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Characterization, and Cytocompatibility Validation of HCOC. (A) Schematic illustration of the development of HCOC. (B) FTIR spectrum of OSA, CMCS and OC hydrogel. (C) Time-dependent evolution of gelation of OC and HCOC. (D) SEM images of HCOC and EDS mapping images of C, N, O and Cu for HCOC. (E) FTIR spectra of HC, OC and HCOC. (F) Dynamic frequency sweep measurements of OC and HCOC. (G) Frequency-dependent viscoelastic behavior of OC and HCOC. (H) Alternating strain sweep with alternating strains of 1% and 1000% at 100s intervals and (I) Self-healing behavior of HCOC. <t>(J)</t> <t>Live/dead</t> staining showing the metabolic activity of L929 and RAW 264.7 cells after treatment with HCOC for 48 h. Rates of proliferation of (K) L929 cells and (L) RAW 264.7 cells after treatment with PBS or HCOC. (∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001).
Dmao Pi Bacterial Live, supplied by Beyotime, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Characterization, and Cytocompatibility Validation of HCOC. (A) Schematic illustration of the development of HCOC. (B) FTIR spectrum of OSA, CMCS and OC hydrogel. (C) Time-dependent evolution of gelation of OC and HCOC. (D) SEM images of HCOC and EDS mapping images of C, N, O and Cu for HCOC. (E) FTIR spectra of HC, OC and HCOC. (F) Dynamic frequency sweep measurements of OC and HCOC. (G) Frequency-dependent viscoelastic behavior of OC and HCOC. (H) Alternating strain sweep with alternating strains of 1% and 1000% at 100s intervals and (I) Self-healing behavior of HCOC. <t>(J)</t> <t>Live/dead</t> staining showing the metabolic activity of L929 and RAW 264.7 cells after treatment with HCOC for 48 h. Rates of proliferation of (K) L929 cells and (L) RAW 264.7 cells after treatment with PBS or HCOC. (∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001).
Live Dead Bacterial Staining Kit, supplied by Beyotime, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Characterization, and Cytocompatibility Validation of HCOC. (A) Schematic illustration of the development of HCOC. (B) FTIR spectrum of OSA, CMCS and OC hydrogel. (C) Time-dependent evolution of gelation of OC and HCOC. (D) SEM images of HCOC and EDS mapping images of C, N, O and Cu for HCOC. (E) FTIR spectra of HC, OC and HCOC. (F) Dynamic frequency sweep measurements of OC and HCOC. (G) Frequency-dependent viscoelastic behavior of OC and HCOC. (H) Alternating strain sweep with alternating strains of 1% and 1000% at 100s intervals and (I) Self-healing behavior of HCOC. <t>(J)</t> <t>Live/dead</t> staining showing the metabolic activity of L929 and RAW 264.7 cells after treatment with HCOC for 48 h. Rates of proliferation of (K) L929 cells and (L) RAW 264.7 cells after treatment with PBS or HCOC. (∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001).
E Click Edu Cell Proliferation Imaging Assay Kit, supplied by Guangzhou JET Bio-Filtration, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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(A) Timeline for tumor injection and drug treatments. Tumor cells were injected on d0. (B) Tumor growth in individual mice treated with DNMTi (RG108) alone, ICI (anti-CTLA4) alone, or dual therapy (ICI+DNMTi). (C) Overall survival of mice receiving ICI (anti-CTLA4), DNMT1i (RG108 or GSK32), or ICI+DNMT1i (RG108 or GSK32) (log-rank Mantel Cox test). (D) UMAP reduction of identified clusters from 4 treatment groups (DNMTi alone (RG108), ICI (anti-CTLA4) alone, dual therapy, and control) with 3 mice per condition and 2 tissues (tdLN and tumor) from each mouse. (E) UMAP reduction of total CD8+ T cells from tdLN from all 4 treatment groups. (F) Dot plot showing expression of key markers defining each CD8 cluster. (G) UMAP reduction of total CD8+ T cells from tdLN from all 4 treatment groups using Monocle3 for trajectory analysis and (H) trajectory analysis colored by pseudotime. (I) Pseudobulk quantification of the proportion of CD8⁺ T cells in the naïve-like cluster (left) and T PEX cluster (right) (n=3).
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Yeasen Biotechnology live dead staining
In vitro and in vivo antibacterial efficacy of the therapeutic platform. (A) Photographs of S. aureus colonies after various treatments in vitro (scale bars: 30 mm). (B) Crystal violet-stained images of S. aureus biofilms (scale bars: 3 mm). (C-D) Quantitative analysis of S. aureus colonies (C) and biofilm staining (D) ( n = 3). (E) <t>Representative</t> <t>live/dead</t> staining images of S. aureus biofilms (scale bars: 400 μm). (F) SEM images of representative S. aureus morphology (scale bars: 2 μm). (G) Schematic illustration of the in vivo antibacterial process of the therapeutic platform. (H) Images of S. aureus colonies from infected wounds treated with different groups formulations combined with external stimuli (scale bars: 30 mm). (I) Photographs of infected wounds during healing and corresponding wound area diagrams (scale bars: 5 mm). (J) Wound closure rates of rats in various treatment groups over time ( n = 3). (K) Representative H&E and Masson's trichrome staining of wound tissues at day 9 post-treatment (scale bars: top-2 mm, mid-500 μm, and bot-500 μm). (L) Schematic diagram of the acoustic-photothermal-enhanced antibacterial mechanism. Data are expressed as the mean ± SD; ∗ P < 0.05, ∗∗∗ P < 0.001.
Live Dead Staining, supplied by Yeasen Biotechnology, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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In vitro and in vivo antibacterial efficacy of the therapeutic platform. (A) Photographs of S. aureus colonies after various treatments in vitro (scale bars: 30 mm). (B) Crystal violet-stained images of S. aureus biofilms (scale bars: 3 mm). (C-D) Quantitative analysis of S. aureus colonies (C) and biofilm staining (D) ( n = 3). (E) <t>Representative</t> <t>live/dead</t> staining images of S. aureus biofilms (scale bars: 400 μm). (F) SEM images of representative S. aureus morphology (scale bars: 2 μm). (G) Schematic illustration of the in vivo antibacterial process of the therapeutic platform. (H) Images of S. aureus colonies from infected wounds treated with different groups formulations combined with external stimuli (scale bars: 30 mm). (I) Photographs of infected wounds during healing and corresponding wound area diagrams (scale bars: 5 mm). (J) Wound closure rates of rats in various treatment groups over time ( n = 3). (K) Representative H&E and Masson's trichrome staining of wound tissues at day 9 post-treatment (scale bars: top-2 mm, mid-500 μm, and bot-500 μm). (L) Schematic diagram of the acoustic-photothermal-enhanced antibacterial mechanism. Data are expressed as the mean ± SD; ∗ P < 0.05, ∗∗∗ P < 0.001.
Live Dead Cell Staining Kit, supplied by Keygen Biotech, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Fisher Scientific live dead viability cytotoxicity kit
Cell-scaffold interaction <t>(A)</t> <t>Live/Dead</t> staining of L-929 fibroblast cultures after 3 and 7 days in 2D conditions and on top of RTU scaffolds rehydrated with PBS and PRGF, respectively (scale bars, 100 μm). Biocompatibility assessment following ISO 10993 standards, evaluated by both direct contact (B) and extract-based (C) assays on L-929 fibroblasts. Cell adhesion and proliferation: SEM imaging and quantification of HDF fibroblast adhesion 24 h post-seeding on the scaffolds (D), followed by proliferation assessment after 72 h (E). Statistical significance is indicated as follows: not significant (ns); ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.
Live Dead Viability Cytotoxicity Kit, supplied by Fisher Scientific, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Cell-scaffold interaction <t>(A)</t> <t>Live/Dead</t> staining of L-929 fibroblast cultures after 3 and 7 days in 2D conditions and on top of RTU scaffolds rehydrated with PBS and PRGF, respectively (scale bars, 100 μm). Biocompatibility assessment following ISO 10993 standards, evaluated by both direct contact (B) and extract-based (C) assays on L-929 fibroblasts. Cell adhesion and proliferation: SEM imaging and quantification of HDF fibroblast adhesion 24 h post-seeding on the scaffolds (D), followed by proliferation assessment after 72 h (E). Statistical significance is indicated as follows: not significant (ns); ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.
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Cell-scaffold interaction <t>(A)</t> <t>Live/Dead</t> staining of L-929 fibroblast cultures after 3 and 7 days in 2D conditions and on top of RTU scaffolds rehydrated with PBS and PRGF, respectively (scale bars, 100 μm). Biocompatibility assessment following ISO 10993 standards, evaluated by both direct contact (B) and extract-based (C) assays on L-929 fibroblasts. Cell adhesion and proliferation: SEM imaging and quantification of HDF fibroblast adhesion 24 h post-seeding on the scaffolds (D), followed by proliferation assessment after 72 h (E). Statistical significance is indicated as follows: not significant (ns); ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.
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Image Search Results


Characterization, and Cytocompatibility Validation of HCOC. (A) Schematic illustration of the development of HCOC. (B) FTIR spectrum of OSA, CMCS and OC hydrogel. (C) Time-dependent evolution of gelation of OC and HCOC. (D) SEM images of HCOC and EDS mapping images of C, N, O and Cu for HCOC. (E) FTIR spectra of HC, OC and HCOC. (F) Dynamic frequency sweep measurements of OC and HCOC. (G) Frequency-dependent viscoelastic behavior of OC and HCOC. (H) Alternating strain sweep with alternating strains of 1% and 1000% at 100s intervals and (I) Self-healing behavior of HCOC. (J) Live/dead staining showing the metabolic activity of L929 and RAW 264.7 cells after treatment with HCOC for 48 h. Rates of proliferation of (K) L929 cells and (L) RAW 264.7 cells after treatment with PBS or HCOC. (∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001).

Journal: Bioactive Materials

Article Title: Smart microenvironment-adaptive nanocatalytic hydrogel for sequential antibacterial, anti-inflammatory, and regenerative therapy of biofilm-infected wounds

doi: 10.1016/j.bioactmat.2026.02.043

Figure Lengend Snippet: Characterization, and Cytocompatibility Validation of HCOC. (A) Schematic illustration of the development of HCOC. (B) FTIR spectrum of OSA, CMCS and OC hydrogel. (C) Time-dependent evolution of gelation of OC and HCOC. (D) SEM images of HCOC and EDS mapping images of C, N, O and Cu for HCOC. (E) FTIR spectra of HC, OC and HCOC. (F) Dynamic frequency sweep measurements of OC and HCOC. (G) Frequency-dependent viscoelastic behavior of OC and HCOC. (H) Alternating strain sweep with alternating strains of 1% and 1000% at 100s intervals and (I) Self-healing behavior of HCOC. (J) Live/dead staining showing the metabolic activity of L929 and RAW 264.7 cells after treatment with HCOC for 48 h. Rates of proliferation of (K) L929 cells and (L) RAW 264.7 cells after treatment with PBS or HCOC. (∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001).

Article Snippet: Following the protocol of the DMAO/PI Bacterial Live/Dead Staining Kit (Beyotime Biotechnology), the bacteria were incubated with a working solution containing both DMAO and PI dyes in the dark at room temperature for 15-20 min. Fluorescence microscopy imaging was subsequently carried out.

Techniques: Biomarker Discovery, Staining, Activity Assay

pH Self-Adaptive Antioxidant Capacity of HCOC (Stage II: anti-inflammation). Cu ion release behavior of (A) HC (1 mg/mL) and (B) HCOC (1 mg/mL) at different pH levels. (C) ABTS + and (D) H 2 O 2 scavenging activity at different pH of Cu 5.4 O, HC and HCOC. (E) O 2 ∙ - , (F)∙OH scavenging activity of Cu 5.4 O, HAs, HC, HCOC. (G) SOD-like, (H) CAT-like and (I) GPx-like activities of HCOC. (J) Fluorescence images showing intracellular ROS detection by DCFH-DA staining, live/dead staining images and (K) cell viability of L929 cells with different treatments (All groups received 500 μM H 2 O 2 and different HCOC concentrations (I: PBS; II: 0; III: 0.25; IV: 0.50; V: 1.0 mg/mL HCOC). (L) Quantitative analysis of the cells under different treatments. (∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗∗∗P < 0.0001) (M) Schematic illustration of pH-responsive activity and ROS scavenging and alleviating cellular oxidative stress of HCOC.

Journal: Bioactive Materials

Article Title: Smart microenvironment-adaptive nanocatalytic hydrogel for sequential antibacterial, anti-inflammatory, and regenerative therapy of biofilm-infected wounds

doi: 10.1016/j.bioactmat.2026.02.043

Figure Lengend Snippet: pH Self-Adaptive Antioxidant Capacity of HCOC (Stage II: anti-inflammation). Cu ion release behavior of (A) HC (1 mg/mL) and (B) HCOC (1 mg/mL) at different pH levels. (C) ABTS + and (D) H 2 O 2 scavenging activity at different pH of Cu 5.4 O, HC and HCOC. (E) O 2 ∙ - , (F)∙OH scavenging activity of Cu 5.4 O, HAs, HC, HCOC. (G) SOD-like, (H) CAT-like and (I) GPx-like activities of HCOC. (J) Fluorescence images showing intracellular ROS detection by DCFH-DA staining, live/dead staining images and (K) cell viability of L929 cells with different treatments (All groups received 500 μM H 2 O 2 and different HCOC concentrations (I: PBS; II: 0; III: 0.25; IV: 0.50; V: 1.0 mg/mL HCOC). (L) Quantitative analysis of the cells under different treatments. (∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗∗∗P < 0.0001) (M) Schematic illustration of pH-responsive activity and ROS scavenging and alleviating cellular oxidative stress of HCOC.

Article Snippet: Following the protocol of the DMAO/PI Bacterial Live/Dead Staining Kit (Beyotime Biotechnology), the bacteria were incubated with a working solution containing both DMAO and PI dyes in the dark at room temperature for 15-20 min. Fluorescence microscopy imaging was subsequently carried out.

Techniques: Activity Assay, Fluorescence, Staining

(A) Timeline for tumor injection and drug treatments. Tumor cells were injected on d0. (B) Tumor growth in individual mice treated with DNMTi (RG108) alone, ICI (anti-CTLA4) alone, or dual therapy (ICI+DNMTi). (C) Overall survival of mice receiving ICI (anti-CTLA4), DNMT1i (RG108 or GSK32), or ICI+DNMT1i (RG108 or GSK32) (log-rank Mantel Cox test). (D) UMAP reduction of identified clusters from 4 treatment groups (DNMTi alone (RG108), ICI (anti-CTLA4) alone, dual therapy, and control) with 3 mice per condition and 2 tissues (tdLN and tumor) from each mouse. (E) UMAP reduction of total CD8+ T cells from tdLN from all 4 treatment groups. (F) Dot plot showing expression of key markers defining each CD8 cluster. (G) UMAP reduction of total CD8+ T cells from tdLN from all 4 treatment groups using Monocle3 for trajectory analysis and (H) trajectory analysis colored by pseudotime. (I) Pseudobulk quantification of the proportion of CD8⁺ T cells in the naïve-like cluster (left) and T PEX cluster (right) (n=3).

Journal: bioRxiv

Article Title: Targeting DNMT1 augments anti-tumor CD8⁺ T cell function

doi: 10.64898/2026.07.03.736412

Figure Lengend Snippet: (A) Timeline for tumor injection and drug treatments. Tumor cells were injected on d0. (B) Tumor growth in individual mice treated with DNMTi (RG108) alone, ICI (anti-CTLA4) alone, or dual therapy (ICI+DNMTi). (C) Overall survival of mice receiving ICI (anti-CTLA4), DNMT1i (RG108 or GSK32), or ICI+DNMT1i (RG108 or GSK32) (log-rank Mantel Cox test). (D) UMAP reduction of identified clusters from 4 treatment groups (DNMTi alone (RG108), ICI (anti-CTLA4) alone, dual therapy, and control) with 3 mice per condition and 2 tissues (tdLN and tumor) from each mouse. (E) UMAP reduction of total CD8+ T cells from tdLN from all 4 treatment groups. (F) Dot plot showing expression of key markers defining each CD8 cluster. (G) UMAP reduction of total CD8+ T cells from tdLN from all 4 treatment groups using Monocle3 for trajectory analysis and (H) trajectory analysis colored by pseudotime. (I) Pseudobulk quantification of the proportion of CD8⁺ T cells in the naïve-like cluster (left) and T PEX cluster (right) (n=3).

Article Snippet: On day 7, live CD8+ T cells were enriched using a dead-cell removal kit (Miltenyi) and added to tumor cells at a 1:10 T-cell:tumor ratio.

Techniques: Injection, Control, Expressing

(A) Schematic of in vitro primary P14 CD8+ T cell culture model. (B) Schematic describing abbreviated nomenclature for in vitro cell states (T M , T EX , T EX+D , T M* , T EX* , T EX+D* ). (C) P14 CD8⁺ T cells were isolated on d7 of culture and restimulated with gp33 peptide for flow cytometry analysis of IFNγ and TNFα production (left) or co-cultured with gp33-expressing mouse melanoma line YUMM-G1-gp33 to assess tumor cell killing (right) by flow cytometry (n=3). (D) Chronic stimulation promotes proliferation of CD8+ T cells as shown by CellTrace Violet dilution (left) and quantified as proportion of cells in each generation (right) (n=3). (E-F) Violin plots showing differentially expressed genes between T EX+D and T EX (E) and between T EX+D* and T EX* (F) with RG108 (left) or with GSK32 (right). An adjusted p-value cutoff of 0.05 and log2FC cutoff of 0.5 were used. (G) UMAP depicting clusters obtained using PhenoGraph for concatenated samples (top left) and density plots for TEX* (top right), TEX+D* (GSK-32) (bottom left), and TEX+D* (RG108). (H) Proportion of live, CD45+ cells in MC4 (left) and MC14 (right) across samples. (I) Heatmap representing the relative expression of markers across clusters. (J) Schematic showing consensus nonnegative matrix factorization (cNMF) matrices. (K) Gene by program matrix from cNMF showing loadings for genes in the top 150 ranked gene list for each module. (L) Comparison of T EX vs T EX+D usage of Program S (left) and Program E1(right). (M) Comparison of T EX vs T EX+D usage of Program E2 (left) and Program E3 (right). (N) Comparison of T EX* vs T EX+D* usage of Program E1 (left) and Program E3 (right).

Journal: bioRxiv

Article Title: Targeting DNMT1 augments anti-tumor CD8⁺ T cell function

doi: 10.64898/2026.07.03.736412

Figure Lengend Snippet: (A) Schematic of in vitro primary P14 CD8+ T cell culture model. (B) Schematic describing abbreviated nomenclature for in vitro cell states (T M , T EX , T EX+D , T M* , T EX* , T EX+D* ). (C) P14 CD8⁺ T cells were isolated on d7 of culture and restimulated with gp33 peptide for flow cytometry analysis of IFNγ and TNFα production (left) or co-cultured with gp33-expressing mouse melanoma line YUMM-G1-gp33 to assess tumor cell killing (right) by flow cytometry (n=3). (D) Chronic stimulation promotes proliferation of CD8+ T cells as shown by CellTrace Violet dilution (left) and quantified as proportion of cells in each generation (right) (n=3). (E-F) Violin plots showing differentially expressed genes between T EX+D and T EX (E) and between T EX+D* and T EX* (F) with RG108 (left) or with GSK32 (right). An adjusted p-value cutoff of 0.05 and log2FC cutoff of 0.5 were used. (G) UMAP depicting clusters obtained using PhenoGraph for concatenated samples (top left) and density plots for TEX* (top right), TEX+D* (GSK-32) (bottom left), and TEX+D* (RG108). (H) Proportion of live, CD45+ cells in MC4 (left) and MC14 (right) across samples. (I) Heatmap representing the relative expression of markers across clusters. (J) Schematic showing consensus nonnegative matrix factorization (cNMF) matrices. (K) Gene by program matrix from cNMF showing loadings for genes in the top 150 ranked gene list for each module. (L) Comparison of T EX vs T EX+D usage of Program S (left) and Program E1(right). (M) Comparison of T EX vs T EX+D usage of Program E2 (left) and Program E3 (right). (N) Comparison of T EX* vs T EX+D* usage of Program E1 (left) and Program E3 (right).

Article Snippet: On day 7, live CD8+ T cells were enriched using a dead-cell removal kit (Miltenyi) and added to tumor cells at a 1:10 T-cell:tumor ratio.

Techniques: In Vitro, Cell Culture, Isolation, Flow Cytometry, Expressing, Comparison

In vitro and in vivo antibacterial efficacy of the therapeutic platform. (A) Photographs of S. aureus colonies after various treatments in vitro (scale bars: 30 mm). (B) Crystal violet-stained images of S. aureus biofilms (scale bars: 3 mm). (C-D) Quantitative analysis of S. aureus colonies (C) and biofilm staining (D) ( n = 3). (E) Representative live/dead staining images of S. aureus biofilms (scale bars: 400 μm). (F) SEM images of representative S. aureus morphology (scale bars: 2 μm). (G) Schematic illustration of the in vivo antibacterial process of the therapeutic platform. (H) Images of S. aureus colonies from infected wounds treated with different groups formulations combined with external stimuli (scale bars: 30 mm). (I) Photographs of infected wounds during healing and corresponding wound area diagrams (scale bars: 5 mm). (J) Wound closure rates of rats in various treatment groups over time ( n = 3). (K) Representative H&E and Masson's trichrome staining of wound tissues at day 9 post-treatment (scale bars: top-2 mm, mid-500 μm, and bot-500 μm). (L) Schematic diagram of the acoustic-photothermal-enhanced antibacterial mechanism. Data are expressed as the mean ± SD; ∗ P < 0.05, ∗∗∗ P < 0.001.

Journal: Bioactive Materials

Article Title: A multimodal ROS logic-gated therapeutic platform disrupts the vicious cycle of senescence to promote aged bone defect repair

doi: 10.1016/j.bioactmat.2026.02.002

Figure Lengend Snippet: In vitro and in vivo antibacterial efficacy of the therapeutic platform. (A) Photographs of S. aureus colonies after various treatments in vitro (scale bars: 30 mm). (B) Crystal violet-stained images of S. aureus biofilms (scale bars: 3 mm). (C-D) Quantitative analysis of S. aureus colonies (C) and biofilm staining (D) ( n = 3). (E) Representative live/dead staining images of S. aureus biofilms (scale bars: 400 μm). (F) SEM images of representative S. aureus morphology (scale bars: 2 μm). (G) Schematic illustration of the in vivo antibacterial process of the therapeutic platform. (H) Images of S. aureus colonies from infected wounds treated with different groups formulations combined with external stimuli (scale bars: 30 mm). (I) Photographs of infected wounds during healing and corresponding wound area diagrams (scale bars: 5 mm). (J) Wound closure rates of rats in various treatment groups over time ( n = 3). (K) Representative H&E and Masson's trichrome staining of wound tissues at day 9 post-treatment (scale bars: top-2 mm, mid-500 μm, and bot-500 μm). (L) Schematic diagram of the acoustic-photothermal-enhanced antibacterial mechanism. Data are expressed as the mean ± SD; ∗ P < 0.05, ∗∗∗ P < 0.001.

Article Snippet: Live/dead staining (40747ES76) was purchased by Yeasen Biotechnology Co., Ltd (Shanghai, China).

Techniques: In Vitro, In Vivo, Staining, Infection

Cell-scaffold interaction (A) Live/Dead staining of L-929 fibroblast cultures after 3 and 7 days in 2D conditions and on top of RTU scaffolds rehydrated with PBS and PRGF, respectively (scale bars, 100 μm). Biocompatibility assessment following ISO 10993 standards, evaluated by both direct contact (B) and extract-based (C) assays on L-929 fibroblasts. Cell adhesion and proliferation: SEM imaging and quantification of HDF fibroblast adhesion 24 h post-seeding on the scaffolds (D), followed by proliferation assessment after 72 h (E). Statistical significance is indicated as follows: not significant (ns); ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.

Journal: iScience

Article Title: Ready-to-use 3D bioprinted scaffolds from natural materials loaded with patient’s PRGF for personalized skin regeneration

doi: 10.1016/j.isci.2026.116185

Figure Lengend Snippet: Cell-scaffold interaction (A) Live/Dead staining of L-929 fibroblast cultures after 3 and 7 days in 2D conditions and on top of RTU scaffolds rehydrated with PBS and PRGF, respectively (scale bars, 100 μm). Biocompatibility assessment following ISO 10993 standards, evaluated by both direct contact (B) and extract-based (C) assays on L-929 fibroblasts. Cell adhesion and proliferation: SEM imaging and quantification of HDF fibroblast adhesion 24 h post-seeding on the scaffolds (D), followed by proliferation assessment after 72 h (E). Statistical significance is indicated as follows: not significant (ns); ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.

Article Snippet: LIVE/DEAD® viability/cytotoxicity kit , Fisher Scientific , Cat# L3224.

Techniques: Staining, Imaging