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elisa kits for pge2  (Elabscience Biotechnology)


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    Structured Review

    Elabscience Biotechnology elisa kits for pge2
    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, <t>PGE2,</t> 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.
    Elisa Kits For Pge2, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 280 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Mesenchymal stromal cells-loaded 3D radially aligned composite scaffold with potentiated paracrine signaling for sequential bone regeneration"

    Article Title: Mesenchymal stromal cells-loaded 3D radially aligned composite scaffold with potentiated paracrine signaling for sequential bone regeneration

    Journal: Bioactive Materials

    doi: 10.1016/j.bioactmat.2026.02.059

    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.
    Figure Legend 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.

    Techniques Used: Confocal Microscopy, Fluorescence, Staining, Cell Culture, Expressing



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    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, <t>PGE2,</t> 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.
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    A, Basal <t>PGE</t> <t>2</t> quantified in NSCLC PDE supernatants (pg/mL), shown as a heatmap illustrating inter-lesion variability. B, Correlation between basal PGE 2 and MSLN-BiTE-induced CD8+ T cell activation in NSCLC PDEs, expressed as FC in CD8 + CD137 + frequencies relative to UT CTRL (Holm-corrected P value shown). C, Correlation between basal PGE 2 and MSLN-BiTE-induced granzyme B release in NSCLC PDEs, expressed as log2 FC relative to UT CTRL per patient (r and P value shown). D, COX blockade rescue experiment in two NSCLC cases (Lung 31 and Lung 33): PDEs were pretreated with ketorolac (COXi, 1 µM) for 1 h prior to co-culture with MSLN-BiTE T cells, and CD8 + CD137 + activation together with granzyme B, CXCL9, and CXCL10 were quantified as FC over UT CTRL. E, Pharmacodynamic verification of prostanoid pathway inhibition in the HGSOC validation cohort (n = 11), showing PGE 2 levels at baseline and after COXi (ketorolac, 1 µM) or EP2/EP4 inhibition (EP2/4i, 1 µM). F, CD8 + T cell activation in HGSOC PDE co-cultures, reported as %CD8 + CD137 + among CD8 + cells across conditions (condition matrix shown). G-H, FLAG-based discrimination of engineered versus bystander/resident CD8 + T cells in HGSOC PDEs, showing frequencies of CD8 + CD137 + FLAG + exogenous cells ( G ) and CD8 + CD137 + FLAG - bystander/ endogenous cells ( H ). (I) IFNγ secretion in HGSOC PDE co-cultures, expressed as FC over UT CTRL across conditions. ( J ) Cytokine and chemokine coordination across HGSOC PDEs visualized as Pearson correlation matrices for untreated, MSLN-BiTE, MSLN-BiTE + COXi, and MSLN-BiTE + EP2/4i conditions (circle size indicates correlation magnitude; color indicates direction). K, Myeloid polarization in HGSOC PDEs quantified as %CD68 + CD80 + among CD68 + macrophages across conditions. ( L-N ) TNFα ( L ), GM-CSF ( M ), and IL-10 ( N ) secretion in HGSOC PDE co-cultures, expressed as FC over UT CTRL. Boxplots show median and interquartile range with whiskers as displayed; each dot represents one patient. For HGSOC panels ( E-N ), statistics were performed on patient-level values using one-way repeated-measures ANOVA with multiple-comparisons correction as indicated (GraphPad Prism v10.1.2). Figure generated with BioRender.
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    A, Basal <t>PGE</t> <t>2</t> quantified in NSCLC PDE supernatants (pg/mL), shown as a heatmap illustrating inter-lesion variability. B, Correlation between basal PGE 2 and MSLN-BiTE-induced CD8+ T cell activation in NSCLC PDEs, expressed as FC in CD8 + CD137 + frequencies relative to UT CTRL (Holm-corrected P value shown). C, Correlation between basal PGE 2 and MSLN-BiTE-induced granzyme B release in NSCLC PDEs, expressed as log2 FC relative to UT CTRL per patient (r and P value shown). D, COX blockade rescue experiment in two NSCLC cases (Lung 31 and Lung 33): PDEs were pretreated with ketorolac (COXi, 1 µM) for 1 h prior to co-culture with MSLN-BiTE T cells, and CD8 + CD137 + activation together with granzyme B, CXCL9, and CXCL10 were quantified as FC over UT CTRL. E, Pharmacodynamic verification of prostanoid pathway inhibition in the HGSOC validation cohort (n = 11), showing PGE 2 levels at baseline and after COXi (ketorolac, 1 µM) or EP2/EP4 inhibition (EP2/4i, 1 µM). F, CD8 + T cell activation in HGSOC PDE co-cultures, reported as %CD8 + CD137 + among CD8 + cells across conditions (condition matrix shown). G-H, FLAG-based discrimination of engineered versus bystander/resident CD8 + T cells in HGSOC PDEs, showing frequencies of CD8 + CD137 + FLAG + exogenous cells ( G ) and CD8 + CD137 + FLAG - bystander/ endogenous cells ( H ). (I) IFNγ secretion in HGSOC PDE co-cultures, expressed as FC over UT CTRL across conditions. ( J ) Cytokine and chemokine coordination across HGSOC PDEs visualized as Pearson correlation matrices for untreated, MSLN-BiTE, MSLN-BiTE + COXi, and MSLN-BiTE + EP2/4i conditions (circle size indicates correlation magnitude; color indicates direction). K, Myeloid polarization in HGSOC PDEs quantified as %CD68 + CD80 + among CD68 + macrophages across conditions. ( L-N ) TNFα ( L ), GM-CSF ( M ), and IL-10 ( N ) secretion in HGSOC PDE co-cultures, expressed as FC over UT CTRL. Boxplots show median and interquartile range with whiskers as displayed; each dot represents one patient. For HGSOC panels ( E-N ), statistics were performed on patient-level values using one-way repeated-measures ANOVA with multiple-comparisons correction as indicated (GraphPad Prism v10.1.2). Figure generated with BioRender.
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    A, Basal <t>PGE</t> <t>2</t> quantified in NSCLC PDE supernatants (pg/mL), shown as a heatmap illustrating inter-lesion variability. B, Correlation between basal PGE 2 and MSLN-BiTE-induced CD8+ T cell activation in NSCLC PDEs, expressed as FC in CD8 + CD137 + frequencies relative to UT CTRL (Holm-corrected P value shown). C, Correlation between basal PGE 2 and MSLN-BiTE-induced granzyme B release in NSCLC PDEs, expressed as log2 FC relative to UT CTRL per patient (r and P value shown). D, COX blockade rescue experiment in two NSCLC cases (Lung 31 and Lung 33): PDEs were pretreated with ketorolac (COXi, 1 µM) for 1 h prior to co-culture with MSLN-BiTE T cells, and CD8 + CD137 + activation together with granzyme B, CXCL9, and CXCL10 were quantified as FC over UT CTRL. E, Pharmacodynamic verification of prostanoid pathway inhibition in the HGSOC validation cohort (n = 11), showing PGE 2 levels at baseline and after COXi (ketorolac, 1 µM) or EP2/EP4 inhibition (EP2/4i, 1 µM). F, CD8 + T cell activation in HGSOC PDE co-cultures, reported as %CD8 + CD137 + among CD8 + cells across conditions (condition matrix shown). G-H, FLAG-based discrimination of engineered versus bystander/resident CD8 + T cells in HGSOC PDEs, showing frequencies of CD8 + CD137 + FLAG + exogenous cells ( G ) and CD8 + CD137 + FLAG - bystander/ endogenous cells ( H ). (I) IFNγ secretion in HGSOC PDE co-cultures, expressed as FC over UT CTRL across conditions. ( J ) Cytokine and chemokine coordination across HGSOC PDEs visualized as Pearson correlation matrices for untreated, MSLN-BiTE, MSLN-BiTE + COXi, and MSLN-BiTE + EP2/4i conditions (circle size indicates correlation magnitude; color indicates direction). K, Myeloid polarization in HGSOC PDEs quantified as %CD68 + CD80 + among CD68 + macrophages across conditions. ( L-N ) TNFα ( L ), GM-CSF ( M ), and IL-10 ( N ) secretion in HGSOC PDE co-cultures, expressed as FC over UT CTRL. Boxplots show median and interquartile range with whiskers as displayed; each dot represents one patient. For HGSOC panels ( E-N ), statistics were performed on patient-level values using one-way repeated-measures ANOVA with multiple-comparisons correction as indicated (GraphPad Prism v10.1.2). Figure generated with BioRender.
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    A, Basal <t>PGE</t> <t>2</t> quantified in NSCLC PDE supernatants (pg/mL), shown as a heatmap illustrating inter-lesion variability. B, Correlation between basal PGE 2 and MSLN-BiTE-induced CD8+ T cell activation in NSCLC PDEs, expressed as FC in CD8 + CD137 + frequencies relative to UT CTRL (Holm-corrected P value shown). C, Correlation between basal PGE 2 and MSLN-BiTE-induced granzyme B release in NSCLC PDEs, expressed as log2 FC relative to UT CTRL per patient (r and P value shown). D, COX blockade rescue experiment in two NSCLC cases (Lung 31 and Lung 33): PDEs were pretreated with ketorolac (COXi, 1 µM) for 1 h prior to co-culture with MSLN-BiTE T cells, and CD8 + CD137 + activation together with granzyme B, CXCL9, and CXCL10 were quantified as FC over UT CTRL. E, Pharmacodynamic verification of prostanoid pathway inhibition in the HGSOC validation cohort (n = 11), showing PGE 2 levels at baseline and after COXi (ketorolac, 1 µM) or EP2/EP4 inhibition (EP2/4i, 1 µM). F, CD8 + T cell activation in HGSOC PDE co-cultures, reported as %CD8 + CD137 + among CD8 + cells across conditions (condition matrix shown). G-H, FLAG-based discrimination of engineered versus bystander/resident CD8 + T cells in HGSOC PDEs, showing frequencies of CD8 + CD137 + FLAG + exogenous cells ( G ) and CD8 + CD137 + FLAG - bystander/ endogenous cells ( H ). (I) IFNγ secretion in HGSOC PDE co-cultures, expressed as FC over UT CTRL across conditions. ( J ) Cytokine and chemokine coordination across HGSOC PDEs visualized as Pearson correlation matrices for untreated, MSLN-BiTE, MSLN-BiTE + COXi, and MSLN-BiTE + EP2/4i conditions (circle size indicates correlation magnitude; color indicates direction). K, Myeloid polarization in HGSOC PDEs quantified as %CD68 + CD80 + among CD68 + macrophages across conditions. ( L-N ) TNFα ( L ), GM-CSF ( M ), and IL-10 ( N ) secretion in HGSOC PDE co-cultures, expressed as FC over UT CTRL. Boxplots show median and interquartile range with whiskers as displayed; each dot represents one patient. For HGSOC panels ( E-N ), statistics were performed on patient-level values using one-way repeated-measures ANOVA with multiple-comparisons correction as indicated (GraphPad Prism v10.1.2). Figure generated with BioRender.
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    A, Basal <t>PGE</t> <t>2</t> quantified in NSCLC PDE supernatants (pg/mL), shown as a heatmap illustrating inter-lesion variability. B, Correlation between basal PGE 2 and MSLN-BiTE-induced CD8+ T cell activation in NSCLC PDEs, expressed as FC in CD8 + CD137 + frequencies relative to UT CTRL (Holm-corrected P value shown). C, Correlation between basal PGE 2 and MSLN-BiTE-induced granzyme B release in NSCLC PDEs, expressed as log2 FC relative to UT CTRL per patient (r and P value shown). D, COX blockade rescue experiment in two NSCLC cases (Lung 31 and Lung 33): PDEs were pretreated with ketorolac (COXi, 1 µM) for 1 h prior to co-culture with MSLN-BiTE T cells, and CD8 + CD137 + activation together with granzyme B, CXCL9, and CXCL10 were quantified as FC over UT CTRL. E, Pharmacodynamic verification of prostanoid pathway inhibition in the HGSOC validation cohort (n = 11), showing PGE 2 levels at baseline and after COXi (ketorolac, 1 µM) or EP2/EP4 inhibition (EP2/4i, 1 µM). F, CD8 + T cell activation in HGSOC PDE co-cultures, reported as %CD8 + CD137 + among CD8 + cells across conditions (condition matrix shown). G-H, FLAG-based discrimination of engineered versus bystander/resident CD8 + T cells in HGSOC PDEs, showing frequencies of CD8 + CD137 + FLAG + exogenous cells ( G ) and CD8 + CD137 + FLAG - bystander/ endogenous cells ( H ). (I) IFNγ secretion in HGSOC PDE co-cultures, expressed as FC over UT CTRL across conditions. ( J ) Cytokine and chemokine coordination across HGSOC PDEs visualized as Pearson correlation matrices for untreated, MSLN-BiTE, MSLN-BiTE + COXi, and MSLN-BiTE + EP2/4i conditions (circle size indicates correlation magnitude; color indicates direction). K, Myeloid polarization in HGSOC PDEs quantified as %CD68 + CD80 + among CD68 + macrophages across conditions. ( L-N ) TNFα ( L ), GM-CSF ( M ), and IL-10 ( N ) secretion in HGSOC PDE co-cultures, expressed as FC over UT CTRL. Boxplots show median and interquartile range with whiskers as displayed; each dot represents one patient. For HGSOC panels ( E-N ), statistics were performed on patient-level values using one-way repeated-measures ANOVA with multiple-comparisons correction as indicated (GraphPad Prism v10.1.2). Figure generated with BioRender.
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    A, Basal <t>PGE</t> <t>2</t> quantified in NSCLC PDE supernatants (pg/mL), shown as a heatmap illustrating inter-lesion variability. B, Correlation between basal PGE 2 and MSLN-BiTE-induced CD8+ T cell activation in NSCLC PDEs, expressed as FC in CD8 + CD137 + frequencies relative to UT CTRL (Holm-corrected P value shown). C, Correlation between basal PGE 2 and MSLN-BiTE-induced granzyme B release in NSCLC PDEs, expressed as log2 FC relative to UT CTRL per patient (r and P value shown). D, COX blockade rescue experiment in two NSCLC cases (Lung 31 and Lung 33): PDEs were pretreated with ketorolac (COXi, 1 µM) for 1 h prior to co-culture with MSLN-BiTE T cells, and CD8 + CD137 + activation together with granzyme B, CXCL9, and CXCL10 were quantified as FC over UT CTRL. E, Pharmacodynamic verification of prostanoid pathway inhibition in the HGSOC validation cohort (n = 11), showing PGE 2 levels at baseline and after COXi (ketorolac, 1 µM) or EP2/EP4 inhibition (EP2/4i, 1 µM). F, CD8 + T cell activation in HGSOC PDE co-cultures, reported as %CD8 + CD137 + among CD8 + cells across conditions (condition matrix shown). G-H, FLAG-based discrimination of engineered versus bystander/resident CD8 + T cells in HGSOC PDEs, showing frequencies of CD8 + CD137 + FLAG + exogenous cells ( G ) and CD8 + CD137 + FLAG - bystander/ endogenous cells ( H ). (I) IFNγ secretion in HGSOC PDE co-cultures, expressed as FC over UT CTRL across conditions. ( J ) Cytokine and chemokine coordination across HGSOC PDEs visualized as Pearson correlation matrices for untreated, MSLN-BiTE, MSLN-BiTE + COXi, and MSLN-BiTE + EP2/4i conditions (circle size indicates correlation magnitude; color indicates direction). K, Myeloid polarization in HGSOC PDEs quantified as %CD68 + CD80 + among CD68 + macrophages across conditions. ( L-N ) TNFα ( L ), GM-CSF ( M ), and IL-10 ( N ) secretion in HGSOC PDE co-cultures, expressed as FC over UT CTRL. Boxplots show median and interquartile range with whiskers as displayed; each dot represents one patient. For HGSOC panels ( E-N ), statistics were performed on patient-level values using one-way repeated-measures ANOVA with multiple-comparisons correction as indicated (GraphPad Prism v10.1.2). Figure generated with BioRender.
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    A, Basal <t>PGE</t> <t>2</t> quantified in NSCLC PDE supernatants (pg/mL), shown as a heatmap illustrating inter-lesion variability. B, Correlation between basal PGE 2 and MSLN-BiTE-induced CD8+ T cell activation in NSCLC PDEs, expressed as FC in CD8 + CD137 + frequencies relative to UT CTRL (Holm-corrected P value shown). C, Correlation between basal PGE 2 and MSLN-BiTE-induced granzyme B release in NSCLC PDEs, expressed as log2 FC relative to UT CTRL per patient (r and P value shown). D, COX blockade rescue experiment in two NSCLC cases (Lung 31 and Lung 33): PDEs were pretreated with ketorolac (COXi, 1 µM) for 1 h prior to co-culture with MSLN-BiTE T cells, and CD8 + CD137 + activation together with granzyme B, CXCL9, and CXCL10 were quantified as FC over UT CTRL. E, Pharmacodynamic verification of prostanoid pathway inhibition in the HGSOC validation cohort (n = 11), showing PGE 2 levels at baseline and after COXi (ketorolac, 1 µM) or EP2/EP4 inhibition (EP2/4i, 1 µM). F, CD8 + T cell activation in HGSOC PDE co-cultures, reported as %CD8 + CD137 + among CD8 + cells across conditions (condition matrix shown). G-H, FLAG-based discrimination of engineered versus bystander/resident CD8 + T cells in HGSOC PDEs, showing frequencies of CD8 + CD137 + FLAG + exogenous cells ( G ) and CD8 + CD137 + FLAG - bystander/ endogenous cells ( H ). (I) IFNγ secretion in HGSOC PDE co-cultures, expressed as FC over UT CTRL across conditions. ( J ) Cytokine and chemokine coordination across HGSOC PDEs visualized as Pearson correlation matrices for untreated, MSLN-BiTE, MSLN-BiTE + COXi, and MSLN-BiTE + EP2/4i conditions (circle size indicates correlation magnitude; color indicates direction). K, Myeloid polarization in HGSOC PDEs quantified as %CD68 + CD80 + among CD68 + macrophages across conditions. ( L-N ) TNFα ( L ), GM-CSF ( M ), and IL-10 ( N ) secretion in HGSOC PDE co-cultures, expressed as FC over UT CTRL. Boxplots show median and interquartile range with whiskers as displayed; each dot represents one patient. For HGSOC panels ( E-N ), statistics were performed on patient-level values using one-way repeated-measures ANOVA with multiple-comparisons correction as indicated (GraphPad Prism v10.1.2). Figure generated with BioRender.
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    A, Basal <t>PGE</t> <t>2</t> quantified in NSCLC PDE supernatants (pg/mL), shown as a heatmap illustrating inter-lesion variability. B, Correlation between basal PGE 2 and MSLN-BiTE-induced CD8+ T cell activation in NSCLC PDEs, expressed as FC in CD8 + CD137 + frequencies relative to UT CTRL (Holm-corrected P value shown). C, Correlation between basal PGE 2 and MSLN-BiTE-induced granzyme B release in NSCLC PDEs, expressed as log2 FC relative to UT CTRL per patient (r and P value shown). D, COX blockade rescue experiment in two NSCLC cases (Lung 31 and Lung 33): PDEs were pretreated with ketorolac (COXi, 1 µM) for 1 h prior to co-culture with MSLN-BiTE T cells, and CD8 + CD137 + activation together with granzyme B, CXCL9, and CXCL10 were quantified as FC over UT CTRL. E, Pharmacodynamic verification of prostanoid pathway inhibition in the HGSOC validation cohort (n = 11), showing PGE 2 levels at baseline and after COXi (ketorolac, 1 µM) or EP2/EP4 inhibition (EP2/4i, 1 µM). F, CD8 + T cell activation in HGSOC PDE co-cultures, reported as %CD8 + CD137 + among CD8 + cells across conditions (condition matrix shown). G-H, FLAG-based discrimination of engineered versus bystander/resident CD8 + T cells in HGSOC PDEs, showing frequencies of CD8 + CD137 + FLAG + exogenous cells ( G ) and CD8 + CD137 + FLAG - bystander/ endogenous cells ( H ). (I) IFNγ secretion in HGSOC PDE co-cultures, expressed as FC over UT CTRL across conditions. ( J ) Cytokine and chemokine coordination across HGSOC PDEs visualized as Pearson correlation matrices for untreated, MSLN-BiTE, MSLN-BiTE + COXi, and MSLN-BiTE + EP2/4i conditions (circle size indicates correlation magnitude; color indicates direction). K, Myeloid polarization in HGSOC PDEs quantified as %CD68 + CD80 + among CD68 + macrophages across conditions. ( L-N ) TNFα ( L ), GM-CSF ( M ), and IL-10 ( N ) secretion in HGSOC PDE co-cultures, expressed as FC over UT CTRL. Boxplots show median and interquartile range with whiskers as displayed; each dot represents one patient. For HGSOC panels ( E-N ), statistics were performed on patient-level values using one-way repeated-measures ANOVA with multiple-comparisons correction as indicated (GraphPad Prism v10.1.2). Figure generated with BioRender.
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    Image Search Results


    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.

    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), TGF-β (Cat. No. E-EL-0162), VEGF (Cat. No. E-EL-R2603), and HGF (Cat. No. E-EL-R0496) were purchased from Elabscience (Wuhan, China).

    Techniques: Confocal Microscopy, Fluorescence, Staining, Cell Culture, Expressing

    A, Basal PGE 2 quantified in NSCLC PDE supernatants (pg/mL), shown as a heatmap illustrating inter-lesion variability. B, Correlation between basal PGE 2 and MSLN-BiTE-induced CD8+ T cell activation in NSCLC PDEs, expressed as FC in CD8 + CD137 + frequencies relative to UT CTRL (Holm-corrected P value shown). C, Correlation between basal PGE 2 and MSLN-BiTE-induced granzyme B release in NSCLC PDEs, expressed as log2 FC relative to UT CTRL per patient (r and P value shown). D, COX blockade rescue experiment in two NSCLC cases (Lung 31 and Lung 33): PDEs were pretreated with ketorolac (COXi, 1 µM) for 1 h prior to co-culture with MSLN-BiTE T cells, and CD8 + CD137 + activation together with granzyme B, CXCL9, and CXCL10 were quantified as FC over UT CTRL. E, Pharmacodynamic verification of prostanoid pathway inhibition in the HGSOC validation cohort (n = 11), showing PGE 2 levels at baseline and after COXi (ketorolac, 1 µM) or EP2/EP4 inhibition (EP2/4i, 1 µM). F, CD8 + T cell activation in HGSOC PDE co-cultures, reported as %CD8 + CD137 + among CD8 + cells across conditions (condition matrix shown). G-H, FLAG-based discrimination of engineered versus bystander/resident CD8 + T cells in HGSOC PDEs, showing frequencies of CD8 + CD137 + FLAG + exogenous cells ( G ) and CD8 + CD137 + FLAG - bystander/ endogenous cells ( H ). (I) IFNγ secretion in HGSOC PDE co-cultures, expressed as FC over UT CTRL across conditions. ( J ) Cytokine and chemokine coordination across HGSOC PDEs visualized as Pearson correlation matrices for untreated, MSLN-BiTE, MSLN-BiTE + COXi, and MSLN-BiTE + EP2/4i conditions (circle size indicates correlation magnitude; color indicates direction). K, Myeloid polarization in HGSOC PDEs quantified as %CD68 + CD80 + among CD68 + macrophages across conditions. ( L-N ) TNFα ( L ), GM-CSF ( M ), and IL-10 ( N ) secretion in HGSOC PDE co-cultures, expressed as FC over UT CTRL. Boxplots show median and interquartile range with whiskers as displayed; each dot represents one patient. For HGSOC panels ( E-N ), statistics were performed on patient-level values using one-way repeated-measures ANOVA with multiple-comparisons correction as indicated (GraphPad Prism v10.1.2). Figure generated with BioRender.

    Journal: bioRxiv

    Article Title: Actionable spatial prostanoid barriers constrain BiTE-driven adoptive T cell immunity in intact human tumors

    doi: 10.64898/2026.03.26.713601

    Figure Lengend Snippet: A, Basal PGE 2 quantified in NSCLC PDE supernatants (pg/mL), shown as a heatmap illustrating inter-lesion variability. B, Correlation between basal PGE 2 and MSLN-BiTE-induced CD8+ T cell activation in NSCLC PDEs, expressed as FC in CD8 + CD137 + frequencies relative to UT CTRL (Holm-corrected P value shown). C, Correlation between basal PGE 2 and MSLN-BiTE-induced granzyme B release in NSCLC PDEs, expressed as log2 FC relative to UT CTRL per patient (r and P value shown). D, COX blockade rescue experiment in two NSCLC cases (Lung 31 and Lung 33): PDEs were pretreated with ketorolac (COXi, 1 µM) for 1 h prior to co-culture with MSLN-BiTE T cells, and CD8 + CD137 + activation together with granzyme B, CXCL9, and CXCL10 were quantified as FC over UT CTRL. E, Pharmacodynamic verification of prostanoid pathway inhibition in the HGSOC validation cohort (n = 11), showing PGE 2 levels at baseline and after COXi (ketorolac, 1 µM) or EP2/EP4 inhibition (EP2/4i, 1 µM). F, CD8 + T cell activation in HGSOC PDE co-cultures, reported as %CD8 + CD137 + among CD8 + cells across conditions (condition matrix shown). G-H, FLAG-based discrimination of engineered versus bystander/resident CD8 + T cells in HGSOC PDEs, showing frequencies of CD8 + CD137 + FLAG + exogenous cells ( G ) and CD8 + CD137 + FLAG - bystander/ endogenous cells ( H ). (I) IFNγ secretion in HGSOC PDE co-cultures, expressed as FC over UT CTRL across conditions. ( J ) Cytokine and chemokine coordination across HGSOC PDEs visualized as Pearson correlation matrices for untreated, MSLN-BiTE, MSLN-BiTE + COXi, and MSLN-BiTE + EP2/4i conditions (circle size indicates correlation magnitude; color indicates direction). K, Myeloid polarization in HGSOC PDEs quantified as %CD68 + CD80 + among CD68 + macrophages across conditions. ( L-N ) TNFα ( L ), GM-CSF ( M ), and IL-10 ( N ) secretion in HGSOC PDE co-cultures, expressed as FC over UT CTRL. Boxplots show median and interquartile range with whiskers as displayed; each dot represents one patient. For HGSOC panels ( E-N ), statistics were performed on patient-level values using one-way repeated-measures ANOVA with multiple-comparisons correction as indicated (GraphPad Prism v10.1.2). Figure generated with BioRender.

    Article Snippet: Basal prostaglandin E2 levels in culture supernatants from PDEs were quantified using a PGE 2 ELISA kit (Cayman Chemical, 514010) according to the manufacturer’s instructions.

    Techniques: Activation Assay, Co-Culture Assay, Inhibition, Biomarker Discovery, Generated