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  • 93
    MedChemExpress lps cit cit
    Lps Cit Cit, supplied by MedChemExpress, 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/lps cit cit/product/MedChemExpress
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    lps cit cit - by Bioz Stars, 2023-06
    93/100 stars
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    97
    Cell Signaling Technology Inc cit h3
    ( A ) Increased TLR4 expression in neutrophils from blood or pericontusional brain tissue at 24 hours after sham (blue)/TBI (red). Scatterplots show % TLR4 + neutrophils from n = 5 mice per group. ( B ) Extracellular expression <t>of</t> <t>MPO,</t> NE, and <t>Cit-H3</t> in CD11b + Ly6G + neutrophils derived from blood or brain from C3H/OuJ (blue) or C3H/HeJ (red) mice after sham/TBI. Representative flow cytometry scatterplots are provided along with quantified data. Brain panels are depicted as % total brain cells, and blood panels are shown as % leukocytes [% white blood cell (WBC)]. ( C ) Cerebral perfusion and cerebral edema were quantified by MRI in C3H/OuJ or C3H/HeJ mice at 24 hours after TBI. Cerebral hypoperfusion, cerebral edema, and the region of slow flow are attenuated in C3H/HeJ mice, indicative of improved cerebrovascular function following TLR4 inhibition. MPO-DNA binding, a quantitative marker of NET formation, was measured in blood from mice immediately following the final imaging session. ( D ) Carboxyfluorescein diacetate succinimidyl ester (CFSE)–labeled wild-type (WT; C3H/OuJ) or mutant (MUT; C3H/HeJ) neutrophils were administered to WT or MUT mice at the time of TBI. NET formation was elevated in WT > WT and WT > MUT mice, as assessed by flow cytometry, as compared to MUT > MUT and MUT > WT mice. ( E and F ) Representative images showing changes in cerebral edema (top) and CBF (bottom), as assessed by MRI and LSCI, respectively. For all panels, data are means ± SEM from n = 8 mice per group from two independent experiments. Data were analyzed using a Student’s t test or one-way analysis of variance (ANOVA) followed by Tukey’s post hoc test (* P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; ns, not statistically significant).
    Cit H3, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cit h3/product/Cell Signaling Technology Inc
    Average 97 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    cit h3 - by Bioz Stars, 2023-06
    97/100 stars
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    85
    Thermo Fisher gene exp cit hs00392339 m1
    ( A ) Increased TLR4 expression in neutrophils from blood or pericontusional brain tissue at 24 hours after sham (blue)/TBI (red). Scatterplots show % TLR4 + neutrophils from n = 5 mice per group. ( B ) Extracellular expression <t>of</t> <t>MPO,</t> NE, and <t>Cit-H3</t> in CD11b + Ly6G + neutrophils derived from blood or brain from C3H/OuJ (blue) or C3H/HeJ (red) mice after sham/TBI. Representative flow cytometry scatterplots are provided along with quantified data. Brain panels are depicted as % total brain cells, and blood panels are shown as % leukocytes [% white blood cell (WBC)]. ( C ) Cerebral perfusion and cerebral edema were quantified by MRI in C3H/OuJ or C3H/HeJ mice at 24 hours after TBI. Cerebral hypoperfusion, cerebral edema, and the region of slow flow are attenuated in C3H/HeJ mice, indicative of improved cerebrovascular function following TLR4 inhibition. MPO-DNA binding, a quantitative marker of NET formation, was measured in blood from mice immediately following the final imaging session. ( D ) Carboxyfluorescein diacetate succinimidyl ester (CFSE)–labeled wild-type (WT; C3H/OuJ) or mutant (MUT; C3H/HeJ) neutrophils were administered to WT or MUT mice at the time of TBI. NET formation was elevated in WT > WT and WT > MUT mice, as assessed by flow cytometry, as compared to MUT > MUT and MUT > WT mice. ( E and F ) Representative images showing changes in cerebral edema (top) and CBF (bottom), as assessed by MRI and LSCI, respectively. For all panels, data are means ± SEM from n = 8 mice per group from two independent experiments. Data were analyzed using a Student’s t test or one-way analysis of variance (ANOVA) followed by Tukey’s post hoc test (* P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; ns, not statistically significant).
    Gene Exp Cit Hs00392339 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/gene exp cit hs00392339 m1/product/Thermo Fisher
    Average 85 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    gene exp cit hs00392339 m1 - by Bioz Stars, 2023-06
    85/100 stars
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    93
    MedChemExpress maleimidocaproyl val cit pabc monomethyl auristatin e
    ( A ) Increased TLR4 expression in neutrophils from blood or pericontusional brain tissue at 24 hours after sham (blue)/TBI (red). Scatterplots show % TLR4 + neutrophils from n = 5 mice per group. ( B ) Extracellular expression <t>of</t> <t>MPO,</t> NE, and <t>Cit-H3</t> in CD11b + Ly6G + neutrophils derived from blood or brain from C3H/OuJ (blue) or C3H/HeJ (red) mice after sham/TBI. Representative flow cytometry scatterplots are provided along with quantified data. Brain panels are depicted as % total brain cells, and blood panels are shown as % leukocytes [% white blood cell (WBC)]. ( C ) Cerebral perfusion and cerebral edema were quantified by MRI in C3H/OuJ or C3H/HeJ mice at 24 hours after TBI. Cerebral hypoperfusion, cerebral edema, and the region of slow flow are attenuated in C3H/HeJ mice, indicative of improved cerebrovascular function following TLR4 inhibition. MPO-DNA binding, a quantitative marker of NET formation, was measured in blood from mice immediately following the final imaging session. ( D ) Carboxyfluorescein diacetate succinimidyl ester (CFSE)–labeled wild-type (WT; C3H/OuJ) or mutant (MUT; C3H/HeJ) neutrophils were administered to WT or MUT mice at the time of TBI. NET formation was elevated in WT > WT and WT > MUT mice, as assessed by flow cytometry, as compared to MUT > MUT and MUT > WT mice. ( E and F ) Representative images showing changes in cerebral edema (top) and CBF (bottom), as assessed by MRI and LSCI, respectively. For all panels, data are means ± SEM from n = 8 mice per group from two independent experiments. Data were analyzed using a Student’s t test or one-way analysis of variance (ANOVA) followed by Tukey’s post hoc test (* P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; ns, not statistically significant).
    Maleimidocaproyl Val Cit Pabc Monomethyl Auristatin E, supplied by MedChemExpress, 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/maleimidocaproyl val cit pabc monomethyl auristatin e/product/MedChemExpress
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    maleimidocaproyl val cit pabc monomethyl auristatin e - by Bioz Stars, 2023-06
    93/100 stars
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    94
    Dojindo Labs cell counting cit 8
    ( A ) Increased TLR4 expression in neutrophils from blood or pericontusional brain tissue at 24 hours after sham (blue)/TBI (red). Scatterplots show % TLR4 + neutrophils from n = 5 mice per group. ( B ) Extracellular expression <t>of</t> <t>MPO,</t> NE, and <t>Cit-H3</t> in CD11b + Ly6G + neutrophils derived from blood or brain from C3H/OuJ (blue) or C3H/HeJ (red) mice after sham/TBI. Representative flow cytometry scatterplots are provided along with quantified data. Brain panels are depicted as % total brain cells, and blood panels are shown as % leukocytes [% white blood cell (WBC)]. ( C ) Cerebral perfusion and cerebral edema were quantified by MRI in C3H/OuJ or C3H/HeJ mice at 24 hours after TBI. Cerebral hypoperfusion, cerebral edema, and the region of slow flow are attenuated in C3H/HeJ mice, indicative of improved cerebrovascular function following TLR4 inhibition. MPO-DNA binding, a quantitative marker of NET formation, was measured in blood from mice immediately following the final imaging session. ( D ) Carboxyfluorescein diacetate succinimidyl ester (CFSE)–labeled wild-type (WT; C3H/OuJ) or mutant (MUT; C3H/HeJ) neutrophils were administered to WT or MUT mice at the time of TBI. NET formation was elevated in WT > WT and WT > MUT mice, as assessed by flow cytometry, as compared to MUT > MUT and MUT > WT mice. ( E and F ) Representative images showing changes in cerebral edema (top) and CBF (bottom), as assessed by MRI and LSCI, respectively. For all panels, data are means ± SEM from n = 8 mice per group from two independent experiments. Data were analyzed using a Student’s t test or one-way analysis of variance (ANOVA) followed by Tukey’s post hoc test (* P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; ns, not statistically significant).
    Cell Counting Cit 8, supplied by Dojindo Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cell counting cit 8/product/Dojindo Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    cell counting cit 8 - by Bioz Stars, 2023-06
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    Image Search Results


    ( A ) Increased TLR4 expression in neutrophils from blood or pericontusional brain tissue at 24 hours after sham (blue)/TBI (red). Scatterplots show % TLR4 + neutrophils from n = 5 mice per group. ( B ) Extracellular expression of MPO, NE, and Cit-H3 in CD11b + Ly6G + neutrophils derived from blood or brain from C3H/OuJ (blue) or C3H/HeJ (red) mice after sham/TBI. Representative flow cytometry scatterplots are provided along with quantified data. Brain panels are depicted as % total brain cells, and blood panels are shown as % leukocytes [% white blood cell (WBC)]. ( C ) Cerebral perfusion and cerebral edema were quantified by MRI in C3H/OuJ or C3H/HeJ mice at 24 hours after TBI. Cerebral hypoperfusion, cerebral edema, and the region of slow flow are attenuated in C3H/HeJ mice, indicative of improved cerebrovascular function following TLR4 inhibition. MPO-DNA binding, a quantitative marker of NET formation, was measured in blood from mice immediately following the final imaging session. ( D ) Carboxyfluorescein diacetate succinimidyl ester (CFSE)–labeled wild-type (WT; C3H/OuJ) or mutant (MUT; C3H/HeJ) neutrophils were administered to WT or MUT mice at the time of TBI. NET formation was elevated in WT > WT and WT > MUT mice, as assessed by flow cytometry, as compared to MUT > MUT and MUT > WT mice. ( E and F ) Representative images showing changes in cerebral edema (top) and CBF (bottom), as assessed by MRI and LSCI, respectively. For all panels, data are means ± SEM from n = 8 mice per group from two independent experiments. Data were analyzed using a Student’s t test or one-way analysis of variance (ANOVA) followed by Tukey’s post hoc test (* P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; ns, not statistically significant).

    Journal: Science Advances

    Article Title: Neutrophil extracellular traps exacerbate neurological deficits after traumatic brain injury

    doi: 10.1126/sciadv.aax8847

    Figure Lengend Snippet: ( A ) Increased TLR4 expression in neutrophils from blood or pericontusional brain tissue at 24 hours after sham (blue)/TBI (red). Scatterplots show % TLR4 + neutrophils from n = 5 mice per group. ( B ) Extracellular expression of MPO, NE, and Cit-H3 in CD11b + Ly6G + neutrophils derived from blood or brain from C3H/OuJ (blue) or C3H/HeJ (red) mice after sham/TBI. Representative flow cytometry scatterplots are provided along with quantified data. Brain panels are depicted as % total brain cells, and blood panels are shown as % leukocytes [% white blood cell (WBC)]. ( C ) Cerebral perfusion and cerebral edema were quantified by MRI in C3H/OuJ or C3H/HeJ mice at 24 hours after TBI. Cerebral hypoperfusion, cerebral edema, and the region of slow flow are attenuated in C3H/HeJ mice, indicative of improved cerebrovascular function following TLR4 inhibition. MPO-DNA binding, a quantitative marker of NET formation, was measured in blood from mice immediately following the final imaging session. ( D ) Carboxyfluorescein diacetate succinimidyl ester (CFSE)–labeled wild-type (WT; C3H/OuJ) or mutant (MUT; C3H/HeJ) neutrophils were administered to WT or MUT mice at the time of TBI. NET formation was elevated in WT > WT and WT > MUT mice, as assessed by flow cytometry, as compared to MUT > MUT and MUT > WT mice. ( E and F ) Representative images showing changes in cerebral edema (top) and CBF (bottom), as assessed by MRI and LSCI, respectively. For all panels, data are means ± SEM from n = 8 mice per group from two independent experiments. Data were analyzed using a Student’s t test or one-way analysis of variance (ANOVA) followed by Tukey’s post hoc test (* P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; ns, not statistically significant).

    Article Snippet: Cells were incubated with conjugated antibodies against the following markers to detect the extracellular presence of TLR4 (BioLegend, catalog no. 145409), CD11b (BioLegend, catalog no. 101212), F4/80 (BioLegend, catalog no. 123107), Ly6G (BioLegend, catalog no. 127608), NE (Bioss, catalog no. bs-6982R), MPO (Invitrogen, catalog no. PA5-16672), and Cit-H3 (Cell Signaling Technology, catalog no. 9715).

    Techniques: Expressing, Derivative Assay, Flow Cytometry, Inhibition, Binding Assay, Marker, Imaging, Labeling, Mutagenesis

    ( A ) Blood and pericontusional brain tissue were collected at 24 hours after sham/TBI, and a population of TLR4 + PAD4 + neutrophils were selected by flow cytometry. This population was further gated for the extracellular expression of NE and MPO and for intracellular expression of interleukin-8 (IL-8; nine- and eightfold increase in blood and brain, respectively, after TBI), an activated neutrophil marker and autocrine inducer of NETs. The % TLR4 + PAD + neutrophils expressing IL-8 and extracellular NE/MPO are shown. ( B ) Placebo or Cl-amidine (30 to 50 mg/kg i.p.) was administered at 10 min after sham/TBI, and pericontusional brain tissue was collected for flow cytometry at 24 hours after injury. Representative histograms and quantified data indicate that Cl-amidine reduces total neutrophil infiltration and attenuates both extracellular MPO and Cit-H3 expression in Ly6G + CD11b + neutrophils. ( C ) Placebo or Cl-amidine (10 to 50 mg/kg i.p.) was administered at 10 min after sham/TBI. Representative LSCI (top) and MRI (bottom) images show a reduction in cerebral edema (24 hours after injury) and improved cerebral perfusion (1 to 24 hours after injury) following Cl-amidine (50 mg/kg) treatment. Data are means ± SEM from n = 8 mice per group. ( D ) Administration of Cl-amidine (50 mg/kg) at 10 min after TBI reduced the time to cross a narrow beam and improved both revolutions per minute (RPM) attained and time spent on the rotarod, as compared to placebo-treated mice after TBI. Data are means ± SEM from n = 10 to 12 mice per group. For all panels, data were analyzed by one-way ANOVA followed by Tukey’s post hoc test (* P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; ns, not statistically significant). SSC, side scatter; FSC, forward scatter.

    Journal: Science Advances

    Article Title: Neutrophil extracellular traps exacerbate neurological deficits after traumatic brain injury

    doi: 10.1126/sciadv.aax8847

    Figure Lengend Snippet: ( A ) Blood and pericontusional brain tissue were collected at 24 hours after sham/TBI, and a population of TLR4 + PAD4 + neutrophils were selected by flow cytometry. This population was further gated for the extracellular expression of NE and MPO and for intracellular expression of interleukin-8 (IL-8; nine- and eightfold increase in blood and brain, respectively, after TBI), an activated neutrophil marker and autocrine inducer of NETs. The % TLR4 + PAD + neutrophils expressing IL-8 and extracellular NE/MPO are shown. ( B ) Placebo or Cl-amidine (30 to 50 mg/kg i.p.) was administered at 10 min after sham/TBI, and pericontusional brain tissue was collected for flow cytometry at 24 hours after injury. Representative histograms and quantified data indicate that Cl-amidine reduces total neutrophil infiltration and attenuates both extracellular MPO and Cit-H3 expression in Ly6G + CD11b + neutrophils. ( C ) Placebo or Cl-amidine (10 to 50 mg/kg i.p.) was administered at 10 min after sham/TBI. Representative LSCI (top) and MRI (bottom) images show a reduction in cerebral edema (24 hours after injury) and improved cerebral perfusion (1 to 24 hours after injury) following Cl-amidine (50 mg/kg) treatment. Data are means ± SEM from n = 8 mice per group. ( D ) Administration of Cl-amidine (50 mg/kg) at 10 min after TBI reduced the time to cross a narrow beam and improved both revolutions per minute (RPM) attained and time spent on the rotarod, as compared to placebo-treated mice after TBI. Data are means ± SEM from n = 10 to 12 mice per group. For all panels, data were analyzed by one-way ANOVA followed by Tukey’s post hoc test (* P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; ns, not statistically significant). SSC, side scatter; FSC, forward scatter.

    Article Snippet: Cells were incubated with conjugated antibodies against the following markers to detect the extracellular presence of TLR4 (BioLegend, catalog no. 145409), CD11b (BioLegend, catalog no. 101212), F4/80 (BioLegend, catalog no. 123107), Ly6G (BioLegend, catalog no. 127608), NE (Bioss, catalog no. bs-6982R), MPO (Invitrogen, catalog no. PA5-16672), and Cit-H3 (Cell Signaling Technology, catalog no. 9715).

    Techniques: Flow Cytometry, Expressing, Marker