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Fig. 4 in The anti-TMV potency of the tobacco-derived fungus Aspergillus versicolor and its active alkaloids, as anti-TMV activity inhibitors
Fig. 4. Docking poses (left) and interactions (right) of compound 10 (yellow) at the binding site of TMV (blue, PDB code 2OM3). The ligand with TMV A chain amino GLY-135 (1.92 Å) form three hydrogen bonds (green dotted line), Hydrogen bonding distance had been hidden for clarity. The binding energy of compound 10 for between ligands and TMV. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)
Fig. 2. The key 1H–1H in The anti-TMV potency of the tobacco-derived fungus Aspergillus versicolor and its active alkaloids, as anti-TMV activity inhibitors
Fig. 2. The key 1H–1H COSY (bold lines), HMBC (solid arrows), and ROESY (dashed arrows) correlations of compounds 1–5.
Fig. 6 in The healing bitterness of Gentiana lutea L., phytochemistry and biological activities: A systematic review
Fig. 6. Amarogentin was demonstrated to stimulate keratinocyte differentiation and reduce inflammation by up-regulating endothelial bitter taste receptors expressed on keratinocytes and mast cells.
Fig. 5. G in The healing bitterness of Gentiana lutea L., phytochemistry and biological activities: A systematic review
Fig. 5. G. lutea extract and its constituents could inhibit vascular smooth muscle cells proliferation acting downstream of PDGF-receptor but upstream ERK1/2 leading to the slackening of the atherosclerotic process. At the same time, amarogentin could inhibit MAPKs and PLCγ activation avoiding platelet activation.
Fig. 3 in The anti-TMV potency of the tobacco-derived fungus Aspergillus versicolor and its active alkaloids, as anti-TMV activity inhibitors
Fig. 3. Docking poses (left) and interactions (right) of compound 1 (yellow) at the binding site of TMV (blue, PDB code 2OM3). The ligand with TMV. A chain amino ASN-73 (2.81 Å) and TYR-139 (3.04 Å) form four hydrogen bonds (green dotted line), Hydrogen bonding distance had been hidden for clarity. The binding energy of strong affinity between ligands and TMV. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article
Fig. 4 in The healing bitterness of Gentiana lutea L., phytochemistry and biological activities: A systematic review
Fig. 4. Down-regulation genes implied in adipocyte differentiation. G. lutea extract and its constituent loganic acid are implied in the inhibition of the messenger ribonucleic acid (mRNA) involved in the regulation of genes, including CCAAT/enhancer-binding protein α (Cebpα), adiponectin (Adipoq), glucose transporter type 4 (GLUT4), lipoprotein lipase (Lpl), proliferator-activated receptor γ (PPARγ), perilipin1 (Plin1), and fatty acid-binding protein 4 (Fabp4). On the other hand, amarogentin indirectly down-regulating PPARγ expression throughout the inhibition of recombinant aldose reductase (ALR2).
Fig. 3 in The healing bitterness of Gentiana lutea L., phytochemistry and biological activities: A systematic review
Fig. 3. The quality assessment is based on a checklist adapted from the Cochrane Handbook for Systematic Reviews of Interventions. The in vivo (indicated by blue bar) and clinical studies (indicated by red bar) have been classified in high, medium, and low risk of bias. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
Fig. 2 in The healing bitterness of Gentiana lutea L., phytochemistry and biological activities: A systematic review
Fig. 2. (a) Schematic representation of author origin country distribution, (b) number of articles per argument, (c) distribution of the selected studies by year of publication.
Fig. 6. C3 activated the Nrf2 in Triterpenoids from Uncaria macrophylla as ferroptosis inhibitors
Fig. 6. C3 activated the Nrf2/SLC7A11/GPx4 axis. (A) C3 increased the protein levels of Nrf2, SLC7A11 and GPx4 in a dose-dependent manner. (B) ML385 treatment abolished the neuroprotective effect of C3 in PC12 cells. (C) ML385 blocked the activation of Nrf2, SLC7A11 and GPx4.
Fig. 1 in The healing bitterness of Gentiana lutea L., phytochemistry and biological activities: A systematic review
Fig. 1. Diagram of systematic review literature search results based on the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement.
Fig. 6 in Abietane diterpenes from the twigs and leaves of Cephalotaxus oliveri Mast. with antitumor activity
Fig. 6. Apoptosis assay of HepG2 cells exposed to metaglyptin A (19) (0, 10, 20, and 30 μM). **p <0.01, compared to control group.
Fig. 5 in Abietane diterpenes from the twigs and leaves of Cephalotaxus oliveri Mast. with antitumor activity
Fig. 5. Colony formation assay of HepG2 cells exposed to metaglyptin A (19) (0, 10, 20, and 30 μM) for 7 days. *p <0.05, **p <0.01, compared to control group.
Fig. 2 in Abietane diterpenes from the twigs and leaves of Cephalotaxus oliveri Mast. with antitumor activity
Fig. 2. Key correlations in HMBC (red arrows) and 1H–1H COSY (black bold) of 1–4, 16, 20, and 21. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)
Fig. 2. 1H–1H in Antitumoral activity of 1,2,4-oxadiazoles compounds isolated from the Neowerdermannia vorwerkii in liver and colon human cancer cells
Fig. 2. 1H–1H COSY and HMBC key correlations of 3-(pyridin-3-yl)-5-(tiophen-3-yl)-1,2,4-oxadiazole (1), 5-(3-methoxyphenyl)-3-(pyridin-3-yl)-1,2,4-oxadiazole (2) and 5-(3-hydroxyphenyl)-3-(pyridin-3-yl)-1,2,4-oxadiazole (3).
Fig. 1. 3 in Antitumoral activity of 1,2,4-oxadiazoles compounds isolated from the Neowerdermannia vorwerkii in liver and colon human cancer cells
Fig. 1. 3-(pyridin-3-yl)-5-(tiophen-3-yl)-1,2,4-oxadiazole (1), 5-(3-methoxyphenyl)-3-(pyridin-3-yl)-1,2,4-oxadiazole (2) and 5-(3-hydroxyphenyl)-3-(pyridin-3-yl)- 1,2,4-oxadiazole (3).
Fig. 6 in Bioactive constituents from the leaves of Metapanax delavayi with anti-benign prostatic hyperplasia activities
Fig. 6. Molecular docking simulations obtained at the lowest energy conformation, highlighting potential hydrogen contacts of compound 1 with 5α-reductase (A) and COX-2 (B) proteins and finasteride with 5α-reductase (C) and COX-2 (D) proteins. (Coloured by atom: carbon is cyan; nitrogen is blue; oxygen is red; hydrogen is grey; sulfur is orange). For clarity, only interacting residues are labelled. Hydrogen bonding interactions are shown by dashes. These figures were created by PyMOL. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
Fig. 5 in Bioactive constituents from the leaves of Metapanax delavayi with anti-benign prostatic hyperplasia activities
Fig. 5. The inhibitory effect of compounds 1–12 on the growth of BPH-1 cells (n = 3). *p <0.05, **p <0.01, and ***p <0.001 compared with 50 μM group; Finasteride was used as positive control.
Fig. 4 in Bioactive constituents from the leaves of Metapanax delavayi with anti-benign prostatic hyperplasia activities
Fig. 4. Calculated and experimental ECD spectra of compounds 1 (A), 2 (B), 4 (C), and 5 (D) in MeOH.
Fig. 9 in Bridged cassane derivatives from the seeds of Caesalpinia sappan L. and their cytotoxic activities
Fig. 9. Cell cycle distribution and apoptosis induced by 8 in HepG2 cells. (A) Cell cycle analysis of PI-stained cells treated with different concentrations of 8 for 48 h by flow cytometry. (B) Apoptosis analysis of Annexin V-FITC/PI-stained cells treated with different concentrations of 8 for 48 h by flow cytometry. (C) Apoptosis analysis of Annexin V-FITC/PI-stained cells treated with 8 μM 8 for 6, 12, 24 and 48 h by flow cytometry. (D) Quantification of each stage of the cell cycle after treatment with 8. (E) Quantitative analysis of apoptotic cells treated with 3, 6 and 12 μM 8. (F) Quantitative analysis of apoptotic cells treated with 8 μM 8 for 6, 12, 24 and 48 h **P <0.01, ***P <0.001 versus control group.
Fig. 10. Compounds 1–8 in Bisabolane-type sesquiterpenes from Vernonia amygdalina: Absolute configuration and anti-inflammatory activity
Fig. 10. Compounds 1–8 inhibited the activation of PI3K/AKT signaling pathways in LPS-induced RAW 264.7 cells. A: The expression of relative proteins related to the PI3K/AKT signaling pathways involved inflammation, including PI3K, NF-κB (p65), and AKT RAW 264.7 cells. B–D: The relative levels of p-PI3K/PI3K, p-AKT/ AKT, and p-p65/p65 were quantified (mean ± SD. ###p <0.001, compared with the group untreated with LPS; *p <0.05, **p <0.01 and ***p <0.001 compared with the group treated with LPS.).
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.