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0.419539 | 541d5538c1b6440186ac80d9b4361b4b | CBCT images of impacted teeth before treatment(A, the sagittal image of #11. B, the sagittal image of #12. C, the sagittal image of #13. D, the sagittal image of #26. E, the coronal image of #26.) | PMC10362615 | 12903_2023_3226_Fig3_HTML.jpg |
0.406161 | 2a66822127e446869ab7197d7b56b578 | Intraoral photographs during treatment | PMC10362615 | 12903_2023_3226_Fig4_HTML.jpg |
0.45894 | 1d37d94399bd4cd0834b6870fbec5b30 | A, Initial (black), and final (red) cephalometric tracings are superimposed on the anterior cranial base. B and C, Initial (green) and final (yellow) 3D models of tracings are superimposed | PMC10362615 | 12903_2023_3226_Fig5_HTML.jpg |
0.38087 | 510799d7e967401e97200b1cf3859ce0 | Intraoral photographs of proband at one year recall | PMC10362615 | 12903_2023_3226_Fig6_HTML.jpg |
0.413155 | 86e15f6d080a41b9a7f8ce9b80124b87 | Clinical and radiographic information of the proband’ bother. (A, intraoral left view. B, panoramic radiograph. C, sagittal image of #46. D, coronal image of #46. “*” represent the PFE involved tooth. ) | PMC10362615 | 12903_2023_3226_Fig7_HTML.jpg |
0.454201 | c4146bf993f842ed8c16507328a514f4 | Clinical and radiographic information of the proband’ father. (A, intraoral right view. B, the sagittal image of 16. C, the coronal image of 16. D, intraoral left view. E, the sagittal image of #36. F, the coronal image of #36. G, panoramic radiograph. “*” represent the PFE involved tooth.) | PMC10362615 | 12903_2023_3226_Fig8_HTML.jpg |
0.422051 | 895e7249140b41afa42976eaf711bd64 | Phenotype and genetic testing results. (A, PFE-involved teeth position of the PFE patients in this family. I:1 represent the father, I:2 represent the mother, II:1 represent the brother of the proband, and II:2 represent the proband. B, pedigree of this family. C, representative electropherogram of the PTH1R sequence segregating. A double peak occurred at the black arrow, indicating that there is a normal single strand of the PTH1R gene and a mutated one. The mutations of three patients are at the same site of the electropherogram.) | PMC10362615 | 12903_2023_3226_Fig9_HTML.jpg |
0.491798 | f0e5e31ca6e24b318bda2e0bcfaa8fa5 | The schematic chart for the pipeline of the study. The data and software used in this study were in solid-line box and dashed box, respectively | PMC10362629 | 13007_2023_1048_Fig1_HTML.jpg |
0.404893 | fb512e35a1e14a6b82f4c951a3465f89 | Quantification of intron retention (IR) in an upland cotton population. a Percent spliced in (PSI) scores were calculated by taking the ratios of junctions observed over annotated splice junctions. The two examples show one intron region in two different accessions. n2 is the count of junction reads for the single intron, and n1 is the count for surrounding exons. b Pie plot showing the distribution of IR-coupled genes of TM-1 expressed genes. c IGV visualization of intron retention in two genes with different PSI scores. The red dotted box indicates the intron of interest; PSI was calculated in two accessions. d The distribution of PSI difference (PSI (max) − PSI [4]) among the population. e Principal component analysis (PCA) based on PSI scores, which shows a distinct separation of wild and cultivar groups. f Number of IR events identified for each gene. The x-axis and y-axis represent the number of IR events identified per gene and the number of genes in each group, respectively. g Box plot of Pearson’s correlation coefficient (PCC) for the PSI scores of different samples. “Same” and “diff” indicate whether the two samples are biological replicates. Boxes span the first to third quartiles and center lines indicate the second quartile (median) | PMC10362629 | 13007_2023_1048_Fig2_HTML.jpg |
0.432239 | a776da39ab3348508e52de45fcaa012a | sQTL mapping and assessment. a Scater plot showing the number of sQTLs. The x-axis and y-axis indicate the physical position of the lead SNP of the sQTL and its associated splice junction, respectively. Each dot represents a sQTL. Dots on the diagonal line indicate intrachromosomal associations. b Pie chart of cis- and trans-sQTLs. c Pie chart of IR-coupled genes with cis- and/or trans-sQTLs. d Histogramm of the sQTLs identified for each IR-coupled gene. The x-axis and y-axis represent the number of sQTLs identified for each gene and the number of genes in each group, respectively. e The density distribution of cis-sQTLs along the span between associated cis-SNP and IR splicing sites. f Significances of cis-sQTLs and trans-sQTLs. For boxplots, the lower and upper horizon lines are the minimum and maximum values of − log10 (p), respectively; the boxes span from the first to third quartiles; and the center line indicates the second quartile (median) | PMC10362629 | 13007_2023_1048_Fig3_HTML.jpg |
0.485716 | b48e284b0bba47cfa93e0b34d7a6ce38 | Relative independence in the genetic control of cis-sQTLs and cis-eQTLs. a Distribution of Pearson’s correlation values relating PSI with gene expression. Case: PCC was calculated for PSI and expression of the same gene. Control: PCC was calculated for PSI and expression of a randomly selected gene. b Venn diagram showing the overlap between genes with cis-sGenes and those with cis-eGenes. From c to e, Manhattan plots show GWAS results for splicing level [51] and overall expression level of each gene (bottom). For boxplots, the lower and upper horizon lines are minimum and maximum values, respectively; the boxes span from the first to third quartiles; and the center line indicates the second quartile (median). p-values were calculated by two-sided Student’s t-test. c Manhattan plot showing a gene (GhVTE5/GH_A05G2930) detected to have a cis-sQTL without effect on expression level. Box plots display the association of sSNP haplotype (A05:35150218; AA, GG, and AG) with splicing level as indicated by PSI score [51] and with total mRNA level (bottom). d Manhattan plot showing a gene (GhSQN /GH_A02G1850) detected to have a cis-eQTL without effect on splicing. Box plots display the association of sSNP haplotype (A02:106438154; AA, GG, and AG) with splicing level as indicated by PSI score [51] and with total mRNA level (bottom). e Manhattan plot showing a gene (GhFBP/GH_A04G1526) detected to have both a cis-sQTL and cis-eQTL. Box plots display the association of sSNP haplotype (A04:85359924; AA, GG, and AG) with splicing level as indicated by PSI score [51] and with total mRNA level (bottom) | PMC10362629 | 13007_2023_1048_Fig4_HTML.jpg |
0.421718 | 60085695df1f42a997993435c1cd849f | The IR event in GhLRRK1 (GH_A06G0890) and its association with cotton lint percentage (LP). a Manhattan plots for lint percentage (LP) based on GWAS [51] and sQTL mapping (bottom). The GWAS plot shows a signal on chromosome A06 that is associated with lint percentage, and the cis-sQTL plot a signal in GhLRRK1 (A06:23710348:23710428:clu_38722). b Local Manhattan plot [51] and LD heat map (bottom) for the sSNP (A06:23513733). The arrowhead indicates the SNP in the candidate gene. The horizontal dashed line indicates the significance threshold (p-value < 1 × 10−5). Red box shows the sSNP locus, the orange box shows the pSNP locus, the blue box shows the GhLRRK1.
c Visualization of GhLRRK1 transcript structure and genotype-specific splicing (GG, GA, and AA). The IGV screenshot [51] shows the total read numbers for each junction among individuals of different haplotypes. The structural schematic (bottom) shows the impact of IR on the GhLRRK1 protein. Retention of the 6th intron alters the predicted protein sequence and produces a premature stop codon (PTC). Red dotted box shows the IR locus. d Boxplot showing the difference of PSI explained by the haplotype (GG, GA, and AA) of sSNP A06:23513733. Boxes in box plots span from the first to third quartiles, and center lines indicate the second quartile (median). p-values were calculated by two-sided Student’s t-test. e Boxplot showing the difference in lint percentage (%) explained by the haplotype (GG, GA, and AA) of sSNP A06:23513733. Boxes in box plots span from the first to third quartiles, and center lines indicate the second quartile (median). p-values were calculated by two-sided Student’s t-test. f Transcriptomic level of GhLRRK1 in different tissues, including R (root), S (stem), and L (leaf), during ovule and fiber development, based on the FPKM values from a single experiment | PMC10362629 | 13007_2023_1048_Fig5_HTML.jpg |
0.433479 | 74f3499c61f2491ba3858f168a6cfe87 | The IR event in GhGC1 (GH_D03G1277) and its association with cotton lint percentage (LP). a Manhattan plots for LP based on GWAS [51] and sQTL mapping (bottom). Each dot represents a single SNP. The GWAS plot shows a signal on chromosome D03 that is associated with lint percentage, and the cis-sQTL plot shows a signal in GhGC1 (D03:43241915:43241985:clu_81849). b Local Manhattan plot [51] and LD heat map (bottom) for the sSNP (D03:43244243). The arrowhead indicates the SNP in the candidate gene. The horizontal dashed line indicates the significance threshold (p-value < 1 × 10−5). Red box shows the sSNP locus, the orange box shows the pSNP locus, the blue box shows the GhGC1. c Visualization of GhGC1 transcript structure and genotype-specific splicing (TT, TC, and CC). The IGV screenshot [51] shows the total read numbers for each junction among individuals of different haplotypes. The structural schematic (bottom) shows the impact of IR on the GhGC1 protein. Retention of the 1st intron alters the predicted protein sequence and produces a premature stop codon (PTC). The red dotted box shows the IR locus. d Boxplot showing the difference of PSI explained by the haplotype (TT, TC, and CC) of sSNP D03:43244243. Boxes in box plots span from the first to third quartiles, and center lines indicate the second quartile (median). p-values were calculated by two-sided Student’s t-test. e Boxplot showing the difference in lint percentage (%) explained by the haplotype (TT, TC, and CC) of sSNP D03:43244243. Boxes in box plots span from the first to third quartiles, and center lines indicate the second quartile (median). p-values were calculated by two-sided Student’s t-test. f Transcriptomic level of GhGC1 in different tissues, including R (root), S (stem), and L (leaf), during ovule and fiber development, based on the FPKM values from a single experiment | PMC10362629 | 13007_2023_1048_Fig6_HTML.jpg |
0.444914 | 7e8b4ecfd890439ca28d64b97dc8ecad | Impacts of IR on transcription factors. a Bar plot showing the number of cis-sQTL genes encoding transcription factors. b Bar plot showing the number of cis-sQTL genes belonging to different TF families. c An example of a gene (GhARF3/GH_A06G1554) with a significant cis-sQTL (A06:104984673:104984791:clu_39823) encoding an ARF transcription factor. The IGV screenshot [51] shows the total read numbers for each junction among individuals of different haplotypes, red dotted box shows the IR locus. The structural schematic (bottom) shows the impact of IR on the GhARF3 protein. For the transcript model, blue boxes indicate coding sequence, and lines indicate introns. In the bottom, protein 2 denotes the new structure produced by IR, which lacks the ARP domain present in the original protein 1. d Distribution of gene expression (left) and PSI according to haplotype (AA, AG, and GG) of sSNP A06:105487159. Data are presented as median (minimum to maximum). p-values were calculated by two-sided Student’s t-test | PMC10362629 | 13007_2023_1048_Fig7_HTML.jpg |
0.477084 | 91f700d6259541dda3838a41135d5b9f | Association of IR with miRNA-mediated regulation. a Pie plot showing the distribution of potential miRNA target sites in IR-coupled genes (left) and cis-sQTL genes [2]. b An example of the IR-coupled miRNA mechanism. GhDCL4 (GH_A05G0514) was detected to have a significant cis-sQTL (A05:4805506:4806040:clu_24377). The IGV screenshot [51] shows the total read numbers for each junction among individuals of different haplotypes, red dotted box shows the IR locus. The transcript model (bottom) shows the impact of IR on predicted miRNA targeting of GhDCL4. Blue boxes indicate the coding sequence, and lines indicate introns. Transcripts labeled “IR” are produced from intron retention. The red box indicates the predicted miRNA target site. c Distribution of PSI (left) and gene expression [2] according to haplotype (CC, CT, and TT) of sSNP A05:4938322. Boxes in box plots span from the first to third quartiles, and center lines indicate the second quartile (median). p-values were calculated by two-sided Student’s t-test | PMC10362629 | 13007_2023_1048_Fig8_HTML.jpg |
0.394259 | 2a36ddf0d7194a29ba1a74c00c778b6e | A prior pelvic hematoma segmentation algorithm correctly labeled hemorrhage in three examples with human error in manual training data (A-C). The expert missed a small volume of presacral blood in case A, inadvertently labeled a small segment of bladder wall in case B and missed a small volume of left pelvic sidewall hematoma in case C (thin arrows). The model, trained in 5-fold cross-validation, labeled these areas correctly in inference (open arrows). | PMC10362988 | fradi-03-1202412-g001.jpg |
0.423272 | 03dc9efc0a684babadaf379c2f5741a7 | Automated labeling errors. Two slices are shown for each case example, one with an error and one without. (A) Pelvic hematoma (red). Arrow (left) shows extension of label into the right pelvic sidewall, requiring minimal edits. (B) Hemoperitoneum (yellow). Arrows show extension of label into the bladder margins, requiring minimal edits. (C) Hemothorax (blue). Open arrow, image right, shows unlabeled hemothorax from beam hardening artifact requiring more substantial editing. This artifact was not appreciated for hemoperitoneum or pelvic hematoma and may be related to the comparably small number of hemothorax training cases. | PMC10362988 | fradi-03-1202412-g002.jpg |
0.457194 | 997d4c6e9741453a8cf294f4a0a0f970 | Hemothorax. The independent observer correctly classified the hemothorax label source as AI-only or expert for case A, but not for case B. Both cases received scores in the 7–9 range and were considered adequate for clinical use. | PMC10362988 | fradi-03-1202412-g003a.jpg |
0.432823 | 06a50d3d42374833833de068bc7598a0 | Hemoperitoneum. The independent observer correctly classified the hemothorax label sources in A. Both AI-only and expert labels received scores in the excellent range. In case B, hemoperitoneum in the right paracolic gutter is incompletely labeled. The observer believed this to be due to algorithm error. | PMC10362988 | fradi-03-1202412-g003b.jpg |
0.443411 | 07d3cb38a8f8487f843232e4431bfe4a | Pelvic hematoma. The independent observer correctly classified case A, but not case B. The expert annotator under-segmented blood along the right pelvic sidewall. The independent observer interpreted this as machine error. | PMC10362988 | fradi-03-1202412-g003c.jpg |
0.424242 | 45d6e573ac294469a2397ddf944829c2 | Preprocedural surface electrocardiogram. | PMC10363462 | gr1.jpg |
0.464714 | 71009a46a2044d52865e18f01b3c72f5 | Preprocedural computed tomographic (CT) images. A: Two-dimensional CT image at the level of inferior pulmonary veins. B: A posterior view of a 3-dimensional CT image. C: A modified right lateral view of a 3-dimensional CT image. LAA = left atrial appendage; LIPV = left inferior pulmonary vein; LSPV = left superior pulmonary vein; RIPV = right inferior pulmonary vein; RSPV = right superior pulmonary vein. | PMC10363462 | gr2.jpg |
0.421145 | 0366efd057b04ea6b16093a3e19ee465 | Intraprocedural fluoroscopy images and postprocedural esophageal endoscopic images. A, B: Right anterior oblique 35° views during contrast injection to the right superior pulmonary vein (A) and right inferior pulmonary vein (B). C, D: Left anterior oblique 45° views during contrast injection to the left superior pulmonary vein (C) and left inferior pulmonary vein (D). E: An esophageal endoscopic image obtained 2 days after the procedure. F: An image obtained 1 week after the procedure. No abnormal finding was observed in the esophageal mucosa in both images. | PMC10363462 | gr3.jpg |
0.374585 | 3fe81f22cd234c99bbe31752be73a79e | PV Solar energy demand. The data obtained for the solar PV system for the year round is tabulated in Table 1 | PMC10365978 | gr1.jpg |
0.374458 | b14d07dfa9114020b7b7dae8f28a2922 | SMA Controller data measurement. | PMC10365978 | gr10.jpg |
0.421965 | 9cd1b38cecf8458288e23754183a0909 | Overall system structure. | PMC10365978 | gr11.jpg |
0.485634 | c4f4af0c9b6f406f8cf5900c7b74de1a | Carbon emission savings. | PMC10365978 | gr2.jpg |
0.385794 | 80625fbf36a946009dc2f9a7be707b02 | Diesel engine energy demand. | PMC10365978 | gr3.jpg |
0.444459 | e5f14bcf6c764dd9b1ad14d0ec9d58f6 | public utility energy demand. | PMC10365978 | gr4.jpg |
0.430898 | f27399d7866443ad957acf9fc2109e7b | Synchronized diesel generators. | PMC10365978 | gr5.jpg |
0.457872 | f749be0a64854a11ab7b6246f6ca4fee | Arial view of the roof-top PV solar system. | PMC10365978 | gr6.jpg |
0.512256 | 56bad5d59192449ca6376417f84e1b44 | Public utility energy grid. | PMC10365978 | gr7.jpg |
0.462634 | 427591587c3648b59b676b94f4fb15dc | The combiner system. | PMC10365978 | gr8.jpg |
0.372564 | 69571ff106e24608936f2bf623fe3326 | Data measurement for the three sources of energy. | PMC10365978 | gr9.jpg |
0.432074 | b05f97384a9b4cb180aa5b26d8d2a139 | Scheme depicting some key activities within the T04247750 clinical trial (A), along with the timing of SARS-CoV-2 vaccination (orange triangles) and blood sampling (yellow arrows) considered in this report. The large longitudinal arrow in panel A identifies the sirolimus treatment that usually started 20 days after the administration of the second dose of the mRNA-1273 (Moderna) vaccine. (B) HPLC analysis of the hemoglobins of EPO-cultured ErPCs isolated from the sirolimus-treated patient at V6 (left side of panel (B)) and V8 (right side of panel (B)) and cultured as described by Zuccato et al. [19] and by Gamberini et al. [32]. | PMC10366771 | hematolrep-15-00044-g001.jpg |
0.43181 | c952c94381844a47bad405b0c0f4c25a | Humoral immune response (AU/mL) quantifying the anti-SARS-CoV-2 IgG at BS1, BS2, BS3, and BS4. The days from mRNA-1273 (Moderna) dose #2 (BS1 and BS2) and booster dose #3 (BS3 and BS4) are indicated in parenthesis. A blood sampling was programmed (BS0) just before the vaccination in order to exclude SARS-CoV-2 infection. Two blood samplings (BS1 and BS2) were programmed after 30–50 (BS1) and 150–200 (BS2) days from BNT162b2 dose #2. Two blood samplings (BS3 and BS4) were programmed after 30–50 (BS3) and 110–160 (BS4) days from BNT162b2 booster dose #3. | PMC10366771 | hematolrep-15-00044-g002.jpg |
0.385731 | c64c7c3d543c46edb68ac59e3668fb69 | Three key networks involved in goal-directed behaviour and planning which are affected by apathy in Alzheimer’s disease. PFC: Prefrontal Cortex. | PMC10366907 | geriatrics-08-00075-g001.jpg |
0.474478 | 0cb8f7ecbbda4a5aad7ca8a87b698c1c | Illustration of the four major central dopaminergic modulatory systems. ACC: Anterior Cingulate Cortex. DLPFC: Dorsolateral Prefrontal Cortex. | PMC10366907 | geriatrics-08-00075-g002.jpg |
0.463645 | 1e237caa13af4ce6a5b6d0acd7e45c45 | Illustration of the locus coeruleus-noradrenaline central modulatory system. | PMC10366907 | geriatrics-08-00075-g003.jpg |
0.443238 | c823da8694b643b4b3be4595a83add11 | Effect of liraglutide on Biochemical parameters: (A–I). (A) FBG, (B) serum insulin, (C) BMI, (D) HbA1c, (E) HOMA-IR, (F) TAG, (G) TC, (H) HDL, (I) LDL and (J) Cumulative body weight change. Data are expressed as means ± SEM. N = 8. *, **, ***, **** indicate significant difference (p < 0.05, p < 0.01, and p < 0.001). | PMC10367011 | fphar-14-1224985-g001.jpg |
0.490134 | 6165ca8ed14a4cbe87aee6457b076f94 | Effect of liraglutide on Inflammatory mediators and oxidative stress markers: (A–D). (A) TNFα, (B) IL6, (C) MDA, and (D) GSH. Data are expressed as means ± SEM. N = 8. *, **, *** indicate significant difference (p < 0.05, p < 0.01, and p < 0.001). | PMC10367011 | fphar-14-1224985-g002.jpg |
0.383141 | 92bde9d8b9e24ce99f48a949cc6b4e9d | Effect of liraglutide on Hormonal profile: (A–C). (A) total testosterone, (B) FSH, and (C) LH. Data are expressed as means ± SEM. N = 8. *, **, *** indicate significant difference (p < 0.05, p < 0.01, and p < 0.001). and 3.4. H&E stain histological results. | PMC10367011 | fphar-14-1224985-g003.jpg |
0.441107 | b3a43c7eeebb46e9bd2adf1e520baa89 | H&E staining of testicular tissues of control, STZ rats, and STZ rats treated with liraglutide (A–H). (A) A stained section in the control group: shows closely packed seminiferous tubules (st) which are lined by spermatogenic epithelium and have patent lumina (L). The tubules are separated from each other by interstitial connective tissue (arrowhead) containing the Leydig cells (Ic); (B) stained section in the control group: higher magnification of the squared area of the figure (a) shows different stages of spermatogenic cells in the form of spermatogonia (sp.g), primary spermatocytes (sp.c.1), secondary spermatocytes (sp.c.2), spermatids and sperms (sp). Sertoli cells with their large pale nuclei were noticed in between (se.c). The tubules were ensheathed by a well-defined basement membrane and connective tissue (arrowhead) containing flattened myoid cells with flattened nuclei (mc). Clusters of Leydig cells (Ic) are seen in the interstitial tissue; (C) Stained section in the diabetic group: shows irregular contour (thick arrow) of seminiferous tubules, vacuolated germinal epithelial cells (star), and damaged, disorganized tubules (st*); (D) Stained section in the diabetic group: higher magnification of the squared area of figure (C) shows homogenous eosinophilic exudate (ex) with vacuolation (bent arrow) in the interstitium. Large empty spaces are seen between spermatogenic cells (star), which appear disorganized with detached cells (zigzag arrow) and pyknotic nuclei (arrow). Sperm flagella are hardly noticed in the lumens of seminiferous tubules (sp*); (E,F) Other fields of rat testicular tissue sections in the diabetic group: show parts of the tubules with thin detached basal lamina (curved arrow) and depleted of most of the spermatogenic cells with large empty spaces in between the cells (star) are seen. Many germ cells are detached (zigzag arrow), and shrunken with pyknotic nuclei (arrow). Sperm flagella are hardly noticed in the lumen of seminiferous tubules (sp*). Large homogenous eosinophilic exudate (ex) with vacuolation (bent arrow) is seen in the interstitium; (G) Stained section in diabetic + liraglutide group: shows most of the seminiferous tubules (st) restore the normal architecture, their regular wall (arrowhead) is formed of nearly normally arranged germinal epithelium. Most of their lumina (L) contained aggregation of sperms, and a few seminiferous tubules were still disorganized and damaged (st*). Interstitium in-between the tubules show normal width except for little homogenous vacuolated eosinophilic material between a few tubules (thick arrow); (H) Stained section in diabetic + liraglutide group: higher magnification of the squared area of figure (G) exhibits different stages of spermatogenic cells resting on regular basal lamina (arrowhead), in the form of spermatogonia (sp.g), primary spermatocytes (sp.c.1), secondary spermatocytes (sp.c.2), spermatids and sperms (sp). Leydig cells (Ic) are noticed in the interstitial connective tissue. | PMC10367011 | fphar-14-1224985-g004.jpg |
0.446502 | c5850a97e6e84609a653836c4dfcb360 | Immunohistochemical staining of testicular tissues of control, STZ rats, and STZ rats treated with liraglutide (A–T). (A) Testicular immunohistochemical stained sections of Nrf2 in control groups Scale bar = 200 μm, x100, (B) Testicular immunohistochemical stained sections of Nrf2 in Diabetic group Scale bar = 200 μm, x100, (C) Testicular immunohistochemical stained sections of Nrf2 in Diabetic + liraglutide group Scale bar = 200 μm, x100, (D) Immunostaining intensity of testicular Nrf2 (% area), (E) Testicular immunohistochemical stained sections of TNFα in control groups Scale bar = 200 μm, x100, (F) Testicular immunohistochemical stained sections of TNFα in Diabetic group Scale bar = 200 μm, x100, (G) Testicular immunohistochemical stained sections of TNFα in Diabetic + liraglutide group Scale bar = 200 μm, x100, (H) Immunostaining intensity of testicular TNFα (% area), (I) Testicular immunohistochemical stained sections of Ki67 in control groups Scale bar = 200 μm, x100, (J) Testicular immunohistochemical stained sections of Ki67 in Diabetic group Scale bar = 200 μm, x100, (K) Testicular immunohistochemical stained sections of Ki67 in Diabetic + liraglutide group Scale bar = 200 μm, x100, (L) Immunostaining intensity of testicular Ki67 (% area), (M) Testicular immunohistochemical stained sections of Kisspeptin in control groups Scale bar = 200 μm, x100, (N) Testicular immunohistochemical stained sections of Kisspeptin in Diabetic group Scale bar = 200 μm, x100, (O) Testicular immunohistochemical stained sections of Kisspeptin in Diabetic + liraglutide group Scale bar = 200 μm, x100, (P) Immunostaining intensity of testicular Kisspeptin (% area), (Q) Testicular immunohistochemical stained sections of androgen receptors in control groups Scale bar = 200 μm, x100, (R) Testicular immunohistochemical stained sections of androgen receptors in Diabetic group Scale bar = 200 μm, x100, (S) Testicular immunohistochemical stained sections of androgen receptors in Diabetic + liraglutide group Scale bar = 200 μm, x100, (T) Immunostaining intensity of testicular androgen receptors (% area), Data are expressed as means ± SEM. *, **, *** indicate significant difference (p < 0.05, p < 0.01, and p < 0.001). | PMC10367011 | fphar-14-1224985-g005.jpg |
0.440879 | bb64ed74b5a7446db82589322934964a | Effect of liraglutide on Hypothalamic and Pituitary expression of GLP-1/leptin/kiss1/GnRH pathway (A–J). (A) GLP-1R, (B) PGC-1α, (C) PPAR-α, (D) leptin, (E) leptin R, (F) kiss, (G) kiss1R, (H) GnRH, (I) GnRHr, and (J) GnIH. Data are expressed as means ± SEM. *, **, *** indicate significant difference (p < 0.05, p < 0.01, and p < 0.001). | PMC10367011 | fphar-14-1224985-g006.jpg |
0.448511 | 13b8bfb1886b46058b1f0b6c4676ec6e | Effect of liraglutide on Testicular expression of GLP-1/kiss1 and steroidogenesis pathway (A–J). (A) GLP-1R, (B) PGC-1α, (C) PPAR-α, (D) kiss1, (E) kiss1R, (F) STAR, (G) CYP11A1, (H) CYP17A1, (I) HSD17B3, and (J) CYP19A1. Data are expressed as means ± SEM. *, **, *** indicate significant difference (p < 0.05, p < 0.01, and p < 0.001). | PMC10367011 | fphar-14-1224985-g007.jpg |
0.50992 | a241939c78334f578c8197209e9caa4b | Effect of liraglutide on Testicular expression of TGF- β/Smad pathway (A–C). (A) TGF- β, (B) Smad2, and (C) Smad7. Data are expressed as means ± SEM. *, **, ***indicate significant difference (p < 0.05, p < 0.01, and p < 0.001). | PMC10367011 | fphar-14-1224985-g008.jpg |
0.433577 | 5c0c4b189e8949dcaf780e65180aaa61 | Pathogenesis of nasopharyngeal carcinoma. Genetically susceptible nasopharyngeal epithelial cells undergo malignant transformation upon acquisition of persistent latent Epstein-Barr virus infection and exposure to environmental carcinogens, which enable cellular transformation and clonal expansion. The figure was created with BioRender. LMP1/2, latent membrane protein 1/2; BARF1, BamH1-A right frame 1; EBNA, Epstein-Barr nuclear antigen 1; MHC, major histocompatibility complex. | PMC10367053 | IJO-63-2-05545-g00.jpg |
0.533491 | f09f19f56d9948febe6b7b7422463381 | Treatment for NPC. Conventional treatment for nasopharyngeal carcinoma includes radiotherapy, chemotherapy, surgery and targeted therapy. Immunotherapy has emerged as a new strategy for the treatment of advanced NPC in recent years. The figure was created with BioRender. NPC, nasopharyngeal carcinoma. | PMC10367053 | IJO-63-2-05545-g01.jpg |
0.474326 | 034c18f22e8545ed9719821ac623ad07 | Classification of immunotherapy for NPC. NPC, nasopharyngeal carcinoma; EBV, Epstein-Barr virus; PD-1, programmed cell death protein-1; PD-L1, programmed death ligand-1; CTLA-4, cytotoxic T-lymphocyte-associated antigen-4; LAG-3, Lymphocyte activation gene-3; TIM-3, T-cell immunoglobulin- and mucin-domain-containing molecule-3; CTL, cytotoxic T lymphocytes; TIL, tumor-infiltrating lymphocytes; CIK, cytokine-induced killer; NK, natural killer; CAR-T, chimeric antigen receptor-modified T; TCR-T, T-cell receptor-engineered T. | PMC10367053 | IJO-63-2-05545-g02.jpg |
0.402728 | 53d223f054734634a625f0a9c6fc020f | Mechanism of (A) immune checkpoint inhibitors (CTLA-4, PD-1 and PD-L1 inhibitors) and (B) adoptive cell transfer of cytotoxic T lymphocytes. The figure was created with BioRender. MHC, major histocompatibility complex; TCR, T-cell receptor; CTLA-4, cytotoxic T-lymphocyte-associated antigen-4; PD-1, programmed cell death protein-1; PD-L1, programmed death ligand-1; EBV, Epstein-Barr virus; LCL, lymphoblastoid B-cell line; CTLs, cytotoxic T-lymphocytes; PBMCs, peripheral blood mononuclear cells. | PMC10367053 | IJO-63-2-05545-g03.jpg |
0.43497 | 0bcd180fbfca42a296de1942814855e9 | Immunofluorescent images for Tuj-1 (A-1), NF200 (B-1) and CS56 (C-1) at the lesion sites of the control group and NGP group, Left: scale bars = 500 μm. Right: scale bars = 20 μm. Percentage of Tuj-1 (A-2), NF200 (B-2) and CS56 (C-2) positive area in each group, *P < 0.05, error bars represent standard deviation for n = 3 | PMC10367392 | 13036_2023_368_Fig10_HTML.jpg |
0.47283 | bd5f5b944f6d4863a8584b50eb21db79 |
A Images of the SAO and NGP solutions and the NGP hydrogels. B Adhesion of NGP hydrogels to spinal cord tissue. (A) FITR spectra of NH2-Gelatin, NH2-Gelatin-PANI, SAO and NGP hydrogels. D SEM images of NGP hydrogels, scale bar lengths are 100 μm | PMC10367392 | 13036_2023_368_Fig1_HTML.jpg |
0.397362 | 49aaf23188c24877a611ec7e96b2d027 |
A The display of the self-healing ability of NGP hydrogels. B The electrical conductivity results of NGP hydrogels | PMC10367392 | 13036_2023_368_Fig2_HTML.jpg |
0.446549 | 06a2056c7f8a47829618879219dde0e3 |
A In vivo degradation images of NGP hydrogels at different time points. B Effect of NGP hydrogel on surrounding skin tissue after subcutaneous implantation, a: Normal mice b: 4 days c: 8 days d: 16 days, scale bar lengths are 200 μm | PMC10367392 | 13036_2023_368_Fig3_HTML.jpg |
0.461082 | 147beb52ac254ec0b35dfa239be3727e | In vitro drug (DPL) release of the NGP hydrogel over 8 days; error bars represent the standard deviation for n = 3 | PMC10367392 | 13036_2023_368_Fig4_HTML.jpg |
0.519092 | ef2bdac9fb57444496803e0de764873f |
A Morphology of NSCs under a light microscope. Left: ruler: 200 μm; right: ruler: 100 μm. B Nestin immunofluorescence identification of NSCs. C Live and dead cell staining of NSCs on NGP hydrogels; scale bar lengths are 100 μm. D Cell proliferation of NSCs cultured in the control, NGP, DPL and NGP + DPL groups, *P < 0.05, error bars represent the standard deviation for n = 3 | PMC10367392 | 13036_2023_368_Fig5_HTML.jpg |
0.443089 | 2182757e8f344202be102a7e8ddd013d | Quantitative real-time PCR analysis of Tuj-1, OSP and GFAP expression in NSCs seeded in different groups. *P < 0.05, error bars represent standard deviation for n = 4 | PMC10367392 | 13036_2023_368_Fig6_HTML.jpg |
0.405681 | 55e94af063754242b2752ae6397e5639 |
A Immunofluorescent images for Tuj-1, OSP and GFAP expression by NSCs seeded on different groups. DAPI staining for nuclei (blue) and Cy3-conjugated secondary antibody for protein (red), scale bar lengths are 50 μm. B Axon length of new neurons and the proportion of new neurons, oligodendrocytes and astrocytes in each group, P < 0.05, error bars represent standard deviation for n = 3 | PMC10367392 | 13036_2023_368_Fig7_HTML.jpg |
0.435496 | 480aec0aea8f4e1e873804df7c60f73e |
A BBB scores of different treatment groups at ten weeks postinjury. B The results of MEP amplitude measurement in each group. C Electromyography of rats in each experimental group. *P < 0.05, error bars represent standard deviation for n = 6 | PMC10367392 | 13036_2023_368_Fig8_HTML.jpg |
0.396967 | 3c2cc74b75fb4680a4adcc7917921e54 |
A Image of spinal tissue specimen. B H&E staining of spinal cord tissues in different groups; scale bar lengths are 1000 μm. C LFB staining of spinal cord tissue in different groups, Left: scale bars = 500 μm; right: scale bars = 50 μm. D Semiquantitative analysis of the cystic cavity area in different groups, *P < 0.05, error bars represent standard deviation for n = 3. E Semiquantitative analysis of the LFB staining area in different groups, *P < 0.05, error bars represent standard deviation for n = 3 | PMC10367392 | 13036_2023_368_Fig9_HTML.jpg |
0.536374 | 5f5ffa1e688c4e6185252e1225b1b3d2 | A brief schematic drawing of the application of NSCs and DPL-loaded NGP hydrogels for SCI repair | PMC10367392 | 13036_2023_368_Sch1_HTML.jpg |
0.428561 | 23735f7805824accb1fa70cd4f0a2097 | Study Schema. Representative schematic of patients with PAH in the EXPEDITE study who initiated parenteral treprostinil and transitioned to oral treprostinil at Week 8. Transition could occur at Week 2, 4, or 8. The mean (SD) duration of parenteral treprostinil exposure, which includes the parenteral treprostinil induction and the cross‐titration phases, was 55 (13) days. Post‐transition visit occurred 1−2 weeks after the transition visit. The mean (SD) duration of oral treprostinil exposure, which includes the cross‐titration and oral treprostinil optimization phases, was 64 (16) days. | PMC10368085 | PUL2-13-e12255-g001.jpg |
0.416067 | d5a91ee02ae94b6292041b633c1f0fd1 | Parenteral Treprostinil Induction. Median (Q1, Q3) parenteral treprostinil dose during EXPEDITE study at Baseline, Week 2, 4, and 8. Clinicians were instructed to initiate parenteral treprostinil at 2 ng/kg/min SC or IV at the Baseline visit in an inpatient or outpatient setting. Clinicians chose the frequency and dose increments for up‐titration with a goal to improve PAH symptomology. In the EXPEDITE study, SC up‐titration of parenteral treprostinil results in higher doses at a faster rate than IV up‐titration. *IV = intravenous, SC = subcutaneous † One patient transitioned at Week 2, four patients transitioned at Week 4, and 14 patients transitioned at Week 8. ‡ One patient transitioned at Week 4, and nine patients transitioned at Week 8. No patients transitioned at Week 2. | PMC10368085 | PUL2-13-e12255-g002.jpg |
0.400392 | 5a1211646e264c9cac0104204659d6b4 | Representative Inpatient Transition Dosing Schedule. For inpatient patients who transitioned from parenteral treprostinil to oral treprostinil, the median parenteral treprostinil dose at transition was 30 ng/kg/min. Inpatient patients gradually discontinued parenteral treprostinil over 1‐2 days while increasing oral treprostinil to the target dosage. Here, the target dose of oral treprostinil is 6 mg TDD for a patient weighing 70 kg, based on oral treprostinil total daily dose (mg) = 0.0072 x parenteral treprostinil daily dose (ng/kg/min) x weight (kg). *AM, morning; PM, afternoon; HS, evening, TDD, total daily dose. | PMC10368085 | PUL2-13-e12255-g003.jpg |
0.386199 | 09626905453a45118d62046493d0e1f0 | Dosing Conversion Steps (with an example). Use the following formula to estimate a target total daily dose of oral treprostinil in mg using a patient's dose of intravenous (IV)/subcutaneous (SC) treprostinil (in ng/kg/min) and weight (in kg)(6). | PMC10368085 | PUL2-13-e12255-g004.jpg |
0.445133 | 39ab4b54b3d94140861bd725827fb3bd | Representative Outpatient Transition Dosing Schedule. For outpatient patients who transitioned from parenteral treprostinil to oral treprostinil, the median parenteral treprostinil dose at transition was 22 ng/kg/min. Outpatient patients gradually discontinued parenteral treprostinil over 5 days while increasing oral treprostinil to the target dosage. Here, the target total daily dose of oral treprostinil is 12.625 mg for a patient weighing 70 kg, based on oral treprostinil total daily dose (mg) = 0.0072 x parenteral treprostinil daily dose (ng/kg/min) x weight (kg). *AM, morning, PM, afternoon, HS, evening, TDD, total daily dose. | PMC10368085 | PUL2-13-e12255-g005.jpg |
0.397871 | 49f713f916e14a2fb2d13d1ce8b515f5 | Patient Disposition in Phase-I Study on Flubentylosin. | PMC10368248 | pntd.0011392.g001.jpg |
0.520306 | ee284c0501564f02ada5f66823af43c1 | Mean Blood Flubentylosin Concentrations Versus Time Profiles after Single Oral Administration of Ascending Doses from 40 mg to 1000 mg (Part 1), Linear (top) and Log-linear (bottom) Scales. | PMC10368248 | pntd.0011392.g002.jpg |
0.47097 | c3d919b3ff754a02bb69c9e7f516c296 | Mean Dose-normalized Cmax and AUC of Flubentylosin after Single Oral Administration of Ascending Doses from 40 mg to 1000 mg (Part 1). | PMC10368248 | pntd.0011392.g003.jpg |
0.516234 | c99b5a9984c84035868fdb244146b402 | Mean Blood Flubentylosin Concentrations versus Time Profiles after Administration of Flubentylosin 1000 mg under Fasting and Fed Conditions in Part 2 (Food Effect), Linear (top) and Log-linear (bottom) Scales. | PMC10368248 | pntd.0011392.g004.jpg |
0.556175 | 0ebb240a260647d1a7cd6e718e13a4b1 | Mean Blood Flubentylosin Concentrations versus Time Profiles after Administration of Multiple Ascending Doses of Flubentylosin in Part 3 (Upper Panels Linear Scale—Lower Panels Log-Linear Scale) | PMC10368248 | pntd.0011392.g005.jpg |
0.461306 | 05f163dfa1b942459c2568b0337dbcbb | (A) Red blood cell distribution width (RDW) by outcome. All comparisons between means of each binary outcome were significant by Wilcoxon signed-rank test (P < 2e−16, denoted by ****). (B) RDW by outcomes by age group. All comparisons between means within each of the 3 age groups were significant by Wilcoxon signed-rank test, with all but Floor versus ICU for age <45 (P = 3e−4) and Floor versus ICU for age 45–65 (P = 1.3e−13) achieving P < 2e−16. Elevated RDW, as defined by the healthcare system (>15.5), is shown by the red dotted line. Thick line represents the median; box represents the interquartile range (IQR); and whiskers represent the 1.5 × IQR from the first and third quartile. | PMC10368803 | ooad053f1.jpg |
0.397879 | e064ebcda65a46b7aadd89e0f273dc96 | Red blood cell distribution width (RDW) by final diagnosis. (A) Ten diagnoses with the highest mean RDW. (B) Ten most frequent diagnoses. (C) Preselected diagnoses of interest. The mean RDW by outcome for every diagnosis category, as well as its standard deviation and P-value for difference across outcomes, is available in Supplementary Table S1. | PMC10368803 | ooad053f2.jpg |
0.386008 | 9fc1cce1dde741089301cd34f9007502 | (A) Variables with highest scaled weights by absolute value in logistic regression (LR) model predicting admission. Positive weights are shown in blue, negative in red. Medical conditions represent comorbidities, not final diagnoses. (B) Variables with highest scaled weights by absolute value in LR model predicting in-hospital mortality. (C) Variables with highest information gain in XGBoost model predicting admission. (D) Variables with highest information gain in XGBoost model predicting in-hospital mortality. 95% confidence intervals are shown by gray bars. ADHD: attention-deficit/hyperactivity disorder; BMI: body mass index; BP: blood pressure; BUN: blood urea nitrogen; MCHC: mean corpuscular hemoglobin concentration; MCV: mean corpuscular volume; MI: myocardial infarction; PTSD: post-traumatic stress disorder; RDW: red blood cell distribution width; WBC: white blood cell count. | PMC10368803 | ooad053f3.jpg |
0.407747 | 0c11c228cdf140869cc73e7b51a0916b | Flowchart of included and excluded patients and the matching process. ACLR, anterior cruciate ligament reconstruction; IB, internal brace. | PMC10369099 | 10.1177_23259671231178026-fig1.jpg |
0.487707 | 56df75ca2be348d3b62557bcabb9f693 | An intraoperative photograph of an all–soft tissue quadriceps tendon autograft prepared for both proximal and distal suspensory fixation with additional independent internal brace augmentation. The pull suture (white arrow) is used to pass the femoral cortical button (black arrowhead) through the femoral socket. The femoral shortening strands (black arrow) are used for docking the graft into the socket and retensioning the graft proximally to achieve final graft fixation. The internal brace is passed through 2 holes on the femoral button where it then runs parallel to the graft (asterisks). A nitinol wire (not pictured) is used to pass the internal brace under 1 suture on the graft both proximally and distally on both sides (white arrowheads). | PMC10369099 | 10.1177_23259671231178026-fig2.jpg |
0.503974 | 9364eff795dd41c1bfa36f25927c64be | Intraoperative arthroscopic views of a right knee from the anterolateral portal of 2 quadriceps tendon autografts at 60° of flexion with internal brace augmentation (asterisk). | PMC10369099 | 10.1177_23259671231178026-fig3.jpg |
0.508132 | 0ca22d596eb84a0daa474d0bae194296 | Kaplan-Meier survival curve for the available time frame. Censored data are denoted by a plus (+) symbol. | PMC10369099 | 10.1177_23259671231178026-fig4.jpg |
0.427452 | 1ff5434680bb4c4faa92b2b156a5e7e2 | Flow chart of study participants. | PMC10369353 | fendo-14-1232618-g001.jpg |
0.39153 | ed861b48d42143769714f03f7e7483ea | Effect of terminal drought stress on (A) Ci (B) Pn of studied chickpea genotypes, where Ci and Pn indicate internal CO2 concentration and photosynthesis rate, respectively. | PMC10302310 | life-13-01405-g002.jpg |
0.382638 | 0de09e77c8104b64a21b6ac36281d0d7 | Effect of terminal drought stress on (A) gs and (B) Tr of studied chickpea genotypes, where gs and Tr indicate stomatal conductance and transpiration rate, respectively. | PMC10302310 | life-13-01405-g003.jpg |
0.374606 | eaaf0868fa0e4771a23c988b4f7a780d | Effect of terminal drought stress on (A) Chl a and (B) Chl b content of studied chickpea genotypes, where Chl a and Chl b indicate chlorophyll a and chlorophyll b, respectively. | PMC10302310 | life-13-01405-g004.jpg |
0.380912 | 46323c8d0705445c85be374bf3de1496 | Effect of terminal drought stress on (A) protein content and (B) H2O2 content of studied chickpea genotypes, where H2O2 indicates hydrogen peroxide. | PMC10302310 | life-13-01405-g005.jpg |
0.390796 | 6ab63a83c35848bd823a1902b7249490 | Effect of terminal drought stress on (A) EL (%) and (B) MDA content of studied chickpea genotypes, where EL and MDA indicate electrolyte leakage and malondialdehyde, respectively. | PMC10302310 | life-13-01405-g006.jpg |
0.370601 | e60263a272de4f1dad310df088f7de62 | Effect of terminal drought stress on (A) TSS content and (B) proline content of studied chickpea genotypes, where TSS indicates total soluble sugar. | PMC10302310 | life-13-01405-g007.jpg |
0.383264 | ffa38cd21cc448578bd08f91aaa30f40 | Effect of terminal drought stress on (A) SOD and (B) POD activity of studied chickpea genotypes, where SOD and POD indicate superoxide dismutase and peroxidise. | PMC10302310 | life-13-01405-g008.jpg |
0.443411 | c5c885fb392e41cb92e5cdac576f5f0d | Effect of terminal drought stress on (A) CAT and (B) APX activity of studied chickpea genotypes, where CAT and APX indicate catalase and ascorbate peroxidise, respectively. | PMC10302310 | life-13-01405-g009.jpg |
0.417831 | 65d2de4de4b44381bc8858d6b7b7d2f3 | Effect of terminal drought stress on (A) DTF and (B) DTM of studied chickpea genotypes, where DTF and DTM indicate days to 50% flowering and days to maturity, respectively. | PMC10302310 | life-13-01405-g010.jpg |
0.420021 | 0f0cc3187abe4a52af0da254d14e1a29 | Effect of terminal drought stress on (A) NOP and (B) SYPP of studied chickpea genotypes, where NOP and SYPP indicate number of pods and seed yield per plant, respectively. | PMC10302310 | life-13-01405-g011.jpg |
0.430971 | f05cc2b9b5124798b93b2a6210daccd2 | Effect of terminal drought stress on (A) BYPP and (B) HI (%) of studied chickpea genotypes, where BYPP and HI indicate biological yield per plant and harvest index, respectively. | PMC10302310 | life-13-01405-g012.jpg |
0.492585 | dbb9f17ecd354c00baa3680b31b51618 | PCA biplots depicting (A) relationships between the traits measured, (B) performance of chickpea genotypes, and (C) combined (A + B) under terminal drought stressed condition. In the active variables, RWC, CTD, Ci, Pn, gs, Tr, Chla, Chlb, EL, MDA, H2O2, SOD, POD, APX, DTF, DTM, NOP, SY, BY, and HI indicate the relative water content, canopy temperature depression, internal CO2 concentration, photosynthesis rate, stomatal conductance, transpiration rate, chlorophyll a, chlorophyll b, electrolyte leakage, malondialdehyde, hydrogen peroxide, superoxide dismutase, peroxidase, ascorbate peroxidase, days to 50% flowering, days to maturity, number of pods, seed yield, biological yield and harvest index, respectively. | PMC10302310 | life-13-01405-g013.jpg |
0.531866 | 28373b249e6844bebaf73a7ebf5614c9 | Agglomerative clustering of studied chickpea genotypes under terminal drought-stressed condition. | PMC10302310 | life-13-01405-g014.jpg |
0.539198 | 82ee5de2e90d4d748ea18086ae3599f0 | The constructive shape of the steel die tool used in the experiment. | PMC10302561 | materials-16-04240-g001.jpg |
0.52065 | 594bbe05e1ab48edb4a0565c0f87bef3 | The sintering regimes for Ti-xNb-10Zr with low and high porosities. | PMC10302561 | materials-16-04240-g002.jpg |
0.430967 | 9d4aefdb532d4206a14e36963c38b392 | General porosity results of the alloys. | PMC10302561 | materials-16-04240-g003.jpg |
0.468062 | 3b5ca0c916664760863547fe9b4a163b | X-ray diffraction spectra for (a) Ti-xNb-10Zr (x: 10 and 20; at. %) with low porosities; (b) Ti-xNb-10Zr (x: 10 and 20; at. %) with high porosities. | PMC10302561 | materials-16-04240-g004.jpg |
0.424586 | 6a31416482a942daaae85735ac32f5de | EDS analysis showing SEM micrograph and EDS points for (a) Ti-10Nb-10Zr with low porosity; (b) Ti-20Nb-10Zr with low porosity. | PMC10302561 | materials-16-04240-g005.jpg |
0.405962 | 2a2f7cdb0e19454f8ac3392947438dbd | SEM micrographs for (a)Ti-10Nb-10Zr with low porosity, (b) Ti-10Nb-10Zr with high porosity, (c) Ti-20Nb-10Zr with low porosity, and (d) Ti-20Nb-10Zr with high porosity. | PMC10302561 | materials-16-04240-g006.jpg |
0.435805 | c73afb1119404b4b9467aa38c4656b33 | EBSD data showing the microstructure (IQ map), grain morphology (IPF map), and phase constituents and distribution (Phase map) for both Ti-10Nb-10Zr alloy and Ti-20Nb-10Zr alloy: (a,d) IQ map; (b,e) IPF map; (c,f) Phase map. | PMC10302561 | materials-16-04240-g007.jpg |
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