tnfr1  (Hycult Biotech)


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    Hycult Biotech tnfr1
    EHD2-scTNF R2 enhances the therapeutic effect of ATROSIMAB on EAE. Hu/m <t>TNFR1-ki</t> x hu/m TNFR2-ki mice were immunized with MOG 35-55 and treated either with saline ( n = 13), EHD2-scTNF R2 (TNFR2 agonist; n = 8), ATROSIMAB <t>(TNFR1</t> antagonist; n = 11) or a combination (E + A; n = 9). Schematic representation of EAE induction, development and treatment regimen ( A ). EHD2-scTNF R2 [10 mg/kg] was injected i.p. at 6, 9 and 12 days post-immunization (dpi; blue and green arrows) while ATROSIMAB [20 mg/kg] was injected at 12, 15 and 18 dpi (red and green arrows). Body weight (BW; B ) and disease development ( C ) were measured daily until 25 dpi. EAE development is represented as sum of EAE scores over 25 days ( D ) but also as mean score at the different treatment days and at killing day ( E ). On the first day of symptoms, disease onset was recorded ( F ). Linear regression curves of disease development ( C ) are shown together with dashed lines representing 95% confidence intervals. Statistical difference between slopes is shown at the bottom right of the graph. Data are presented as mean ± SEM and differences between groups were assessed with Mann–Whitney or Kruskal–Wallis tests, except for relative body weight for which two-way ANOVA and Tukey’s post-test were used. # = PBS vs E + A; $ = PBS vs ATROSIMAB. * /#/$ p < 0.05, ** /##/$$ p < 0.01
    Tnfr1, supplied by Hycult Biotech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/tnfr1/product/Hycult Biotech
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    tnfr1 - by Bioz Stars, 2024-04
    93/100 stars

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    1) Product Images from "Sequential treatment with a TNFR2 agonist and a TNFR1 antagonist improves outcomes in a humanized mouse model for MS"

    Article Title: Sequential treatment with a TNFR2 agonist and a TNFR1 antagonist improves outcomes in a humanized mouse model for MS

    Journal: Journal of Neuroinflammation

    doi: 10.1186/s12974-023-02785-y

    EHD2-scTNF R2 enhances the therapeutic effect of ATROSIMAB on EAE. Hu/m TNFR1-ki x hu/m TNFR2-ki mice were immunized with MOG 35-55 and treated either with saline ( n = 13), EHD2-scTNF R2 (TNFR2 agonist; n = 8), ATROSIMAB (TNFR1 antagonist; n = 11) or a combination (E + A; n = 9). Schematic representation of EAE induction, development and treatment regimen ( A ). EHD2-scTNF R2 [10 mg/kg] was injected i.p. at 6, 9 and 12 days post-immunization (dpi; blue and green arrows) while ATROSIMAB [20 mg/kg] was injected at 12, 15 and 18 dpi (red and green arrows). Body weight (BW; B ) and disease development ( C ) were measured daily until 25 dpi. EAE development is represented as sum of EAE scores over 25 days ( D ) but also as mean score at the different treatment days and at killing day ( E ). On the first day of symptoms, disease onset was recorded ( F ). Linear regression curves of disease development ( C ) are shown together with dashed lines representing 95% confidence intervals. Statistical difference between slopes is shown at the bottom right of the graph. Data are presented as mean ± SEM and differences between groups were assessed with Mann–Whitney or Kruskal–Wallis tests, except for relative body weight for which two-way ANOVA and Tukey’s post-test were used. # = PBS vs E + A; $ = PBS vs ATROSIMAB. * /#/$ p < 0.05, ** /##/$$ p < 0.01
    Figure Legend Snippet: EHD2-scTNF R2 enhances the therapeutic effect of ATROSIMAB on EAE. Hu/m TNFR1-ki x hu/m TNFR2-ki mice were immunized with MOG 35-55 and treated either with saline ( n = 13), EHD2-scTNF R2 (TNFR2 agonist; n = 8), ATROSIMAB (TNFR1 antagonist; n = 11) or a combination (E + A; n = 9). Schematic representation of EAE induction, development and treatment regimen ( A ). EHD2-scTNF R2 [10 mg/kg] was injected i.p. at 6, 9 and 12 days post-immunization (dpi; blue and green arrows) while ATROSIMAB [20 mg/kg] was injected at 12, 15 and 18 dpi (red and green arrows). Body weight (BW; B ) and disease development ( C ) were measured daily until 25 dpi. EAE development is represented as sum of EAE scores over 25 days ( D ) but also as mean score at the different treatment days and at killing day ( E ). On the first day of symptoms, disease onset was recorded ( F ). Linear regression curves of disease development ( C ) are shown together with dashed lines representing 95% confidence intervals. Statistical difference between slopes is shown at the bottom right of the graph. Data are presented as mean ± SEM and differences between groups were assessed with Mann–Whitney or Kruskal–Wallis tests, except for relative body weight for which two-way ANOVA and Tukey’s post-test were used. # = PBS vs E + A; $ = PBS vs ATROSIMAB. * /#/$ p < 0.05, ** /##/$$ p < 0.01

    Techniques Used: Injection, MANN-WHITNEY

    Modulating TNFRs selectively does not lead to major changes in leukocytes subsets. Hu/m TNFR1-ki x hu/m TNFR2-ki mice treated either with saline, EHD2-scTNF R2 (TNFR2 agonist), ATROSIMAB (TNFR1 antagonist) or a combination (E + A) were killed either 18 (acute) or 25 (chronic) days post-immunization (dpi; n = 3–5 animals/treatment group/killing timepoint). Immune cells from inguinal lymph nodes (on the left) and spleen (on the right) were analyzed by flow cytometry to reveal the frequencies of CD3 + T cells ( A and B ), CD19 + B cells ( C and D ), CD3 + FoxP3 + Treg ( E and F ) and CD3 + CD8 + IFN-γ + cytotoxic T cells ( G and H ). Representative contour plots depict interferon gamma (IFN-γ) expression of CD8 + T cells in spleen samples from animals killed at 18 dpi ( I ). The percentage of CD3 + CD8 + IFN-γ + cells is reported at the bottom right of each plot. Data are presented as mean ± SEM and differences between groups were assessed with one-way ANOVA and Tukey’s post-test. *p < 0.05, **p < 0.01
    Figure Legend Snippet: Modulating TNFRs selectively does not lead to major changes in leukocytes subsets. Hu/m TNFR1-ki x hu/m TNFR2-ki mice treated either with saline, EHD2-scTNF R2 (TNFR2 agonist), ATROSIMAB (TNFR1 antagonist) or a combination (E + A) were killed either 18 (acute) or 25 (chronic) days post-immunization (dpi; n = 3–5 animals/treatment group/killing timepoint). Immune cells from inguinal lymph nodes (on the left) and spleen (on the right) were analyzed by flow cytometry to reveal the frequencies of CD3 + T cells ( A and B ), CD19 + B cells ( C and D ), CD3 + FoxP3 + Treg ( E and F ) and CD3 + CD8 + IFN-γ + cytotoxic T cells ( G and H ). Representative contour plots depict interferon gamma (IFN-γ) expression of CD8 + T cells in spleen samples from animals killed at 18 dpi ( I ). The percentage of CD3 + CD8 + IFN-γ + cells is reported at the bottom right of each plot. Data are presented as mean ± SEM and differences between groups were assessed with one-way ANOVA and Tukey’s post-test. *p < 0.05, **p < 0.01

    Techniques Used: Flow Cytometry, Expressing

    Sequential treatment decreases demyelination while single treatments interfere with lymphocytes recruitment to the CNS. Immunohistochemical analysis of spinal cord sections of hu/m TNFR1-ki x hu/m TNFR2-ki mice immunized with MOG 35-55 and treated either with saline, EHD2-scTNF R2 (TNFR2 agonist), ATROSIMAB (TNFR1 antagonist) or a combination (E + A). Demyelination degree was measured with Klüver Barrera staining at 18 days post-immunization (dpi; n = 5–6/group; A and B ) and at 25 dpi ( n = 7–10/group; G and H ). The number of T cells present in the sections was measured by automated counting of CD3 + cells at 18 dpi ( n = 6–7/group; C and D ) and 25 dpi ( n = 6–9/group; I and J ). B-cell clustering was assessed by counting the number of perivascular cuffs (black stars) at 18 dpi ( n = 5–7/group; E and F ) and 25 dpi ( n = 5/group; K and L ). Data are presented as mean ± SEM and differences between groups were assessed with Mann–Whitney test. *p < 0.05
    Figure Legend Snippet: Sequential treatment decreases demyelination while single treatments interfere with lymphocytes recruitment to the CNS. Immunohistochemical analysis of spinal cord sections of hu/m TNFR1-ki x hu/m TNFR2-ki mice immunized with MOG 35-55 and treated either with saline, EHD2-scTNF R2 (TNFR2 agonist), ATROSIMAB (TNFR1 antagonist) or a combination (E + A). Demyelination degree was measured with Klüver Barrera staining at 18 days post-immunization (dpi; n = 5–6/group; A and B ) and at 25 dpi ( n = 7–10/group; G and H ). The number of T cells present in the sections was measured by automated counting of CD3 + cells at 18 dpi ( n = 6–7/group; C and D ) and 25 dpi ( n = 6–9/group; I and J ). B-cell clustering was assessed by counting the number of perivascular cuffs (black stars) at 18 dpi ( n = 5–7/group; E and F ) and 25 dpi ( n = 5/group; K and L ). Data are presented as mean ± SEM and differences between groups were assessed with Mann–Whitney test. *p < 0.05

    Techniques Used: Immunohistochemical staining, Staining, MANN-WHITNEY

    TNFR2 stimulation leads to an increased number of Tregs in the spinal cord at 18 dpi. Immunohistochemical analysis of FoxP3 staining of hu/m TNFR1-ki x hu/m TNFR2-ki mice immunized with MOG 35-55 and treated either with saline, EHD2-scTNF R2 (TNFR2 agonist), ATROSIMAB (TNFR1 antagonist) or a combination (E + A). FoxP3 + cells (black) were counted in spinal cord sections of mice killed at 18 days post-immunization (dpi; n = 5/group; A and B ) and at 25 dpi ( n = 5–7/group; C and D ). Data are presented as mean ± SEM and differences between groups were assessed with Mann–Whitney test. *p < 0.05
    Figure Legend Snippet: TNFR2 stimulation leads to an increased number of Tregs in the spinal cord at 18 dpi. Immunohistochemical analysis of FoxP3 staining of hu/m TNFR1-ki x hu/m TNFR2-ki mice immunized with MOG 35-55 and treated either with saline, EHD2-scTNF R2 (TNFR2 agonist), ATROSIMAB (TNFR1 antagonist) or a combination (E + A). FoxP3 + cells (black) were counted in spinal cord sections of mice killed at 18 days post-immunization (dpi; n = 5/group; A and B ) and at 25 dpi ( n = 5–7/group; C and D ). Data are presented as mean ± SEM and differences between groups were assessed with Mann–Whitney test. *p < 0.05

    Techniques Used: Immunohistochemical staining, Staining, MANN-WHITNEY

    tnf  (Hycult Biotech)


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    Hycult Biotech tnf
    Tnf, supplied by Hycult Biotech, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/tnf/product/Hycult Biotech
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    tnf - by Bioz Stars, 2024-04
    86/100 stars

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    tnf alpha  (Hycult Biotech)


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    Hycult Biotech tnf alpha
    Logarithmic transformation of <t>TNF-alpha</t> activity normalized using total protein in the inflamed paw: \documentclass[12pt]{minimal} \usepackage{wasysym} \usepackage[substack]{amsmath} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage[mathscr]{eucal} \usepackage{mathrsfs} \DeclareFontFamily{T1}{linotext}{} \DeclareFontShape{T1}{linotext}{m}{n} {linotext }{} \DeclareSymbolFont{linotext}{T1}{linotext}{m}{n} \DeclareSymbolFontAlphabet{\mathLINOTEXT}{linotext} \begin{document} ${\mathrm{y' = }}\root {\mathrm{3}} \of {\mathrm{Y}} $\end{document} . TNF-alpha levels were measured 48 hours post-induction of inflammation and normalized using total protein (n=6 for control, n=8 for all other groups). <t>ELISA</t> sensitivity = 10.9 to 700 pg/mL. *p<0.05. **p<0.01. ***p<0.001. Data is displayed as mean ± SD. TNF-alpha data derived from same mouse hind-paw recorded in edema measurements.
    Tnf Alpha, supplied by Hycult 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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    1) Product Images from "Umbilical Cord Stem Cell Lysate: A New Biologic Injectate for the Putative Treatment of Acute Temporomandibular Joint Inflammation"

    Article Title: Umbilical Cord Stem Cell Lysate: A New Biologic Injectate for the Putative Treatment of Acute Temporomandibular Joint Inflammation

    Journal: Journal of Inflammation Research

    doi: 10.2147/JIR.S420741

    Logarithmic transformation of TNF-alpha activity normalized using total protein in the inflamed paw: \documentclass[12pt]{minimal} \usepackage{wasysym} \usepackage[substack]{amsmath} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage[mathscr]{eucal} \usepackage{mathrsfs} \DeclareFontFamily{T1}{linotext}{} \DeclareFontShape{T1}{linotext}{m}{n} {linotext }{} \DeclareSymbolFont{linotext}{T1}{linotext}{m}{n} \DeclareSymbolFontAlphabet{\mathLINOTEXT}{linotext} \begin{document} ${\mathrm{y' = }}\root {\mathrm{3}} \of {\mathrm{Y}} $\end{document} . TNF-alpha levels were measured 48 hours post-induction of inflammation and normalized using total protein (n=6 for control, n=8 for all other groups). ELISA sensitivity = 10.9 to 700 pg/mL. *p<0.05. **p<0.01. ***p<0.001. Data is displayed as mean ± SD. TNF-alpha data derived from same mouse hind-paw recorded in edema measurements.
    Figure Legend Snippet: Logarithmic transformation of TNF-alpha activity normalized using total protein in the inflamed paw: \documentclass[12pt]{minimal} \usepackage{wasysym} \usepackage[substack]{amsmath} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage[mathscr]{eucal} \usepackage{mathrsfs} \DeclareFontFamily{T1}{linotext}{} \DeclareFontShape{T1}{linotext}{m}{n} {linotext }{} \DeclareSymbolFont{linotext}{T1}{linotext}{m}{n} \DeclareSymbolFontAlphabet{\mathLINOTEXT}{linotext} \begin{document} ${\mathrm{y' = }}\root {\mathrm{3}} \of {\mathrm{Y}} $\end{document} . TNF-alpha levels were measured 48 hours post-induction of inflammation and normalized using total protein (n=6 for control, n=8 for all other groups). ELISA sensitivity = 10.9 to 700 pg/mL. *p<0.05. **p<0.01. ***p<0.001. Data is displayed as mean ± SD. TNF-alpha data derived from same mouse hind-paw recorded in edema measurements.

    Techniques Used: Transformation Assay, Activity Assay, Enzyme-linked Immunosorbent Assay, Derivative Assay

    tnfr1  (Hycult Biotech)


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    Hycult Biotech tnfr1
    EHD2-scTNF R2 enhances the therapeutic effect of ATROSIMAB on EAE. Hu/m <t>TNFR1-ki</t> x hu/m TNFR2-ki mice were immunized with MOG 35-55 and treated either with saline ( n = 13), EHD2-scTNF R2 (TNFR2 agonist; n = 8), ATROSIMAB <t>(TNFR1</t> antagonist; n = 11) or a combination (E + A; n = 9). Schematic representation of EAE induction, development and treatment regimen ( A ). EHD2-scTNF R2 [10 mg/kg] was injected i.p. at 6, 9 and 12 days post-immunization (dpi; blue and green arrows) while ATROSIMAB [20 mg/kg] was injected at 12, 15 and 18 dpi (red and green arrows). Body weight (BW; B ) and disease development ( C ) were measured daily until 25 dpi. EAE development is represented as sum of EAE scores over 25 days ( D ) but also as mean score at the different treatment days and at killing day ( E ). On the first day of symptoms, disease onset was recorded ( F ). Linear regression curves of disease development ( C ) are shown together with dashed lines representing 95% confidence intervals. Statistical difference between slopes is shown at the bottom right of the graph. Data are presented as mean ± SEM and differences between groups were assessed with Mann–Whitney or Kruskal–Wallis tests, except for relative body weight for which two-way ANOVA and Tukey’s post-test were used. # = PBS vs E + A; $ = PBS vs ATROSIMAB. * /#/$ p < 0.05, ** /##/$$ p < 0.01
    Tnfr1, supplied by Hycult Biotech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/tnfr1/product/Hycult Biotech
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    tnfr1 - by Bioz Stars, 2024-04
    93/100 stars

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    1) Product Images from "Sequential treatment with a TNFR2 agonist and a TNFR1 antagonist improves outcomes in a humanized mouse model for MS"

    Article Title: Sequential treatment with a TNFR2 agonist and a TNFR1 antagonist improves outcomes in a humanized mouse model for MS

    Journal: Journal of Neuroinflammation

    doi: 10.1186/s12974-023-02785-y

    EHD2-scTNF R2 enhances the therapeutic effect of ATROSIMAB on EAE. Hu/m TNFR1-ki x hu/m TNFR2-ki mice were immunized with MOG 35-55 and treated either with saline ( n = 13), EHD2-scTNF R2 (TNFR2 agonist; n = 8), ATROSIMAB (TNFR1 antagonist; n = 11) or a combination (E + A; n = 9). Schematic representation of EAE induction, development and treatment regimen ( A ). EHD2-scTNF R2 [10 mg/kg] was injected i.p. at 6, 9 and 12 days post-immunization (dpi; blue and green arrows) while ATROSIMAB [20 mg/kg] was injected at 12, 15 and 18 dpi (red and green arrows). Body weight (BW; B ) and disease development ( C ) were measured daily until 25 dpi. EAE development is represented as sum of EAE scores over 25 days ( D ) but also as mean score at the different treatment days and at killing day ( E ). On the first day of symptoms, disease onset was recorded ( F ). Linear regression curves of disease development ( C ) are shown together with dashed lines representing 95% confidence intervals. Statistical difference between slopes is shown at the bottom right of the graph. Data are presented as mean ± SEM and differences between groups were assessed with Mann–Whitney or Kruskal–Wallis tests, except for relative body weight for which two-way ANOVA and Tukey’s post-test were used. # = PBS vs E + A; $ = PBS vs ATROSIMAB. * /#/$ p < 0.05, ** /##/$$ p < 0.01
    Figure Legend Snippet: EHD2-scTNF R2 enhances the therapeutic effect of ATROSIMAB on EAE. Hu/m TNFR1-ki x hu/m TNFR2-ki mice were immunized with MOG 35-55 and treated either with saline ( n = 13), EHD2-scTNF R2 (TNFR2 agonist; n = 8), ATROSIMAB (TNFR1 antagonist; n = 11) or a combination (E + A; n = 9). Schematic representation of EAE induction, development and treatment regimen ( A ). EHD2-scTNF R2 [10 mg/kg] was injected i.p. at 6, 9 and 12 days post-immunization (dpi; blue and green arrows) while ATROSIMAB [20 mg/kg] was injected at 12, 15 and 18 dpi (red and green arrows). Body weight (BW; B ) and disease development ( C ) were measured daily until 25 dpi. EAE development is represented as sum of EAE scores over 25 days ( D ) but also as mean score at the different treatment days and at killing day ( E ). On the first day of symptoms, disease onset was recorded ( F ). Linear regression curves of disease development ( C ) are shown together with dashed lines representing 95% confidence intervals. Statistical difference between slopes is shown at the bottom right of the graph. Data are presented as mean ± SEM and differences between groups were assessed with Mann–Whitney or Kruskal–Wallis tests, except for relative body weight for which two-way ANOVA and Tukey’s post-test were used. # = PBS vs E + A; $ = PBS vs ATROSIMAB. * /#/$ p < 0.05, ** /##/$$ p < 0.01

    Techniques Used: Injection, MANN-WHITNEY

    Modulating TNFRs selectively does not lead to major changes in leukocytes subsets. Hu/m TNFR1-ki x hu/m TNFR2-ki mice treated either with saline, EHD2-scTNF R2 (TNFR2 agonist), ATROSIMAB (TNFR1 antagonist) or a combination (E + A) were killed either 18 (acute) or 25 (chronic) days post-immunization (dpi; n = 3–5 animals/treatment group/killing timepoint). Immune cells from inguinal lymph nodes (on the left) and spleen (on the right) were analyzed by flow cytometry to reveal the frequencies of CD3 + T cells ( A and B ), CD19 + B cells ( C and D ), CD3 + FoxP3 + Treg ( E and F ) and CD3 + CD8 + IFN-γ + cytotoxic T cells ( G and H ). Representative contour plots depict interferon gamma (IFN-γ) expression of CD8 + T cells in spleen samples from animals killed at 18 dpi ( I ). The percentage of CD3 + CD8 + IFN-γ + cells is reported at the bottom right of each plot. Data are presented as mean ± SEM and differences between groups were assessed with one-way ANOVA and Tukey’s post-test. *p < 0.05, **p < 0.01
    Figure Legend Snippet: Modulating TNFRs selectively does not lead to major changes in leukocytes subsets. Hu/m TNFR1-ki x hu/m TNFR2-ki mice treated either with saline, EHD2-scTNF R2 (TNFR2 agonist), ATROSIMAB (TNFR1 antagonist) or a combination (E + A) were killed either 18 (acute) or 25 (chronic) days post-immunization (dpi; n = 3–5 animals/treatment group/killing timepoint). Immune cells from inguinal lymph nodes (on the left) and spleen (on the right) were analyzed by flow cytometry to reveal the frequencies of CD3 + T cells ( A and B ), CD19 + B cells ( C and D ), CD3 + FoxP3 + Treg ( E and F ) and CD3 + CD8 + IFN-γ + cytotoxic T cells ( G and H ). Representative contour plots depict interferon gamma (IFN-γ) expression of CD8 + T cells in spleen samples from animals killed at 18 dpi ( I ). The percentage of CD3 + CD8 + IFN-γ + cells is reported at the bottom right of each plot. Data are presented as mean ± SEM and differences between groups were assessed with one-way ANOVA and Tukey’s post-test. *p < 0.05, **p < 0.01

    Techniques Used: Flow Cytometry, Expressing

    Sequential treatment decreases demyelination while single treatments interfere with lymphocytes recruitment to the CNS. Immunohistochemical analysis of spinal cord sections of hu/m TNFR1-ki x hu/m TNFR2-ki mice immunized with MOG 35-55 and treated either with saline, EHD2-scTNF R2 (TNFR2 agonist), ATROSIMAB (TNFR1 antagonist) or a combination (E + A). Demyelination degree was measured with Klüver Barrera staining at 18 days post-immunization (dpi; n = 5–6/group; A and B ) and at 25 dpi ( n = 7–10/group; G and H ). The number of T cells present in the sections was measured by automated counting of CD3 + cells at 18 dpi ( n = 6–7/group; C and D ) and 25 dpi ( n = 6–9/group; I and J ). B-cell clustering was assessed by counting the number of perivascular cuffs (black stars) at 18 dpi ( n = 5–7/group; E and F ) and 25 dpi ( n = 5/group; K and L ). Data are presented as mean ± SEM and differences between groups were assessed with Mann–Whitney test. *p < 0.05
    Figure Legend Snippet: Sequential treatment decreases demyelination while single treatments interfere with lymphocytes recruitment to the CNS. Immunohistochemical analysis of spinal cord sections of hu/m TNFR1-ki x hu/m TNFR2-ki mice immunized with MOG 35-55 and treated either with saline, EHD2-scTNF R2 (TNFR2 agonist), ATROSIMAB (TNFR1 antagonist) or a combination (E + A). Demyelination degree was measured with Klüver Barrera staining at 18 days post-immunization (dpi; n = 5–6/group; A and B ) and at 25 dpi ( n = 7–10/group; G and H ). The number of T cells present in the sections was measured by automated counting of CD3 + cells at 18 dpi ( n = 6–7/group; C and D ) and 25 dpi ( n = 6–9/group; I and J ). B-cell clustering was assessed by counting the number of perivascular cuffs (black stars) at 18 dpi ( n = 5–7/group; E and F ) and 25 dpi ( n = 5/group; K and L ). Data are presented as mean ± SEM and differences between groups were assessed with Mann–Whitney test. *p < 0.05

    Techniques Used: Immunohistochemical staining, Staining, MANN-WHITNEY

    TNFR2 stimulation leads to an increased number of Tregs in the spinal cord at 18 dpi. Immunohistochemical analysis of FoxP3 staining of hu/m TNFR1-ki x hu/m TNFR2-ki mice immunized with MOG 35-55 and treated either with saline, EHD2-scTNF R2 (TNFR2 agonist), ATROSIMAB (TNFR1 antagonist) or a combination (E + A). FoxP3 + cells (black) were counted in spinal cord sections of mice killed at 18 days post-immunization (dpi; n = 5/group; A and B ) and at 25 dpi ( n = 5–7/group; C and D ). Data are presented as mean ± SEM and differences between groups were assessed with Mann–Whitney test. *p < 0.05
    Figure Legend Snippet: TNFR2 stimulation leads to an increased number of Tregs in the spinal cord at 18 dpi. Immunohistochemical analysis of FoxP3 staining of hu/m TNFR1-ki x hu/m TNFR2-ki mice immunized with MOG 35-55 and treated either with saline, EHD2-scTNF R2 (TNFR2 agonist), ATROSIMAB (TNFR1 antagonist) or a combination (E + A). FoxP3 + cells (black) were counted in spinal cord sections of mice killed at 18 days post-immunization (dpi; n = 5/group; A and B ) and at 25 dpi ( n = 5–7/group; C and D ). Data are presented as mean ± SEM and differences between groups were assessed with Mann–Whitney test. *p < 0.05

    Techniques Used: Immunohistochemical staining, Staining, MANN-WHITNEY

    mouse monoclonal immunoglobulin ig g1 antibody  (Hycult Biotech)


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    Hycult Biotech mouse monoclonal immunoglobulin ig g1 antibody
    Mouse Monoclonal Immunoglobulin Ig G1 Antibody, supplied by Hycult Biotech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 93 stars, based on 1 article reviews
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    mouse monoclonal immunoglobulin ig g1 antibody - by Bioz Stars, 2024-04
    93/100 stars

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    tnf alpha  (Hycult Biotech)


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    Hycult Biotech tnf alpha
    Histological changes induced by the new 4-clone cocktail (CII-3, CII-6, C2B-14, and C2A-12) . DBA/1J mice were injected with the new 4-clone cocktail on day 0 followed by LPS. On day 10, the front paws were amputated for histological examination. The tissues were stained with H&E and for immunohistochemistry <t>(TNF-alpha</t> and IL-1beta). Results shown are representative histological pictures of five mice ankle joints in each group. A: normal paw, B: arthritis, C: normal ankle joint, D: arthritic ankle joint, E: normal TNF- alpha, F: arthritic TNF- alpha, G: normal IL-1 beta, H: arthritic IL-1 beta.
    Tnf Alpha, supplied by Hycult Biotech, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Arthrogenicity of type II collagen monoclonal antibodies associated with complement activation and antigen affinity"

    Article Title: Arthrogenicity of type II collagen monoclonal antibodies associated with complement activation and antigen affinity

    Journal: Journal of Inflammation (London, England)

    doi: 10.1186/1476-9255-8-31

    Histological changes induced by the new 4-clone cocktail (CII-3, CII-6, C2B-14, and C2A-12) . DBA/1J mice were injected with the new 4-clone cocktail on day 0 followed by LPS. On day 10, the front paws were amputated for histological examination. The tissues were stained with H&E and for immunohistochemistry (TNF-alpha and IL-1beta). Results shown are representative histological pictures of five mice ankle joints in each group. A: normal paw, B: arthritis, C: normal ankle joint, D: arthritic ankle joint, E: normal TNF- alpha, F: arthritic TNF- alpha, G: normal IL-1 beta, H: arthritic IL-1 beta.
    Figure Legend Snippet: Histological changes induced by the new 4-clone cocktail (CII-3, CII-6, C2B-14, and C2A-12) . DBA/1J mice were injected with the new 4-clone cocktail on day 0 followed by LPS. On day 10, the front paws were amputated for histological examination. The tissues were stained with H&E and for immunohistochemistry (TNF-alpha and IL-1beta). Results shown are representative histological pictures of five mice ankle joints in each group. A: normal paw, B: arthritis, C: normal ankle joint, D: arthritic ankle joint, E: normal TNF- alpha, F: arthritic TNF- alpha, G: normal IL-1 beta, H: arthritic IL-1 beta.

    Techniques Used: Injection, Staining, Immunohistochemistry

    tnf α  (Hycult Biotech)


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    Hycult Biotech tnf α
    Effect of hemin treatment on proinflammatory cytokines concentration. Notes: One-way analysis of variance and Tukey’s post hoc test; * P <0.05; *** P <0.001 compared to the TNBS group or between groups. Abbreviations: IL-1β, interleukin 1β; TNBS, 2,4,6-trinitrobenzene sulfonic <t>acid;</t> <t>TNF-α,</t> tumor necrosis factor α.
    Tnf α, supplied by Hycult 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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    1) Product Images from "Hemin reduces inflammation associated with TNBS-induced colitis"

    Article Title: Hemin reduces inflammation associated with TNBS-induced colitis

    Journal: Clinical and Experimental Gastroenterology

    doi: 10.2147/CEG.S166197

    Effect of hemin treatment on proinflammatory cytokines concentration. Notes: One-way analysis of variance and Tukey’s post hoc test; * P <0.05; *** P <0.001 compared to the TNBS group or between groups. Abbreviations: IL-1β, interleukin 1β; TNBS, 2,4,6-trinitrobenzene sulfonic acid; TNF-α, tumor necrosis factor α.
    Figure Legend Snippet: Effect of hemin treatment on proinflammatory cytokines concentration. Notes: One-way analysis of variance and Tukey’s post hoc test; * P <0.05; *** P <0.001 compared to the TNBS group or between groups. Abbreviations: IL-1β, interleukin 1β; TNBS, 2,4,6-trinitrobenzene sulfonic acid; TNF-α, tumor necrosis factor α.

    Techniques Used: Concentration Assay

    tnf α  (Hycult Biotech)


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    Hycult Biotech tnf α
    Caspase3 (pg/ml), IL6 (pg/ml), <t> TNFα </t> (pg/ml), INFγ (ng/100 mg), and HSP70 (ng/100 mg) in the brain homogenates of the two groups of rats
    Tnf α, supplied by Hycult 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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    1) Product Images from "Etiology of autistic features: the persisting neurotoxic effects of propionic acid"

    Article Title: Etiology of autistic features: the persisting neurotoxic effects of propionic acid

    Journal: Journal of Neuroinflammation

    doi: 10.1186/1742-2094-9-74

    Caspase3 (pg/ml), IL6 (pg/ml),  TNFα  (pg/ml), INFγ (ng/100 mg), and HSP70 (ng/100 mg) in the brain homogenates of the two groups of rats
    Figure Legend Snippet: Caspase3 (pg/ml), IL6 (pg/ml), TNFα (pg/ml), INFγ (ng/100 mg), and HSP70 (ng/100 mg) in the brain homogenates of the two groups of rats

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    mouse tnf α elisa kit  (Hycult Biotech)


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    Hycult Biotech mouse tnf α elisa kit
    Caspase3 (pg/ml), IL6 (pg/ml), <t> TNFα </t> (pg/ml), INFγ (ng/100 mg), and HSP70 (ng/100 mg) in the brain homogenates of the two groups of rats
    Mouse Tnf α Elisa Kit, supplied by Hycult Biotech, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Etiology of autistic features: the persisting neurotoxic effects of propionic acid"

    Article Title: Etiology of autistic features: the persisting neurotoxic effects of propionic acid

    Journal: Journal of Neuroinflammation

    doi: 10.1186/1742-2094-9-74

    Caspase3 (pg/ml), IL6 (pg/ml),  TNFα  (pg/ml), INFγ (ng/100 mg), and HSP70 (ng/100 mg) in the brain homogenates of the two groups of rats
    Figure Legend Snippet: Caspase3 (pg/ml), IL6 (pg/ml), TNFα (pg/ml), INFγ (ng/100 mg), and HSP70 (ng/100 mg) in the brain homogenates of the two groups of rats

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    mouse tnf α  (Hycult Biotech)


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    Hycult Biotech mouse tnf α
    Caspase3 (pg/ml), IL6 (pg/ml), <t> TNFα </t> (pg/ml), INFγ (ng/100 mg), and HSP70 (ng/100 mg) in the brain homogenates of the two groups of rats
    Mouse Tnf α, supplied by Hycult 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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    1) Product Images from "Etiology of autistic features: the persisting neurotoxic effects of propionic acid"

    Article Title: Etiology of autistic features: the persisting neurotoxic effects of propionic acid

    Journal: Journal of Neuroinflammation

    doi: 10.1186/1742-2094-9-74

    Caspase3 (pg/ml), IL6 (pg/ml),  TNFα  (pg/ml), INFγ (ng/100 mg), and HSP70 (ng/100 mg) in the brain homogenates of the two groups of rats
    Figure Legend Snippet: Caspase3 (pg/ml), IL6 (pg/ml), TNFα (pg/ml), INFγ (ng/100 mg), and HSP70 (ng/100 mg) in the brain homogenates of the two groups of rats

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    human tnf α  (Hycult Biotech)


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    Hycult Biotech human tnf α
    Caspase3 (pg/ml), IL6 (pg/ml), <t> TNFα </t> (pg/ml), INFγ (ng/100 mg), and HSP70 (ng/100 mg) in the brain homogenates of the two groups of rats
    Human Tnf α, supplied by Hycult 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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    1) Product Images from "Etiology of autistic features: the persisting neurotoxic effects of propionic acid"

    Article Title: Etiology of autistic features: the persisting neurotoxic effects of propionic acid

    Journal: Journal of Neuroinflammation

    doi: 10.1186/1742-2094-9-74

    Caspase3 (pg/ml), IL6 (pg/ml),  TNFα  (pg/ml), INFγ (ng/100 mg), and HSP70 (ng/100 mg) in the brain homogenates of the two groups of rats
    Figure Legend Snippet: Caspase3 (pg/ml), IL6 (pg/ml), TNFα (pg/ml), INFγ (ng/100 mg), and HSP70 (ng/100 mg) in the brain homogenates of the two groups of rats

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    Hycult Biotech tnfr1
    EHD2-scTNF R2 enhances the therapeutic effect of ATROSIMAB on EAE. Hu/m <t>TNFR1-ki</t> x hu/m TNFR2-ki mice were immunized with MOG 35-55 and treated either with saline ( n = 13), EHD2-scTNF R2 (TNFR2 agonist; n = 8), ATROSIMAB <t>(TNFR1</t> antagonist; n = 11) or a combination (E + A; n = 9). Schematic representation of EAE induction, development and treatment regimen ( A ). EHD2-scTNF R2 [10 mg/kg] was injected i.p. at 6, 9 and 12 days post-immunization (dpi; blue and green arrows) while ATROSIMAB [20 mg/kg] was injected at 12, 15 and 18 dpi (red and green arrows). Body weight (BW; B ) and disease development ( C ) were measured daily until 25 dpi. EAE development is represented as sum of EAE scores over 25 days ( D ) but also as mean score at the different treatment days and at killing day ( E ). On the first day of symptoms, disease onset was recorded ( F ). Linear regression curves of disease development ( C ) are shown together with dashed lines representing 95% confidence intervals. Statistical difference between slopes is shown at the bottom right of the graph. Data are presented as mean ± SEM and differences between groups were assessed with Mann–Whitney or Kruskal–Wallis tests, except for relative body weight for which two-way ANOVA and Tukey’s post-test were used. # = PBS vs E + A; $ = PBS vs ATROSIMAB. * /#/$ p < 0.05, ** /##/$$ p < 0.01
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    Hycult Biotech tnf
    EHD2-scTNF R2 enhances the therapeutic effect of ATROSIMAB on EAE. Hu/m <t>TNFR1-ki</t> x hu/m TNFR2-ki mice were immunized with MOG 35-55 and treated either with saline ( n = 13), EHD2-scTNF R2 (TNFR2 agonist; n = 8), ATROSIMAB <t>(TNFR1</t> antagonist; n = 11) or a combination (E + A; n = 9). Schematic representation of EAE induction, development and treatment regimen ( A ). EHD2-scTNF R2 [10 mg/kg] was injected i.p. at 6, 9 and 12 days post-immunization (dpi; blue and green arrows) while ATROSIMAB [20 mg/kg] was injected at 12, 15 and 18 dpi (red and green arrows). Body weight (BW; B ) and disease development ( C ) were measured daily until 25 dpi. EAE development is represented as sum of EAE scores over 25 days ( D ) but also as mean score at the different treatment days and at killing day ( E ). On the first day of symptoms, disease onset was recorded ( F ). Linear regression curves of disease development ( C ) are shown together with dashed lines representing 95% confidence intervals. Statistical difference between slopes is shown at the bottom right of the graph. Data are presented as mean ± SEM and differences between groups were assessed with Mann–Whitney or Kruskal–Wallis tests, except for relative body weight for which two-way ANOVA and Tukey’s post-test were used. # = PBS vs E + A; $ = PBS vs ATROSIMAB. * /#/$ p < 0.05, ** /##/$$ p < 0.01
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    Hycult Biotech tnf alpha
    Logarithmic transformation of <t>TNF-alpha</t> activity normalized using total protein in the inflamed paw: \documentclass[12pt]{minimal} \usepackage{wasysym} \usepackage[substack]{amsmath} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage[mathscr]{eucal} \usepackage{mathrsfs} \DeclareFontFamily{T1}{linotext}{} \DeclareFontShape{T1}{linotext}{m}{n} {linotext }{} \DeclareSymbolFont{linotext}{T1}{linotext}{m}{n} \DeclareSymbolFontAlphabet{\mathLINOTEXT}{linotext} \begin{document} ${\mathrm{y' = }}\root {\mathrm{3}} \of {\mathrm{Y}} $\end{document} . TNF-alpha levels were measured 48 hours post-induction of inflammation and normalized using total protein (n=6 for control, n=8 for all other groups). <t>ELISA</t> sensitivity = 10.9 to 700 pg/mL. *p<0.05. **p<0.01. ***p<0.001. Data is displayed as mean ± SD. TNF-alpha data derived from same mouse hind-paw recorded in edema measurements.
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    Hycult Biotech mouse monoclonal immunoglobulin ig g1 antibody
    Logarithmic transformation of <t>TNF-alpha</t> activity normalized using total protein in the inflamed paw: \documentclass[12pt]{minimal} \usepackage{wasysym} \usepackage[substack]{amsmath} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage[mathscr]{eucal} \usepackage{mathrsfs} \DeclareFontFamily{T1}{linotext}{} \DeclareFontShape{T1}{linotext}{m}{n} {linotext }{} \DeclareSymbolFont{linotext}{T1}{linotext}{m}{n} \DeclareSymbolFontAlphabet{\mathLINOTEXT}{linotext} \begin{document} ${\mathrm{y' = }}\root {\mathrm{3}} \of {\mathrm{Y}} $\end{document} . TNF-alpha levels were measured 48 hours post-induction of inflammation and normalized using total protein (n=6 for control, n=8 for all other groups). <t>ELISA</t> sensitivity = 10.9 to 700 pg/mL. *p<0.05. **p<0.01. ***p<0.001. Data is displayed as mean ± SD. TNF-alpha data derived from same mouse hind-paw recorded in edema measurements.
    Mouse Monoclonal Immunoglobulin Ig G1 Antibody, supplied by Hycult Biotech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Hycult Biotech tnf α
    Effect of hemin treatment on proinflammatory cytokines concentration. Notes: One-way analysis of variance and Tukey’s post hoc test; * P <0.05; *** P <0.001 compared to the TNBS group or between groups. Abbreviations: IL-1β, interleukin 1β; TNBS, 2,4,6-trinitrobenzene sulfonic <t>acid;</t> <t>TNF-α,</t> tumor necrosis factor α.
    Tnf α, supplied by Hycult 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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    Hycult Biotech mouse tnf α elisa kit
    Caspase3 (pg/ml), IL6 (pg/ml), <t> TNFα </t> (pg/ml), INFγ (ng/100 mg), and HSP70 (ng/100 mg) in the brain homogenates of the two groups of rats
    Mouse Tnf α Elisa Kit, supplied by Hycult Biotech, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Caspase3 (pg/ml), IL6 (pg/ml), <t> TNFα </t> (pg/ml), INFγ (ng/100 mg), and HSP70 (ng/100 mg) in the brain homogenates of the two groups of rats
    Mouse Tnf α, supplied by Hycult 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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    Caspase3 (pg/ml), IL6 (pg/ml), <t> TNFα </t> (pg/ml), INFγ (ng/100 mg), and HSP70 (ng/100 mg) in the brain homogenates of the two groups of rats
    Human Tnf α, supplied by Hycult 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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    EHD2-scTNF R2 enhances the therapeutic effect of ATROSIMAB on EAE. Hu/m TNFR1-ki x hu/m TNFR2-ki mice were immunized with MOG 35-55 and treated either with saline ( n = 13), EHD2-scTNF R2 (TNFR2 agonist; n = 8), ATROSIMAB (TNFR1 antagonist; n = 11) or a combination (E + A; n = 9). Schematic representation of EAE induction, development and treatment regimen ( A ). EHD2-scTNF R2 [10 mg/kg] was injected i.p. at 6, 9 and 12 days post-immunization (dpi; blue and green arrows) while ATROSIMAB [20 mg/kg] was injected at 12, 15 and 18 dpi (red and green arrows). Body weight (BW; B ) and disease development ( C ) were measured daily until 25 dpi. EAE development is represented as sum of EAE scores over 25 days ( D ) but also as mean score at the different treatment days and at killing day ( E ). On the first day of symptoms, disease onset was recorded ( F ). Linear regression curves of disease development ( C ) are shown together with dashed lines representing 95% confidence intervals. Statistical difference between slopes is shown at the bottom right of the graph. Data are presented as mean ± SEM and differences between groups were assessed with Mann–Whitney or Kruskal–Wallis tests, except for relative body weight for which two-way ANOVA and Tukey’s post-test were used. # = PBS vs E + A; $ = PBS vs ATROSIMAB. * /#/$ p < 0.05, ** /##/$$ p < 0.01

    Journal: Journal of Neuroinflammation

    Article Title: Sequential treatment with a TNFR2 agonist and a TNFR1 antagonist improves outcomes in a humanized mouse model for MS

    doi: 10.1186/s12974-023-02785-y

    Figure Lengend Snippet: EHD2-scTNF R2 enhances the therapeutic effect of ATROSIMAB on EAE. Hu/m TNFR1-ki x hu/m TNFR2-ki mice were immunized with MOG 35-55 and treated either with saline ( n = 13), EHD2-scTNF R2 (TNFR2 agonist; n = 8), ATROSIMAB (TNFR1 antagonist; n = 11) or a combination (E + A; n = 9). Schematic representation of EAE induction, development and treatment regimen ( A ). EHD2-scTNF R2 [10 mg/kg] was injected i.p. at 6, 9 and 12 days post-immunization (dpi; blue and green arrows) while ATROSIMAB [20 mg/kg] was injected at 12, 15 and 18 dpi (red and green arrows). Body weight (BW; B ) and disease development ( C ) were measured daily until 25 dpi. EAE development is represented as sum of EAE scores over 25 days ( D ) but also as mean score at the different treatment days and at killing day ( E ). On the first day of symptoms, disease onset was recorded ( F ). Linear regression curves of disease development ( C ) are shown together with dashed lines representing 95% confidence intervals. Statistical difference between slopes is shown at the bottom right of the graph. Data are presented as mean ± SEM and differences between groups were assessed with Mann–Whitney or Kruskal–Wallis tests, except for relative body weight for which two-way ANOVA and Tukey’s post-test were used. # = PBS vs E + A; $ = PBS vs ATROSIMAB. * /#/$ p < 0.05, ** /##/$$ p < 0.01

    Article Snippet: The mouse monoclonal immunoglobulin (Ig) G1 antibody (HM1097) against TNFR1 was purchased from Hycult Biotech (Uden, The Netherlands).

    Techniques: Injection, MANN-WHITNEY

    Modulating TNFRs selectively does not lead to major changes in leukocytes subsets. Hu/m TNFR1-ki x hu/m TNFR2-ki mice treated either with saline, EHD2-scTNF R2 (TNFR2 agonist), ATROSIMAB (TNFR1 antagonist) or a combination (E + A) were killed either 18 (acute) or 25 (chronic) days post-immunization (dpi; n = 3–5 animals/treatment group/killing timepoint). Immune cells from inguinal lymph nodes (on the left) and spleen (on the right) were analyzed by flow cytometry to reveal the frequencies of CD3 + T cells ( A and B ), CD19 + B cells ( C and D ), CD3 + FoxP3 + Treg ( E and F ) and CD3 + CD8 + IFN-γ + cytotoxic T cells ( G and H ). Representative contour plots depict interferon gamma (IFN-γ) expression of CD8 + T cells in spleen samples from animals killed at 18 dpi ( I ). The percentage of CD3 + CD8 + IFN-γ + cells is reported at the bottom right of each plot. Data are presented as mean ± SEM and differences between groups were assessed with one-way ANOVA and Tukey’s post-test. *p < 0.05, **p < 0.01

    Journal: Journal of Neuroinflammation

    Article Title: Sequential treatment with a TNFR2 agonist and a TNFR1 antagonist improves outcomes in a humanized mouse model for MS

    doi: 10.1186/s12974-023-02785-y

    Figure Lengend Snippet: Modulating TNFRs selectively does not lead to major changes in leukocytes subsets. Hu/m TNFR1-ki x hu/m TNFR2-ki mice treated either with saline, EHD2-scTNF R2 (TNFR2 agonist), ATROSIMAB (TNFR1 antagonist) or a combination (E + A) were killed either 18 (acute) or 25 (chronic) days post-immunization (dpi; n = 3–5 animals/treatment group/killing timepoint). Immune cells from inguinal lymph nodes (on the left) and spleen (on the right) were analyzed by flow cytometry to reveal the frequencies of CD3 + T cells ( A and B ), CD19 + B cells ( C and D ), CD3 + FoxP3 + Treg ( E and F ) and CD3 + CD8 + IFN-γ + cytotoxic T cells ( G and H ). Representative contour plots depict interferon gamma (IFN-γ) expression of CD8 + T cells in spleen samples from animals killed at 18 dpi ( I ). The percentage of CD3 + CD8 + IFN-γ + cells is reported at the bottom right of each plot. Data are presented as mean ± SEM and differences between groups were assessed with one-way ANOVA and Tukey’s post-test. *p < 0.05, **p < 0.01

    Article Snippet: The mouse monoclonal immunoglobulin (Ig) G1 antibody (HM1097) against TNFR1 was purchased from Hycult Biotech (Uden, The Netherlands).

    Techniques: Flow Cytometry, Expressing

    Sequential treatment decreases demyelination while single treatments interfere with lymphocytes recruitment to the CNS. Immunohistochemical analysis of spinal cord sections of hu/m TNFR1-ki x hu/m TNFR2-ki mice immunized with MOG 35-55 and treated either with saline, EHD2-scTNF R2 (TNFR2 agonist), ATROSIMAB (TNFR1 antagonist) or a combination (E + A). Demyelination degree was measured with Klüver Barrera staining at 18 days post-immunization (dpi; n = 5–6/group; A and B ) and at 25 dpi ( n = 7–10/group; G and H ). The number of T cells present in the sections was measured by automated counting of CD3 + cells at 18 dpi ( n = 6–7/group; C and D ) and 25 dpi ( n = 6–9/group; I and J ). B-cell clustering was assessed by counting the number of perivascular cuffs (black stars) at 18 dpi ( n = 5–7/group; E and F ) and 25 dpi ( n = 5/group; K and L ). Data are presented as mean ± SEM and differences between groups were assessed with Mann–Whitney test. *p < 0.05

    Journal: Journal of Neuroinflammation

    Article Title: Sequential treatment with a TNFR2 agonist and a TNFR1 antagonist improves outcomes in a humanized mouse model for MS

    doi: 10.1186/s12974-023-02785-y

    Figure Lengend Snippet: Sequential treatment decreases demyelination while single treatments interfere with lymphocytes recruitment to the CNS. Immunohistochemical analysis of spinal cord sections of hu/m TNFR1-ki x hu/m TNFR2-ki mice immunized with MOG 35-55 and treated either with saline, EHD2-scTNF R2 (TNFR2 agonist), ATROSIMAB (TNFR1 antagonist) or a combination (E + A). Demyelination degree was measured with Klüver Barrera staining at 18 days post-immunization (dpi; n = 5–6/group; A and B ) and at 25 dpi ( n = 7–10/group; G and H ). The number of T cells present in the sections was measured by automated counting of CD3 + cells at 18 dpi ( n = 6–7/group; C and D ) and 25 dpi ( n = 6–9/group; I and J ). B-cell clustering was assessed by counting the number of perivascular cuffs (black stars) at 18 dpi ( n = 5–7/group; E and F ) and 25 dpi ( n = 5/group; K and L ). Data are presented as mean ± SEM and differences between groups were assessed with Mann–Whitney test. *p < 0.05

    Article Snippet: The mouse monoclonal immunoglobulin (Ig) G1 antibody (HM1097) against TNFR1 was purchased from Hycult Biotech (Uden, The Netherlands).

    Techniques: Immunohistochemical staining, Staining, MANN-WHITNEY

    TNFR2 stimulation leads to an increased number of Tregs in the spinal cord at 18 dpi. Immunohistochemical analysis of FoxP3 staining of hu/m TNFR1-ki x hu/m TNFR2-ki mice immunized with MOG 35-55 and treated either with saline, EHD2-scTNF R2 (TNFR2 agonist), ATROSIMAB (TNFR1 antagonist) or a combination (E + A). FoxP3 + cells (black) were counted in spinal cord sections of mice killed at 18 days post-immunization (dpi; n = 5/group; A and B ) and at 25 dpi ( n = 5–7/group; C and D ). Data are presented as mean ± SEM and differences between groups were assessed with Mann–Whitney test. *p < 0.05

    Journal: Journal of Neuroinflammation

    Article Title: Sequential treatment with a TNFR2 agonist and a TNFR1 antagonist improves outcomes in a humanized mouse model for MS

    doi: 10.1186/s12974-023-02785-y

    Figure Lengend Snippet: TNFR2 stimulation leads to an increased number of Tregs in the spinal cord at 18 dpi. Immunohistochemical analysis of FoxP3 staining of hu/m TNFR1-ki x hu/m TNFR2-ki mice immunized with MOG 35-55 and treated either with saline, EHD2-scTNF R2 (TNFR2 agonist), ATROSIMAB (TNFR1 antagonist) or a combination (E + A). FoxP3 + cells (black) were counted in spinal cord sections of mice killed at 18 days post-immunization (dpi; n = 5/group; A and B ) and at 25 dpi ( n = 5–7/group; C and D ). Data are presented as mean ± SEM and differences between groups were assessed with Mann–Whitney test. *p < 0.05

    Article Snippet: The mouse monoclonal immunoglobulin (Ig) G1 antibody (HM1097) against TNFR1 was purchased from Hycult Biotech (Uden, The Netherlands).

    Techniques: Immunohistochemical staining, Staining, MANN-WHITNEY

    Logarithmic transformation of TNF-alpha activity normalized using total protein in the inflamed paw: \documentclass[12pt]{minimal} \usepackage{wasysym} \usepackage[substack]{amsmath} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage[mathscr]{eucal} \usepackage{mathrsfs} \DeclareFontFamily{T1}{linotext}{} \DeclareFontShape{T1}{linotext}{m}{n} {linotext }{} \DeclareSymbolFont{linotext}{T1}{linotext}{m}{n} \DeclareSymbolFontAlphabet{\mathLINOTEXT}{linotext} \begin{document} ${\mathrm{y' = }}\root {\mathrm{3}} \of {\mathrm{Y}} $\end{document} . TNF-alpha levels were measured 48 hours post-induction of inflammation and normalized using total protein (n=6 for control, n=8 for all other groups). ELISA sensitivity = 10.9 to 700 pg/mL. *p<0.05. **p<0.01. ***p<0.001. Data is displayed as mean ± SD. TNF-alpha data derived from same mouse hind-paw recorded in edema measurements.

    Journal: Journal of Inflammation Research

    Article Title: Umbilical Cord Stem Cell Lysate: A New Biologic Injectate for the Putative Treatment of Acute Temporomandibular Joint Inflammation

    doi: 10.2147/JIR.S420741

    Figure Lengend Snippet: Logarithmic transformation of TNF-alpha activity normalized using total protein in the inflamed paw: \documentclass[12pt]{minimal} \usepackage{wasysym} \usepackage[substack]{amsmath} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage[mathscr]{eucal} \usepackage{mathrsfs} \DeclareFontFamily{T1}{linotext}{} \DeclareFontShape{T1}{linotext}{m}{n} {linotext }{} \DeclareSymbolFont{linotext}{T1}{linotext}{m}{n} \DeclareSymbolFontAlphabet{\mathLINOTEXT}{linotext} \begin{document} ${\mathrm{y' = }}\root {\mathrm{3}} \of {\mathrm{Y}} $\end{document} . TNF-alpha levels were measured 48 hours post-induction of inflammation and normalized using total protein (n=6 for control, n=8 for all other groups). ELISA sensitivity = 10.9 to 700 pg/mL. *p<0.05. **p<0.01. ***p<0.001. Data is displayed as mean ± SD. TNF-alpha data derived from same mouse hind-paw recorded in edema measurements.

    Article Snippet: Supernatants were tested for MPO using MPO ELISA kit (Hycult Biotech, Cat HK210) and TNF-alpha using TNF-alpha Quantikine ELISA kit (R&D Systems, Cat. MTA00B).

    Techniques: Transformation Assay, Activity Assay, Enzyme-linked Immunosorbent Assay, Derivative Assay

    Effect of hemin treatment on proinflammatory cytokines concentration. Notes: One-way analysis of variance and Tukey’s post hoc test; * P <0.05; *** P <0.001 compared to the TNBS group or between groups. Abbreviations: IL-1β, interleukin 1β; TNBS, 2,4,6-trinitrobenzene sulfonic acid; TNF-α, tumor necrosis factor α.

    Journal: Clinical and Experimental Gastroenterology

    Article Title: Hemin reduces inflammation associated with TNBS-induced colitis

    doi: 10.2147/CEG.S166197

    Figure Lengend Snippet: Effect of hemin treatment on proinflammatory cytokines concentration. Notes: One-way analysis of variance and Tukey’s post hoc test; * P <0.05; *** P <0.001 compared to the TNBS group or between groups. Abbreviations: IL-1β, interleukin 1β; TNBS, 2,4,6-trinitrobenzene sulfonic acid; TNF-α, tumor necrosis factor α.

    Article Snippet: The TNF-α, IL-1β, and IL-10 levels were measured spectrophotometrically at 450 nm (ELISA kit Quantikine, Hycult Biotechnology) and expressed as pg/mL.

    Techniques: Concentration Assay

    Caspase3 (pg/ml), IL6 (pg/ml),  TNFα  (pg/ml), INFγ (ng/100 mg), and HSP70 (ng/100 mg) in the brain homogenates of the two groups of rats

    Journal: Journal of Neuroinflammation

    Article Title: Etiology of autistic features: the persisting neurotoxic effects of propionic acid

    doi: 10.1186/1742-2094-9-74

    Figure Lengend Snippet: Caspase3 (pg/ml), IL6 (pg/ml), TNFα (pg/ml), INFγ (ng/100 mg), and HSP70 (ng/100 mg) in the brain homogenates of the two groups of rats

    Article Snippet: TNF α was measured using a mouse TNF α ELISA kit (Hycult Biotech, Uden, Netherlands.

    Techniques:

    Caspase3 (pg/ml), IL6 (pg/ml),  TNFα  (pg/ml), INFγ (ng/100 mg), and HSP70 (ng/100 mg) in the brain homogenates of the two groups of rats

    Journal: Journal of Neuroinflammation

    Article Title: Etiology of autistic features: the persisting neurotoxic effects of propionic acid

    doi: 10.1186/1742-2094-9-74

    Figure Lengend Snippet: Caspase3 (pg/ml), IL6 (pg/ml), TNFα (pg/ml), INFγ (ng/100 mg), and HSP70 (ng/100 mg) in the brain homogenates of the two groups of rats

    Article Snippet: One unit of Hycult Biotech Mouse TNF α approximates the bioactivity of 16 units of human TNF α according to the standard L929 cytotoxicity assays for TNF α prepared by the World Health Organization (WHO).

    Techniques:

    Caspase3 (pg/ml), IL6 (pg/ml),  TNFα  (pg/ml), INFγ (ng/100 mg), and HSP70 (ng/100 mg) in the brain homogenates of the two groups of rats

    Journal: Journal of Neuroinflammation

    Article Title: Etiology of autistic features: the persisting neurotoxic effects of propionic acid

    doi: 10.1186/1742-2094-9-74

    Figure Lengend Snippet: Caspase3 (pg/ml), IL6 (pg/ml), TNFα (pg/ml), INFγ (ng/100 mg), and HSP70 (ng/100 mg) in the brain homogenates of the two groups of rats

    Article Snippet: One unit of Hycult Biotech Mouse TNF α approximates the bioactivity of 16 units of human TNF α according to the standard L929 cytotoxicity assays for TNF α prepared by the World Health Organization (WHO).

    Techniques: