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0.462674 | 6d3273c7cd114ba38c3b2ead2e07c2d5 | Prognosis value of the eight necroptosis-related lncRNAs signature. (A). The outcome of the Kaplan-Meier curves. (B). The AUC values for predicting OS survival rates at 1, 2, and 3 years. (C). The AUC values of the risk variables. (D). Distribution of patient risk ratings. (E). The PCA plot. (F). Plot of risk survival status. (G). The t-SNE plot. (H). Heatmap of lncRNAs associated with necroptosis in high- and low-risk groups. | PMC9465333 | fphar-13-944158-g004.jpg |
0.439648 | 6820456883b74400babd8c0117bb3ec8 | Independent prognostic value of the novel prognostic signature. (A–F). Kaplan–Meier survival curves are stratified by age, gender, and metastasis status. (G). Univariate analysis result. (H). Multivariate analysis result. | PMC9465333 | fphar-13-944158-g005.jpg |
0.411693 | d976c059aa244e46a162d3088c01682a | Construction and calibration of a nomogram. (A). Nomogram integrating risk score and clinical characteristics. (B–D), calibration of the nomogram at 1-year, 2-years, and 3-years survival. | PMC9465333 | fphar-13-944158-g006.jpg |
0.450372 | 6502579681f9454c8a8285786a80dd9e | The GSEA analysis results between the high-risk group and low-risk group. (A). Top five enriched pathways in the high-risk group. (B). Top five enriched pathways in the low-risk group. | PMC9465333 | fphar-13-944158-g007.jpg |
0.418088 | 786aa7b9e68c4c96b9b54e7b27dceae5 | The investigation of immune status in OS. (A–D). Comparisons between the two risk groups regarding stomal score, immune score, ESTIMATE score, and tumor purity. (E–H). The correlation between risk score and stomal score, immune score, ESTIMATE score, and tumor purity. (I–L). (K–M) survival outcome is based on different stomal scores, immune scores, ESTIMATE scores, and tumor purity. (M). The boxplot of tumor-infiltrating immune cell types in low- and high-risk groups. (N). Boxplots of immune cells and immune-associated functions in low- and high-risk groups. (O). Heatmap for immune status based ESTIMATE and ssGSEA among two risk subgroups. | PMC9465333 | fphar-13-944158-g008.jpg |
0.547369 | 319a6056fc1a4a6581793e0c5f079198 | Drug sensitivity analysis. (A–L). The candidate anticancer drugs with significant treatment differences in the high- and low-risk groups. | PMC9465333 | fphar-13-944158-g009.jpg |
0.480879 | 92846fb4c64f4c28adb8836739d91ccc |
(A–H). Validation of the expression of signature genes in OS cell lines. (A). LBX2-AS1. (B). AL133371.2. (C). GAS5. (D). AC007383.1. (E). AC087623.1. (F). AC027348.1. (G). LINC00963. (H). VPS9D1-AS1. | PMC9465333 | fphar-13-944158-g010.jpg |
0.455102 | 07d3d6aeace54b889e9d9648df243beb | Abdominal ultrasound showed a huge mass in the right adrenal gland | PMC9465864 | 12887_2022_3594_Fig1_HTML.jpg |
0.456442 | f1075fb6eb974384b13e4b6e42bc9434 | Abdominal MRI showed the adrenal hemorrhage(3.1*3.6 cm) | PMC9465864 | 12887_2022_3594_Fig2_HTML.jpg |
0.48054 | 427d071c6d314d05bdf25bdc101434df | Formation of PMNs. The PMNs in cancer can be divided into three major temporal phases following a sequential order. First, the metastatic microenvironment is deternmined by the primary tumour. Second, the secondary sites recruit immunosuppressive cells. Finally, circulating tumour cells invade and colonize distant organs or tissues | PMC9465880 | 12964_2022_945_Fig1_HTML.jpg |
0.393955 | ec16355c69ed49fcaecfa20af9017ca3 | Role of exosomal PD-L1 in breast cancer. On the one hand, tumour cell surface-specific antigens are recognized by antigen-presenting cells (APCs), and apoptosis occurs; on the other hand, the combination of PD-1 on the surface of T cells and PD-L1 on the surface of tumour cells inhibits T-cell proliferation, and breast cancer cells secret sEVs that carry PD-L1 to bind to PD-1 on T cells, inhibiting T-cell activation and cell-killing activities | PMC9465880 | 12964_2022_945_Fig2_HTML.jpg |
0.381025 | c2eb34b36e3f4e97bf61d2bf08a809d7 | Effect of sEVs on the pre-metastatic niche in breast cancer. An overview of the effects of sEVs on the PMN of breast cancer can be summarized as follows: inflammation, immunosuppression, angiogenesis and vascular permeability, stromal remodelling and organotropism. a The sEVs secrete inflammatory factors, such as IL-6 and IL-8, promoting angiogenesis and recruiting immunosuppressive cells to promote the formation of breast cancer PMNs. In turn, inflammatory molecules can affect the distribution of sEVs and thus influence the PMN. b The sEVs not only inhibit T cells and induce immune escape by transporting PD-L1, but also exert immunosuppressive effects by recruiting MDSCs, altering DC cell activity, and transforming macrophages. sEVs also stimulate immune cells such as TANs to secrete cytokines, which suppress the antitumour immunity. c Through proangiogenic factors, including MMPs, and VE-cadherin, as well as miRNAs, sEVs are believed to act on angiogenesis and vascular permeability in the PMN of breast cancer. d In breast cancer, sEVs facilitate the turnover of CAFs to remodel the ECM and create the PMN. e The sEVs of breast cancer can provide a measure of organtropism, such as specific exosomal integrin combinations (there is a link between exosomal α6β4 and α6β1 integrins and lung metastasis/exosomal αvβ5 integrin with liver metastasis/exosomal αvβ3 integrin with brain metastasis). In addition, exosomal IBSP and miRNAs are involved in breast cancer brain metastasis | PMC9465880 | 12964_2022_945_Fig3_HTML.jpg |
0.508692 | 0af89150a93f411696f0ff75a9788952 | The mean serum creatinine measurement trends (mg/dl) across different months of the follow-up in patients with diabetes mellitus. | PMC9467309 | pone.0274495.g001.jpg |
0.469647 | 22a06cd0443445cab5d09a826acb9ab2 | Kaplan–Meier cumulative hazard rate curves depict the doubling of serum creatinine levels compared the baseline in patients with diabetics. | PMC9467309 | pone.0274495.g002.jpg |
0.437202 | f4d8fe2c80924cf9af0b71c9c5218a4e | Two approaches for reservoir computing. (a) Bio-inspired plasticity is used to adjust the structural and dynamical properties of the reservoir in the unsupervised fashion. (b) Task performance feedback is used to optimize the interconnection topology of the reservoir. The detailed description of the feedback is presented in the Results section (see also Fig. 4). | PMC9468161 | 41598_2022_19386_Fig1_HTML.jpg |
0.388841 | 7356d1d418034cbfb802ef3331fcfd11 | The collective behavior of the network of \documentclass[12pt]{minimal}
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\begin{document}$$N = 100$$\end{document}N=100 spin-torque oscillators with coupling parameters \documentclass[12pt]{minimal}
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\begin{document}$$\alpha = 0.075$$\end{document}α=0.075 and \documentclass[12pt]{minimal}
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\begin{document}$$\beta = 0.01$$\end{document}β=0.01 in the absence of external input. The adjacency matrix A is randomly filled with ones with probability 1/40. (a) Time series of the real (top panel) and imaginary (bottom panel) parts of \documentclass[12pt]{minimal}
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\begin{document}$$i \in {{\mathscr {V}}}$$\end{document}i∈V. (b) Phase portrait of (3). (c) Correlation matrices for the time-series of real (top panel) and imaginary (bottom panel) parts of \documentclass[12pt]{minimal}
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\begin{document}$$\Delta T = 1/12\,\hbox {ns}$$\end{document}ΔT=1/12ns taken at the beginning (left figures), middle (middle figures), and at the end (right figures) of simulation. Please see section Methods for the description of the clusterization method used for correlation matrices. (d) Graphical representation of the graph \documentclass[12pt]{minimal}
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\begin{document}$${{\mathscr {G}}}$$\end{document}G. | PMC9468161 | 41598_2022_19386_Fig2_HTML.jpg |
0.39 | 526c863a6c6743bc8c080b4910014d18 | Comparison of different dynamical regimes for the all-to-all network of \documentclass[12pt]{minimal}
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\begin{document}$$N=28$$\end{document}N=28 spin torque oscillators depending on the coupling parameters. (a) Order parameter \documentclass[12pt]{minimal}
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\begin{document}$$r_x$$\end{document}rx depending on the coupling parameters \documentclass[12pt]{minimal}
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\begin{document}$$\alpha \in [0,0.3]$$\end{document}α∈[0,0.3] and \documentclass[12pt]{minimal}
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\begin{document}$$\beta \in [-0.02,0.02]$$\end{document}β∈[-0.02,0.02]. (b) Probability distributions in three qualitatively different scenarios: Subcritical (top figure, \documentclass[12pt]{minimal}
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\begin{document}$$\beta =0.0167$$\end{document}β=0.0167), critical (middle figure, \documentclass[12pt]{minimal}
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\begin{document}$$\beta =0.0192$$\end{document}β=0.0192), and supercritical (bottom figure, \documentclass[12pt]{minimal}
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\begin{document}$$\beta =-0.0192$$\end{document}β=-0.0192) regimes. The critical regime is characterized by the power law probability distribution of cluster sizes (close to the straight line in the log-log coordinates). | PMC9468161 | 41598_2022_19386_Fig3_HTML.jpg |
0.437233 | baaee302d1e64462905243b7f0f70064 | Scheme of the algorithm for the structural plasticity that is driven by the interaction of the reservoir (STOs network) with the environment (performance in solving hand-written digits classification task). | PMC9468161 | 41598_2022_19386_Fig4_HTML.jpg |
0.428551 | 45d52b0d57ce46a8b6edf24011750efa | Behavior of the STO-network under the MNIST-input. (a) Time series of the real and imaginary parts of z under two different interconnection topologies (before and after the training). The switch between the topologies is performed at \documentclass[12pt]{minimal}
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\begin{document}$$t=2$$\end{document}t=2 ns. (b) Phase space representation of z. (c) Graphical representation of the used MNIST digit. (d) Periodic input u that corresponds to the chosen MNIST digit (see section Methods for details on the input construction). | PMC9468161 | 41598_2022_19386_Fig5_HTML.jpg |
0.454687 | 99e99f5a82f14f59ac8b9f9976859a29 | Only \documentclass[12pt]{minimal}
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\begin{document}$$\approx 6\%$$\end{document}≈6% of removed edges lead to significant qualitative changes in the network’s behavior (from (b) to (c)). The input applied to the original all-to-all network does not qualitatively change the collective behavior (from (b) to (a)). The trained network without any external input resides in a vicinity of the critical state (c) and reaches the criticality under the external input (d). This is additionally demonstrated in Fig. 7. Nodes’ labels on the graph (e) indicate the difference between the number of the node’s outgoing edges for the initial and the trained topology. These removed edges are highlighted with red color. | PMC9468161 | 41598_2022_19386_Fig6_HTML.jpg |
0.511434 | 2786628818f24a99aeca10410a111ded | Power law exponent and standard deviation of the power law fitting for different inputs. External inputs do not change the mean exponent of the power law distribution, however, the standard deviation of the power law fitting decreases under the input. This indicates that the trained network without an input resides in the vicinity of the critical state and the external input brings it closer to criticality. | PMC9468161 | 41598_2022_19386_Fig7_HTML.jpg |
0.461355 | 3402396d5d4848a983b2a77d3e6865e9 | Evolution of the task performance and graph-theoretic characteristics in course of training: (a) Classification loss; (b) Classification accuracy; (c) Network’s average degree; (d) Entropy; (e) ’In’-’in’-, ’in’-’out’, ’out’-’in’-, and ’out’-’out’- assortativity; (f) Average clustering coefficient; (g) A comparison of the trained interconnection topologies (blue dots) to some selected classes of graphs against the entropy, ’out’-’out’ assortativity, and clustering. | PMC9468161 | 41598_2022_19386_Fig8_HTML.jpg |
0.404054 | 4e96d49ef3f841398c483a6c89edefd2 | Power law exponent and standard deviation of the power law fitting for different tasks, inputs, and networks from Table 1. Figure (a) is a zoom-in of a region from Figure (b) that corresponds to the STO network. In all cases, the trained networks exhibit criticality signatures, and the standard deviation of the power law fitting decreases under the external input. | PMC9468161 | 41598_2022_19386_Fig9_HTML.jpg |
0.470876 | 4f3184b30f024725996fed2c462912c9 | Research methodology | PMC9468252 | 10669_2022_9878_Fig1_HTML.jpg |
0.403134 | 62513cfeb3a0463984b1db97e8571775 | The important levels of criteria | PMC9468252 | 10669_2022_9878_Fig2_HTML.jpg |
0.43173 | ab95a1add45243ed9ee58f0412d735bf | The most important five criteria-Pareto analysis | PMC9468252 | 10669_2022_9878_Fig3_HTML.jpg |
0.464459 | 73e0017462744bf9b20a0f0b64d042b7 | Effect of 180-day UUO and treatment with EPL on lung histology and fibrosis. (A) H&E staining of histological changes in the lung. (B) Masson's staining of fibrosis. (C) Immunohistochemistry staining for α-SMA. Magnification, x200. (D) Immunohistochemistry staining for collagen I. Magnification, x400. (E) Ashcroft score for each group. (F) Collagen volume fraction for each group. (G) α-SMA and (H) collagen I positive expression area. Data are presented as the mean ± standard deviation (n=6). #P<0.05 vs. Sham; *P<0.05 vs. UUO. α-SMA, α-smooth muscle actin; UUO, unilateral ureteral obstruction; H&E, hematoxylin and eosin; EPL, eplerenone. | PMC9468786 | etm-24-04-11560-g00.jpg |
0.407851 | 47283468c9144c2b9a55687183f5cf80 | Lymphangiogenesis in the lung of UUO rats. (A) Immunohistochemical staining of lymphatic vessel marker LYVE-1. Magnification, x200. Immunohistochemical staining for (B) podoplanin and (C) VEGFR-3. Magnification, x400. (D) LYVE-1, (E) podoplanin and (F) VEGFR-3 positive expression. (G) Protein expression of podoplanin, LYVE-1, VEGF-C and VEGFR-3 in lung tissue of UUO rats as detected by western blotting. (H) podoplanin, (I) LYVE-1, (J) VEGF-C and (K) VEGFR-3 protein expression. Data are presented as the mean ± standard deviation (n=6). #P<0.05 vs. Sham; *P<0.05 vs. UUO. UUO, unilateral ureteral obstruction; LYVE-1, lymphatic vessel endothelial receptor-1; VEGFR, VEGF receptor; EPL, eplerenone. | PMC9468786 | etm-24-04-11560-g01.jpg |
0.409253 | 0abee8dc86fb40f299a23431c6f4b79d | Effect of UUO and EPL on expression of F4/80, CD68, MCP-1, IL-1β and TNF-α in the lung of UUO rats. Immunohistochemical staining of (A) F4/80, (B) CD68, (C) MCP-1, (D) IL-1β and (E) TNF-α. Magnification, x400. (F) F4/80, (G) CD68, (H) MCP-1, (I) IL-1β and (J) TNF-α positive expression area. Expression of (K) MCP-1, (L) IL-1β and (M) TNF-α mRNA as detected by RT-qPCR. (N) Protein expression of IL-1β, TNF-α and MCP-1 as detected by western blotting. (O) IL-1β, (P) TNF-α and (Q) MCP-1 protein expression. Data are presented as the mean ± standard deviation (n=6). #P<0.05 vs. Sham; *P<0.05 vs. UUO. MCP-1, monocyte chemotactic protein 1; UUO, unilateral ureteral obstruction; RT-q, reverse transcription-quantitative; TNF, tumor necrosis factor; EPL, eplerenone. | PMC9468786 | etm-24-04-11560-g02.jpg |
0.405179 | edd15d07891c41f0a995116b26f8a592 | Effect of UUO and EPL on expression of downstream molecules of MRs in lung tissue. Immunohistochemical staining for (A) SGK-1 and (B) NF-κB. Magnification, x400. (C) Protein expression of p-SGK-1, SGK-1, MR and NF-κB as detected by western blotting. (D) SGK-1 and (E) NF-κB positive expression. (F) p-SGK-1 and (G) SGK-1 protein expression in each group. (H) Ratio of p-SGK-1 to SGK-1. (I) MR and (J) NF-κB protein expression. mRNA expression of (K) SGK-1 and (L) NF-κB as detected by RT-qPCR. Data are presented as the mean ± standard deviation (n=6). #P<0.05 vs. Sham; *P<0.05 vs. UUO. UUO, unilateral ureteral obstruction; SGK-1, serum- and glucocorticoid-inducible kinase-1; RT-q, reverse transcription-quantitative; p-, phosphorylated; EPL, eplerenone; MR, mineralocorticoid receptor. | PMC9468786 | etm-24-04-11560-g03.jpg |
0.429104 | ea38bcf5df3945489995bf6b8635f8b0 | EndMT in the lung of UUO rats. Co-expression of lymphatic vessel (LYVE-1, green) and myofibroblast (α-SMA, red) markers was detected by two-color immunofluorescence staining and indicated EndMT. Magnification, x400. Representative image of LYVE-1 +/α-SMA + EndMT cells is magnification, x8. Nuclei were stained blue with DAPI. UUO, unilateral ureteral obstruction; EndMT, endothelial-mesenchymal transition; LYVE-1, lymphatic vessel endothelial receptor-1; α-SMA, α-smooth muscle actin; EPL, eplerenone. | PMC9468786 | etm-24-04-11560-g04.jpg |
0.394336 | 8472943465d34580bc7b93637cd99b82 | Cells undergoing endothelial-mesenchymal transition produce collagen in the lung tissue of UUO rats. Three-color confocal laser scanning microscopy of cells co-expressing LYVE-1 (green), α-SMA (red) and collagen I (blue). Lymphatic vessels co-expressing LYVE-1 and α-SMA are surrounded by collagen I. Magnification, x400. LYVE-1, lymphatic vessel endothelial receptor-1; α-SMA, α-smooth muscle actin; UUO, unilateral ureteral obstruction; EPL, eplerenone. | PMC9468786 | etm-24-04-11560-g05.jpg |
0.451137 | c8d420287a6b4e12937489e8a1e86207 | Expression difference and gene mutation of CRGs in LUAD. (A) Expression differences of 10 CRGs in LUAD and normal lung tissues. *, p < 0.05; ***, p < 0.001. (B,C) Gene mutation and classification of 10 CRGs in LUAD. (D) Transition (Ti) and transversion (Tv) classification of the SNVs of 10 CRGs in LUAD. (E) Interactive network of CRGs; the darker the color is, the larger the circle is, indicating that it belongs to the central target in the whole network. | PMC9468865 | fphar-13-971867-g001.jpg |
0.482853 | e72ce3bd45674813bf88ab4545056edc | GO and KEGG enrichment analyses of 10 CRGs in LUAD. (A) Bubble plot of GO enrichment results of 10 CRGs in LUAD. (B) Bubble plot of KEGG enrichment results of 10 CRGs in LUAD. (C) Interactive network of GO entries and CRGs. (D) Interactive network of KEGG entries and CRGs. | PMC9468865 | fphar-13-971867-g002.jpg |
0.437003 | 870281413b504a77bbaab2fb4b2ab400 | Prognostic value of 10 CRGs in LUAD. The OS curves of GLS (A), CDKN2A (B), PDHA1 (C), DLAT (D), MTF1 (E), LIAS (F), FDX1 (G), LIPT1 (H), PDHB (I), and DLD (J) in patients with LUAD in the low and high expression groups. | PMC9468865 | fphar-13-971867-g003.jpg |
0.391465 | f5c6dcd5b9964e41b329fd0219062815 | Construction of a prognostic signature model of CRGs in LUAD. (A) LASSO coefficients of the six prognostic CRGs. (B) PLD of the six prognostic CRGs. (C) Distribution of risk score, survival status, and expression of the six prognostic CRGs. (D) OS curve of patients with LUAD in the low and high expression groups. (E) 1-, 3-, and 5-year ROC prediction curves for patients with LUAD. | PMC9468865 | fphar-13-971867-g004.jpg |
0.438796 | e6b82c27d530451eb9ae15c9a6f030ad | Correlation between the six prognostic CRGs and immune infiltration in LUAD. The correlation between LIPT1 (A), DLD (B), PDHA1 (C), MTF1 (D), GLS (E), CDKN2A (F), and the degree of immune infiltration of 24 immune cell types in patients with LUAD. | PMC9468865 | fphar-13-971867-g005.jpg |
0.423639 | 1ca83552dba646fd8daded04607fad6a | Enrichment scores of the six prognostic CRGs in 24 immune cell types in LUAD. The six prognostic CRGs were LIPT1 (A), DLD (B), PDHA1 (C), MTF1 (D), GLS (E), and CDKN2A (F). | PMC9468865 | fphar-13-971867-g006.jpg |
0.497694 | 32ae4756f9424fb28c6c3d6273c8fdcd | Correlation analysis of the six CRGs with TMB and MSI in LUAD. (A–F) Correlation between the six CRGs and TMB in LUAD. (G–L) Correlation between the six CRGs and MSI in LUAD. | PMC9468865 | fphar-13-971867-g007.jpg |
0.406834 | 0b15e8f9a71a42a59abc327fb2d68e4b | Association analysis of the six CRGs and different clinical parameters in patients with LUAD. The different clinical factors included pathologic stage (A), T stage (B), M stage (C), gender (D), age (E), OS event (F), smoker (G), and race (H). | PMC9468865 | fphar-13-971867-g008.jpg |
0.409748 | ed8c40b06300439bb7fe44b9671633d9 | Construction of the ceRNA regulatory axis. (A) Differential expression of DLD protein in LUAD and normal lung tissues (HPA). (B) Ten miRNAs associated with DLD. (C) Differential expression of the 10 miRNAs in LUAD and normal lung tissues. ns, p ≥ 0.05; *, p < 0.05; ***, p < 0.001. (D) OS curves of DLD in patients with LUAD in the low and high expression groups. (E) Identification of 20 lncRNAs by the Starbase and lncbasev3 databases. (F) The 27 miRNAs associated with miR-1-3p. (G) OS curves of UCA1 in patients with LUAD in the low and high expression groups. | PMC9468865 | fphar-13-971867-g009.jpg |
0.431697 | b831a8cbaf014044b55b44b127c4e748 | Active ingredients of traditional Chinese medicine with a potential effect on DLD. | PMC9468865 | fphar-13-971867-g010.jpg |
0.38638 | d4a75b38178b42bb8297eaaec027aaba | Validation of In vitro cell experiment and molecular docking. (A) The differential expression of lncRNA UCA1, miR-1-3p and DLD in normal lung epithelial cells (BEAS-2B) and different LUAD cell lines (A549 and H1299) were detected by in vitro cell experiments. **, p < 0.01. (B) The interaction between nine TCM active components and DLD protein was simulated by molecular docking. | PMC9468865 | fphar-13-971867-g011.jpg |
0.449624 | 6b4424daf03241cfa1090505128f27ae | PRISMA Flow Chart showing the selected Papers. | PMC9468903 | fphys-13-888233-g001.jpg |
0.465593 | 51fb6c070a2a48d69ff861539633dd67 | Interaction of dominant regulatory focus (promotion vs. prevention) with motivational direction (approach vs. avoidance motivation) and the fit or non-fit between the two variables. | PMC9468904 | fpsyg-13-807875-g001.jpg |
0.418011 | b0c16a35f3d3429abd153841d5b48311 | Effects of RFI and MI on elaboration, perceived autonomy support, satisfaction, and relationship conflict for Study 1. (*)p < 0.10, *p > 0.05, **p > 0.01. Elaboration: Simple slopes showed that for individuals high on promotion, approach or avoidance did not make a significant difference (p = 0.824), but individuals high on prevention (p = 0.004) elaborated the ideas in more detail when they were high on avoidance compared to high on approach. For individuals high on approach (p = 0.539) promotion compared to prevention focus did not make a significant difference. Individuals high on avoidance (p = 0.012) elaborated the ideas in more detail when they were high on prevention compared to high on promotion. Perceived autonomy support: Simple slopes showed that for individuals high on promotion (p = 0.386), approach or avoidance did not make a significant difference. Individuals high on prevention (p = 0.088) tended to feel more supported in their autonomy when they were high on avoidance compared to high on approach. Individuals high on approach (p = 0.004) felt more supported in their autonomy when they were high on promotion compared to high on prevention. For individuals high on avoidance (p = 0.631), promotion or prevention did not make a significant difference. Satisfaction: Simple slopes showed that for individuals high on promotion (p = 0.371), approach or avoidance did not make a significant difference, but individuals high on prevention (p = 0.081) tended to be more satisfied when they were high on avoidance compared to high on approach. Individuals high on approach (p = 0.010) were more satisfied with the ideas when they were high on promotion compared to high on prevention. For individuals high on avoidance (p = 0.990), promotion or prevention did not make a significant difference. Relationship conflict: Simple slopes showed that neither for individuals high on promotion (p = 0.253), nor for individuals high on prevention (p = 0.220), approach or avoidance made a difference. For individuals high on approach (p = 0.627), promotion or prevention did not make a difference, but individuals high on avoidance (p = 0.030) perceived less relationship conflicts when they were also high on prevention compared to high on promotion. | PMC9468904 | fpsyg-13-807875-g002.jpg |
0.449733 | 5e81f29f2208429ea4fd480da3f579a5 | Effects of RFI and manipulated avoidance on perceived autonomy support, satisfaction, and task conflict for Study 2. (*)p < 0.10, *p > 0.05, **p > 0.01. Perceived autonomy support: Simple slopes showed that individuals high on promotion (p = 0.005) perceived lower autonomy support when they were high on avoidance, but for individuals high on prevention (p = 0.786) approach or avoidance did not make a difference. Individuals in the avoidance condition (p = 0.059) tended to be perceive more autonomy support when they were high on prevention than high on promotion. For individuals in the other conditions (p = 0.611), prevention or promotion did not make a significant difference. Satisfaction: Simple slopes showed that individuals high on promotion (p = 0.086) tended to be less satisfied when they were high on avoidance, and individuals high on prevention (p = 0.057) tended to be more satisfied when they were high on avoidance. Individuals in the avoidance condition (p = 0.005) were more satisfied when they were high on prevention than high on promotion. For individuals in the other conditions (p = 0.834), prevention or promotion did not make a significant difference. Task conflict: Simple slopes showed that individuals high on promotion (p = 0.005) perceived more conflicts when they were high on avoidance, but for individuals high on prevention (p = 0.748) approach or avoidance did not make a difference. Individuals in the avoidance condition (p = 0.010) perceived less conflicts when they were high on prevention than high on promotion. For individuals in the other conditions (p = 0.813), prevention or promotion did not make a significant difference. | PMC9468904 | fpsyg-13-807875-g003.jpg |
0.450696 | 4bdfd2b9b82d4ca0ae8d1a22224f81f9 | Effects of RFI and manipulated approach on satisfaction for Study 2. *p < 0.05. Simple slopes showed that neither for individuals high on promotion (p = 0.147), nor for individuals high on prevention (p = 0.122), approach or avoidance made a difference. For individuals in the approach condition (p = 0.286), promotion or prevention did not make a difference either but individuals in the other conditions were more satisfied when they were high on prevention than high on promotion (p = 0.026). | PMC9468904 | fpsyg-13-807875-g004.jpg |
0.424725 | 1e77f383826749ddbdc8173d9ae926ee | Effects of RFI and MI on satisfaction for Study 2. *p > 0.05, **p > 0.01. Simple slopes showed that for individuals high on promotion (p = 0.591), approach or avoidance did not make a significant difference, but individuals high on prevention (p = 0.010) were more satisfied when they were high on approach compared to high on avoidance. Individuals high on approach (p = 0.006) were more satisfied with the ideas when they were high on prevention compared to high on promotion. For individuals high on avoidance (p = 0.834), promotion or prevention did not make a significant difference. | PMC9468904 | fpsyg-13-807875-g005.jpg |
0.386415 | 247121b07deb40ad85377ebf905d370a | Biochemical characterization of decellularized extracellular matrices (dECMs). (A) Freeze-dried ECM was tough and follicular cavities were observed (black arrows). (B) DNA content analysis. (C) H&E staining and DAPI staining showed that there were no residual cellular materials after decellularization. (D) Masson staining and TB staining showed that there were collagen and proteoglycan in the dECMs. (E) SDS-PAGE revealed the existence of various proteins within the dECMs. (F) Microarchitecture of decellularized ovary matrix by SEM. The extracellular matrix structure was intact. Collagen (white arrow) and flexible fibronectin fibers (black arrow) were found in the pore wall. | PMC9469198 | IJB-8-3-597-g001.jpg |
0.431424 | 350d187fad7b4d4cbb9dab1db306d8a8 | The preparation of ovary-derived decellularized extracellular matrix (dECM)-based bioink and the printing of porous cylindrical 3D scaffold constructs. | PMC9469198 | IJB-8-3-597-g002.jpg |
0.431901 | 46405a9195354c5a9da559981a1797cc | Characterization and biocompatibility of the dECMs-based bioink. (A) Microarchitecture of the bioink by SEM. (B) Circular dichroism spectrum was used to determine the protein structure and thermal stability of the bioink. (C) Rheological properties were measured to assess the mechanical properties of the bioink before (D2) and after (D3) cross-linking of calcium chloride compared with those of dECM solution (D1). (D) Blood vessels were clearly visible on 1 week after implantation. (E) The biocompatibility of the bioink was assessed by H&E staining and CD45 (a marker for inflammatory cells) immunostaining. | PMC9469198 | IJB-8-3-597-g003.jpg |
0.43991 | 619baf2aa55b4e6ab35c135a59f5a2aa | Viability of primary ovarian cells (POCs) in the 3D scaffold in vitro. (A) The isolated POCs included a vast majority of stromal cells (POCs-1) and a large number of follicles at different developmental stages (POCs-2 and POCs-3). (B) Using the live/dead assay to examine the POCs survival in the 3D scaffolds in vitro. Green fluorescence refers to living cells containing calcein AM, while red fluorescence refers to dead cells containing EthD-1. | PMC9469198 | IJB-8-3-597-g004.jpg |
0.48888 | 971376032ff74562a252e67438b7e391 | General view of grafts before and after transplantation. At 4 weeks after implantation, the constructs maintained their shape and developed functional blood vessels (black arrow). | PMC9469198 | IJB-8-3-597-g005.jpg |
0.412906 | 76007a084e0f4ee488335808dde82ab0 | Evaluation of the neoangiogenesis and cell proliferation. (A-C) The effects of 3D scaffolds, 3D scaffold encapsulating POCs, and hydrogel encapsulating POCs constructs on blood revascularization (CD31, red arrows). (D-F) Immunostaining for the cell proliferation-specific marker (Ki67, cells in brown), in the implanted 3D scaffold encapsulating POCs and hydrogel encapsulating POCs constructs. (G) Expression of CD31, Ki67. *P < 0.05, **P < 0.0001. (H) Identification of the apoptosis of sections from grafts treated with 3D scaffold encapsulating POCs and hydrogel encapsulating POCs (white arrows). | PMC9469198 | IJB-8-3-597-g006.jpg |
0.553498 | 2a71de5ba128447bb6829e930161c227 | Hormone assessment and the vaginal smear. (A-C) The comparison of serum hormone levels of samples from five different groups. *P < 0.05, **P < 0.0001. # means statistical differences exist in pairwise comparison between the groups (P ≤ 0.001), but not in the 3D scaffold encapsulating POCs group vs. non-OVX group (P = 0.684). (D-G) The vaginal smear at 4 weeks after implantation. (D) A large number of keratinized cells can be observed in the non-OVX group mice on estrus. (E) The OVX-C group mice were on anestrus for a long time, and a large number of leukocytes can be seen. (F) A high level of anestrus was observed in three mice of the 3D scaffold encapsulating POCs group. (G) A lower level of estrus in one mice of the 3D scaffold encapsulating POCs group was observed. | PMC9469198 | IJB-8-3-597-g007.jpg |
0.381828 | 805e2a9ac8c6437cbacc645064f0babe | Detection of the expression of ER-α, PR, inhibin-α and FSHR within the 3D scaffold encapsulating POCs and hydrogel encapsulating POCs constructs after 4-week implantation. DAPI located in the nucleus (blue), the specific primary antibody located in the cell membrane and cytoplasm (green). Green and blue superimposed to appear white, representing the expression of steroid hormone receptors in the groups (white arrows). The expression of ER-α, Inhibin-α and FSHR were more in the 3D scaffold encapsulating POCs group than in the hydrogel encapsulating POCs group. However, there was no significant difference in the expression of PR (P = 0.12). *P < 0.05. | PMC9469198 | IJB-8-3-597-g008.jpg |
0.428588 | e792d5c513ea4162825dab4e160ffd58 | Visual representation of the formulation. In explaining the neurobiology of FND to MT and her parents, we used this visual metaphor alongside the following language: “The red ball represents the brain regions that underpin salience detection, arousal, and emotional states—the brain stress systems, for short. The pink ball represents brain areas involved in motor processing—motor-processing regions, for short. The yellow ball represents brain areas involved in sensory processing—sensory-processing regions, for short. The spikey ball represents pain-processing regions—pain maps, for short. When all is well, the brain stress systems get on with their job, as do the motor-, sensory-, and pain-processing regions, and they interact together in a balanced way. In FND the relationship between the brain stress systems and motor-, sensory, and pain- processing regions changes and becomes unbalanced. The brain stress systems become larger and stronger, and they disrupt motor and sensory processing and amplify pain.” © Kasia Kozlowska 2019. | PMC9470039 | hrp-30-303-g001.jpg |
0.460759 | 17bc0baf1f164e9a85dc28d4be7ec95c | Visual representation of the time frame of MT’s constantly changing functional symptoms during the six months of her illness. PNES, psychogenic non-epileptic seizures (current term: functional seizures). | PMC9470039 | hrp-30-303-g002.jpg |
0.443844 | d1b3a6e9b41249ed847f9ab683feb50c | A PchD catalyzes the adenylation of salicylate as the first step in pyochelin biosynthesis. B Salicyl-AMS, originally described by Ferreras et al. as an inhibitor of siderophore producing NRPS adenylation domains in M. tuberculosis and Y. pestis has been modified by the addition of a cyano group at C4 of the salicylate ring to produce 4-cyano-salicyl-AMS | PMC9470617 | 775_2022_1941_Fig1_HTML.jpg |
0.397316 | 044a930d799d44ba8fb10820e51660e5 | A PchD bound to salicyl-AMS (salmon) shown in midnight blue. B PchD bound to 4-cyanosalicylAMS (orange) shown in skyblue | PMC9470617 | 775_2022_1941_Fig2_HTML.jpg |
0.442085 | d1d0390f61104156916a308dbfeea8df | A The adenylation conformation represented by the full NRPS module from AB3403 (4ZXI) with the adenylation domain shown in green, the condensation domain shown in light grey, the PCP domain shown in light purple, and the thioesterase domain shown in dark grey. Ligands shown in the adenylation domain include AMP (grey), Mg2+ (orange) and glycine (cyan) (B). The thioester-forming conformation represented by the EntF NRPS module (5T3D) with the adenylation domain shown in plum/pink, the condensation domain shown in light grey, and the PCP domain shown in light purple. The mechanism-based inhibitor Ser-AVS is shown in fuchsia | PMC9470617 | 775_2022_1941_Fig3_HTML.jpg |
0.450501 | 28453b21672e46c8955ad1b26cb01935 | A PchD (blue) closely aligns with the adenylating conformation demonstrated by the AB3403 adenylation domain (green). 4-cyano-salicyl-AMS ligand of PchD shown in teal. B The EntF adenylation domain (Acore:plum, Asub: pink) demonstrates the thioester-forming conformation and was co-crystalized with the ligand serine adenosine vinylsulfonamide (magenta). The Asub of MbtA (wheat; Acore: orange) does not align with either the C adenylation or the D thioester conformation | PMC9470617 | 775_2022_1941_Fig4_HTML.jpg |
0.432927 | 06a2a4aac212478a8e5de60ac41235fe | A Relative position of Cys250 to the salicyl-AMS inhibitor. B Relative position of the 4-cyano-salicyl-AMS inhibitor. Inhibitor densities are shown with a polder map drawn at 3σ | PMC9470617 | 775_2022_1941_Fig5_HTML.jpg |
0.470106 | 0bddd1ad49b348fe96935b5d27eee5f3 | DhbE adenylation domain bound to DHB-adenylate (1MDB) shown in yellow overlayed with both salicyl-AMS PchD (salmon inhibitor, midnight blue structure) and 4-cyano-salicyl-AMS bound PchD (orange inhibitor, skyblue structure). Residues conferring specificity for salicylate are Cys250 and Ile347. For the DhbE structure these positions are a conserved serine and a valine which are hypothesized to more readily accommodate the second hydroxyl of DHB | PMC9470617 | 775_2022_1941_Fig6_HTML.jpg |
0.508659 | caa78c53e03f48babc1e2796c0ab68af | Contacts between active site residues and the inhibitor | PMC9470617 | 775_2022_1941_Fig7_HTML.jpg |
0.446691 | 66b5e85475ae44678e84daaa9c7907a3 | SPECT/CT imaging of free [111In]DTPA complex and [111In]DTPA‐labeled B16F10 exosomes in melanoma‐bearing mice. (A) Mice were injected intravenously with free [111In]DTPA complex as control. (B) Mice were injected intravenously with [111In]DTPA‐labeled B16F10 exosomes. Imaging was conducted at 30 min, 4 h, and 24 h post‐injection. Tumors are highlighted by white circles. Adapted from Ref. [74] with permission. Copyright 2019, Ivyspring International Publisher. | PMC9471060 | OPEN-11-e202200124-g001.jpg |
0.374712 | b437eb090b934218afd0180e94ff7269 | Bioluminescence imaging of CAL62/Rluc‐labeled EVs in naïve or CAL62/Effluc tumor‐bearing mice. Imaging was carried out at 5 min, 30 min, 60 min, and 120 min post‐injection. Tumors are highlighted by black circles. Adapted from Ref. [65] with permission. Copyright 2021, Springer Nature. | PMC9471060 | OPEN-11-e202200124-g004.jpg |
0.45456 | 7eb41f94c55f45298ad6ffb1117a4731 | Various molecular imaging techniques to label extracellular vesicles for in vivo tracking. Lipophilic fluorescent dyes and genetically engineered fluorescent protein are used for fluorescence imaging; luciferase is used for bioluminescence imaging; radionuclide and contrast agents can be inserted into the membrane of EVs or loaded into the cavity of EVs for nuclear imaging or magnetic resonance imaging. | PMC9471060 | OPEN-11-e202200124-g006.jpg |
0.447992 | f0bf1528b7d14434b2ff3d5cb5da1e80 | Fluorescence imaging of DiR and DiR‐labeled NEs‐Exos in brain tissue of C6‐Luc glioma‐bearing mice. Images were obtained at 30 min and 1, 2, 4, 8, 12, and 24 h post‐injection. Adapted from Ref. [58] with permission. Copyright 2021, Elsevier. | PMC9471060 | OPEN-11-e202200124-g007.jpg |
0.38143 | 51496990cc5e429da9582323d7e53270 | Magnetic resonance imaging of control, ESIONs‐PEG, ESIONs‐RGD and ESIONs‐RGD@EVs in tumor‐bearing mice. Imaging was conducted at 0 h and 2 h post‐injection. Tumors are highlighted by white circles. Adapted from Ref. [89] with permission. Copyright 2021, Ivyspring International Publisher. | PMC9471060 | OPEN-11-e202200124-g008.jpg |
0.414118 | f4ba8a6d2faf4e59b1cbc7c36b662c70 | Overview of expression of m6A regulators in NAFLD. (A) Expression levels of m6A regulators in liver tissues. The t-test analyzed the difference in the expression levels of m6A regulators between the healthy and NAFLD tissues. (B) Boxplot showed the association of expression with clinical stages for m6A regulators. Turkey’s post hoc test was used for comparison between groups to analyze the difference in the expression of m6A regulators among different clinical stages of NAFLD. The results of significant difference analysis: *p < 0.05; **p < 0.01; and ***p < 0.001. | PMC9471244 | fphar-13-973116-g001.jpg |
0.482994 | 25749962afd24b7ead558e3d44ff5df6 | Correlations between the expression of m6A regulators and BMI as well as waist. Pearson’s correlation was performed to calculate the correlation between the expression of m6A regulators and BMI as well as waist. The results of significant difference analysis: ns ≥ 0.05; *p < 0.05; **p < 0.01; and ***p < 0.001. | PMC9471244 | fphar-13-973116-g002.jpg |
0.51718 | 51bc1efd1f0249958bce901f31b6e447 | Correlations between m6A regulators and steatosis as well as inflammation. Pearson’s correlation was performed to calculate the correlation between the expression of m6A regulators and hepatic steatosis. Spearman’s correlation was performed to calculate the correlation between the expression of m6A regulators as well as lobular inflammation. The results of significant difference analysis: ns ≥ 0.05; *p < 0.05; **p < 0.01; and ***p < 0.001. | PMC9471244 | fphar-13-973116-g003.jpg |
0.426842 | 8be4ef046eeb416a9f99451fdf768497 | Correlations of levels of m6A regulators with immune infiltration by combination with a single-cell dataset. (A) Distinct cell clusters were revealed in healthy human liver. (B) Heatmap showed the expression of the m6A regulator in each cell. (C) Histogram showed the relative percentage of different types of cells in each sample of GSE89632. (D) t-tests were performed to analyze the difference in cell percent between healthy control and NAFLD. The results of significant difference were showed as *p < 0.05; **p < 0.01; or ***p < 0.001. (E) Pearson’s test was conducted to analyze the correlations of the m6A regulators’ expression level with the cell percent. The ratio of correlation was shown in color. Blue was a positive correlation and red was negative correlation. Color darker, circle bigger implied a stronger correlation. Demerit marks showed p > 0.05. | PMC9471244 | fphar-13-973116-g004.jpg |
0.368474 | b7e96ea5868d4b8aabe960335eec0dbe | Explore the coexpression relationship of m6A regulators as well as the target genes and enrichment pathways of m6A related. (A) Pearson’s test was conducted to analyze the coexpression relationship of m6A regulators. (B) Intersection of KEGG enrichment pathways, which were analyzed by GSEA according to stratify by the median expression level of RBM15, YTHDC2, HNRNPA2B1, and HNRNPC, was visualized as a Venn diagram. (C) Intersection of DEGs which were screened according to stratify by the median expression level of RBM15, YTHDC2, HNRNPA2B1, and HNRNPC, was visualized as a Venn diagram. (D) PPI network was construed by common DEGs as well as RBM15, YTHDC2, HNRNPA2B1, and HNRNPC, with the disconnected proteins being hidden. Wider lines indicated stronger evidence of protein interaction. | PMC9471244 | fphar-13-973116-g005.jpg |
0.499373 | 6a4530c5bb844ad383a134d6f1238c03 | MYC expression profile in NAFLD. (A) Difference was analyzed in the expression of MYC between different clinical stages of NAFLD. The ANOVA was performed to the difference among the multiple clinical stages. Turkey’s post hoc test was used for comparison between groups. (B) Correlations between the expression of MYC and patients’ clinical characteristics. The correlations were all analyzed by Pearson’s test except for fibrosis, lobular inflammation, and ballooning. The correlations between the MYC expression and the characteristic of fibrosis, lobular inflammation, and ballooning were conducted by Spearman’s test. The results of significant difference analysis: ns ≥ 0.05; *p < 0.05; **p < 0.01; and ***p < 0.001. | PMC9471244 | fphar-13-973116-g006.jpg |
0.485579 | af63c3fd51ff4c47b70d8393292ae53b | MYC expression profile in NAFLD by using four datasets. (A) PCA showed the datasets of GSE164770, GSE37031, GSE48452, and GSE63067 were merged and adjusted in batches. (B) -test was conducted to analyze the difference in the expression of MYC between healthy controls and NAFLD. (C) Pearson’s test was performed to analyze the correlation between MYC and m6A regulators. The results of significant difference analysis: ns ≥ 0.05; *p < 0.05; **p < 0.01; and ***p < 0.001. | PMC9471244 | fphar-13-973116-g007.jpg |
0.42116 | 8dd9ef6ce2284227913165238f95d2c9 | Socioecological model for the Using PrEP: Doing it for Ourselves (UPDOs) Protective Styles intervention. PrEP: pre-exposure prophylaxis. | PMC9472057 | resprot_v11i8e34556_fig1.jpg |
0.411287 | 8e809b1cc81346318b12f095f68f1fa2 | Study design schematic. PrEP: pre-exposure prophylaxis. | PMC9472057 | resprot_v11i8e34556_fig2.jpg |
0.424226 | 73cf59f0712c45dfa1e062dc5fd1fece | The Cherenkov imaging system commissioned for clinical use in our hospital. The left panel shows a Cherenkov camera mounted to the right of the treatment couch. The Right panel shows the Cherenkov image display at the treatment console. | PMC9472078 | gr1.jpg |
0.426595 | 5e2fdfabe65e48aead11e22cc79b0aca | Cherenkov image from Case #1 shows exit dose from a LPO field into the right breast. | PMC9472078 | gr2.jpg |
0.412664 | 0f78181c39e74466ae6281a34a6265b1 | Case #3, Utilization of cumulative Cherenkov image outline from first day approved treatment as reference treatment area to monitor patient motion. | PMC9472078 | gr3.jpg |
0.425493 | c6cb66dfd736434fbf3235697f7cbeb7 | Cherenkov images from Case #4 show chin and arm position variations between two treatments. | PMC9472078 | gr4.jpg |
0.445398 | 851fd342b60a43bea44e3efb6ed02567 | Using Cherenkov imaging to monitor, gate and verify electron DIBH treatment delivery in Case #5. | PMC9472078 | gr5.jpg |
0.434492 | 2110f289c07e4c648ebf3c1179b98a0b | Flowchart of COMET patients included in the study | PMC9472195 | 13054_2022_4153_Fig1_HTML.jpg |
0.470687 | 150799b5840f43cda18553454eb94aa8 | Correlation matrix for plasma biomarker and N-antigen concentrations. Biomarkers are presented on the log10 scale. Spearman correlation coefficients are presented above the diagonal. RAGE, n = 235; IL-10, n = 230; IP-10, n = 231. P value for all correlations = 0.01 when adjusted for multiple comparisons | PMC9472195 | 13054_2022_4153_Fig2_HTML.jpg |
0.448226 | d61edec7c315458e94c16c64cea4d6f2 | a Plasma SARS-CoV-2 N-antigen concentration on D0 by change in clinical status on the World Health Organization ordinal scale. b Plasma viral N-antigen concentration on D0 in patients who were not initially admitted to the ICU at the time of study recruitment, stratified by ICU admission during hospitalization. c Plasma SARS-CoV-2 N-antigen concentration on D0 stratified by mechanical ventilation at 28 days. d Plasma SARS-CoV-2 N-Antigen concentration on D0 stratified by death at 28 days. Plasma N-antigen concentration is presented on log10 scale. P values represent the results of the Wilcoxon rank-sum test | PMC9472195 | 13054_2022_4153_Fig3_HTML.jpg |
0.444358 | e2c7d98a3b154706a2f8748a1892fe49 | Types of case files of the study population from the years 2009 to 2014 | PMC9472304 | UA-14-241-g001.jpg |
0.440556 | 6fe9dd29e74f43929c50a952f979d67d | The most common congenital anomalies of the kidney and urinary tract diagnosis during antenatal follow-up | PMC9472304 | UA-14-241-g002.jpg |
0.4867 | 2c2da3c9202f425c9cb52f05cf1a9b99 | Gestational age at diagnosis of congenital anomalies of the kidney and urinary tract | PMC9472304 | UA-14-241-g003.jpg |
0.415824 | e3cde2ae2d38428c82e9e02a9405d8a1 | Distribution of population estimates of men who have sex with men by age group and UNICEF region. | PMC9473434 | pone.0269780.g001.jpg |
0.419656 | 4a5a56209d5041338714c57d07fe93b5 | Distribution of population size estimates of female sex workers by age group and UNICEF. | PMC9473434 | pone.0269780.g002.jpg |
0.445995 | e7732018b95b47058d408b4db8ab9e11 | Preservation of propene over multiple runs. aFraction of propene in the (propene + propane) fraction. Conditions: RuBr3·xH2O (2 mol%), propene (1 bar), Bu4PBr (577 mg, 3.4 mmol). Pretreatment: CO gas (1 bar) 40 bar H2, 0.5 h, 180 °C. Each hydrogenation uses a fresh charge of propene gas (1 bar), 40 bar H2, 1 h, 220 °C. bCO pretreatment before first run. cCO pretreatment before each run. | PMC9473539 | d2sc02150a-f1.jpg |
0.528978 | 8bcec696dab3410eb7c0ec0a009c2548 | XANES (a) and magnitudes of Fourier-transformed (4–15 Å−1) phase-uncorrected FT-EXAFS (b) data for RuBr3 (red) and RuCl3 (blue), before (dashed lines) and after (solid lines) dissolution in Bu4PBr. | PMC9473539 | d2sc02150a-f2.jpg |
0.464342 | 1f303c1e82f749f4a99c9557220094b9 | XANES (a) and magnitudes of Fourier-transformed (4–15 Å−1) phase-uncorrected FT-EXAFS (b) data for [RuBr2(CO)3]2 (red) and [RuCl2(CO)3]2 (blue), before (dashed lines) and after (solid lines) dissolution in Bu4PBr. | PMC9473539 | d2sc02150a-f3.jpg |
0.476337 | 16c05a1685f84cffad89ab4b4b8f8e28 | XANES (a) and phase-uncorrected FT-EXAFS (b) data for the reference RuBr3 salt (dashed black) and [RuBr2(CO)3]2 compound (dashed red), and RuBr3 salt dissolved in Bu4PBr without (dashed grey) and with (solid blue) addition of CO gas. | PMC9473539 | d2sc02150a-f4.jpg |
0.555234 | fabcbf3eb989407391aa03f241898e7d | Relative fractions of Br (shown in red) vs. CO (in blue) in the Ru coordination sphere, for different samples, as obtained by LCF analysis. | PMC9473539 | d2sc02150a-f5.jpg |
0.493362 | 9891847cf357445589ffeb0042025452 | XANES (a) and phase-uncorrected FT-EXAFS (b) data for RuBr3 salt dissolved in IL before (solid red) and after (solid purple) reaction with propene. Dashed grey lines correspond to metallic Ru reference. | PMC9473539 | d2sc02150a-f6.jpg |
0.45244 | 894889a968c34b50957df368b64c09b7 | (a) XANES spectra of pure Ru-species (solid coloured lines) extracted by MCR-ALS plotted together with the reference spectra of RuBr3, [RuBr2(CO)3]2, and Ru foil (dashed red, green and blue lines respectively). (b) Concentration profiles of the three Ru-species extracted from MCR-ALS. (c) A list of experimental conditions applied during in situ XAS data collection. Conditions were varied within the described boundary conditions (see ESI,† “boundary conditions”): CO (0–5 bar), H2 (0–30 bar) and temperature (180–220 °C). Dashed lines indicate when the sample was changed. aA high concentration of RuBr3 was used, with 68 mg RuBr3 in 2 g IL. bFor all other entries, low concentrations of Ru were measured (13.6 mg in 2 g IL, similar to catalytic results presented in Table 1). cFormaldehyde (100 μL) was thermally decomposed to generate in situ CO gas. dIsopropanol (IPA, 250 μL) was added as propene precursor. | PMC9473539 | d2sc02150a-f7.jpg |
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