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  • 95
    Sino Biological cd36
    Results from multiple bond flow assay obtained at 37 and 41°C. Shown is the cellular lifetime against shear stress for IRBC-ICAM-1 and <t>IRBC-CD36</t> bonds at 37°C ( a and b ) and 41°C ( c and d ). Shown is an overlay of cellular lifetime against force graphs of IRBC-ICAM-1 and IRBC-CD36 interactions at all three temperatures ( e and f ), 37°C, and 41°C, respectively. Cellular lifetimes are plotted as mean ± SEM. To see this figure in color, go online.
    Cd36, supplied by Sino Biological, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cd36/product/Sino Biological
    Average 95 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    cd36 - by Bioz Stars, 2021-04
    95/100 stars
      Buy from Supplier

    94
    Sino Biological icam 1
    CCI-TBI increases BBB permeability to fibrinogen and decreases tight junction protein detection with a rescue or preservation of barrier function with <t>anti-ICAM-1/catalase.</t> Immunohistochemical detection of plasma protein fibrinogen in brain parenchyma at 48 hr following moderate CCI-TBI. ( A,B ) Naive and sham controls show absent fibrinogen detection in the brain parenchyma, as the BBB is healthy and intact. Absence of staining maintained at 20X. ( C ) Following CCI-TBI, BBB hyperpermeability permits the extravasation of fibrinogen into the brain tissue. Black arrowheads indicate areas of dense fibrinogen staining in the perivascular space. ( D ) Anti-ICAM-1/catalase reduces parenchymal and perivascular fibrinogen detection in the brain by 48 hrs post-CCI-TBI. ( E , F ) Anti-ICAM-1 antibody and catalase alone do not appear to reduce fibrinogen extravasation as indicated by intense fibrinogen detection in the impact site with dense staining in perivascular space. Scale bar equals 50 microns. (Top panels 2X, bottom panels 20X). ( G ) Western blot analysis of tight junction protein expression for occludin and claudin-5 in the cortex ipsilateral to the site of CCI-TBI for sham, CCI-TBI and CCI-TBI+anti-ICAM-1/catalase groups. The whole membrane was cut at 75 kDa and between 37 and 25 kDa to minimize antibody use. Membranes were separately probed for occludin and claudin-5. The membrane probed for occludin was striped, reblocked, and then probed for GAPDH. Full length blots are presented in Supplementary Figure 1 . ( H , I ) Densitometry quantification for occludin and claudin-5 normalized to GAPDH presented as mean ± SD (Ordinary one-way ANOVA with multiple comparisons occludin F = 5.779, P = 0.0399. Claudin-5 F = 17.42, P = 0.0032).
    Icam 1, supplied by Sino Biological, 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/icam 1/product/Sino Biological
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    icam 1 - by Bioz Stars, 2021-04
    94/100 stars
      Buy from Supplier

    93
    Sino Biological ox 40
    CCI-TBI increases BBB permeability to fibrinogen and decreases tight junction protein detection with a rescue or preservation of barrier function with <t>anti-ICAM-1/catalase.</t> Immunohistochemical detection of plasma protein fibrinogen in brain parenchyma at 48 hr following moderate CCI-TBI. ( A,B ) Naive and sham controls show absent fibrinogen detection in the brain parenchyma, as the BBB is healthy and intact. Absence of staining maintained at 20X. ( C ) Following CCI-TBI, BBB hyperpermeability permits the extravasation of fibrinogen into the brain tissue. Black arrowheads indicate areas of dense fibrinogen staining in the perivascular space. ( D ) Anti-ICAM-1/catalase reduces parenchymal and perivascular fibrinogen detection in the brain by 48 hrs post-CCI-TBI. ( E , F ) Anti-ICAM-1 antibody and catalase alone do not appear to reduce fibrinogen extravasation as indicated by intense fibrinogen detection in the impact site with dense staining in perivascular space. Scale bar equals 50 microns. (Top panels 2X, bottom panels 20X). ( G ) Western blot analysis of tight junction protein expression for occludin and claudin-5 in the cortex ipsilateral to the site of CCI-TBI for sham, CCI-TBI and CCI-TBI+anti-ICAM-1/catalase groups. The whole membrane was cut at 75 kDa and between 37 and 25 kDa to minimize antibody use. Membranes were separately probed for occludin and claudin-5. The membrane probed for occludin was striped, reblocked, and then probed for GAPDH. Full length blots are presented in Supplementary Figure 1 . ( H , I ) Densitometry quantification for occludin and claudin-5 normalized to GAPDH presented as mean ± SD (Ordinary one-way ANOVA with multiple comparisons occludin F = 5.779, P = 0.0399. Claudin-5 F = 17.42, P = 0.0032).
    Ox 40, supplied by Sino Biological, 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/ox 40/product/Sino Biological
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    ox 40 - by Bioz Stars, 2021-04
    93/100 stars
      Buy from Supplier

    99
    Illumina Inc 180 bp next generation illumina sequence
    CCI-TBI increases BBB permeability to fibrinogen and decreases tight junction protein detection with a rescue or preservation of barrier function with <t>anti-ICAM-1/catalase.</t> Immunohistochemical detection of plasma protein fibrinogen in brain parenchyma at 48 hr following moderate CCI-TBI. ( A,B ) Naive and sham controls show absent fibrinogen detection in the brain parenchyma, as the BBB is healthy and intact. Absence of staining maintained at 20X. ( C ) Following CCI-TBI, BBB hyperpermeability permits the extravasation of fibrinogen into the brain tissue. Black arrowheads indicate areas of dense fibrinogen staining in the perivascular space. ( D ) Anti-ICAM-1/catalase reduces parenchymal and perivascular fibrinogen detection in the brain by 48 hrs post-CCI-TBI. ( E , F ) Anti-ICAM-1 antibody and catalase alone do not appear to reduce fibrinogen extravasation as indicated by intense fibrinogen detection in the impact site with dense staining in perivascular space. Scale bar equals 50 microns. (Top panels 2X, bottom panels 20X). ( G ) Western blot analysis of tight junction protein expression for occludin and claudin-5 in the cortex ipsilateral to the site of CCI-TBI for sham, CCI-TBI and CCI-TBI+anti-ICAM-1/catalase groups. The whole membrane was cut at 75 kDa and between 37 and 25 kDa to minimize antibody use. Membranes were separately probed for occludin and claudin-5. The membrane probed for occludin was striped, reblocked, and then probed for GAPDH. Full length blots are presented in Supplementary Figure 1 . ( H , I ) Densitometry quantification for occludin and claudin-5 normalized to GAPDH presented as mean ± SD (Ordinary one-way ANOVA with multiple comparisons occludin F = 5.779, P = 0.0399. Claudin-5 F = 17.42, P = 0.0032).
    180 Bp Next Generation Illumina Sequence, supplied by Illumina Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/180 bp next generation illumina sequence/product/Illumina Inc
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    180 bp next generation illumina sequence - by Bioz Stars, 2021-04
    99/100 stars
      Buy from Supplier

    Image Search Results


    Results from multiple bond flow assay obtained at 37 and 41°C. Shown is the cellular lifetime against shear stress for IRBC-ICAM-1 and IRBC-CD36 bonds at 37°C ( a and b ) and 41°C ( c and d ). Shown is an overlay of cellular lifetime against force graphs of IRBC-ICAM-1 and IRBC-CD36 interactions at all three temperatures ( e and f ), 37°C, and 41°C, respectively. Cellular lifetimes are plotted as mean ± SEM. To see this figure in color, go online.

    Journal: Biophysical Journal

    Article Title: Temperature-Induced Catch-Slip to Slip Bond Transit in Plasmodium falciparum-Infected Erythrocytes

    doi: 10.1016/j.bpj.2019.11.016

    Figure Lengend Snippet: Results from multiple bond flow assay obtained at 37 and 41°C. Shown is the cellular lifetime against shear stress for IRBC-ICAM-1 and IRBC-CD36 bonds at 37°C ( a and b ) and 41°C ( c and d ). Shown is an overlay of cellular lifetime against force graphs of IRBC-ICAM-1 and IRBC-CD36 interactions at all three temperatures ( e and f ), 37°C, and 41°C, respectively. Cellular lifetimes are plotted as mean ± SEM. To see this figure in color, go online.

    Article Snippet: Furthermore, the binding affinity between IRBC and CD36 is largely reduced at 41°C.

    Techniques:

    CCI-TBI increases BBB permeability to fibrinogen and decreases tight junction protein detection with a rescue or preservation of barrier function with anti-ICAM-1/catalase. Immunohistochemical detection of plasma protein fibrinogen in brain parenchyma at 48 hr following moderate CCI-TBI. ( A,B ) Naive and sham controls show absent fibrinogen detection in the brain parenchyma, as the BBB is healthy and intact. Absence of staining maintained at 20X. ( C ) Following CCI-TBI, BBB hyperpermeability permits the extravasation of fibrinogen into the brain tissue. Black arrowheads indicate areas of dense fibrinogen staining in the perivascular space. ( D ) Anti-ICAM-1/catalase reduces parenchymal and perivascular fibrinogen detection in the brain by 48 hrs post-CCI-TBI. ( E , F ) Anti-ICAM-1 antibody and catalase alone do not appear to reduce fibrinogen extravasation as indicated by intense fibrinogen detection in the impact site with dense staining in perivascular space. Scale bar equals 50 microns. (Top panels 2X, bottom panels 20X). ( G ) Western blot analysis of tight junction protein expression for occludin and claudin-5 in the cortex ipsilateral to the site of CCI-TBI for sham, CCI-TBI and CCI-TBI+anti-ICAM-1/catalase groups. The whole membrane was cut at 75 kDa and between 37 and 25 kDa to minimize antibody use. Membranes were separately probed for occludin and claudin-5. The membrane probed for occludin was striped, reblocked, and then probed for GAPDH. Full length blots are presented in Supplementary Figure 1 . ( H , I ) Densitometry quantification for occludin and claudin-5 normalized to GAPDH presented as mean ± SD (Ordinary one-way ANOVA with multiple comparisons occludin F = 5.779, P = 0.0399. Claudin-5 F = 17.42, P = 0.0032).

    Journal: Scientific Reports

    Article Title: Acute administration of catalase targeted to ICAM-1 attenuates neuropathology in experimental traumatic brain injury

    doi: 10.1038/s41598-017-03309-4

    Figure Lengend Snippet: CCI-TBI increases BBB permeability to fibrinogen and decreases tight junction protein detection with a rescue or preservation of barrier function with anti-ICAM-1/catalase. Immunohistochemical detection of plasma protein fibrinogen in brain parenchyma at 48 hr following moderate CCI-TBI. ( A,B ) Naive and sham controls show absent fibrinogen detection in the brain parenchyma, as the BBB is healthy and intact. Absence of staining maintained at 20X. ( C ) Following CCI-TBI, BBB hyperpermeability permits the extravasation of fibrinogen into the brain tissue. Black arrowheads indicate areas of dense fibrinogen staining in the perivascular space. ( D ) Anti-ICAM-1/catalase reduces parenchymal and perivascular fibrinogen detection in the brain by 48 hrs post-CCI-TBI. ( E , F ) Anti-ICAM-1 antibody and catalase alone do not appear to reduce fibrinogen extravasation as indicated by intense fibrinogen detection in the impact site with dense staining in perivascular space. Scale bar equals 50 microns. (Top panels 2X, bottom panels 20X). ( G ) Western blot analysis of tight junction protein expression for occludin and claudin-5 in the cortex ipsilateral to the site of CCI-TBI for sham, CCI-TBI and CCI-TBI+anti-ICAM-1/catalase groups. The whole membrane was cut at 75 kDa and between 37 and 25 kDa to minimize antibody use. Membranes were separately probed for occludin and claudin-5. The membrane probed for occludin was striped, reblocked, and then probed for GAPDH. Full length blots are presented in Supplementary Figure 1 . ( H , I ) Densitometry quantification for occludin and claudin-5 normalized to GAPDH presented as mean ± SD (Ordinary one-way ANOVA with multiple comparisons occludin F = 5.779, P = 0.0399. Claudin-5 F = 17.42, P = 0.0032).

    Article Snippet: All sections were incubated in primary antibody prepared in Dako Antibody Diluent either for 1 hr at RT (NeuN, Iba1, Fibrinogen, 3-NT), or O/N at 4 °C (GFAP and ICAM-1) at the following dilutions: NeuN (1:500, Covance), Iba1 (1:400, Wako Chemicals), Fibrinogen (1:400, Dako), GFAP (1:2000, Cell Signaling), 3-NT (1:1000, Abcam) and ICAM-1 (1:250, Sino Biologicals).

    Techniques: Permeability, Preserving, Immunohistochemistry, Staining, Western Blot, Expressing

    Two-photon imaging detection of microglia in CX3CR1-GFP mice and morphometric analysis of cellular morphology in CCI-TBI and anti-ICAM-1/catalase administration. CX3CR1-GFP mice (B6.129P- Cx3cr1 tm1Litt /J, The Jackson Laboratory) were subjected to moderate CCI-TBI with and without anti-ICAM-1/catalase conjugate administration 30 min after impact. No craniectomy (naive) CX3CR1-GFP mice served as control. At 48 hrs following CCI-TBI, subjects were perfusion fixed, brain tissue was collected and subsequently sectioned into 1 mm segments for two-photon imaging. ( A ) Representative single slice images depict microglial ramification in the area of impact for naive, CCI-TBI, and CCI-TBI+anti-ICAM-1/catalase mice. Arrowheads point to microglial processes, which are finely ramified in the naive condition and thicken and retract following CCI-TBI. Anti-ICAM-1/catalase attenuates changes in microglia cell body enlargement and process retraction. Scale bar 20 μm. Imaris (Bitplane) software was utilized for 3D reconstruction of GFP-expressing microglia from z-stack images obtained by two-photon microscopy. ( B ) Surface rendering was performed for microglia based on GFP signal threshold to measure cellular surface area ( D ) (only objects with surface area > 1000 μm 2 were analyzed) and sphericity ( E ). ( C ) Imaris FilamentTracer was employed to map microglial processes to quantify changes in cell ramification in CCI-TBI. Microglial total filament length ( F ) and number of filament branching points (complexity, ( G ) and were assessed for naive, CCI-TBI, and CCI-TBI+anti-ICAM-1/catalase groups. Data presented at mean ± SD. (Ordinary one-way ANOVA. Surface area: F = 73.12, P

    Journal: Scientific Reports

    Article Title: Acute administration of catalase targeted to ICAM-1 attenuates neuropathology in experimental traumatic brain injury

    doi: 10.1038/s41598-017-03309-4

    Figure Lengend Snippet: Two-photon imaging detection of microglia in CX3CR1-GFP mice and morphometric analysis of cellular morphology in CCI-TBI and anti-ICAM-1/catalase administration. CX3CR1-GFP mice (B6.129P- Cx3cr1 tm1Litt /J, The Jackson Laboratory) were subjected to moderate CCI-TBI with and without anti-ICAM-1/catalase conjugate administration 30 min after impact. No craniectomy (naive) CX3CR1-GFP mice served as control. At 48 hrs following CCI-TBI, subjects were perfusion fixed, brain tissue was collected and subsequently sectioned into 1 mm segments for two-photon imaging. ( A ) Representative single slice images depict microglial ramification in the area of impact for naive, CCI-TBI, and CCI-TBI+anti-ICAM-1/catalase mice. Arrowheads point to microglial processes, which are finely ramified in the naive condition and thicken and retract following CCI-TBI. Anti-ICAM-1/catalase attenuates changes in microglia cell body enlargement and process retraction. Scale bar 20 μm. Imaris (Bitplane) software was utilized for 3D reconstruction of GFP-expressing microglia from z-stack images obtained by two-photon microscopy. ( B ) Surface rendering was performed for microglia based on GFP signal threshold to measure cellular surface area ( D ) (only objects with surface area > 1000 μm 2 were analyzed) and sphericity ( E ). ( C ) Imaris FilamentTracer was employed to map microglial processes to quantify changes in cell ramification in CCI-TBI. Microglial total filament length ( F ) and number of filament branching points (complexity, ( G ) and were assessed for naive, CCI-TBI, and CCI-TBI+anti-ICAM-1/catalase groups. Data presented at mean ± SD. (Ordinary one-way ANOVA. Surface area: F = 73.12, P

    Article Snippet: All sections were incubated in primary antibody prepared in Dako Antibody Diluent either for 1 hr at RT (NeuN, Iba1, Fibrinogen, 3-NT), or O/N at 4 °C (GFAP and ICAM-1) at the following dilutions: NeuN (1:500, Covance), Iba1 (1:400, Wako Chemicals), Fibrinogen (1:400, Dako), GFAP (1:2000, Cell Signaling), 3-NT (1:1000, Abcam) and ICAM-1 (1:250, Sino Biologicals).

    Techniques: Imaging, Mouse Assay, Software, Expressing, Microscopy

    CCI-TBI results in increased hydrogen peroxide production and 3-nitrotyrosine detection in the ipsilateral cortex area of impact. ( A ) OxiSelect™ Hydrogen Peroxide/Peroxidase Assay Kit was used to measure hydrogen peroxide levels in fresh mouse cortical tissue ipsilateral to the area of impact 4 hrs following CCI-TBI, CCI-TBI+anti-ICAM-1/catalase, catalase only, and antibody only administration or from naive and sham controls. The naive condition provides basal hydrogen peroxide levels in uninjured cortical tissue which are not significantly different from sham. CCI-TBI results in a nearly 3-fold increase in hydrogen peroxide level detection. Anti-ICAM-1/catalase quenches hydrogen peroxide levels in the area of injury to physiological levels comparable to that of naive and sham, an effect not achieved with anti-ICAM-1 antibody and catalase alone. Immunohistochemical chomogen staining of 3-NT demonstrates increased tyrosine nitration following CCI-TBI ( D ) compared to naive and sham controls ( B and C , respectively). Anti-ICAM-1/catalase significantly decreased 3-NT detection ( E ). 3-NT levels in anti-ICAM-1 antibody and catalase only groups did not significantly differ from CCI-TBI alone ( F and G , respectively). Positive signal detection was pseudo-colored red for better visualization. All images taken at 20X. Scale bar equals 50 microns. ( H ) Quantification of 3-NT signal detection was analyzed by percent area and normalized to total tissue area per image. Data are presented as mean ± SD. (Ordinary one-way ANOVA with multiple comparisons for hydrogen peroxide data F = 25.95, P

    Journal: Scientific Reports

    Article Title: Acute administration of catalase targeted to ICAM-1 attenuates neuropathology in experimental traumatic brain injury

    doi: 10.1038/s41598-017-03309-4

    Figure Lengend Snippet: CCI-TBI results in increased hydrogen peroxide production and 3-nitrotyrosine detection in the ipsilateral cortex area of impact. ( A ) OxiSelect™ Hydrogen Peroxide/Peroxidase Assay Kit was used to measure hydrogen peroxide levels in fresh mouse cortical tissue ipsilateral to the area of impact 4 hrs following CCI-TBI, CCI-TBI+anti-ICAM-1/catalase, catalase only, and antibody only administration or from naive and sham controls. The naive condition provides basal hydrogen peroxide levels in uninjured cortical tissue which are not significantly different from sham. CCI-TBI results in a nearly 3-fold increase in hydrogen peroxide level detection. Anti-ICAM-1/catalase quenches hydrogen peroxide levels in the area of injury to physiological levels comparable to that of naive and sham, an effect not achieved with anti-ICAM-1 antibody and catalase alone. Immunohistochemical chomogen staining of 3-NT demonstrates increased tyrosine nitration following CCI-TBI ( D ) compared to naive and sham controls ( B and C , respectively). Anti-ICAM-1/catalase significantly decreased 3-NT detection ( E ). 3-NT levels in anti-ICAM-1 antibody and catalase only groups did not significantly differ from CCI-TBI alone ( F and G , respectively). Positive signal detection was pseudo-colored red for better visualization. All images taken at 20X. Scale bar equals 50 microns. ( H ) Quantification of 3-NT signal detection was analyzed by percent area and normalized to total tissue area per image. Data are presented as mean ± SD. (Ordinary one-way ANOVA with multiple comparisons for hydrogen peroxide data F = 25.95, P

    Article Snippet: All sections were incubated in primary antibody prepared in Dako Antibody Diluent either for 1 hr at RT (NeuN, Iba1, Fibrinogen, 3-NT), or O/N at 4 °C (GFAP and ICAM-1) at the following dilutions: NeuN (1:500, Covance), Iba1 (1:400, Wako Chemicals), Fibrinogen (1:400, Dako), GFAP (1:2000, Cell Signaling), 3-NT (1:1000, Abcam) and ICAM-1 (1:250, Sino Biologicals).

    Techniques: Immunohistochemistry, Staining, Nitration

    In vivo sodium fluorescein assay further elucidates changes in BBB permeability with increased barrier permeability following moderate CCI-TBI and rescue of barrier function with anti-ICAM-1/catalase. Sodium fluorescein was administered IV at 48 hrs post-CCI-TBI to evaluate barrier integrity at this time point. The small molecular weight fluorescent tracer was allowed to circulate for 15 min before tissue perfusion and collection. Fluorescent images captured using short wave UV light demonstrate sodium fluorescein leakage into brain tissue in naive (( A ), no craniectomy) and sham ( B ) mice and mice sustaining moderate CCI-TBI events at 48 hr following injury ( C ) CCI-TBI only, D: CCI-TBI+Anti-ICAM-1/catalase, ( E ) CCI-TBI+anti-ICAM-1 antibody, and F: CCI-TBI+catalase). The dashed circle in B demarcates where the craniectomy was performed. Sodium fluorescein leakage into the brain extends beyond the area of impact following moderate CCI-TBI, highlighted by white arrowheads. Black arrowheads indicate areas of hemorrhage, edema, or swelling of the brain following injury. Coup and contrecoup mechanisms of injury resulting from CCI-TBI can be appreciated by comparing sodium fluorescein signal detection in the area of impact (top of brain section) to the base of the brain directly opposite of the area of impact in CCI-TBI and CCI-TBI+Catalase groups ( C , F ).

    Journal: Scientific Reports

    Article Title: Acute administration of catalase targeted to ICAM-1 attenuates neuropathology in experimental traumatic brain injury

    doi: 10.1038/s41598-017-03309-4

    Figure Lengend Snippet: In vivo sodium fluorescein assay further elucidates changes in BBB permeability with increased barrier permeability following moderate CCI-TBI and rescue of barrier function with anti-ICAM-1/catalase. Sodium fluorescein was administered IV at 48 hrs post-CCI-TBI to evaluate barrier integrity at this time point. The small molecular weight fluorescent tracer was allowed to circulate for 15 min before tissue perfusion and collection. Fluorescent images captured using short wave UV light demonstrate sodium fluorescein leakage into brain tissue in naive (( A ), no craniectomy) and sham ( B ) mice and mice sustaining moderate CCI-TBI events at 48 hr following injury ( C ) CCI-TBI only, D: CCI-TBI+Anti-ICAM-1/catalase, ( E ) CCI-TBI+anti-ICAM-1 antibody, and F: CCI-TBI+catalase). The dashed circle in B demarcates where the craniectomy was performed. Sodium fluorescein leakage into the brain extends beyond the area of impact following moderate CCI-TBI, highlighted by white arrowheads. Black arrowheads indicate areas of hemorrhage, edema, or swelling of the brain following injury. Coup and contrecoup mechanisms of injury resulting from CCI-TBI can be appreciated by comparing sodium fluorescein signal detection in the area of impact (top of brain section) to the base of the brain directly opposite of the area of impact in CCI-TBI and CCI-TBI+Catalase groups ( C , F ).

    Article Snippet: All sections were incubated in primary antibody prepared in Dako Antibody Diluent either for 1 hr at RT (NeuN, Iba1, Fibrinogen, 3-NT), or O/N at 4 °C (GFAP and ICAM-1) at the following dilutions: NeuN (1:500, Covance), Iba1 (1:400, Wako Chemicals), Fibrinogen (1:400, Dako), GFAP (1:2000, Cell Signaling), 3-NT (1:1000, Abcam) and ICAM-1 (1:250, Sino Biologicals).

    Techniques: In Vivo, Permeability, Molecular Weight, Mouse Assay

    CCI-TBI induces local and temporal increase in ICAM-1 expression in mouse cerebral cortex and underlying brain structures. ( A ) Immunohistochemical detection of ICAM-1 time course of expression in cerebral vasculature (solid arrows) and aberrant expression in astrocytes (open arrows) in area of impact in naive (no craniectomy control), sham (surgical control without impact) and at 8, 24, and 48 hr post-CCI-TBI (20X). Included is a stitched coronal section through the CCI-TBI impact site 48 hrs following CCI-TBI (boxed, 4X). Increased ICAM-1 expression detection can also be visualized in hippocampal regions underlying the impact site. ( B ) Quantification of ICAM-1 staining optical density (OD) normalized to vessel caliber and length for naive, sham, and 48 hr post-CCI-TBI groups. Scale bar equals 50 microns. Data are presented as mean ± SD. (Ordinary one-way ANOVA with multiple comparisons F = 96.35, P

    Journal: Scientific Reports

    Article Title: Acute administration of catalase targeted to ICAM-1 attenuates neuropathology in experimental traumatic brain injury

    doi: 10.1038/s41598-017-03309-4

    Figure Lengend Snippet: CCI-TBI induces local and temporal increase in ICAM-1 expression in mouse cerebral cortex and underlying brain structures. ( A ) Immunohistochemical detection of ICAM-1 time course of expression in cerebral vasculature (solid arrows) and aberrant expression in astrocytes (open arrows) in area of impact in naive (no craniectomy control), sham (surgical control without impact) and at 8, 24, and 48 hr post-CCI-TBI (20X). Included is a stitched coronal section through the CCI-TBI impact site 48 hrs following CCI-TBI (boxed, 4X). Increased ICAM-1 expression detection can also be visualized in hippocampal regions underlying the impact site. ( B ) Quantification of ICAM-1 staining optical density (OD) normalized to vessel caliber and length for naive, sham, and 48 hr post-CCI-TBI groups. Scale bar equals 50 microns. Data are presented as mean ± SD. (Ordinary one-way ANOVA with multiple comparisons F = 96.35, P

    Article Snippet: All sections were incubated in primary antibody prepared in Dako Antibody Diluent either for 1 hr at RT (NeuN, Iba1, Fibrinogen, 3-NT), or O/N at 4 °C (GFAP and ICAM-1) at the following dilutions: NeuN (1:500, Covance), Iba1 (1:400, Wako Chemicals), Fibrinogen (1:400, Dako), GFAP (1:2000, Cell Signaling), 3-NT (1:1000, Abcam) and ICAM-1 (1:250, Sino Biologicals).

    Techniques: Expressing, Immunohistochemistry, Staining

    Diminished neuropathology indices with acute anti-ICAM-1/catalase administration following CCI-TBI demonstrated by immunohistochemical staining for neurons, astrocytes, and microglia. ( A ) NeuN staining identifies viable neurons within the cerebral cortex and demonstrates substantial neuronal loss 48 hrs following CCI-TBI. Primary injury mechanisms invariably result in cell death, as indicated by persistently decreased NeuN detection, based on particle count analysis, that is rescued with targeted antioxidant enzyme intervention. NeuN detection following anti-ICAM-1/catalase administration was significantly higher than CCI-TBI alone or in combination with recombinant catalase and anti-ICAM-1. Green arrows point to nuclear stain of NeuN. ( B ) Microglia are finely ramified with small cell bodies in the sham condition. Following CCI-TBI, number of activated microglia per 5.61 × 10 5 microns squared is significantly increased as indicated by threshold increases in cell body size and Iba1 staining intensity. Anti-ICAM-1/catalase reduced the number of amoeboid microglia per frame, while catalase and anti-ICAM-1 alone did not. Red arrows point to amoeboid microglia. ( C ) GFAP expression indicating astrocyte activation shows significant increase at 48 hrs following CCI-TBI compared to optical density readouts per 5.61 × 10 5 microns squared for the sham group. Anti-ICAM-1/catalase significantly reduced optical density of GFAP detection at 48 hrs after CCI-TBI compared to CCI-TBI alone. Non-targeted catalase and anti-ICAM-1 controls did not offer benefit regarding astrocyte activation following CCI-TBI, with no significant difference from CCI-TBI alone. Yellow arrows point to astrocytes with robust GFAP staining detection. Scale bars equal 50 microns. ( D ) Associated bar graphs display imaging quantification. Naive animals were included in image analysis and quantification but are not displayed in the montage. Data are presented as mean ± SD. (Ordinary one-way ANOVA. NeuN: F = 39.83, P

    Journal: Scientific Reports

    Article Title: Acute administration of catalase targeted to ICAM-1 attenuates neuropathology in experimental traumatic brain injury

    doi: 10.1038/s41598-017-03309-4

    Figure Lengend Snippet: Diminished neuropathology indices with acute anti-ICAM-1/catalase administration following CCI-TBI demonstrated by immunohistochemical staining for neurons, astrocytes, and microglia. ( A ) NeuN staining identifies viable neurons within the cerebral cortex and demonstrates substantial neuronal loss 48 hrs following CCI-TBI. Primary injury mechanisms invariably result in cell death, as indicated by persistently decreased NeuN detection, based on particle count analysis, that is rescued with targeted antioxidant enzyme intervention. NeuN detection following anti-ICAM-1/catalase administration was significantly higher than CCI-TBI alone or in combination with recombinant catalase and anti-ICAM-1. Green arrows point to nuclear stain of NeuN. ( B ) Microglia are finely ramified with small cell bodies in the sham condition. Following CCI-TBI, number of activated microglia per 5.61 × 10 5 microns squared is significantly increased as indicated by threshold increases in cell body size and Iba1 staining intensity. Anti-ICAM-1/catalase reduced the number of amoeboid microglia per frame, while catalase and anti-ICAM-1 alone did not. Red arrows point to amoeboid microglia. ( C ) GFAP expression indicating astrocyte activation shows significant increase at 48 hrs following CCI-TBI compared to optical density readouts per 5.61 × 10 5 microns squared for the sham group. Anti-ICAM-1/catalase significantly reduced optical density of GFAP detection at 48 hrs after CCI-TBI compared to CCI-TBI alone. Non-targeted catalase and anti-ICAM-1 controls did not offer benefit regarding astrocyte activation following CCI-TBI, with no significant difference from CCI-TBI alone. Yellow arrows point to astrocytes with robust GFAP staining detection. Scale bars equal 50 microns. ( D ) Associated bar graphs display imaging quantification. Naive animals were included in image analysis and quantification but are not displayed in the montage. Data are presented as mean ± SD. (Ordinary one-way ANOVA. NeuN: F = 39.83, P

    Article Snippet: All sections were incubated in primary antibody prepared in Dako Antibody Diluent either for 1 hr at RT (NeuN, Iba1, Fibrinogen, 3-NT), or O/N at 4 °C (GFAP and ICAM-1) at the following dilutions: NeuN (1:500, Covance), Iba1 (1:400, Wako Chemicals), Fibrinogen (1:400, Dako), GFAP (1:2000, Cell Signaling), 3-NT (1:1000, Abcam) and ICAM-1 (1:250, Sino Biologicals).

    Techniques: Immunohistochemistry, Staining, Recombinant, Expressing, Activation Assay, Imaging