agonist vs. response –variable slope (four parameters) nonlinear fit graphpad prism 10.1.2 Search Results


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Brain penetration (B/P-ratio) of each drug as a function of inhibitor plasma level. The drugs are classified as: (I) Abcb1 only substrates, (II) Abcb1 and weak Abcg2 substrates and (III) Abcb1 and strong Abcg2 substrates, as shown below. The inhibitor concentration vs. brain-to-plasma ratios curves were fitted using the [Agonist] vs. response <t>–Variable</t> <t>slope</t> <t>(four</t> <t>parameters)</t> <t>nonlinear</t> <t>fit</t> in Graphpad Prism 10.1.2. The dashed lines indicate the 90% CI around the curves
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Lipid accumulation and adipogenic marker mRNA in response to chemical exposure during adipocyte differentiation . C3H10T1/2 cells were differentiated for 6 days in the presence of 0, 0.3, or 1 % ( A ) ethanol or ( B ) ethylene glycol. Cells were compared to an undifferentiated control. Gene expression analysis by RT-qPCR was performed for adipocyte markers ( Pparg2 , Adipoq , Fabp4 , Slc2a4 ) using SYBR Green assay ( n = 4). ( C ) Differentiation of human ASCs was induced with either high (2 μM) or low (0.1 μM) concentrations of rosiglitazone in the adipogenic medium. During differentiation, cells were exposed to 0, 0.3, or 1 % ethanol. Lipids were stained with Oil Red O at day 12 of differentiation, visualized by microscopy, and quantified ( n = 4). The graphs show means ± SEM. Asterisk (*) and hash (#) indicate statistically significant differences compared to the differentiated unexposed control cells <t>using</t> <t>Dunnett's</t> test or two-way <t>ANOVA</t> followed by Dunnett's test, respectively (p < 0.05).
Two Way Analysis Of Variance (Anova), supplied by GraphPad Software Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Lipid accumulation and adipogenic marker mRNA in response to chemical exposure during adipocyte differentiation . C3H10T1/2 cells were differentiated for 6 days in the presence of 0, 0.3, or 1 % ( A ) ethanol or ( B ) ethylene glycol. Cells were compared to an undifferentiated control. Gene expression analysis by RT-qPCR was performed for adipocyte markers ( Pparg2 , Adipoq , Fabp4 , Slc2a4 ) using SYBR Green assay ( n = 4). ( C ) Differentiation of human ASCs was induced with either high (2 μM) or low (0.1 μM) concentrations of rosiglitazone in the adipogenic medium. During differentiation, cells were exposed to 0, 0.3, or 1 % ethanol. Lipids were stained with Oil Red O at day 12 of differentiation, visualized by microscopy, and quantified ( n = 4). The graphs show means ± SEM. Asterisk (*) and hash (#) indicate statistically significant differences compared to the differentiated unexposed control cells <t>using</t> <t>Dunnett's</t> test or two-way <t>ANOVA</t> followed by Dunnett's test, respectively (p < 0.05).
Anova Test, supplied by GraphPad Software Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Lipid accumulation and adipogenic marker mRNA in response to chemical exposure during adipocyte differentiation . C3H10T1/2 cells were differentiated for 6 days in the presence of 0, 0.3, or 1 % ( A ) ethanol or ( B ) ethylene glycol. Cells were compared to an undifferentiated control. Gene expression analysis by RT-qPCR was performed for adipocyte markers ( Pparg2 , Adipoq , Fabp4 , Slc2a4 ) using SYBR Green assay ( n = 4). ( C ) Differentiation of human ASCs was induced with either high (2 μM) or low (0.1 μM) concentrations of rosiglitazone in the adipogenic medium. During differentiation, cells were exposed to 0, 0.3, or 1 % ethanol. Lipids were stained with Oil Red O at day 12 of differentiation, visualized by microscopy, and quantified ( n = 4). The graphs show means ± SEM. Asterisk (*) and hash (#) indicate statistically significant differences compared to the differentiated unexposed control cells <t>using</t> <t>Dunnett's</t> test or two-way <t>ANOVA</t> followed by Dunnett's test, respectively (p < 0.05).
Graphpad Prism 10.1.0, supplied by GraphPad Software Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Lipid accumulation and adipogenic marker mRNA in response to chemical exposure during adipocyte differentiation . C3H10T1/2 cells were differentiated for 6 days in the presence of 0, 0.3, or 1 % ( A ) ethanol or ( B ) ethylene glycol. Cells were compared to an undifferentiated control. Gene expression analysis by RT-qPCR was performed for adipocyte markers ( Pparg2 , Adipoq , Fabp4 , Slc2a4 ) using SYBR Green assay ( n = 4). ( C ) Differentiation of human ASCs was induced with either high (2 μM) or low (0.1 μM) concentrations of rosiglitazone in the adipogenic medium. During differentiation, cells were exposed to 0, 0.3, or 1 % ethanol. Lipids were stained with Oil Red O at day 12 of differentiation, visualized by microscopy, and quantified ( n = 4). The graphs show means ± SEM. Asterisk (*) and hash (#) indicate statistically significant differences compared to the differentiated unexposed control cells <t>using</t> <t>Dunnett's</t> test or two-way <t>ANOVA</t> followed by Dunnett's test, respectively (p < 0.05).
Agonist Vs. Response –Variable Slope Analysis In Graphpad Prism Software, supplied by GraphPad Software Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Lipid accumulation and adipogenic marker mRNA in response to chemical exposure during adipocyte differentiation . C3H10T1/2 cells were differentiated for 6 days in the presence of 0, 0.3, or 1 % ( A ) ethanol or ( B ) ethylene glycol. Cells were compared to an undifferentiated control. Gene expression analysis by RT-qPCR was performed for adipocyte markers ( Pparg2 , Adipoq , Fabp4 , Slc2a4 ) using SYBR Green assay ( n = 4). ( C ) Differentiation of human ASCs was induced with either high (2 μM) or low (0.1 μM) concentrations of rosiglitazone in the adipogenic medium. During differentiation, cells were exposed to 0, 0.3, or 1 % ethanol. Lipids were stained with Oil Red O at day 12 of differentiation, visualized by microscopy, and quantified ( n = 4). The graphs show means ± SEM. Asterisk (*) and hash (#) indicate statistically significant differences compared to the differentiated unexposed control cells <t>using</t> <t>Dunnett's</t> test or two-way <t>ANOVA</t> followed by Dunnett's test, respectively (p < 0.05).
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Lipid accumulation and adipogenic marker mRNA in response to chemical exposure during adipocyte differentiation . C3H10T1/2 cells were differentiated for 6 days in the presence of 0, 0.3, or 1 % ( A ) ethanol or ( B ) ethylene glycol. Cells were compared to an undifferentiated control. Gene expression analysis by RT-qPCR was performed for adipocyte markers ( Pparg2 , Adipoq , Fabp4 , Slc2a4 ) using SYBR Green assay ( n = 4). ( C ) Differentiation of human ASCs was induced with either high (2 μM) or low (0.1 μM) concentrations of rosiglitazone in the adipogenic medium. During differentiation, cells were exposed to 0, 0.3, or 1 % ethanol. Lipids were stained with Oil Red O at day 12 of differentiation, visualized by microscopy, and quantified ( n = 4). The graphs show means ± SEM. Asterisk (*) and hash (#) indicate statistically significant differences compared to the differentiated unexposed control cells <t>using</t> <t>Dunnett's</t> test or two-way <t>ANOVA</t> followed by Dunnett's test, respectively (p < 0.05).
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Lipid accumulation and adipogenic marker mRNA in response to chemical exposure during adipocyte differentiation . C3H10T1/2 cells were differentiated for 6 days in the presence of 0, 0.3, or 1 % ( A ) ethanol or ( B ) ethylene glycol. Cells were compared to an undifferentiated control. Gene expression analysis by RT-qPCR was performed for adipocyte markers ( Pparg2 , Adipoq , Fabp4 , Slc2a4 ) using SYBR Green assay ( n = 4). ( C ) Differentiation of human ASCs was induced with either high (2 μM) or low (0.1 μM) concentrations of rosiglitazone in the adipogenic medium. During differentiation, cells were exposed to 0, 0.3, or 1 % ethanol. Lipids were stained with Oil Red O at day 12 of differentiation, visualized by microscopy, and quantified ( n = 4). The graphs show means ± SEM. Asterisk (*) and hash (#) indicate statistically significant differences compared to the differentiated unexposed control cells <t>using</t> <t>Dunnett's</t> test or two-way <t>ANOVA</t> followed by Dunnett's test, respectively (p < 0.05).
Agonist Vs. Response –Variable Slope (Four Parameters) Nonlinear Fit, supplied by GraphPad Software Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Lipid accumulation and adipogenic marker mRNA in response to chemical exposure during adipocyte differentiation . C3H10T1/2 cells were differentiated for 6 days in the presence of 0, 0.3, or 1 % ( A ) ethanol or ( B ) ethylene glycol. Cells were compared to an undifferentiated control. Gene expression analysis by RT-qPCR was performed for adipocyte markers ( Pparg2 , Adipoq , Fabp4 , Slc2a4 ) using SYBR Green assay ( n = 4). ( C ) Differentiation of human ASCs was induced with either high (2 μM) or low (0.1 μM) concentrations of rosiglitazone in the adipogenic medium. During differentiation, cells were exposed to 0, 0.3, or 1 % ethanol. Lipids were stained with Oil Red O at day 12 of differentiation, visualized by microscopy, and quantified ( n = 4). The graphs show means ± SEM. Asterisk (*) and hash (#) indicate statistically significant differences compared to the differentiated unexposed control cells <t>using</t> <t>Dunnett's</t> test or two-way <t>ANOVA</t> followed by Dunnett's test, respectively (p < 0.05).
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Lipid accumulation and adipogenic marker mRNA in response to chemical exposure during adipocyte differentiation . C3H10T1/2 cells were differentiated for 6 days in the presence of 0, 0.3, or 1 % ( A ) ethanol or ( B ) ethylene glycol. Cells were compared to an undifferentiated control. Gene expression analysis by RT-qPCR was performed for adipocyte markers ( Pparg2 , Adipoq , Fabp4 , Slc2a4 ) using SYBR Green assay ( n = 4). ( C ) Differentiation of human ASCs was induced with either high (2 μM) or low (0.1 μM) concentrations of rosiglitazone in the adipogenic medium. During differentiation, cells were exposed to 0, 0.3, or 1 % ethanol. Lipids were stained with Oil Red O at day 12 of differentiation, visualized by microscopy, and quantified ( n = 4). The graphs show means ± SEM. Asterisk (*) and hash (#) indicate statistically significant differences compared to the differentiated unexposed control cells <t>using</t> <t>Dunnett's</t> test or two-way <t>ANOVA</t> followed by Dunnett's test, respectively (p < 0.05).
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Lipid accumulation and adipogenic marker mRNA in response to chemical exposure during adipocyte differentiation . C3H10T1/2 cells were differentiated for 6 days in the presence of 0, 0.3, or 1 % ( A ) ethanol or ( B ) ethylene glycol. Cells were compared to an undifferentiated control. Gene expression analysis by RT-qPCR was performed for adipocyte markers ( Pparg2 , Adipoq , Fabp4 , Slc2a4 ) using SYBR Green assay ( n = 4). ( C ) Differentiation of human ASCs was induced with either high (2 μM) or low (0.1 μM) concentrations of rosiglitazone in the adipogenic medium. During differentiation, cells were exposed to 0, 0.3, or 1 % ethanol. Lipids were stained with Oil Red O at day 12 of differentiation, visualized by microscopy, and quantified ( n = 4). The graphs show means ± SEM. Asterisk (*) and hash (#) indicate statistically significant differences compared to the differentiated unexposed control cells <t>using</t> <t>Dunnett's</t> test or two-way <t>ANOVA</t> followed by Dunnett's test, respectively (p < 0.05).
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Brain penetration (B/P-ratio) of each drug as a function of inhibitor plasma level. The drugs are classified as: (I) Abcb1 only substrates, (II) Abcb1 and weak Abcg2 substrates and (III) Abcb1 and strong Abcg2 substrates, as shown below. The inhibitor concentration vs. brain-to-plasma ratios curves were fitted using the [Agonist] vs. response –Variable slope (four parameters) nonlinear fit in Graphpad Prism 10.1.2. The dashed lines indicate the 90% CI around the curves

Journal: Fluids and Barriers of the CNS

Article Title: ATP-binding cassette transporter inhibitor potency and substrate drug affinity are critical determinants of successful drug delivery enhancement to the brain

doi: 10.1186/s12987-024-00562-4

Figure Lengend Snippet: Brain penetration (B/P-ratio) of each drug as a function of inhibitor plasma level. The drugs are classified as: (I) Abcb1 only substrates, (II) Abcb1 and weak Abcg2 substrates and (III) Abcb1 and strong Abcg2 substrates, as shown below. The inhibitor concentration vs. brain-to-plasma ratios curves were fitted using the [Agonist] vs. response –Variable slope (four parameters) nonlinear fit in Graphpad Prism 10.1.2. The dashed lines indicate the 90% CI around the curves

Article Snippet: The inhibitor concentration vs. brain-to-plasma ratios curves were fitted using the [Agonist] vs. response –Variable slope (four parameters) nonlinear fit in Graphpad Prism 10.1.2.

Techniques: Clinical Proteomics, Concentration Assay

Potency of elacridar and tariquidar to inhibit Abcg2 and Abcb1a/b. The drugs are classified as: (I) Abcb1 only substrates, (II) Abcb1 and weak Abcg2 substrates and (III) Abcb1 and strong Abcg2 substrates, as shown below. The accumulation of the substrates in Abcb1 KO mice (blue bars), Abcg2 KO mice (green bars) and WT mice (black bars). The color-filled bars show the maximum gain with elacridar or tariquidar. The red dotted line (100%) designates the accumulation of drugs in Abcg2;Abcb1a/b KO mice. The inhibitor concentration vs. brain-to-plasma ratio were fitted using the [Agonist] vs. response –Variable slope (four parameters) nonlinear fit in Graphpad Prism 10.1.2

Journal: Fluids and Barriers of the CNS

Article Title: ATP-binding cassette transporter inhibitor potency and substrate drug affinity are critical determinants of successful drug delivery enhancement to the brain

doi: 10.1186/s12987-024-00562-4

Figure Lengend Snippet: Potency of elacridar and tariquidar to inhibit Abcg2 and Abcb1a/b. The drugs are classified as: (I) Abcb1 only substrates, (II) Abcb1 and weak Abcg2 substrates and (III) Abcb1 and strong Abcg2 substrates, as shown below. The accumulation of the substrates in Abcb1 KO mice (blue bars), Abcg2 KO mice (green bars) and WT mice (black bars). The color-filled bars show the maximum gain with elacridar or tariquidar. The red dotted line (100%) designates the accumulation of drugs in Abcg2;Abcb1a/b KO mice. The inhibitor concentration vs. brain-to-plasma ratio were fitted using the [Agonist] vs. response –Variable slope (four parameters) nonlinear fit in Graphpad Prism 10.1.2

Article Snippet: The inhibitor concentration vs. brain-to-plasma ratios curves were fitted using the [Agonist] vs. response –Variable slope (four parameters) nonlinear fit in Graphpad Prism 10.1.2.

Techniques: Concentration Assay, Clinical Proteomics

Lipid accumulation and adipogenic marker mRNA in response to chemical exposure during adipocyte differentiation . C3H10T1/2 cells were differentiated for 6 days in the presence of 0, 0.3, or 1 % ( A ) ethanol or ( B ) ethylene glycol. Cells were compared to an undifferentiated control. Gene expression analysis by RT-qPCR was performed for adipocyte markers ( Pparg2 , Adipoq , Fabp4 , Slc2a4 ) using SYBR Green assay ( n = 4). ( C ) Differentiation of human ASCs was induced with either high (2 μM) or low (0.1 μM) concentrations of rosiglitazone in the adipogenic medium. During differentiation, cells were exposed to 0, 0.3, or 1 % ethanol. Lipids were stained with Oil Red O at day 12 of differentiation, visualized by microscopy, and quantified ( n = 4). The graphs show means ± SEM. Asterisk (*) and hash (#) indicate statistically significant differences compared to the differentiated unexposed control cells using Dunnett's test or two-way ANOVA followed by Dunnett's test, respectively (p < 0.05).

Journal: Biochemistry and Biophysics Reports

Article Title: Effects of ethanol or ethylene glycol exposure on PPARγ and aromatase expression in adipose tissue

doi: 10.1016/j.bbrep.2024.101742

Figure Lengend Snippet: Lipid accumulation and adipogenic marker mRNA in response to chemical exposure during adipocyte differentiation . C3H10T1/2 cells were differentiated for 6 days in the presence of 0, 0.3, or 1 % ( A ) ethanol or ( B ) ethylene glycol. Cells were compared to an undifferentiated control. Gene expression analysis by RT-qPCR was performed for adipocyte markers ( Pparg2 , Adipoq , Fabp4 , Slc2a4 ) using SYBR Green assay ( n = 4). ( C ) Differentiation of human ASCs was induced with either high (2 μM) or low (0.1 μM) concentrations of rosiglitazone in the adipogenic medium. During differentiation, cells were exposed to 0, 0.3, or 1 % ethanol. Lipids were stained with Oil Red O at day 12 of differentiation, visualized by microscopy, and quantified ( n = 4). The graphs show means ± SEM. Asterisk (*) and hash (#) indicate statistically significant differences compared to the differentiated unexposed control cells using Dunnett's test or two-way ANOVA followed by Dunnett's test, respectively (p < 0.05).

Article Snippet: Statistical significance was assessed by Dunnett's multiple comparisons test or two-way analysis of variance (ANOVA) using GraphPad Prism 10.1.2, depending on the number of variables.

Techniques: Marker, Control, Gene Expression, Quantitative RT-PCR, SYBR Green Assay, Staining, Microscopy

Aromatase mRNA level in response to ethanol or ethylene glycol exposure . Gene expression analysis of aromatase ( CYP19A1 ) and adipocyte markers ( ADIPOQ and FASN ) was performed by RT-qPCR using SYBR Green assay. ( A ) Undifferentiated or ( B ) differentiated A41 cells were exposed to 1 % ethanol or ethylene glycol for 24 h (both panels). The graphs present means ± SEM ( n = 3). Asterisk (*) and hash (#) indicate statistically significant differences compared to control cells using Dunnett's test or two-way ANOVA followed by Dunnett's test, respectively ( p < 0.05).

Journal: Biochemistry and Biophysics Reports

Article Title: Effects of ethanol or ethylene glycol exposure on PPARγ and aromatase expression in adipose tissue

doi: 10.1016/j.bbrep.2024.101742

Figure Lengend Snippet: Aromatase mRNA level in response to ethanol or ethylene glycol exposure . Gene expression analysis of aromatase ( CYP19A1 ) and adipocyte markers ( ADIPOQ and FASN ) was performed by RT-qPCR using SYBR Green assay. ( A ) Undifferentiated or ( B ) differentiated A41 cells were exposed to 1 % ethanol or ethylene glycol for 24 h (both panels). The graphs present means ± SEM ( n = 3). Asterisk (*) and hash (#) indicate statistically significant differences compared to control cells using Dunnett's test or two-way ANOVA followed by Dunnett's test, respectively ( p < 0.05).

Article Snippet: Statistical significance was assessed by Dunnett's multiple comparisons test or two-way analysis of variance (ANOVA) using GraphPad Prism 10.1.2, depending on the number of variables.

Techniques: Gene Expression, Quantitative RT-PCR, SYBR Green Assay, Control