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0.420871 | 3625c39179604264b9f1469d09ce52a3 | Unsupervised learning capability of neural network constructed based on artificial neuron and synapse.a Schematics of neuron (FG-com) and synapse (MT-FGMEM) array for unsupervised learning simulation of MNIST data sets without labels. b Accuracy variation along the nonlinearity factor (β) and the number of post-neurons. c Conductance potentiation of synapse along the number of spikes at different nonlinearity factors (β = 0 ~ 10). d Visualized synaptic conductance after 60,000 MNIST (no labels) training. The number of post-neurons is 10 (top panel) and 30 (bottom panel). e The number of neuronal fires in 10, 20, 30 and 100 post-neurons for the test label. | PMC10224934 | 41467_2023_38667_Fig6_HTML.jpg |
0.446515 | 42ef139ca7ac46999b6d6eec3026c1e7 | Fabrication process and photos of Ag2Se network.a Schematic of the two-step impregnation process, showing the in-situ synthesis of Ag2Se network by silvering and then selenizing. b A large Ag2Se network with a size of 1.8 × 0.9 m2. c Ag2Se networks are processed to special shapes. | PMC10224941 | 41467_2023_38852_Fig1_HTML.jpg |
0.449538 | f29c24a309d249da8863310b1a85b6e2 | Mechanical, and thermoelectric properties of Ag2Se network.a–c Photos (inset) and cross-section micrographs of the Ag2Se network in different states, showing the deformation of network structure under stress. d Tensile stress (σt)–strain (εt) curve and compressive stress (σc)–strain (εc) curve with corresponding resistance change (R/R0). e Cyclic σc–εc curves with strain varying from 50% to 80% (bottom left), and σt–εt curves with strain from 40% to 100% (top right). f Cyclic strain-stress curves at a maximum εc of 80% (bottom left) and a maximum εt of 100% (top right). g
R/R0 upon cyclic compressing (top) and stretching (bottom) under different strain rates. h Thermoelectric performance of Ag2Se network including electrical resistivity (ρ), Seebeck coefficient (S), power factor (PF), and zT value. i Comparison of the present zT value with reported 3D flexible thermoelectric materials. The inset shows the larger version of the zT values of CNT-based materials. Error bars represent the standard deviation. Source data are provided as a Source Data file. | PMC10224941 | 41467_2023_38852_Fig2_HTML.jpg |
0.51121 | bcdde985f4ec4ad98f4a46f15fe48bf3 | Output performance of Ag2Se network-based FTEG.The simulated internal temperature distribution of the full filled (a), 10% filled (b) bulk FTEGs and the network-based FTEG (c) at an ambient temperature of 290 K. Further simulation details are provided in the supplementary materials. d, e, The simulated single leg voltage and power density in an ambient temperature range from 273 K to 305 K. f The infrared image and optical photograph (inset) of a network-based FTEG dressed on a human wrist. The top electrode was removed to avoid the effect caused by its low emissivity. g, h The measured voltage and power density at an ambient temperature of 290 K and 297 K. Inset shows a device under test. i Summary of the FTEG’s power generation at different ambient temperatures. All the measurements were performed on human skin without heat sinks. Red line and red circles respectively represent the simulated and measured values of the Ag2Se network-based FTEG. Source data are provided as a Source Data file. | PMC10224941 | 41467_2023_38852_Fig3_HTML.jpg |
0.38805 | ee49fae8ed3f438f9024f10efd0cb8be | Thermoelectric jacket and fabrics.a A thermoelectric jacket filled with the Ag2Se network-based FTEG. b Detailed photograph of the thermoelectric-device area. c Schematic of the thermoelectric modules in series. d,
e The thermoelectric jacket’s open-circuit voltage and output power under different thermal conditions. f–h The optical photos and morphologies (inset) of various thermoelectric fabrics. Further micrographs and thermoelectric performances are shown in Figs. S13 and S14. Ruler scale unit: mm. Source data are provided as a Source Data file. | PMC10224941 | 41467_2023_38852_Fig4_HTML.jpg |
0.411137 | 8a882c7abd7a4a31a5dff2027c6d8bd1 | forest plot displaying pooled prevalence undiagnosed hypertension among adults in Ethiopia, 2023 | PMC10225092 | 12872_2023_3300_Fig17_HTML.jpg |
0.534223 | 06b387e3f6c446b2b641ebeda129ed40 | forest plot displaying subgroup analysis on the pooled prevalence of undiagnosed hypertension by region among adults in Ethiopia, 2022 | PMC10225092 | 12872_2023_3300_Fig18_HTML.jpg |
0.452691 | c56531da7cfc4bd0a0d5a09e2677b571 | forest plot displaying subgroup analysis by study setting for the pooled undiagnosed hypertension among adults in Ethiopia, 2023 | PMC10225092 | 12872_2023_3300_Fig19_HTML.jpg |
0.426117 | 0cff99c859d649cfac5c81f201cb57b8 | PRISMA flow diagram of articles screened and the selection process on undiagnosed hypertension and Associated Factors among adults in Ethiopia, 2023 | PMC10225092 | 12872_2023_3300_Fig1_HTML.jpg |
0.445985 | 5152f924dbca4739b3cb9bb1bc994a24 | funnel plot displaying publication bias of studies reporting the pooled undiagnosed hypertension among adults in Ethiopia, 2023 | PMC10225092 | 12872_2023_3300_Fig20_HTML.jpg |
0.380986 | 80f5336adde24023825cd08b991f5838 | Sensitivity analysis on the studies included in systematic review and meta-analysis on prevalence of undiagnosed hypertension by region among adults in Ethiopia, 2023 | PMC10225092 | 12872_2023_3300_Fig21_HTML.jpg |
0.416187 | 0d8716926eee42dd89c756a96fd8cce5 | The pooled odd ratio of the association between age and undiagnosed hypertension among adults in Ethiopia, 2023 | PMC10225092 | 12872_2023_3300_Fig22_HTML.jpg |
0.424688 | f65e7a39c0ad4506b6be72368cee84a1 | The pooled odd ratio of the association between body mass index and undiagnosed hypertension among adults in Ethiopia, 2023 | PMC10225092 | 12872_2023_3300_Fig23_HTML.jpg |
0.540136 | daebcc530bdd40b1b0880f4c5c1e8e16 | The pooled odd ratio of the association between family history of hypertension and undiagnosed hypertension among adults in Ethiopia, 2023 | PMC10225092 | 12872_2023_3300_Fig24_HTML.jpg |
0.508566 | a80276f786424423b5641ebb7689ab0a | The pooled odd ratio of the association between presence of DM comorbidity and undiagnosed hypertension among adults in Ethiopia, 2023 | PMC10225092 | 12872_2023_3300_Fig25_HTML.jpg |
0.407219 | 5bc15740cb134c8ab27b9daa99464308 | The economies’ environment efficiency of three trade patterns and seven sectors under two scenarios. | PMC10225307 | gr10_lrg.jpg |
0.405735 | 563e577ea70b4961a1d4e2ea7f0aebc6 | The carbon emission calculating under trade and no-trade scenarios. | PMC10225307 | gr1_lrg.jpg |
0.462171 | a3f1795ffcb24fccafe20de6765b307e | Modling framework of environmental performance assessment. | PMC10225307 | gr2_lrg.jpg |
0.445023 | f12725a7e74642ad8337a9fc0180c843 | Structure of CO2, SO2, and NOX direct emissions of the 15 economies (million tons). Notes: the length of bars refers to emissions embodied in domestic production and three export links. The color of bars corresponds to the share of emissions induced by exports, from the smallest share in yellow to the largest share in red. | PMC10225307 | gr3_lrg.jpg |
0.440691 | 73522d4d0ced40548ccae6c1b65c1622 | The structure and changing trend of emissions. Notes: (1) the area graphs above show the changing trends of embodied CO2, SO2, and NOX emissions, and the colors correspond to three specific export links respectively. (2) The histograms blow are the changing rate of embodied emissions during 2008–2011. | PMC10225307 | gr4_lrg.jpg |
0.460154 | 51bf10102a9547f5af003eba649c3a09 | Three trade patterns’ effects on embodied emissions. Notes: The negative value means that the emissions in trade scenario are less than that in no-trade scenario. The histograms on the right are country-level decomposition of the left 2014 results. | PMC10225307 | gr5_lrg.jpg |
0.422845 | b8cf6f5bc547439688809e9115f91a55 | Three trade patterns’ effects on sectors’ embodied emissions. Note: The value is the difference between the emissions under the trade scenario and no-trade scenario. A negative value means that the sector's emissions under the trade scenario are less than that under the no-trade scenario. The three rows represent the calculation results of CO2, SO2 and NOX emissions respectively. The three columns represent emissions caused by final products, last-stage intermediate products, and GVC-related intermediate products trade. | PMC10225307 | gr6_lrg.jpg |
0.356444 | 75b4589db009475295dee92f7cbf8998 | Three trade patterns’ effects on countries’ embodied emissions. Note, the value is the difference between the environmental efficiency under the trade scenario and no-trade scenario in 2014. The column ‘R_ing’ denotes the average impacts of the developing economies other than China, Russia, and India. The column ‘R_ed’ denotes the average impacts of the developed economies other than the European Union, the United States and Japan. | PMC10225307 | gr7_lrg.jpg |
0.446102 | 3893d550a891463d806f686fe05c68bf | The economies’ environment efficiency under two scenarios. | PMC10225307 | gr8_lrg.jpg |
0.439883 | 29fc1705d198405793a02a78dca75372 | The economies’ environment efficiency of three trade patterns under two scenarios. Note, the value corresponding to the color is the calculation result in 2014. | PMC10225307 | gr9_lrg.jpg |
0.409438 | ccc51343151948fca256424f9c511bc0 | Correlation of MRD between qPCR and ddPCR. Spearman’s correlation shows a significant concordance (r = 0.95, P < 0.0001). Thirteen time points out of 26 time points were scored positive by one method or both methods, 11 of which were fully concordantly positive. The other 13 time points were scored negative by one method or both methods, including three time points below the quantitative range (BQR) of qPCR. The wavy line is on 1E-4. ¶, Major qualitative discordance; §, ddPCR-MRD negative due to less sensitivity than primer/probe set | PMC10225364 | 12185_2023_3566_Fig1_HTML.jpg |
0.512772 | 3475a2886e41484286941fb67e8dcd49 | Representative results of MRD detection discordances in the follow-up samples of T-ALL patients. Comparison of MRD level evaluated by qPCR (gray lines with circle points) and ddPCR (black square or triangle). First time point indicates the onset of disease. A, C–D: Two different primer/probe sets for ddPCR were used in each case. B: One primer/probe set for ddPCR was used. A–C: Patients with fully concordant follow-up samples. D: A patient in which the results of two ddPCR MRDs deviated through the medical course. The results of second, third and fourth time point were all negative less than the primer/probe sensitivity (Table S2). ddPCR-1 was positive at the fifth time point, but PRC-MRD was negative. ddPCR-2 was negative at the sixth time point, but PCR-MRD was positive | PMC10225364 | 12185_2023_3566_Fig2_HTML.jpg |
0.445207 | e5229db5441b4ae6ba4900143bfee2ec | Results of ddPCR MRD positive case of ovarian tissue. The tumor-specific SNV (WDR87 c.G8501A) was observed in 19.8% of tumor cells in UPN1 and detected in ovarian tissues at a variant allele frequency of 0.21%. Error bars represent 95% confidence intervals | PMC10225364 | 12185_2023_3566_Fig3_HTML.jpg |
0.414895 | 36a5f531ece44b14b40da32b9d507a31 | Percentage of the Studied Nurse's Perception About coronavirus disease 2019 (COVID-19) Vaccine (n = 189). | PMC10225959 | 10.1177_23779608231177560-fig1.jpg |
0.436935 | 3235d7b8ed7147599e0947d38d8133d3 | Percentage of the studied nurse's acceptance regarding coronavirus disease 2019 (COVID-19) (n = 189). | PMC10225959 | 10.1177_23779608231177560-fig2.jpg |
0.553034 | d5d4c367b54742808c23975e730c5b3f | Schematic of biosensor mode of action.Vaginal swab from mother, or neonatal swab taken either in the nose or
pharynx is introduced into vesicle solution. After 45 min, Group B
Streptococcus (GBS) virulence factors have caused lysis
of vesicles allowing for release of fluorescent 5(6)-carboxyfluorescein. | PMC10226325 | 10.1177_20499361231175821-fig1.jpg |
0.436794 | 2a3a0adaaba341069cf4972514d50932 | Biosensor fluorescence response for 51 participants in study.Green shows true Group B Streptococcus (GBS) negative
samples (using enriched medium culture (ECM)) and red shows GBS positive
samples (using ECM). Values over the lowest positive threshold are deemed
GBS positive using the biosensor test, while samples under the highest
negative threshold are deemed GBS negative using the biosensor test.
Thresholds are set arbitrary. | PMC10226325 | 10.1177_20499361231175821-fig2.jpg |
0.486337 | 8b76800203414fbba19e9370ce634475 | Standards for reporting of diagnostic accuracy (STARD) flow diagram. | PMC10226325 | 10.1177_20499361231175821-fig3.jpg |
0.605092 | 7a0510d61ead43e191ad06029f419e83 | CS, coronary sinus; LAA, left atrial appendage; PW, posterior wall; SVC, superior vena cava. | PMC10226376 | euad136_ga1.jpg |
0.432663 | 0dfb7e04db644458924778fd6e806668 | Lamin-A L:N responds to changes in actomyosin contractility prior to lineage segregation.a,
b 3D immunofluorescence and quantification of Lamin-A/C lamina:nucleoplasm levels (Lamin-A/C L:N) in intact mouse embryos shows that Lamin-A/C L:N increases during development prior to lineage segregation. This is accompanied by changes in nuclear shape, with nuclei becoming more spherical over time. Treatment with H-1152 (50 µM, 4 h) causes a reduction in Lamin-A/C L:N and nuclear sphericity. Insets show 1 µm sections of the nucleus and 3D segmentation of the lamina (transparent) and nucleoplasm (opaque). Dots represent the mean and error bars represent SD (n = 10 for 2-cell, n = 34 for 4-cell, n = 59 for pre-compaction 8-cell, n = 54 for post-compaction 8-cell; P = 0.0002, Kruskal-Wallis test). c,
d Immunofluorescence and quantification (fluorescence intensity standardized to DAPI) shows rising phosphorylated-myosin II between the 2-, 8-, and 16-cell stages. Dots represent the mean and error bars represent SD. n = 4 for 2-cell, n = 14 for 8 cell, and n = 16 for 16-cell. P = 0.0007 Kruskal-Wallis test. e Lamin-A/C L:N decreases after treatment with H-1152 at the 8-cell stage. n = 17 for control and H-1152. ****P < 0.0001, Mann-Whitney U test. f, Live-imaging of 4-cell and 8-cell cleavage divisions reveals greater deformation of cell shape at early stages. Utrophin-GFP allows 3D segmentation and analysis of local curvature. n = 11 for 4-8 cell, n = 8 for 8-16 cell. **P = 0.006, Mann-Whitney U test. Staining with phalloidin reveals an F-actin meshwork throughout the cytoplasm in early-stage mouse (g) and human (h) embryos. The meshwork extends from the cell cortex to the nucleus and the cytoplasmic density remains similar between the 2- and 8-cell stages. Representative examples selected from phalloidin stainings of >100 mouse embryos (g) and 9 human embryos (h). i, j Disrupting the contractility of the F-actin meshwork causes a reduction in mRuby-Lamin-A L:N. Spatiotemporally controlled stimulation of azido-blebbistatin was performed using a 860 nm laser targeting the F-actin meshwork between the nucleus and cortex (i). Graph shows mRuby-Lamin-A L:N following photostimulation. n = 4 for apical and basolateral, p = 0.0286, Mann-Whitney U test. All statistical tests are two-tailed. Bars in dot plots represent median and interquartile range. Scale bars, 10 µm. Source data are provided as a Source Data file. | PMC10226985 | 41467_2023_38770_Fig1_HTML.jpg |
0.459768 | 52414f1ba1384edf84f12c0d5cf97f82 | Differences in Lamin-A L:N identify lineage segregation in mouse and human embryos.a, b, Immunofluorescence for Lamin-A/C in fixed mouse embryos (a) and live-imaging of mRuby-Lamin-A (b) at different developmental stages. Images show thin confocal sections to illustrate inner-outer differences. Lamin-A L:N plotted against distance to embryo center of mass. For (a) n = 6 for 16-cell inner, n = 40 for 16-cell outer, n = 21 for blastocyst ICM, n = 33 for blastocyst trophectoderm. For (b) n = 29 for 16-cell inner, n = 48 for 16-cell outer, n = 18 for blastocyst ICM, n = 32 for blastocyst trophectoderm. ****P < 0.0001, Mann-Whitney U test. c, Live-imaging and quantification of mRuby-Lamin-A in embryos treated with H-1152 or blebbistatin show reduced mRuby-Lamin-A L:N. Conversely, embryos expressing the constitutively active RhoA mutant Q63L show increased mRuby-Lamin-A L:N. n = 11 for control outer, n = 5 for control inner, n = 11 for H-1152 outer, n = 6 for H-1152 inner, n = 10 for blebbistatin outer, n = 6 for blebbistatin inner, n = 13 for RhoA Q63L outer and n = 6 for RhoA Q63L inner. ***P < 0.0007, *P = 0.0343 for control outer vs blebbistatin outer, *P = 0.0410 for control outer vs RhoA Q63L outer. *P = 0.0418 control inner vs RhoA Q63L inner. Mann-Whitney U test. d, Human blastocyst immunostained for Lamin-A/C shows lower Lamin-A L:N in the ICM versus trophectoderm (TE). Quantification shows the relationship between Lamin-A/C L:N and distance to embryo center of mass. n = 19 for ICM, n = 108 for trophectoderm (two human blastocysts were analyzed and therefore statistical analysis was not performed). e, Human blastocysts treated with ROCK inhibitor H-1152 have reduced Lamin-A/C L:N (one human blastocyst per group, trophectoderm cells n = 199 for control, n = 95 for H-1152. All statistical tests are two-tailed. Bars in dot plots represent median and interquartile range. Scale bars, 10 µm. Source data are provided as a Source Data file. | PMC10226985 | 41467_2023_38770_Fig2_HTML.jpg |
0.434725 | 6b5278b050384a589b625498ad703023 | Lamin-A controls the transcriptional regulators Yap and Cdx2.a, Cytoplasmic intensity of phospho-Yap and nuclear Cdx2 correlate with Lamin-A/C L:N. Open arrowhead indicates a cell undergoing internalization via apical constriction. n = 48 for phospho-Yap, n = 71 for Cdx2, R2 = 0.42 for phospho-Yap, R2 = 0.66 for Cdx2. b–d, Knockdown of Lamin-A by siRNA causes an increase in cytoplasmic phospho-Yap levels (b), a reduction in nuclear Cdx2 levels (c) and a reduction in nuclear:cytoplasmic Yap levels (d). siRNAs were microinjected into a single cell of the 2-cell embryo. Membrane-GFP or H2B-GFP was used to label injected cells (arrowheads). For (b) n = 9 for control outer, n = 6 for control inner, n = 10 for Lamin-A siRNA outer, n = 4 for Lamin-A siRNA inner. ***P = 0.0004 for control inner vs control outer, ***P = 0.0006 for control outer vs Lamin-A siRNA outer, NS > 0.999. For (c) n = 8 for control outer, n = 6 control inner, n = 6 Lamin-A siRNA outer, n = 4 Lamin-A siRNA inner. ***P = 0.0007 for control inner vs control outer, ***P = 0.0007 for control outer vs Lamin-A siRNA outer, NS = 0.9143. For (d) n = 9 for control outer, n = 6 for control inner, n = 7 for Lamin-A siRNA outer, n = 4 for Lamin-A siRNA inner. ***P = 0.0004 for control inner vs control outer, ***P = 0.0003 for control outer vs Lamin-A siRNA outer, NS = 0.0727. All statistical tests are two-tailed. Fluorescence intensities represent results standardized to DAPI. Bars in dot plots represent median and interquartile range. Scale bars, 10 µm Source data are provided as a Source Data file. | PMC10226985 | 41467_2023_38770_Fig3_HTML.jpg |
0.394381 | 50de2987e9764d528a047833f238f9bf | Lamin-A regulates the F-actin meshwork, which serves as a scaffold to stabilize cytoplasmic Amot.a, Amot levels are increased in the cytoplasm of inner cells. Immunofluorescence images of Amot in fixed mouse embryos with standardized Amot intensity, n = 18 for outer, n = 5 for inner **P = 0.0011, Mann-Whitney U test. b, Knockdown of Lamin-A by siRNA causes an increase in cytoplasmic levels of Amot in outer cells. siRNAs were microinjected at the 1-cell stage. n = 18 for control, n = 10 for Lamin-A siRNA **P = 0.003, Mann-Whitney U test. c, F-actin meshwork density increases in the cytoplasm of inner cells at the 16-cell stage and in the ICM at the blastocyst stage. Insets show detail of cytoplasmic meshwork (cyt) and absence of actin in the nucleus (nuc). n = 5 for 16-cell inner, n = 6 for 16-cell outer, n = 8 for blastocyst ICM, n = 25 for blastocyst trophectoderm **P = 0.0087, ***P = 0.001, Mann-Whitney U test. d, Latrunculin A causes Amot disruption. Note the decrease in cytoplasmic Amot in the inner cell cytoplasm. n = 9 for control, n = 10 Latrunculin A, **P = 0.0061 Mann-Whitney U test. e, Knockdown of Lamin-A by siRNA causes an increase in cytoplasmic F-actin levels. siRNA was microinjected into a single cell of the 2-cell embryo. H2B-GFP labels injected cells. Inset shows detailed view of cytoplasmic F-actin. n = 12 for control, n = 10 for Lamin-A siRNA. ****P < 0.0001, Mann-Whitney U test. f, g, Human blastocysts immunostained for Amot (f) and stained with phalloidin (g) show increased levels of cytoplasmic Amot and F-actin in the ICM compared to trophectoderm (TE). For Amot (f), n = 2 human embryos (no statistical comparison performed). For phalloidin (g), n = 3 human embryos. P = 0.0025 by paired two-tailed t-test. For human embryos, dots represent individual cells. Fluorescence intensities represent results standardized to DAPI. Bars in dot plots represent median and interquartile range. All statistical tests are two-tailed. Scale bars, 10 µm. Source data are provided as a Source Data file. | PMC10226985 | 41467_2023_38770_Fig4_HTML.jpg |
0.395663 | 20eee556456c430fafd91c72ca24cb0d | Lamin-A regulates fate by controlling actin nucleator localization.a, Formin 2 shows a high nuclear:cytoplasmic ratio, which is increased in outer cells following cell internalization. n = 4 for all stages. *P = 0.0286, Mann-Whitney U test. b, Knockdown of Lamin-A by siRNA reduces nuclear:cytoplasmic Formin 2. siRNA was microinjected at the 1-cell stage. Insets show reduced levels of Lamin-A in siRNA. n = 14 for control, n = 10 for Lamin-siRNA. *P = 0.0470, Mann-Whitney U test. c, Treatment with SMIFH2 reduces inner cell F-actin and increases nuclear:cytoplasmic Yap. 16-cell embryos were either treated with DMSO (control) or 250 µM SMIFH2 and immunostained for Yap and with phalloidin. Insets highlight the differences between inner cell cytoplasmic phalloidin intensity and nuclear Yap intensity between control and treated embryos. *P = 0.0364, **P = 0.0024, Mann-Whitney U test. d, e, Emerald-Formin 2 overexpression. Emerald-Formin 2 RNA was microinjected into a single cell of the 2-cell embryo, fixed at the 16-cell stage and immunostained for either Yap or Amot. Injected cells can be identified by Emerald-Formin 2 expression (arrowheads). Injected outer cells show increases in cytoplasmic phalloidin, nuclear Yap and cytoplasmic Amot intensities compared to uninjected cells. For panel (d) n = 10 for Emerald-Formin 2 (injected cells), n = 9 for control (uninjected cells). ***P = 0.0006, *P = 0.0244, Mann-Whitney U test. For panel (e) n = 9 for control (uninjected cells), n = 10 for Emerald-Formin 2 (injected cells). **P = 0.0063, *P = 0.0414, Mann-Whitney U test. Fluorescence intensities represent results standardized to DAPI. Bars in dot plots represent median and interquartile range. All statistical tests are two-tailed. Scale bars, 10 µm. Source data are provided as a Source Data file. | PMC10226985 | 41467_2023_38770_Fig5_HTML.jpg |
0.434576 | 55ca65f3a76348dabaec93d59091df54 | Schematic summary of main results.Schematic summary shows the main events allowing Lamin-A to link changes in mechanical forces to cell fate in the embryo. | PMC10226985 | 41467_2023_38770_Fig6_HTML.jpg |
0.414897 | a72fefe75f1f4003b8e47124e1e5e4b6 | PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) flowchart. Selection procedure and search results. | PMC10227696 | jmir_v25i1e46084_fig1.jpg |
0.416052 | 33855ceb1d384770b0cfe11ad08cd3d2 | In the normal physiology, quiescent CD8+ T lymphocytes become activated when antigen presenting cells (APCs) present major histocompatibility complex–bound antigen fragments to T cell receptors. The secondary activation/co-stimulatory signals (involving CD80/86 and CD28) generate effective immune response. CTLA4 receptors on the inactive T cells inhibit the activation process binding to the CD80/86 complex on the APCs resulting in T cell anergy. Monoclonal antibodies (Mabs) against CTLA4 (ipilimumab/tremelimumab) remove the inhibitory signal facilitating the activation of CD8+ T cells. In the tumor micro-environment, the cancer cells evade the T cell response by increased expression of ligands (eg.PD-L1) which bind to immune checkpoints (eg. PD-1) on the T cells preventing the immune response. This immune tolerance by the cancer cells is inhibited by the Mabs against PD-1 (pembrolizumab/nivolumab) and PD-L1 (atezolizumab/avelumab). In the presence of ICI, T cells can lose their tolerance against normal renal tubular epithelium leading on to kidney injury. | PMC10229281 | sfad014fig1.jpg |
0.49047 | 2d589a82aa4a4889b3b83d76dd0f4b90 | Potential mechanisms of kidney injury in patients treated with ICI. | PMC10229281 | sfad014fig2.jpg |
0.462269 | 4115fc30ba544608a71192c02b45563c | Spectrum of kidney diseases associated with ICI. | PMC10229281 | sfad014fig3.jpg |
0.371505 | 8836a82b2eae416dbf0e2b7447303857 | Sample principal components and correlation analysis. (A) Principal component analysis (PCA) of five groups of muscle samples. (B) Heatmap of Pearson correlation between samples based on gene expression. | PMC10229883 | fphys-14-1199311-g001.jpg |
0.517138 | 2f9f150be6624719a4e6211dc557a44c | Identification of DEGs in five groups of muscle samples. (A) Distribution of gene expression levels in different groups. (B) Volcano plots of DEGs in the PJFXL vs. PJFTL, PJFXL vs. PJFXS, PJFXL vs. PJMXL, and PJFXS vs. JHFXS groups (Sig_Up: significantly upregulated; Sig_Up: significantly downregulated; NoDiff: no significant difference). (C) Upset diagram of four group comparatives DEGs (The horizontal bars on the left indicate the number of DEGs required for each group comparison. The individual points in the middle matrix represent the DEGs specific to each group comparison, and the lines between points represent the DEGs common to different group comparisons. The vertical bars represent the number of DEGs specific to or common to different group comparisons). | PMC10229883 | fphys-14-1199311-g002.jpg |
0.423336 | 0458764141de4b298ffa88cc97888795 | GO functional enrichment results of DEGs in (A) PJFXL vs. PJFTL, (B) PJFXL vs. PJFXS, (C) PJFXL vs. PJMXL, and (D) PJFXS vs. JHFXS group comparisons (The vertical coordinate is −log10 (Qvalue), the horizontal coordinate is the up-down normalization value: the difference between the number of differentially up-regulated genes and the number of differentially down-regulated genes as a percentage of the total differential genes, and the size of the bubble indicates the number of target genes currently enriched by the GO term). | PMC10229883 | fphys-14-1199311-g003.jpg |
0.477159 | 122fc891bcd24bb1893e84a970c6f34e | KEGG pathway enrichment results of DEGs in (A) PJFXL vs. PJFTL, (B) PJFXL vs. PJFXS, (C) PJFXL vs. PJMXL, and (D) PJFXS vs. JHFXS group comparisons (Rich Factor indicates the ratio of the number of differential genes to the number of all genes in the background gene set that are enriched in the pathway). | PMC10229883 | fphys-14-1199311-g004.jpg |
0.431475 | 4f76ba4e2cb24be0bbd684253bf8a0e8 | Module identification and trait correlation analysis. (A) Gene modules based on phylogenetic clustering tree. (B) Correlation analysis of 12 modules and muscle phenotypes. (C) Heatmap of gene co-expression network (the heatmap area indicates the dissimilarity between genes, the smaller the value, the darker the color). (D) Gene significance in the module. | PMC10229883 | fphys-14-1199311-g005.jpg |
0.443719 | d0385ba0c52e4d5d848d5050c0e3e758 | Hub genes screening and functional analysis in brown, midnightblue, red, and yellow modules. Scatter plot of gene significance and module membership for (A)-1 (brown), (B)-1 (midnightblue), (C)-1 (yellow), and (D)-1 (red) modules. GO functional enrichment analysis (BP: biological processes; CC: cellular components; MF: molecular functions) of hub genes in (A)-2 (brown), (B)-2 (midnightblue), (C)-2 (yellow), and (D)-2 (red) modules. KEGG pathway enrichment analysis of hub genes in (A)-3 (brown), (B)-3 (midnightblue), (C)-3 (yellow), and (D)-3 (red) modules (red nodes are key genes enriched in the pathway). | PMC10229883 | fphys-14-1199311-g006.jpg |
0.449035 | 4f6821116a5b4866b334622c242c9a08 | Functional gene identification. (A) Upset Venn diagram of hub genes and DEGs in four important modules. (B) Correlation of 14 DEGs with IMP and cooking loss (The value in the upper left corner of the figure is the correlation coefficient, and the value in the lower right corner is −log10 (p-value)). Tissue expression of (C) TGIF1 and (D) THBS1 in Jingyuan chickens. The protein interaction network of (E) TGIF1 and (F) THBS1 (Network nodes represent proteins: splice isoforms or post-translational modifications are collapsed, i.e., each node represents all the proteins produced by a single, protein-coding gene locus. Edges represent protein-protein associations: associations are meant to be specific and meaningful, i.e., proteins jointly contribute to a shared function). | PMC10229883 | fphys-14-1199311-g007.jpg |
0.45445 | 910aa3a1a75541ebb0a49a55b47a655d | The basic Green Cross template. Reproduced with permission.17 | PMC10230969 | bmjoq-2022-002247f01.jpg |
0.440554 | 3c131718fb2a4f6bab9869df2015b9c6 | Expression analysis and molecular validation of miRNAs identified in the A. c. cerana 4-, 5-, and 6-day-old larval guts. (A) Venn analysis of miRNAs discovered in the 4-, 5-, and 6-day-old larval guts; (B) expression clustering of miRNAs expressed in the 4-, 5-, and 6-day-old larval guts; (C) Sanger sequencing of six miRNAs shared by the 4-, 5-, and 6-day-old larval guts. | PMC10231108 | insects-14-00469-g001.jpg |
0.427535 | 62b60bbe2ce14532b1491aaf5792a279 | Structural characteristics of miRNAs in A. c. cerana 4-, 5-, and 6-day-old larval guts. (A) Length distribution of miRNAs; (B) first nucleotide bias of miRNAs; (C) bias of each nucleotide of miRNAs. | PMC10231108 | insects-14-00469-g002.jpg |
0.457304 | 62f69a98f864412c8a2e8f72d2ce112d | Radar maps of DEmiRNAs in the Ac4 vs. Ac5 (A) and Ac5 vs. Ac6 (B) comparison groups. Blue circles represent downregulation, while orange circles represent upregulation. The larger the circles, the greater the difference. | PMC10231108 | insects-14-00469-g003.jpg |
0.445184 | 3181f2320cee4d598edff7e43d40a25a | GO terms annotated by the DEmiRNA-targeted mRNAs in the Ac4 vs. Ac5 and Ac5 vs. Ac6 comparison groups. Different colors indicate different functional terms. The numbers inside the chord diagram indicate target mRNAs annotated to corresponding terms. | PMC10231108 | insects-14-00469-g004.jpg |
0.409291 | b316b80868eb4e8a9a802a66d4d03081 | KEGG pathways annotated by the targets of DEmiRNAs in the Ac4 vs. Ac5 (A) and Ac5 vs. Ac6 (B) comparison groups. Bubbles indicate target mRNAs enriched in corresponding pathways; the larger the bubbles, the greater the amount of target mRNAs, and the smaller the bubbles, the fewer the target mRNAs. Different colors represent the p-values of different pathways; the red color indicates higher p-values, while the purple color indicates lower p-values. | PMC10231108 | insects-14-00469-g005.jpg |
0.369342 | e970c8a6cf784e23971e2cf05fafb409 | DEmiRNA–mRNA networks relevant to development-associated signaling pathways in the Ac4 vs. Ac5 (A) and Ac5 vs. Ac6 (B) comparison groups. Orange diamonds represent target mRNAs, while purple circles represent DEmiRNAs. Grey lines indicate potential targeting relationships between DEmiRNAs and target mRNAs. | PMC10231108 | insects-14-00469-g006.jpg |
0.421949 | 24d946410f684a6fa8cfbf9e98697b97 | DEmiRNA-mRNA networks involved in the cellular and humoral immune in the Ac4 vs. Ac5 (A) and Ac4 vs. Ac5 (B) comparison groups. Orange circles represent target mRNAs, red circles represent miRNAs, and green circles represent annotated pathway. Grey lines indicate potential targeting relationships between the miRNAs–mRNAs pathway. | PMC10231108 | insects-14-00469-g007.jpg |
0.547051 | b14f50bbed6d458e94fa7247e632bf98 | RT-qPCR validation of five DEmiRNAs. Both qPCR data and RNA-seq data were presented as mean ± standard deviation (SD) and subjected to Student’s t test, * p < 0.05; ** p < 0.01. | PMC10231108 | insects-14-00469-g008.jpg |
0.41514 | f1abe86edefa40cfb69ef4a2e2bc0d12 | Intratracheally delivered liposomes and nintedanib liposomes are nontoxic in vivo. Toxicity studies were performed at 24 h. Naive murine lung is compared to nebulized LPS (a positive control for injury), intratracheal instillation of nintedanib‐loaded liposomes (0.5 mg kg−1 drug and 0.73 mg kg−1 lipid) in sucrose, empty liposomes (2.5 mg kg−1 lipid) in saline, empty liposomes (2.5 mg kg−1 lipid) in sucrose, saline buffer, or sucrose buffer. a) BALF leukocyte count; b) BALF protein concentration; c) weight change from baseline. N = 3 mice per group, one‐way ANOVA; **** p <= 0.0001, ** p <= 0.01. d–g) H&E histology shows no observable toxicity from intratracheal liposomes compared to acid instillation positive control; representative images, n = 3 mice per group with the exception of acid instillation, n = 1 and saline instillation, n = 2. | PMC10231510 | ANBR-3-2200106-g001.jpg |
0.420682 | 5d2fd7f6b2fa49a5b30c62fab9befb30 | Inhaled liposomes home to both alveolar leukocytes and lung parenchymal cells. Mice were given fluorescent liposomes (empty and drug‐loaded) via intratracheal instillation, and then at 20 h whole lung was analyzed. a–f) Prior to harvest and preparation of single‐cell suspension for flow cytometry, BAL and perfusion were performed. a,b) Greater than 75% of alveolar leukocyte populations were associated with liposomes, but only macrophages (B, right panel) demonstrated a large shift in fluorescence, indicating significant uptake. c,d) Comparatively, parenchymal leukocytes (those embedded in the lung parenchyma, or at least firmly attached) were significantly less associated with liposomes (<15%), but parenchymal macrophages still demonstrated a significant shift (D, right panel). e,f) Cells of the lung parenchyma, such as epithelial cells and endothelial cells, were approximately 10% and 35% associated with liposomes, respectively, though with a much smaller shift in fluorescence compared to macrophages. g,h) IHC demonstrates liposomes (red) in all layers of lung tissue in both h) alveolated tissue and g) conducting airways. Airspace leukocytes are seen with significant liposome uptake (arrows). Scale bar = 50 μm. N = 2, error bars = SEM. | PMC10231510 | ANBR-3-2200106-g002.jpg |
0.470536 | 1ad6a57d1d344775b100411d187264b2 | Inhaled nintedanib‐loaded liposomes confer massive increases in lung half‐life and AUC compared to inhaled or oral free nintedanib. Mice were given one of three nintedanib formulations, shown in a): intratracheal instillation of liposome‐loaded nintedanib (red), intratracheal instillation of free nintedanib (orange), or oral gavage of free nintedanib (blue; noting that clinically the drug is orally administered). Lung and plasma were harvested at time points up to 24 h, and then nintedanib concentration was measured by LC/MS. b,c) Nintedanib concentration over 24 h is shown for each formulation, measured by LC/MS; b) in the lung and c) in plasma. d) AUC and half‐life were calculated using GastroPlus noncompartmental modeling software from data obtained by LC/MS in panels (b) and (c). For oral dosing, AUC is shown for the dose given (60 mg kg−1) and then also normalized to the dose given by intratracheal administration (0.5 mg kg−1). e) Instilled liposomal nintedanib has a 35‐fold and 8000‐fold higher lung AUC compared to oral and instilled free drug (no nanocarrier), respectively. f) Instilled liposomal nintedanib has an eightfold and tenfold increase in lung half‐life compared to free instilled and oral drug, respectively. N = 3, error bars = SEM. | PMC10231510 | ANBR-3-2200106-g003.jpg |
0.408241 | 78817e240abc4626a92b452e1107e596 | Liposomes remain intact and do not aggregate following intratracheal instillation. Mice were given 10 mg kg−1 lipid of fluorescent liposomes or nintedanib‐loaded fluorescent liposomes via intratracheal instillation, and then BALF was harvested and analyzed by NTA. a) Example primary data showing NTA of endogenous particles in BALF by light scattering (left) and liposomes in BAL by fluorescence scattering (right). b) Normalized histogram of nintedanib‐loaded liposomes in their native form (before being given to mice, dotted green line, fluorescence emission), compared to nintedanib‐loaded liposomes present in BALF 15 min after instillation (solid green line, fluorescence scattering), compared to endogenous particles + nintedanib‐loaded liposomes present in BALF 15 min after instillation (dotted red line). Nintedanib liposomes have the same size distribution before and after lung delivery. c–e) Size distribution of c) BAL‐extracted empty liposomes and e) nintedanib liposomes at 15 min, 4, and 20 h after liposome instillation, each compared to their preinstillation size distribution. d) Average size of liposomes over time [data from histograms in (c) and (e)], noting small size increase with increased time the liposomes have dwelled in the BALF layer of the lungs in vivo. f) Liposomes recovered in BAL over time, as a percentage of initial dose, showing that at least ≈20–30% of liposomes are recoverable intact in BALF as long as 20 h after instillation; inset is the same data depicted as averages. N = 3–6 for empty liposomes; N = 3 for nintedanib liposomes; error bars = SEM. | PMC10231510 | ANBR-3-2200106-g005.jpg |
0.399153 | 71109ed8281b42c8ab1255f1ff4e928f | Nintedanib‐loaded liposomes have advantageous drug‐loading properties and are stable in ex vivo BALF. a) Schematic of liposome showing phospholipid bilayer with small molecule drug within the aqueous core. b) Negative stain electron microscopy of nintedanib‐loaded liposomes; scale bar, 500 nm. c) Hydrodynamic diameter, PDI, and zeta potential (mV) of empty and NTD‐loaded liposomes. d) Graph adapted from Chemicalize (Copyright 2022 Chemaxon) demonstrates nintedanib species at different pH. Shown in orange at pH 2–6, nintedanib's tertiary amine is protonated; this form is encapsulated in liposomes. Shown in blue at pH ≈9, nintedanib's tertiary amine is in a neutral state. e) Nintedanib leak out of liposomes over 24 h at varied pH shows less leak at neutral pH (as in serum and alveolar surfactant) versus acidic pH (as in endosomes), n = 1 preparation per pH. f) Assessment of fluorescent liposomes in ex vivo BALF up to 24 h, n = 1 per time point. Liposome elution by size exclusion chromatography shows no difference after incubation in BALF, and no free fluorophore peak. g,h) Assessment of fluorescent liposomes in ex vivo BALF up to 24 h, n = 5 technical replicates per time point. g) Size distribution and h) fluorescence intensity by size show complete overlap of all conditions, and therefore no difference after incubation in BALF. Error bars represent SEM. | PMC10231510 | ANBR-3-2200106-g006.jpg |
0.525219 | 9b6d145ffcf2426c96dc71654b8f2df1 | Inhaled liposomes behavior in BALF, alveolar macrophages, and lung parenchyma: over time, lung parenchyma's share of total lung dose increases; over dose range, macrophages do not demonstrate saturability. Mice were given liposomes labeled with 125I radiotracer via intratracheal instillation, then BALF was collected and organs were harvested at various time points as shown. Liposome localization was measured by a gamma counter. a) Schematic demonstrating intratracheal delivery into lungs with division into two initial compartments: the intra‐alveolar compartment (blue), consisting of liposomes taken up by intra‐alveolar leukocytes or suspended in the cell‐free BALF layer; and the parenchymal compartment (pink), which is composed of all lung cells except intra‐alveolar leukocytes. b) Biodistribution over time in blood, lung, stomach, and, in inset graph due to low total levels, in liver, spleen, and intestine. Lipid dose: 2.5 mg kg−1. c–f) Saturability study with varied lipid dose from 1.25 to 30 mg kg−1. Lung compartment biodistribution is divided into c) lung parenchyma, d) total BALF, e) BAL supernatant, and f) BAL pellet. N = 3, error bars = SEM. | PMC10231510 | ANBR-3-2200106-g007.jpg |
0.492483 | b75551ce9cc7471da8508d908f08410b | (a) The upper panel shows two coupled resonators. The left resonator (red) has resonance frequency ωA and nonlinear saturable gain g(|ψA|) (see the discussions in Section 8 of the online supplementary material), and the other resonator (blue) has resonance frequency ωB and linear loss. Such a nonlinear non-Hermitian system can be mapped into a PT symmetric three-resonator system as shown in the lower panel with linear gain (G) and neutral (N) and loss (L) resonators. (b) Steady-state solution of (1) with κ=1, ωB = 0 and all the other parameters normalized by κ. The red and blue regions represent stable and unstable states, respectively. The yellow lines represent EAs that are also boundaries of the stable and unstable states. The two yellow lines merge at an EX (black star), where two stable states and one unstable state coalesce. (c) (SNR)−1 as a function of the detuning for a linear scheme (green dashed line), and a nonlinear saturable scheme (purple line). Here sensing is viewed as a scattering process of the input photon. The linear Hamiltonian is provided in Equation (S24) of the online supplementary material. (d) Purple asterisks show the SNR retrieved from the system dynamics and the cyan background represents the line width limit introduced by the finite recording time. Details are provided in Section 4 of the online supplementary material. | PMC10232044 | nwac259fig1.jpg |
0.509894 | 34f6ef1481fa4c8d810dfa67cec528d0 | (a–d) Real part of the solutions of (2) versus the detuning and loss, where the red and blue solid lines represent stable and unstable steady states, respectively, and the red and blue dashed lines represent complex solutions of (2) with positive and negative imaginary parts, respectively. In (a) l = 0.7, in (b) Δω = 0.22, in (c) l = 1, in (d) Δω = 0, and all the other parameters are the same as in Fig. 1(b). (e–h) Phase rigidities of the corresponding states in (a–d), respectively. | PMC10232044 | nwac259fig2.jpg |
0.431759 | 741340dab5b843178653684c75a4624a | (a,d,g) The dynamics of Re[ψA] (red lines) for the nonlinear Hamiltonian in (1) for different magnitudes of noise and detuning. (b,e,h) The dynamics of Re[ψA] (green lines) for the corresponding linear Hamiltonian in Equation (S24) within the online supplementary material. The amplitudes of noise are given with the blue lines in the first two columns. (c,f,i) The corresponding Fourier spectra for the nonlinear (red) and linear (green) systems. Here the spectra are averaged over 100 independent noise realizations. The dynamics all begin with a small kick-start amplitude ψA = 10−2 and follow the corresponding linear or nonlinear Schrödinger equations thereafter. The Fourier spectra of the nonlinear systems (red lines) are obtained with the corresponding dynamics of Re[ψA] within the period 0 ≤ t ≤ 300. For the linear systems, the wave magnitudes are increasing functions of time. We record the dynamics of Re[ψA] until Max[|ψA|2] = 100 is reached, and then perform the Fourier transform. In (a–f) Δω=0 and in (g–i) Δω = 0.01. For (a–c), D = ζ = 0; for (d and g) and the solid red lines in (f and i), D = ζ = 0.3; and for (e and h), the solid green lines in (f and i), and the dashed red lines in (f and i), D = ζ = 0.1. For the nonlinear Hamiltonian, l = 1, ωB = 2, and the gain saturation model is given by Equation (S6) within the online supplementary material. | PMC10232044 | nwac259fig3.jpg |
0.379644 | 4f444979e85744a29c6fe164f383142b | (a) Circuit used for experimental verification, showing the inductors (L), capacitors (C), resistors (R), diodes (D) and amplifier (A). (b) Photo of the experimental setup. (c–f) Measured resonance frequencies (open circles and diamonds) of the system together with the steady-state eigenfrequencies from the simulations (solid lines). Loss = 35.7 (Ω · mF)−1 in (c), detuning = 0.36 (kHz) in (d), loss = 47.5 (Ω · mF)−1 in (e) and detuning = 0 (kHz) in (f). (g–j) The critical behavior near the corresponding EPs and EX in (c–f), respectively. The solid lines are the theoretical predictions. The estimated experimental errors (standard deviation obtained from eight independent measurements) in (c–j) are smaller than the marker sizes. For demonstration purposes, we exaggerate the error bars by factors of 100, 100, 50, 50, 10, 10, 10 and 10 in (c–j), respectively. (k–n) The corresponding SNR-1 for different detuning and loss values. The cyan background represents the theoretical fitting as shown similarly in Fig. 1(d). | PMC10232044 | nwac259fig4.jpg |
0.453199 | c96c21b91c4f4ccf8ed4e45ad118e1cb | Functional, structural, and haemodynamic components reflected in artificial intelligence-enabled electrocardiogram (AI-ECG) for aortic stenosis (AS) are summarized. | PMC10232245 | ztad009_ga1.jpg |
0.437465 | 9f5c70ca8fcf42d8a889d6a4455cd54c | IgM response to infection is totally abolished in aged mice irrespective of TLR2 expression: C57BL/6 wild-type (WT) mice and Toll-like receptor 2-deficient (TLR2−/−) mice of both sexes, aged from 13–28 weeks (young) and 73–89 weeks (old). (a) IgM levels (mg/ml) in healthy condition (WT-young n = 4, WT-old n = 4, TLR2−/−-young n = 4, and TLR2−/−-old n = 4). (b) IgM levels (mg/ml) at day 10 post-infection of S. aureus Newman strain at a dose of 1.5 × 106 CFU/mouse, bacteremia infection, (WT-young n = 8, WT-old n = 9, TLR2−/−-young n = 9, and TLR2−/−-old n = 9). (c) Fold change of IgM levels in bacteremia infection compared to healthy conditions. Statistical evaluations were performed using the student t test. Data are presented as box plots and whiskers. **P < 0.01, ***P < 0.001. The data shown are a combination of two individual experiments. | PMC10232519 | 41598_2023_35970_Fig1_HTML.jpg |
0.410142 | 06a39fb29de8401690451126afeda4fc | IgG response to S. aureus bacteremia is age- and TLR2-dependent: C57BL/6 wild-type (WT) mice and Toll-like receptor 2-deficient (TLR2−/−) mice of both sexes, aged from 13–28 weeks (young) and 73–89 weeks (old). (a) IgG levels (mg/ml) in healthy condition (WT-young n = 4, WT-old n = 4, TLR2−/−-young n = 4, and TLR2−/−-old n = 4). (b) IgG levels (mg/ml) at day 10 post-infection of S. aureus Newman strain at a dose of 1.5 × 106 CFU/mouse, bacteremia infection, (WT-young n = 8, WT-old n = 9, TLR2−/−-young n = 9, and TLR2−/−-old n = 9). (c) Fold change of IgG levels in bacteremia infection compared to healthy conditions. Statistical evaluations were performed using the student t test. Data are presented as box plots and whiskers. **P < 0.01, ***P < 0.001. The data shown are a combination of two individual experiments. | PMC10232519 | 41598_2023_35970_Fig2_HTML.jpg |
0.404762 | 05868784a71742359f6fca783ed62959 | The impact of aging and TLR2 on IgG subclasses in healthy and S. aureus bacteremia: C57BL/6 wild-type (WT) mice and Toll-like receptor 2-deficient (TLR2−/−) mice of both sexes, aged from 13–28 weeks (young) and 73–89 weeks (old). (a) IgG1 levels (mg/ml) in healthy condition (WT-young n = 4, WT-old n = 4, TLR2−/−-young n = 4, and TLR2−/−-old n = 4). (b) IgG1 levels (mg/ml) at day 10 post-infection of S. aureus Newman strain at a dose of 1.5 × 106 CFU/mouse, bacteremia infection, (WT-young n = 8, WT-old n = 9, TLR2−/−-young n = 9, and TLR2−/−-old n = 9). (c) Fold change of IgG1 levels in bacteremia infection compared to healthy conditions. (d) IgG2a levels (mg/ml) in healthy conditions. (e) IgG2a levels (mg/ml) in bacteremia infection. (f) Fold change of IgG2a levels in bacteremia infection compared to healthy conditions. (g) IgG2b levels (mg/ml) in healthy condition. (h) IgG2b levels (mg/ml) in bacteremia infection. (i) Fold change of IgG2b levels in bacteremia infection compared to healthy conditions. Statistical evaluations were performed using the student t test Data are presented as box plots and whiskers. *P < 0.05, **P < 0.01, ***P < 0.001. The data shown are a combination of two individual experiments. | PMC10232519 | 41598_2023_35970_Fig3_HTML.jpg |
0.423643 | 16b2a94b01d14a969ab0a8f60d950657 | S. aureus-specific anti-IgM but not anti-IgG levels are dependent on age and TLR2: C57BL/6 wild-type (WT) mice and Toll-like receptor 2-deficient (TLR2−/−) mice of both sexes, aged from 13–28 weeks (young) and 73–89 weeks (old). (a) S. aureus-specific anti-IgM levels (A450) in healthy conditions (WT-young n = 4, WT-old n = 4, TLR2−/−-young n = 4, and TLR2−/−-old n = 4). (b) S. aureus-specific anti-IgM levels (A450) at day 10 post-infection of S. aureus Newman strain at a dose of 1.5 × 106 CFU/mouse, bacteremia infection, (WT-young n = 8, WT-old n = 9, TLR2−/−-young n = 9, and TLR2−/−-old n = 9). (c) Fold change of S. aureus-specific anti-IgM levels in bacteremia infection compared to healthy conditions. (d) S. aureus-specific anti-IgG levels (A450) in healthy conditions. (e) S. aureus-specific anti-IgG levels (A450) in bacteremia infection. (f) Fold change of S. aureus-specific anti-IgG levels in bacteremia infection compared to healthy conditions. Statistical evaluations were performed using the student t test Data are presented as box plots and whiskers. *P < 0.05, **P < 0.01. The data shown are a combination of two individual experiments. | PMC10232519 | 41598_2023_35970_Fig4_HTML.jpg |
0.3957 | 95b4f8927c6845ddbcd9c0a4bdc42be6 | Sialylated IgG levels are dependent on age and TLR2 rather than S. aureus bacteremia: C57BL/6 wild-type (WT) mice and Toll-like receptor 2-deficient (TLR2−/−) mice of both sexes, aged from 13–28 weeks (young) and 73–89 weeks (old). (a) Sialic acid on IgG in healthy condition (WT-young n = 4, WT-old n = 4, TLR2−/−-young n = 4, and TLR2−/−-old n = 4). (b) Sialic acid on IgG at day 10 post-infection of S. aureus Newman strain at a dose of 1.5 × 106 CFU/mouse, bacteremia infection, (WT-young n = 8, WT-old n = 9, TLR2−/−-young n = 9, and TLR2−/−-old n = 9). (c) Fold change Sialic acid on IgG levels in bacteremia infection compared to healthy conditions. Statistical evaluations were performed using the student t test. Data are presented as box plots and whiskers. **P < 0.01, ***P < 0.001. The data shown are a combination of two individual experiments. | PMC10232519 | 41598_2023_35970_Fig5_HTML.jpg |
0.474676 | 8f3f20c15dd747b893e0e1a020997688 | Result summary: Immunoglobulins response concerning age and TLR2: (A) healthy, and (B) fold changes of immunoglobulins response for age and TLR2 to S. aureus bacteremia in comparison to respective groups of healthy mice. | PMC10232519 | 41598_2023_35970_Fig6_HTML.jpg |
0.468666 | 868f4e00dd70424880ad197e69dd3d57 | Bacterial abundance (A,B) and richness (C,D) in soybean field trials at the flowering–podding stage (A,C) and maturity stage (B,D). CK: non-inoculated control in soil; PK, superphosphorus and potassium chloride; PK + N, PK chemical fertilizers plus urea; PK + R, PK chemical fertilizers plus Bradyrhizobium japonicum 5821. Different letters above bars indicate significant differences (one-way ANOVA, p < 0.05, Duncan’s multiple-range test) among different treatments at each growth stage. The overall effects of growth stage (G), rhizosphere effect (R), and treatment (T) on bacterial abundance and Shannon index were evaluated by three-way ANOVA, with the results shown at the top of the figure. *0.01 < p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001. | PMC10232743 | fmicb-14-1161983-g001.jpg |
0.502685 | 5e495c4cb14247a9a9498a96905234ad | Linear regression relationships between bacterial abundance (A,C,E,G) and richness (B,D,F,H), and soybean yield, in bulk (A,B,E,F) and rhizosphere soil (C,D,G,H), at the flowering–podding stage (A–D) and at the maturity stage (E–H). | PMC10232743 | fmicb-14-1161983-g002.jpg |
0.431659 | 257fcfa277af4d83a4296dbe1c08cae7 | Principal coordinate analysis (PCoA) ordinations of bacterial community composition from the bulk soil and the rhizosphere of soybean under different fertilization levels at the flowering–podding stage (A) and the maturity stage (B). Differences in bacterial beta diversity among different fertilization treatments were determined through PERMANOVA based on the Bray–Curtis distance matrix. CK: non-inoculated control in soil; PK, superphosphorus and potassium chloride; PK + N, PK chemical fertilizers plus urea; PK + R, PK chemical fertilizers plus Bradyrhizobium japonicum 5821. The effects of growth stage (G), rhizosphere effect (R), and treatment (T) on bacterial community composition were evaluated by three-way ANOVA, with the results shown at the top of the figure. *0.01 < p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001. | PMC10232743 | fmicb-14-1161983-g003.jpg |
0.441772 | a5d337dad68045f8b1828878bbfa58af | Relative abundance of dominant bacteria at the class level (relative abundance >1%) (A,B) for each treatment at the flowering–podding stage (A) and at the maturity stage (B). CK: non-inoculated control in soil; PK, superphosphorus and potassium chloride; PK + N, PK chemical fertilizers plus urea; PK + R, PK chemical fertilizers plus Bradyrhizobium japonicum 5821. | PMC10232743 | fmicb-14-1161983-g004.jpg |
0.492079 | 651b7ec84e2547fab3612fa738541661 | Relative abundances of top 20 dominant genera in different treatments at flowering–podding (A,B) and maturity (C,D) stages in bulk (A,C) and rhizosphere (B,D) soil. CK: non-inoculated control in soil; PK, superphosphorus and potassium chloride; PK + N, PK chemical fertilizers plus urea; PK + R, PK chemical fertilizers plus Bradyrhizobium japonicum 5821. | PMC10232743 | fmicb-14-1161983-g005.jpg |
0.444082 | bcceb84e738843019d15ea1421650fb6 | Spearman correlation coefficients between soybean yield and dominant bacteria at class (relative abundance >1%) (A–D) and genus level (20 most abundant) (E–H) in bulk soil (A,C,E,G) and rhizosphere soil (B,D,F,H) at the flowering–podding stage (A,B,E,F) and maturity stage (C,D,G,H). Bold font indicates classes and genera with significant differences among different treatments. *0.01 < p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001. | PMC10232743 | fmicb-14-1161983-g006.jpg |
0.377994 | 88b67014e53c401d80144e026781b999 | Redundancy analysis (RDA) profile constructed from the OTU composition of bacteria and soil properties in the bulk and rhizosphere soil samples under different fertilization levels at the flowering–podding stage (A) and the maturity stage (B). The position and length of the arrows indicate the direction and strength of the influence of soil variables on bacterial communities, respectively. The significant variables are shown by red arrows (p < 0.01). CK, non-inoculated control in soil; PK, superphosphorus and potassium chloride; PK + N, PK chemical fertilizers plus urea; PK + R, PK chemical fertilizers plus Bradyrhizobium japonicum 5821. | PMC10232743 | fmicb-14-1161983-g007.jpg |
0.440409 | b5a18f364b004d889a40fd628712b511 | Structural equation model (SEM) showing the hypothesized causal relationships among soil properties (OM, TN, pH, AP), nodule dry weight, soybean yield and bacterial abundance, diversity, and composition (A). This model resulted in a good fit to the data, with a model χ2 = 24, df = 18, p = 0.16, GFI = 0.92, RMSEA = 0.08. Red arrows indicate significant positive correlations, while blue indicates significant negative relationships (p < 0.05). R2 values represent the proportion of the variance explained for each endogenous variable. The direct and indirect effects of factors on bacterial composition were determined using SEM (B). | PMC10232743 | fmicb-14-1161983-g008.jpg |
0.469347 | 7edada4f928f42d7af31390f2d1550ac | Map of the bidirectional association between epilepsy, gut microbiota, and circadian rhythms. | PMC10232836 | fneur-14-1157358-g001.jpg |
0.435481 | 573a60b91bc14dddafe7183c5da56f8e | Structure of FOXO transcription factors and common mutations across B cell malignancies. Domain structure of FOXO1 (655 aa) and FOXO3 (673 aa), consisting of a conserved region (CR1), a forkhead DNA-binding domain (DBD), a nuclear localization signal (NLS), a nuclear export sequence (NES) and a C-terminal transactivation domain (TAD). Markers show FOXO1 driver mutations across B cell malignancies (CLL, DLBCL, FL, BL, MZL) and variants of uncertain significance (VUS) in FOXO3, with phosphorylation sites highlighted in bold. Occurrence of respective mutations in FOXO1 and FOXO3 across B cell malignancies are shown below the relevant structural schematic [data from combined studies, 2298 samples (16–18)]. | PMC10233034 | fimmu-14-1179101-g001.jpg |
0.443772 | c06d3fd321414e48b151d04336fa3e33 | FOXO expression is critical for early B-cell development. B-cells undergo a specific set of developmental stages in the bone marrow (BM), which are tightly controlled by the expression of particular FOXO transcription factors, enabling differentiation and proliferation at distinct stages of lymphopoiesis. FOXO3 regulates commitment of CLP cells to the B-cell lineage, whereupon FOXO1 expression enables pro-B cell differentiation via E2A and HEB activity. FOXO1, in conjunction with EBF1, promotes B-cell lineage commitment via activation of PAX5, alongside positive regulators such as IL-7R. Cells advancing to the pre-B cell stage are coordinated by SYK activity, which promotes proliferation or differentiation via activation of PI3K or BLNK respectively. PI3K signalling inactivates FOXO1, leading to an upregulation of MYC and CCND2 expression driving pre-B cell proliferation, while BLNK induces cell cycle arrest via FOXO1 and BCL6 upregulation. FOXO1 expression is ablated to allow for differentiation of small pre-B cells into immature B-cells primed to leave the BM to further mature and differentiate in GC reactions. Figure produced in BioRender. | PMC10233034 | fimmu-14-1179101-g002.jpg |
0.413518 | 32df830030624cf79303186cbfe07d2c | FOXO expression assists in germinal centre (GC) B-cell differentiation. The formation of the GC is crucial for the generation of B-cells that produce high affinity antibodies towards specific antigens and differentiate into plasma cells (PCs) and memory B-cells. This occurs through GC-centralised processes: SHM, affinity maturation and clonal expansion. GCs consist of two distinct compartments: the DZ, in which B-cells cycle between proliferation and SHM, and the LZ, in which cells undergo evaluation and selection processes. FOXO1 expression is critical for forming and retaining cells in the DZ. Cells then enter the LZ, where the modified/mutated antibody is tested for high-affinity towards antigen: this process requires FOXO1 downregulation via SYK. Here, B-cells interact with FDCs to evaluate antigen affinity and BCR function, while Tfh-cell interactions aid in B-cell differentiation and proliferation by providing the appropriate signals. Of note, the LZ requires specific regulation of FOXO1 expression to allow for correct LZ proliferation via BATF induction. B-cells from the LZ gain re-entry into the DZ to undergo clonal expansion regulated by FOXO1 and CCND3. All the while, FOXO3 expression maintains GC Th-cell populations and allows for the differentiation of PCs. Red arrows and malignant-like cells indicate stages in GC B-cell differentiation where B-cell malignancy can originate. Figure produced in BioRender. | PMC10233034 | fimmu-14-1179101-g003.jpg |
0.40847 | e6482de1f83a4dfebcd09cea05474165 | Pan-cancer frequency of FOXO mutations. (A) The frequency of FOXO1 mutations across malignancies [data from MSK-IMPACT, 10945 samples; (83)] highlight that FOXO1 mutations are most prevalent in B-cell neoplasms. Within the B-cell malignancy subset, (B)
FOXO1 is most frequently mutated in Burkitt's lymphoma, and (C)
FOXO3 is most frequently mutated in marginal zone lymphoma. Mutations encompass, in-frame, missense and truncating mutations, and deep deletion indicates a deep loss, possibly a homozygous deletion. | PMC10233034 | fimmu-14-1179101-g004.jpg |
0.461145 | 75513b7c466b44adbf1a3dd703b8f203 | Schematic presentation of the experimental time scale: intermittent Theta Burst Stimulation (iTBS) treatment of streptozotocin (STZ)-induced Alzheimer-like disease rat model. | PMC10233102 | fnagi-15-1161678-g001.jpg |
0.437664 | 3dfa9829282444ba956639ffb560f628 | Streptozotocin induces oxidative stress and suppresses antioxidative defense. Evaluation of (А) Superoxide anion radical (O2•−; nmol red NBT/min/mg protein), (B) total Superoxide dismutase (tSOD; U/mg protein), and (C) Sulfhydryl groups (SH; nmol SH/mg protein) in the cortex, striatum, hippocampus, and cerebellum of the Wistar rats. The Control group received Saline solution intracerebroventricularly (icv) and Streptozotocin (STZ) group received icv streptozotocin (3 mg/kg). Bars in the graphs represent means ± SD values (unpaired t-test) for 6 animals in each group. *p < 0.05, **p < 0.01, ***p < 0.001. | PMC10233102 | fnagi-15-1161678-g002.jpg |
0.450288 | 2c9f0589950347fdb503fee45b7a6612 | Intermittent Theta Burst Stimulation (iTBS) attenuates STZ-induced oxidative/nitrosative stress. Evaluation of (A) Superoxide anion radical (O2•−; nmol red NBT/min/mg protein), (B) malondialdehyde (MDA; mmol MDA/mg protein), and (C) nitrite and nitrate concentration (NO2 + NO3; μmol/mg protein) in the cortex, striatum, hippocampus, and cerebellum of the Wistar rats. The STZ + Placebo group represents STZ-administrated animals (3 mg/kg) subjected to noise artifact, and the STZ + iTBS group represents STZ-administrated rats (3 mg/kg) with applied iTBS protocol. Bars in the graphs represent means ± SD values (unpaired t-test) for 6 animals in each group. *p < 0.05, **p < 0.01, ***p < 0.001. | PMC10233102 | fnagi-15-1161678-g003.jpg |
0.440519 | ea713c9ce1b8424ba0f731d1e77a6a8d | Intermittent Theta Burst Stimulation (iTBS) attenuates STZ-induced nucleic acid damage. Evaluation of 8-hydroxy-2′-deoxyguanosine (A) (8-OHdG; ng/mg protein) and Early growth response protein 1 (B) (EGR1; pg./mg protein) in the cortex, striatum, hippocampus, and cerebellum of the Wistar rats. The STZ + Placebo group represents STZ-administrated animals (3 mg/kg) subjected to noise artefict, and the STZ + iTBS group represents STZ-administrated rats (3 mg/kg) with applied iTBS protocol. Bars in the graphs represent means ± SD values (unpaired t-test and Mann–Whitney) for 6 animals in each group. *p < 0.05, **p < 0.01, ***p < 0.001. | PMC10233102 | fnagi-15-1161678-g004.jpg |
0.428693 | 6820f45cf08b40c1b76f306740b3d107 | Intermittent Theta Burst Stimulation (iTBS) attenuates STZ-induced Aß deposition. Evaluation of (A) Amyloid ß precursor protein (APP; ng/mg protein) and (B)
ß-amyloid1-42 (Aß1-42; pg./mg protein) in the cortex, striatum, hippocampus, and cerebellum of the Wistar rats. Evaluation of (C)
ß-amyloid1-42 in the hippocampus using Dot Blot. The STZ + Placebo group represents STZ-administrated animals (3 mg/kg) subjected to noise artifact, and the STZ + iTBS group represents STZ-administrated rats (3 mg/kg) with applied iTBS protocol. Bars in the graphs represent means. ± SD values (unpaired t-test and Mann–Whitney) for 6 animals in each group. *p < 0.05, **p < 0.01, ***p < 0.001. | PMC10233102 | fnagi-15-1161678-g005.jpg |
0.50629 | fe8c1d82a27d468b8866b3e58fc6f298 | Intermittent Theta Burst Stimulation (iTBS) enhances antioxidative capacity in STZ-administrated rats. Evaluation of (A) total Superoxide dismutase (tSOD; U/mg protein), copper-zinc Superoxide dismutase (B) (CuZnSOD; U/mg protein), (C) manganese Superoxide dismutase (MnSOD; U/mg protein), (D) catalase (CAT; U/mg protein), (E) glutathione (GSH; nmol GSH/mg protein), (F) sulfhydryl groups (SH; nmol SH/mg protein), and (G) Nuclear factor erythroid-derived 2-like 2 (Nrf2; pg./mg protein) in the cortex, striatum, hippocampus, and cerebellum of the Wistar rats. The STZ + Placebo group represents STZ-administrated animals (3 mg/kg) subjected to noise artifact, and the STZ + iTBS group represents STZ-administrated rats (3 mg/kg) with applied iTBS protocol. Bars in the graphs represent means ± SD values (unpaired t-test and Mann–Whitney) for 6 animals in each group. *p < 0.05, **p < 0.01, ***p < 0.001. | PMC10233102 | fnagi-15-1161678-g006.jpg |
0.439819 | 1bba8ddf211e4b28b9d2e9edf85ea14a | Intermittent Theta Burst Stimulation increases BDNF expression in STZ-administrated rats. Evaluation Brain-derived neurotrophic factor (BDNF; pg./mg protein) in the cortex, striatum, hippocampus, and cerebellum of the Wistar rats. The STZ + Placebo group represents STZ-administrated animals (3 mg/kg) subjected to noise artifact, and the STZ + iTBS group represents STZ-administrated rats (3 mg/kg) with applied iTBS protocol. Bars in the graphs represent means. ± SD values (unpaired t-test) for 6 animals in each group. *p < 0.05, **p < 0.01, ***p < 0.001. | PMC10233102 | fnagi-15-1161678-g007.jpg |
0.403575 | 0aec73eacd1e49d692d9f64019ca6015 | Effects of Theta Burst Stimulation on Streptozotocin induced reactive astrogliosis in the hippocampus (fimbria). Triple immunofluorescence labeling directed to astrocyte marker GFAP (red), vimentin—VIM (blue), and C3 (green). The number of tested rats was 3 for each group. The micrographs were taken at a magnification of 40X. The scale bar corresponds to 50 μm. | PMC10233102 | fnagi-15-1161678-g008.jpg |
0.452322 | 8e9c3efda2be4621a8c72952b1d10431 | Sequence of lateral autozooid budding in mature branch of Hornera sp. 1 (abfrontal view, distal at right), showing four generations of autozooids (L1 to L4) and lines of associated cancelli (marked with dots). Cancelli are color‐coded to indicate from which autozooid its hypostegal pore originates within the sulcus (Some cancelli connect to two zooids). Exomural budding sites marked by arrows. The cancelli arise from the most recently budded of the two zooids forming the sulcus, the transition taking place at the zooidal budding site. (Image: micro‐computed tomography back‐face isosurface render; cancellus openings outlined with thin black lines to aid interpretation) | PMC10234448 | JMOR-283-783-g001.jpg |
0.41943 | 3f31f77a26e64d0f800b74a33d44218f | Interior skeletal reconstructions of exomural budding sites on abfrontal branch surface. Each budding locus is marked with a yellow dot. (a) Part of fenestrate branch of Hornera foliacea. Note the difference in crossbar composition: the upper‐central branch anastomosis results from branch fusion; the lower crossbar lacks exomural buds, having been formed solely by peristomial anastomosis. (b) Hornera. sp. 1. Multiple lines of exomural budding sites associated with increased branch width. Denser concentrations of exomural buds result in shorter autozooids and higher zooidal divergence angles, evident in the pinnule on the center‐right (micro‐computed tomography‐derived, back‐face, isosurface renders) | PMC10234448 | JMOR-283-783-g002.jpg |
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