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0.411487 | 36766111047f4638959a38921ee400c9 | Oncostatin M affected FGF23 regulators in UMR106 cells. Arithmetic means ± SEM (n = 8) of Phex (A), Dmp1 (B), Pth1r (C), Vdr (D), and Epor (E) mRNA expression relative to Tbp in UMR106 cells treated with or without 30 ng/ml oncostatin M for 24 h (one-sample t test). *** p < 0.001 indicates significant difference from vehicle control. a. u. arbitrary units; ctr control; Dmp1 dentin matrix acidic phosphoprotein 1; Epor erythropoietin receptor; OSM oncostatin M; Phex phosphate regulating endopeptidase X-linked; Pth1r PTH receptor; Vdr vitamin d receptor. | PMC10209182 | 41598_2023_34858_Fig2_HTML.jpg |
0.633697 | c8aaa53ee89b48349479d65ed9e7ca35 | Oncostatin M induced FGF23 protein secretion by UMR106 cells. (A) Arithmetic means ± SEM of Fgf23 mRNA levels relative to Tbp in UMR106 cells pretreated for 24 h with 10 nM PTH and then additionally treated with or without 100 ng/ml oncostatin M for another 24 h (n = 6; one-sample t test). Arithmetic means ± SEM of C-terminal (B; n = 5) and intact (C; n = 5) FGF23 concentration in the supernatant of UMR106 cells pretreated for 24 h with 10 nM PTH and then additionally treated with or without 100 ng/ml oncostatin M for another 24 h (n = 5; paired t test). (D) Representative original Western blots and arithmetic means ± SEM of normalized FGF23 over GAPDH protein ratio in lysates of UMR106 cells pretreated for 24 h with 10 nM PTH and then treated with or without 100 ng/ml oncostatin M for another 24 h (n = 5; paired t test). ** p < 0.01 indicates significant difference from vehicle control. a. u. arbitrary units; ctr control; GAPDH glyceraldehyde-3-phosphate dehydrogenase; n. d. not detectable; OSM oncostatin M. | PMC10209182 | 41598_2023_34858_Fig3_HTML.jpg |
0.51596 | 125c377aff504aaab315cc145297f078 | Oncostatin M receptor knockdown attenuated oncostatin M-dependent Fgf23 gene expression. Arithmetic means ± SEM of Fgf23 expression relative to Tbp in UMR106 cells treated for 24 h with or without 10 ng/ml oncostatin M in the presence of non-target siRNA (left bars) or siRNA specifically targeting the oncostatin M receptor (osmr) (right bars) (n = 11; Wilcoxon one-sample test and paired t test with Bonferroni adjustment for multiple comparisons). * p < 0.05, ** p < 0.01 indicate significant difference from vehicle control (1st bar); # p < 0.05 indicates significant difference from the absence of siRNA targeting the oncostatin M receptor (2nd bar vs. 4th bar). a. u. arbitrary units; ctr control; osmr oncostatin M receptor. | PMC10209182 | 41598_2023_34858_Fig4_HTML.jpg |
0.534576 | 2d5e03048356485ba8410832275b914a | Gp130 inhibitor SC144 blunted oncostatin M-dependent Fgf23 gene expression. Arithmetic means ± SEM of Fgf23 mRNA abundance relative to Tbp in UMR106 cells treated with or without 30 ng/ml oncostatin M for 24 h in the presence or absence of 1 µM gp130 inhibitor SC144 (n = 7; one-sample t test and Wilcoxon signed-rank test with Bonferroni adjustment for multiple comparisons). ** p < 0.01 indicates significant difference from vehicle control (1st bar); # p < 0.05 indicates significant difference from the absence of SC144 (2nd bar vs. 4th bar). a. u. arbitrary units; ctr control. | PMC10209182 | 41598_2023_34858_Fig5_HTML.jpg |
0.476767 | 7dcbd7c3d29e4511b3f9288781ae41c5 | STAT3 inhibitor nifuroxazide reduced oncostatin M-dependent Fgf23 gene expression. Arithmetic means ± SEM of Fgf23 mRNA abundance relative to Tbp in UMR106 cells treated with or without 10 ng/ml oncostatin M for 24 h in the presence or absence of 10 µM STAT3 inhbitor nifuroxazide (n = 6; one-sample t test and paired t test with Bonferroni adjustment for multiple comparisons). * p < 0.05, ** p < 0.01 indicate significant difference from vehicle control (1st bar); ## p < 0.01 indicates significant difference from the absence of nifuroxazide (2nd bar vs. 4th bar). a. u. arbitrary units; ctr control. | PMC10209182 | 41598_2023_34858_Fig6_HTML.jpg |
0.524414 | f4db903f0ed44cdfbf261af5bda6debd | MEK1/2 inhibitor trametinib attenuated oncostatin M-dependent Fgf23 gene expression. Arithmetic means ± SEM of Fgf23 mRNA abundance relative to Tbp in UMR106 cells treated with or without 10 ng/ml oncostatin M for 24 h in the presence or absence of 10 µM MEK1/2 inhibitor trametinib (n = 5; one-sample t test and paired t test with Bonferroni adjustment for multiple comparisons). * p < 0.05 indicates significant difference from vehicle control (1st bar); ## p < 0.01 indicates significant difference from the absence of trametinib (2nd bar vs. 4th bar). a. u. arbitrary units; ctr control. | PMC10209182 | 41598_2023_34858_Fig7_HTML.jpg |
0.409646 | 06e85d2000c64993839a4a4b9315f6b6 | Representation of the cortical mask optimised for the measurement of [18F]Flutemetamol | PMC10209381 | 13550_2023_994_Fig1_HTML.jpg |
0.407302 | b27de0b0548d43f2b194f062e2de71da | Composite SUVr of 11 patients (4 dots per patient) from pilot data using the pons as reference region with pre-existing cortical masks for all four software packages, the data is ranked by the patient’s mean SUVr across the four software packages | PMC10209381 | 13550_2023_994_Fig2_HTML.jpg |
0.417139 | d62b0728a5e3415fb13f8f69a7ec5c99 | Composite SUVr of 11 patients from pilot data using the pons as reference region with harmonised cortical mask for all four software packages, the data is ranked by the patient’s mean SUVr across the four software packages | PMC10209381 | 13550_2023_994_Fig3_HTML.jpg |
0.493126 | e9ad9c212cfa4935b43b99f2351d1c99 | Boxplot showing composite SUVr using the pons as a reference region for each of the 4 software packages analysed | PMC10209381 | 13550_2023_994_Fig4_HTML.jpg |
0.423948 | 253cf391415b4f8996d7bf236df970b0 | Z-score correlation analysis between the only two software packages assessed in this paper which offer composite z-scores | PMC10209381 | 13550_2023_994_Fig5_HTML.jpg |
0.433734 | 7e164d808581403185f58e8c084550c2 | Bland–Altmann plots for the highest (Software 1 and 2) and lowest (Software 3 and 4) agreement scores, according to Cohen’s kappa. Y-axis shows the difference between the composite SUVr for each software package and the x-axis shows the mean composite SUVr of the two software packages | PMC10209381 | 13550_2023_994_Fig6_HTML.jpg |
0.386784 | 7d72a938317643b1bf460f7beb5f7977 | PAGE gels illustrate genetic differences detected by RFLP analysis in out-break strains of C. hepaticus. (A) Historically prominent outbreak Clades 1 and 2 of C. hepaticus that were recurrently detected on free range farms in S.E. Queensland (F1, F2, F3, F5, F6) and NSW (F7) over the 4 yr of the study. (B) demonstrates that both clades were detected in on-farm fauna and layer hen feces. Procedures were as described in Materials and Methods. | PMC10209450 | gr1.jpg |
0.429331 | 44c820613fc64d39b1cb4938d64162a2 | (a) Coronary artery aneurysm and extravasation of contrast media. (b) Anomalous vessel indicating the coronary-pulmonary artery fistula. | PMC10209525 | ivad067f1.jpg |
0.430899 | cf9660f7c56b4d6a8c62ba8058ebca75 | (a) Ligation of inlet and outlet vessels. (b) Identification of residual branch and ligation of it. (c) Closure of the aneurysm. The saphenous vein graft was ligated and dissected finally. (d) In the postoperative computed tomography, the aneurysm is not shown. | PMC10209525 | ivad067f2.jpg |
0.403105 | 9c4c2d1b76e040ada3a043c785b6c55e | AUROC according to cumulative moving-average window size. (a) COx for infarction status. (b) Coherence for infarction status. (c) COx for hyperperfusion status. (d) Coherence for hyperperfusion status. | PMC10212684 | BMRI2022-3091660.001.jpg |
0.418906 | 03f4f7b1757a4b95b294824f2369b2fc | ROC curve and AUROC for infarction status according to cumulative moving-average intervals. (a, c) ROC curve and AUROC for infarction status according to cumulative mean calculation interval of COx. (b, d) The corresponding information for coherence. Two-sided statistical comparisons were performed using the Hanley-McNeil test. ∗∗∗ denotes a p value < 0.1, and all other values have a p value greater than 0.1. | PMC10212684 | BMRI2022-3091660.002.jpg |
0.408245 | edb66465c7204d55b969282126bf6b36 | Illustrative cases of the moving average of COx with varying window sizes. The graphs on the left are from a patient who developed postoperative infarction, and the graphs on the right are from a patient who did not develop postoperative infarction. The graphs at the top show real-time COx, and the graphs at the bottom show the cumulative moving average of COx. The rest are moving-average graphs over varying window sizes. | PMC10212684 | BMRI2022-3091660.003.jpg |
0.412771 | 21b5e771c84c4eb3925272530c288c80 | Illustrative cases of the moving average of coherence (Coh) within the VLF range with varying window sizes. The graphs on the left are from a patient who developed postoperative infarction, and the graphs on the right are from a patient who did not develop postoperative infarction. The graphs at the top show real-time coherence, and the graphs at the bottom show the cumulative moving average of coherence. The rest are moving-average graphs over varying window sizes. | PMC10212684 | BMRI2022-3091660.004.jpg |
0.420794 | 281973c36153455c8d35d6b99a4595cd | PRISMA flow diagram. | PMC10213267 | fimmu-14-1170569-g001.jpg |
0.455832 | 9dd805bd01f54299833519bae35ec711 | Forest Plot of (A) R0 and (B) Pathological Complete Response (pCR). | PMC10213267 | fimmu-14-1170569-g002.jpg |
0.403391 | 0a84082ba148444f85395967abe662aa | Forest Plot of (A) Major Pathological Response (mPR) and (B) Death within 30 Days after Surgery. | PMC10213267 | fimmu-14-1170569-g003.jpg |
0.509458 | ad8e675cc05e400c80c5f91262e93528 | Forest Plot of (A) 1-year Overall Survival (OS) and (B) 1-year Disease Free Survival (DFS). | PMC10213267 | fimmu-14-1170569-g004.jpg |
0.397217 | 0ac43e34f9a74485bd35b7c34783621b | Results of Comparisons by Risk Ratio (RR) and 95% Confidence Interval (CI) among Four Neoadjuvant Therapies. (*The number of events in the calculation of the RR value is the number of survivors rather than the number of deaths. RR and 95% CI > 1 indicates that treatment is more conducive to survival, while RR and 95% CI < 1 indicates that treatment is more detrimental to survival.) Pathological Complete Response (pCR), Major Pathological Response (mPR), Overall Survival (OS), Disease Free Survival (DFS). | PMC10213267 | fimmu-14-1170569-g005.jpg |
0.573506 | 604e072385164a9b9ac669ff50b52f4e | Forest Plot of Traditional Neoadjuvant Therapy (left) and Neoadjuvant Immunotherapy (right). (A) R0, (B) Pathological Complete Response (pCR), (C) Major Pathological Response (mPR), (D) Death within 30 Days after Surgery, (E) 1-year Overall Survival (OS) and (F) 1-year Disease Free Survival (DFS). (For 1-year OS and 1-year DFS, the number of events in the calculation of the RR value is the number of survivors rather than the number of deaths. RR and 95% CI > 1 indicates that treatment is more conducive to survival, while RR and 95% CI < 1 indicates that treatment is more detrimental to survival.). | PMC10213267 | fimmu-14-1170569-g006.jpg |
0.42271 | 199ff89ce1fd4c5fa8e475aa35d49765 | The B. multicinctus genome indicated that toxin protein families originated independently from local tandem duplication. (A) The layers of the circus plot represent the chromosome length, repeat content, gene density and GC content (%) of the genome from the outside to the inside. Regions with repeat content greater than the third quantile are shown in brown and those with higher-than-average GC content are shown in blue. (B) Venom families identified in the genome. The identified proteins include members not expressed in the venom. Glycosyl hydrolase families (13,37,56) were presented as one. (C) Phylogenetic tree constructed using 387 single-copy orthologous genes conserved across 12 species speculates divergence times for each species. (D) Synteny maps of B. multicinctus aligned with H. sapiens and G. gallus. Light grey lines exhibit the synteny blocks. Dark grey lines exhibit the synteny blocks with venom genes. Red, yellow and green lines exhibit blocks with 3FTx, PLA2, and kunitz families respectively. (E) The incremental (red) and global (purple) tests show significant clustering of venom genes. | PMC10213816 | gr1.jpg |
0.441941 | 6759fa282d5740918eab30ab25bbada0 | 3D chromatin organization and histone modification indicated the global epigenetic regulation of B. multicinctus genes. (A) Chromatin interaction in different tissues (red, venom gland; blue, muscle). (B) The increased ratio of chromosomal interactions in different chromosome groups when compare venom gland with muscle. (C, D) Whole-genome distance-contact frequency diagram with a 100-kb resolution in the venom gland (−0.94) and muscle (−0.88). Color: contact decay curve of different chromosomes; horizontal axis: distance between different sites on the chromosome; vertical axis: contact frequency. (E) Hi-C interaction map and colocalization of the genomic composition and various epigenetic marks on Chr7. The heatmap denotes the intrachromosomal Hi-C interaction frequencies among the pairwise 100-kb bins shown on the top. The PCA eigenvectors of the A and B compartments and genomic and epigenetic feature tracks are shown below in separate 100-kb bins, including abundances of genes and TEs, different histone modifications and mRNA expression levels (normalized by FPKM). (F) Bubble pattern of enriched pathways in the differential and conserved compartment domains (venom gland: A; muscle: B). The Y-axis represents the name of the pathway or function, and the X-axis represents the q values of each enriched gene family. The size of the bubble represents the number of genes in a signaling pathway or involved in a GO annotation. The color of the bubble indicates the ratio of the number of enriched genes. | PMC10213816 | gr2.jpg |
0.400146 | 3fee4841f84a4b0899c42af154711075 | A truncation event in an ancient duplicated LY6 member shaped modern 3FTxs. (A) Genomic position for the 3FTx tandem arrays across vertebrates. Genes belong to the uPAR/LY6/CD59/snake toxin-receptor superfamily (Pfam: CL0117) and containing a glycosylphosphatidylinositol (GPI)-anchor tail were labeled using cyan, and those without GPI-anchor tail were labeled as red. Other genes were labeled as grey. (B) The statistics of 3FTxs. Gene labeled in purple indicate genes containing the glycosylphosphatidylinositol (GPI)-anchor tail; gene labeled in grey indicate genes losing the GPI-anchor tail. Numbers on labels denote the chromosome number. Following three columns show the gene length, transposable element (TE) number and the first intron size. For heatmaps, characteristic expression with amounts ≥100 are all marked as red. | PMC10213816 | gr3.jpg |
0.464196 | 7a1f86051ba74c1b99ab850c2176fc3b | Sturcture features of 3FTxs in B. multicinctus. (A) Predicted tertiary structure of BM20242 (a LY6E ortholog in B. multicinctus) the GPI-anchor domain was indicated in black rectangle frame in dash, and the labled animo acid remain indicated the C-terminal of protein. (B) Predicted tertiary structure of BM20245 (the α-BgTx) unlike BM20242, its C-terminal GPI-anchor domain was missed. (C) Sequence alignment of the uPAR/LY6/CD59/snake toxin-receptor superfamily proteins in B. multicinctus. Purple shading shows the three-finger domain while the bluish grey shading shows the predicted GPI anchor. Yellow highlightings represent the cysteine pairs. | PMC10213816 | gr4.jpg |
0.42302 | 61d60299691f4c96a827f004b8369183 | Genome phasing of B. multicinctus Chr7:94,000,000‒96,000,000. (A) Syntenies between refence and the haplotypes (P scaffold and H scaffold). (B) Heterozygous sites in different genes. The purple square represents Toxin_TOLIP domain, the orange square represents the UPAR_LY6 domain, the green dot represents nonsynonymous mutaitions, and the blue dot represents synonymous mutations. | PMC10213816 | gr5.jpg |
0.457779 | ea9f4821f8d8491097a74c288b86e96c | The unit A of β-bungarotoxin lacked the Cys11‒Cys70 pair and were under global epigenetic regulation. (A) The ML phylogenetic tree and the amino acid sequence alignment of the GI-PLA2. (B, C) The expression characteristics of the many-banded krait GI-PLA2 in venom gland b and muscle c. Tracks from the top to bottom are H3ac counts (the red histogram), H3K27me3 counts (the navy histogram), the reads count of transcriptome (blue histogram) and gene structures (green blocks, where GI-PLA2 were indicated using red). Loops were displayed using arcs. Heatmaps implicated the contact frequency between chromosomal regions. The large square frames implicated the TADs and small square frame implicated peak loci. | PMC10213816 | gr6.jpg |
0.403112 | 8c71ee7f835745bd9025652959c0c468 | Simulated vibrational spectra of ammonium metavanadate: IR spectrum (black), Raman spectrum (red), and VDOS (blue). | PMC10214109 | d3ra02053c-f1.jpg |
0.411157 | dfc071f424e34d6393ce7981aaaabe5f | Four examples of vibrational modes at 44–312 cm−1. The green arrows represent the direction of vibration, where the size of each arrow is proportional to the vibrational amplitude. The number below each mode indicates its wavenumber. | PMC10214109 | d3ra02053c-f2.jpg |
0.466595 | e51459afbe3c47a1b0579e88fc0e02b7 | Four examples of vibrational modes at 317–489 cm−1. The first three modes represent VO3− bending, and the last one represents a skeletal rotation. | PMC10214109 | d3ra02053c-f3.jpg |
0.469243 | f239217c7e4642a4af611bbb54c30675 | Four examples of vibrational modes. The first two correspond to VO3− stretching, the third to NH4+ bending, and the last to NH4+ stretching. | PMC10214109 | d3ra02053c-f4.jpg |
0.423462 | 32cda63d905d4e099fab7e66da22c890 | a) In vivo imaging system (IVIS) images of visualized MHS@PPKHF in the articular cavity of rat at different time points; b) images of rat knee slices under fluorescence microscope; c) fluorescence images of PPKHF at different concentrations; and d) graph of fluorescence intensity–drug concentration. | PMC10214257 | ADVS-10-2207438-g001.jpg |
0.463042 | 02dd8297ab5d44b4b11370b038eb610e | a) Photo of finished POSS‐SH product; b) nuclear magnetic hydrogen (NMH) spectrum of POSS‐SH; c) Fourier transform infrared (FTIR) spectroscopy of POSS‐SH; d) synthesis process of PPKHF; e) NMH spectrum of PPKHF; f) silicon spectrum of PPKHF; g) mass spectrum of PPKHF; h) TEM images of PPKHF; i) fluorescence photos of PPKHF at series of concentrations under 365 nm UV lamp; and j) fluorescence intensity of different concentrations of PPKHF. | PMC10214257 | ADVS-10-2207438-g002.jpg |
0.415258 | 1c713f131eb543c69fb36efd47660eeb | a) Cell proliferation under different concentrations of PPKHF (n = 3, * p < 0.05, ** p < 0.01, and ***p < 0.001); b) representative fluorescence images of MHS, MHS@PPKHF, and PPKHF co‐cultured BMSCs by live‐dead staining assay; c) CCK8 values measured with live‐dead staining (n = 3, * p < 0.05, ** p < 0.01, and *** p < 0.001); d) viable cell count results (n = 3, * p < 0.05, ** p < 0.01, and *** p < 0.001); e) fluorescence confocal microscopic images of cell clusters induced by MHS@PPKHF and TGF‐β; f) mRNA relative expression levels of Collagen II, Aggrecan, and Sox9 (n = 3, * p < 0.05, ** p < 0.01, and *** p < 0.001, compared with TGF‐β group). | PMC10214257 | ADVS-10-2207438-g004.jpg |
0.460657 | c6ac7bd9541f4474ac59eb88a37cda95 | a) State of MHS@PPKHF after standing and precipitating, shaken into suspension and under UV light irradiation; b) hydrogel microspheres under bright field microscope, fluorescence microscope, and electron microscope; c) flight secondary ion mass spectroscopy(F‐SIMS) results of MHS@PPKHF; d) degradation curve of MHS@PPKHF; e) drug release profile; f) friction test diagram; and g–j) friction curves and statistical graphs. (* p < 0.05, ** p < 0.01, and *** p < 0.001). | PMC10214257 | ADVS-10-2207438-g005.jpg |
0.456093 | c9bc7f29763341038f6cd376b50aa8dc | a) Lateral X‐ray films of rat knees at 1st and 8th week after destabilization of medial meniscus (MMx), b) micro‐CT tomographic images and 3D reconstruction images of rat knee joints at 8 weeks postoperation, c) relative joint gap width of each group at 1‐week postoperation, d) relative joint gap width of each group at 8 weeks postoperation, and e) total volume of knee osteophytes in each group at 8 weeks postoperation. (n = 3, *** and ### indicate p < 0.001 when compared with Sham group and PBS group, respectively). | PMC10214257 | ADVS-10-2207438-g006.jpg |
0.463113 | ca5ab0c1efb64ce9bde9f76d0a07d163 | a) H&E staining, Safranin O‐fast green staining, and type II collagen immunohistochemical staining of each group; b) cartilage wear depth; c) relative glycosaminoglycan (GAG) content; d) OARSI score of each group, and e) relative type II collagen content. (n = 3, ns: no significance). | PMC10214257 | ADVS-10-2207438-g008.jpg |
0.408641 | 7e70ca0329c24c1b87664ed91d2b32d8 | Antitumor efficacy and immunoactivity of αPD‐L1/GEM NPs in an orthotopic pancreatic cancer model. A–C) Panc02 and 4T1 cells were treated with 50 nm free GEM or 500 IU mL−1 recombinant mouse IFN‐γ and incubated for 6, 24, and 48 h. PD‐L1 expression was measured by (A) qPCR and (B and C) flow cytometric analysis. For (B) and (C), the cells were treated with free GEM or IFN‐γ for 24 h at the abovementioned concentration. The results are presented as histograms in (B), and the corresponding MFI values are compared in (C). Cells treated with recombinant mouse IFN‐γ (500 IU mL−1) served as a positive control, as IFN‐γ has been reported to upregulate PD‐L1 expression.[
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] D) In vivo bioluminescence imaging of Panc02‐Luci tumor growth in the different treatment groups (n = 5). E) Tumor growth curves for the different treatment groups (n = 5). Tumor growth was quantified by the total luminescence flux as measured with an IVIS imaging system. The intensity fold change (Y axis) was normalized to the average luminescence flux on day 0. F) On day 35, the mice from different groups were first intraperitoneally injected with D‐luciferin at a dose of 75 mg kg−1/mouse and then sacrificed. Tumors with pancreatic tissues were harvested for ex vivo inspection. G) Survival curves for the different treatment groups (n = 5). H) Body weight was recorded at different time points. I) Flow cytometry plots and J) statistical chart presenting the proportions of IFN‐γ
+ CD8a+ T cells across different treatment groups. K) Flow cytometry plots and L) statistical chart presenting the proportions of CD25+ Foxp3+ Treg cells across the different treatment groups. The proportions of the above immune cell subsets were compared across the different treatment groups by the Kruskal–Wallis test. *p<0.05, **p < 0.01, and ***p < 0.001. | PMC10214259 | ADVS-10-2204890-g001.jpg |
0.449727 | 0df48018c0b040618cf7c88f6fa258ee | GPS therapy inflamed the TME and achieved recurrence‐free survival in a triple‐negative breast cancer model. A) Schematic of the experimental timeline and the different treatment groups. B,C) Relative tumor volumes were determined at different time points (n = 8). D) Breast cancer tissues were excised on day 18. E) In vivo bioluminescence imaging of 4T1 recurrence and metastasis in different treatment groups (n = 8). F) Survival in different treatment groups (n = 8). G) Gross examination of major organs (lung, liver, and spleen) collected from different treatment groups. Lung metastatic nodules (indicated by the green arrows), liver inflammatory infiltration, splenomegaly, and focal metastasis (indicated by the dashed and arrow‐indicated areas) were observed. H) H&E staining of lungs, spleens, and livers. The dashed areas indicate metastatic lesions in the lungs and spleens and granulocytic infiltration in the livers. Scale bars: 100 µm. I) Flow cytometry plots and statistical chart for CD80+ CD86+ DCs (distributed in the upper right quadrants in the flow cytometry plots) isolated from TILs. J) IFN‐β, IL‐6, IFN‐γ, CXCL9, and CXCL10 levels in the 4T1 TME were measured by a bead‐based multiplex LEGENDplex assay. The data shown are the mean ± s.e.m. values (n = 5). Statistical analysis was performed with one‐way ANOVA. *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001. | PMC10214259 | ADVS-10-2204890-g002.jpg |
0.410329 | d882203bb4de4863bcc03cd9ddad9061 | Development of a combinatorial immunogenic nanovesicle for cancer chemoimmunotherapy. A) Schematic illustration showing the preparation of a triple therapy‐integrated nanoparticle composed of a cytotoxic polymeric gemcitabine (GEM) prodrug and a diamidobenzimidazole‐based STING agonist (diABZI) surface‐modified with an anti‐PD‐L1 antibody (αPD‐L1). The integrated nanoparticle combining these components is designated GPS based on the concatenated single initials G (GEM), P (αPD‐L1), and S (STING agonist). αPD‐L1 conjugation not only augments cellular uptake and intratumor drug delivery but also improves the overall antitumor efficacy. B) Upon systemic administration, cytotoxic GEM induces cancer cell apoptosis to generate tumor cell debris, while the diABZI agonist activates the STING signaling pathway to induce DC maturation, cell debris uptake, and cytokine release. These events transform an immunosuppressed “cold” tumor microenvironment (TME) into a “hot” TME and result in robust immune activation, which can further synergize with immune checkpoint blockade with an anti‐PD‐L1 antibody (αPD‐L1). | PMC10214259 | ADVS-10-2204890-g003.jpg |
0.433398 | 29e68c53ed3a4bd59961e3375dd5825e | GPS eradicates large tumors and elicits tumor‐specific immunity in an aggressive melanoma model. A) Schematic of the experimental timeline for a rechallenged B16‐OVA melanoma model. B) The relative volumes of primary tumors were determined at different time points (n = 6). “IR” refers to “immune response”, which is defined as the tumor volume on day 9 being smaller than the baseline tumor volume on day 0. C) Primary melanoma tissues were excised on day 9. D) The volumes of rechallenged melanoma tumors were determined at different time points (n = 5). “TF” refers to “tumor free”, which is defined as those without any tumor growth on the contralateral side on day 19 after rechallenge. E) Rechallenged melanoma tissues were excised on day 42. The dashed area indicates that GPS treatment resulted in complete elimination of reinoculated melanoma tumors. F,G) Maturation of DCs, as indicated by the expression levels of CD80, CD86, and CD83, was evaluated in the primary TME, and the results are presented on statistical charts (n = 5). H,I) CD103+ DCs were quantified in primary TMEs and tdLNs, and the results are presented in statistical charts (n = 5). J–M) Activation of OVA‐specific CD8+ T cells was evaluated after ex vivo restimulation of splenic lymphocytes with OVA (peptide sequence: SIINFKEL) for 6 h. The proportions of (J, K) IFN‐γ+ CD8+ T cells and (L, M) CD107a+ CD8+ T cells were quantified by flow cytometry. CD107a constitutes a marker of cytotoxic degranulation in CD8+ T cells. The proportions of the above immune cell subsets were compared across the different treatment groups by the Kruskal–Wallis test. *p<0.05, **p < 0.01, and ***p < 0.001. | PMC10214259 | ADVS-10-2204890-g004.jpg |
0.44056 | 4539f77a5da84852af3150b2fd5e004d | Preparation and characterization of polymeric GEM‐loaded immunogenic NPs. A) Schematic illustration of GEM NP and αPD‐L1/GEM NP generation. B) TEM images of GEM NPs (first row) and αPD‐L1/GEM NPs (second row). The area enclosed in the green dashed lines was further enlarged and is presented on the right. After antibody conjugation, an electron‐dense shell was observed on the outer layer of αPD‐L1/GEM NPs, as marked with red arrows in the enlarged image. The C) Size distribution and D) zeta potential of GEM NPs and αPD‐L1/GEM NPs were measured using DLS analysis. E) The D
H of GEM NPs and αPD‐L1/GEM NPs was determined by DLS analysis at different time points. Both NPs were dissolved in saline medium supplemented with 20% FBS to mimic the physiological environment. F) αPD‐L1 conjugation was confirmed by Coomassie Brilliant Blue staining. Lane 1: GEM NPs were incubated with iminothiolated αPD‐L1 without prior maleimide functionalization; lane 2: resuspended αPD‐L1/GEM NPs after ultracentrifugation; lane 3: supernatant solution after ultracentrifugation with excess αPD‐L1; lane 4: αPD‐L1/GEM NPs before ultracentrifugation; lane 5: iminothiolated αPD‐L1 solution used as the positive control. (G‐H) Panc02 cells were treated with DiI@GEM NPs or DiI@αPD‐L1/GEM NPs at different time points (e.g., 0.5, 2, 4, and 6 h), and the cellular uptake of both NPs was assessed by flow cytometric analysis. G) The results are presented as histograms, and H) the MFI value of the DiI dye is compared (n = 3). I) Panc02, B16.F10, 4T1, and RAW 247.6 cells were treated with free GEM, the PLA‐GEM conjugate, GEM NPs, and αPD‐L1/GEM NPs for 72 h, and cell viability was determined using a CCK‐8 assay. The X‐axis shows the equivalent concentration of GEM (n = 6). The data shown are the mean ± s.e.m. values. Statistical analysis was performed with the Mann–Whitney test. *p<0.05, **p < 0.01, ***p < 0.001 and ****p < 0.0001. | PMC10214259 | ADVS-10-2204890-g006.jpg |
0.432968 | 1852f2b707854f67b70655bb4e5b5c01 | Design and characterization of the GPS therapeutic. A) Schematic illustration of the generation of GPS. B) TEM images of GPS NPs. Scale bars: 100 nm. C) D
H of GPS as determined by DLS analysis (diABZI was loaded at different mass ratios; the ratios are presented as diABZI:GEM). D) D
H of GPS NPs (loaded at a mass ratio of 1:5) as determined by DLS analysis. NPs were dissolved in saline medium supplemented with 20% FBS, which mimics the physiological environment. E,F) qPCR analysis of IFN‐β, cGAS, IRF7, and IL‐6 gene expression in (E) BMDCs and (F) 4T1 after treatment with diABZIs or a physical mixture of free diABZI, GEM, and αPD‐L1 (referred to as 3 free). The X axis shows the equivalent dose of diABZI. The gene expression of Gapdh was defined as an internal reference; all treatment group data were compared to the data in untreated BMDCs or 4T1 (control). Statistical analysis was performed with ANOVA. *p<0.05, **p < 0.01, and ***p < 0.001. | PMC10214259 | ADVS-10-2204890-g007.jpg |
0.43953 | a663c47571a3477b978659c8287e13fa | Phase space reconstructed results and performance evaluated by Lyapunov exponent and correlation dimension. a–c) Phase space reconstructed by x(t), y(t), and z(t), the diagonal plot represents the output of x(t), y(t), and z(t) under different moments. d–g) Influence of embedded dimension (Dim = [9, 10]), delay time (τ = [1, 5, 10, 20, 30, 50, 100, 200, 500, 1000]), sampling rate (F
s = [100, 200, 300, 500, 600, 700, 800, 1000, 1500, 2000]), and expansion range (eR = [10, 50, 100, 150, 200, 250, 300, 500, 800, 1000]) on Lyapunov exponent (L
y) in the natural exponential chaotic system. h–k) Influence of Dim, τ, N
p (within the scope of [10, 50, 100, 150, 200, 250, 300, 500, 800, 1000]) and logarithm of N
p on C
d in the natural exponential chaotic system. | PMC10214267 | ADVS-10-2204269-g001.jpg |
0.451965 | f13767550cb64236b1ab586e364a733d | Mapping and bifurcation characterization of the natural exponential 3D chaotic system. a) 3D mapping of natural exponential chaotic system. b) Dynamic trajectory in the x–y plane. c) Poincare map in the x–y plane. d) Poincare map in the x–z plane. e) Poincare map in the y–z plane. f–h) Bifurcation map under different main system parameters (a = −0.4:0.001:−0.005), b = 0.1:0.001:0.5, c = 30:0.01:40, d = 0.005:0.01:2, α = 0.005:0.01:2, β = 0.005:0.01:2). Results for x(t), y(t), and z(t) are expressed in (f), (g), and (h), separately. | PMC10214267 | ADVS-10-2204269-g002.jpg |
0.368364 | 04d412ea11db4d058cfdfcc56292ba65 | Grid entropy (GE) measurement for x(t) and y(t). a–d) GE for x(t) when the system parameter of a, b, c, and d changes as mentioned in Figure 7. e–h) GE for y(t) when the parameter of a, b, c, and d changes as mentioned in Figure 7. The range shown in each box is x∈[−500, 500] and y∈[−500, 500]. | PMC10214267 | ADVS-10-2204269-g004.jpg |
0.474941 | b15d43c035064c5b83007cc39dcc4f15 | Sensitivity of natural exponential chaotic system to initial conditions. a) Plane graph of the natural exponential chaotic system attractor. b) 3D attractor of the natural exponential chaotic system. c) Output signals of x(t) under different initial conditions. The curves in the first three lines are the output results from traditional Duffing system and the lower rows with three signals are the comparison results from the natural exponential chaotic model under different initial conditions. These three curves of Duffing and the new model are all calculated with initial value (x(t), y(t), z(t)) of (1, 1, 0.1), (1.05, 1, 0.1), (1.1, 1, 0.1) from top to bottom lines. d) Error of output x(t) when the initial input difference of x
0 changes. e) Error of output y(t) when y
0 changes. f) Change trends of output errors for x(t) and y(t) when x
0 varies with the element of [0.001, 0.002, 0.005, 0.01, 0.02, 0.05, 0.1, 0.2, 0.5, 0.9]. | PMC10214267 | ADVS-10-2204269-g005.jpg |
0.435447 | 3cfea9a821d4435fb1c699816d69728a | Application of the natural exponential chaotic system in time series prediction. a–d) Time series prediction results of x(t) through convolutional and recurrent combined neural network (CNN‐RNN) with time series lengths of 3000, 5000, 10 000, and 30 000. The root mean square error (RMSE) for the predicted time series of T
1 to T
4 is 0.1671, 0.1427, 0.1489, and 0.2741, respectively. e–h) Time series prediction results of x(t) by long‐short term memory neural network (LSTM) with time series lengths of 3000, 5000, 10 000, and 30 000. The RMSE for the predicted T
1 to T
4 is 0.03464, 0.08105, 0.06720, and 0.08517, respectively. The first line box shows the original signals and the forecast new signal, the second line box is a local show for the forecast new signal and corresponding original signal segments, and the third line box represents the error between the original signal and forecast new signal. | PMC10214267 | ADVS-10-2204269-g006.jpg |
0.384743 | 1fa9488dcdc243b4bd0cb647b65dad85 | Comparison of noise induced phase. a) Noise induced phase by traditional chaotic method. b) Noise induced phase unwrapped by natural exponential and 3D chaotic system. | PMC10214267 | ADVS-10-2204269-g007.jpg |
0.445218 | 6ea89f0161344cfe90a63f5aa476aebf | Application of the natural exponential chaotic system in image encryption and decryption. a) Original image before and after encrypted. b) RGB values of the image before and after encrypted. c) Mean square error (MSE) and peak signal‐to‐noise ratio (PSNR) of the encrypted image under different noise density. d) RGB values of the decrypted image. e) Decrypted image under different noise density. f) Correlation analysis for the original image in three dimensions. g) Correlation analysis for the encrypted image in three dimensions. H, V, and D in (f) and (g) means the horizontal, vertical, and diagonal correlation results, separately. The labels marked in (e) represent the Gaussian noise intensity added to the original image before decrypted. | PMC10214267 | ADVS-10-2204269-g008.jpg |
0.539585 | 4c7ae260fb6b4cc8806cb76de9d1739b | Heterogeneous and cross recurrence analysis. a) Heterogeneous recurrence results under different ending time of T. b) Change trends of heterogeneous recurrence rate (Rr), heterogeneous entropy (En), and heterogeneous mean (Mean) under different T. c–e) CRP results for x(t), y(t), and z(t). f–h) TCRP and synchronization lines for x(t), y(t), and z(t). i) Cross recurrence results for x(t)–x(t) (labeled as xx), y(t)–y(t) (labeled as yy) and z(t)−z(t) (labeled as zz). j) Cross recurrence results for x(t)−y(t) (labeled as xy), x(t)−z(t) (labeled as xz) and y(t)−z(t) (labeled as yz). The variables in (i) and (j) are determinism (De), entropy (En), length of longest vertical (V
m) and horizontal (H
m) line, length of longest (L) and average (L
v) diagonal line, laminarity of vertical (L
m) and horizontal (L
h) lines, recurrence rate (Rr), trapping time of vertical lines (T) and horizontal lines (Th), respectively. | PMC10214267 | ADVS-10-2204269-g009.jpg |
0.384161 | 039eef1d6716440d9f8de8dfd1750690 | Time series entropy (TSE) measurement for x(t) and y(t). a–d) TSE results for x(t) when the system parameter of a, b, c, and d changes. e–h) TSE for y(t) when the parameter of a, b, c, and d changes. These parameters are set as a = [−5, −1, −0.5, −0.3, −0.1, −0.01, 0.01, 0.1], b = [0.1, 0.2, 0.3, 0.5, 1, 3, 5, 7], c = [−10, −5, −1, 0, 1, 5, 10, 20], d = [−7, −5, −1, 0, 1, 3, 5, 15]. The red line represents the number of circles in the circled TSE measurement, and the blue dots express 15‐degree of difference plot, which calculate these data fall over the circled‐pieced area. | PMC10214267 | ADVS-10-2204269-g010.jpg |
0.437439 | c4966000b10e4a5a97a08543104e40c8 | Entropy analysis and comparison of the chaotic systems. a) Chordal graph for topological entropy (TE). b) Chordal graph for approximate entropy (AE). xL and xr represent the AE computation results of x(t) when the parameters of L and r vary within the scope of [2, 4, 6, 8, 10, 12, 14, 16, 18, 20] and [0.01, 0.1, 0.2, 0.3, 0.4, 0.5, 0.6, 0.7, 0.8, 0.9]. c) Chordal graph for Shannon entropy (SE). xq and xw mean the SE computation results of x(t) when the parameters of q and w varies within the scope of [2, 4, 6, 8, 10, 12, 14, 16, 18, 20] and [1, 2, 3, 4, 5, 6, 7, 8, 9, 10]. xa, xb, xc, and xd in (a)–(c) express the corresponding entropy of x(t) when the system parameters of a, b, c, and d varies within the scope of [−5, −1, −0.5, −0.3, −0.2, −0.1, −0.01, 0, 0.01, 0.1], [0.1, 0.2, 0.3, 0.5, 1, 2, 3, 5, 7, 10], [−10, −5, −1, 0, 1, 5, 10, 20, 30, 50], and [−7, −5, −1, 0, 1, 3, 5, 15, 20, 50], respectively. A–J represent different groups of system parameters. d) Fuzzy entropy of x(t) (upper row, FE(x)), y(t) (middle row, FE(y)), and z(t) (lower row, FE(z)), where dim = [2, 4, 6, 8, 10, 12, 14, 16, 18, 20], wid = [2, 4, 6, 8, 10, 12, 14, 16, 18, 20], and st = [1, 2, 3, 4, 5, 6, 7, 8, 9, 10]. | PMC10214267 | ADVS-10-2204269-g011.jpg |
0.416864 | 430ef61a057a4cf5b5b04e3b6c4f008a | The amplification and standard curves of the pentaplex qRT-PCR assay. A, B, C, D, and E are the amplification curves of HBV, HCV, HEV, T. pallidum, and RNase P, respectively, using serial tenfold dilutions of plasmid standards ranging from 106 to 101 copies/µL, and F, G, H, I, and J are the standard curves of HBV, HCV, HEV, T. pallidum, and RNase P, respectively | PMC10214662 | 12879_2023_8240_Fig1_HTML.jpg |
0.489659 | 55052ced03e142fb807bd4ffe19b68e7 | The analytical specificity of the pentaplex qRT-PCR assay. Only HBV, HCV, HEV, and T. pallidum had amplification curves. HAV, EBV, HSV, CMV, HIV, and negative controls had no fluorescence signal.1, T. pallidum; 2, HBV; 3, HEV; 4, HCV; 5–9, HAV, EBV, HSV, CMV, and HIV; 10, negative control | PMC10214662 | 12879_2023_8240_Fig2_HTML.jpg |
0.449801 | 4fa263547f78484a9451e764d5b28125 | Venn diagram of the results of serology versus pentaplex qRT-PCR assays. The serology and pentaplex qRT-PCR assays were performed to detect HBV(A), HCV(B), HEV (C), and T. pallidum(D) in 2400 blood samples. Number of samples positive by serology only (blue), positive by pentaplex qRT-PCR only(yellow), or positive by both serology and pentaplex qRT-PCR (green). Number of samples negative by both serology and pentaplex qRT-PCR(grey) | PMC10214662 | 12879_2023_8240_Fig3_HTML.jpg |
0.418282 | b6454e2f0e0f4cb5acbbd254db4aa4e6 | Schematic of experimental design. Three-month-old pigs were fed either standard pig chow (Lean) or a high-fat/high-fructose diet (Obese) for 16 weeks (n = 6 each). Mesenchymal stem/stromal cells (MSCs) were isolated from subcutaneous abdominal fat, expanded in vitro, and characterized for surface markers. Hydroxymethylated DNA immunoprecipitation sequencing (hMeDIP-seq) was performed on Lean- and Obese-MSCs (n = 3 each), and again on Obese-MSCs (n = 3) cultured with epigenetic modulator vitamin-C, to determine levels of the 5-hydroxymethylcytosine (5hmC) epigenetic mark. (Illustrations were created with BioRender.com and exported under a paid subscription through the Mayo Clinic) | PMC10214739 | 13287_2023_3372_Fig1_HTML.jpg |
0.483166 | 0bbbcd0ac61a41f78557c3236d1675e7 | Obesity and dyslipidemia induce epigenetic changes in 5-hydroxymethylcytosine (5hmC) in swine adipose-derived MSCs. A Volcano plot of genes with significant changes in overall exonic 5hmC peak levels in Obese-MSCs versus Lean-MSCs, as defined by the following thresholds (dashed lines): p-value ≤ 0.05 and fold change (Obese-MSCs/Lean-MSCs) ≥ 1.4 (high 5hmC levels) or ≤ 0.7 (low 5hmC levels). Genes with high (n = 467) or low (n = 591) 5hmC levels in Obese- versus Lean-MSCs are represented with red or blue circles, respectively, while blank circles indicate genes without significant alterations. Outlier genes with very large fold change values (often due to undetectable 5hmC levels in Lean-MSCs) are displayed as triangles. B Heat map of genes with higher (left) or lower (right) 5hmC levels in Obese-MSCs versus Lean-MSCs. C Integrative Genomics Viewer (IGV) outputs displaying 5hmC profiles for two representative genes. n = 3 per group | PMC10214739 | 13287_2023_3372_Fig2_HTML.jpg |
0.485369 | b93d1a13df5341cfa5689f3ab862fec0 | Obesity/dyslipidemia-induced 5hmC marks correlate with changes in gene expression in pathways related to apoptotic process, cell proliferation, and leukocyte-mediated cytotoxicity. A Scatterplot of gene sets from the Molecular Signatures Database identifying those with concordant dysregulation of 5hmC levels and mRNA expression in swine Obese- versus Lean-MSCs. For each gene set, the normalized enrichment score (NES) is separately calculated for hMeDIP-seq (vertical axis) and mRNA-seq (horizontal axis) using Gene Set Enrichment Analysis. Based on thresholds (dashed lines) of NES > 1.4 and NES < -1.4, gene sets with higher (n = 95) or lower (n = 7) levels of both 5hmC and mRNA in Obese- versus Lean-MSCs were marked as red or blue dots, respectively. Genes from the gene sets with B NES > 1.4 or C NES < -1.4 for both hMeDIP-seq and mRNA-seq were extracted, and classified via Gene Ontology (GO): Biological Process overlap analysis. In panels (B, C), salient overlapping gene categories are highlighted in yellow | PMC10214739 | 13287_2023_3372_Fig3_HTML.jpg |
0.423789 | 7e0e32758a574e2daadc7a2d1744ddd6 | Obesity/dyslipidemia associates with dysregulated 5hmC levels in swine MSCs on genes related to apoptotic process. A Volcano plot showing differential 5hmC levels in Obese- versus Lean-MSCs for genes filtered by the Gene Ontology (GO) term for apoptotic process (GO:0006915). For a given gene, differential 5hmC levels entail p-value ≤ 0.05 and fold change (Obese-MSCs/Lean-MSCs) ≥ 1.4 (high 5hmC levels) or ≤ 0.7 (low 5hmC levels). Genes with high (n = 58) or low (n = 46) 5hmC levels in Obese-MSCs versus Lean-MSCs are represented with red or blue markers, respectively. High 5hmC genes with undetectable 5hmC levels in Lean-MSCs are presented as outliers (red triangles). B Heat map of genes filtered by apoptotic process (GO:0006915) showing higher (left) or lower (right) 5hmC levels in Obese-MSCs versus Lean-MSCs. C Venn diagram analysis shows regulators of apoptotic process among genes with higher (left) or lower (right) 5hmC levels in Obese- versus Lean-MSCs, grouped based on GO terms: positive (GO:0043065) and negative (GO:0043066) regulation of apoptotic process | PMC10214739 | 13287_2023_3372_Fig4_HTML.jpg |
0.409415 | 283596ec675e464ebd396d032f82bec3 | Cellular senescence-associated genes with differential 5hmC levels in swine Obese- versus Lean-MSCs interact richly with canonical markers of senescence. A Volcano plot showing differential 5hmC levels in Obese- versus Lean-MSCs for genes filtered by the Cellular Senescence REACTOME Superpath or the GO term for Cellular Senescence (GO:0090398). For a given gene, differential 5hmC levels entail p-value ≤ 0.05 and fold change (Obese-MSCs/ Lean-MSCs) ≥ 1.4 (high 5hmC) or ≤ 0.7 (low 5hmC), as shown with dashed lines. Senescence-associated genes with high (n = 12) or low (n = 5) 5hmC levels in Obese- versus Lean-MSCs are represented with red or blue markers, respectively. B Heat map of genes filtered for Cellular Senescence showing higher (left) or lower (right) 5hmC levels in Obese-MSCs versus Lean-MSCs. C Functional network analysis of genes with differential 5hmC levels in Obese- versus Lean-MSCs using the STRING database. Network edges indicate both functional and physical protein associations, and color indicates the type of interaction evidence. Inclusion of three classic markers of senescence (p16, p21, and p53), along with stress kinase p38α, in the interaction analysis reveals salient interactions with the epigenetically dysregulated genes | PMC10214739 | 13287_2023_3372_Fig5_HTML.jpg |
0.373963 | 5f73f94743f74e9a9cd9351c6a85dd84 | Functional assays indicate increased senescence in swine Obese-MSCs. A Cell proliferation, given as change in % confluence across 24 h (mean ± SEM; Obese-MSCs: n = 6, Lean-MSCs: n = 5) was not significantly different between Obese- and Lean-MSCs. B Obese-MSCs, but not Lean-MSCs, showed resistance to induction of apoptosis by staurosporine (dissolved in DMSO; 20 nM for 24 h in vitro; DMSO: n = 5 each; staurosporine: n = 6 each). C Percentage of senescence-associated beta-galactosidase (SA-β-Gal) positively stained cells was increased in Obese- versus Lean-MSCs (n = 4 per group). D Obese-MSCs also showed increased p16 immunoreactivity (% staining area), compared with Lean-MSCs (n = 6 per group). *p-value ≤ 0.05 versus Lean-MSCs; #p-value ≤ 0.05 versus Lean-MSCs + DMSO; ‡p-value ≤ 0.05 versus Obese-MSCs + DMSO | PMC10214739 | 13287_2023_3372_Fig6_HTML.jpg |
0.465143 | ea559ff933014d4cb401f0c8b84bb6ed | Epigenetic reprogramming of swine MSCs with vitamin-C partly reverses obesity/dyslipidemia-induced changes in hydroxymethylation of genes related to apoptosis and cell proliferation/senescence. A Scatterplot of genes in which vitamin-C induced differential 5hmC levels in Obese-MSCs. Genes showing differential 5hmC levels both in Obese- versus Lean-MSCs (x-axis) and in vitamin-C-treated Obese-MSCs versus untreated Obese-MSCs (y-axis) are colored. Differential 5hmC levels entail p-value ≤ 0.05 and fold change ≥ 1.4 (high 5hmC levels) or ≤ 0.7 (low 5hmC levels). Outliers (with very large fold change values) are represented with triangle markers. Green points (n = 40) represent genes with low 5hmC levels in Obese- versus Lean-MSCs, which are reversed upon vitamin-C treatment, while orange points (n = 28) represent genes with high 5hmC levels in Obese- versus Lean-MSCs, which are reversed upon vitamin-C treatment. B Heat map of genes for which vitamin-C treatment reverses the differential 5hmC levels observed in Obese-MSCs (orange and green clusters from panel A), filtered for apoptotic process (GO:0006915), cell cycle (GO:0007049), cell population proliferation (GO:0008283), and cellular senescence [REACTOME SuperPath + (GO:0090398)]. n = 3 per group | PMC10214739 | 13287_2023_3372_Fig7_HTML.jpg |
0.435095 | 146e679917414a90950dcba81db966ff | Obesity/dyslipidemia-driven dysregulation of 5hmC epigenetic marks on apoptosis- and senescence-related genes in human adipose-derived MSCs. A Heat maps showing high (left; n = 16) and low (right; n = 52) 5hmC levels in genes filtered by apoptotic process (GO:0006915) in human Obese- versus Lean-MSCs. B Heat map showing high (AAAS, n = 1) and low (n = 15) 5hmC levels in genes filtered by the Cellular Senescence REACTOME Superpath or the GO term for Cellular Senescence (GO:0090398) in human Obese- versus Lean-MSCs. n = 5 per group | PMC10214739 | 13287_2023_3372_Fig8_HTML.jpg |
0.437243 | 6ec034c4dd3b4ba8b4e887430e3c3b84 |
NbCORE silencing removes csp22 responsiveness and increases transient protein production in older N. benthamiana plants. (a) TRV::NbCSPR and TRV::NbCORE plants have no additional developmental phenotype compared to TRV::GUS plants. Scale bars, 1 cm. *, removed sample leaves. (b) The csp22‐induced oxidative burst is absent from 6‐week‐old TRV::NbCORE plants but present in TRV::GUS and TRV::NbCSPR plants. Error shades represent the standard error of n = 6 leaf discs. (c) NbCORE depletion causes bright GFP fluorescence upon agroinfiltration of 6‐week‐old plants. The image was taken 5 days agroinfiltration with 35S:eGFP. Scale bar, 1 cm. (d) Significant increase in GFP fluorescence upon NbCORE depletion. GFP fluorescence was quantified from images of n = 4 biological replicates of 6‐week and 8‐week‐old VIGS plants agroinfiltrated with 35S:eGFP 5 days before fluorescence scanning. Fluorescence was quantified using ImageJ and normalized by leaf area. ****, P value = 0.0000084 (t‐test). (e) TRV::NbCORE plants accumulate much more GFP protein upon agroinfiltration than TRV::GUS plants. Total leaf proteins were extracted from VIGS plants, 5 days after agroinfiltration with 35S:eGFP, and analysed by anti‐GFP western blot. CBB, Coomassie brilliant blue. | PMC10214749 | PBI-21-1103-g001.jpg |
0.467218 | 38bc427ab8374be98a775cd60f82126c | Progress curves for the hydrolysis of (a) 100 µM imipenem (IMI) and (b) 25 µM ceftazidime (CAZ) by KPC-2 and the D179Y and D179N variants (2 µM enzyme) at 25 °C obtained using a stopped-flow apparatus. | PMC10215400 | antibiotics-12-00892-g001.jpg |
0.397782 | 32706d7ec1be411592154b77f3cc80a1 | Time-based mass spectrometry (A) 1:1 ratio of the D179Y and D179N variants to imipenem. (B) 1:50 ratio of variant to ceftazidime. | PMC10215400 | antibiotics-12-00892-g002.jpg |
0.396349 | 0dedbcab90644a0d865ec94cdf4a6984 | Time-based mass spectrometry (A) 1:1 ratio of the D179Y and D179N variants to relebactam. (B) 1:1 ratio of variant to avibactam. | PMC10215400 | antibiotics-12-00892-g003.jpg |
0.449015 | c5d1aa4de4d34abcbda4b1e34c24774d | The acyl–enzyme complexes of the D179Y variant (left) and the D179N variant (right) with imipenem (cyan). | PMC10215400 | antibiotics-12-00892-g004.jpg |
0.413422 | 249970e262464904ba908f0135604225 | The number of articles identified by searching for keyword combinations. | PMC10215522 | biomedicines-11-01237-g001.jpg |
0.423012 | c7c19bc1be0c47a2a63bab4411b96488 | Conserved motif arrangement in proteins of the TFPI family. | PMC10215522 | biomedicines-11-01237-g002.jpg |
0.521098 | 4af110f704474426a8fcde232d704d4b | Concentrations of TF, TFPI1, and TFPI2 in maternal blood and placental tissue from healthy pregnant women and preeclamptic patients. The thicker the arrow in the figure, the greater the production volume. | PMC10215522 | biomedicines-11-01237-g003.jpg |
0.425689 | 6c1572cb3a6045348fa4955b36bd968c | Cumulative gas production curves of cassava chip and winged bean tuber treated with various modified starch methods. CSC-untreated = Cassava chip-untreated, CSC-Steam = Cassava chip-steam treated, CSC-NaOH = Cassava chip-sodium hydroxide treated, CSC-CaOH2 = Cassava chip-calcium hydroxide treated, CSC-LA = Cassava chip-lactic acid treated, WBT-untreated = Winged bean tuber-untreated, WBT-Steam = Winged bean tuber-steam treated, WBT-NaOH = Winged bean tuber-sodium hydroxide treated, WBT-CaOH2 = Winged bean tuber-calcium hydroxide treated, WBT-LA = Winged bean tuber- lactic acid treated. | PMC10215758 | animals-13-01640-g001.jpg |
0.383379 | 69d5690d39464c10a0c0dfaa59037536 | Percentage of XP patients with internal tumors in each complementation group among the French XP patients. The blue bars represent the true number of XP patients and the orange bars are the percentage of internal tumors for each of the 7 complementation groups available among the French XP patients. | PMC10216379 | cancers-15-02706-g001.jpg |
0.393304 | 922d57d22da34204bcaf483c2f50d3cd | Full face protection of XP patients. Full ultraviolet protections of the face of XP patients have been constructed allowing them to be outside on a sunny day without any danger and without any sunlight-protective cream. The XP patients can participate in a normal activity with this protection (a), such as skating (b) or cycling, at noon time, on the Comorian Island Mayotte very close to the equator (c). Photographs are shown with the agreement of the XP patients and their families. Thanks to Fabrice Dimier for shooting the (a,b) pictures. | PMC10216379 | cancers-15-02706-g002.jpg |
0.43274 | 736cd093f5da4d63a7bb3aad159baeaa | Incidence of combined myelodysplasia (MDS) and Acute Myeloid Leukemia (AML) in the French general population and number of XP-C patients with MDS and/or AML. In orange, incidence of MDS and AML in the French population according to the ages for 100,000 person-years (data have been compiled in 2018 and are available as “National estimates of cancer incidence and mortality in metropolitan France between 1990 and 2018”; Vol. 2, Hematological Malignancies; https://www.e-cancer.fr/; accessed on 18 January 2023 [28]). In blue, the true number of XP-C patients with MDS and/or AML: 3 patients for ages 0–14, 2 for 15–19, 4 for 20–24, and 7 for 25–29 (see Table 1). | PMC10216379 | cancers-15-02706-g003.jpg |
0.454748 | a7a86e224dde46e3a627b870228aec08 | Kaplan–Meier distribution of survival for XP-C patients with brain tumors (blue curve) or MDS/AML (red curve). Three XP-C patients developed early brain tumors (median ages of 10y) and 16 XP-C patients developed MDS and/or AML (median ages of 25y). The two curves are statistically different (p = 0.002; X2 test). | PMC10216379 | cancers-15-02706-g004.jpg |
0.502316 | 5b0ce2378b284c4fbf176cc568a5cebb | Somatic chromosomal abnormalities in the AML with myelodysplasia-related changes in the XP185VI patient. Patient XP185VI first developed MDS (at 24 years old) followed by AML-6 at 25y. One can see numerous chromosomal changes, especially in chromosomes 5q and 7q. Below the centered-line one can see loss of genomic materials in blue and above the centered-line one can see gain of genomic materials in red. | PMC10216379 | cancers-15-02706-g005.jpg |
0.432239 | d4a2c954d0e64bed98a9063b89cfa41a | Timing of the appearance of major hematological abnormalities in French XP patients. Often XP patients develop anemia before the appearance of MDS (RAEB-1 and -2 correspond to the old name for MDS, meaning Refractory Anemia with Excess Blasts) which occurs with a median age of around 24 years old. MDS are rapidly transformed into AML. Numerous driver gene mutations and chromosomal abnormalities are associated with these hematological malignancies. | PMC10216379 | cancers-15-02706-g006.jpg |
0.455481 | 06d4f3683bae4c07a49f483f623feaab | Basic BsAb structure showing the antigen-binding site that harbors the complementarity-determining region (CDR) segment, disulfide bond, light chains (L) and heavy chains (H); C: constant domain; V: variable domain, Fab: fragment antigen-binding domain; Fc: fragment-crystallizable domain. Figure created by BioRender.com (accessed on 14 May 2023). | PMC10216491 | cancers-15-02824-g001.jpg |
0.433151 | 7b1988293a254d8396b58205ea8a306d | (A) BsAbs without FC portion connected via a linker. Example is blinatumomab. (B) Classic BsAbs with FC portion that requires antigen-presenting cells and activation of which results in ADCC. Example is catumaxomab. Figure created by BioRender.com (accessed on 14 May 2023). | PMC10216491 | cancers-15-02824-g002.jpg |
0.428634 | 87f0760469d442d08cb162c7f804bb9c | Techniques under investigation for targeting intracellular tumor antigens using antibodies. (A) Liposomal coating of antibodies. (B) Cell-penetrating peptides that adhere to the phospholipid bilayers. (C) Nanoparticles. (D) Cytosol-penetrating antibodies. (E) TCR-like antibodies that can target low-concentration intracellular peptide fragments that are presented to extracellular space via MHC. (F) Viral vectors that incorporate into the genome and produce intracellular antibodies. Figure created by BioRender.com (accessed on 14 May 2023). | PMC10216491 | cancers-15-02824-g003.jpg |
0.469201 | 51565a53bbfa48ee8674c858cacc8b46 | Therapeutic targets for bi- and trispecific antibodies. Figure created by BioRender.com (accessed on 14 May 2023). | PMC10216491 | cancers-15-02824-g004.jpg |
0.483364 | 12501bd445b646998bc108a18d66e06c | Structure of As-Conv. (a) Diagram of enhancement of asymmetric convolution effect; (b) Schematic diagram of As-Conv. | PMC10216973 | entropy-25-00808-g001.jpg |
0.467728 | 6761f929240b42b5ba30e9b5d995a11b | Diagram of the structure of the MSIA module. | PMC10216973 | entropy-25-00808-g002.jpg |
0.517011 | f039de07fb8d4cb6aa5eabe1994cd37e | Structure of the DPP module. | PMC10216973 | entropy-25-00808-g003.jpg |
0.428301 | 78d02d7f2b6f442cbbc3f213d8dc25ce | Structure of the SPPF module. | PMC10216973 | entropy-25-00808-g004.jpg |
0.494548 | a1bf01ce1a7a4c6c82a975527d74cc04 | Information compensation branch. | PMC10216973 | entropy-25-00808-g005.jpg |
0.435462 | d09cd741f63048318bb7a057262ed504 | Structure of CA. (Where different colors represent different weights.) | PMC10216973 | entropy-25-00808-g006.jpg |
0.493352 | a8fc9e36ac134d67a22588cbe29c4cad | Several FPN diagrams. (a) FPN; (b) PA-net; (c) LIR-FPN; (d) PCM. | PMC10216973 | entropy-25-00808-g007.jpg |
0.430575 | 75c703b20985421f818518665ea8268e | Network structure diagram for MSIA-Net. The numbers in parentheses are the numbers of modules. | PMC10216973 | entropy-25-00808-g008.jpg |
0.394191 | 8a89841320df48d5940feeb6ceeac7d5 | Bar diagram of the target instances. | PMC10216973 | entropy-25-00808-g009.jpg |
0.408514 | 7f79a712eb82447db022d9add47fb4b5 | The Mosaic data augmentation method. | PMC10216973 | entropy-25-00808-g010.jpg |
0.453864 | 99f6ec81ae584a0ea56e0f403fd71795 | Anchor boxes optimization diagram. | PMC10216973 | entropy-25-00808-g011.jpg |
0.404355 | c246be0b82ea49a28b103854c52314c9 | Decay curve of the learning rate. | PMC10216973 | entropy-25-00808-g012.jpg |
0.443368 | 13189393130f424a84390311b9446b11 | Visual detection results of the proposed MSIA-Net. (a) Infrared images and their labels; (b) model detection results. (The green triangle is the false detection result of the network.) | PMC10216973 | entropy-25-00808-g013.jpg |
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