dedup-isc-ft-v107-score
float64 0.3
1
| uid
stringlengths 32
32
| text
stringlengths 1
17.9k
| paper_id
stringlengths 8
11
| original_image_filename
stringlengths 7
69
|
|---|---|---|---|---|
0.376135 | ee8a523cbaa04cfa89fe2061d995167f | Effect of the steam-to-biomass ratio on the gaseous product composition
(T = 1100 K, ER = 0.25, Dp = 100 μm, P = 1 atm). | PMC10099456 | ao3c00908_0005.jpg |
0.418709 | 2d96f4843fde4512a1b178aa68f7c3dd | Effect of particle size on the gaseous
product composition (T = 1100 K, ER = 0.25, SBR =
1, P = 1 atm). | PMC10099456 | ao3c00908_0006.jpg |
0.403281 | a830b3426d864e23927f16fdcd240bdd | Effect of the equivalence ratio on the gaseous
product composition
(T = 1100 K, SBR = 1, Dp = 100 μm, P = 1 atm). | PMC10099456 | ao3c00908_0007.jpg |
0.465423 | a0b77c17239a40f897e6eafa182d8acd | Effect
of pressure on gaseous product composition (T = 1100
K, ER = 0.25, SBR = 1, and Dp = 100 μm). | PMC10099456 | ao3c00908_0008.jpg |
0.429704 | 1d6d4c00f257471299fee281043c2c55 | Validation run at the optimum conditions of operating parameters
(P = 1 atm, ER = 0, SBR = 0.75, Dp = 100 μm, T = 1100 K). | PMC10099456 | ao3c00908_0009.jpg |
0.419077 | 9e8d154ead9a4693a77c5a9f81e5b247 | Effects of BOD1L/SETD1A loss on PARP inhibitor sensitivity in BRCA1-deficient cells. (A) H3K4me mediated by the BOD1L/SETD1A complex promotes RIF1 localisation at DNA double-strand breaks (DSBs) and stimulates NHEJ. In BRCA1-deficient cells, DNA-end resection and RAD51 loading are inhibited and lesions cannot be repaired by homologous recombination (HR), resulting in sensitivity to PARP inhibition and cell death. (B) Depletion of the BOD1L/SETD1A complex results in loss of H3K4me and decreased RIF1 localisation to DSBs. This allows DNA end-resection and RAD51 loading, partially restoring HR. This mediates resistance to PARP inhibition and allows cells to survive. Me: Methylation; PARP: poly(ADP) ribose polymerase; NHEJ: non-homologous end joining; KDMs: lysine demethylases. | PMC10099596 | cdr-6-1-35.fig.1.jpg |
0.420424 | db724e1e5c8b4fb6b4fb25f9b865da5a | Future strategies to restore PARP inhibitor efficacy in BRCA1-deficient cells upon loss of SETD1A function. Sensitivity to PARP inhibition following loss of the BOD1L/SETD1A complex or H3K4me perturbation could potentially be restored via 3 mechanisms including: (1) inhibition of the lysine demethylases (KMD5 and LSD1) responsible for removing H3K4me; (2) inhibiting nucleases such as MRE11 to prevent DNA-end resection which facilitates HR; and (3) exploiting collateral vulnerabilities using chemotherapeutics, e.g., cisplatin. Me: Methylation; PARP: poly(ADP) ribose polymerase; HR: homologous recombination; NHEJ: non-homologous end joining; DSB: double-strand break; KDMs: lysine demethylases. | PMC10099596 | cdr-6-1-35.fig.2.jpg |
0.444622 | a5aa6dd4e9d3444bbc1cc9e544b36300 | Radiomics score workflow and study flowchart. Tumor was manually drawn ROI from the axis ABUS images by using the SEG3D2 software. Next, 837 features, including first-order statistics, textural and wavelet features, were extracted by pyradiomics. ICC > 0.75, correlation coefficient ≥ 0.9, tenfold cross-test, and the LASSO regression were applied to data dimension reduction and select the most significant ALN tumor burden related radiomics features. Univariable and multivariate logistic regression analysis was used to develop the predicting model. We incorporated all independent predictors, and this was presented as ABUS radiomics nomogram | PMC10100322 | 12885_2023_10743_Fig1_HTML.jpg |
0.553838 | f5e5dae66b1241e3bd174e529d8259c9 | Radiomics features selection using tenfold cross-test and LASSO regression. A Tuning parameter(λ) selection in the LASSO regression used tenfold cross-test based on the minimum criterion. Dotted vertical lines indicated the optimal values using the minimum criteria and the1-SE criteria. A λ value of 0.024(log(λ) = -3.715) was chosen (minimum criterion) according to tenfold cross-test. B A coefficient profile plot was produced against the log(λ) sequence. Dotted vertical lines indicated the value obtained by the above tenfold cross-test, which resulted in 13 radiomics features with nonzero coefficients. C After tenfold cross-test and LASSO regression, the name and coefficient of selected radiomics features showed by a bar diagram | PMC10100322 | 12885_2023_10743_Fig2_HTML.jpg |
0.517073 | 13eb62cafb85434cb8b58cd42b43675f | Distribution of radiomics score in high and low tumor burden patients. The patients with high tumor burden had significantly higher score than those with low tumor burden (P < 0.001) | PMC10100322 | 12885_2023_10743_Fig3_HTML.jpg |
0.446296 | dcee73ad79154b8a929f2a64fcd7af3c | Developed ABUS radiomics nomogram. The ABUS radiomics nomogram was developed in the training set, incorporating the radiomics score, US-reported ALN status and retraction phenomenon. US, ultrasound; ALN, axillary lymph node | PMC10100322 | 12885_2023_10743_Fig4_HTML.jpg |
0.437328 | 11d40478548640a98aca1f4f61c7c16e | ROC Curves and Calibration curves of the model in the training and test sets. A ROC Curves of radiomics nomogram (blue, AUC:0.876), radiomics score (red, AUC:0.794), and ABUS model (black, AUC:0.772) in the training set. B ROC Curves of the radiomics nomogram (blue, AUC:0.851), radiomics score (red, AUC:0789), and ABUS model (black, AUC:0.736) in the test set. C, D Calibration curves of radiomics nomogram in the training (C) and test set (D). ROC, Receiver operating characteristic; US, ultrasound; ALN, axillary lymph node | PMC10100322 | 12885_2023_10743_Fig5_HTML.jpg |
0.458097 | 003db089f30941ef90b4322e82f555e6 | Decision curve of the radiomics nomogram (red line), radiomics score (purple line), ABUS model (blue line) and US-reported ALN status (yellow line) in the training set (A) and test (B) set. The vertical axis indicates the net benefit, the x-axis indicates the threshold probability. The black line indicates the presume that no patients showed ALN high burden, and the grey line indicates the presume that all patients showed ALN high burden | PMC10100322 | 12885_2023_10743_Fig6_HTML.jpg |
0.455885 | 9ec01872a6584c8fa5a7d2562e8c4705 | A case of radiomics nomogram. A 77-year-old woman who has a 3.1 cm diameter lesion, radiomics score = -1.301, retraction phenomenon positive and US-reported ALN positive, indicates a low burden, with a low probability of less than 45%. Pathology confirmed only one metastatic ALN in the patient. A coronal plane of ABUS examination. B axial plane of ABUS examination. C sagittal plane of ABUS examination. D Axillary US examination revealed suspiciously positive ALN (cortical thickening and lymphatic hilum disappeared). E The nomogram showed a low probability of high burden (< 45%), indicating ALN low tumor burden | PMC10100322 | 12885_2023_10743_Fig7_HTML.jpg |
0.408704 | 684019f525c849448e57b9dd5ddc00dc | Schematic representation of identifying critical factors of pathogenic Leptospira upon interaction with human macrophages by integrating transcriptomics and proteomics techniques. (A) In vitro macrophage infection model. (B) Integration of transcriptome and proteome data. (C) Bioinformatics analysis. (D) Validation of OMICs data. | PMC10100824 | spectrum.03135-22-f001.jpg |
0.448812 | a91db606fbdc4a79a5f0580b4edb8e71 | Transcriptome analysis of Leptospira during interaction with human macrophages. (A) Box plot of logCPM expression values across the samples. (B) Volcano plot representation of differential expression analysis of Leptospira gene in bacterial mock samples and host adopted bacterial samples. Genes with a significance (Padj) of ≤0.05 and genes with a significance (Padj) of ≤0.05 and a log2-fold change greater than 1 are represented in red and green, respectively. (C) Heatmap of most variable genes across the samples (D) Subcellular localization of DEGs. | PMC10100824 | spectrum.03135-22-f002.jpg |
0.438703 | fa8165fd196d43899c2fd9cfa5302ee3 | Dynamic profiling of the proteome of Leptospira during interaction with human macrophages. (A to D) Distributions of the molecular weight (A), number of unique peptides (B), calculated pI (C), and sequence coverage (D) of the identified proteins. (E) Volcano plots displaying proteins changing in leptospiral protein abundance at 24 h after host adaptation. Proteins with a Log2FC of >1 are in the green area. Proteins with a Log2FC of <−1 are in the red area. Proteins with a P value of <0.05 or a –log10(P value) of >1.3 are indicated above the horizontal black dotted line. (F) Subcellular localization of proteins that are dysregulated in Leptospira during the host adaptation. | PMC10100824 | spectrum.03135-22-f003.jpg |
0.446527 | ea2747d4a0274100bf7cc292a5e9257e | Correlation and conjoint analysis of transcriptome and proteome. (A) Venn diagram displaying the common and the unique genes found at transcriptome and proteome level. (B) Comparisons of the expression ratios from transcriptomic (y axis) and proteomic (x axis) profiling. Log2FC expression ratios are calculated as the mRNA or protein changes in Leptospira at 24 h after host adaptation. Significant changes in expression are indicated as follows: quadrants 2 and 8, proteins only; quadrants 4 and 6, transcripts only; quadrant 3, green; and quadrant 7, red. Both red and green lines represent an mRNA fold change of ±1 and a protein fold change of ±1. (C) Heat maps representing the changes in the abundance of the genes in both quadrants 3 and 7 during L. interrogans Icterohaemorrhagiae interaction with human macrophage Thp1 cells. | PMC10100824 | spectrum.03135-22-f004.jpg |
0.435195 | b3f24f74f8164c6485e5f670b5872ba8 | Gene ontology and KEGG pathway analysis of RNA-protein pairs. (A) The functional classification of the common 130 transcript-protein pairs DEGs was analyzed by GO enrichment analysis. (B) KEGG pathway analysis was performed to investigate the significant pathways enriched by the 130 common differentially expressed genes in transcriptomes and proteomes. | PMC10100824 | spectrum.03135-22-f005.jpg |
0.4445 | dee19dfdf81b49e88fb4449b07b9057c | qRT-PCR validation. (A) Heatmap showing the 08 RNA-protein pairs DEGs of LEPIRGA at different times points after interaction with the host (THP-1/HBPM/HWB). (B to D) Gene expression correlation between qRT-PCR (THP-1/HBPM/HWB) and RNA-Seq data. | PMC10100824 | spectrum.03135-22-f006.jpg |
0.423482 | 5a78cd6575e54364a970ee5e0cf2f475 | The discovery on IgAN biomarkers. | PMC10101996 | 41598_2023_32910_Fig1_HTML.jpg |
0.444795 | 8e2075361f844e588f37f097e6906e32 | (A) Comparison of miR-16-5p expression levels between the IgAN group and normal group in a confirmation cohort. IgAN group, n = 30, Normal control, n = 30. (B) Comparison of miR-16-5p expression levels between the IgAN group and Disease control group and normal control group in a validation cohort. IgAN group, n = 144, Disease control, n = 100, Normal control, n = 67. *, P < 0.05; ****, P < 0.0001. | PMC10101996 | 41598_2023_32910_Fig2_HTML.jpg |
0.459562 | 9dd0148886e24da0897975acc01202a3 | (A) Levels of urinary miR-16-5p in patients with different grade of Endocapillary hypercellularity. (B) Comparison of urinary sediment miR-16-5p expression levels between the IgAN progressors and non-progressors. IgANp (progressor), IgANnp (non-progressor). | PMC10101996 | 41598_2023_32910_Fig3_HTML.jpg |
0.407883 | 0c496fb1dfb84259b07c4fc372edd03a | Compound eye types and development. (A)
D. melanogaster has a neural-superposition eye, the optics of which follows typical apposition organization, with individual lenses (L) that each project a tiny image fragment onto the tips of underlying photoreceptor rhabdomeres (R). Underneath the lens, there is a pseudocone (PC) and four Semper cell (SC) bodies. (B)
T. marmoratus has an optical superposition eye, in which sets of lenses synergistically project image points onto corresponding underlying closed rhabdoms. In this organization, the SC bodies are located in close proximity to the lens and above the photoreceptor cell bodies. The optics require the presence of pronounced crystalline cones (CCs) and a clear zone. (C) Compound eye development is best understood in D. melanogaster, in which specific cell types are sequentially recruited from a precursor epithelium. Top: Diagram of cell fate specification and differentiation in the Drosophila compound eye. Bottom: The four SCs within each ommatidium show Cut immunoreactivity (green) in the larval, pupal, and adult stages. For better orientation, counterstained tissue is illustrated in magenta: ELAV in larvae, E-cadherin in pupae, and drosocrystallin (lenses) in adults. | PMC10102356 | fcell-11-1104620-g001.jpg |
0.47535 | bcece68f71034c7e9e161b900959d97d | Cut expression and RNAi-driven knockdown in D. melanogaster and T. marmoratus compound eyes. (A). In D. melanogaster, a quartet of Cut-positive Semper cells (green) are situated within the distal-most portion of developing ommatidia (at ∼37% pupal development). DAPI and N-cadherin counterstaining are used to identify the correct layer within the eye. As illustrated in representative images, efficient cut knockdown is achieved by two different SC-directed RNAis, with overlapping phenotypes consisting of an irregular ommatidial array. Incidences of laterally displaced rhabdoms are indicated via N-cadherin staining (arrowhead). (B). In T. marmoratus, at a comparable developmental stage, four Cut-positive SCs are similarly organized near the distal margin of each ommatidium. At this stage, the closed rhabdom (red; confirmed by actin staining) still resides in close proximity to the SCs. The nuclear localization of Cut is confirmed by complete overlap with DAPI. cutRNAi treated individuals show a strong but incomplete reduction of Cut, with irregularities in the ommatidial array. In some instances at this level, only a triad of Cut-positive nuclei are visible (arrow), and rhabdoms appear to be laterally displaced (arrowhead). Scale bars = 10 µm. | PMC10102356 | fcell-11-1104620-g002.jpg |
0.436257 | b0cba69e62024727987701030e9153be |
Cut knockdown affects lens organization in insect compound eyes. (A–F) Scanning electron micrographs of adult D. melanogaster compound eyes. Overview of a control individual (A) illustrates a typical completely regular ommatidium array, whereas ct
GD
(B) and ct
V20
(C) exhibit major irregularities in ommatidial placement and lens formation. The latter is illustrated in a magnified view of the anterior region of the compound eye. In control individuals (D), lenses appear precisely shaped with properly formed lens surfaces. In ct
GD
(E) and ct
V20
(F), irregularities exist in ommatidium separation, with some neighboring units fused (arrows). In some instances, the lens surface exhibits deformities typical of the blueberry phenotype (arrowheads), which are particularly pronounced in the ct
V20 line. (G–K) Scanning electron micrographs of adult T. marmoratus compound eyes. Overview of a control beetle (G) shows an intact eye with a smooth surface. In cutRNAi individuals (H), surface dimples (arrow) are more common than in controls (I). A high-resolution image of the anterior region of the compound eye illustrates precise placement and smooth transitions between neighboring ommatidia (J), whereas cutRNAi injected individuals show irregularities in ommatidium size and more delineated borders (K). Additionally, some neighboring units are fused (arrow). Scale bars = 100 µm (A–C), 40 µm (D–F), 500 µm (G, H), and 50 µm (J, K). | PMC10102356 | fcell-11-1104620-g003.jpg |
0.474575 | 8f325571639c46f88fdaff10db83659f | Morphological lens defects lead to profound optical deficits. Isolated lens arrays were used to visualize the back surfaces of lenses (A–F) and images of an object with three stripes were then produced by these lens arrays (A′–F′). In D. melanogaster, control lenses have smooth and accurately formed back surfaces (A) that lead to regularly spaced and equally sized images with a uniform focal plane across the lens array (A′). In contrast, the lenses of the cut knockdown lines show visible defects in morphology (B, C) and optics, with images that vary in placement, image magnification (arrowheads), focal plane, and blurriness (B′, C′). For ct
V20, several lenses show dimple-like indentations on the back surfaces (arrowhead) and other lenses appear dark and necrotic (C). Such necrotic lenses (exemplified by the cluster marked with *) lead to gaps in the resulting image array * in (C′). In T. marmoratus, a similar pattern is observed, with controls having smooth and even lens back surfaces (D) that result in pristine regular image arrays (D′). In contrast, cutRNAi individuals exhibit lens irregularities (E) that lead to irregularities in the corresponding lens array (E′), including greatly displaced images (arrowhead). Lens back surfaces frequently show dimple-like lens indentations arrowheads in (E, F), which are also present in individuals with fewer irregularities in lens placement (F). Even in this morphologically less severe phenotype, major deficiencies in the lens array optics occur, resulting in many blurry images and some differently sized images (arrowhead) (F′). Scale bars = 50 µm. | PMC10102356 | fcell-11-1104620-g004.jpg |
0.500193 | 6487c36a472f4b088f883decbb124d00 |
Cut knockdown leads to rhabdom misplacement in both eye types. (A). In D. melanogaster, rhabdoms typically extend along the majority of the ommatidia, from close to the pseudocone to the basement membrane. (B). Rhabdoms, visualized with phalloidin, appear well developed and regular in control individuals. In ct
GD
(C) and ct
V20
(D) individuals, rhabdoms appear truncated and frequently misplaced, with many extending well below the basement membrane (arrowheads). (E). In T. marmoratus, rhabdoms are situated much deeper in the eye to make room for a clear zone, which is necessary to allow many lenses to contribute to the image formed at the distal end of the PRs. (F). Phalloidin staining in control individuals illustrates precisely aligned rhabdoms that extend from below the clear zone to well above the basement membrane (BM). PR nuclei are aligned precisely along a concentric circle between the rhabdoms and lenses. (G). In cutRNAi individuals, PR placement is less regular, at the levels of both PR nuclei and rhabdoms. As in D. melanogaster, rhabdoms are displaced toward the basement membrane and occasionally traverse it (arrowhead). Scale bars = 50 µm (B–D) and 100 µm (F, G). | PMC10102356 | fcell-11-1104620-g005.jpg |
0.431927 | 9aa5a27759494e08962c6a6455071cf0 |
Cut knockdown leads to ultrastructural defects of rhabdoms in both eye types. (A). As illustrated by a control individual, D. melanogaster has an open rhabdom that, at any cross-sectional plane, is formed by seven rhabdomeres. (B). At higher magnification, it is apparent that the smaller central rhabdomere extends into the center of an extracellular lumen, which is bordered by larger and approximately evenly sized outer rhabdomeres. (C). Overview of a ct
GD knockdown individual illustrates ommatidial displacements (with a compromised interommatidial space) and deformed or missing rhabdomeres (exemplified by the unit marked with *). (D). Several units characterized by relatively extended or even split rhabdomeres (arrowhead). (E). Other units showing unusually small rhabdomeres (arrowhead). (F). Overview of a ct
V20 knockdown individual illustrates ommatidia with relatively sparse rhabdomeres, large extracellular spaces between rhabdomeres, and sparse and degenerate interommatidial tissue. Non-etheless, ct
V20 individuals also show laterally extended rhabdoms (G), arrow, split rhabdomeres (G), arrowhead, and possibly fused rhabdomeres (H), arrow. (I). As illustrated by a control individual, the superposition eyes of T. marmoratus are characterized by closed rhabdoms (two units with similar rhabdom diameters in close proximity are marked with *). (J) The rhabdom is positioned centrally within a healthy ommatidium. (K). In cutRNAi individuals, neighboring units (marked with *) show relatively different rhabdom organization. (L) An unusually shaped rhabdom with central deficiencies. (M) A laterally displaced and strongly degenerate rhabdom. (N) Overview of several ommatidia in a different individual shows the complete absence of a rhabdom (^) next to two neighboring semi-intact rhabdoms (*). (O) A laterally degenerate rhabdom. (P) A rhabdom with a displaced portion (arrowhead). Scale bars = 5 µm (A,C, F), 2 µm (B, D, E, G, H, J, L, M, O, P), and 10 µm (I, K, N); Rh = rhabdomere (B, D) or rhabdom (J, M, O, P). | PMC10102356 | fcell-11-1104620-g006.jpg |
0.437287 | af7d5d1654c64a3f9fbdd9833f8db303 | Despite major structural deficits, electroretinograms of cut knockdown individuals show relatively intact physiological responses in D. melanogaster and relatively minor deficiencies in T. marmoratus. (A). Example recordings from two control and two test flies illustrate comparable responses. (B). Average responses (with standard error) to increasing light intensities suggest a comparable dynamic range across the four tested fly lines (n = 10 each). (C). Example responses at two different light intensities. (D). Quantification of cutRNAi injected beetles shows inverted responses at all (dark red) or higher (medium red) light intensities. (E). Example recordings of a control individual and one of each of the three phenotypes in (D). (F). Average responses (with standard error) to increasing light intensities suggest a comparable dynamic range between control and cutRNAi individuals, albeit with generally lower responses in the knockdowns (*p < 0.05, **p < 0.005; based on Wilcoxon’s rank sum test). (G). Example responses at two different light intensities. (H). Example of cutRNAi individuals showing different response dynamics when multiple pulses are presented. | PMC10102356 | fcell-11-1104620-g007.jpg |
0.401054 | 5bb5ac554c4b42c9b81e628e022a8f4e | Schematic summary of SC-mediated effects of cut. | PMC10102356 | fcell-11-1104620-g008.jpg |
0.410496 | 1bdd0721493e4416875eabfae16bb50f | CHRONOS19 study design and patient disposition | PMC10102503 | gr1_lrg.jpg |
0.432099 | 59193bb6f4ca4137b1fb74f389b9fba9 | Overall survival in patients with various types of hematologic malignancies and COVID-19 who were eligible for the primary endpoint assessment in CHRONOS19. Survival analysis was performed with Kaplan-Maier estimates. Abbreviations: AL, acute leukemia; CLL, chronic lymphocytic leukemia; CML, chronic myeloid leukemia; CMPN, chronic myeloproliferative neoplasms; HL, Hodgkin's lymphoma; MDS, myelodysplastic syndrome; MM, multiple myeloma; NHL, non-Hodgkin lymphoma | PMC10102503 | gr2_lrg.jpg |
0.487647 | 8a2ccde3946e4d4d8c00595c56f74136 | Overall survival in the evaluable population of patients who were eligible for the primary endpoint assessment in CHRONOS19, n = 626: survival estimates (95% CI) at 1, 3, and 6 months after the COVID-19 diagnosis. Survival analysis was performed with Kaplan-Maier estimates. | PMC10102503 | gr3_lrg.jpg |
0.403604 | de1f022ebfd04da5b5f12b765aeda7c9 | Forrest plot representing risk factors for COVID-19 mortality (univariate analysis). Abbreviations: ARDS, acute respiratory distress syndrome; CRS, cytokine release syndrome; ECOG, Eastern Cooperative Oncology Group; ICU, intensive care unit; MTA, myelotoxic agranulocytosis. | PMC10102503 | gr4_lrg.jpg |
0.431712 | d628e6858ef04aea84f44cf8337add34 | Impact of a hematologic disease treatment and its schedule change on overall survival. Survival analysis was performed with Kaplan-Maier estimates. | PMC10102503 | gr5_lrg.jpg |
0.474285 | 0af4d60b988549c8819bc83065aa86df | A. Delayed estimation working memory task. Participants were asked to remember the orientation of a teardrop-shaped object and reproduce the orientation after a varying delay period. The orientation of a given target was selected with equal likelihood from a set of 12 equally spaced values. Each trial began with a 1.2 s fixation dot, followed by a teardrop object presented at the center for 0.2 s. This was followed by a delay of 0, 2, 4, or 8 s, during which only the fixation dot was visible. At the end of the delay, participants reproduced the orientation of the target using a computer mouse. This report was followed by a 0.5 s intertrial interval. B. Response Variability. Average standard deviation of response errors. This variability (inverse precision) increased in magnitude over time. C. Drift Rate. This was calculated as the slope of the function relating standard deviation to delay period. D. Bias-corrected Response Variability. E. Bias-corrected Drift Rate. | PMC10104073 | nihpp-2023.04.04.535597v1-f0001.jpg |
0.479365 | 1e608ee74af24e1aa67077387a75db9c | A. Serial dependence by group and delay duration. Serial dependence is calculated as the mean response error as a function of the difference in orientation between the previous and current trial. The single-subject means and the group means are plotted for each delay. Solid lines indicate the means, with shading being ± s.e.m. Dots indicate single-subject means. B. Small Orientation Differences. The mean bias index (mean response error averaged over trials with orientation differences of ≤90°) is plotted for each group (dots indicate single-subject means) at each delay, showing that the bias became progressively more positive over delays in HCS and progressively more negative over delays in PSZ. | PMC10104073 | nihpp-2023.04.04.535597v1-f0002.jpg |
0.409589 | 169807593b414b69ae8772663e795872 | Correlations with neurocognitive and clinical measures in PSZA. In PSZ, serial dependence bias was associated with the working memory cognitive domain from the MATRICS battery. B. In PSZ, serial dependence bias was also associated with visual working memory capacity (K) from a change localization task. Greater repulsion was associated with lower scores on WM measures in PSZ. C. In PSZ, serial dependence bias in this task was correlated with the bias index from the within-trial task. D. Correlation between bias and medication dose (not significant). | PMC10104073 | nihpp-2023.04.04.535597v1-f0003.jpg |
0.464806 | 487a65f4abdd40a8b8c7373dcb30204c | Schematic illustration of the plus-strand RNA life cycle.① Virus (V) enters the cell via receptor-mediated endocytosis (ke). ② The viral genome (RP) is released (kf). Virus within the endosome (VE) degrades with rate constant μVE. ③ Ribosomes (Ribo) bind at the viral genome and form (k1) a translation initiation complex (TC) that degrades with rate constant μTC. ④ The viral genome (RP) is translated (k2) into a polyprotein (PP) that ⑤ is subsequently cleaved (kc) into structural and non-structural viral proteins, PS and PN, respectively. To measure translation activity, luciferase (L) is integrated into the viral genome and produced with RNA translation. Viral proteins degrade with rate constant μP; luciferase degrades with rate constant μL. ⑥ Non-structural proteins and freshly translated viral RNA form (kPin) replicase complexes (RC) that are associated with replication organelles (ROs) and ⑦ serve as a template for the minus-strand synthesis (k4m) leading to double-stranded RNA (RDS).⑧ Viral non-structural proteins, such as the RdRp, within the replication organelle (PNRO) bind to double-stranded RNA, forming (k5) a minus-strand replication intermediate complex (RIDS) that ⑨ initiates the plus-strand RNA synthesis (k4p) giving rise to multiple copies of viral plus-strand RNA (RPRO). All species within the replication organelle degrade with the same rate constant μRO. ⑩ The viral genome can remain within the replication organelle, where it undergoes multiple rounds of genome replication (k3), ⑪ it can be exported (kPout) out of the replication organelle into the cytoplasm starting with the translation cycle again, or ⑫ the plus-strand RNA genome (RPRO) is packaged together with structural proteins (PS) into virions (VR) that are released from the cell (kp) and ⑬ may re-infect the same cell or infect naïve cells (kre). Extracellular infectious viral species (V and VR) degrade with rate constant μV. | PMC10104377 | pcbi.1010423.g001.jpg |
0.411954 | 14216c39cd274166ad59a158da98d239 | Best fit of the model to the data with standard deviation (left panel) and model prediction of plus-strand RNA allocation between the cytoplasm and replication organelle (RO) (right panel). For parameter values, see Table 2. [LEFT: green: (+)RNA = RPtot=(VE+RP+TC+RC+RDS+RIDS+RPRO), red: (-)RNA = RMtot=(RDS+RIDS), blue: A) Virus = Vtot = VR, B) and C) Virus = Vtot = (V+VR), yellow: Luc = L; RIGHT: yellow: RNA in cytoplasm = (RP+TC)/RPtot, purple: RNA within replication organelle (RO) = RC+RDS+RIDS+RPRO)/RPtot; Infectious virus was measured in PFU/mL, (+) and (-)RNA were measured in molecules/mL or relative RNA concentration, luciferase was measured in relative light unit (RLU)]. | PMC10104377 | pcbi.1010423.g002.jpg |
0.471089 | 8990b142748e4dd28f8874f1f0cf93ce | Uncertainty analysis of the best-fit model.For parameter values and 95% confidence intervals, see Table 2. The best fit is shown in Fig 2. | PMC10104377 | pcbi.1010423.g003.jpg |
0.46191 | d74e11c7e3a74ccea32beb10a9e26d03 | Infectious virus concentration with parameter adjustments.A) HCV concentration with estimated parameters (solid), the number of ribosomes taken from CVB3 (dashed), and the RNA synthesis rate taken from CVB3 (dotted). B) CVB3 concentration with estimated parameters (solid), the number of ribosomes taken from HCV (dashed), and the RNA synthesis rate taken from HCV (dotted). | PMC10104377 | pcbi.1010423.g004.jpg |
0.415811 | 3dd551cc9d2d4943b1c18b25c1f984d8 | Replicase complexes over time.Dynamics of replicase complexes for A) hepatitis C and dengue virus, B) coxsackievirus B3. The dashed grey line represents the carrying capacity or the maximum number of formed replicase complexes. | PMC10104377 | pcbi.1010423.g005.jpg |
0.425615 | 87633ea6a0f84e3c9bc44b06c2223bb0 | Global sensitivity profile for the model species plus-strand RNA throughout infection (CVB3 = 10 hours, HCV = DENV = 72 hours). | PMC10104377 | pcbi.1010423.g006.jpg |
0.460408 | 927c8c10faf54ee2b6a6c9f9e97da140 | Effects of drug interventions applied to two different time points: at infection beginning (left) and in steady state (right). A successful drug treatment leads to more than 99% viral eradication (light yellow), while an ineffective drug treatment leads to 100% remaining virus (black). | PMC10104377 | pcbi.1010423.g007.jpg |
0.464924 | 1929700ae069401a92faccb7975233b8 | Combined drug effect on A) vRNA synthesis and formation of translation complex (TC), B) vRNA synthesis and translation, and C) viral RNA synthesis and polyprotein cleavage. Initiation of treatment was in steady state (100 h pi). A successful drug treatment leads to more than 99% viral eradication (light yellow), while an ineffective drug treatment leads to 100% remaining virus (black). | PMC10104377 | pcbi.1010423.g008.jpg |
0.405717 | 60fb695798e44c3ba2c1174c1c0cc745 | Relative virus decay under combination therapy that clears HCV, DENV, and CVB3 infections.A combined drug effect on A) vRNA synthesis and formation of translation complex (TC), B) vRNA synthesis and translation, and C) viral RNA synthesis and polyprotein cleavage. Initiation of treatment was in steady state (100 h pi). The drug efficacy constant (εA and εB) were chosen as minimal efficacies to clear all three viruses. For comparability, virus-specific concentrations in steady state have been normalized to their virus-specific pre-treatment steady-state concentration. A successful drug treatment leads to more than 99% viral eradication (light yellow), while an ineffective drug treatment leads to 100% remaining virus (black). | PMC10104377 | pcbi.1010423.g009.jpg |
0.403162 | 8755b17076064f8e95def2b005f038e9 | The antimicrobial susceptibility of clinical K. pneumoniae isolates to different antibiotics by disk diffusion method. | PMC10105274 | IJM-15-27-g001.jpg |
0.407036 | c16469c5d34f470291a5527df6b744c1 | Antibiogram pattern of K. pneumoniae isolates against antimicrobial agents.* R: resistant – I: Intermediate resistant – S: sensitive. | PMC10105274 | IJM-15-27-g002.jpg |
0.458993 | 0692932e1cd94bd4bc1313bc79fc2812 | Electrophoretic graph of conventional PCR products on 1.5% agarose gel stained with ethidium bromide of some representative K. pneumoniae isolates for the detection of integron I. Lanes M: represent 100 bp DNA ladder, Lane 18: positive control (reagent control mixture with DNA of the standard strain), Lane 19: negative control (reagent control mixture without DNA), Lanes 1–17 and 20–38: clinical K. pneumoniae isolates. | PMC10105274 | IJM-15-27-g003.jpg |
0.433848 | 6cac670cce1042a2af535f7a5145e95a | Correlation between the susceptibility of the tested K. pneumoniae isolates to different antimicrobials agents and the presence or absence of: (a) integron I and (b) integron III | PMC10105274 | IJM-15-27-g004.jpg |
0.491038 | d6866fcfe9cc40e6a823b1c5aac3a3ff | Model of a serial connection | PMC10105445 | 12874_2023_1919_Fig1_HTML.jpg |
0.47889 | e60ddd7feb784c60ae1d4841ded355b5 | Model of a parallel connection | PMC10105445 | 12874_2023_1919_Fig2_HTML.jpg |
0.491445 | c39c83b175b848a8add98b6303609875 | The parallel and serial-connection model of a complex event with an observed factor, a trigger factor and a confounding factor. A pattern for exposed group; B pattern for non-exposed group. The expectation that the incidence in the exposure group may be not 1: (A) due to an observed factor acting with a trigger factor; and (B) the expectation that the incidence in the non-exposure group may be not zero due to confounding factors acting with a trigger factor | PMC10105445 | 12874_2023_1919_Fig3_HTML.jpg |
0.476315 | 74160e64772e406f96721e4fe16fd856 | Displaying the relationship and strength of causal factors based on the parallel and serial connection of switches | PMC10105445 | 12874_2023_1919_Fig4_HTML.jpg |
0.486195 | 40b35fa3c357432eb030c18ee84d9938 | Information visualization for displaying the relationship and strength between HLADQB1*03 and schizophrenia | PMC10105445 | 12874_2023_1919_Fig5_HTML.jpg |
0.488746 | f2632754fe4f4af18a3756400d352aea | Information visualization for displaying the relationship and strength between aging with 5 years and all-cause death | PMC10105445 | 12874_2023_1919_Fig6_HTML.jpg |
0.440082 | e2d681a1f7b64999b4994cefd01837f2 | Sample dendrogram of GSE137943 dataset. | PMC10105563 | peerj-11-15093-g001.jpg |
0.44771 | 07e8c0526ae34b70a690cebffab7c14a | Gene co expression network was constructed by GSE137943 dataset.Analysis of the scale-free fit index for soft-thresholding powers (left) and the mean connectivity for various soft-thresholding powers (right); (B) Gene expression clustering tree and recognition module in co-expression network; (C) network heatmap plot in the co-expression modules. | PMC10105563 | peerj-11-15093-g002.jpg |
0.429418 | a3db15a5f12f4bb1ad258bfd506fa393 | Module-trait correlations analysis in muscle tissue (GSE137943).(A) Heat map of correlation between GSE137943 data set module and muscle tissue; (B) Significance of genes related to muscle tissue in the magenta module (each dot represents a gene in the magenta module); (C) Module eigengene (y-axis) across samples (x-axis) from the magenta module (associated to muscle tissue). | PMC10105563 | peerj-11-15093-g003.jpg |
0.454393 | 87053c70a8d84269a3af8c08d2f6fd04 | GO and KEGG analysis.The visualization results of (A) partial GO biological function analysis and (B) partial KEGG analysis of magenta module gene. The first 10 important enrichment pathways are shown. | PMC10105563 | peerj-11-15093-g004.jpg |
0.46616 | eaff06b9fd6644589cc0f5c19c4b1bd9 | Identification of Hub gene.(A) Correlation of the top 20 genes with high MM and GS in the magenta module; (B) the top 20 genes with the highest connection degree in magenta module were identified by Cytoscape software; (C) identify the common genes in the co-expression network and PPI network. | PMC10105563 | peerj-11-15093-g005.jpg |
0.40107 | 34c21d2cffef4fcea6d49bd24bff4f6e | The gene set enrichment analysis results of hub gene.Pathway enrichment analysis of genes positively associated with (A) Atp2a1, (B) Tmod4, (C) Lmod3, (D) Mybpc2 and (E) Ryr1 in the GSE137943 dataset. | PMC10105563 | peerj-11-15093-g006.jpg |
0.497774 | 786339418dff4b0da3be2e6ace863822 | Expression of hub genes in dataset GSE137943.(A–E) Expression levels of (A) Atp2a1, (B) Tmod4, (C) Lmod3, (D) Mybpc2, and (E) Ryr1 were significantly increased in muscle tissue. | PMC10105563 | peerj-11-15093-g007.jpg |
0.453014 | f5c6962b1761402fba6a869c4172baa9 | Expression of hub genes in dataset GSE116775.(A–E) Expression levels of (A) Atp2a1, (B) Tmod4, (C) Lmod3, (D) Mybpc2, and (E) Ryr1 were significantly increased in muscle tissue. | PMC10105563 | peerj-11-15093-g008.jpg |
0.475208 | e9ca17781e22435f98cf72875b411c99 | The expression level of hub gene in newborn calf tissue samples was detected.(A–E) Compared with other tissues, the expression levels of (A) Atp2a1, (B) Tmod4, (C) Lmod3, (D) Mybpc2, and (E) Ryr1 in muscle tissue were significantly increased. | PMC10105563 | peerj-11-15093-g009.jpg |
0.46355 | 11ed6441a2664b278e2dc3d86d38daec | Expression levels of hub genes were examined in tissue samples from 2.5 year old cattle.(A–E) Compared with other tissues, the expression levels of (A) Atp2a1, (B) Tmod4, (C) Lmod3, (D) Mybpc2, and (E) Ryr1 in muscle tissue were significantly increased. | PMC10105563 | peerj-11-15093-g010.jpg |
0.443223 | bf32fd26e3a940a9bd9748808daebf6e | To induce myogenic differentiation of bovine skeletal muscle satellite cells.(A) Cell state map of bovine BSMSCs in different culture periods; GM: Proliferative phase, DM1-5: Cell differentiation day 1 to day 5; (B–C) The mRNA expression levels of MyOG and MyHC in different culture periods were detected; (D) The bovine BSMSCs differentiated for 0 (D0), 3 (D3) and 5 days (D5) were analyzed by immunofluorescence staining (x200). Compared with the control, two asterisks (**) means extremely significant difference (P < 0.01). | PMC10105563 | peerj-11-15093-g011.jpg |
0.429263 | c97be5e473f54e55af24291832af928d | Expression levels of hub genes in bovine skeletal muscle satellite cells at different culture periods.(A–E) Compared with that before differentiation, the expression levels of (A) Atp2a1, (B) Tmod4, (C) Lmod3, (D) Mybpc2, and (E) Ryr1 were significantly increased after induction. | PMC10105563 | peerj-11-15093-g012.jpg |
0.480779 | c36761e414644d8abd9ddac77c1716d4 | Circos plot to indicate the relationship between hub genes and KEGG pathways. | PMC10105563 | peerj-11-15093-g013.jpg |
0.427986 | b6eec07f45644ccb856c43a6f5265420 | Area under the ROC curve of D-dimer cutoff ≥500 ng/mL of 0.6836. ROC, receiver operating characteristic. | PMC10106564 | fsurg-10-1041578-g001.jpg |
0.414574 | 754266251f7a4c6aa396247ccbd47016 | Area under the ROC curve at Wells score ≥3 cutoff point of 0.4964. ROC, receiver operating characteristic. | PMC10106564 | fsurg-10-1041578-g002.jpg |
0.402457 | 958fcc6dad064d21afbb4103a253ddbd | Area under the ROC curve at Caprini score ≥11 of 0.4988. ROC, receiver operating characteristic. | PMC10106564 | fsurg-10-1041578-g003.jpg |
0.409518 | 27880688f5774e7db0e46c5b9d127582 | Area under the ROC curve of D-dimers with the new cutoff value at 795 ng/mL of 0.7536. ROC, receiver operating characteristic. | PMC10106564 | fsurg-10-1041578-g004.jpg |
0.445993 | 5ebd03fbae6340c8aca66210025e88f0 | Roles of HSF1 in atherosclerosis. Macrophages uptake oxLDL through lipid uptake transporters and accumulate lipids intracellularly. Macrophages remove excessive intracellular lipids through lipid efflux transporters. Unbalanced lipid homeostasis leads macrophages to form foam cells, leading to the formation of atherosclerosis plaques. Chronic inflammation, PSR, and ROS induce the transcriptional function of HSF1 to express HSPs, such as HSP27 and HSP72. Intercellular HSPs (iHSPs) promote cholesterol efflux and inhibit lipid uptake. Secreted extracellular HSPs (eHSPs) play dual roles in atherosclerosis. HSPs inhibit atherogenesis during the early stage of atherosclerosis but promote atherosclerosis during the late stage of atherosclerosis. HSF1 non-transcriptionally promotes lipogenesis and cholesterol synthesis via SREBP1/2 by interacting with and inhibiting AMPK. ABCA1, ATP binding cassette subfamily A member 1; ABCG1, ATP binding cassette subfamily G member 1; AMPK, AMP-activated protein kinase; CD36, cluster of differentiation 36; eHSPs, extracellular heat shock proteins; HSE, heat shock element; HSF1, heat shock factor 1; HSPs, heat shock proteins; iHSPs, intracellular heat shock proteins; LDLR, low-density lipoprotein receptor; oxLDL, oxidized low-density lipoprotein; p, phosphorylation; PSR, proteotoxic stress response; ROS, reactive oxygen species; SR-A, scavenger receptor type A; SR-BI, scavenger receptor class B type I; SREBP1/2, sterol regulatory element binding protein 1/2. Images were created with BioRender.com. | PMC10106699 | fcvm-10-1155444-g001.jpg |
0.424772 | 2e2b4ade548c418fbd577001f94aa7eb | HSF1 regulatory domains and post-translational modifications. HSF1 is composed of several functional domains, including a DNA-binding domain (DBD), a regulatory domain (RD), a heptad repeat (HR), and a transactivating domain (AD). Specific sites for serine/threonine phosphorylation (P), acetylation (AC), and SUMOylation (S) that activate or inhibit HSF1's activity are shown. These post-translational modifications are mediated by a variety of kinases, de-acetylases, and SUMOylases. AMPK, AMP-activated protein kinase, Akt, protein kinase B; CaMKII, calcium/calmodulin-dependent protein kinase II; CK2, casein kinase 2; ERK, extracellular signal-regulated kinase; GSK3, glycogen synthase kinase 3; JNK, c-Jun N-terminal kinase; mTOR, mammalian target of rapamycin; MEK, mitogen-activated protein kinase; PKA, protein kinase A; PKC, protein kinase C; PLK1, polo-like kinase 1; SIRT1, sirtuin 1; UBC9, ubiquitin-conjugating enzyme E2I. Images were created with BioRender.com. | PMC10106699 | fcvm-10-1155444-g002.jpg |
0.40441 | afa3ae548891422e8bd2a25aa097e98b | Grapevine embryogenic callus system (cv. Thompson Seedless) and stable transformation with the GFP gene. (a) Unopened leaves cultured on initiation medium (bar = 6 mm) produced (b) sectors of embryogenic and non-embryogenic callus (bar = 2 mm). (c) Embryogenic callus proliferated and (d) produced somatic embryos ready for transformation (bars = 1 mm). (e) Somatic embryos after 72 h of co-cultivation with Agrobacterium tumefaciens under white light and (f) UV light (bars = 0.5 mm). (g) Embryogenic callus induced from somatic embryos under white light and (h) UV light (bars = 0.75 mm). | PMC10108004 | uhac240f1.jpg |
0.44771 | b5f829c1a5984c308bad851cb1134e74 | Isolation of grapevine protoplasts (cv. Thompson seedless) overexpressing GFP, and the subsequent regeneration stages. (a) Embryogenic callus overexpressing GFP under white light and (b) UV light (bars = 1 mm). (c) Protoplasts isolated from transgenic callus, viewed under white light and (d) UV light (bars = 20 μm). (e) Protoplasts stained with Fluorescent Brightener 28 under white light and (f) UV light (bars = 20 μm). (g) The first protoplast cell division occurred after 3 days, viewed under white light and (h) UV light (bars = 30 μm). (i) Somatic embryos at the globular stage of embryo development under white light and (j) UV light (bars = 70 μm). (k) Somatic embryos at the heart stage of embryo development under white light and (l) UV light (bars = 70 μm). | PMC10108004 | uhac240f2.jpg |
0.418444 | 60f8eda27ba248e6a9cb33a95e233941 | Regeneration of plants from protoplasts overexpressing GFP. (a) Mature cotyledonary somatic embryos under white light and (b) UV light (bars = 0.5 mm). (c) Germinated somatic embryos under white light and (d) UV light (bars = 0.8 mm). (e) Apical young leaves of a regenerated plantlet under white light and (f) UV light (bars = 1 mm). (g) Transgenic plantlet regenerated in vitro. (h) Regenerated whole transgenic plant in the greenhouse. (i) Wild-type plantlet regenerated in vitro. (j) Wild-type plant in the greenhouse. | PMC10108004 | uhac240f3.jpg |
0.385958 | ba15613d5052423ab0d554049244ace7 | Nuclear localization of Cas9-GFP in grapevine (cv. Thompson Seedless) protoplasts and somatic embryos, and the regeneration of plantlets from protoplasts transfected with RNP2 and RNP4. (a) Nuclear localization of Cas9-GFP in protoplasts 1, 24, 48 and 72 h post-transfection, viewed under white light (bright field), with nuclear staining (Hoechst 33342), under UV light (GFP) and a merged view of the Hoechst 33342 and GFP images (merged), compared to a PEG-only transfection control (bars = 5 μm). (b) Germinated somatic embryos regenerated from protoplasts overexpressing GFP (control), from protoplasts transfected with RNP2 and lacking GFP activity (OFF-GFP RNP2) and from protoplasts transfected with RNP4 and lacking GFP activity (OFF-GFP RNP4) under white light (bright field) and UV light (GFP) (bars = 0.8 mm). (c) Phenotype of plantlets regenerated in vitro from PEG-transfected protoplasts (control) and from those transfected with RNP2 (OFF-GFP RNP2) and RNP4 (OFF-GFP RNP4). | PMC10108004 | uhac240f4.jpg |
0.394596 | 1ea6337767fe475b97cca3e631ba1e9d | Analysis of GFP mutations in edited plants. (a) Adenine and thymidine insertions (red boxes) in plants regenerated from protoplasts transfected with RNP2 (E2) and RNP4 (E4), both lacking GFP activity, compared to plants regenerated from PEG-transfected protoplasts (control). The PAM sequence is underlined in violet. (b) GFP amino acid sequence frameshift in plants E2 and E4 compared to control. (c) GFP fluorescence intensity based on total protein extracted from plants E2 and E4 compared to wild-type (WT) plants (lacking GFP) and control (C) transgenic plants expressing GFP. The (+) lane is an additional positive control of total protein extracted from GFP-overexpressing tobacco plants. Data are means ± SE (n = 3). (d) Western blots of total protein extracted from E2 and E4 leaves compared to WT and C samples, probed with an anti-GFP polyclonal antibody. The same polyclonal antibody is used here as an additional positive control for the detection step. The anticipated molecular weight of GFP is 27 kDa. M, marker (PageRuler Pre-stained Protein Ladder, 10—180 kDa; Thermo Fisher Scientific). | PMC10108004 | uhac240f5.jpg |
0.389318 | c2fbe0aa6123472f8411f95466ffcbdf | Flow chart of CRISPR/Cas9-mediated gene editing in grapevine, including a step-by-step protocol based on the direct delivery of RNPs to protoplasts. The entire procedure takes ~18 months. | PMC10108004 | uhac240f6.jpg |
0.399951 | 92b37fb42c7c44c6a11f787b4bb55b5e | A) Upconversion mechanism and subsequent FRET sensitization of pinacolone resulting in a Norrish type I reaction and formation of isobutylene. B) Absorption spectra (solid line) of pinacolone (dark red), acetone (green), and normalized emission (dotted line) of bTIPS‐Bz in cyclohexane with the spectral overlap being highlighted. Inset: Stern–Volmer plot corresponding to quenching of upconverted bTIPS‐Bz emission by the carbonyl compounds. C) NMR scale experiment of 100 μM 4CzIPN, 10 mM bTIPS‐Bz, and 100 mM pinacolone in Ar‐saturated cyclohexane:toluene (9 : 1) with control experiments before and after 30 min irradiation at 447 nm with 1.1 W. Shown are the 1H NMR signals of isobutylene as a stable product of the UC‐FRET‐driven Norrish reaction. D) Comparison of FRET efficiencies between pinacolone and acetone. E) and F) Mechanistic LFP experiments with 355 nm laser pulses of ≈10 ns duration of 20 μM 4CzIPN and 10 mM bTIPS‐Bz in Ar‐saturated cyclohexane:toluene (9 : 1) with different concentrations of pinacolone and acetone used for the Stern–Volmer plots in the inset of panel B). E) Time‐resolved emission at 318 nm. F) Normalized time‐gated (delay, 6 μs; integration over 500 μs) emission spectra. | PMC10108172 | ANIE-62-0-g001.jpg |
0.39222 | c16c063c23c6468ca528b242c66f3d6e | Photon upconversion studies with deoxygenated solutions containing 44 or 88 μM 4CzIPN and 10 mM bTIPS‐Bz in cyclohexane:toluene (9 : 1) using a cw laser for excitation at 447 nm or 445 nm. A) Power‐dependent spectra of the normalized upconverted emission. Inset: Photostability measurement at different sensitizer concentrations at a cw laser power of 471 mW cm−2. B) External upconversion quantum yield, Φ
UC, plotted against the laser power (with 44 μM 4CzIPN). C) Normalized UC emission plotted against the laser power on a double‐logarithmic scale (with 44 μM 4CzIPN). The threshold intensity I
th was determined from the crossing point. See Supporting Information for details. | PMC10108172 | ANIE-62-0-g002.jpg |
0.402916 | e558fac5d4754ad1bfb5e08f26767aa9 | Structures and emission spectra of recently used annihilators for blue‐to‐UV upconversion. This work: Novel benzene‐based annihilator (bTIPS‐Bz) suitable for blue‐to‐UVB upconversion that has been successfully employed as an energy donor in a subsequent FRET activation of UVB‐absorbing carbonyls. | PMC10108172 | ANIE-62-0-g003.jpg |
0.45716 | de5b0af86eca46b6b5da7e139e038003 | Mechanistic LFP experiments with 355 nm laser pulses of ≈5 ns duration. If not stated otherwise 20 μM 4CzIPN and 10 mM bTIPS‐Bz in Ar‐saturated cyclohexane:toluene (9 : 1) were used. A) Luminescence quenching experiments of 4CzIPN (detection wavelength, 477 nm) at different annihilator concentrations. Inset: corresponding Stern–Volmer plot. B) Transient absorption spectra of only 4CzIPN (cyan) recorded 1 μs after the laser pulse and combined with bTIPS‐Bz after 6 μs (purple) and oscillator strength of
3
bTIPS‐Bz computed by TD‐DFT. Inset: Computed spin density of the triplet state of bTIPS‐Bz with λ
max,DFT of the predicted main absorption bands. C) Normalized time‐gated (delay, 6 μs; integration over 500 μs) emission spectra of the complete upconversion system (pink), only 4CzIPN (cyan), and only bTIPS‐Bz (dark blue). Inset: Time‐resolved upconversion emission plotted logarithmically at different sensitizer concentrations under pulsed excitation at 445 nm. D) Time‐resolved emission (319 nm) and transient absorption (342 nm) traces upon excitation of the UC system. The asterisk marks laser stray light. | PMC10108172 | ANIE-62-0-g005.jpg |
0.448132 | 4a2d5e84b5984250b56f4f1c8a875abd | A) Structures of TIPS‐Bz, tTIPS‐Bz and Bz. B) Energy diagram visualizing the lowest triplet‐excited state energies of 4CzIPN, unsubstituted benzene, and TIPS‐ethinyl substituted benzenes. C) Structures, absorption (solid line), and normalized emission (dotted line) spectra of bTIPS‐Bz and 4CzIPN in cyclohexane. The excitation wavelengths (445 nm and 447 nm) used for upconversion measurements are indicated by blue vertical lines. | PMC10108172 | ANIE-62-0-g006.jpg |
0.448193 | 34b706cc9cce4ee8a1accf00ad56f9b4 | The comparison of post-training test results of both groups. Score of the performance of outpatient service including physical examination assessment and inquiry assessment. Score of the management of chronic condition including SOAP medical record writing and presentation of chronic condition management | PMC10108467 | 12909_2023_4210_Fig1_HTML.jpg |
0.469255 | 5598e376562c4464b6934f7ac6900b33 | Upper airway, with areas of the nasopharynx (between skull base and
hard palate), oropharynx (soft palate to the upper border of the
epiglottis), and hypopharynx or laryngopharynx (from the tongue base to
the lower border of the cricoid cartilage). | PMC10108585 | 2177-6709-dpjo-28-01-e23spe1-gf1.jpg |
0.44334 | ac5576b8794d4a1786bbb7b39085bb90 | A, B, C) Intraoral view of a patient in maximum
intercuspation. D, E, F) The same patient using a mandibular
advancement device. | PMC10108585 | 2177-6709-dpjo-28-01-e23spe1-gf2.jpg |
0.418837 | 1b62fe9fcc8548d4b2bc8ff79287916e | Different mandibular advancement devices (individualized
bi-blocks made of rigid acrylic plates that allow
titration). | PMC10108585 | 2177-6709-dpjo-28-01-e23spe1-gf3.jpg |
0.368199 | 17f6493e169f427787097ac63510c91b | Some sleep assessment technology devices presented in a
systematic review,
22
available on Google Play and iOS platforms. | PMC10108585 | 2177-6709-dpjo-28-01-e23spe1-gf4.jpg |
0.509201 | 502c60c5516f4b94845068c072fefc88 | NAD+ competitive inhibitor RBN2397 blocks PARP7-mediated ADP-ribosylation of the AR in cells. A, Effect of RBN2397 (12 pmol/L to 81 nmol/L) on androgen-induced AR ADP-ribosylation in PC3-AR cells treated for 17 hours. AR and PARP7 were detected using Western blotting method. ADPr-AR was detected using Fl-Af521. B, RBN2397 inhibits androgen-dependent AR ADP-ribosylation and AR/DTX3L/PARP9 complex formation in PC3-AR cells cotreated with R1881 for 17 hours. Flag-AR was immunoprecipitated and blotted. C, RBN2397 inhibits androgen-dependent AR ADP-ribosylation in VCaP prostate cancer cells. AR was immunoprecipitated and protein and ADP-ribose were detected. D, Dose–response and RBN2397 EC50 values for recombinant PARP7 and PARP1 ADP-ribosyltransferase activities measured in vitro, using Histone H2A and H2B as a substrate. E, Heatmaps depicting the effect of RBN2397 (7.6 nmol/L) on the ADP-ribosyltransferase activity of individual PARP family members in vitro (left), and compared with the expression levels of PARP family members in human prostate cancers (TCGA; RNA-seq data; right). F, Protein half-life measurements of HA-PARP7 determined in the absence and presence of RBN2397. Cells were pretreated with RBN2397 for 1 hour prior to addition of cycloheximide (0.1 mg/mL). Error bars reflect the SD of biological triplicates. G, Auto-ADP-ribosylation of ectopically expressed PARP7 detected in HA-immunoprecipitates from PC3-AR(HA-PARP7) cells treated with RBN2397. Proteasome inhibition with MG132 (10 μmol/L, 4 hours) was used to increase PARP7 levels. | PMC10108886 | crc-23-0086_fig1.jpg |
0.407059 | bcfda22df9b646f7811b2604615a37e8 | Growth-inhibitory effect of RBN2397 in AR-positive prostate cancer cells in the presence of androgen. A, Cell growth (MTT assay) in response to combinations of RBN2397 and R1881. Each condition reflects eight biological replicates. For A–C, the error bars depict the SD. ****, P < 0.0001; ***, P < 0.001; n.s., not significant. B, RBN2397 dose–response growth curves from VCaP, CWR22Rv1, PC3-AR, and PC3 in the presence of the R1881. C, Phase contrast microscopy showing the morphology of cells in the presence or absence of RBN2397 and R1881 for 6 days (slower growing VCaP and CWR22Rv1) and 3 days (faster growing PC3-AR and PC3). D, Dead cell detection by Trypan blue staining after culturing cells as in C. The experiments were performed in triplicate. | PMC10108886 | crc-23-0086_fig2.jpg |
0.494132 | 97b63e3be7bc4c8b98d647f962c0c943 | Growth inhibition by RBN2397 is PARP7 dependent and associated with elevated CDKN1A (p21) expression. A, Treating PC3-AR cells with siPARP7 partially reduces the growth inhibitory effect of RBN2397. PARP7 knockdown in the cell growth experiments (A–C) was confirmed by immunoblotting for PARP7, with TUBULIN as a loading control (top). For the cell growth in A–C and E and F, each condition reflects eight biological replicates, error bars show the SD, and the statistical differences between cell lines at each RBN concentration are ****, P < 0.0001; ***, P < 0.001; **, <0.01; *, <0.05 (bottom). B, Stable knockdown of PARP7 in PC3-AR treated with R1881 partially protects cells from the growth-inhibitory effects of RBN2397. C, Stable knockdown of PARP7 in CWR22Rv1 treated with R1881 partially protects cells from the growth-inhibitory effects of RBN2397. D, Immunoblot detection of CDK inhibitor CDKN1A and PARP7 in prostate cancer lines grown ±R1881 and ±RBN2397 for 24 hours. E, Treating PC3-AR cells with si-CDKN1A (20 nmol/L) partially reverses the growth-inhibitory effect of RBN2397. The expression levels of CDKN1A and PARP7 ±R1881 and ±RBN2397 were determined by immunoblotting (top). F, CRISPR knockout of CDKN1A in PC3-AR cells reduces the growth-inhibitory effect of RBN2397. The knockout was validated by immunoblotting for CDKN1A (top). | PMC10108886 | crc-23-0086_fig3.jpg |
0.42381 | b56af389b61c42cca548e4d54f006e85 | PARP7 induction using AHR agonists sensitizes prostate cancer cells to growth inhibition by RBN2397. A, Effect of RBN2397 on AR− (PC3, DU145) and AR+ (CWR22Rv1, VCaP) prostate cancer lines treated with AHR agonists BBQ and FICZ to induce PARP7. In A, D–H, each condition reflects eight biological replicates, error bars show the SD, and ****, P < 0.0001; ***, P < 0.001; **, <0.01. B, Dead cell detection by Trypan blue staining after culturing cells in the presence or absence of RBN2397 and BBQ for 6 days (slower growing VCaP and CWR22Rv1) and 3 days (faster growing PC3-AR and PC3). The experiments were performed in triplicate, error bars show the SD, and ***, P < 0.001; **, <0.01, *, <0.05; ns, not significant. C, Phase contrast microscopy showing the morphology of cells treated with AHR agonist and RBN2397. The treatments for CWR22Rv1 were performed as part of the experiments shown in Fig. 2C involving R1881 and RBN2397. A similar image for CWR22Rv1 cells with vehicle alone (−) is used in both Fig. 2C and 4C. D, RBN2397 dose–response curve of PC3-AR cells treated with BBQ. E, RBN2397 dose–response curve of DU145 cells treated with BBQ. F, RBN2397 dose–response curve of VCaP cells treated with BBQ. G, Stable knockdown of PARP7 blunts the growth-inhibitory effects of RBN2397 in CWR22Rv1 cells treated with BBQ. H, Stable knockdown of PARP7 blunts the growth-inhibitory effects of RBN2397 in PC3-AR cells treated with BBQ. | PMC10108886 | crc-23-0086_fig4.jpg |
0.362439 | abeedcf557ed413fb98917f090cebc49 | RBN2397 traps PARP7 in the nucleus. A, IF microscopy of PARP7 in PC3 cells after treatment with RBN2397 and BBQ. B, IF of PARP7 in CWR22Rv1 after treatment with RBN2397 and R1881. C, Biochemical fractionation of PC3-AR cells with RBN2397 and R1881 treatment and immunoblot detection of PARP7, AR, TUBULIN, and LAMIN A. D, Biochemical fractionation of PC3 cells treated with RBN2397 and BBQ, and immunoblot detection of PARP7, AHR, TUBULIN, and LAMIN A. E, IF of HA-PARP7 in PC3-AR(HA-PARP7) cells after treatment with RBN2397. The left panel shows cells directly fixed and processed for IF microscopy. The right panel shows cells extracted with TX-100 buffer prior to fixation. F, Biochemical fractionation of PC3-AR(HA-PARP7) cells with RBN2397 treatment and immunoblot detection of HA-PARP7, TUBULIN, and LAMIN A. | PMC10108886 | crc-23-0086_fig5.jpg |
0.482204 | cb12a394425d44ef8f892093959bd7ab | PARP7 expression in prostate cancer. A, Violin plots (boxplot inserted) showing PARP7 expression levels in CPM in normal prostate, primary tumors and metastatic AR− and AR+ tumors. The red line indicates the level of PARP7 in the VCaP cell line required for RBN2397-mediated growth inhibition and the gray line shows the basal level of PARP7 in VCaP cells. P values calculated for pairwise comparisons using the Wilcoxon test are indicated (***, <0.001; **, <0.01; *, < 0.05; ns, not significant). All compared values come from the recount3 project. B, Scatter plots comparing expression of PARP7 with AR and AHR in primary tumors (left), metastatic AR− tumors (middle), and metastatic AR+ tumors (right). Spearman correlation coefficients and P values are shown on the plots. C, Boxplots comparing enrichment scores for HALLMARK_INTERFERON_ALPHA_RESPONSE gene set, calculated using GSVA method between lung (LUAD) and prostate (PRAD) primary tumor samples (left); between high PARP7 expression (top quartile, n = 124) and low PARP7 expression (bottom quartile, n = 124) in prostate primary tumor samples (middle); between high PARP7 expression (top quartile, n = 128) and low PARP7 expression (bottom quartile, n = 128) in lung primary tumor samples (right). The P values from Wilcoxon rank-sum tests are shown on the plots. | PMC10108886 | crc-23-0086_fig6.jpg |
0.550433 | afd01ba5790544f6aa893bc110e9ea36 | Flow diagram of participants’ enrollment, assessment, and allocation. KQIDS-SR, Korean Quick Inventory of Depressive Symptomatology Self-Report; STAI-S, State–Trait Anxiety Inventory-State; HRSD, Hamilton Rating Scale for Depression; HAS, Hamilton Anxiety Scale; ECG, Electrocardiogram. | PMC10109339 | fpsyt-14-1124550-g001.jpg |
Subsets and Splits
No community queries yet
The top public SQL queries from the community will appear here once available.