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0.435534 | 55b38836c7e348d1aa9cbfdee626e049 | Gall formation and stable DsRed expression in citrus epicotyl tissue transformed with wild-type Agrobacterium fabrum strain 1D1416 harboring the binary vector pCTAGV-KCN3. Left panel, gall viewed under white light. Right panel, same gall displaying DsRed expression. The binary plasmid and the protocol used for citrus transformation were previously published (1). | PMC10353357 | mra.00264-23-f001.jpg |
0.427933 | e080c236b314438eae7a02ac85ce08ea | Venn’s diagram showing the relations among the answers to the question “what do you think is happening?”. Some volunteers answered more than one name to our inquiry | PMC10355005 | 12883_2023_3327_Fig1_HTML.jpg |
0.436108 | fda5ec4adff44aa79ca5532838b4791d | Approach to study design, performed tests, and diagnostic classification after long follow-up. | PMC10356105 | fneur-14-1211812-g001.jpg |
0.479162 | 3f3ff7987e12425ea9843c75732cb59b | Frequency of autoantibodies in different diagnostic groups. | PMC10356105 | fneur-14-1211812-g002.jpg |
0.405428 | 19a54fff05c94f9990af8d8a9cd22e06 | Indirect immunofluorescence on unfixed murine brain sections. (A) Cerebrospinal fluid (CSF) of patient A24 showed strong binding of cerebellar granule cells and neuropil in the hippocampus (insert), reflecting the characteristic anti-NMDAR autoantibody pattern. (B) Anti-GFAP antibody-positive CSF of patient B1 displayed the characteristic astrocytic pattern in the brain including Bergmann glia and white matter astrocytes (star-like formation in insert). (C) CSF of patient A38 exhibited strong binding to brain vasculature (insert: higher magnification of a capillary). (D) Serum of patient A36 showed binding of myelinated fibers in white matter tracts (insert), cerebellar white matter (arrows), and around cerebellar Purkinje neurons (arrowheads). (E) Serum of patient A19 displayed binding to nuclear antigens of neurons in the cerebellar cortex (insert: Purkinje cell layer). (F) CSF of Patient A32 exhibited a cytoplasmatic binding pattern in Purkinje neurons also involving proximal dendrites (insert). Scale bars: (A–C,E,F) 100 μm; (D) 50 μm. | PMC10356105 | fneur-14-1211812-g003.jpg |
0.44406 | 97f2893374144f5fb97b1d3d9078c29d | Free running rhythms and periods of PcoaE-, PftsZ-, and PmntH::luxCDABE reporters taken from the center of each culture well. Detrended records of bioluminescence from PcoaE::luxCDABE in standard media [(A), n = 12] and media supplemented with 1 nM melatonin [(A′), n = 12]. Detrended bioluminescence traces from PftsZ::luxCDABE in standard media [(B), n = 12] and 1 nM melatonin-supplemented media [(B′), n = 11]. Detrended bioluminescence traces from PmntH::luxCDABE in standard media [(C), n = 4] and 1 nM melatonin-supplemented media [(C′), n = 4]. Period analysis for PcoaE::luxCDABE
(A″), PftsZ::luxCDABE
(B″), and PmntH::luxCDABE
(C″) comparing cultures in the absence (EMB) or presence (MEL) of melatonin. | PMC10356819 | fmicb-14-1181756-g001.jpg |
0.459771 | 4e29edf68a7f41f496e2f83ca561d9c5 | Free running rhythms and periods of PcoaE-, PftsZ-, and PmntH::luxCDABE reporters taken from the each of four peripheral ROIs in each culture well. Detrended records of bioluminescence from PcoaE::luxCDABE in standard media [(A), n = 12 for top, right, and left, n = 10 for Bottom] and media supplemented with 1 nM melatonin [(A′), n = 12 for top, right, bottom, and left]. Detrended bioluminescence traces from PftsZ::luxCDABE in standard media [(B), n = 12 for top, bottom, and left, n = 8 for right] and 1 nM melatonin-supplemented media [(B′), n = 12 for top, right, bottom, and left]. Detrended bioluminescence traces from PmntH::luxCDABE in standard media [(C), n = 4 for top, n = 14 for right, n = 8 for bottom, n = 9 for left] and 1 nM melatonin-supplemented media [(C′), n = 13 for top, n = 10 for right, n = 7 for bottom, n = 12 for left]. Period analysis for PcoaE::luxCDABE
(A″), PftsZ::luxCDABE
(B″), and PmntH::luxCDABE
(C″) comparing cultures in the absence (EMB) or presence (MEL) of melatonin for each peripheral ROI. | PMC10356819 | fmicb-14-1181756-g002.jpg |
0.470105 | 718ef67aa8614dc9be617a3e9a88276c | Population growth in K. aerogenes. (A) Copy number stability over 144 h in cultures incubated with Tetracycline (blue) or in standard media (grey) [adapted from Graniczkowska and Cassone (2021)]. (B) Culture growth, as seen by colony forming units (CFUs, blue) compared to bioluminescence (grey) over 48-h. | PMC10356819 | fmicb-14-1181756-g003.jpg |
0.470504 | 5f787b2585aa4825900cecb169d6545d | One-dimensional representation of the relationship between the Lie group \documentclass[12pt]{minimal}
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\begin{document}$$\mathfrak{g}$$\end{document}g. | PMC10356829 | 41598_2023_36628_Fig1_HTML.jpg |
0.444668 | ba6c2b3666e048e3b9749c6f70b07680 | Visual representation of the toral subalgebra \documentclass[12pt]{minimal}
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\begin{document}$$p=2$$\end{document}p=2 planes of rotations. The broken line marks the search curve. The matrices \documentclass[12pt]{minimal}
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\begin{document}$${W}_{2}$$\end{document}W2, are defined as in (41). | PMC10356829 | 41598_2023_36628_Fig2_HTML.jpg |
0.485489 | 2ef7aeca3e474d979da1fcc027aee7cf | The constellation patterns corresponding to (a) five transmitted signals, (b) five of the eight received signals and (c) the five recovered signals using proposed algorithm. | PMC10356829 | 41598_2023_36628_Fig3_HTML.jpg |
0.458657 | 671663157a1b4b409c9eb6585bbd7503 | Examples of the evolution of the cost function (12) (a) and Amari Performance Index (b) for different algorithms used in the simulation. | PMC10356829 | 41598_2023_36628_Fig4_HTML.jpg |
0.383258 | 55614c1f049144e5b40dc57716610d9b | Comparison of the average convergence times and API of the tested algorithms for (a) M and (b) F criterion, respectively versus number of sources in symmetrical MIMO system. | PMC10356829 | 41598_2023_36628_Fig5_HTML.jpg |
0.529157 | 91ba15b79def4457a90a3eea9ce2c38d | Comparison of the average convergence times of the tested algorithms for (a) M and (b) F criterion, respectively versus type of non-symmetrical MIMO system. | PMC10356829 | 41598_2023_36628_Fig6_HTML.jpg |
0.395687 | a85b2bc47d194f0f927d3fcf87bf8bfc | SINR performance comparison of ICA algorithms for: (a) symmetrical 3 × 3 MIMO system and AWGN channel, (b) non-symmetrical 5 × 8 MIMO system and AWGN channel, (c) symmetrical 3 × 3 MIMO system and Rayleigh channel, (d) non-symmetrical 5 × 8 MIMO system and Rayleigh channel. | PMC10356829 | 41598_2023_36628_Fig7_HTML.jpg |
0.525065 | db4292ea1c384f87884adab0e34b8a8b | BER performance of separated signals in (a) AWGN and (b) Rayleigh fading channel. | PMC10356829 | 41598_2023_36628_Fig8_HTML.jpg |
0.461744 | 3f5cccdae6a94331b601020c66fcaeda | Average BER performance comparison of ICA algorithms for: (a) symmetrical 3 × 3 MIMO system and AWGN channel, (b) non-symmetrical 5 × 8 MIMO system and AWGN channel, (c) symmetrical 3 × 3 MIMO system and Rayleigh channel, (d) non-symmetrical 5 × 8 MIMO system and Rayleigh channel. | PMC10356829 | 41598_2023_36628_Fig9_HTML.jpg |
0.480644 | d68139feb9b4441c9220d444ab11e1b8 | Overview of 15-day study period. BMI, body mass index; CT, computed tomography; DEXA, dual-energy X-ray absorptiometry; MRI, magnetic resonance imaging, OGTT, oral glucose tolerance testing. | PMC10357167 | jnd-10-jnd230036-g001.jpg |
0.444049 | 25d770f8696044bcbb32689e38f62515 | Comparison of fat ratio between myotonic dystrophy type 1 (DM1) patients and healthy age-, sex- and BMI-matched controls, based on full-body MRI measurements. | PMC10357167 | jnd-10-jnd230036-g002.jpg |
0.43612 | 89eb131403cf4b4298c08f6b9156dd6c | Comparison of full body MRI images between a myotonic dystrophy type 1 (DM1) patient and a healthy age-, sex- and BMI-matched control. Visceral adipose tissue (VAT) deposition is highlighted in pink. VAT volume was 5,59L in the displayed DM1 patient versus 4,28 L in the healthy matched control. Subcutaneous fat deposition is highlighted in blue, as part of the total adipose tissue volume. Also note the difference in shoulder and leg musculature: thigh lean muscle volume was 11,1 L in the DM1 patient versus 15,1 L in the healthy control, as part of total lean tissue volume. | PMC10357167 | jnd-10-jnd230036-g003.jpg |
0.425986 | a9ea41323c3848aa85cfaa09ca54e331 | Comparison between A) 24 h resting energy expenditure measured by whole room calorimetry, B) 24 h total energy expenditure under free living conditions measured using doubly labeled water, and C) number of steps per 24 h measured by accelerometer, in myotonic dystrophy type 1 patients and healthy age-, sex- and BMI-matched controls. DM1, myotonic dystrophy type 1. | PMC10357167 | jnd-10-jnd230036-g004.jpg |
0.420587 | 3dbf623f12e5461fb1764094f400e887 | Solid deposits accumulated
behind the surface choke. | PMC10357422 | ao3c03149_0002.jpg |
0.362733 | afb709faaaf046c38dc5b5daf0966f61 | Images of solubility
measurement tests with different solvents:
(a) images of 1 g of solid deposits in a beaker at the start of experiments;
(b) images of different volumes of solvents added to each beaker at
the start of experiments; (c) images of different solutions during
filtration after 72 h; and (d) images of solid residues after filtration. | PMC10357422 | ao3c03149_0003.jpg |
0.408389 | 2f4a3387bd4d49059a40d8b137fae081 | Effect of solvent volume on the efficiency of
solvents. | PMC10357422 | ao3c03149_0004.jpg |
0.498688 | aab7bd54da674b4bb540a03030bd0323 | (a) Efficiency of the mixture of xylene
and gas condensate in dissolving
solid deposits; (b) efficiency of the mixture of gasoline and gas
condensate in dissolving solid deposits. | PMC10357422 | ao3c03149_0005.jpg |
0.486664 | 90bf0275615a4e9e89957c60ebc6d471 | FT-IR analysis of asphaltene, diesel, and asphaltene + diesel samples;
circled areas highlight regions of O–H and N–H bonds. | PMC10357422 | ao3c03149_0006.jpg |
0.452347 | 788085b646d74b73a52e95b41791a593 | Schematic diagram of permeability reduction
by asphaltene adsorption
on the dolomite rock surface. | PMC10357422 | ao3c03149_0007.jpg |
0.562974 | ded73468884345dd9f200dfe4b58b7af | FT-IR analysis of AECO, WECO, and AESC samples. | PMC10357422 | ao3c03149_0008.jpg |
0.450101 | 3d398c712a954b4685873d11e7643377 | Efficiency of xylene,
gasoline, and kerosene in reversing the damaged
permeability. | PMC10357422 | ao3c03149_0009.jpg |
0.423045 | 389fb38c71a84e35847de7f6ca423174 | GAS6-CAR-T cells target cells overexpressing TAM members. A Flow cytometry analysis of TAM family (AXL, TYRO3, and MERTK) protein levels in various pancreatic cancer cell lines (PANC1, MIA PaCa2, BxPC3, and ASPC1), human embryonic kidney cell 293 T (HEK-293 T), ASPC1-gemcitabine-resistant (ASPC1-Gem) cells, and cell line-derived cancer stem cells (PANC1-CSC and MIA PaCa2-CSC). B The level of TAM protein overexpression in HEK-293 T and BxPC3 cell lines was tested by western blot, and GAPDH was used as a loading control. Cytotoxicity of GAS6-CAR-T cells on TAM-overexpressing HEK-293 T (C) and BxPC3 (D) cells at an E/T ratio of 4:1 for 24 h (n = 3). Enzyme-linked immunosorbent assay (ELISA) was used to analyze IFN-γ (E& F) and TNF-α (G& H) release by either Mock T cells or GAS6-CAR-T cells in coculture supernatant | PMC10357739 | 13045_2023_1467_Fig1_HTML.jpg |
0.434349 | c400905f5bd54041904f84d1785d4d65 | GAS6-CAR-T cells efficiently lyse TAM-positive human pancreatic cancer cell lines. The cytotoxicity of GAS6-CAR-T cells on TAM-low ASPC1 (A) and BxPC3 (B), TAM-high MIA PaCa2 (C), and PANC1 (D) cell lines was tested at varying effector-to-target (E/T) ratios for 24 h (n = 3). Quantification of IFN-γ and TNF-α release in response to coculture with Mock T cells or GAS6-CAR-T cells at an E/T ratio of 4:1 in ASPC1 (E), BxPC3 (F), MIA PaCa2 (G), and PANC1 (H), as measured by ELISA | PMC10357739 | 13045_2023_1467_Fig2_HTML.jpg |
0.415084 | 50751f09e704480685d7a8e4646e2804 | GAS6-CAR-T cells cytotoxicity is abolished by silencing AXL. A The knockdown efficiency of shRNAs targeting AXL, TYRO3, or MERTK was tested by flow cytometry. Cytotoxicity of GAS6-CAR-T cells on target cells PANC1-shRNA (B) and MIA PaCa2-shRNA (C) was tested at an E/T ratio of 4:1 for 24 h (n = 3). ELISA-based quantification of IFN-γ (D& E) and TNF-α (F& G) release in response to coculture with Mock T cells or GAS6-CAR-T cells | PMC10357739 | 13045_2023_1467_Fig3_HTML.jpg |
0.431007 | 88a9a2793ae04471a69ff7a815ca55d8 | GAS6-CAR-T cells efficiently kill drug-resistant cells and cancer stem-like cells. A The levels of TAM proteins in ASPC1 and ASPC1-gemcitabine-resistant (ASPC1-Gem) cells were determined by western blot with GAPDH used as a loading control. B The cytotoxicity of GAS6-CAR-T cells on target cells was assessed an E/T ratio of 4:1 for 24 h (n = 3). ELISAs were used to detect IFN-γ (C) and TNF-α (D) release by T cells in coculture supernatants. E The levels of TAM proteins in parental cells (PANC1, MIA PaCa2) and cell line-derived cancer stem cells (PANC1-CSC and MIA PaCa2-CSC) were determined by western blot with GAPDH used as a loading control. The cytotoxicity of GAS6-CAR-T cells on luciferase-expressing target cells PANC1-CSC (F) and MIA PaCa2-CSC (G) was quantified at an E/T ratio of 4:1 for 24 h (n = 3). ELISAs were used to detect IFN-γ (H& I) and TNF-α (J&K) release by T cells in coculture supernatants | PMC10357739 | 13045_2023_1467_Fig4_HTML.jpg |
0.422965 | 3c73ec7a02504071b5804c1e52fdeb61 | Antitumor effects of GAS6-CAR-T cells are analyzed in vivo. A Photographs of NCG mice subcutaneously injected with 5 × 105 PANC1 cells; after receiving CAR-T-cell treatment, tumor volumes were monitored with bioluminescence at the indicated times. B Quantification of tumor bioluminescence levels (n = 5–6). C DNA copies of Mock T cells and GAS6-CAR-T cells in peripheral blood of mice were determined by real-time PCR. The expression of target genes was normalized GAPDH. 50 μL of venous blood collected from tail veins was collected after (days 7, 14, 21, 28, 35, 42) injecting GAS6-CAR-T cells into mice (n = 3–6). D Immunohistochemistry analysis of COX IV in tumor (n = 3), and the tumor weight at day 5 post-CAR-T cells infusion (the right). NCG mice subcutaneously injected with 5 × 105 PANC1 cells received an infusion of CAR-T cells (1 × 107 cells/mouse) at day 7, and the tumors were harvested after 5 days. E Immunohistochemistry analysis of CD3 in tumor (n = 3), and CD3 + T-cell numbers were counted in five randomly captured pictures of each mouse by ImageJ. F Co-immunofluorescence staining of AXL (green) and OCT4 (red) (n = 3) | PMC10357739 | 13045_2023_1467_Fig5_HTML.jpg |
0.372036 | 827e318f52fe46d69e249f50912be7ee | Cytotoxicity of GAS6-CAR-T cells on pancreatic cancer patient-derived in vivo xenograft model. A Tumor volumes were monitored at the indicated time points (n = 3–4). NCG mice were subcutaneously implanted with pancreatic tumor tissues and received an infusion of T cells (1 × 107 cells/mouse) at days 14 and 23. B DNA copies of Mock T cells and GAS6-CAR-T cells in peripheral blood of mice were determined by real-time PCR. The expression of target genes was normalized GAPDH. 50 μL of venous blood collected from tail veins was collected after (days 3, 10, 17, 24, 31, 38, 45, 52) injecting GAS6-CAR-T cells into mice (n = 3–4). C Immunohistochemistry analysis of COX IV in tumor (n = 3). D Co-immunofluorescence staining of AXL (green) and CK19 (red) was used to test the cytotoxicity of CAR-T cells against AXL-positive tumor cells (n = 3). E Co-immunofluorescence staining of AXL (green) and CD68 (red) was used to test cytotoxic activity of CAR-T cells against AXL-positive tumor-associated macrophages (n = 3) | PMC10357739 | 13045_2023_1467_Fig6_HTML.jpg |
0.422469 | 04a3feeb20244394806c812fdf8614c0 | Safety of GAS6-CAR-T cells in mice. A PCR analysis of TAM expression in a non-cancerous mouse cell line (NIH 3T3) and mouse tumor cell lines (4 T-1, Hepa1-6). B The cytotoxicity of GAS6-CAR-T cells on mouse cell lines at an E/T ratio of 4:1 for 24 h (n = 3). ELISA-based quantification of T-cell-induced IFN-γ (C) and TNF-α (D) release in the culture supernatants. Body weights in PANC1 xenograft mice (n = 3–6) (E) and PDX model (n = 3–4) (F) after receiving CAR-T cells. Pathological analysis of the indicated organs following hematoxylin and eosin staining at the experimental endpoint of PANC1 xenograft (G) and PDX model (H) | PMC10357739 | 13045_2023_1467_Fig7_HTML.jpg |
0.483284 | e7d68898169e46c397e42c0b21b1b3e5 | Safety of GAS6-CAR-T cells in nonhuman primate. A Transduction efficiency of GAS6-CAR into macaques T cells and non-transduced T (NT) cells was used as control. B DNA copies of GAS6-CAR-T cells in the peripheral blood of macaques were quantified by real-time PCR. GAS6-CAR-T cells (2 × 106 cells/kg) were autologously infused to rhesus macaques, and the peripheral blood was collected before (day 0) and after (days 1, 3, 5, 7, 14, 21, 28, and 35) injecting GAS6-CAR-T cells into rhesus macaques (n = 3). C Analysis of physiological indexes (diastolic and systolic blood pressure, heart rate, anus temperature, body weight). Biochemical indicators for D alanine transaminase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), γ-glutamine acylase (GGT), total protein (TP), albumin (ALB), globulin (GLO), ALB/GLO (A/G), total bilirubin (TBIL), E blood glucose (GLU), F blood urea nitrogen (BUN) and creatinine (CRE), G cholesterol (CHOL) and triacylglycerol (TRIG), H creatine kinase (CK) were tested. Blood routines for I red blood cell (RBC), hemoglobin (HGB), hematocrit (HCT), mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC), J platelet count (PLT), platelet distribution density (PDW), mean platelet volume (MPV), platelet volume ratio (PCT), K white blood cell (WBC), L monocyte, and M lymphocyte were analyzed | PMC10357739 | 13045_2023_1467_Fig8_HTML.jpg |
0.431718 | c6b145c33b1f4d67b75b6d5c3573139b | Two-level linear regression model of influencing factors of OOPE in TB patients in Sichuan Province | PMC10357819 | 12889_2023_16180_Fig1_HTML.jpg |
0.386748 | 667e404713474a008ce101bbcf1c53cb | Two-level linear regression model of influencing factors of TOOPE in patients in Sichuan Province | PMC10357819 | 12889_2023_16180_Fig2_HTML.jpg |
0.423646 | fdc8322d86234cf6a610950da2e9e2bc | PCR-amplified RAPD pattern of four tomato genotypes using five RAPD primers (S119; OPV19; S6; OPV18 and S22). L, ladder; O, Opal; P, Permata F1; R, Rewako; M, Mutiara. | PMC10358481 | 10.1177_00368504221122364-fig1.jpg |
0.427609 | 62b0b24ed1694acb88d49fbc436e53e9 | Unweighted pair group method with arithmetic mean (UPGMA) dendrogram illustrating the genetic relationship between four genotypes of Indonesian tomatoes based on RAPD fingerprinting. | PMC10358481 | 10.1177_00368504221122364-fig2.jpg |
0.464684 | 8a6da3eb489c4493a11899e0ba62a3c4 | Effect of pb contamination on root length of the Indonesian tomato genotypes at 32 days after planting (DAP). The value represents means of plant height ± SD. Different letters indicate statistically significant differences (p < 0.05). | PMC10358481 | 10.1177_00368504221122364-fig3.jpg |
0.465269 | 1d39ea42651242fd8df5c621681ee5eb | Effect of pb stress treatment on plant height of the Indonesian tomato genotypes at 32 days after planting (DAP). Value represents means of plant height ± SD. Different letters indicate statistically significant differences (p < 0.05). | PMC10358481 | 10.1177_00368504221122364-fig4.jpg |
0.466703 | 04dd3a5868474fa6806572bacd76e7b9 | Root length of the Indonesian tomato (Solanum lycopersicum L.) genotypes after being treated with Pb stress at 32 days after planting. | PMC10358481 | 10.1177_00368504221122364-fig5.jpg |
0.448056 | da2e44f343204b6a84d2fb2725938922 | GDF-15 interferes with T cell adhesion to activated endothelial cells.a Effects of recombinant human (rh)GDF-15 (added for 10 min) on CXCL12α−mediated adhesion of whole blood-derived CD45+ cells to activated human lymphatic endothelial cells (huLEC) were analyzed. Adherence was calculated based on the number of CD45+ cells as enumerated by flow cytometry (n = 7 experiments). In b, adhering leukocytes were further characterized by multicolor staining (n = 10 experiments). c Stimulated T cells from 6 donors were treated or not with rhGDF-15 for 20 min before being run in µ-slides over a layer of activated huLEC. 10 predefined fields of view were video-imaged for 5 s and the number of T cells adhering under hydrodynamic flow conditions was counted. Different shadings indicate different T cell donors. For reference, adhesion to non-activated huLEC is shown for one donor. d Enumeration of T cells adhering to human umbilical vein endothelial cells (HUVEC). 5 predefined fields of view per sample were analyzed in a representative experiment. In e, CXCL9 and CXCL10 were used to induce adhesion of untreated or GDF-15-treated CD8+ T cells from 3 different donors on stimulated huLEC. In f, stimulated CD8+ T cells from 3 different donors were treated with rhGDF-15 and anti-GFRAL or isotype control antibodies for 20 min before being run in µ-slides over a layer of activated huLEC. In g–j, phase-contrast microscopy in chamber slides to assess effects of rhGDF-15 on T cell adhesion to activated HUVEC. An EC50 value for rhGDF-15-mediated adhesion inhibition on pan T cells from 3 different donors was determined in g (logICF=logIC50 + (1/HillSlope)*log(F/(100-F)). h–j Using pan T cells from 9 different donors, effects of rhGDF-15 on T cell adhesion (h), transmigration (i) and recruitment (j) were analyzed. Statistical analyses were performed by one-way ANOVA in a, d, f, by two-sided paired Student´s t-tests in b, e, h, i, j, by mixed-effects analysis in c. To correct for multiple comparisons, Tukey´s post hoc test was applied in a, c, d, Bonferroni´s method in b. In c, d, g, mean values with SEM, in e, f, median values are indicated as horizontal lines. Source data are provided as a Source Data file. | PMC10359308 | 41467_2023_39817_Fig1_HTML.jpg |
0.466426 | 854da1ffaefc46ec955f6b1a04c0155c | GDF-15 interferes with LFA-1-dependent adhesion of human T cells.a–c µ-slides were coated with CXCL12α and vehicle or ICAM-1-Fc (a–c), MAdCAM-1-Fc (b), or VCAM-1-Fc (c). Stained primary human T cells were stimulated with anti-CD3/CD28 before GDF-15, or vehicle, or antibodies against adhesion molecules LFA-1, α4β7 integrin, or VCAM-1 were added for 30 min. T cells were perfused for 6 min over the coated µ-slides. Adhesion was recorded by live microscopy and analyzed using CellProfiler software. In d, e, CD4+ and CD8+ T cells were pre-treated for 20 min with GDF-15, or blocking anti-LFA-1 antibody TS1/18, or both, and run over activated HUVEC as in (1e–i). f, g Binding of conformation-specific anti-active LFA-1 antibody mAb24 (f) or ICAM-Fc (g) to CD8+ T cells was analyzed. Whole blood from healthy volunteers was maintained at 37 °C and treated or not with GDF-15 10 min prior to LFA-1 activation. Fluorescence-conjugated antibodies and complexed soluble ICAM-1-Fc were added for another 10 min. Cells were fixed and analyzed on an Attune Nxt flow cytometer. Mean fluorescent intensity (MFI) values were normalized to control conditions by z-transformation. h, i, j Human PBMC were stimulated for 30 min with CXCL12α and Mg2+ ± rhGDF-15. Cells were stained with the conformation-specific Alexa Fluor 647-labeled anti-LFA-1 antibody mAb24 (h) or hICAM-1-Fc-AF647 (i). The number of active LFA-1 molecules per single CD3+ T cell was quantified by direct stochastic optical reconstruction microscopy. Representative single cell images are shown in h, i. Data obtained with mAb24 across three different donors are summarized in j. k, l T cells were added to ICAM-1- and E-Selectin-coated Protein G beads, in the absence or presence of GDF-15. After lysis, Talin phosphorylation was assessed by Western blotting, with CD3ε as loading control. A representative blot is shown in k. Protein quantification data from 7 different samples normalized to vehicle (human serum albumin) control are displayed in l. Statistics were calculated by Kruskal–Wallis with Dunn´s post hoc test (a), by one-way ANOVA with Tukey´s correction for multiple comparisons (b–e), and by two-sided paired t-tests (f, g, j, l). Horizontal bars indicate mean (a, f, g) or median (d, e, j, l) values. Source data are provided as Source Data file. | PMC10359308 | 41467_2023_39817_Fig2_HTML.jpg |
0.459801 | 644292d4911c49a598f57608c68a78f3 | GDF-15 interferes with immune infiltration and immune-mediated tumor rejection in the MC38 colon cancer model in vivo.a, b NCInu/nu-mice (6 mice/group) were subcutaneously injected with 5 × 105 MC38blank or MC38tghGDF-15 colon cancer cells. Body weight (a) and tumor sizes (b) were determined twice weekly. c–h C57BL/6NCrl–mice were subcutaneously injected with 5 × 105 MC38blank or MC38tghGDF-15 cells. c Tumor take rates. d Representative survival curves (termination criterion: tumor volume > 1200 mm3) shown as Kaplan–Meier plot (detailed statistics in Supplementary Table 1). e hGDF-15 serum levels on day 28 were analyzed by ELISA and f correlated with tumor size. g Antibodies against hGDF-15 were assessed in sera and h correlated with hGDF-15 levels. i–t C57BL/6NCrl–mice were subcutaneously injected with MC38blank or MC38tghGDF-15 cells. In i–k, tumors were explanted when ≥1000 mm3. Tumor-infiltrating CD45+ and CD8+ cells were stained (i) and quantified (j, k). In l–o, effects of anti-hGDF-15 antibody on tumor growth (l), and infiltration by CD45+ (m), CD4+ (n) and CD8+ (o) cells are shown. Infiltration was analyzed by flow cytometry from gently dissociated, 300–500 mm3-sized tumors. Preferential rejection of MC38blank tumors and tumor-unrelated deaths caused imbalances between the groups. In p–r, MC38tghGDF-15 tumors were treated with vehicle/anti-hGDF-15/anti-PD-1/anti-hGDF-15+anti-PD1. Representative pictures (p), the percentage of tumor-infiltrating CD8+ T cells (q) and a score for perinecrotic CD8+ T cell infiltration (r) are shown. s, t C57BL/6NCRL mice were subcutaneously inoculated with 5 × 105 MC38blank or MC38tghGDF-15 cells. Mice were randomized across the different treatment groups and treated or not with anti-PD-1 antibody ± anti-GDF-15 antibody (t). Kaplan–Meier plots based on survival are displayed. a, b, c, h, q, and r were analyzed by two-sided unpaired t-tests, d and s by log-rank (Mantel-Cox) test. Wilcoxon–Mann–Whitney test was applied to e, g, j, and k. Pearson’s linear regression was calculated in f. In t, tumor growth was compared by Cox proportional hazard models. Individual tumor growth curves for s and t are shown in Supplementary Fig. S4. Horizontal bars depict mean values ± SEM in a, b, l, and median values in c, e, g, j, k, m, n, o, q, r. All experiments were performed at least three times. In a, b, d–t, representative experiments are shown. Source data are provided as a Source Data file. | PMC10359308 | 41467_2023_39817_Fig3_HTML.jpg |
0.425647 | f87071ff23c747de999be0b2b2c8e1c6 | GDF-15 blockade synergizes with anti-PD-1 in orthotopic Panc02 tumors and enhances T cell recruitment in syngeneic and humanized mice.In a, c, d, e, 1 × 104 luciferase-transgenic Panc02 cells (Panc02-luc) were inoculated into the pancreatic head of male albino C57Bl/6J mice. In b, female albino C57Bl/6J mice received 1 × 106 Panc02-Luc cells into the pancreatic tail. After bioluminescence-based randomization on day 5, animals were treated twice weekly with vehicle/anti-hGDF-15/anti-PD-1/anti-hGDF-15+anti-PD1. Bioluminescent in vivo imaging (1–2 times/week) enabled monitoring of tumor growth (countsfinal measurement/countsrandomization). In a, animals were euthanized when symptomatic or on day 29 (see x-axis), in b on day 35. CD4+ (c) and CD8+ (d) T cell infiltration on day 12 were assessed by flow cytometry from disseminated tumors. e Representative stainings for tumor-infiltrating CD8+, Granzyme B+ and Foxp3+ cells. f–i 2 × 105 EMT6 murine breast cancer cells were orthotopically injected in female 7–10-week-old BALB/c mice. Anti-GDF-15 or isotype control were administered on days 6, 9, 12. Carboxyfluorescein-succinimidylester (CFSE)-labeled T cells were adoptively transferred on day 13. On day 14, infiltration of transferred CD3+, CD4+ and CD8+ T cells into (explanted) axillary (f) and brachial (g) lymph nodes was assessed by flow cytometry. Tumor size (h) and weight (i) were recorded. j–m NOD/SCID/γc-/-FcRγ-/- mice were reconstituted with human hematopoietic stem cells (HSC), injected with patient-derived HV-18-MK (GDF-15high) melanoma transplants, and treated with anti-hGDF-15 or control antibody. Day 24 hGDF-15 serum levels (j) correlated with tumor size for the 3 isotype-treated tumors that could be explanted without being disrupted (Pearson correlation) (k). Tumor-infiltrating human CD45+, CD3+, and CD19+ cells were determined by flow cytometry. Two independent experiments (n = 9 mice/group) are summarized in l. Colors relate to CD34+ HSC donors. In m, the composition of CD3+ T cell immune infiltrates on day 24 is shown for the mice from the second independent experiment. In a, b, tumor growth was analyzed by pairwise Mann–Whitney tests with Bonferroni–Holm correction. In c, d, f, g, h, i, groups were compared by unpaired Student´s t-test. In l and m, Mann–Whitney U-test was performed, using overall cell percentages in m. Horizontal bars indicate mean ± SEM in c, d, f, g, h, i, median values in j, l, m. Source data are provided as a Source Data file. | PMC10359308 | 41467_2023_39817_Fig4_HTML.jpg |
0.423337 | 3090c83d1f814164941b2cec5d44d9db | GDF-15 expression is negatively correlated with intratumoral T cell infiltration in brain metastases from melanoma patients and in HPV+ oropharyngeal squamous cell carcinomas.a–d Formalin-fixed paraffin-embedded tissues from melanoma brain metastases from 70 patients were stained by immunohistochemistry for GDF-15 and for the T cell marker proteins CD3 and CD8. Exemplary stainings are shown in a. b–d For hGDF-15 expression, a score was based on frequency (0–1% → score 0; 1–10% → score 1; 10–25% → score 2; 25–50% → score 3; >50% → score 4) multiplied with staining intensity (weak → 1, moderate → 2, strong → 3)). e–h GDF-15 serum levels were assessed from patients with human papilloma virus (HPV)+ or HPV- oropharyngeal squamous cell carcinomas (OPSCC). Tumor-infiltrating CD8+ T cells per area were quantitated for 37 HPV+ tumors and correlated with the corresponding GDF-15 serum levels (e). f–h GDF-15 serum levels were divided into two groups with either GDF-15 < 1.0 ng/ml or GDF-15 ≥ 1.0 ng/ml. Kaplan–Meier plots for disease-specific survival were plotted for these two groups for patients with OPSCC irrespective of HPV status (n = 86) (f), as well as for HPV- (n = 32) (g) and HPV+(n = 54) (h) OPSCC. Spearman´s rank-correlation coefficients (ρ) and p-values are indicated for b–e. Dotted trend lines were added for visualization. Kaplan–Meier curves were compared by log-rank (Mantel-Cox) test (f–h). Source data for b–h are provided as a Source Data file. | PMC10359308 | 41467_2023_39817_Fig5_HTML.jpg |
0.51991 | 0adc991331c64a0db41a019e511bb3a0 | In human melanoma patients GDF-15 serum levels predict response to and survival under therapy with anti-PD-1 antibodies.a, b GDF-15 levels were analyzed in 37 melanoma patients at baseline of ipilimumab treatment, and correlated with clinical responses based on RECIST v1.1 criteria (a), including durability of initial responses (b). c–j GDF-15 levels were analyzed in pre-treatment sera from 34 melanoma patients prior to pembrolizumab treatment (Zurich cohort, c–e), and from 88 patients (Tübingen cohort, f–j) prior to treatment with pembrolizumab (n = 48) or nivolumab (n = 40). GDF-15 serum levels were correlated with responses according to RECIST v1.1 (c, f). Black circles indicate patients with ongoing responses at the time of analysis. Groups were compared by Mann–Whitney test in a–c. In d, g, h, logistic regression models were fitted for response (d, g) or disease control (h) under anti-PD-1 treatment. Dotted vertical lines indicate GDF-15 serum levels (continuous predictor) corresponding to a 50% probability of treatment response. Two extreme values ([GDF-15] ≫ 100 ng/ml) are displayed at the upper end of the scale. In e and i, overall survival of 34 (e), respectively 88 (i) patients was analyzed by Cox proportional hazards model with overall survival (time to death) as outcome variable and GDF-15 as continuous predictor. Kaplan–Meier plots (cut-off: 2.0 ng/ml GDF-15) are shown for visualization (e, i). Further Kaplan–Meier curves including serum lactate dehydrogenase (sLDH) as additional predictor were calculated for the Tübingen cohort (j). Censoring is indicated by vertical lines. In f, p-values were calculated by Kruskal–Wallis test. In f, g, h, one patient whose clinical course contradicted the RECIST1.1-, and therefore target lesion-based classification as complete responder was omitted from statistical consideration. One further patient could not be staged and is therefore neither displayed nor assigned to any group. In i, j, overall survival between groups was compared using two-sided log-rank tests, including all patients. Horizontal bars in a, b, c, f depict median values. Source data for b–h are provided as a Source Data file. | PMC10359308 | 41467_2023_39817_Fig6_HTML.jpg |
0.468736 | 712ff728056b496fa13171e26c130d65 | Stalled HK97 packaging complexes. (A) DNAse protection assay for the HK97 packaging motor using a cos containing substrate at variable ATP concentrations. (B) Sample visualised by negative stain electron microscopy. (C) Sample visualised by cryo-EM. Red arrows highlight DNA packaging centres. (D) External and cross-sectional views of the asymmetric reconstruction. | PMC10359639 | gkad480fig1.jpg |
0.447949 | acfa4893d253454ca8eb47d6172061a6 | Icosahedral reconstruction of the HK97 prohead II at 3.06 Å resolution. (A) EM density viewed along the five-fold axis. (B) Ribbon diagram of the asymmetric capsomere unit shown alone (bottom) and fit into the corresponding density map (top). (C) Representative EM map shown for a prohead segment fitted with corresponding atomic model. | PMC10359639 | gkad480fig2.jpg |
0.432743 | cb43e6eca68d4fc78d1d596e8d4b192b | Structure of the portal protein. (A–C) C12 reconstruction of the in-situ portal protein at 2.98 Å resolution. (A) Ribbon diagram with only two opposing subunits. (B, C) Portal density. (D) Comparison of portal protein maps in the presence and absence of the motor, viewed from the clip (left) and perpendicular to the portal axis (right). | PMC10359639 | gkad480fig3.jpg |
0.446874 | 6da8da19043f481ea027464001618ac3 | Asymmetric reconstruction of the HK97 DNA packaging motor. (A) Pentameric motor surrounding DNA substrate. The terminase ring is tilted 10° relative to the portal. (B) The portal-terminase motor complex. (C) Cross sectional views of the portal-motor complex. (D) Result of the rigid body docking of terminase domains, derived from the crystal structure of the HK97 large terminase, into the EM density with the fitted models shown as ribbon diagrams coloured by subunit. | PMC10359639 | gkad480fig4.jpg |
0.454757 | ee09769e6e474daf8e978ffe742716e5 | Packaging termination in vivo and in vitro. (A) Initiation complex of HK97 DNA packaging in vivo. (B) Termination complex of HK97 packaging in vivo. (C) HK97 stalled packaging complex present in vitro, after cleavage of DNA with the large terminase assembly remaining attached, releasing the cleaved DNA into the prohead interior. | PMC10359639 | gkad480fig5.jpg |
0.443948 | 0a21055e1d664affa3980e552f9a00fa | Structural comparison of HK97 large terminase monomers of the motor. (A) Proposed nucleoside binding pattern. (B) Comparison of proposed ATP and ADP bound subunits. (C) Overlay of large terminase monomers after aligning the nuclease domain. | PMC10359639 | gkad480fig6.jpg |
0.547337 | e846b52680d94007b54c76ec85f7b532 | Comparison of domain adjustments in HK97, Φ29 and Ftsk DNA translocation motors. Subunits are coloured differently and shown as molecular surfaces. DNA (Φ29 and Ftsk) or DNA density (HK97) is in dark grey. For each motor (A – HK97, B – Φ29 and C – Ftsk) two orthogonal views of the assembly are on the left, and individual subunits along with DNA are shown on the right. | PMC10359639 | gkad480fig7.jpg |
0.436455 | 2cc661a802d54cbab88a3da1d33ec71f | Integrate solution by control element. | PMC10360599 | gr1.jpg |
0.428741 | 398877c7c43647df8f5e3d93b761c47f | Before sampling: Strain equivalent target (simulated by FEM) vs Stress equivalent using ANN. | PMC10360599 | gr10.jpg |
0.419733 | 34bdafd67f524808909fbd30e0769029 | After sampling: Strain equivalent (simulated by FEM) vs Stress equivalent using ANN (feedforward matched at the layer N°6). | PMC10360599 | gr11.jpg |
0.430058 | 3fde6d0035a941a3ad6d54c9ccc7a076 | (a) Upscaling structure; (b) Asymmetry model. | PMC10360599 | gr2.jpg |
0.408723 | 6f5e49b24287440cbe99e5c243003438 | Procedure used for the application and optimization of the ANN model. | PMC10360599 | gr3.jpg |
0.434701 | 36b6d1adb78c4cabaeec848523ee40d9 | Workflow numerical twin. | PMC10360599 | gr4.jpg |
0.457535 | 0fc8a7198f5947ae8cd5e43312e64ad9 | Temperature distribution using FEM. | PMC10360599 | gr5.jpg |
0.424231 | 62e79f0bd28a4257b3eb03bfc2418fb9 | Before sampling: Temperature distribution “target” (simulated by FEM) vs multi scenarios of Temperature distribution using ANN. | PMC10360599 | gr6.jpg |
0.421725 | b65c3301a5b4433287920cba58ced176 | Before sampling: Temperature distribution (simulated by FEM) vs multi scenarios Temperature distribution using ANN (feedforward at the layer N°8). | PMC10360599 | gr7.jpg |
0.462843 | 47d9d08eb66c48d1a64a7b98e9e016dd | Before sampling: Stress equivalent (simulated by FEM) vs multi scenarios Stress equivalent using ANN. | PMC10360599 | gr8.jpg |
0.436577 | a7c62e6490274d5ab6381eabb1f18d2b | After sampling: Stress equivalent (simulated by FEM) vs Stress equivalent using ANN (feedforward matched at the layer N°5). | PMC10360599 | gr9.jpg |
0.426629 | 4f622e79de6b4b729b0454a32a4968ec | Model construction and experimental flow chart. | PMC10361039 | gr1.jpg |
0.535143 | 1a72277fe7874c2bb77f1110ae047875 | Comparison of prediction results between the XGBoost and Decision Tree models. | PMC10361039 | gr10.jpg |
0.49748 | b0240a1bd678427491601e4d63baa479 | Comparison of prediction results between the XGBoost and IHBA-SVM models. | PMC10361039 | gr11.jpg |
0.497899 | fdbf2e95a40a447d9c57bf79153ec3bc | Comparison of prediction results between the XGBoost and LSTM models. | PMC10361039 | gr12.jpg |
0.496641 | 13cac9573c7140cd8a87df5c54ef1d84 | Comparison of prediction results between the XGBoost and TCN models. | PMC10361039 | gr13.jpg |
0.497342 | dafceac5ed7a4cffba51eb725b91c541 | Comparison of prediction results between the XGBoost and GRU models. | PMC10361039 | gr14.jpg |
0.418422 | 69844b3e45f143368e69b6c14d303bf1 | Standard K-line detail chart. | PMC10361039 | gr2.jpg |
0.424793 | 5d9efee29325420cbc3e56c651a550a5 | Wind power K-line construction schematic. | PMC10361039 | gr3.jpg |
0.477653 | 2d23d9f399004293bc6ace65fdc30da1 | Variational ant colony algorithm running flowchart. | PMC10361039 | gr4.jpg |
0.562992 | 6a178223e2e84e1cb2d6971e9917c737 | Schematic diagram of the effect of parameter optimization with MACD-s as an example (Group I). | PMC10361039 | gr5.jpg |
0.553424 | 2e97d2546f634cbb8cc25882d6feae3c | Schematic diagram of the effect of parameter optimization with MACD-s as an example (Group II). | PMC10361039 | gr6.jpg |
0.572362 | 6be11f15f01f488e9e66dc4c15174e4c | Schematic diagram of the effect of parameter optimization with MACD-s as an example (Group III). | PMC10361039 | gr7.jpg |
0.442146 | 9ef280265e2a4f2aa0257093afa0e662 | Predictive effect of FTIs obtained by different methods in the model. | PMC10361039 | gr8.jpg |
0.473494 | 54f9749c80124accb75ca40f30fa8233 | Comparison of prediction results between the XGBoost and LightGBM models. | PMC10361039 | gr9.jpg |
0.451755 | d9362f2560474b1f82df2ff3936c0330 | Path analysis model | PMC10361049 | BNJ-7-4-267-g001.jpg |
0.461963 | 7208b064fb9242989ead317d8236e2e9 | Frequency of monocyte subsets and expression intensity of CD14 and CD16 in each subset. The graphs represent the four study groups: HC (n = 39), TB (n = 34), HIV (n = 35), TB/HIV (n = 12). A) Monocytes subset frequency in health and dis disease, B) MFI of CD14 and, C) MFI of CD16 within CM, IM and NCM subsets in HC, TB, HIV and TB/HIV co-infection. The insert figures in the direction of the arrow (B, C) are zoomed pictures of the same figure to enhance the visibility of low-frequency subpopulations. Asterisks represent P-values of: * 0.05, **0.01, ***0.001, ****0.0001. | PMC10361379 | gr1.jpg |
0.396318 | 8bc071199e704e13b303f7931661ad8b | Expression of chemokine receptors on total monocytes in HC, TB, HIV and TB/HIV patients MFI of A) CCR2, B) CX3CR1 C) CCR4 and D) CCR5 on total monocytes was determined. The middle line in each dot plot represents median values. Group comparison was computed by the Kruskal-Wallis test followed by Dunn's multiple comparison test. Asterisks represent p-value of 0.05*, 0.01**, 0.001***, and 0.0001****. | PMC10361379 | gr2.jpg |
0.41931 | 49ba7d193adf4e23a98bfbca38b2751c | Correlation of CCR4 and CCR5 with CD4+T cell count and HIV-1 plasma RNA viral load in HIV patients. Correlation of A) CCR4 vs CD4, B) CCR5 vs CD4, C) CCR4 vs HIV-1 RNA viral load and D) CCR5 vs HIV-1 RNA viral load. CD4+ T cell count presented as number of cells/mm3, HIV-1 plasma RNA viral load as number of viral copies/milliliter are depicted. Non-parametric Spearman correlation test used to assess correlation. | PMC10361379 | gr3.jpg |
0.385502 | 6f1b055d816c4113915ba220abc8e402 | Chemokine receptors expression on CM, IM and NCM in health and disease. A) CCR2, B) CX3CR1, C) CCR4 and D) CCR5. The y-axis represents MFI of each marker. Each symbol in the plots represents patient specific values and the middle line represents the median. Comparisons across cohorts was made by the Kruskal-Wallis test followed by Dunn's adjustment. Asterisks represent p-value of 0.05*, 0.01**, 0.001*** and 0.0001****. | PMC10361379 | gr4.jpg |
0.402912 | 3c6db755427049529f07ceaa97e0a7e0 | Correlation of chemokine receptors with monocyte subsets. Figures in row represent chemokine receptors: A) CCR2, B) CX3CR1, C) CCR4 and D) CCR5. Figures in a column are from a single monocyte subset either: CM-classical monocytes, IM-intermediate monocyte, NCM-non-classical monocyte In figures, the y-axis represents percentage of monocyte subsets; the x-axis represents median fluorescence intensity (MFI) of chemokine receptors. Correlations were made on total participants without stratifying the data into study groups. | PMC10361379 | gr5.jpg |
0.47635 | 3a226e4621e54eb4b373573ebcde39e7 | Positivity of antineutrophil cytoplasmic antibodies (ANCA) tests performed at diagnosis. This analysis includes all study participants that had ANCA tests performed at diagnosis. The positivity rate was 32.0% (10/31) for indirect immunofluorescence (IIF)-ANCA tests performed at the Immuno-Rheumatology laboratory (A), 75.0% (9/12) for IIF-ANCA tests performed by other laboratories (B), and 72.8% (8/11) for ELISA tests performed at diagnosis by other laboratories (C). Analyses were performed with Fisher's exact test. | PMC10361643 | 1414-431X-bjmbr-56-e12636-gf001.jpg |
0.445664 | 2361f001afc441d086c5a1c749e80809 | Positivity of indirect immunofluorescence-antineutrophil cytoplasmic antibodies (IIF-ANCA) tests using the standard technique. The IIF-ANCA using the standard technique was positive in 26.7% (8/18) of ANCA associated vasculitis (AAV) patients and in 5.3% (1/19) of ulcerative colitis (UC) patients, while no patient with type 1 autoimmune hepatitis (type 1 AIH) had a positive test. Analyses were performed with Fisher's exact test. | PMC10361643 | 1414-431X-bjmbr-56-e12636-gf002.jpg |
0.498998 | 9a50aea0382f40d7bbcf445da07d1f3d | The positivity of indirect immunofluorescence-antineutrophil cytoplasmic antibodies (IIF-ANCA) tests using standard and improved techniques in each disease. The overall positivity rate improved significantly from the standard to the improved technique (A) [10/61(16%) to 21/61(34%)]. Although the positivity rate of IIF-ANCA tests remained stable in granulomatosis with polyangiitis (GPA) patients (B) [8/18(44%) to 9/18(50%)], it improved in microscopic polyangiitis (MPA) patients (C) [0/6 (0%) to 1/6 (17%)], in eosinophilic granulomatosis with polyangiitis (EGPA) patients (D) [0/5 (0%) to 1/5 (20%)], in type 1 autoimmune hepatitis (AIH) patients (E) [0/12 (0%) to 3/12 (25%)], and in ulcerative colitis (UC) patients (F) [1/19 (5%) to 7/19 (37%)]. Statistical analyses were performed with McNemar's test. | PMC10361643 | 1414-431X-bjmbr-56-e12636-gf003.jpg |
0.551077 | 75b02461afe445e5b04077c6eb5d60ad | Changes in indirect immunofluorescence-antineutrophil cytoplasmic antibodies (IIF-ANCA) titers using the standard and improved IIF techniques. The median IIF-ANCA titers among positive tests increased from 1/40 (1/30-1/160) to 1/80 (1/40-1/80) using the standard and the improved IIF techniques, respectively. Data were analyzed with the Wilcoxon signed-rank test. | PMC10361643 | 1414-431X-bjmbr-56-e12636-gf004.jpg |
0.429901 | c4c1b312b8f04438aa70717a5a86da2a | Bright field microscopic images of ICO culture maintenance after tissue or cryopreserved organoid culture initiation(A) Immediately after tissue-derived ICO initiation and SEM addition, showing residual cellular debris and only small potential ICO structures (Ø 5–10 μm; zoom in black squared box).(B) While residual cellular debris is still present, the SEM media is switched for EM after day 3 of initiation, showing ICO structures arising (Ø 10–100 μm; zoom in black squared box).(C) The maximum density of the residual cellular debris level upon tissue-derived ICO initiation, which will still result in viable ICO culture (zoom in black squared box).(D) ICO initiation from previously established cryopreserved ICO with an overall 50% debris density upon thawing. Only few small potential ICO structures are visible (Ø 5–10 μm; zoom in black squared box).(E) Upon multiple small ICO structures (Ø 10–100 μm; zoom in black squared box) the SEM media is switched for EM, after approximately 5 days.(F) 95% ICO density within the BME dome with a collapsed darkened ICO within the zoom in black squared box, indicating that passaging the culture is desired.(G) Examples of ICO cultures with densities <80% that only require media refreshment, no passaging yet, showing entrapped debris within an ICO in the zoom in black squared box.(H) Examples of ICO cultures with densities >80% that require passaging for culture expansion, in which the zoom in black squared box indicates the formation of thickened ICO borders within a dense ICO culture. (All images: 2× magnification; scale bar indicates 2,000 μm). | PMC10362172 | gr1.jpg |
0.389015 | 0c50bb064c1a4d7e8d6dcf38b8eb551d | Bright field microscopic images of the branching initiation process in ICO cultures(A) The lay-out of the BME dome seeding in a well of a 12-wells plate upon branching initiation.(B) The desired (20%–50%) ICO seeding size and density to promote successful BRCO initiation.(C) After 3 days of EM and the presence of small ICOs (Ø 10–100 μm), the media is switched to BM.(D) BM incubation of 3 days will result in darkened ICO structures with a thickened border (blue arrow). The blue squared box tracks the branching formation of one of the BRCO over 2 weeks’ time. This specific ICO line already showed clear small tubular branching structures (Ø 100–500 μm) after 2 weeks of BM refreshment, while the EM control maintained exponential growth and required passaging after 1 week.(E) Tracking the outgrowth of branching structures until 1.5 weeks after manual BRCO clone selection, showing the formation of tubular structures after careful structure breaking during picking (blue squared box).(F) The 6 day outgrowth of BRCO after normal passaging procedures for the expansion of BRCO up to 1,000 μm (zoomed scale bar indicated 1,000 μm at 4× magnification), these results have been published as supplementary data in Roos et al., 2022; Supplementary figure S11 (All images, except for A and zoom in: 2× magnification; scale bar indicates 2,000 μm). | PMC10362172 | gr2.jpg |
0.417897 | 409f72c4b6914536941852c770c8819a | The manual clone selection of BRCO to enable the outgrowth of larger BRCO structures and the purification of the BRCO culture from cystic ICO structures(A) The BRCO density (<70%) without overlapping structures that could be picked by applying an inverted microscope, as indicated by the example in the picture.(B) The manual BRCO selection of high density BRCO cultures (>70%) with overlapping structures utilizing an automated hybrid microscope cell imaging system (EVOS Cell Imaging System, Thermo Fisher Scientific). The blue arrows indicate the BRCO structures that should be manually picked. (All bright field images; 2× magnification; scale bar indicates 2,000 μm). | PMC10362172 | gr3.jpg |
0.449179 | e5763843b0624e619de74d0480859a3f | Bright field microscopic images of the expected outcomes of a successful BRCO initiation procedure(A) The formation of an elaborate tubular network of BRCO structures within one healthy ICO line (zoomed scale bar indicates 1,000 μm at 4× magnification).(B) Upon BM media switch, the percentage of BRCO outgrow differs between different healthy ICO lines, ranging from 70%‒25% of total organoid structures within the BME dome including different size ranges of (100–500 μm), these results have been published as supplementary data in Roos et al., 2022; Supplementary figure S1.1(C) Successful branching of BRCCAO, showing the distinct dense branching structures without large elaborate networks or tubular formations reaching outwards (zoomed scale bar indicates 1,000 μm at 4× magnification).(D) The successful branching of PCLDO showing large elaborate tubular networks exceeding the 3,000 μm (zoomed scale bar indicates 1,000 μm at 4× magnification). (All images, except zoom in; 2× magnification; scale bar indicates 2,000 μm). | PMC10362172 | gr4.jpg |
0.380139 | 54c3527a97e245ddb3f2aadfab1d2445 | An overview of bright field microscopic images presenting potential problems that could arise during the BRCO initiation procedure(A) The presence of large cystic ICO structures (Ø 1,000 μm) only, even after 4 weeks of BM culture. The blue arrows indicate the somewhat thickened border and darkened coloring of the cystic organoids after 4 weeks of BM culture.(B) Exceeding the advised ICO seeding density >70% for BRCO initiation will result in the formation of smaller, dense and seemingly less viable BRCO structure, creating an overall less successful BRCO culture.(C) While decreasing the ICO seeding to <20% could result in the outgrowth of faster growing cystic ICO cultures, with only 1 or 2 BRCO that would be eligible for manual clone selection (increasing overall procedure times drastically).(D) When BRCO are not broken or passaged on time, the BRCO structure will start to expire over time showing very dark dense thickened tubular structures. The zoomed in black square indicates the release of dying cells into the BME dome.(E) Mycoplasma contamination of an ICO culture showing the distinct bearded ICO structures and the small dots (Ø 1–5 μm) that are both clear indicators for mycoplasma contamination (20× magnification; scale bar indicates 200 μm) (All images, except zoom in; 2× magnification; scale bar indicates 2,000 μm). | PMC10362172 | gr5.jpg |
0.426952 | 0f5a8093c36643b19c61259af6ec332a | A, the distribution of PPR exons and the position of c.1325-1336del. The normal sequence and corresponding amino acid sequence of the gene are in the left corner. The red part shows the missing segment. B, the 3D structure of PPR which contain 7 segments ofαhelices embedded between the lipid bilayer. The variant occurs in the red transmembrane region indicated by the black box. C, the specific location of the variant on the helix and the green globules represent the missing amino acids | PMC10362615 | 12903_2023_3226_Fig10_HTML.jpg |
0.411962 | e603efb93e654e42baae140d464ea1b5 | Pretreatment intraoral photographs | PMC10362615 | 12903_2023_3226_Fig1_HTML.jpg |
0.470163 | a6c1382b7b22447fb0a4a0f4b3d31f73 | Pretreatment panoramic radiograph | PMC10362615 | 12903_2023_3226_Fig2_HTML.jpg |
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