12 −/− (HO) and the littermate control (WT, Stx12 +/+ ) mice. F. The expression of IL-6, S100A9 and GAPDH by western blot in lung lysate from Stx12 −/− (HO) and the littermate control (WT, Stx12 +/+ ) mice. G. Quantification of the levels of IL-6 and S100A9 normalized to GAPDH. H. Heatmap showing upregulated inflammation-related gene including neutrophil-related gene, interleukin, tumor necrosis factor (TNF)-related gene, complement(C) - related gene, colony stimulating factor (CSF)-related gene and chemokines in WT and Stx12 −/− lung tissue. I. The picture of newborn mice after drug intervention. Results are presented as mean ± SEM; statistical significance was assessed by Student’s t-test.

Article Snippet: The primary antibodies used included the following: rabbit anti-STX12 monoclonal antibody (1:1000, Custom-made), mouse anti-β-actin (1:5000; Proteintech, #60008-1-Ig), mouse anti-GAPDH (1:20000, Proteintech, #60004-1-Ig), anti-OXPHOS antibody (1:1000; Abcam, #ab110413), anti-cGAS (1:1000; Cell Signaling Technology, #31659), anti-TBK1(1:1000, Cell Signaling Technology, #3504S), anti-pTBK1(1:1000; Cell Signaling Technology, # 5483S), anti-IRF3(1:1000; Proteintech, #11312-1-AP), anti-pIRF3(1:1000; Cell Signaling Technology, #29047), anti-IL-6 (1:1000; Abcam, #ab229381), anti-S100A9 (1:1000; Boster, #PB0718).

Techniques: RNA Sequencing Assay, Control, Activation Assay, Enzyme-linked Immunosorbent Assay, Expressing, Western Blot

Journal: Molecules

Article Title: Targeting Chondroitin Sulphate Synthase 1 (Chsy1) Promotes Axon Growth Following Neurorrhaphy by Suppressing Versican Accumulation

doi: 10.3390/molecules28093742

Figure Lengend Snippet: Confocal photomicrographs of the distribution of S100 and Chsy1 in regenerating axons at one and three months following ESN. Arrow indicated S100-positive cells. Arrow head indicated distribution of Chsy1.The recipient nerve tissue (distal end of McN) was immunostained with anti-S100 antibody (green) and anti-Chsy1 antibody (red) in the sham operation group ( A – C ), ES1M-saline group ( D – F ), and ES3M-saline group ( G – I ). After labeling the sections, nuclei DNA were counterstained with Hoechst33342 (blue). S100-positive Schwann cell and Chsy1 expression appear in the regenerating axons of ES1M group. Scale bar = 25 μm. Immunoblots ( J ) and histogram ( K ) showing versican V1, Chsy1, and S100 expressions in the nerve tissues of sham-operated and 1- to 3-month ESN rats. β-actin was used as a loading control. Data are present as mean ± SD from three independent experiments. * p < 0.05, compared with the sham operation group. # p < 0.05, compared with the ES1M si-ctrl group.

Article Snippet: After the protein blocking step, the sections were incubated in rabbit polyclonal anti-S100 antibody (1:1000, Taiclone Biotech Corp, Taipei, Taiwan), rabbit polyclonal anti-Chsy1 antibody (1:1000, Origene, Rockville, MD, USA), rabbit polyclonal anti-versicanV 1 antibody (1:500, Invitrogen, ThermoFisher, Waltham, MA, USA), and rabbit polyclonal anti-β3-tubulin antibody (1:1000, Proteintech, Manchester, UK), with the blocking solution for 24 h at 4 °C.

Techniques: Saline, Labeling, Expressing, Western Blot, Control

Journal: Molecules

Article Title: Targeting Chondroitin Sulphate Synthase 1 (Chsy1) Promotes Axon Growth Following Neurorrhaphy by Suppressing Versican Accumulation

doi: 10.3390/molecules28093742

Figure Lengend Snippet: Protein expressions in the recipient nerve tissue one month after the siRNA treatment. ( A ) Western blots showing versican V1 expression and S100, PGP9.5, and β3-tubulin distribution in the sham operation, ES1M si-ctrl, and ES1M si-Chsy1 groups. ( B ) Histogram showing the expression of each protein in the sham-op, ES1M si-ctrl, and ES1M si-Chsy1 groups. β-Actin was used as a loading control. Data are present as mean ± standard deviation from three independent experiments. * p < 0.05, compared to the sham operation group. # p < 0.05, compared to the ES1M si-ctrl group.

Article Snippet: After the protein blocking step, the sections were incubated in rabbit polyclonal anti-S100 antibody (1:1000, Taiclone Biotech Corp, Taipei, Taiwan), rabbit polyclonal anti-Chsy1 antibody (1:1000, Origene, Rockville, MD, USA), rabbit polyclonal anti-versicanV 1 antibody (1:500, Invitrogen, ThermoFisher, Waltham, MA, USA), and rabbit polyclonal anti-β3-tubulin antibody (1:1000, Proteintech, Manchester, UK), with the blocking solution for 24 h at 4 °C.

Techniques: Western Blot, Expressing, Control, Standard Deviation

Journal: Journal of Clinical Pathology

Article Title: Unusual fusion gene rearrangements in patients with nodular fasciitis: a study of rare and novel USP6 fusion partners with a review of the literature

doi: 10.1136/jcp-2023-208768

Figure Lengend Snippet: Patient characteristics and clinical findings in USP6::MYH9 fusion cases

Article Snippet: Thin histological sections (3 μm thick) were used, and each sample was stained using the following antibodies and protocols: anti-smooth muscle actin (SMA) mouse monoclonal antibodies (clone 1A4, BioSB— Bioscience for the World, dilution 1:75; pretreatment: heating up to 99°C in a pH 6 buffer in a water bath); anti-H-caldesmon mouse monoclonal antibodies (clone BSB-19|, BioSB, dilution 1:100; pretreatment: heating up to 99°C in a pH 9 buffer in a water bath); anti-desmin mouse monoclonal antibodies (clone D33, BioSB, dilution 1:100; pretreatment: heating up to 99°C in a pH 9 buffer in a water bath); anti-S100-β rabbit monoclonal antibodies (clone EP32, BioSB, dilution 1:300; pre-treatment: heating up to 99 ◦C in a pH 9 buffer in a water bath); anti-Ki-67 mouse monoclonal antibodies (clone MIB-1, BioSB, dilution 1:150; pretreatment: heating up to 99°C in a pH 6 buffer in a water bath).

Techniques: