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0.42179 | 8aa42827c76c49b3ab73f8345bf77197 | Protein network of the differentially expressed genes (red), showing the main proteins with which, they interact. There were proteins that were present more than once (blue) among these groups of networks. The networks were obtained from the STRING database based on the functional enrichment analysis of the protein–protein interaction networks. | PMC9854435 | animals-13-00308-g004.jpg |
0.412496 | d0b713bb00a8483ebd14335e14ba5faf | Pathways of the innate and adaptative immune system that contain genes that were differentially expressed by the acute physical exercise in horses. (A) The Th1 and Th2 cell differentiation signaling pathways, which are mainly driven by cytokines IL2 and IL4, respectively. (B) The NF-kappa B signaling pathway, which is considered as a regulator of innate immunity and links pathogenic signals and cellular danger signals, thus organizing cellular resistance to invading pathogens. (C) The chemokine signaling pathway, which is associated with the activation, differentiation, and migration of immune cells [13]. | PMC9854435 | animals-13-00308-g005.jpg |
0.49776 | d8e6cf44cfc947658d27f8ec10f817f3 | Historical potential prices and official housing prices. Note: The solid line in this figure shows the estimated historical potential price of the samples, and the dotted line shows second-hand housing price from the Beijing Bureau of Statistics. The base period for both curves is the first quarter of 2012. | PMC9854462 | behavsci-13-00055-g001.jpg |
0.460018 | adf0d1e2e2724892a38e7c2191a8354e | Systematic screening stages of literature review on Opuntia humifusa (OH). | PMC9854510 | antioxidants-12-00174-g001.jpg |
0.470389 | 0631c881ce224f038b3facd56b5e6b43 | Risk of bias in individual studies graph. | PMC9854510 | antioxidants-12-00174-g002.jpg |
0.450927 | 77789c2c54704425a0c47af20d22b52a | Comparison of reducing skin-aging signal between OH treatment and control groups [5,19,20,21]. | PMC9854510 | antioxidants-12-00174-g003.jpg |
0.419551 | 20277918d1af45cd81904891b3d54018 | Comparisons of inhibiting the growth of cancer between OH treatment and control groups [6,7,15,21,22,23,24,25,26]. | PMC9854510 | antioxidants-12-00174-g004.jpg |
0.371226 | 9831863c78ef447aaf0e5d989cce63ea | Comparisons of inhibiting the development of diabetes between OH treatment and control groups [9,11,13]. | PMC9854510 | antioxidants-12-00174-g005.jpg |
0.480115 | 9b8fa7512d9a45d1bc075a23d7767c26 | Subgroup analysis for the reduction of cancer cell proliferation based on four sub-criteria: raw materials, extraction methods, types of cancer cell lines, and concentrations of OH treatment. | PMC9854510 | antioxidants-12-00174-g006.jpg |
0.451338 | 53e82322d06a4c7cb961b36671c3f4f2 | Publication bias of included studies for the effectiveness of using OH for the treatment of skin aging, cancer, and diabetes. | PMC9854510 | antioxidants-12-00174-g007.jpg |
0.420068 | fbc579d168134592aa7d6f42ab4d4a24 | Effects of AMSC therapy on mice exposed to 500 mg/kg APAP. (A) Representative HE-staining and quantitation of the necrosis area in liver sections obtained from normal control (NC group), APAP-overdosed (vehicle group), AMSC-injected (AMSC group), and NAC-treated (NAC group) mice for 24 h. (B) Serum ALT and AST. (C) Hepatic GSH level. (D) Representative Ly6G IHC analysis. The positive cells were pointed out by arrowheads. Quantification of positive cells in each group per medium power field (MPF) using a 20× objective. Data were expressed as mean ± SD; n = 5; #### p < 0.0001 vs. NC group; **** p < 0.0001 versus vehicle group; ns: no significance versus NAC group. | PMC9854665 | antioxidants-12-00158-g001.jpg |
0.478154 | 9d15962310654a8d871c01931a3b5b0e | AMSC treatment prevents APAP-induced mitochondrial dysfunction. (A) Hepatic ATP levels in each group. Mice were sacrificed after APAP overdosing and AMSC treatment for 6 h. (B) JC-1 staining for detecting ΔΨm in each group. (C) Distinctive mitochondrial morphological changes were detected by electron microscopy in mouse livers treated with APAP and AMSC. Data are expressed as mean ±SD; n = 5; **** p < 0.0001 and ns: no significance vs. NC group; ### p < 0.001 and #### p < 0.0001 vs. vehicle group. NC group: normal control mice; vehicle group: APAP-overdosed mice; AMSC group: AMSC-treated mice. | PMC9854665 | antioxidants-12-00158-g002.jpg |
0.456176 | 7818795b35b1423e80e3ca1c44b6519b | The APAP-induced mitochondrial retrograde pathway limits therapeutic potential of AMSCs. (A) Representative HE-staining of delayed AMSCs injection at 1 h, 2 h, 4 h, and 6 h after APAP exposure. (B) Serum ALT and AST. (C) The protein expression levels of p-JNK and γH2AX at different times after the APAP challenge. Data are presented as the mean ± SD; n = 3–5; ** p < 0.01, *** p < 0.001, **** p < 0.0001 and ns: no significance vs. 0 h group. | PMC9854665 | antioxidants-12-00158-g003.jpg |
0.454391 | 5ee3f5b6ea1444d5be897c109ec232d1 | AMSCs inhibit JNK activation and mitochondrial translocation in AILI. (A) The enrichment maps of KEGG pathways of differentially expressed genes in the vehicle group versus the NC group and the AMSC group versus the vehicle group. (B) Heat maps of the MAPK signaling pathway gene subset in each group plotted with cohort means of Z scores. (C) The pathway of JNK signaling up was among significant differences in GSEA of AMSC group vs. vehicle group. Genes with the highest enrichment score are shown as a gene expression-based heat map. (D) The Western blot analysis of p-JNK level in isolated mitochondria and liver tissue after 6 h APAP exposure and AMSC treatment. NC group: normal control mice; vehicle group: APAP-overdosed mice; AMSC group: AMSC-treated mice. | PMC9854665 | antioxidants-12-00158-g004.jpg |
0.403282 | 0057a10e49d843fc9b546f07a5a4758e | Inhibition of JNK activation alleviates APAP-induced mitochondrial dysfunction in AML12 cells. (A) Western blot analysis of p-JNK and JNK levels in AML12 cells treated with anisomycin, APAP, and SP600125 for 24 h. (B) The cells were stained by DCFH-DA and MitoSOX to visualize intracellular ROS. (C) The representative fluorescent microscopic analysis of ΔΨm by JC-1 staining of each group. Data are presented as the mean ± SD; n = 3; * p < 0.05, **** p < 0.0001 and ns: no significance vs. NC group; # p < 0.05 vs. APAP group. AN: anisomycin; SP: SP600125. | PMC9854665 | antioxidants-12-00158-g005.jpg |
0.44465 | 2e5c8d3d587e4dd3b33fafac92635ccd | AMSCs inhibit ROS production and restore mitochondrial function. (A) Western blot analysis of p-Src and Src levels in isolated mitochondria from mouse liver tissues after treating with APAP and AMSCs for 6 h. (B) The measurement of ROS content in liver tissue by DHE staining and quantification by measuring the mean gray value of DHE. (C) GSEA plots of significantly different mitochondrial pathway gene sets in the vehicle group versus the NC group and the AMSC group versus the vehicle group. Data are presented as the mean ± SD; n = 3–5; ** p < 0.01, **** p < 0.0001 and ns: no significance vs. NC group; ## p < 0.01 and #### p < 0.0001 vs. APAP group. NC group: normal control mice; vehicle group: APAP-overdosed mice; AMSC group: AMSC-treated mice. | PMC9854665 | antioxidants-12-00158-g006.jpg |
0.413679 | d50f4b42264d4e6bac9afde651a01a67 | APAP-induced ATM retrograde pathway can be inhibited by inactivating JNK in AML12 cells. (A) Immunoblots and quantitative histograms showing the results of Western blotting analysis for the expression of p-ATM, ATM, γH2AX, and H2AX proteins. (B) Representative images showing the immunofluorescence staining for γH2AX (red) and p-ATM (green) among different groups. (C) The number of γH2AX foci per nucleus was quantitated using ImageJ (Fiji). In each sample, at least 100 nuclei cells were scored. The expression of p-ATM was quantified by measuring the mean gray value. Data are presented as the mean ± SD; n = 3; * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001 vs. APAP group; ## p < 0.01 and #### p < 0.0001 vs. AN group. AN: anisomycin; SP: SP600125; KU: KU-55933. | PMC9854665 | antioxidants-12-00158-g007.jpg |
0.477493 | 225030a9b52647f2a6b21802621e1556 | AMSCs inhibit the JNK-ATM mitochondrial retrograde pathway in AILI. (A) Immunoblots and quantitative histograms showing the results of Western blotting analysis for p-ATM, ATM, γH2AX, H2AX and p21 protein expression. (B) The AST and ALT levels after treating with AMSCs and AN. (C) Representative H&E staining of each group. (D) Liver tissues were stained for γH2AX and quantified. Representative IHC images are shown. Data are presented as the mean ± SD; n = 3–5; ** p < 0.01, *** p < 0.001, **** p < 0.0001 and ns: no significance vs. NC group and vehicle group; ## p < 0.01, ### p < 0.001 and #### p < 0.0001 vs. APAP group and AMSC + AN group. AN: anisomycin; NC group: normal control mice; vehicle group: APAP-overdosed mice; AMSC group: AMSC-treated mice; AMSC + AN group: AMSC-injected mice pretreated with anisomycin. | PMC9854665 | antioxidants-12-00158-g008.jpg |
0.446143 | a5b748c585274ab9b03b3545d8b1daa3 | Average activity of total alkaline protease (a) and amylase (b) (U/g live weight) in the intestines of C. labrosus and L. aurata juveniles (n = 36). Data expressed as means ± standard deviation (SD). Significant differences between species (p < 0.05) are indicated using lowercase letters (a, b). | PMC9855105 | animals-13-00287-g001.jpg |
0.57153 | 31e5d45c35b0425790d36a160be3c310 | Release of amino acids (AA) from L. aurata and C. labrosus when simulating the different feeding frequencies in vitro (n = 18). Data expressed as means ± SD. Significant differences between species (p < 0.05) are indicated using lowercase letters (a, b). | PMC9855105 | animals-13-00287-g002.jpg |
0.452702 | b58c5cf94b124618b2450057d73304ee | Release of reducing sugars from L. aurata (a) and C. labrosus (b) when the different feeding frequencies in vitro (n = 18). Data expressed as means ± SD. Significant differences between feeding patterns (p < 0.05) are indicated using uppercase letters (A, B). | PMC9855105 | animals-13-00287-g003.jpg |
0.454729 | 91261c3effeb4def8ea9234232c939ae | The mechanisms of rTMS in the treatment of PSP. Schematic illustration of the underlying mechanism of rTMS in the treatment of PSP. rTMS modulates the abnormal excitability of the cerebral cortex by modulating the pain network, improving interhemispheric inhibition, and increasing the number of GABA receptors, BDNF expression, and the number of NMDA receptors to alter brain plasticity, ultimately relieving PSP. VPL, ventral posterolateral nucleus; S1, primary somatosensory cortex; S2, secondary somatosensory cortex; MD, mediodorsal nucleus; IHI, interhemispheric inhibition; ICI, intracortical inhibition; GABA receptor, gamma-aminobutyric acid receptor; BDNF, brain-derived neurotrophic factor; NMDA receptor, N-methyl-D-aspartate receptor; LTP, long-term potentiation. | PMC9855274 | fnmol-15-1091402-g0001.jpg |
0.416214 | c33ee48d02c049d292c38ed8460b2ffe | The structure of JAK. Schematic illustrating the four functional domains of JAK, FERM, SH2, pseudokinase, and Kinase. Figure prepared using information from various sources [20,21]. | PMC9855819 | biomolecules-13-00119-g001.jpg |
0.40962 | 5efb6dee6a1944d39eeb04552b8690d8 | The structure of STAT. Schematic illustrating the conserved domain structure of STAT, including N-terminal domain (NTD), coiled-coil domain, DNA binding domain, transcriptional activation domain, SH2 domain, tyrosine activation domain (TAD). Figure prepared using information from various sources [20,26]. | PMC9855819 | biomolecules-13-00119-g002.jpg |
0.444899 | 2d08da92b539416a97349c03045150b4 | The activation of the JAK/STAT signaling pathway by cytokines. Schematic illustrating the preference of cytokines to bind JAK family. Figure prepared using information from various sources [21,34]. | PMC9855819 | biomolecules-13-00119-g003.jpg |
0.455861 | 6d6fcb8fa5c1472ba9d7a2b85fe03686 | The role of JAK/STAT in renal fibrosis. Schematic illustrating the main JAK/STAT members may involve in renal fibrosis, primarily through ischemia reperfusion injury, inflammatory infiltration, and diabetic nephropathy to modulate renal fibrosis. | PMC9855819 | biomolecules-13-00119-g004.jpg |
0.410544 | 8025d320df41437a826d78466ce153fb | Male and female G2019S mice display hyperlocomotion at different ages. Total distance covered in the open field test during 60 min by male (A) and female (B) WT and G2019S mice at the ages indicated above the graphs (m: months). N = 4–23 mice in each group. ** p < 0.001 unpaired Student’s t-test. Circles represent data of male. Squares represent data of female. Colors indicate different ages. | PMC9856037 | biomolecules-13-00051-g001.jpg |
0.398616 | 9f6834fb71a840fca074306bd7bf3b06 | Male and female G2019S mice display fine motor impairment at different ages. Fine motor coordination was assessed with the pole test in male (A) and female (B) mice at four age ranges. Tturn: time taken by the mice to turn downward from the top of a vertical pole; Ttotal: total time to descend the pole. N = 4–14 mice in each group. * p < 0.05; ** p < 0.01; *** p < 0.001 unpaired Student’s t-test. ##
p < 0.01 Mann-Whitney U test. | PMC9856037 | biomolecules-13-00051-g002.jpg |
0.396943 | 5bf446b682a447e0afc7df777eb471b9 | Old male G2019S mice display decreased DAT amount in the striatum. Western blotting of TH and DAT in the striatum of 10–12 months old and 20–21 months old male (A) and female (B) WT and G2019S mice. N = 4–25 mice in each group. * p < 0.05 unpaired Student’s t-test. | PMC9856037 | biomolecules-13-00051-g003.jpg |
0.434808 | 3eb27d15068044eb8af03a4cc57ed8c0 | Intact cell counts in the SNc of old WT and G2019S male and female mice. (A) Confocal images showing immunofluorescence for TH in midbrain sections containing the SNc (dotted lines) of 20–21 months old WT and G2019S male and female mice; scale bars: 500 µm. (B) Number of TH-positive neurons in the SNc of 20–21 months old mice. N = 6 WT male mice, N = 4 G2019S male mice, N = 4 WT female mice, and N = 4 G2019S female mice. | PMC9856037 | biomolecules-13-00051-g004.jpg |
0.422121 | b8ea5855eae14236b800aa9fdf9ec9ca | Scheme of the transition zone (Obersteiner–Redlich zone) between the central and peripheral zone of myelination of the cranial nerve. Zone of peripheral myelination lateral, centrifugal, to the transition zone is the site of vestibular schwannoma origin. | PMC9856152 | biomedicines-11-00032-g001.jpg |
0.382408 | ddd2a58bb6e441788bbbd0ce71ea7850 | Histology of VS, sections from the same tumor. Arrows show tumor cell nuclei; triangles point to macrophage nuclei. (a) Hematoxylin–eosin staining of tumor cell-rich Antoni A area (400× magnification). High density of tumor cells, presence of elongated cell nuclei. (b) CD163 immunohistochemical staining of Antoni A area (400× magnification), low CD163+ macrophage density (brown). (c) Hematoxylin–eosin staining-Antoni A area (1000× magnification). (d) Hematoxylin–eosin staining of Antoni B area (400× magnification). The disorganization of cellular arrangement, presence of microcystic pattern, and different shapes of cell nuclei. The stroma is loose. Immune cells are abundant. (e) CD163 immunohistochemical staining of Antoni B area (400× magnification), high CD163+ macrophage density (brown). (f) Hematoxylin–eosin staining-Antoni B area (1000× magnification). Bar is 50 μm (a,b,d,e) and 20 μm (c,f). This figure was provided by the Department of Pathology and Molecular Medicine, 2nd Faculty of Medicine, Charles University and Motol University Hospital. | PMC9856152 | biomedicines-11-00032-g002.jpg |
0.698179 | badfc479651545a5b6b4d50522ab11d3 | Schema of the VS tumor microenvironment. The tumor microenvironment is composed of the tumor cells themselves and the cellular and non-cellular components of the tumor stroma. The cellular component of the tumor microenvironment of VS is a compound of immune cells and mesenchymal cells. The non-cellular component involves structural proteins of the extracellular matrix, regulatory proteins, and communication molecules such as cytokines, chemokines, and growth factors. | PMC9856152 | biomedicines-11-00032-g003.jpg |
0.400117 | b583ea8f3f354753876121bcb4ca444c | Gross images of type III vasa previa. Reproduced and updated data from Clin Case Rep. 2019; 7: 2263–2264. Hara et al. [39] with copyright permission. (a) Marginal cord insertion with an unprotected cord vessel running along the extraplacental membrane (white arrow). (b) The placenta and membranes were filled with water to visualize the 3D images of the fetal vessels. The vessels indicated with white arrows were running near the internal cervical os and were diagnosed as vasa previa. | PMC9856204 | biomedicines-11-00152-g001.jpg |
0.479177 | 55e4ba2675a2461bbe0725c7754fbae0 | Schema of type I, II, and III vasa previa. The passage of unprotected blood vessels across or near the internal cervical os is common to all three types. Typical characteristics of type I, II, and III vasa previa are shown in the scheme. In general, type I is caused by velamentous cord insertion, type II is caused by a multilobed placenta or placenta with a succenturiate lobe, and type III is caused by a defective placenta and unprotected fetal vessels running outside of the placenta. | PMC9856204 | biomedicines-11-00152-g002.jpg |
0.390855 | ae4fb4da38e6467a82923be74f8f37b5 | Study selection scheme of the systematic search of previous studies. | PMC9856204 | biomedicines-11-00152-g003.jpg |
0.40071 | 3ae2e2e449a54c11be8c34f6d30c7356 | Meta-analysis of the characteristics and outcomes of types I and III vasa previa. Pooled odds ratios for (A) maternal age (years), (B) the rate of ART pregnancy (unadjusted), (C) the rate of antenatal diagnosis (unadjusted), (D) the rate of emergent cesarean delivery (unadjusted), and (E) gestational age at delivery (weeks) among patients with type I and type III vasa previa. The Forest Plot is ordered by publication year and relative weight (%) of the studies within the strata. The position of colored boxes is a point of the estimated odds ratio and the size represents the weight of study. Heterogeneity among the studies in each analysis was defined as substantial heterogeneity in unadjusted random effect analysis ((A): I2 = 56%), no heterogeneity in unadjusted fixed-effect analysis ((B): I2 = 0%), moderate heterogeneity in unadjusted random effect analysis ((C): I2 = 48%), moderate heterogeneity in unadjusted random effect analysis ((D): I2=32%), and no heterogeneity ((E): I2 = 0%). The above results were calculated using the RevMan ver. 5.4.1. and may vary slightly from their original values. CI, confidence interval; Type III, type III vasa previa; Type I, type I vasa previa; ART, assisted reproductive technology; CD, cesarean delivery; GA, gestational age. | PMC9856204 | biomedicines-11-00152-g004.jpg |
0.434477 | e91b458a603246b68f19f5e75ec89b75 | Drafting arrows. A biological–psychological interface model for borderline pd. | PMC9856504 | brainsci-13-00013-g001.jpg |
0.416207 | 749a1c11d45a4d4f8e1c34fc53371b2d | Linking dots. Images from a dissipating style of existence. | PMC9856504 | brainsci-13-00013-g002.jpg |
0.380366 | bfe3f7b8cd564d54bc88808a7b3dc8f6 | Stages of T cell selection during the establishment of central tolerance. T cell precursor double-negative (DN) T cells enter the cortex of the thymus through a blood vessel to undergo positive selection. Due to the interaction between antigen-presenting cells (APCs) present on cortical thymic epithelial cells (cTECs) and migratory dendritic cells (DCs), double-positive (DP) T cells are differentiated into CD4+ or CD8+ single-positive (SP) T cells and migrate to the medulla of the thymus to undergo negative selection. As they interact with APCs (medulla thymic epithelial cells (mTECs), migratory or resident DCs, and B cells), CD4+ T cells become CD4+ naïve T cells or T regulatory cells (Tregs) and leave the thymus. Negative selection is schematically shown only for SP CD4+ T cells. | PMC9856717 | cells-12-00314-g001.jpg |
0.499807 | a77ebc3805854faf84984462e9fa7704 | MHC-II maturation and antigenic peptide loading. MHC-II molecules are synthesized in the endoplasmic reticulum (ER) and loaded with an invariant chain (Ii). The MHC-II complex with Ii is transported through the Golgi to the late endosome. Endosomal proteases process antigens to short peptides and Ii to shorter class II-associated invariant chain peptide (CLIP). The binding of a nonclassical HLA-DM (DM) molecule to MHC-II promotes CLIP exchange to the antigenic peptide with an optimal binding register. The formed pMHC complex is transported to the surface of the APC for CD4+ T cell recognition. | PMC9856717 | cells-12-00314-g002.jpg |
0.492625 | 5b54ccc344f94065a768d8f0e2e7ed6e | The role of a nonclassical DM molecule in the editing of the self-antigen repertoire presented by MHC-II. (A) In a thymic APC, the self-antigen is processed through a classical pathway under exposure to cellular proteolytic enzymes. Next, CLIP is exchanged to the high-affinity fragment in late endosomes under DM control. The stable pMHC complex is then transferred to the APC surface, where the T cells specific to this pMHC undergo clonal deletion. (B) If an excessive amount of certain self-antigens, processed outside APCs, is present in peripheral tissues, then these self-antigen fragments can be loaded on MHC-II molecules in early endosomes or on the surface of APCs without the recruitment of DM. The absence of DM editing allows the emergence of either stable or unstable pMHC complexes. The pMHCs, containing high-affinity fragments, do not elicit a T cell response due to the deletion of autoreactive T cells in the thymus. Unstable complexes with low-affinity fragments can bind autoreactive T cells since such T cells are not susceptible to clonal deletion. | PMC9856717 | cells-12-00314-g003.jpg |
0.410171 | 99a964d073dd44518fa415cfdba2e6a3 | Effect of posttranslational modifications of self-antigens on trimolecular complex assembly. Certain self-antigen fragments do not bind to MHC-II molecules, or their binding affinity is low. Similar self-antigen with posttranslational modifications (iodination, acetylation, glycosylation, citrullination, generation of hybrid peptides, etc.) exhibiting increased affinity for MHC-II molecules, can appear in peripheral tissues. The resulting pMHC complexes can bind autoreactive T cells that have not undergone negative selection in the thymus. | PMC9856717 | cells-12-00314-g004.jpg |
0.441838 | 53f3724c588249f9916b836126e927e2 | The development of autoreactive CD4+ T cells in a proinflammatory environment. The proinflammatory environment caused by viral or bacterial infection entails IFN-γ production, which results in increased MHC-II and costimulatory molecule expression compared to normal conditions. Therefore, rare self-antigens are present in a greater number, which can lead to the potential activation of autoreactive T cells. | PMC9856717 | cells-12-00314-g005.jpg |
0.434051 | 9e57f19f08ad4e11adf02044dc260bc7 | The expansion of autoreactive CD4+ T cells due to the molecular mimicry between foreign and self-antigens. The presentation of viral or bacterial antigenic peptides on MHC-II molecules, structurally similar to self-antigens, may result in the expansion of CD4+ T cells, specific to exogenous pMHC. Expanded CD4+ T cells, specific for foreign peptides, can bind the self-antigen pMHC, which results in the development of autoimmunity. | PMC9856717 | cells-12-00314-g006.jpg |
0.422566 | 77ff749cf9064aa68299ff1ffeeb92be | The role of protective MHC-II molecules in the suppression of autoreactive T cell development. (A) Recognition of the self-antigen presented on the product of the protective allele by CD4+ T cell results in negative selection or Treg development in the thymus. (B) The slow loading rate of self-antigen on the MHC-II molecule of the protective allele results in the failure of pMHC complex assembly on the surface of thymic or peripheral APCs. | PMC9856717 | cells-12-00314-g007.jpg |
0.47443 | 31ae98a8b2954afa91500ae452b78976 | CGI mean score in the 4 measurements during treatment. | PMC9857282 | children-10-00150-g001.jpg |
0.465302 | 675253d05a554f118b14d957037b4e2c | Total ion chromatogram (A) and MS/MS spectra (B–D) of CCSKO. | PMC9857420 | foods-12-00293-g001.jpg |
0.487355 | c6b0b0afd1de4099bb58bf45e81af237 | DSC curve (A) and FTIR spectrum (B) of CCSKO. | PMC9857420 | foods-12-00293-g002.jpg |
0.501416 | c0bb599888b54352a0e585bac63d4281 | The relationship between the dose of CCSKO (μg/dish) and the number of reverse bacteria colonies in the experimental group. (A) The preliminary test in the absence of S9 (−S9). (B) The preliminary test in the presence of S9 (+S9). (C) The main test in the absence of S9 (−S9). (D) The main test in the presence of S9 (+S9). Data are expressed as mean ± SD. | PMC9857420 | foods-12-00293-g003.jpg |
0.476553 | 13358f15f2244b34bdac819810c4b772 | L5178Y cell TK gene mutation frequency and cell toxicity of in vitro mammalian cell TK gene mutation test of CCSKO. (A) L5178Y cell TK gene mutation frequency in the absence of S9 (−S9) induced by CCSKO. (B) L5178Y cell TK gene mutation frequency in the presence of S9 (+S9) induced by CCSKO. (C) The cell toxicity of in vitro mammalian cell TK gene mutation test of CCSKO in the absence of S9 (−S9). (D) The cell toxicity of in vitro mammalian cell TK gene mutation test of CCSKO in the presence of S9 (+S9). NC, negative control. Data in Figure 4A,B are expressed as mean ± SD; Values with different letters in the same color indicate significant differences (p < 0.05). | PMC9857420 | foods-12-00293-g004.jpg |
0.55935 | f8c0b17ea0e7485d9417bf147d97bce0 | (a) Time response curves of reference displacement velocity Xm(t). (b) Time response curves of reference stiffness vibration Lm(t). | PMC9857604 | entropy-25-00115-g001.jpg |
0.477654 | 6b249b2f71054af6a8047775ec18ae92 | The time response curves of the model following errors for the displacement velocity X(t)−Xm(t) without a controller. | PMC9857604 | entropy-25-00115-g002.jpg |
0.465386 | 159316a7f8f143088be6dc763f9e9adc | The time response curves of the model following errors for the stiffness vibration L(t)−Lm(t) without a controller. | PMC9857604 | entropy-25-00115-g003.jpg |
0.574853 | 17c1d2775639452290aba74953bf98fb | (a) Time response curves of displacement velocity X(t) for a controlled elastic beam with a controller and coupling term. (b) Time response curves of stiffness vibration L(t) for a controlled elastic beam with a controller and coupling term. | PMC9857604 | entropy-25-00115-g004.jpg |
0.516238 | 46d262fda3294770a57256666d862624 | (a) Model following error curves of displacement velocity X(t)−Xm(t) for a controlled elastic beam with a controller and coupling term. (b) Model following error curves of stiffness vibration L(t)−Lm(t) for a controlled elastic beam with a controller and coupling term. | PMC9857604 | entropy-25-00115-g005.jpg |
0.466743 | 6510c0de570445c7a1951063e51ba3b2 | The time response curve of the estimate value δ^. | PMC9857604 | entropy-25-00115-g006.jpg |
0.478423 | 3457e951c1b9424b946ee2fbf683a77e | The time response curve for the norm of estimate matrix Kp in the controller. | PMC9857604 | entropy-25-00115-g007.jpg |
0.416521 | b187def5b0f04eaeb62bb121165918be | The framework of hypernetwork link prediction method for fusion topology and attributes (TA-HLP). | PMC9858157 | entropy-25-00089-g001.jpg |
0.540355 | ecdbd351f4954043a511da7367112475 | Overall framework of attribute encoder based on hypergraph neural network. | PMC9858157 | entropy-25-00089-g002.jpg |
0.452258 | ea4905d5cb2347e9999596a1a715a1ba | AUC score results of ablation study. | PMC9858157 | entropy-25-00089-g003.jpg |
0.424729 | 5200fa839bc34920b785cd53ed4f31cd | Topology of e543. | PMC9858157 | entropy-25-00089-g004.jpg |
0.398312 | 26847edf6c0b4073a24d8f47515396fe | Attention weight of component nodes of e543. | PMC9858157 | entropy-25-00089-g005.jpg |
0.501007 | b1de4962518b49939065eb138be84266 | Impact of different dimensions of embedded vectors for hyperlink prediction. | PMC9858157 | entropy-25-00089-g006.jpg |
0.399104 | 476dd32d645543378a91acef6b2e929e | The process of manufacturing an anthropomorphic phantom. (A) 3D modeling process using DICOM images in all three planes with bone thresholds; (B) After exporting the STL file, it is loaded into PreForms to create supports and prepare for printing; (C) the printed anthropomorphic paediatric head phantom with supports. | PMC9858362 | diagnostics-13-00328-g001.jpg |
0.474367 | 4fe99ece650e452fa78dda7c8761666a | Evaluation of the manufactured phantom accuracy: (a) regions of interest used for evaluation of soft tissue and skull (A), brain (B), and lateral size (C); (b) profile of 10-pixel average of CT numbers along the x-axis in measurement region A. Curves representing CT numbers for patient, adult phantom and manufactured phantom are denoted by dotted, dashed and solid curves, respectively. | PMC9858362 | diagnostics-13-00328-g002.jpg |
0.471872 | 3bfeca7087e6497fa08fa4c03ec348bf | (a) Dependence of CT numbers variance (σ2) on volume computed tomography air kerma index (CVOL) obtained using different tube loadings (mAs) and voltages (kV) on a 16-slice Toshiba Astelion computed tomography unit, measured in the centre of the adult and paediatric head phantom. Coefficients of determination for two fitting curves are Ra2=0.957 and Rp2=0.965. Data for adult and paediatric phantom are given by symbols + and ×, respectively, while fitted curves for adult and paediatric phantom data are given by solid and dashed curves, respectively; (b) tube loading for paediatric patients at different tube voltages corresponding to adult volume computed tomography air kerma index (CVOL) at 120 kV with the same image noise as the 16-slice Toshiba Astelion computed tomography unit. The four curves account for 80 kV (solid curve with symbol +), 100 kV (dashed with symbol ×), 120 kV (dotted with symbol *), and for 135 kV (dash-dotted with □). | PMC9858362 | diagnostics-13-00328-g003.jpg |
0.421765 | 1f4e52b855bd486ba1ba6ba09828a05d | The box plot represents the distribution of dose descriptors for infant patients who underwent head computed tomography examination: (a) volume computed tomography air kerma index (CVOL); (b) air kerma length product (PKL,CT). In both box plots, the left-hand side stands for unoptimised protocol data and the right-hand side stands for the optimised one. Outliers are represented with circles. | PMC9858362 | diagnostics-13-00328-g004.jpg |
0.392587 | e63cf299d1ec4ea2a11ef22246557898 | Subjective image quality grades for unoptimised and optimised scanning protocol: (a) mean grades of five criteria explained in Section 2.6 of the main text and (b) box plot of total grade. No significant differences in quality of patient images using unoptimised and optimised scanning protocol (Mann–Whitney U test, p=0.379). In both diagrams, the left-hand side stands for unoptimised protocol data and the right-hand side stands for the optimised one. | PMC9858362 | diagnostics-13-00328-g005.jpg |
0.454089 | b408207a597c4c77a46cb51827879293 | (a) Location of the study site in the Iberian Peninsula and the topographic map of the nearby area, and (b) the meteorological station and the radon measurement system at Bilbao. | PMC9859108 | ijerph-20-00917-g001.jpg |
0.402557 | 0118b493e0224d0f94e8cc49aeba5207 | (a) Hourly 222Rn concentration evolution and (b) diurnal composite of average hourly radon concentrations in Bilbao during the period 2017–2018. | PMC9859108 | ijerph-20-00917-g002.jpg |
0.525415 | 1cb6daf5420f4d75af744715b388f607 | Seasonal box plots of 222Rn hourly concentrations at Bilbao. The rectangle represents 50% of data (interquartile range from 25th to 75th percentile), the small cross identifies the mean, the continuous horizontal line inside the rectangle identifies the median (50th percentile), the squares and circles identify the 90th and 10th percentiles respectively, and the whiskers extend between the 95th and 5th values. | PMC9859108 | ijerph-20-00917-g003.jpg |
0.411157 | 5aba11c05c884f42b9d6029f80879ca5 | (a) Evolution of the 222Rn baseline and maximum daily values at Bilbao, considering the average of the afternoon minimum (16:00–20:00 UTC) and morning maximum (06:00–10:00) measurements during the whole sampling period; (b) monthly difference between 222Rn baseline and maximum daily values. | PMC9859108 | ijerph-20-00917-g004.jpg |
0.52042 | 88e78ee80b9d4b20abdadd49381245e7 | Diurnal composite of average hourly radon concentrations for each range of different daily concentrations in Bilbao. | PMC9859108 | ijerph-20-00917-g005.jpg |
0.400604 | 7ef6367b30df462ca494718c6f8bba59 | Scatter plot precipitation vs daily differences between maximum and background hourly 222Rn concentrations. | PMC9859108 | ijerph-20-00917-g006.jpg |
0.426166 | dda810c0132b4bd0b89794e5fc15d02c | Daily cycles of wind direction (top) and speed for each range (bottom). | PMC9859108 | ijerph-20-00917-g007.jpg |
0.443904 | c1098c582e324de4879a39e0bf9880db | Air mass backward trajectory clusters (computed with HYSPLIT) and their frequencies (in brackets) for each 222Rn range. | PMC9859108 | ijerph-20-00917-g008.jpg |
0.423832 | d48cedfe41304064ad3c5dbad339ac69 | (a) Angular concentration and contribution profile for 222Rn based on the TSA method, and (b) PSCF method identifying those areas more influencing the occurrence of the highest 222Rn activity concentrations at Bilbao. | PMC9859108 | ijerph-20-00917-g009.jpg |
0.455135 | 49edec7aca104b9987ab0a645fe05f3d | (a) 222Rn exhalation rate map of European soils, for July 2006 calculated with the monthly mean soil moisture estimates from the GLDAS Noah LSM for July 2006, from [20]; (b) Screenshot of the European Map of Uranium in soil available on REMONwebportal (https://remon.jrc.ec.europa.eu/About/Atlas-of-Natural-Radiation/Digital-Atlas/Uranium-in-soil/Uranium-concentration-in-soil-, accessed on 10 October 2022). | PMC9859108 | ijerph-20-00917-g010.jpg |
0.435981 | 0069e3f6625b4881ae43953cb328a4a3 | Study design and somatic ERBB2 exon 16 skipping (ERBB2ΔEx16) analyzed in this study. (A) A diagram of study workflow. (B) Number of ERBB2ΔEx16+ patients from Cohorts 1 (upper panel) and 2 (lower panel) per tumor type, shown above the bars are the tumor type-specific prevalence (number of ERBB2ΔEx16+ patients/number of screened patients). (C) Diagram of the 22 unique sequence variants detected in the Chinese cancer patients cohort. The exon 16 (between nucleotides 1899 to 1946) and the flanking regions are shown, in which the gray bars correspond to each unique ERBB2ΔEx16 isoform as shown by the sequence variant on the right column. | PMC9859631 | fonc-12-1064598-g001.jpg |
0.449855 | 709bdb4419ad426eb850f7a71165450d | Molecular characteristics of patients harboring ERBB2 exon 16 skipping (ERBB2ΔEx16). (A) An oncoprint of somatic mutation landscape of ERBB2ΔEx16+ patients from Cohort 1. Each row represents a gene indicated on the left, with the mutation rate indicated on the right. Each column represents a patient. Different colors denote the mutation types. Bar plots on top of the oncoprint summarize the number of mutations each patient carries. The cancer type, ERBB2ΔEx16 variant type, and patient ID of each patient were indicated by various colors at the bottom. (B) Relative allele frequency (RAF), (C) mutation frequencies of TP53, and (D) number of somatic mutations in lung cancer (LC) patients before systemic therapy, LC patients after progression on EGFR tyrosine kinase inhibitors (TKIs), and in gastric cancer (GC) patients. (E) Genomic alterations harbored by ERBB2ΔEx16+ patients from TCGA were categorized by pathway and analyzed for the proportion of mutated among all pathway-related genes and the corresponding mutation frequency in patients. Number pairs in the middle (e.g. “10/85” for the RTK-RAS pathway), indicate the number of genes encoding for members of the indicated pathway that were found altered in ERBB2ΔEx16+ patients and number of genes encoding for members of the pathway, respectively. Number pairs at the rightmost (e.g. “7/9” for the RTK-RAS pathway), indicate the number of ERBB2ΔEx16+ patients carrying ≥1 alteration in genes in the indicated pathway and the number of ERBB2ΔEx16+ patients, respectively. | PMC9859631 | fonc-12-1064598-g002.jpg |
0.415631 | 715e052c80c540219b3acd8b7491c7ba | Schematic presentation of the courses of management for two ERBB2ΔEx16+ lung cancer patients (A) P03 and (B) P05 from Cohort 1. CN, copy number. NSCLC, non-small cell lung cancer. PD, progressive disease. | PMC9859631 | fonc-12-1064598-g003.jpg |
0.450937 | 3b35de712f6c4c0897b1afb0a65404c8 | Pharmacokinetic evaluation and biodistribution of CorA after administration of 30, 60 and 100 mg/kg IP as well as after 100 mg/kg SC in CD-1. Concentrations in plasma (a), heart (b), brain (c), spleen (d), kidney (e), liver (f), lung (g) and thigh (h) are displayed as mean and standard deviation (n = 3 per time point). | PMC9860980 | pharmaceutics-15-00131-g001.jpg |
0.441191 | 140b33df169a451f818b86e53027559d | CorA shows efficacy in the neutropenic lung infection model with MRSA. Bacterial burden expressed as log10 cfu/g lung tissue is shown for vehicle control group, CorA 60 mg/kg IP TID, CorA 60 mg/kg IP QD + 100 mg/kg SC BID and Levofloxacin 100 mg/kg IP. (a). Bacterial burden reduction compared to vehicle control group is displayed for CorA 60 mg/kg IP TID, CorA 60 mg/kg IP QD + 100 mg/kg SC BID and Levofloxacin 100 mg/kg IP (b). Compound concentrations in blood (c), kidney (d) and lung (e) are shown for CorA 60 mg/kg IP TID, CorA 60 mg/kg IP QD + 100 mg/kg SC BID and Levofloxacin 100 mg/kg IP. *: p < 0.05, **: p < 0.01 using a Kruskal–Wallis test. | PMC9860980 | pharmaceutics-15-00131-g002.jpg |
0.390402 | fd6b072e7a1149a3a850abcdee12d78c | Subject disposition from the three SAKURA trials. a A total of 2786 subjects received at least 1 DAXI treatment (202 subjects received their first DAXI treatment in SAKURA 1, 204 in SAKURA 2, and 2380 in SAKURA 3); of these, 2737 were evaluable subjects with baseline assessment and at least 1 post-baseline antibody assessment. b A total of 2823 subjects were exposed to RTP004 (2786 received RTP004 in the DAXI formulation in the three trials, and 203 received RTP004 in placebo in SAKURA 1 or SAKURA 2); of these, 2772 were evaluable subjects with baseline assessment and at least 1 post-baseline antibody assessment. DAXI, DaxibotulinumtoxinA for Injection. | PMC9862169 | toxins-15-00060-g001.jpg |
0.433868 | 612a05ca246a468c8578d574a289ae31 | Binding antibodies to daxibotulinumtoxinA and FWS status over time in subjects with treatment-related binding antibodies to daxibotulinumtoxinA. The dotted line represents the median duration of glabellar line response (time to loss of FWS none or mild by both investigator and subject assessment) to DAXI in treatment cycles 1 and 2 in this subgroup. ADA, anti-drug antibody; BoNTA, botulinum neurotoxin type A; DAXI, DaxibotulinumtoxinA for Injection; FWS, Frown Wrinkle Severity (assessed by either subject or investigator). | PMC9862169 | toxins-15-00060-g002.jpg |
0.462764 | b0163fe02aa9465b98e24f27c40e33b1 | Binding antibodies to RTP004 and FWS status over time in subjects with treatment-induced binding antibodies to RTP004. The dotted line represents the median duration of glabellar line response (time to loss of FWS none or mild by both investigator and subject assessment) to DAXI in treatment cycles 1 and 2 in this subgroup. ADA, anti-drug antibody; DAXI, DaxibotulinumtoxinA for Injection; FWS, Frown Wrinkle Severity (assessed by either subject or investigator). | PMC9862169 | toxins-15-00060-g003.jpg |
0.40094 | 1895f47ce758499aa879f5363c4e9274 | Anti-drug antibody three-tiered testing paradigm comprised (1) screening assay to identify samples positive for reactive antibodies, (2) confirmatory assay for positive samples to confirm binding specificity, and (3) titration assay to estimate antibody titer. Samples confirmed positive for anti-daxibotulinumtoxinA binding antibodies were assessed for the presence of neutralizing antibodies in the validated mouse protection assay. ADA, anti-drug antibody; DAXI, DaxibotulinumtoxinA for Injection; Nab, neutralizing antibody. | PMC9862169 | toxins-15-00060-g004.jpg |
0.397025 | 38d3479f0e2c4431bd14301cc671c20c | Three-tiered testing paradigm comprised (1) screening assay to identify samples positive for reactive antibodies, (2) confirmatory assay for positive samples to confirm binding specificity, and (3) titration assay to estimate antibody titer. Samples confirmed positive for anti-daxibotulinumtoxinA binding antibodies were assessed for the presence of neutralizing antibodies in the validated mouse protection assay. MPA, mouse protection assay. | PMC9862169 | toxins-15-00060-g005.jpg |
0.415968 | e509e3a35eed4725a429c7ace3a71c86 | Interactions between the sample and leaf surface. A Retention mass of EB aqueous dispersion in water, EB@AM-zein, and EB@AM-zein-SA on cucumber leaves, B Simulation of the retention rates of EB aqueous dispersion, EB@AM-zein, and EB@ AM-zein-SA on cucumber leaves were after erosion by rain. C Contact angles of EB aqueous dispersion, EB@AM-zein, and EB@AM-zein-SA on cucumber leaves. The experimental data were measured three replicates; a statistically significant difference between treatments compared with control is indicated by different small alphabets (a, b). Error bars indicate the least considerable value (LSD) at p ≤ 0.05 among the treatments | PMC9862550 | 12951_2023_1777_Fig10_HTML.jpg |
0.463595 | 7a59e43c777b4e4485dda20eba7c368e | Changes in the contents of antioxidant enzymes, POD and SOD, in cucumber under 60 mmol salt stress of different concentrations of A AM-zein and B AM-zein-SA and C the MDA content depicts the degree of damage to the cell lipid membrane. The experimental data were measured three replicates; a statistically significant difference between treatments compared with control is indicated by different small alphabets (a–l). Error bars indicate the least considerable value (LSD) at p ≤ 0.05 among the treatments | PMC9862550 | 12951_2023_1777_Fig11_HTML.jpg |
0.415373 | 1b0fd667719b418babd3d721c930ebae | Germination rate of cucumber seeds under salt stress for A 72 h and B 120 h in different concentrations of AM-zein and AM-zein-SA solutions and C Germination rate and germination potential of cucumber seeds treated with different concentrations of carrier under 120 mmol salt stress after 72 h. The experimental data were measured three replicates; a statistically significant difference between treatments compared with control is indicated by different small alphabets (a–i). Error bars indicate the least considerable value (LSD) at p ≤ 0.05 among the treatments | PMC9862550 | 12951_2023_1777_Fig12_HTML.jpg |
0.443882 | acdc0369408f4219a97e03e46442e2d9 | Slow release curve of A EB@AM-zein-SA and B EB@AM-zein at different pH values, C Photodegradation curve of EB in EB@AM-zein and EB@AM-zein-SA solutions | PMC9862550 | 12951_2023_1777_Fig13_HTML.jpg |
0.370791 | 65ceb73bcb914159968fae84bf74928a | A, B Distribution of EB in cucumber after 24/48 h of application, C Translocation Factors (TFs) of EB/EB@AM-zein/EB@AM-zein-SA in cucumber with root treatments. The experimental data were measured three replicates; a statistically significant difference between treatments compared with control is indicated by different small alphabets (a–c). Error bars indicate the least considerable value (LSD) at p ≤ 0.05 among the treatments | PMC9862550 | 12951_2023_1777_Fig14_HTML.jpg |
0.441007 | d324879e47c04202b392e07a249dc06a | Cytotoxicity of samples zein, AM-zein, AM-zein-SA. The experimental data were measured three replicates; a statistically significant difference between treatments compared with control is indicated by different small alphabets (a–d). Error bars indicate the least considerable value (LSD) at p ≤ 0.05 among the treatments | PMC9862550 | 12951_2023_1777_Fig15_HTML.jpg |
0.419363 | 5337bdbcfedd4f949e96017a174b1dac | Spraying of EB@AM-zein-SA on cucumber plants under salt stress enhanced salt tolerance, drug release property, and uptake of nanoparticles | PMC9862550 | 12951_2023_1777_Fig1_HTML.jpg |
0.424362 | c3d815862cb3418fbb8530459f1c6645 | The proposed route for the synthesis of AM-zein-SA | PMC9862550 | 12951_2023_1777_Fig2_HTML.jpg |
0.471803 | c74fa2f2fad442f4b30f26dac283bc2f | Structures of the cut parts of the cucumber plant | PMC9862550 | 12951_2023_1777_Fig3_HTML.jpg |
0.485291 | e95c981ce384409baaa36c97e84ccfc5 | A FTIR, B UV, C Raman, and D Fluorescence spectra of zein, AM-zein, SA, and AM-zein-SA | PMC9862550 | 12951_2023_1777_Fig4_HTML.jpg |
0.489871 | 0cdc25bf1a9e43f0822c7169f7495e02 | A SDS–PAGE gel electrophoresis results of the Marker, zein, AM-zein, and AM-zein-SA. B Free amino contents of zein, AM-zein, and AM-zein-SA. The experimental data were measured three replicates; a statistically significant difference between treatments compared with control is indicated by different small alphabets (a–c). Error bars indicate the least considerable value (LSD) at p ≤ 0.05 among the treatments | PMC9862550 | 12951_2023_1777_Fig5_HTML.jpg |
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