methanol Search Results


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Cell Signaling Technology Inc methanol fixed cryosections
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Cell Signaling Technology Inc methanol
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Cell Signaling Technology Inc 47746s fetal bovines serum bio
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Cayman Chemical polyphenolic transstilbene resveratrol analog cay10512
FIGURE 4. Differential activation NF-B and Sp1 and miRNA-146a, IRAK-1, or IRAK-2 gene promoter-luciferase reporter activities in IL- 1A42-stressed HAG primary cells. A, the NF-B p50/p65 complex is up-regulated in IL-1A42-stressed HAG primary cells: p65 (upper arrow- head), p50 (middle arrowhead). Sp1 activation is unchanged after any treat- ment condition (lower arrowhead). B, activation of miRNA-146a luciferase reporter expression by IL-1A42 and inhibition by <t>CAY10512,</t> curcumin, or PDTC is shown. C, differential activation of IRAK-1 and IRAK-2 gene pro- moter-luciferase reporters (pGL3-promoter-IRAK-1, pGL3-promoter-IRAK-2 constructs) by IL-1A42 and inhibition by CAY10512, curcumin, or PDTC is shown. n 4–5; significance over control: *, p 0.05 (ANOVA).
Polyphenolic Transstilbene Resveratrol Analog Cay10512, supplied by Cayman Chemical, 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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Croda International Plc chloroform
FIGURE 4. Differential activation NF-B and Sp1 and miRNA-146a, IRAK-1, or IRAK-2 gene promoter-luciferase reporter activities in IL- 1A42-stressed HAG primary cells. A, the NF-B p50/p65 complex is up-regulated in IL-1A42-stressed HAG primary cells: p65 (upper arrow- head), p50 (middle arrowhead). Sp1 activation is unchanged after any treat- ment condition (lower arrowhead). B, activation of miRNA-146a luciferase reporter expression by IL-1A42 and inhibition by <t>CAY10512,</t> curcumin, or PDTC is shown. C, differential activation of IRAK-1 and IRAK-2 gene pro- moter-luciferase reporters (pGL3-promoter-IRAK-1, pGL3-promoter-IRAK-2 constructs) by IL-1A42 and inhibition by CAY10512, curcumin, or PDTC is shown. n 4–5; significance over control: *, p 0.05 (ANOVA).
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Cayman Chemical azd8055 cayman chemicals 16978
FIGURE 4. Differential activation NF-B and Sp1 and miRNA-146a, IRAK-1, or IRAK-2 gene promoter-luciferase reporter activities in IL- 1A42-stressed HAG primary cells. A, the NF-B p50/p65 complex is up-regulated in IL-1A42-stressed HAG primary cells: p65 (upper arrow- head), p50 (middle arrowhead). Sp1 activation is unchanged after any treat- ment condition (lower arrowhead). B, activation of miRNA-146a luciferase reporter expression by IL-1A42 and inhibition by <t>CAY10512,</t> curcumin, or PDTC is shown. C, differential activation of IRAK-1 and IRAK-2 gene pro- moter-luciferase reporters (pGL3-promoter-IRAK-1, pGL3-promoter-IRAK-2 constructs) by IL-1A42 and inhibition by CAY10512, curcumin, or PDTC is shown. n 4–5; significance over control: *, p 0.05 (ANOVA).
Azd8055 Cayman Chemicals 16978, supplied by Cayman Chemical, 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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Cayman Chemical iso60147

Iso60147, supplied by Cayman Chemical, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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93
Cayman Chemical cbd
( A ) Representative in vivo bovine oviduct histoarchitecture at Day 5, showing cannabinoid receptor 1 (CB1) and 2 (CB2) expression. ( B ) Representative control group organoid CB1 and CB2 expression. ( C ) Independent experimental variables – ( i ) 17β-estradiol (E2) with medroxyprogesterone acetate (MPA); ( ii ) E2 and MPA plus Δ⁹-tetrahydrocannabinol (THC) and cannabidiol <t>(CBD)</t> supplementation; or ( iii <t>)</t> <t>methanol</t> (control) supplementation for 144 h. ( D ) Representative organoid brightfield images across treatments and time. Note: Yellow borders are software generated. ( E - G ) Mean (±SEM) organoid (n=4) morphometric kinetics – ( E ) count, ( F ) circularity, and ( G ) area. Select differences observed [ P ≤0.05 (*) and P ≤0.0001 (****)]. ( H ) Representative organoid Ki67 expression following pathological mimic (THC+CBD) supplementation. ( I ) Heatmap of differentially expressed genes (DEG) by treatment, grouped into six clusters. ( J ) Multivariate plot of DEG pathway significance and impact according to cluster. Bubble size is proportional to the impact ratio (number of genes divided by total pathway size), whereas the vertical axis unit is inverse false discovery rate (FDR). ( K - M ) DEG between organoid treatments – ( K ) control vs . E2+MPA, ( L ) control vs . THC+CBD, and ( M ) E2+MPA vs . THC+CBD. Yellow, purple, and teal indicate control, E2+MPA, and THC+CBD gene upregulation, respectively. ( N ) Parametric gene set enrichment analysis using gene ontology resource molecular function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway annotations, highlighting activated (red) and suppressed (blue) processes in E2+MPA vs . THC+CBD treated organoids. All scale bars: 100 µm.
Cbd, supplied by Cayman Chemical, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Toronto Research Chemicals losartan
( A ) Representative in vivo bovine oviduct histoarchitecture at Day 5, showing cannabinoid receptor 1 (CB1) and 2 (CB2) expression. ( B ) Representative control group organoid CB1 and CB2 expression. ( C ) Independent experimental variables – ( i ) 17β-estradiol (E2) with medroxyprogesterone acetate (MPA); ( ii ) E2 and MPA plus Δ⁹-tetrahydrocannabinol (THC) and cannabidiol <t>(CBD)</t> supplementation; or ( iii <t>)</t> <t>methanol</t> (control) supplementation for 144 h. ( D ) Representative organoid brightfield images across treatments and time. Note: Yellow borders are software generated. ( E - G ) Mean (±SEM) organoid (n=4) morphometric kinetics – ( E ) count, ( F ) circularity, and ( G ) area. Select differences observed [ P ≤0.05 (*) and P ≤0.0001 (****)]. ( H ) Representative organoid Ki67 expression following pathological mimic (THC+CBD) supplementation. ( I ) Heatmap of differentially expressed genes (DEG) by treatment, grouped into six clusters. ( J ) Multivariate plot of DEG pathway significance and impact according to cluster. Bubble size is proportional to the impact ratio (number of genes divided by total pathway size), whereas the vertical axis unit is inverse false discovery rate (FDR). ( K - M ) DEG between organoid treatments – ( K ) control vs . E2+MPA, ( L ) control vs . THC+CBD, and ( M ) E2+MPA vs . THC+CBD. Yellow, purple, and teal indicate control, E2+MPA, and THC+CBD gene upregulation, respectively. ( N ) Parametric gene set enrichment analysis using gene ontology resource molecular function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway annotations, highlighting activated (red) and suppressed (blue) processes in E2+MPA vs . THC+CBD treated organoids. All scale bars: 100 µm.
Losartan, supplied by Toronto Research Chemicals, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Toronto Research Chemicals hydroxymidazolam
( A ) Representative in vivo bovine oviduct histoarchitecture at Day 5, showing cannabinoid receptor 1 (CB1) and 2 (CB2) expression. ( B ) Representative control group organoid CB1 and CB2 expression. ( C ) Independent experimental variables – ( i ) 17β-estradiol (E2) with medroxyprogesterone acetate (MPA); ( ii ) E2 and MPA plus Δ⁹-tetrahydrocannabinol (THC) and cannabidiol <t>(CBD)</t> supplementation; or ( iii <t>)</t> <t>methanol</t> (control) supplementation for 144 h. ( D ) Representative organoid brightfield images across treatments and time. Note: Yellow borders are software generated. ( E - G ) Mean (±SEM) organoid (n=4) morphometric kinetics – ( E ) count, ( F ) circularity, and ( G ) area. Select differences observed [ P ≤0.05 (*) and P ≤0.0001 (****)]. ( H ) Representative organoid Ki67 expression following pathological mimic (THC+CBD) supplementation. ( I ) Heatmap of differentially expressed genes (DEG) by treatment, grouped into six clusters. ( J ) Multivariate plot of DEG pathway significance and impact according to cluster. Bubble size is proportional to the impact ratio (number of genes divided by total pathway size), whereas the vertical axis unit is inverse false discovery rate (FDR). ( K - M ) DEG between organoid treatments – ( K ) control vs . E2+MPA, ( L ) control vs . THC+CBD, and ( M ) E2+MPA vs . THC+CBD. Yellow, purple, and teal indicate control, E2+MPA, and THC+CBD gene upregulation, respectively. ( N ) Parametric gene set enrichment analysis using gene ontology resource molecular function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway annotations, highlighting activated (red) and suppressed (blue) processes in E2+MPA vs . THC+CBD treated organoids. All scale bars: 100 µm.
Hydroxymidazolam, supplied by Toronto Research Chemicals, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
Santa Cruz Biotechnology myeloid differentiation protein 2
( A ) Representative in vivo bovine oviduct histoarchitecture at Day 5, showing cannabinoid receptor 1 (CB1) and 2 (CB2) expression. ( B ) Representative control group organoid CB1 and CB2 expression. ( C ) Independent experimental variables – ( i ) 17β-estradiol (E2) with medroxyprogesterone acetate (MPA); ( ii ) E2 and MPA plus Δ⁹-tetrahydrocannabinol (THC) and cannabidiol <t>(CBD)</t> supplementation; or ( iii <t>)</t> <t>methanol</t> (control) supplementation for 144 h. ( D ) Representative organoid brightfield images across treatments and time. Note: Yellow borders are software generated. ( E - G ) Mean (±SEM) organoid (n=4) morphometric kinetics – ( E ) count, ( F ) circularity, and ( G ) area. Select differences observed [ P ≤0.05 (*) and P ≤0.0001 (****)]. ( H ) Representative organoid Ki67 expression following pathological mimic (THC+CBD) supplementation. ( I ) Heatmap of differentially expressed genes (DEG) by treatment, grouped into six clusters. ( J ) Multivariate plot of DEG pathway significance and impact according to cluster. Bubble size is proportional to the impact ratio (number of genes divided by total pathway size), whereas the vertical axis unit is inverse false discovery rate (FDR). ( K - M ) DEG between organoid treatments – ( K ) control vs . E2+MPA, ( L ) control vs . THC+CBD, and ( M ) E2+MPA vs . THC+CBD. Yellow, purple, and teal indicate control, E2+MPA, and THC+CBD gene upregulation, respectively. ( N ) Parametric gene set enrichment analysis using gene ontology resource molecular function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway annotations, highlighting activated (red) and suppressed (blue) processes in E2+MPA vs . THC+CBD treated organoids. All scale bars: 100 µm.
Myeloid Differentiation Protein 2, supplied by Santa Cruz Biotechnology, 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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92
Cayman Chemical n stearoyl taurine
( A ) Representative in vivo bovine oviduct histoarchitecture at Day 5, showing cannabinoid receptor 1 (CB1) and 2 (CB2) expression. ( B ) Representative control group organoid CB1 and CB2 expression. ( C ) Independent experimental variables – ( i ) 17β-estradiol (E2) with medroxyprogesterone acetate (MPA); ( ii ) E2 and MPA plus Δ⁹-tetrahydrocannabinol (THC) and cannabidiol <t>(CBD)</t> supplementation; or ( iii <t>)</t> <t>methanol</t> (control) supplementation for 144 h. ( D ) Representative organoid brightfield images across treatments and time. Note: Yellow borders are software generated. ( E - G ) Mean (±SEM) organoid (n=4) morphometric kinetics – ( E ) count, ( F ) circularity, and ( G ) area. Select differences observed [ P ≤0.05 (*) and P ≤0.0001 (****)]. ( H ) Representative organoid Ki67 expression following pathological mimic (THC+CBD) supplementation. ( I ) Heatmap of differentially expressed genes (DEG) by treatment, grouped into six clusters. ( J ) Multivariate plot of DEG pathway significance and impact according to cluster. Bubble size is proportional to the impact ratio (number of genes divided by total pathway size), whereas the vertical axis unit is inverse false discovery rate (FDR). ( K - M ) DEG between organoid treatments – ( K ) control vs . E2+MPA, ( L ) control vs . THC+CBD, and ( M ) E2+MPA vs . THC+CBD. Yellow, purple, and teal indicate control, E2+MPA, and THC+CBD gene upregulation, respectively. ( N ) Parametric gene set enrichment analysis using gene ontology resource molecular function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway annotations, highlighting activated (red) and suppressed (blue) processes in E2+MPA vs . THC+CBD treated organoids. All scale bars: 100 µm.
N Stearoyl Taurine, supplied by Cayman Chemical, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


FIGURE 4. Differential activation NF-B and Sp1 and miRNA-146a, IRAK-1, or IRAK-2 gene promoter-luciferase reporter activities in IL- 1A42-stressed HAG primary cells. A, the NF-B p50/p65 complex is up-regulated in IL-1A42-stressed HAG primary cells: p65 (upper arrow- head), p50 (middle arrowhead). Sp1 activation is unchanged after any treat- ment condition (lower arrowhead). B, activation of miRNA-146a luciferase reporter expression by IL-1A42 and inhibition by CAY10512, curcumin, or PDTC is shown. C, differential activation of IRAK-1 and IRAK-2 gene pro- moter-luciferase reporters (pGL3-promoter-IRAK-1, pGL3-promoter-IRAK-2 constructs) by IL-1A42 and inhibition by CAY10512, curcumin, or PDTC is shown. n 4–5; significance over control: *, p 0.05 (ANOVA).

Journal: Journal of Biological Chemistry

Article Title: Differential Regulation of Interleukin-1 Receptor-associated Kinase-1 (IRAK-1) and IRAK-2 by MicroRNA-146a and NF-κB in Stressed Human Astroglial Cells and in Alzheimer Disease

doi: 10.1074/jbc.m110.178848

Figure Lengend Snippet: FIGURE 4. Differential activation NF-B and Sp1 and miRNA-146a, IRAK-1, or IRAK-2 gene promoter-luciferase reporter activities in IL- 1A42-stressed HAG primary cells. A, the NF-B p50/p65 complex is up-regulated in IL-1A42-stressed HAG primary cells: p65 (upper arrow- head), p50 (middle arrowhead). Sp1 activation is unchanged after any treat- ment condition (lower arrowhead). B, activation of miRNA-146a luciferase reporter expression by IL-1A42 and inhibition by CAY10512, curcumin, or PDTC is shown. C, differential activation of IRAK-1 and IRAK-2 gene pro- moter-luciferase reporters (pGL3-promoter-IRAK-1, pGL3-promoter-IRAK-2 constructs) by IL-1A42 and inhibition by CAY10512, curcumin, or PDTC is shown. n 4–5; significance over control: *, p 0.05 (ANOVA).

Article Snippet: As required, 0.5-week-old HAG cells were treated with (a) curcumin (1,7-bis(4-hydroxy-3methoxyphen-yl)-1,6-hepta-diene-3,5-dione diferuloylmethane; purity 98.5%, Axxora, San Diego, CA), dissolved in dimethyl sulfoxide as a 100 mM stock solution, and used at 5 M ambient concentration in the astrocyte basal medium cell medium, (b) the metal chelator, anti-oxidant, and NF- B translocation inhibitor pyrrolidine dithiocarbamate (PTDC; P8765; Sigma) at 25 M PTDC, or with (c) the polyphenolic transstilbene resveratrol analog CAY10512 (10009536; Cayman Chemical, Ann Arbor, MI) as required (Fig. 5).

Techniques: Activation Assay, Luciferase, Expressing, Inhibition, Construct, Control

Journal: iScience

Article Title: Mu-opioid receptor selective superagonists produce prolonged respiratory depression

doi: 10.1016/j.isci.2023.107121

Figure Lengend Snippet:

Article Snippet: Morphine , Cayman Chemical , ISO60147.

Techniques: Recombinant, Expressing, Transfection, Software

( A ) Representative in vivo bovine oviduct histoarchitecture at Day 5, showing cannabinoid receptor 1 (CB1) and 2 (CB2) expression. ( B ) Representative control group organoid CB1 and CB2 expression. ( C ) Independent experimental variables – ( i ) 17β-estradiol (E2) with medroxyprogesterone acetate (MPA); ( ii ) E2 and MPA plus Δ⁹-tetrahydrocannabinol (THC) and cannabidiol (CBD) supplementation; or ( iii ) methanol (control) supplementation for 144 h. ( D ) Representative organoid brightfield images across treatments and time. Note: Yellow borders are software generated. ( E - G ) Mean (±SEM) organoid (n=4) morphometric kinetics – ( E ) count, ( F ) circularity, and ( G ) area. Select differences observed [ P ≤0.05 (*) and P ≤0.0001 (****)]. ( H ) Representative organoid Ki67 expression following pathological mimic (THC+CBD) supplementation. ( I ) Heatmap of differentially expressed genes (DEG) by treatment, grouped into six clusters. ( J ) Multivariate plot of DEG pathway significance and impact according to cluster. Bubble size is proportional to the impact ratio (number of genes divided by total pathway size), whereas the vertical axis unit is inverse false discovery rate (FDR). ( K - M ) DEG between organoid treatments – ( K ) control vs . E2+MPA, ( L ) control vs . THC+CBD, and ( M ) E2+MPA vs . THC+CBD. Yellow, purple, and teal indicate control, E2+MPA, and THC+CBD gene upregulation, respectively. ( N ) Parametric gene set enrichment analysis using gene ontology resource molecular function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway annotations, highlighting activated (red) and suppressed (blue) processes in E2+MPA vs . THC+CBD treated organoids. All scale bars: 100 µm.

Journal: bioRxiv

Article Title: Oviduct fluid metabolic regulation of embryonic genome methylation

doi: 10.1101/2025.06.13.659599

Figure Lengend Snippet: ( A ) Representative in vivo bovine oviduct histoarchitecture at Day 5, showing cannabinoid receptor 1 (CB1) and 2 (CB2) expression. ( B ) Representative control group organoid CB1 and CB2 expression. ( C ) Independent experimental variables – ( i ) 17β-estradiol (E2) with medroxyprogesterone acetate (MPA); ( ii ) E2 and MPA plus Δ⁹-tetrahydrocannabinol (THC) and cannabidiol (CBD) supplementation; or ( iii ) methanol (control) supplementation for 144 h. ( D ) Representative organoid brightfield images across treatments and time. Note: Yellow borders are software generated. ( E - G ) Mean (±SEM) organoid (n=4) morphometric kinetics – ( E ) count, ( F ) circularity, and ( G ) area. Select differences observed [ P ≤0.05 (*) and P ≤0.0001 (****)]. ( H ) Representative organoid Ki67 expression following pathological mimic (THC+CBD) supplementation. ( I ) Heatmap of differentially expressed genes (DEG) by treatment, grouped into six clusters. ( J ) Multivariate plot of DEG pathway significance and impact according to cluster. Bubble size is proportional to the impact ratio (number of genes divided by total pathway size), whereas the vertical axis unit is inverse false discovery rate (FDR). ( K - M ) DEG between organoid treatments – ( K ) control vs . E2+MPA, ( L ) control vs . THC+CBD, and ( M ) E2+MPA vs . THC+CBD. Yellow, purple, and teal indicate control, E2+MPA, and THC+CBD gene upregulation, respectively. ( N ) Parametric gene set enrichment analysis using gene ontology resource molecular function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway annotations, highlighting activated (red) and suppressed (blue) processes in E2+MPA vs . THC+CBD treated organoids. All scale bars: 100 µm.

Article Snippet: These were: ( a ) negative control – comprising Base Medium ( Table S2 ); ( b ) E2 – Base Medium supplemented with E2 (Thermo Scientific Chemicals, L0380103) dissolved in methanol (Fisher Chemical, A4521) at a final concentration of 50 nM with a corresponding vehicle contribution of 0.6 % ( v / v ); ( c ) MPA – Base Medium supplemented with MPA (Thermo Scientific Chemicals, 461120010) dissolved in methanol at a final concentration of 1 µM with a corresponding vehicle contribution of 0.3 % ( v / v ); ( d ) Physiological mimic – Base Medium supplemented with both E2 and MPA as above, with a corresponding cumulative vehicle contribution of 0.9 % ( v / v ); ( e ) Pathological mimic – Base Medium supplemented with E2 and MPA as above, in addition to THC (Cayman Chemical, ISO60157) dissolved in methanol at a final concentration of 6 µM with a corresponding vehicle contribution of 0.2 % ( v / v ); and CBD (Cayman Chemical, ISO60156) dissolved in methanol at a final concentration of 6 µM with a corresponding vehicle contribution of 0.2 % ( v / v ); and ( f ) vehicle control – Base Medium supplemented with 1.3 % ( v / v ) methanol – identical to the largest solvent contribution (Group e ).

Techniques: In Vivo, Expressing, Control, Software, Generated