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0.454502 | ed9898648e584205a7cb5af1d885e98f | Relative energies in kcal mol−1 of the most stable intermediates and first transition state determined for acetone (top) and propene (bottom) hydrogenation reactions. The corresponding relaxed structures and output files are attached in ESI.† | PMC9473539 | d2sc02150a-f8.jpg |
0.43652 | 8fc82329b7bd49f4b0d52e8289404486 |
(
A
) T2-weighted magnetic resonance imaging (MRI) axial view showing a solitary lesion in the right posterior temporal lobe with perilesional edema. (
B
) Diffusion-weighted image showing mild incomplete restriction in the wall of the lesion. (
C
) Postcontrast T1-weighted axial MRI view showing ring enhancement in the lesion.
| PMC9473804 | 10-1055-s-0042-1750384-i23421-1.jpg |
0.433488 | 0fa232513f0b44509e8c1b2a42ffa756 |
(
A
) T2-weighted axial magnetic resonance imaging (MRI) after 3 weeks showing multicentric cystic lesions in the right temporal lobe, right frontal lobe, and left cerebellum. (
B
) Diffusion-weighted images corresponding to the lesions showing marked restriction centrally in the superficial cystic lesion and mild restriction in the deep temporal lesion. (
C
) Spectroscopy image with the voxel placed frontally showing marked lipid lactate peak. (
D
) Spectroscopy image with the voxel placed temporally showing marked choline peak.
| PMC9473804 | 10-1055-s-0042-1750384-i23421-2.jpg |
0.437084 | f6c701891f0040629f30898e5669121c |
(
A
) Gram-positive filamentous rod shape organism suggestive of Nocardia (
black arrow
). (
B
) Microvascular hyperplasia (
blue arrow
). (
C
) Densely cellular glial tumor with pleomorphic astrocytic cells in fibrillary background. (
D
) High K
i
-67 score of 30%. These features were representative of glioblastoma.
| PMC9473804 | 10-1055-s-0042-1750384-i23421-3.jpg |
0.429589 | 4dffa2b8b3c54409a9d430ff1aaa2997 |
(
A
) (
Left to right
) Plain computed tomography (CT) head, T2-weighted axial magnetic resonance imaging (MRI), diffusion-weighted axial MRI, and postcontrast axial MRI showing a mass in the left frontal lobe with marked edema, mild restriction, and heterogeneous peripheral enhancement suggestive of high-grade glioma. (
B
)
(Left to right
) T1-weighted axial MRI, T2-weighted axial MRI, diffusion-weighted axial MRI, and postcontrast axial MRI after 18 months of follow-up showing no recurrence or residue.
| PMC9473804 | 10-1055-s-0042-1750384-i23421-4.jpg |
0.398628 | 06ff85fecb334af5b4990d609649cd45 |
When did respondents tattoo lesions?
| PMC9473856 | 10-1055-a-1914-6197-i2495ei1.jpg |
0.479684 | cccf0ac4d3eb4abcab44bf2408336114 | A flowchart of the selection process. ABPM, ambulatory blood pressure measurement; MRI, magnetic resonance imaging. | PMC9474888 | fneur-13-963648-g0001.jpg |
0.387098 | 5a404e8275b7489cad7275ca1efdc82c | Subregions of temporal GM with significant atrophy associated with night systolic BPV. The left entorhinal cortex (marked in pink, P = 0.010) and the right fusiform gyrus (marked in red, P = 0.039) showed significantly greater atrophy associated with increased night systolic BPV. | PMC9474888 | fneur-13-963648-g0002.jpg |
0.484145 | 6fd987212e354557b1d8e8645ca5bb1b | Schematic of the data analysis pipeline. (A) Discovery of prediction model. Imaging feature extraction for each brain region was based on the Brainnetome atlas and used to establish brain age prediction models. (B) Verification of the prediction model. Determination of the brain age prediction model in SSVD patients and evaluation of the association of brain age with cognitive assessments. (C) Expansion of the model. Establishment of a SVM classification model with brain age-related imaging features and exploration of its neurobiological basis. HCs, healthy controls; SSVD, subcortical small-vessel disease; GMV, gray matter volume; mALFF, mean amplitude of low frequency fluctuation; mfALFF, mean fractional amplitude of low-frequency fluctuation; RVR, relevance vector regression; SVM, support vector machine; SCI, subjective cognitive impairment; MCI, mild cognitive impairment; AUC, area under the curve. | PMC9475066 | fnagi-14-973054-g001.jpg |
0.443475 | 19a014240e234db6afe8c84c79d92807 | Multivariate relevance vector regression analysis. Scatterplot showing the estimated age for each participant derived from their imaging features compared with their chronological age (A: HCs; B: SSVD patients). Distribution of permutation of the prediction R and mean absolute error (C,D: HCs; E,F: SSVD patients). The values obtained using real scores are indicated by the dashed line. HCs, healthy controls; SSVD, subcortical small-vessel disease. | PMC9475066 | fnagi-14-973054-g002.jpg |
0.424097 | 803388aab1c9485ab10fbf4e27218afb | Establishment of SVM classification model. (A) Visualizations of 25 gray matter volume features using relevance vector regression analysis for the prediction of brain age in SSVD patients. (B) Classification Performance of SVM classification model between SCI patients and MCI patients in participants with SSVD. SSVD, subcortical small-vessel disease; SVM, support vector machine; AUC, area under the curve. | PMC9475066 | fnagi-14-973054-g003.jpg |
0.438096 | 01e8bfff2fdf46eb83072617c3b323ec | Correlation between the support vector machine model classification probabilities and MoCA (A), TMT-A (B), TMT-B (C), Stroop-C (D) scores, information processing speed total scores (E), and plasma levels of T-AOC (F) in patients with SSVD. SSVD, subcortical small-vessel disease; MoCA, Montreal Cognitive Assessment; TMT-A, Trail Making Test A; TMT-B, Trail Making Test B; Stroop-C, Stroop Color and Word Test C; T-AOC, total antioxidant capacity. | PMC9475066 | fnagi-14-973054-g004.jpg |
0.44543 | 4d977639d71545708f4fed9c05a4df1b | A: Magnetic resonance imaging. B: Magnetic resonance cholangiopancreatography.. | PMC9475139 | fsurg-09-937682-g001.jpg |
0.390314 | f4f2fa6adcca4380af8d9bda21e390d9 | Preoperative design. A: Layout of “5 trocar-puncture”. B: LCP-removal procedure. C: Schematic diagram of CP pancreatic margin. | PMC9475139 | fsurg-09-937682-g002.jpg |
0.441431 | e7b40b3f69a244b9829251cfece89614 | Pancreatic reconstruction process. | PMC9475139 | fsurg-09-937682-g003.jpg |
0.419195 | bae1f3accf8b442cb101dce2eb06ae69 | Laparoscopic central pancreatectomy (involving A, B, C, D four steps). | PMC9475139 | fsurg-09-937682-g004.jpg |
0.460287 | d343367c041a492bbbb4b7e57b08a67a | The pigtail position. | PMC9475139 | fsurg-09-937682-g005.jpg |
0.444662 | 47bab7d0f85a4e2bad5456076391730a | Postoperative outcome: CT and pathological images. A: CT images, B: pathological images. | PMC9475139 | fsurg-09-937682-g006.jpg |
0.472552 | a782782a10994cd4b30e2c7193f9dea7 | Postoperative outcome: the amylase (A) and volume of abdominal drainage tubes (B). | PMC9475139 | fsurg-09-937682-g007.jpg |
0.450976 | 588546d9bff94118bb8d9db6b878a4f4 | The steps involved in raw ECG signal preprocessing and computation of heart rate variability metrics are illustrated (A) Preprocessing of ECG signal includes R peak detection, artifact correction, interpolation and detrending. Subsequently, time domain (SDNN, RMSSD), frequency domain (LFnu, HFnu), and non-linear (SD1, SD2) metrics are computed. (B) Visual illustration of Poincaré plots in three different experimental situation namely complete autonomic blockade, parasympathetic blockade and balanced sympathetic-parasympathetic activity. | PMC9475489 | nihms-1783240-f0001.jpg |
0.47615 | 55c163b330634ec2a1021ac088e25ba8 | Mean (SEM) of common HRV metrics in the first 48 hours of life in infants with different subtypes of brain injury (color coded). Watershed and Mixed pattern of injury was associated with most severely depressed while basal ganglia injury was associated with moderately depressed short-term (RMSSD, SD1) and overall variability (SDNN, SD2) at all timepoints compared to infants with normal MRI or focal infarct. There were no significant differences in the temporal trends of frequency domain HRV measures between the groups. | PMC9475489 | nihms-1783240-f0002.jpg |
0.467254 | 6d395d020919444083230f6244cfeb1b | Comparing the topography of Poincare maps at 12 hours of life. Each plot from one patient of each brain injury subtype (a) Focal infarct, comet shaped; (b) basal ganglia pattern, cigar shaped; (c) mixed pattern of brain injury, tight cluster; (d) normal brain MRI, comet shaped. | PMC9475489 | nihms-1783240-f0003.jpg |
0.454296 | cabdc0ff059a4d4fb0411df96e57895f | Study design and flow of participants. | PMC9476145 | bmjopen-2022-062722f01.jpg |
0.473199 | a64af3416f344cdf8c1e0eadac9d2b43 | Gas chromatogram of the reaction mixture for
the synthesis of GD
from GL and DMC using KNO3/Al2O3 (30%,
800) as the catalyst. Peaks are as follows: (1) methanol, (2) DMC,
(3) n-butanol, (4) GD, (5) GL;, (6) tetraethylene
glycol, and (7) GC. | PMC9476187 | ao2c02381_0001.jpg |
0.52253 | 75b4f862857947f69d4dc6e955bda07a | (a) XRD patterns of 30%
KNO3/Al2O3 catalysts at different
calcination temperatures. (b) XRD patterns
of KNO3/Al2O3 catalysts with different
loadings (%) of KNO3 at 800 °C and the recovered sample
after the second recycling. (c) FT-IR spectra of KNO3/Al2O3 at different calcination temperatures. (d) FT-IR
spectra of KNO3/Al2O3 catalysts with
different loadings (%) of KNO3 at 800 °C. | PMC9476187 | ao2c02381_0002.jpg |
0.389702 | 88511a88303249d7aeeb2bfb961b7569 | SEM images
of KNO3/Al2O3 catalysts.
(a) KNO3/Al2O3 (30%, 700), (b) KNO3/Al2O3 (30%, 800), (c) KNO3/Al2O3 (30%, 900), and (d) KNO3/Al2O3 (30%, 800) recovered after the second recycling. | PMC9476187 | ao2c02381_0003.jpg |
0.454239 | fd60e459cb6f424288c84a64f57ebd1a | SEM images of KNO3/Al2O3 (30%
KNO3, 800). Images are magnified 10 000–50 000×.
Particle size s are 200–300 nm. | PMC9476187 | ao2c02381_0004.jpg |
0.426246 | 499d1cbdc84247d79c6297bf91978232 | (a) CO2-TPD profiles of KNO3/Al2O3 with a 30% loading of KNO3 at different
calcination temperatures. (b) Effect of reaction temperature on the
transesterification of GL with DMC. (c) The effect of the DMC/GL molar
ratio on the transesterification of GL with DMC. (d) Effect of the
catalyst amount on the transesterification of GL with DMC. | PMC9476187 | ao2c02381_0005.jpg |
0.487272 | 5c21a58dd9614007a8adffdd15fb5ea0 | (a) Effect of the reaction
time on the transesterification of GL
with DMC. (b) Effect of the catalyst reusability on the transesterification
of GL with DMC. | PMC9476187 | ao2c02381_0006.jpg |
0.525066 | 92e88bc6c4f040ac9aa5420ad2cafeb6 | Synthesis of GD from GL and DMC over the KNO3/Al2O3 Solid Base Catalyst | PMC9476187 | ao2c02381_0007.jpg |
0.474798 | b4f14a51fa5f40be893a2defe76717d9 | Proposed
Reaction Mechanism for the One-Pot Synthesis of GD from
GL and DMC Using Nanocatalysts | PMC9476187 | ao2c02381_0008.jpg |
0.462325 | d687ec25d2904145b5810f63ebed08fc | Schematic diagram of the modified MERDOC measurement system. The measurement setup consists of (1) three mixing chambers equipped with silica gel desiccant; (2) exhaled air water trap, and; (3) two high-efficiency particulate filters. A detailed description of the experimental setup is discussed in Madueño et al. [18]. Photos on the right show the actual sampling of study participants in different exposure scenarios, a public transport and b light walking. Please note that the exposure and exhaled BC mass concentrations were measured by separate micro-aethalometers placed in two different backpacks carried by different individuals (study supervisor (BC exposure measurement) and volunteers (exhaled BC mass concentration measurement)) | PMC9476571 | 12989_2022_501_Fig1_HTML.jpg |
0.417711 | 0828a41f2944422f98e3e0504041cac5 | The stationary measurement sites during TAME-BC were located in A Manila North Port, Manila City and B East Avenue, Quezon City. The exposure of study participants was conducted on a predetermined commuting route within a 5 km radius from the stationary measurement sites. The study participants were given the freedom to choose between commuting by riding Jeepney (along the red line) or commuting by walking (along the brown line), or both | PMC9476571 | 12989_2022_501_Fig2_HTML.jpg |
0.424308 | bd2c6136a1ce4db8a44aa77b947bcf19 | Diurnal and daily variation of BC mass concentration in Manila North Port, Manila City (red) and East Avenue, Quezon City (black). Error bars indicate standard deviation | PMC9476571 | 12989_2022_501_Fig3_HTML.jpg |
0.450634 | d0376b48617a49639c816180706935a2 | Spatial distribution of BC mass concentration in TMEs along the routes in A Manila and B Quezon City. Dashed lines correspond to an inner gated area with restricted traffic. The midpoint of the color scale was set to 15 μg m−3 (yellow) to visually represent the areas where the BC mass concentration alone exceeded (orange to red) the World Health Organization suggested PM2.5 daily limit values. Each tile is a 55 m square grid resolution | PMC9476571 | 12989_2022_501_Fig4_HTML.jpg |
0.36684 | 3e0fbc3782e8458195028339eac5fe46 | Relative abundance of bacteria at the phylum level of fermented mutton sausage during natural ripening (the 15 most abundant phyla). | PMC9478030 | fmicb-13-961117-g001.jpg |
0.42479 | 0184f16a285b45f190ba4bb5e6319806 | Relative abundance of bacteria at the genus level of fermented mutton sausage during natural ripening (the 15 most abundant genera). | PMC9478030 | fmicb-13-961117-g002.jpg |
0.513863 | f3656787746c49e2b477d8c22b9eb6a6 | A Venn diagram of fermented mutton sausage during natural ripening based on the OTUs of bacteria. | PMC9478030 | fmicb-13-961117-g003.jpg |
0.432127 | 9b9ae706800448e88642daa8e1fd41c7 | Principal coordinates analysis (PCoA) results of bacterial communities of fermented mutton sausage during natural ripening based on Bray–Curtis distance with 95% confidence level. | PMC9478030 | fmicb-13-961117-g004.jpg |
0.435919 | bc584a9c6cf544d0b2ffe635e7a4dd72 | LEfSe highlights consistently differentia bacteria taxa of fermented mutton sausage during natural ripening within four stages. (A) Cladogram representation; (B) the predominant bacteria of the microbiota, LDA score is over 4. Labels beginning with o_indicate order; f_family; g_genus; s_species. | PMC9478030 | fmicb-13-961117-g005.jpg |
0.438096 | e1bb78c5e2604f38a087cea90916951e | Total ion current chromatogram of fermented mutton sausage on day 26. | PMC9478030 | fmicb-13-961117-g006.jpg |
0.472379 | 1cbec0eb6b794a9f9511f562b1a3ebe8 | The PCA score plot of total volatile compounds of fermented mutton sausage on days 0, 7, 16, and 26. | PMC9478030 | fmicb-13-961117-g007.jpg |
0.475514 | 2a7b1a1e1d534040b196ba9400a13807 | A heatmap of the Spearman rank correlation between genera with relative abundance in the top 15 and the volatile properties in fermented mutton sausage during natural ripening. The intensity of the colors represents the degree of correlation between the genera and volatile compounds, where the blue color represents a negative degree of correlation and red a positive correlation. | PMC9478030 | fmicb-13-961117-g008.jpg |
0.48109 | 9e4a1ef4e97a4ec4a6f958ef5ed6bed9 | Inosine overcomes resistance to immunotherapy by inflaming tumour immune microenvironment.a Volcano plot showing the hazard ratios (HR) of high/low levels of serum metabolites (n = 202, represented as points, high and low are stratified by the median of each metabolite) in CheckMate 025 renal cell carcinoma (RCC) patients with nivolumab (anti-PD1 Ab) treatment (n = 392). Overall survival is used as a Cox proportional hazards model. A cutoff at P = 0.01 is shown as a horizontal line and HR (high/low) = 1 is shown as a vertical line (HR: high/low <1 indicates that a high level of a metabolite is a benefit for ICB patients). b Kaplan–Meier plot of overall survival in RCC patients with nivolumab (anti-PD1 Ab) (High, n = 196, mean OS = 33; Low, n = 195, mean OS = 21) or everolimus (mTOR inhibitor) (High, n = 174, mean OS = 20; Low, n = 174, mean OS = 20) grouped by the inosine level at the median of baseline level. c–e Tumour volume and survival analysis of B16-F0 (c, n = 5), B16-GMCSF (d, n = 5), or 4T1 (e, n = 6) tumour-bearing mice treated with IgG2a (Ctrl), 400 mg/kg of Inosine (Ino), anti-CTLA4 + anti-PD1 (ICB) or ICB + Inosine (Ino + ICB) treatment. f tSNE plot of single-cell RNA sequencing of CD45+ immune cells from 4T1 tumours treated with Ctrl (n = 16199 cells) or Ino+ICB treatment (n = 9842 cells). g The frequency of gp70-specific CD8+ T cells in 4T1 tumour with Ctrl (n = 6), Ino (n = 6), ICB (n = 6), or Ino+ICB (n = 8) treatment for 15 days. Data are presented as Mean ± s.e.m. Statistical significance was determined by one-way ANOVA and Tukey test for multiple comparisons (tumour sized of c–e, g) or log-rank (Mantel–Cox) test (survival analysis of b–e). Source data are provided as a Source Data file. | PMC9478149 | 41467_2022_33116_Fig1_HTML.jpg |
0.417094 | 6e822a4aeb574c40a26d8651ce00d1cb | Inosine sensitises tumour cells to T-cell-mediated killing by modulating tumour immunogenicity.a Experimental strategy to evaluate the ability of inosine to enhance T-cell-mediated tumour killing by modulating T cells. b The relative cell viability of B16-GMCSF-OVA cells was shown. OT-1 T cells were pretreated with indicated concentrations of inosine or vehicle for 24 h, then co-cultured with B16-GMCSF-OVA tumour cells at a 2:1 E: T (Effector: T cells, Target: tumour cells) ratio for 48 h (n = 5). c The relative cell viability of 4T1 cells after incubation with activated CD8+ T cells pretreated with the indicated concentration of inosine at a 5:1 E: T ratio for 48 h (n = 5). d Experimental strategy to evaluate the ability of inosine to enhance T-cell-mediated tumour killing by modulating Tumour cells. e The relative cell viability of B16-GMCSF-OVA cells (left) and 4T1 cells (right) with Ctrl or inosine treatment following the method in a (n = 5). f Experimental strategy to evaluate the direct effect of inosine on tumour cells. g The relative cell viability (left) and apoptosis (right) of B16-GMCSF cells following inosine treatment at indicated concentrations for 48 h in vitro (n = 5). h The relative cell viability (left) and apoptosis (right) of 4T1 cells following inosine treatment at indicated concentrations for 48 h in vitro (n = 5). i Representative flow analysis (left panel) and quantifying (left panel) the intensity of cell surface MHC-I expression in B16-GMCSF cells treated with vehicle and inosine (100 μM) upon IFN-γ (20 ng/ml) treatment (n = 3). j, k Selective represented antigen processing/presentation and interferon-responsive gene expression in B16-GMCSF (j) and 4T1 (k) and tumour cells treated with inosine at indicated concentrations (n = 3). Data are presented as Mean ± s.e.m. Statistical significance was determined by Two-sided Student’s t test (i) and one-way ANOVA and Tukey test for multiple comparisons (b, c, e, g, h). NS no significant. Source data are provided as a Source Data file. | PMC9478149 | 41467_2022_33116_Fig2_HTML.jpg |
0.42104 | 871220f392b046d49380b67c378a4f5a | Inosine directly inhibits tumour UBA6 to sensitise T-cell-mediated killing.a Scheme of chemical proteomics for target identification. b Volcano plots of LiP-SMap experiments with inosine treatment. c Heat-map of the top 23 proteins changed with inosine treatment identified by LiP-SMap. d The effect of deletion of the top 23 genes in e on OT-1 T-cell-mediated tumour cell killing. e The effect of inosine on the interaction between UBA6 and USE1 in HEK293 cells. Data were representative of two independent experiments (n = 2). f The effect of inosine on USE1~S~FAT10 thioester in vitro. Data were representative of two independent experiments (n = 2). g The relative cell viability of WT (sgCtrl), Uba6-null (sgUba6) 4T1, or B16-GMCSF-OVA tumour cells with vehicle (Ctrl) or inosine (100 µM) following the method in a (n = 5). Data are presented as Mean ± s.e.m. Statistical significance was determined by one-way ANOVA and Tukey test for multiple comparisons (g). The P values in b and d were based on log-rank tests. NS no significant. Source data are provided as a Source Data file. | PMC9478149 | 41467_2022_33116_Fig3_HTML.jpg |
0.42375 | c73cc726b6944efca83f77f66cc4994d | Inosine and genetic inhibition of UBA6 stimulate tumour cell-intrinsic immune response signalling.a Volcano plots of upstream regulator analysis of UBA6-dependent genes in 4T1 tumour cells by IPA. b Top-ranked GO terms in the transcriptome of Uba6-null 4T1 tumour cells. c The upregulated GSEA signatures in the Uba6-null 4T1 tumour. d Heat-map of proteins for differential signalling pathways (Red upregulated, blue downregulated). The expression level of these proteins in sgCtrl and sgUba6 4T1 cells is measured by the whole proteomics (n = 3). e The relative mRNA expression of IFNγ response-related genes in sgCtrl and sgUba6 4T1 tumour cells without or with inosine (100 µM) treatment for 48 h (n = 3). f Cell viability of Uba6-null and control 4T1 or B16-GMCSF tumour cells following stimulation with 10 ng/ml TNFα + 10 ng/ml IFNγ treatment for 48 h (n = 4). Data are presented as Mean ± s.e.m. Statistical significance was determined by two-sided Student’s t test (e, f). The P values in a and b were based on log-rank tests. NS no significant. Raw RNA-seq data is available in the GEO database with accession number GSE210225. For the remaining data, source data are provided in a Source Data file. | PMC9478149 | 41467_2022_33116_Fig4_HTML.jpg |
0.437601 | c3b1a2783f9b4042adc5da93d8bdc572 | UBA6 deletion substitutes the effect of inosine on antitumour immunity in vivo.a Tumour volume and survival analysis of sgCtrl and sgUba6 B16-GMCSF tumours in NSG, wild-type (WT) mice (n = 8). b Tumour volume and survival analysis of sgCtrl and sgUba6 B16-GMCSF tumours in WT mice with Ctrl, ICB, or ICB + Ino treatment (n = 8). c Tumour volume and survival analysis of sgCtrl and sgUba6 4T1 tumour-bearing NSG mice (left) or wild-type (WT) mice (right) (n = 10). d Tumour volume and survival analysis of sgCtrl and sgUba6 4T1 tumour-bearing WT mice with Ctrl, ICB, or ICB + Ino treatment (n = 10). Data are presented as mean ± SEM. Statistical significance was determined by ANOVA (tumour volume of a–d) or log-rank (Mantel–Cox) test (survival analysis of a–d). NS no significant. Source data are provided as a Source Data file. | PMC9478149 | 41467_2022_33116_Fig5_HTML.jpg |
0.438163 | 2b4c6eeabc35433aa40549ebe4a37f63 | UBA6 in tumour cells predicts patient outcomes to immunotherapy.a The association between CTL and OS of melanoma patients with distinct UBA6 levels. b Kaplan–Meier plots of PFS of melanoma patients with anti-CTLA4 (n = 42) and OS of melanoma patients with anti-PD1 (n = 47) based on UBA6 level. c Representative UBA6 protein staining tumour sections (top: 100×, bottom: 400×) (left) and CT scans (right) of lung cancer patients with anti-PD1 treatment. CT scans of tumours (top) and mediastinal lymph nodes (bottom) of patient 1 and left pleural effusion (top) and pericardial effusion (bottom) of patient 2 are highlighted by red arrows. Data were representative of three independent experiments (n = 3). d Waterfall plot depicting the responses to anti-PD1 treatment by the best change in the sum of target lesions, in comparison to baseline, in cancer patients with low UBA6 (n = 16) or high UBA expression (n = 6). Every bar represents one patient and the colours correspond to response to anti-PD1 treatment (PR partial response, SD stable disease, PD progressive disease). Dotted black lines indicate the response as described by RECIST1.1. e Pie charts of response fractions for each group of patients with UBA6-low and UBA6-high expression in tumour cells. Data are presented as Mean ± s.e.m. Statistical significance was determined by a log-rank test (a, b). Source data are provided as a Source Data file. | PMC9478149 | 41467_2022_33116_Fig6_HTML.jpg |
0.430595 | 23403f0475824e15b17193cbbacc9643 | A summary model linking inosine and immunotherapy responses.The metabolic imbalance, especially inosine, is associated with immunotherapy responses in mice and humans. Inosine overcomes tumour-intrinsic resistance to immunotherapy by inhibiting UBA6 and increasing tumour immunogenicity in tumours with UBA6-high expression. | PMC9478149 | 41467_2022_33116_Fig7_HTML.jpg |
0.459011 | ff4c0586d4db442e9ccd12fa9ffc5f27 | Flow chart demonstrating the patient cohorts of the indicated trials and the approach for the development of a blood cell count test (BCT)–based score (BCTscore). The internal cohorts are from four international, multicenter studies (OAK, POPLAR, BIRCH, and FIR). Ate, atezelizumab; Dtx, docetaxel. | PMC9478919 | fimmu-13-961926-g001.jpg |
0.449331 | a56cbf44eeb7428da3a6b8b5395f9296 | Forest plot of hazard ratio (HR) for overall survival (OS) and progression-free survival (PFS) of the BCT biomarkers (A) NMR_T2, (B) NMR_T3, (C) NLR_T3, (D) PLR_T3, and (E) LMR_T3 in decile patient fractions in the atezolizumab (Ate) or docetaxel (Dtx) treatment groups of the combined internal cohorts. Mean HRs for OS (white shade) or PFS (gray shade) under univariate (green) or multivariate (red) Cox analysis is indicated by the dots, the range of HR is indicated by the error bar of the forest plot; -log10
p-value of each calculated HR is indicated by the size of the blue dots adjacent to the forest plot. | PMC9478919 | fimmu-13-961926-g002.jpg |
0.496016 | 64f21061210042708fcfe8921a073a11 | Kaplan–Meier analysis of (A) overall survival (OS) and (B) progression-free survival (PFS) between high-risk (hi) and low-risk (lo) patients, as defined with the identified BCTscore candidate 2 (BCTscore #2), treated with atezolizumab (Ate) of the training cohort (OAK) and the internal validation cohorts (BIRCH and POPLAR + FIR). The percentage of survival of high-risk (dark blue) and low-risk (light blue) patients is plotted against the time in months. | PMC9478919 | fimmu-13-961926-g003.jpg |
0.410786 | 4d3b984fb5074a35826e7bdacbb3a0e1 | Time-dependent receiver-operating characteristic (ROC) analysis for overall survival (OS) to obtain the area under curve (AUC) of (A) BCTscore candidate 2 (BCTscore #2) and the BCT biomarkers (B) NLR_T3, (C) NMR_T2, and (D) PLR_T3 of the atezolizumab-treated patients of the training cohort (OAK) and the internal validation cohorts (BIRCH and POPLAR + FIR). Sensitivity is plotted against specificity. | PMC9478919 | fimmu-13-961926-g004.jpg |
0.43836 | 020d218b363543bea2871bc5b1c481de | Kaplan–Meier analysis of overall survival (OS) for (A) BCTscore candidate 2 (BCTscore #2) and the BCT biomarkers (B) NLR_T3, (C) NMR_T2, and (D) PLR_T3 comparing atezolizumab (Ate)–treated patients (dark blue) against docetaxel (Dtx)–treated patients (dark green) in the high-risk (hi) group, and comparing between Ate-treated patients (light blue) against Dtx-treated patients (light green) in the low-risk (lo) group of the training cohort (OAK). | PMC9478919 | fimmu-13-961926-g005.jpg |
0.464839 | e566ce9f381f487dab48c38dc017f3c8 | PRISMA flowchart of the study selection process for the meta-analysis. | PMC9479108 | fphys-13-973304-g001.jpg |
0.42092 | 898e8369bc1b481dba2bcbec203313a8 | Forest plot comparing the MVIC of the neck in the physical exercise and control groups. (A) Flexion. (B) Extension. (C) Right lateral flexion. (D) Left lateral flexion. MVIC, maximal voluntary isometric contractions. | PMC9479108 | fphys-13-973304-g002.jpg |
0.508815 | 269567ff900e4f6d998e70cf0a4c3f8d | Forest plot comparing the prevalence of neck pain in the physical exercise and control groups. (A) Before leave-one-out sensitivity analysis (B) After leave-one-out sensitivity analysis (Jones et al., 2000). (C) After leave-one-out sensitivity analysis (De Loose et al., 2008). | PMC9479108 | fphys-13-973304-g003.jpg |
0.42021 | 3deb3f59d689484782001d229ffdd596 | Subgroup analysis for prevalence of neck pain (type of study). | PMC9479108 | fphys-13-973304-g004.jpg |
0.403749 | a6f3167829e548af9fe62363269b16f6 | Subgroup analysis for prevalence of neck pain (type of aircraft). | PMC9479108 | fphys-13-973304-g005.jpg |
0.426591 | 025ad59d3a07419e9994a821f26f2811 | Subgroup analysis for prevalence of neck pain (training protocol). | PMC9479108 | fphys-13-973304-g006.jpg |
0.395946 | c62d13946d4a4cee8c14082419c27bba | Forest plot comparing MVIC of the shoulder in the physical exercise and control groups. (A) Right elevation. (B) Left elevation. MVIC, maximal voluntary isometric contractions. | PMC9479108 | fphys-13-973304-g007.jpg |
0.386146 | 5d6d548a4bbd40e6bc2e961fcb4409fa | Forest plot comparing the VAS scores of the neck and shoulder in the physical exercise and control groups. (A) Neck. (B) Right shoulder. (C) Left shoulder. VAS, visual analog scale. | PMC9479108 | fphys-13-973304-g008.jpg |
0.414689 | 5774b216ab7849b1ac0cbe555a883195 | Item Parameters and Person Parameters – Partial Credit Model. The Item Parameter graph shows the threshold for each one of the seven items of the IOS. The Person Parameter graph show the absolute raw score frequencies for each one of the three class solutions. | PMC9479453 | fpsyg-13-987931-g001.jpg |
0.550673 | ca9eb7fafa204170a5b81fc8a88e3789 | Item Characteristic Curves of the seven items of the IOS – Grade Response Model. Category response curves for the seven items of the IOS. From left to right in the first column (item 1, item 2, item 3); From left to right in the second column (item 4, item 5, item 6); in the third column (item 7). | PMC9479453 | fpsyg-13-987931-g002.jpg |
0.567434 | b52548e6b357435694a62f1e7423e760 | Test Information Function and Measurement Error Curves – Grade Response Model. The test information curve is represented by the solid line. The standard error of measurement curve is represented by the dotted line. | PMC9479453 | fpsyg-13-987931-g003.jpg |
0.458403 | ef880cb9607a4a3c9fce456bde814a78 | The mechanisms of dual incretin receptor agonists. Glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) are the main incretins. Incretins are hormones released by endothelial cells in the intestine in response to various stimuli. Novel dual incretin receptor agonists, which include GLP-1 receptor agonists (GLP1-RAs) combined with glucose-dependent insulinotropic peptide, also known as gastric inhibitory polypeptide or gastric inhibitory peptide (GIP) receptor agonists (GIPRAs), have a synergic effect. The synergy of dual incretin receptor agonists results in reduced body weight, blood glucose levels as determined by glycated hemoglobin, or hemoglobin A1c (HbA1c), total liver fat content (LFC), and a reduced risk of cardiovascular disease (CVD) through increased expression of the GLP-1 receptor (GLP1R) and the GIPR (GIP receptor) heterodimer. The combined consequence of simultaneous receptor stimulation also results in improved metabolic regulation, including reduced inflammatory responses and reduced insulin resistance. The outcomes of the synergistic effects of dual incretin receptor agonists are to reduce the onset and progression of metabolic dysfunction-associated fatty liver disease (MAFLD). | PMC9479660 | medscimonit-28-e938365-g001.jpg |
0.470652 | cbbfc1ce17cc4155930e32b36da884ed | Schematic representation of fungal moonlight proteins localization and function.Fungal moonlight proteins related to virulence are mostly adhesins with their moonlight function in the cell surface and their canonical function in the cytosol. An asterisk (*) indicates that Als3 and Tsl are moonlight proteins that perform both functions, canonical and moonlight, in the same cellular compartment. | PMC9480056 | peerj-10-14001-g001.jpg |
0.411605 | 36515b53169a4b27b561d3cac43076b6 | Schematic representation of the host ligands that bind to the different fungal moonlighting proteins.The host ligands are located in many cell types and compartments, and many of the pathogen moonlighting proteins are capable of binding to more than one ligand, facilitating the attachment and dissemination of the fungus to different tissues. All the proteins are present on the cell surface of the pathogenic fungus, which is arbitrarily represented by yeast cells. GAPDH, glyceraldehyde-3-phosphate dehydrogenase; Eno, enolase; Gpm, phosphoglycerate mutase; Gpd2, glycerol-3-phosphate dehydrogenase 2; Adh, alcohol dehydrogenase; Cta, peroxisomal catalase; Tef1, transcription elongation factor; Fba, fructose-bisphosphate aldolase; Pgk, phosphoglycerate kinase; Tsa, peroxiredoxin; Eft2, elongation factor 2; Tpi, triosephosphate isomerase; Gpi1, glucose-6-phosphate isomerase 1; Gnd, 6-phosphogluconate dehydrogenase; Fbp, fructose-1, 6-bisphosphatase; Ssa1 and Ssa2: Hsp70, Als3: cell wall agglutinin-like sequence protein 3, HIS-60: Hsp60. | PMC9480056 | peerj-10-14001-g002.jpg |
0.468311 | 8f96d84dbe4e4b97be715ca968c20df0 | Platinum resistant recurrence and early recurrence in 153 patients undergoing interval cytoreductive surgery. | PMC9480093 | fonc-12-951419-g001.jpg |
0.43285 | 95b10a6ccf514ff4b8ded0d0e0376c63 | Figure 1 depicts the median percentage of platelets, red blood cells, immune cells and fibrin of each arterial clot in COVID-19 patients. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.) | PMC9481474 | gr1_lrg.jpg |
0.441171 | 7676e62209824ba6b020fd6292d73225 | Images show an example of the morphological and immunochemistry study of the arterial thrombi, with Hematoxylin and Eosin staining (panel A), CD3 (panel B) and CD20 (panel C) immunostaining for lymphocytes, CD61 immunostaining for platelets (panel D) and myeloperoxydase (MPO) immunostaining for polymoprhonuclear leukocytes (Panel E). | PMC9481474 | gr2_lrg.jpg |
0.479633 | 80c23ad2b19e413cbeaeced7cd13b211 | Long COVID symptoms after three and six months of discharge. | PMC9483130 | 10.1177_10105395221124259-fig1.jpg |
0.402359 | 8a826e77c1114c92929e1c2f6325d4c5 | NPD1 modulates the expression of tight junction (TJ)-associated proteins in the hippocampus and prefrontal cortex after surgery. Representative Western blotting bands of the expression of occludin, claudin-5, and ZO-1 in the hippocampus and prefrontal cortex at 6 and 9 h after surgery (A,B). Quantification analyses of the expression of occludin, claudin-5, and ZO-1 were normalized to that of β-actin as internal control (C–H). Data are presented as mean ± SEM. Statistics: two-way ANOVA followed by Bonferroni post hoc comparison. (C–H)
n = 4–5 per group. **P < 0.01 vs. the control group, #P < 0.05 vs. the surgery group, ##P < 0.01 vs. the surgery group. | PMC9483812 | fnagi-14-934855-g0001.jpg |
0.441823 | 14b13200d9784960b0e1c0f8ca027838 | Dietary Cu supplementation did not reduce CPZ-induced myelin damage. (a) Mice were
administered 0.2% CPZ ± 0.1% copper sulfate (Cu) or 0.1% Cu alone in standard rodent
chow for 3 weeks and the splenium of the corpus callosum was examined via Luxol fast
blue (LFB) staining. (b) All mice were weighed at baseline and once per week
throughout the 3-week experiment. (c) Quantification of myelin content based on LFB
staining. Cu supplementation did not prevent CPZ-induced myelin loss. (d-e) Mice were
administered CPZ ± Cu for an abbreviated 2-week period and brain tissue sections
stained with LFB or anti-citrullinated MBP (citMBP) and anti-microglia/macrophage
(Iba1) antibodies. (f-h) 2 weeks of CPZ did not produce overt demyelination by LFB
staining, but induced microgliosis and hypercitrullination of myelin in the medial
corpus callosum that was not alleviated with Cu supplementation. Cu supplementation in
the absence of CPZ did not cause myelin damage. Each dot on the graph in (c), (f),
(g), and (h) represents one mouse. Error bars indicate SEM. Scale bars are 300 μm. | PMC9483969 | 10.1177_17590914221126367-fig1.jpg |
0.554566 | db21defbab3146ee848bcb624d6d4aea | Other Cu chelators failed to induce cerebral demyelination. (a)The Cu chelators
D-penicillamine (D-Pen), neocuproine (neo), and CPZ each undergo unique color change
in the presence of Cu in aqueous solution. (b) When D-Pen or neocuproine was added to
a deep-blue solution of 1mM CPZ + 0.5mM copper sulfate a marked color change was noted
resembling the hue of each chelator without CPZ. Colors remained stable at room
temperature and did not change with the addition of more CPZ (not shown). (c)
8-week-old male mice were administered 0.16% D-Pen or 0.15% neocuproine (w/w) in
rodent chow for 3 weeks and the splenium examined by Luxol fast blue (LFB) staining.
(d) No myelin loss was observed in the corpus callosum with either chelator, despite
confirmation that both bind Cu even more tightly than CPZ. Each dot on the graph
represents one mouse. (e) The only clinically notable feature was weight loss in the
neocuproine-fed mice. Error bars indicate SEM. Scale bars indicate 300 μm. | PMC9483969 | 10.1177_17590914221126367-fig2.jpg |
0.411035 | ba8e284295694df486aa0043fe7e8ee8 | D-Pen-induced C u deficiency was unlike purported CPZ-induced Cu deficiency. (a-c)
After 4 weeks of 2% D-Pen supplementation in rodent chow, mice exhibited digit
paralysis in both hindlimbs (an inability to grasp the metal wires of the cage top),
along with high hindlimb clasping scores and low wire hang scores. CPZ-treated mice
were clinically unremarkable and behaviourally indistinguishable from untreated
control mice. (d-f) mouse CNS and PNS cryosections labeled with anti-citrullinated MBP
(citMBP) and anti-microglia/macrophage (Iba1) antibodies. (h-i) Mice were administered
either 1% D-Pen or 1% D-Pen + 0.92% copper sulfate for 12 weeks, with digit paralysis
and hindlimb clasping recorded weekly. 1%-D-Pen-treated mice began to exhibit digit
paralysis at week 4, and progressed until week 12 when most mice had digit paralysis
in both hindlimbs. Hindlimb clasping scores became statistically significant by week 6
of treatment. * indicates the first time point at which 1% D-Pen mice have scores that
are significantly different from 1% D-Pen + Cu mice (p < 0.05, repeated
measurements ANOVA with Fisher’s LSD post hoc tests). (j) At week 12, D-Pen-treated
mice had significantly abnormal wire hang scores. Mice administered 1% D-Pen + Cu were
clinically and behaviourally indistinguishable from untreated controls. Each dot on
the graph in (a-c), and (j) represents one mouse. Error bars indicate SEM. Scale bars
are 300 μm. | PMC9483969 | 10.1177_17590914221126367-fig3.jpg |
0.486079 | 20b8aedeacca4dccb21caca549188ea3 | D-Pen supplementation paradoxically prevented CPZ-induced demyelination. (a) Mice
were administered 0.2% CPZ ± D-Pen in rodent chow for 3 weeks and the splenium
examined via Luxol fast blue (LFB) staining. (b) The addition of D-Pen to the CPZ diet
prevented demyelination in a dose-dependent manner. At 0.25% D-Pen prevented all
myelin loss and was statistically indistinguishable from untreated controls. Each dot
on the graph represents one mouse. Error bars indicate SEM. Scale bar is 300 μm. | PMC9483969 | 10.1177_17590914221126367-fig4.jpg |
0.467022 | 62c15dbec3434cf2871db046355ff9d9 | (A) Setting of robotic assisted mirror therapy (RMT); (B) Setting of mirror therapy (MT). | PMC9484120 | rnn-40-rnn221263-g001.jpg |
0.441239 | 5fbb4f13d59544a5b643808ada723ae3 | Study flow chart. | PMC9484120 | rnn-40-rnn221263-g002.jpg |
0.420515 | 5c4cbf976e2f40a0923b76b6671635d4 | Median change scores and interquartile range between groups for FMA-UE Motor Function (p = 0.006**) and Motricity Index (p = 0.108), p < 0.05. | PMC9484120 | rnn-40-rnn221263-g003.jpg |
0.44934 | 790c787c4cc44555a0c1ac4f6d226185 | Flow chart and evolution of the 180 admissions included in the cohort | PMC9484245 | 13054_2022_4165_Fig1_HTML.jpg |
0.399414 | 3dafd399ca1e4eaa83b40d72a33c1452 | A Pruritus numeric rating scale before and after MARS® therapy in the refractory pruritus group. Numeric rating scale ranges from 0 (no itch) to 10 (worst imaginable itch). Patients perception of pruritus was decreased from 9 [8–10] to 2 [0–3] (p < 0.01) after MARS® therapy. Results are shown as median, first quartile, third quartile, minimum and maximum. B Richmond Agitation Sedation Scale (RASS) variation before and after MARS.® therapy in the drug intoxication group. RASS score improved in 11 out of 12 admissions (p < 0.01) | PMC9484245 | 13054_2022_4165_Fig2_HTML.jpg |
0.413458 | 4ed3d28296bf4dc494f779b74764f36f | Brain MRI shows massive cerebral infarction of the right middle cerebral artery area (a). Brain CT shows diffuse brain edema resulting in brain herniation (b), and no cerebral edema after external decompression (c) | PMC9485363 | 40792_2022_1526_Fig1_HTML.jpg |
0.416574 | 9f58b6a9c0b14e88907acde17c3d0c57 | Chest CT shows double-barrel aortic dissection on the day of onset (a) and the dissected right common carotid artery with the false lumen thrombosed (b) | PMC9485363 | 40792_2022_1526_Fig2_HTML.jpg |
0.433354 | de741fa1d4c740bbbed458de2fffafb1 | Postoperative CT shows the graft-replaced ascending aorta (a) and a moderate amount of cerebral spinal fluid (b) | PMC9485363 | 40792_2022_1526_Fig3_HTML.jpg |
0.429377 | 007d0db8d36e4426bd35653de30e3b95 | Schematic illustration of the tissue preparation steps before cryosectioning | PMC9485525 | gr1.jpg |
0.437205 | bf62ba05a7704b2ba633fbbc51660196 | Representative images showing the steps of tissue dissection, fixation, decalcification and dehydration(A) Fixation of femora dissected from 4-week-old Gli1-LacZ mice in 4% PFA in an ice box.(B) Decalcification of femora on a shaker at 4°C, and side by side images of freshly harvested (left) and decalcified (right) bones.(C) Dehydration of femora by 30% sucrose solution, during which the bones will first float for a few minutes and then descend through the solution to the bottom of the tube. | PMC9485525 | gr2.jpg |
0.443692 | 8ca57ee09a164ac480bff603d51bd8b0 | Representative images showing the steps of tissue embedding and cryosectioning(A) Embedding of mouse femur in OCT.(B) Cryosectioning of mouse femur.(C) Flattened tissue section before collection.(D) Collected tissue section on slide. | PMC9485525 | gr3.jpg |
0.416132 | fcf6dec4248d4655a719c7555612b5b6 | Representative images showing the steps of immunofluorescence staining(A) Drawing of hydrophobic barrier around femur section, marked with dotted line.(B) Rehydration in a staining jar.(C) Example of adding solution to section.(D) Mounting with coverslip. | PMC9485525 | gr4.jpg |
0.434556 | 17b012f78b264560a350d2fdb1f07334 | Representative immunofluorescence staining imagesβ-galactosidase immunostaining showing Gli1-LacZ+ cells (red) and CD31 (green) co-immunostaining in the femoral metaphysis of juvenile (4-week-old) and adult (8-week-old) Gli1-LacZ mice, counterstained by Hoechst (blue). Secondary antibody alone is used as the negative control. Scale bars, 50 μm. | PMC9485525 | gr5.jpg |
0.47754 | 9a8dcd2137424654bd65dadb848d6d45 | Representative image describing the study measurements with radial strain. Intraventricular dyssynchrony (IVD) was measured as the time from earliest peak segmental radial strain to latest peak segmental strain (solid line – 15 ms). Electromechanical latency (EML) was measured as the time from the onset of QRS to earliest peak segmental radial strain (dashed horizontal white line – 190 ms). | PMC9485544 | fcvm-09-978341-g001.jpg |
0.439857 | 366fad90ea014429b3186845945a5f45 | Progression of (A) left ventricular ejection fraction, (B) intra-ventricular dyssynchrony and (C) electro-mechanical latency across bigeminal PVCs and sham groups over 12 weeks. This figure demonstrate that while LVEF decreases gradually over the 12 weeks in the PVC-CM group, an early intraventricular LV dyssynchrony is present that pseudo-normalizes after the remodeling of peak cardiac contractility homogenizes in all segments, only identified by prolongation of EML. PVC group n = 11; sham group n = 9. Error lines denote standard deviation. (P values, Friedman’s two-way ANOVA); * P < 0.05 at 4 week. | PMC9485544 | fcvm-09-978341-g002.jpg |
0.446985 | bf963cb8f0594a7ebe401920c08d5f0b | Progression of Intra-ventricular dyssynchrony and Electro-Mechanical Latency from baseline (A) to 4 weeks (B), to 8 weeks (C) and 12 weeks (D) in a single representative animal from the PVC cohort. IVD (solid arrow line) is the time between the earliest and latest peak radial strain amongst different LV segments, while EML (dotted arrow line) is the time between QRS onset and earliest peak radial strain. | PMC9485544 | fcvm-09-978341-g003.jpg |
0.40935 | 82dc43afa16a4f4c864705696edb0235 | Flowchart of the study selection process. | PMC9486298 | 10.1177_20420188221122426-fig1.jpg |
0.479797 | f556c345f75c404a93035fc9baa7a947 | Methodological quality and risk of bias of the included trials. | PMC9486298 | 10.1177_20420188221122426-fig2.jpg |
0.503092 | 509a618b257a4bffbfb83733b0df1501 | Meta-analysis of the effects of a sedentary lifestyle and training on
hepatic enzyme parameters of NAFLD: (a) ALT (U/L), (b) AST (U/L), and
(c) GGT (U/L). | PMC9486298 | 10.1177_20420188221122426-fig3.jpg |
0.483881 | f72ba256de6045fe8662bbbf75f90773 | Meta-analysis of sedentary lifestyle and training serum lipid parameters
of NAFLD: (a) CHOL (mmol/L), (b) TG (mmol/L), and (c) LDL-C
(mmol/L). | PMC9486298 | 10.1177_20420188221122426-fig4.jpg |
0.475083 | fab76ec00bf7457db6ddebba2e0ce83e | Meta-analysis of sedentary lifestyle and training on glucose metabolism
parameters of NAFLD: (a) FBG (mmol/L), (b) Insulin (pmol/L), and (c)
HOMA-IR. | PMC9486298 | 10.1177_20420188221122426-fig5.jpg |
0.460017 | d5001175769440a88652cf38434249f3 | Meta-analysis of sedentary lifestyle and training on BMI, Body fat (%)
and VO2peak levels of NAFLD. (a) BMI (kg/m2), (b)
Body fat (%), and (c) VO2peak (mL/kg/min). | PMC9486298 | 10.1177_20420188221122426-fig6.jpg |
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