balanced salt solution  (Thermo Fisher)


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    Structured Review

    Thermo Fisher balanced salt solution
    Balanced Salt Solution, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 94/100, based on 564 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/balanced salt solution/product/Thermo Fisher
    Average 94 stars, based on 564 article reviews
    Price from $9.99 to $1999.99
    balanced salt solution - by Bioz Stars, 2020-09
    94/100 stars

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    Incubation:

    Article Title: Inhibition of glioblastoma cell proliferation, invasion, and mechanism of action of a novel hydroxamic acid hybrid molecule
    Article Snippet: .. Following treatment, cells were incubated in phenol-free Hanks’ balanced Salt solution containing calcein-AM (0.5 µM, Thermo Fisher Scientific, Eugene, OR, USA) and propidium iodide (3 µM, Sigma-Aldrich, St. Louis, MO, USA) for 30 min at 37 °C. .. The media were replaced with fresh Hanks’ balanced salt solution and cells were imaged using a fluorescence microscope (Leica DMI4000B).

    Cell Culture:

    Article Title: Isoform-specific effects of ApoE on neurite outgrowth in Olfactory Epithelium culture
    Article Snippet: .. Cell culture medium, including Neurobasal A, Hanks’ Balanced Salt Solution, B-27 Supplement and FGF2 were obtained from Invitrogen Corporation (Grand Island, NY). .. Glutamine and fibronectin were purchased from Sigma Chemicals (St. Louis, MO).

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  • 99
    Thermo Fisher bsa
    Pretreatment with ethanol and cholesterol removal do not interfere with the FcεRI expression but affect its internalization. (A) The cells were incubated or not for 15 min with <t>BSS-BSA</t> alone (Ctrl) or supplemented with ethanol (0.5%) and/or Mβ (2 mM) and then stained for surface KIT and FcεRI by direct immunofluorescence followed by flow cytometry analysis. (B) IgE-sensitized cells were incubated with the drugs as above and activated or not with antigen (500 ng/ml). After 15 min the cells were fixed, permeabilized, labeled for IgE and analyzed by confocal microscopy. Bars = 5 μm. (C) Distribution of IgE in individual cells was evaluated and the fraction of IgE detected in the cytoplasm was determined. Each spot represents one cell, bars indicate means. Statistical significance of intergroup differences is also indicated.
    Bsa, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 187 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/bsa/product/Thermo Fisher
    Average 99 stars, based on 187 article reviews
    Price from $9.99 to $1999.99
    bsa - by Bioz Stars, 2020-09
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    94
    Thermo Fisher balanced salt solution hbss
    <t>p5RHH-JNK2</t> siRNA NPs reduce thrombotic risk, restore endothelial integrity, and decrease necrotic plaque area and macrophages. Notes: ( A ) Shorter occlusion times for untreated ApoE −/− mice indicate more aggressive clotting (ie, heightened thrombotic risk) compared to mice treated with p5RHH-JNK2 siRNA NPs (n=6), which manifest prolonged occlusion times compared to <t>HBSS</t> control (n=5, P =0.02). ( B ) 19 F MRS demonstrates significantly less perfluorocarbon (CE volume) NP accumulation in ApoE −/− mice after p5RHH-JNK2 siRNA NP treatment (n=8) compared to those treated with HBSS (n=7) ( P =0.003), confirming restoration of endothelial barrier integrity that now prohibits passive permeation of perfluorocarbon NPs. ( C and D ) Representative aorta sections demonstrate that necrotic plaque area is reduced in p5RHH-JNK2 siRNA NP-treated animals ( D ) (n=8) compared to those treated with HBSS ( C ) (n=4, bar 100 μm). ( E ) Necrotic plaque areas from mice treated with p5RHH-JNK2 siRNA NPs are reduced compared to mice receiving HBSS ( P =0.004). ( F and G ) Representative immunofluorescence stains demonstrate significantly fewer Moma-positive cells in atherosclerotic plaque from ApoE −/− mice treated with p5RHH-JNK2 siRNA NPs ( G ) (n=36) compared to HBSS control mice ( F ) (n=17, P
    Balanced Salt Solution Hbss, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 94/100, based on 61 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/balanced salt solution hbss/product/Thermo Fisher
    Average 94 stars, based on 61 article reviews
    Price from $9.99 to $1999.99
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    91
    Thermo Fisher earle s balanced salt solution ebss
    Effect of anti-inositol 1,4,5-trisphosphate type-1 receptor/BioPORTER ® on progesterone-, zona pellucida-, and calcium ionophore-induced calcium influx. ( a ) Summary graph. The calcium influx curves in this figure represent the change in the average calcium concentration of the groups. Black arrows indicate when inducers were added. The raw intensity values were normalized as ΔF, ΔF = ( F − F baseline )/F baseline . “F” represent the mean FITC fluorescence intensity of each gate and “F baseline ” represents of the mean FITC fluorescence intensity of the initial 2 min. The data are expressed as the mean, n = 3. ( b ) Effect of anti-inositol 1,4,5-trisphosphate type-1 receptor/BioPORTER ® on progesterone-induced calcium influx. The “ * ” represents this curve, and the versus curve treated with inducer only was significantly different. The data are expressed as the mean, n = 3. ( c ) Effect of anti-inositol 1,4,5-trisphosphate type-1 receptor/BioPORTER ® on zona pellucida-induced calcium influx. The data are expressed as the mean, n = 3. ( d ) Effect of anti-inositol 1,4,5-trisphosphate type-1 receptor/BioPORTER ® on calcium ionophore-induced calcium influx. The data are expressed as the mean, n = 3. ( e ) Description of the legends in a , b , c and d . Figure legends are given a series of two-letter groupings. The first letter indicates the pretreatment reagent, and the second letter represents the inducers. For the first letter, “C” indicates <t>Earle's</t> balanced salt solution supplemented with 0.0% BSA <t>(EBSS</t> [0.0% BSA]), and “O” represent anti-IP3R1/BioPORTER®. For the second letter, “P” indicates progesterone, “T” represents ZP, “A” indicates A23187 and “E” indicates EBSS (0.0% BSA). IP3R1: inositol 1,4,5-trisphosphate type-1 receptor; ZP: zona pellucida.
    Earle S Balanced Salt Solution Ebss, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 91/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 91 stars, based on 3 article reviews
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    Image Search Results


    Pretreatment with ethanol and cholesterol removal do not interfere with the FcεRI expression but affect its internalization. (A) The cells were incubated or not for 15 min with BSS-BSA alone (Ctrl) or supplemented with ethanol (0.5%) and/or Mβ (2 mM) and then stained for surface KIT and FcεRI by direct immunofluorescence followed by flow cytometry analysis. (B) IgE-sensitized cells were incubated with the drugs as above and activated or not with antigen (500 ng/ml). After 15 min the cells were fixed, permeabilized, labeled for IgE and analyzed by confocal microscopy. Bars = 5 μm. (C) Distribution of IgE in individual cells was evaluated and the fraction of IgE detected in the cytoplasm was determined. Each spot represents one cell, bars indicate means. Statistical significance of intergroup differences is also indicated.

    Journal: PLoS ONE

    Article Title: Ethanol Inhibits High-Affinity Immunoglobulin E Receptor (FcεRI) Signaling in Mast Cells by Suppressing the Function of FcεRI-Cholesterol Signalosome

    doi: 10.1371/journal.pone.0144596

    Figure Lengend Snippet: Pretreatment with ethanol and cholesterol removal do not interfere with the FcεRI expression but affect its internalization. (A) The cells were incubated or not for 15 min with BSS-BSA alone (Ctrl) or supplemented with ethanol (0.5%) and/or Mβ (2 mM) and then stained for surface KIT and FcεRI by direct immunofluorescence followed by flow cytometry analysis. (B) IgE-sensitized cells were incubated with the drugs as above and activated or not with antigen (500 ng/ml). After 15 min the cells were fixed, permeabilized, labeled for IgE and analyzed by confocal microscopy. Bars = 5 μm. (C) Distribution of IgE in individual cells was evaluated and the fraction of IgE detected in the cytoplasm was determined. Each spot represents one cell, bars indicate means. Statistical significance of intergroup differences is also indicated.

    Article Snippet: For measurement in the presence of extracellular calcium, cells were pelleted by centrifugation 500 x g for 3 min, resuspended in BSS-0.1% BSA and transferred to white polysorp 96 well plate (NUNC, Thermo Scientific).

    Techniques: Expressing, Incubation, Staining, Immunofluorescence, Flow Cytometry, Cytometry, Labeling, Confocal Microscopy

    Pretreatment with ethanol inhibits tyrosine phosphorylation of FcεRI β and γ subunits and some other proteins involved in FcεRI signaling. (A) IgE-sensitized cells were preincubated for 15 min with BSS-BSA alone (Ctrl) or supplemented with ethanol (0.5%) and/or Mβ and then activated or not with antigen (100 ng/ml) in the presence or absence of the compounds. After 5 min the cells were solubilized in 0.2% Triton X-100 and FcεRI was immunoprecipitated (IP) from postnuclear supernatants. The immunoprecipitates were resolved by SDS-PAGE and analyzed by immunoblotting with PY-20-HRP conjugate. For loading controls, the same membrane was stripped and re-blotted with FcεRI-β-chain-specific antibody. Representative immunoblots from three to five independent experiments are shown on the left. The immunoblots were analyzed by densitometry and the fold increase in tyrosine FcεRI-β and -γ chain phosphorylation, normalized to non-activated cells and the amount of FcεRI-β chain, is also shown on the right. (B) IgE-sensitized cells were incubated and activated as above. Five min after triggering the cells were solubilized, size fractionated, and tyrosine phosphorylated proteins were detected by immunoblotting with the phosphoprotein-specific antibodies. Antibodies for the corresponding proteins were used for detection of loading controls. Representative immunoblots from three to four independent experiments are shown. (C) The immunoblots were analyzed by densitometry. Fold increases of protein tyrosine phosphorylation, normalized to control (Ctrl) non-activated cells and the corresponding protein loads are shown. (D and E) IgE-sensitized cells were incubated with the drugs as in A and then activated with antigen (100 ng/ml) in the presence of the drugs for the indicated time intervals. The cells were solubilized, size fractionated, and LYN phosphorylated on Tyr 507 (D) or Tyr 416 (E) was detected by immunoblotting with the corresponding antibodies. After stripping, the membranes were developed for LYN used as a loading control. Fold increase in protein tyrosine phosphorylation, normalized to non-activated cells (Ctrl) and protein load, is also shown. Means ± SEs and the statistical significance of differences in A, C, E, and D were calculated from three to five independent experiments.

    Journal: PLoS ONE

    Article Title: Ethanol Inhibits High-Affinity Immunoglobulin E Receptor (FcεRI) Signaling in Mast Cells by Suppressing the Function of FcεRI-Cholesterol Signalosome

    doi: 10.1371/journal.pone.0144596

    Figure Lengend Snippet: Pretreatment with ethanol inhibits tyrosine phosphorylation of FcεRI β and γ subunits and some other proteins involved in FcεRI signaling. (A) IgE-sensitized cells were preincubated for 15 min with BSS-BSA alone (Ctrl) or supplemented with ethanol (0.5%) and/or Mβ and then activated or not with antigen (100 ng/ml) in the presence or absence of the compounds. After 5 min the cells were solubilized in 0.2% Triton X-100 and FcεRI was immunoprecipitated (IP) from postnuclear supernatants. The immunoprecipitates were resolved by SDS-PAGE and analyzed by immunoblotting with PY-20-HRP conjugate. For loading controls, the same membrane was stripped and re-blotted with FcεRI-β-chain-specific antibody. Representative immunoblots from three to five independent experiments are shown on the left. The immunoblots were analyzed by densitometry and the fold increase in tyrosine FcεRI-β and -γ chain phosphorylation, normalized to non-activated cells and the amount of FcεRI-β chain, is also shown on the right. (B) IgE-sensitized cells were incubated and activated as above. Five min after triggering the cells were solubilized, size fractionated, and tyrosine phosphorylated proteins were detected by immunoblotting with the phosphoprotein-specific antibodies. Antibodies for the corresponding proteins were used for detection of loading controls. Representative immunoblots from three to four independent experiments are shown. (C) The immunoblots were analyzed by densitometry. Fold increases of protein tyrosine phosphorylation, normalized to control (Ctrl) non-activated cells and the corresponding protein loads are shown. (D and E) IgE-sensitized cells were incubated with the drugs as in A and then activated with antigen (100 ng/ml) in the presence of the drugs for the indicated time intervals. The cells were solubilized, size fractionated, and LYN phosphorylated on Tyr 507 (D) or Tyr 416 (E) was detected by immunoblotting with the corresponding antibodies. After stripping, the membranes were developed for LYN used as a loading control. Fold increase in protein tyrosine phosphorylation, normalized to non-activated cells (Ctrl) and protein load, is also shown. Means ± SEs and the statistical significance of differences in A, C, E, and D were calculated from three to five independent experiments.

    Article Snippet: For measurement in the presence of extracellular calcium, cells were pelleted by centrifugation 500 x g for 3 min, resuspended in BSS-0.1% BSA and transferred to white polysorp 96 well plate (NUNC, Thermo Scientific).

    Techniques: Immunoprecipitation, SDS Page, Western Blot, Incubation, Stripping Membranes

    Protective effect of cholesterol against ethanol-mediated inhibition of ROS production in antigen-activated BMMCs. (A) IgE-sensitized cells were incubated for 15 min with the indicated concentrations of ethanol, which was also present during the activation. Then the cells were activated or not with antigen (250 ng/ml) and ROSs were determined using H 2 DCFDA as a substrate. The values on y-axes indicate fluorescence intensities observed 10 min after triggering. (B) The cells were exposed to BSS-BSA supplemented or not with ethanol (0.5%), Mβ (2 mM) and/or sMβ (2 mM), and after 20 min activated or not with antigen (250 ng/ml). ROSs were determined as above. Data are means ± SEs (n = 6–8). The statistical significance of the intergroup differences is also shown.

    Journal: PLoS ONE

    Article Title: Ethanol Inhibits High-Affinity Immunoglobulin E Receptor (FcεRI) Signaling in Mast Cells by Suppressing the Function of FcεRI-Cholesterol Signalosome

    doi: 10.1371/journal.pone.0144596

    Figure Lengend Snippet: Protective effect of cholesterol against ethanol-mediated inhibition of ROS production in antigen-activated BMMCs. (A) IgE-sensitized cells were incubated for 15 min with the indicated concentrations of ethanol, which was also present during the activation. Then the cells were activated or not with antigen (250 ng/ml) and ROSs were determined using H 2 DCFDA as a substrate. The values on y-axes indicate fluorescence intensities observed 10 min after triggering. (B) The cells were exposed to BSS-BSA supplemented or not with ethanol (0.5%), Mβ (2 mM) and/or sMβ (2 mM), and after 20 min activated or not with antigen (250 ng/ml). ROSs were determined as above. Data are means ± SEs (n = 6–8). The statistical significance of the intergroup differences is also shown.

    Article Snippet: For measurement in the presence of extracellular calcium, cells were pelleted by centrifugation 500 x g for 3 min, resuspended in BSS-0.1% BSA and transferred to white polysorp 96 well plate (NUNC, Thermo Scientific).

    Techniques: Inhibition, Incubation, Activation Assay, Fluorescence

    p5RHH-JNK2 siRNA NPs reduce thrombotic risk, restore endothelial integrity, and decrease necrotic plaque area and macrophages. Notes: ( A ) Shorter occlusion times for untreated ApoE −/− mice indicate more aggressive clotting (ie, heightened thrombotic risk) compared to mice treated with p5RHH-JNK2 siRNA NPs (n=6), which manifest prolonged occlusion times compared to HBSS control (n=5, P =0.02). ( B ) 19 F MRS demonstrates significantly less perfluorocarbon (CE volume) NP accumulation in ApoE −/− mice after p5RHH-JNK2 siRNA NP treatment (n=8) compared to those treated with HBSS (n=7) ( P =0.003), confirming restoration of endothelial barrier integrity that now prohibits passive permeation of perfluorocarbon NPs. ( C and D ) Representative aorta sections demonstrate that necrotic plaque area is reduced in p5RHH-JNK2 siRNA NP-treated animals ( D ) (n=8) compared to those treated with HBSS ( C ) (n=4, bar 100 μm). ( E ) Necrotic plaque areas from mice treated with p5RHH-JNK2 siRNA NPs are reduced compared to mice receiving HBSS ( P =0.004). ( F and G ) Representative immunofluorescence stains demonstrate significantly fewer Moma-positive cells in atherosclerotic plaque from ApoE −/− mice treated with p5RHH-JNK2 siRNA NPs ( G ) (n=36) compared to HBSS control mice ( F ) (n=17, P

    Journal: International Journal of Nanomedicine

    Article Title: Anti-JNK2 peptide–siRNA nanostructures improve plaque endothelium and reduce thrombotic risk in atherosclerotic mice

    doi: 10.2147/IJN.S168556

    Figure Lengend Snippet: p5RHH-JNK2 siRNA NPs reduce thrombotic risk, restore endothelial integrity, and decrease necrotic plaque area and macrophages. Notes: ( A ) Shorter occlusion times for untreated ApoE −/− mice indicate more aggressive clotting (ie, heightened thrombotic risk) compared to mice treated with p5RHH-JNK2 siRNA NPs (n=6), which manifest prolonged occlusion times compared to HBSS control (n=5, P =0.02). ( B ) 19 F MRS demonstrates significantly less perfluorocarbon (CE volume) NP accumulation in ApoE −/− mice after p5RHH-JNK2 siRNA NP treatment (n=8) compared to those treated with HBSS (n=7) ( P =0.003), confirming restoration of endothelial barrier integrity that now prohibits passive permeation of perfluorocarbon NPs. ( C and D ) Representative aorta sections demonstrate that necrotic plaque area is reduced in p5RHH-JNK2 siRNA NP-treated animals ( D ) (n=8) compared to those treated with HBSS ( C ) (n=4, bar 100 μm). ( E ) Necrotic plaque areas from mice treated with p5RHH-JNK2 siRNA NPs are reduced compared to mice receiving HBSS ( P =0.004). ( F and G ) Representative immunofluorescence stains demonstrate significantly fewer Moma-positive cells in atherosclerotic plaque from ApoE −/− mice treated with p5RHH-JNK2 siRNA NPs ( G ) (n=36) compared to HBSS control mice ( F ) (n=17, P

    Article Snippet: For in vitro applications, p5RHH-siRNA nanoparticles were formulated by mixing p5RHH and siRNA in Hanks’ Balanced Salt solution (HBSS) (14025-092; Thermo Fisher Scientific) and incubated at 37°C for 40 minutes, followed by albumin stabilization, as previously reported.

    Techniques: Mouse Assay, Coagulation, Immunofluorescence

    p5RHH-JNK2 siRNA NPs neither suppress systemic immune-cell function nor induce innate/adaptive immunoresponses. Notes: ( A ) After seven sequential doses of p5RHH-siRNA NPs over 3.5 weeks, spleens were extracted and splenocytes enumerated 24 hours after the last dose. ApoE −/- mice treated with p5RHH-JNK2 NPs (n=4) exhibit significantly fewer splenocytes compared to HBSS control (n=3) ( P =0.02). ( B ) Spleen sizes of mice treated with p5RHH-JNK2 siRNA NPs (n=19) are significantly smaller than from mice with HBSS treatment (n=12, P =0.001) and approximate spleen sizes of control C57BL/6 mice (n=9, P =0.511; one-way ANOVA followed with Scheffé post hoc test). ( C ) Distribution of splenic immune-cell subpopulations was not affected by the p5RHH-JNK2 siRNA NP treatment (n=4) compared to HBSS control (n=3; FoxP3 + p5RHH-JNK2 siRNA NP treatment, n=6; HBBS, n=5). ( D ) Splenic CD4 + T cells stimulated with anti-CD3 monoclonal antibody responded normally (HBSS, n=5; p5RHH-JNK2 siRNA NPs, n=6). ( E ) C3a assay indicates that p5RHH-JNK2 siRNA NPs (n=5) do not activate complement (innate immune response) compared with DOTAP NPs known to activate strongly (n=5). C3a level of the mice treated with the p5RHH-JNK2 siRNA NPs is significantly smaller than those of mice treated with DOTAP NP ( P

    Journal: International Journal of Nanomedicine

    Article Title: Anti-JNK2 peptide–siRNA nanostructures improve plaque endothelium and reduce thrombotic risk in atherosclerotic mice

    doi: 10.2147/IJN.S168556

    Figure Lengend Snippet: p5RHH-JNK2 siRNA NPs neither suppress systemic immune-cell function nor induce innate/adaptive immunoresponses. Notes: ( A ) After seven sequential doses of p5RHH-siRNA NPs over 3.5 weeks, spleens were extracted and splenocytes enumerated 24 hours after the last dose. ApoE −/- mice treated with p5RHH-JNK2 NPs (n=4) exhibit significantly fewer splenocytes compared to HBSS control (n=3) ( P =0.02). ( B ) Spleen sizes of mice treated with p5RHH-JNK2 siRNA NPs (n=19) are significantly smaller than from mice with HBSS treatment (n=12, P =0.001) and approximate spleen sizes of control C57BL/6 mice (n=9, P =0.511; one-way ANOVA followed with Scheffé post hoc test). ( C ) Distribution of splenic immune-cell subpopulations was not affected by the p5RHH-JNK2 siRNA NP treatment (n=4) compared to HBSS control (n=3; FoxP3 + p5RHH-JNK2 siRNA NP treatment, n=6; HBBS, n=5). ( D ) Splenic CD4 + T cells stimulated with anti-CD3 monoclonal antibody responded normally (HBSS, n=5; p5RHH-JNK2 siRNA NPs, n=6). ( E ) C3a assay indicates that p5RHH-JNK2 siRNA NPs (n=5) do not activate complement (innate immune response) compared with DOTAP NPs known to activate strongly (n=5). C3a level of the mice treated with the p5RHH-JNK2 siRNA NPs is significantly smaller than those of mice treated with DOTAP NP ( P

    Article Snippet: For in vitro applications, p5RHH-siRNA nanoparticles were formulated by mixing p5RHH and siRNA in Hanks’ Balanced Salt solution (HBSS) (14025-092; Thermo Fisher Scientific) and incubated at 37°C for 40 minutes, followed by albumin stabilization, as previously reported.

    Techniques: Cell Function Assay, Mouse Assay

    p5RHH-JNK2 siRNA NPs reduce inflammatory signaling in atherosclerotic plaque. Notes: ( A and B ) Representative confocal images of immunofluorescence stains exhibit reduced nuclear localization of p65 in atherosclerotic plaques from treated ApoE −/− mice ( B ) (n=10) compared to HBSS control ( A ) (n=16, P

    Journal: International Journal of Nanomedicine

    Article Title: Anti-JNK2 peptide–siRNA nanostructures improve plaque endothelium and reduce thrombotic risk in atherosclerotic mice

    doi: 10.2147/IJN.S168556

    Figure Lengend Snippet: p5RHH-JNK2 siRNA NPs reduce inflammatory signaling in atherosclerotic plaque. Notes: ( A and B ) Representative confocal images of immunofluorescence stains exhibit reduced nuclear localization of p65 in atherosclerotic plaques from treated ApoE −/− mice ( B ) (n=10) compared to HBSS control ( A ) (n=16, P

    Article Snippet: For in vitro applications, p5RHH-siRNA nanoparticles were formulated by mixing p5RHH and siRNA in Hanks’ Balanced Salt solution (HBSS) (14025-092; Thermo Fisher Scientific) and incubated at 37°C for 40 minutes, followed by albumin stabilization, as previously reported.

    Techniques: Immunofluorescence, Mouse Assay

    p5RHH-JNK2 siRNA NPs selectively inhibit JNK2 expression at both mRNA and protein levels in aorta from ApoE −/− mice on a Western diet. Notes: ( A ) RT 2 -PCR results demonstrate the JNK2-mRNA knockdown by p5RHH-JNK2 siRNA NPs (n=7) compared to HBSS control (n=6, P =0.044) and p5RHH-scrambled siRNA NPs (n=6, P =0.027; one-way ANOVA followed with Scheffé post hoc test). ( B ) JNK1 mRNA expression is not affected by p5RHH-JNK2 siRNA NP treatment (n=6) compared to HBSS control (n=6). ( C and D ) Western blot results illustrate JNK2 protein knockdown by p5RHH-JNK2 siRNA NPs (n=5) compared to HBSS control (n=6, P =0.042; unpaired two-sided Student’s t -test). GAPDH was used as internal control. Data presented in dot plots with means ± SE. * P

    Journal: International Journal of Nanomedicine

    Article Title: Anti-JNK2 peptide–siRNA nanostructures improve plaque endothelium and reduce thrombotic risk in atherosclerotic mice

    doi: 10.2147/IJN.S168556

    Figure Lengend Snippet: p5RHH-JNK2 siRNA NPs selectively inhibit JNK2 expression at both mRNA and protein levels in aorta from ApoE −/− mice on a Western diet. Notes: ( A ) RT 2 -PCR results demonstrate the JNK2-mRNA knockdown by p5RHH-JNK2 siRNA NPs (n=7) compared to HBSS control (n=6, P =0.044) and p5RHH-scrambled siRNA NPs (n=6, P =0.027; one-way ANOVA followed with Scheffé post hoc test). ( B ) JNK1 mRNA expression is not affected by p5RHH-JNK2 siRNA NP treatment (n=6) compared to HBSS control (n=6). ( C and D ) Western blot results illustrate JNK2 protein knockdown by p5RHH-JNK2 siRNA NPs (n=5) compared to HBSS control (n=6, P =0.042; unpaired two-sided Student’s t -test). GAPDH was used as internal control. Data presented in dot plots with means ± SE. * P

    Article Snippet: For in vitro applications, p5RHH-siRNA nanoparticles were formulated by mixing p5RHH and siRNA in Hanks’ Balanced Salt solution (HBSS) (14025-092; Thermo Fisher Scientific) and incubated at 37°C for 40 minutes, followed by albumin stabilization, as previously reported.

    Techniques: Expressing, Mouse Assay, Western Blot, Polymerase Chain Reaction

    p5RHH-JNK2 siRNA NPs reduce thrombotic risk, restore endothelial integrity, and decrease necrotic plaque area and macrophages. Notes: ( A ) Shorter occlusion times for untreated ApoE −/− mice indicate more aggressive clotting (ie, heightened thrombotic risk) compared to mice treated with p5RHH-JNK2 siRNA NPs (n=6), which manifest prolonged occlusion times compared to HBSS control (n=5, P =0.02). ( B ) 19 F MRS demonstrates significantly less perfluorocarbon (CE volume) NP accumulation in ApoE −/− mice after p5RHH-JNK2 siRNA NP treatment (n=8) compared to those treated with HBSS (n=7) ( P =0.003), confirming restoration of endothelial barrier integrity that now prohibits passive permeation of perfluorocarbon NPs. ( C and D ) Representative aorta sections demonstrate that necrotic plaque area is reduced in p5RHH-JNK2 siRNA NP-treated animals ( D ) (n=8) compared to those treated with HBSS ( C ) (n=4, bar 100 μm). ( E ) Necrotic plaque areas from mice treated with p5RHH-JNK2 siRNA NPs are reduced compared to mice receiving HBSS ( P =0.004). ( F and G ) Representative immunofluorescence stains demonstrate significantly fewer Moma-positive cells in atherosclerotic plaque from ApoE −/− mice treated with p5RHH-JNK2 siRNA NPs ( G ) (n=36) compared to HBSS control mice ( F ) (n=17, P

    Journal: International Journal of Nanomedicine

    Article Title: Anti-JNK2 peptide–siRNA nanostructures improve plaque endothelium and reduce thrombotic risk in atherosclerotic mice

    doi: 10.2147/IJN.S168556

    Figure Lengend Snippet: p5RHH-JNK2 siRNA NPs reduce thrombotic risk, restore endothelial integrity, and decrease necrotic plaque area and macrophages. Notes: ( A ) Shorter occlusion times for untreated ApoE −/− mice indicate more aggressive clotting (ie, heightened thrombotic risk) compared to mice treated with p5RHH-JNK2 siRNA NPs (n=6), which manifest prolonged occlusion times compared to HBSS control (n=5, P =0.02). ( B ) 19 F MRS demonstrates significantly less perfluorocarbon (CE volume) NP accumulation in ApoE −/− mice after p5RHH-JNK2 siRNA NP treatment (n=8) compared to those treated with HBSS (n=7) ( P =0.003), confirming restoration of endothelial barrier integrity that now prohibits passive permeation of perfluorocarbon NPs. ( C and D ) Representative aorta sections demonstrate that necrotic plaque area is reduced in p5RHH-JNK2 siRNA NP-treated animals ( D ) (n=8) compared to those treated with HBSS ( C ) (n=4, bar 100 μm). ( E ) Necrotic plaque areas from mice treated with p5RHH-JNK2 siRNA NPs are reduced compared to mice receiving HBSS ( P =0.004). ( F and G ) Representative immunofluorescence stains demonstrate significantly fewer Moma-positive cells in atherosclerotic plaque from ApoE −/− mice treated with p5RHH-JNK2 siRNA NPs ( G ) (n=36) compared to HBSS control mice ( F ) (n=17, P

    Article Snippet: For in vitro applications, p5RHH-siRNA nanoparticles were formulated by mixing p5RHH and siRNA in Hanks’ Balanced Salt solution (HBSS) (14025-092; Thermo Fisher Scientific) and incubated at 37°C for 40 minutes, followed by albumin stabilization, as previously reported.

    Techniques: Mouse Assay, Coagulation, Immunofluorescence

    p5RHH-JNK2 siRNA NPs reduce inflammatory signaling in atherosclerotic plaque. Notes: ( A and B ) Representative confocal images of immunofluorescence stains exhibit reduced nuclear localization of p65 in atherosclerotic plaques from treated ApoE −/− mice ( B ) (n=10) compared to HBSS control ( A ) (n=16, P

    Journal: International Journal of Nanomedicine

    Article Title: Anti-JNK2 peptide–siRNA nanostructures improve plaque endothelium and reduce thrombotic risk in atherosclerotic mice

    doi: 10.2147/IJN.S168556

    Figure Lengend Snippet: p5RHH-JNK2 siRNA NPs reduce inflammatory signaling in atherosclerotic plaque. Notes: ( A and B ) Representative confocal images of immunofluorescence stains exhibit reduced nuclear localization of p65 in atherosclerotic plaques from treated ApoE −/− mice ( B ) (n=10) compared to HBSS control ( A ) (n=16, P

    Article Snippet: For in vitro applications, p5RHH-siRNA nanoparticles were formulated by mixing p5RHH and siRNA in Hanks’ Balanced Salt solution (HBSS) (14025-092; Thermo Fisher Scientific) and incubated at 37°C for 40 minutes, followed by albumin stabilization, as previously reported.

    Techniques: Immunofluorescence, Mouse Assay

    p5RHH-JNK2 siRNA NPs selectively inhibit JNK2 expression at both mRNA and protein levels in aorta from ApoE −/− mice on a Western diet. Notes: ( A ) RT 2 -PCR results demonstrate the JNK2-mRNA knockdown by p5RHH-JNK2 siRNA NPs (n=7) compared to HBSS control (n=6, P =0.044) and p5RHH-scrambled siRNA NPs (n=6, P =0.027; one-way ANOVA followed with Scheffé post hoc test). ( B ) JNK1 mRNA expression is not affected by p5RHH-JNK2 siRNA NP treatment (n=6) compared to HBSS control (n=6). ( C and D ) Western blot results illustrate JNK2 protein knockdown by p5RHH-JNK2 siRNA NPs (n=5) compared to HBSS control (n=6, P =0.042; unpaired two-sided Student’s t -test). GAPDH was used as internal control. Data presented in dot plots with means ± SE. * P

    Journal: International Journal of Nanomedicine

    Article Title: Anti-JNK2 peptide–siRNA nanostructures improve plaque endothelium and reduce thrombotic risk in atherosclerotic mice

    doi: 10.2147/IJN.S168556

    Figure Lengend Snippet: p5RHH-JNK2 siRNA NPs selectively inhibit JNK2 expression at both mRNA and protein levels in aorta from ApoE −/− mice on a Western diet. Notes: ( A ) RT 2 -PCR results demonstrate the JNK2-mRNA knockdown by p5RHH-JNK2 siRNA NPs (n=7) compared to HBSS control (n=6, P =0.044) and p5RHH-scrambled siRNA NPs (n=6, P =0.027; one-way ANOVA followed with Scheffé post hoc test). ( B ) JNK1 mRNA expression is not affected by p5RHH-JNK2 siRNA NP treatment (n=6) compared to HBSS control (n=6). ( C and D ) Western blot results illustrate JNK2 protein knockdown by p5RHH-JNK2 siRNA NPs (n=5) compared to HBSS control (n=6, P =0.042; unpaired two-sided Student’s t -test). GAPDH was used as internal control. Data presented in dot plots with means ± SE. * P

    Article Snippet: For in vitro applications, p5RHH-siRNA nanoparticles were formulated by mixing p5RHH and siRNA in Hanks’ Balanced Salt solution (HBSS) (14025-092; Thermo Fisher Scientific) and incubated at 37°C for 40 minutes, followed by albumin stabilization, as previously reported.

    Techniques: Expressing, Mouse Assay, Western Blot, Polymerase Chain Reaction

    p5RHH-JNK2 siRNA NPs neither suppress systemic immune-cell function nor induce innate/adaptive immunoresponses. Notes: ( A ) After seven sequential doses of p5RHH-siRNA NPs over 3.5 weeks, spleens were extracted and splenocytes enumerated 24 hours after the last dose. ApoE −/- mice treated with p5RHH-JNK2 NPs (n=4) exhibit significantly fewer splenocytes compared to HBSS control (n=3) ( P =0.02). ( B ) Spleen sizes of mice treated with p5RHH-JNK2 siRNA NPs (n=19) are significantly smaller than from mice with HBSS treatment (n=12, P =0.001) and approximate spleen sizes of control C57BL/6 mice (n=9, P =0.511; one-way ANOVA followed with Scheffé post hoc test). ( C ) Distribution of splenic immune-cell subpopulations was not affected by the p5RHH-JNK2 siRNA NP treatment (n=4) compared to HBSS control (n=3; FoxP3 + p5RHH-JNK2 siRNA NP treatment, n=6; HBBS, n=5). ( D ) Splenic CD4 + T cells stimulated with anti-CD3 monoclonal antibody responded normally (HBSS, n=5; p5RHH-JNK2 siRNA NPs, n=6). ( E ) C3a assay indicates that p5RHH-JNK2 siRNA NPs (n=5) do not activate complement (innate immune response) compared with DOTAP NPs known to activate strongly (n=5). C3a level of the mice treated with the p5RHH-JNK2 siRNA NPs is significantly smaller than those of mice treated with DOTAP NP ( P

    Journal: International Journal of Nanomedicine

    Article Title: Anti-JNK2 peptide–siRNA nanostructures improve plaque endothelium and reduce thrombotic risk in atherosclerotic mice

    doi: 10.2147/IJN.S168556

    Figure Lengend Snippet: p5RHH-JNK2 siRNA NPs neither suppress systemic immune-cell function nor induce innate/adaptive immunoresponses. Notes: ( A ) After seven sequential doses of p5RHH-siRNA NPs over 3.5 weeks, spleens were extracted and splenocytes enumerated 24 hours after the last dose. ApoE −/- mice treated with p5RHH-JNK2 NPs (n=4) exhibit significantly fewer splenocytes compared to HBSS control (n=3) ( P =0.02). ( B ) Spleen sizes of mice treated with p5RHH-JNK2 siRNA NPs (n=19) are significantly smaller than from mice with HBSS treatment (n=12, P =0.001) and approximate spleen sizes of control C57BL/6 mice (n=9, P =0.511; one-way ANOVA followed with Scheffé post hoc test). ( C ) Distribution of splenic immune-cell subpopulations was not affected by the p5RHH-JNK2 siRNA NP treatment (n=4) compared to HBSS control (n=3; FoxP3 + p5RHH-JNK2 siRNA NP treatment, n=6; HBBS, n=5). ( D ) Splenic CD4 + T cells stimulated with anti-CD3 monoclonal antibody responded normally (HBSS, n=5; p5RHH-JNK2 siRNA NPs, n=6). ( E ) C3a assay indicates that p5RHH-JNK2 siRNA NPs (n=5) do not activate complement (innate immune response) compared with DOTAP NPs known to activate strongly (n=5). C3a level of the mice treated with the p5RHH-JNK2 siRNA NPs is significantly smaller than those of mice treated with DOTAP NP ( P

    Article Snippet: For in vitro applications, p5RHH-siRNA nanoparticles were formulated by mixing p5RHH and siRNA in Hanks’ Balanced Salt solution (HBSS) (14025-092; Thermo Fisher Scientific) and incubated at 37°C for 40 minutes, followed by albumin stabilization, as previously reported.

    Techniques: Cell Function Assay, Mouse Assay

    Effect of anti-inositol 1,4,5-trisphosphate type-1 receptor/BioPORTER ® on progesterone-, zona pellucida-, and calcium ionophore-induced calcium influx. ( a ) Summary graph. The calcium influx curves in this figure represent the change in the average calcium concentration of the groups. Black arrows indicate when inducers were added. The raw intensity values were normalized as ΔF, ΔF = ( F − F baseline )/F baseline . “F” represent the mean FITC fluorescence intensity of each gate and “F baseline ” represents of the mean FITC fluorescence intensity of the initial 2 min. The data are expressed as the mean, n = 3. ( b ) Effect of anti-inositol 1,4,5-trisphosphate type-1 receptor/BioPORTER ® on progesterone-induced calcium influx. The “ * ” represents this curve, and the versus curve treated with inducer only was significantly different. The data are expressed as the mean, n = 3. ( c ) Effect of anti-inositol 1,4,5-trisphosphate type-1 receptor/BioPORTER ® on zona pellucida-induced calcium influx. The data are expressed as the mean, n = 3. ( d ) Effect of anti-inositol 1,4,5-trisphosphate type-1 receptor/BioPORTER ® on calcium ionophore-induced calcium influx. The data are expressed as the mean, n = 3. ( e ) Description of the legends in a , b , c and d . Figure legends are given a series of two-letter groupings. The first letter indicates the pretreatment reagent, and the second letter represents the inducers. For the first letter, “C” indicates Earle's balanced salt solution supplemented with 0.0% BSA (EBSS [0.0% BSA]), and “O” represent anti-IP3R1/BioPORTER®. For the second letter, “P” indicates progesterone, “T” represents ZP, “A” indicates A23187 and “E” indicates EBSS (0.0% BSA). IP3R1: inositol 1,4,5-trisphosphate type-1 receptor; ZP: zona pellucida.

    Journal: Asian Journal of Andrology

    Article Title: Participation of the inositol 1,4,5-trisphosphate-gated calcium channel in the zona pellucida- and progesterone-induced acrosome reaction and calcium influx in human spermatozoa

    doi: 10.4103/aja.aja_44_19

    Figure Lengend Snippet: Effect of anti-inositol 1,4,5-trisphosphate type-1 receptor/BioPORTER ® on progesterone-, zona pellucida-, and calcium ionophore-induced calcium influx. ( a ) Summary graph. The calcium influx curves in this figure represent the change in the average calcium concentration of the groups. Black arrows indicate when inducers were added. The raw intensity values were normalized as ΔF, ΔF = ( F − F baseline )/F baseline . “F” represent the mean FITC fluorescence intensity of each gate and “F baseline ” represents of the mean FITC fluorescence intensity of the initial 2 min. The data are expressed as the mean, n = 3. ( b ) Effect of anti-inositol 1,4,5-trisphosphate type-1 receptor/BioPORTER ® on progesterone-induced calcium influx. The “ * ” represents this curve, and the versus curve treated with inducer only was significantly different. The data are expressed as the mean, n = 3. ( c ) Effect of anti-inositol 1,4,5-trisphosphate type-1 receptor/BioPORTER ® on zona pellucida-induced calcium influx. The data are expressed as the mean, n = 3. ( d ) Effect of anti-inositol 1,4,5-trisphosphate type-1 receptor/BioPORTER ® on calcium ionophore-induced calcium influx. The data are expressed as the mean, n = 3. ( e ) Description of the legends in a , b , c and d . Figure legends are given a series of two-letter groupings. The first letter indicates the pretreatment reagent, and the second letter represents the inducers. For the first letter, “C” indicates Earle's balanced salt solution supplemented with 0.0% BSA (EBSS [0.0% BSA]), and “O” represent anti-IP3R1/BioPORTER®. For the second letter, “P” indicates progesterone, “T” represents ZP, “A” indicates A23187 and “E” indicates EBSS (0.0% BSA). IP3R1: inositol 1,4,5-trisphosphate type-1 receptor; ZP: zona pellucida.

    Article Snippet: Earle's balanced salt solution (EBSS), phosphate-buffered saline (PBS), and penicillin–streptomycin were obtained from Thermo Fisher Scientific, Inc. (Waltham, MA, USA).

    Techniques: Concentration Assay, Fluorescence