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noncontact microarray printer  (SCIENION)


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    SCIENION noncontact microarray printer
    <t>Microarray</t> analysis reveals the effects of GFAP mAb treatment on key inflammatory mediators in glaucomatous retina. ( A - C ) The expression of TLR4 and S100A8 was significantly downregulated by 25–50 µg GFAP mAb treatment compared to the vehicle. The marker for microglial activation, CD68, was significantly decreased in the 25 µg GFAP mAb treatment group. ( D - F ) Proteins of the inflammasome pathway, NLRP3, GSDMD and Caspase-1 were significantly downregulated in the 25 µg GFAP mAb treatment group. With the 50 µg dose, these protein expressions showed a similar downward trend, but without statistical significance. ( G ) Expression profiling of inflammation-associated mediators showed that 25 µg GFAP mAb significantly decreased pro-inflammatory factors (TNF-α, IL-1β, IL-8, MMP9, and IFN-γ), and increased the anti-inflammatory cytokine IL-10 compared to the vehicle group. In contrast, the 50 µg dose significantly reduced IFN-γ only. ( H ) Representative images of spots showing IL-1β levels in the subarrays for each group. Image analysis was conducted with Imagene software, using the median intensity from each spot to calculate the mean of the triplicate spots for each marker. For CD68 and TLR4, due to significant heterogeneity in SDs, statistical analysis was performed using Welch’s ANOVA followed by the Tamhane T2 post hoc test. All other data were analyzed using one-way ANOVA with Tukey’s post hoc test. Data are presented as the mean ± SD; n = 4 per group; * p < 0.05, ** p < 0.01, *** p < 0.001; ns = not significant. TLR4 – Toll-Like Receptor 4. S100A8 – S100 Calcium Binding Protein A8. NLRP3 – NLR Family Pyrin Domain Containing 3. GSDMD – Gasdermin D
    Noncontact Microarray Printer, supplied by SCIENION, used in various techniques. Bioz Stars score: 96/100, based on 308 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/noncontact microarray printer/product/SCIENION
    Average 96 stars, based on 308 article reviews
    noncontact microarray printer - by Bioz Stars, 2026-04
    96/100 stars

    Images

    1) Product Images from "Targeting glial fibrillary acidic protein in glaucoma: a monoclonal antibody approach to modulate glial reactivity and neuroinflammation for neuroprotection"

    Article Title: Targeting glial fibrillary acidic protein in glaucoma: a monoclonal antibody approach to modulate glial reactivity and neuroinflammation for neuroprotection

    Journal: Journal of Neuroinflammation

    doi: 10.1186/s12974-025-03482-8

    Microarray analysis reveals the effects of GFAP mAb treatment on key inflammatory mediators in glaucomatous retina. ( A - C ) The expression of TLR4 and S100A8 was significantly downregulated by 25–50 µg GFAP mAb treatment compared to the vehicle. The marker for microglial activation, CD68, was significantly decreased in the 25 µg GFAP mAb treatment group. ( D - F ) Proteins of the inflammasome pathway, NLRP3, GSDMD and Caspase-1 were significantly downregulated in the 25 µg GFAP mAb treatment group. With the 50 µg dose, these protein expressions showed a similar downward trend, but without statistical significance. ( G ) Expression profiling of inflammation-associated mediators showed that 25 µg GFAP mAb significantly decreased pro-inflammatory factors (TNF-α, IL-1β, IL-8, MMP9, and IFN-γ), and increased the anti-inflammatory cytokine IL-10 compared to the vehicle group. In contrast, the 50 µg dose significantly reduced IFN-γ only. ( H ) Representative images of spots showing IL-1β levels in the subarrays for each group. Image analysis was conducted with Imagene software, using the median intensity from each spot to calculate the mean of the triplicate spots for each marker. For CD68 and TLR4, due to significant heterogeneity in SDs, statistical analysis was performed using Welch’s ANOVA followed by the Tamhane T2 post hoc test. All other data were analyzed using one-way ANOVA with Tukey’s post hoc test. Data are presented as the mean ± SD; n = 4 per group; * p < 0.05, ** p < 0.01, *** p < 0.001; ns = not significant. TLR4 – Toll-Like Receptor 4. S100A8 – S100 Calcium Binding Protein A8. NLRP3 – NLR Family Pyrin Domain Containing 3. GSDMD – Gasdermin D
    Figure Legend Snippet: Microarray analysis reveals the effects of GFAP mAb treatment on key inflammatory mediators in glaucomatous retina. ( A - C ) The expression of TLR4 and S100A8 was significantly downregulated by 25–50 µg GFAP mAb treatment compared to the vehicle. The marker for microglial activation, CD68, was significantly decreased in the 25 µg GFAP mAb treatment group. ( D - F ) Proteins of the inflammasome pathway, NLRP3, GSDMD and Caspase-1 were significantly downregulated in the 25 µg GFAP mAb treatment group. With the 50 µg dose, these protein expressions showed a similar downward trend, but without statistical significance. ( G ) Expression profiling of inflammation-associated mediators showed that 25 µg GFAP mAb significantly decreased pro-inflammatory factors (TNF-α, IL-1β, IL-8, MMP9, and IFN-γ), and increased the anti-inflammatory cytokine IL-10 compared to the vehicle group. In contrast, the 50 µg dose significantly reduced IFN-γ only. ( H ) Representative images of spots showing IL-1β levels in the subarrays for each group. Image analysis was conducted with Imagene software, using the median intensity from each spot to calculate the mean of the triplicate spots for each marker. For CD68 and TLR4, due to significant heterogeneity in SDs, statistical analysis was performed using Welch’s ANOVA followed by the Tamhane T2 post hoc test. All other data were analyzed using one-way ANOVA with Tukey’s post hoc test. Data are presented as the mean ± SD; n = 4 per group; * p < 0.05, ** p < 0.01, *** p < 0.001; ns = not significant. TLR4 – Toll-Like Receptor 4. S100A8 – S100 Calcium Binding Protein A8. NLRP3 – NLR Family Pyrin Domain Containing 3. GSDMD – Gasdermin D

    Techniques Used: Microarray, Expressing, Marker, Activation Assay, Software, Binding Assay



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    Image Search Results


    Microarray analysis reveals the effects of GFAP mAb treatment on key inflammatory mediators in glaucomatous retina. ( A - C ) The expression of TLR4 and S100A8 was significantly downregulated by 25–50 µg GFAP mAb treatment compared to the vehicle. The marker for microglial activation, CD68, was significantly decreased in the 25 µg GFAP mAb treatment group. ( D - F ) Proteins of the inflammasome pathway, NLRP3, GSDMD and Caspase-1 were significantly downregulated in the 25 µg GFAP mAb treatment group. With the 50 µg dose, these protein expressions showed a similar downward trend, but without statistical significance. ( G ) Expression profiling of inflammation-associated mediators showed that 25 µg GFAP mAb significantly decreased pro-inflammatory factors (TNF-α, IL-1β, IL-8, MMP9, and IFN-γ), and increased the anti-inflammatory cytokine IL-10 compared to the vehicle group. In contrast, the 50 µg dose significantly reduced IFN-γ only. ( H ) Representative images of spots showing IL-1β levels in the subarrays for each group. Image analysis was conducted with Imagene software, using the median intensity from each spot to calculate the mean of the triplicate spots for each marker. For CD68 and TLR4, due to significant heterogeneity in SDs, statistical analysis was performed using Welch’s ANOVA followed by the Tamhane T2 post hoc test. All other data were analyzed using one-way ANOVA with Tukey’s post hoc test. Data are presented as the mean ± SD; n = 4 per group; * p < 0.05, ** p < 0.01, *** p < 0.001; ns = not significant. TLR4 – Toll-Like Receptor 4. S100A8 – S100 Calcium Binding Protein A8. NLRP3 – NLR Family Pyrin Domain Containing 3. GSDMD – Gasdermin D

    Journal: Journal of Neuroinflammation

    Article Title: Targeting glial fibrillary acidic protein in glaucoma: a monoclonal antibody approach to modulate glial reactivity and neuroinflammation for neuroprotection

    doi: 10.1186/s12974-025-03482-8

    Figure Lengend Snippet: Microarray analysis reveals the effects of GFAP mAb treatment on key inflammatory mediators in glaucomatous retina. ( A - C ) The expression of TLR4 and S100A8 was significantly downregulated by 25–50 µg GFAP mAb treatment compared to the vehicle. The marker for microglial activation, CD68, was significantly decreased in the 25 µg GFAP mAb treatment group. ( D - F ) Proteins of the inflammasome pathway, NLRP3, GSDMD and Caspase-1 were significantly downregulated in the 25 µg GFAP mAb treatment group. With the 50 µg dose, these protein expressions showed a similar downward trend, but without statistical significance. ( G ) Expression profiling of inflammation-associated mediators showed that 25 µg GFAP mAb significantly decreased pro-inflammatory factors (TNF-α, IL-1β, IL-8, MMP9, and IFN-γ), and increased the anti-inflammatory cytokine IL-10 compared to the vehicle group. In contrast, the 50 µg dose significantly reduced IFN-γ only. ( H ) Representative images of spots showing IL-1β levels in the subarrays for each group. Image analysis was conducted with Imagene software, using the median intensity from each spot to calculate the mean of the triplicate spots for each marker. For CD68 and TLR4, due to significant heterogeneity in SDs, statistical analysis was performed using Welch’s ANOVA followed by the Tamhane T2 post hoc test. All other data were analyzed using one-way ANOVA with Tukey’s post hoc test. Data are presented as the mean ± SD; n = 4 per group; * p < 0.05, ** p < 0.01, *** p < 0.001; ns = not significant. TLR4 – Toll-Like Receptor 4. S100A8 – S100 Calcium Binding Protein A8. NLRP3 – NLR Family Pyrin Domain Containing 3. GSDMD – Gasdermin D

    Article Snippet: Briefly, the microarray was prepared using a noncontact microarray printer (SciFLEXARRAYER S3; Scienion, Berlin, Germany).

    Techniques: Microarray, Expressing, Marker, Activation Assay, Software, Binding Assay

    Probing receptor binding specificities of A(H3N2) and A(H1N1)pdm09. a) Collection of glycans printed on succinimide reactive microarray slides. Glycan binding data of b) early A(H3N2) and A(H3N2) 3C.2 viruses; c) A (H3N2) 3C.3 viruses; and d) A(H1N1)pdm09 viruses. Whole viruses were exposed to a glycan microarray, and binding was visualized antistalk antibodies. Bars represent the average relative fluorescence units (RFU) of four replicates ± SD.

    Journal: JACS Au

    Article Title: Asymmetrical Biantennary Glycans Prepared by a Stop-and-Go Strategy Reveal Receptor Binding Evolution of Human Influenza A Viruses

    doi: 10.1021/jacsau.3c00695

    Figure Lengend Snippet: Probing receptor binding specificities of A(H3N2) and A(H1N1)pdm09. a) Collection of glycans printed on succinimide reactive microarray slides. Glycan binding data of b) early A(H3N2) and A(H3N2) 3C.2 viruses; c) A (H3N2) 3C.3 viruses; and d) A(H1N1)pdm09 viruses. Whole viruses were exposed to a glycan microarray, and binding was visualized antistalk antibodies. Bars represent the average relative fluorescence units (RFU) of four replicates ± SD.

    Article Snippet: The glycans, which have an α-amine at the anomeric asparagine moiety, were printed on amine reactive NHS activated glass slides using a noncontact microarray printer ( S3 , Scienion, Inc.).

    Techniques: Binding Assay, Microarray, Glycoproteomics, Fluorescence