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0.423712 | c9cc6a1992f5474580785f25163ff26f | Protective effects of XQG against II/R-induced ileum morphological damage. (A) H&E staining of ileum histological lesion (scale = 50 μm). Goblet cells, lamina propria, and inflammatory cell infiltration were indicated by arrows with green, red and yellow colors, respectively; (B) Chiu’s score of ileum tissue. All values were expressed as mean ± SEM (n ≥ 3). ** p < 0.01 vs. sham group while # p < 0.05 and ## p < 0.01 vs. II/R group. | PMC9415796 | molecules-27-05227-g002.jpg |
0.445639 | 6dfe7647d8e54963be63094ac800b535 | XQG alleviated II/R-induced intestinal barrier injury. (A) The expression level of Occludin in intestinal tissue; (B) Immunohistochemical expression of ZO-1 in intestinal tissue (scale = 100 μm). All values were expressed as mean ± SEM (n ≥ 3). ** p < 0.01 vs. sham group while # p < 0.05 vs. II/R group. | PMC9415796 | molecules-27-05227-g003.jpg |
0.435756 | e017bf12994245febc66c8dd75af0c8c | XQG alleviated oxidative stress and inflammatory response induced by II/R. Effects of XQG on (A) MDA; (B) SOD; (C) GSH; (D) TNF-α; (E) IL-1β; and (F) iNOS in intestinal tissues. All values were expressed as mean ± SEM (n ≥ 3). compared with sham group, * p < 0.05 and ** p < 0.01 vs. sham group, # p < 0.05 and ## p < 0.01 vs. II/R group. | PMC9415796 | molecules-27-05227-g004.jpg |
0.425353 | eeab1006aa20484eb85dfcc755e06041 | XQG alleviated II/R-induced apoptosis. Western Blot analysis of intestinal bcl-2, Bax, and cleaved caspase3. All values were expressed as mean ± SEM (n ≥ 3). ** p < 0.01 vs. sham group, # p < 0.05 and ## p < 0.01 vs. II/R group. | PMC9415796 | molecules-27-05227-g005.jpg |
0.424999 | 2a036a53658f447cbc4fc0030adbac71 | Differentially expressed genes and GO functional annotation. (A,B) Differentially expressed genes after II/R injury (A) and XQG treatment (B); (C,D) GO functional annotation of the differentially expressed genes after II/R injury (C) and XQG treatment (D). | PMC9415796 | molecules-27-05227-g006.jpg |
0.42066 | 0f620c4577f6489bb6718f7589a9881f | KEGG pathway enrichment. (A) KEGG enrichment result of DEGs after XQG administration; (B,C) Enrichment plots of PPAR signaling pathway from GSEA analysis after II/R injury (B) and XQG administration (C); (D) Heat map of gene expression levels of PPARα, NF-κB, Bcl2, TNF-α, IL-1, Gsta1 and SOD; (E) The protein expression levels of PPARα and NF-κB in the intestinal tissue. All values were expressed as mean ± SEM (n ≥ 3). * p < 0.05 vs. sham group, #
p < 0.05 vs. II/R group. | PMC9415796 | molecules-27-05227-g007.jpg |
0.484972 | b8004fc8284e49e7887e7dcb9b1d1cc2 | Diagram expressing steps in β–sito–Alg/Ch/NPs preparation. Aqueous alginate (1 mg/mL) solution pH lined up to 5.2 (A); Incorporation of β–sito solution to the alginate solution (B); Subsequent addition of CaCl2 solution to the alginate solution (C) via injectable needle measuring volume 0.5 mL/min following uninterrupted stirring, 1000 ± 5 rpm for 30 min, consequently entangling β–sito in a complex structure of calcium–alginate (D); Drop-wise addition of the chitosan solution to the alginate solution (E), a self-assembled β–sito–Alg/Ch/NPs formulation resulted (F). | PMC9416187 | pharmaceutics-14-01711-g001.jpg |
0.453189 | 9ccc005b0730479ebd42f20c1bb0fdc4 | Response surface morphology in three-dimensional (3D) plot (A–C) exemplifying the effects of independent variables, X1: Chitosan, %w/v; X2: Sodium alginate, %w/v; and X3: Calcium chloride, mM on responses, Y1: Particle size, nm; Y2: PDI; and Y3: Entrapment efficiency, %. | PMC9416187 | pharmaceutics-14-01711-g002.jpg |
0.519781 | d976b607849d4c998b58c5ef53d796a5 | Two-dimensional contour plots (A–C) exhibiting the effect of X1: Chitosan, %w/v; X2: Sodium alginate, %w/v; and X3: Calcium chloride, mM on responses, Y1: Particle size, nm; Y2: PDI; and Y3: Entrapment efficiency, %. | PMC9416187 | pharmaceutics-14-01711-g003.jpg |
0.458953 | a489a472888c413fb608b09b36a31882 | Particle size distribution indicated by red bar (A); Zeta potential (mV) (B); and transmission electron microscopic image of optimized β–sito–Alg/Ch/NPs (C). | PMC9416187 | pharmaceutics-14-01711-g004.jpg |
0.48803 | 7493591b87f9485180af54bc4308256e | DSC thermogram expressing melting-point of β–sitosterol (A); Chitosan (B); sodium alginate (C); and β–sito–Alg/Ch/NPs (D). | PMC9416187 | pharmaceutics-14-01711-g005.jpg |
0.44171 | 54b4c8ca232e41a1b340987c1d7a346d | TGA analysis of β–sitosterol (A); Chitosan (B); Sodium alginate (C); and β–sito–Alg/Ch/NPs (D). Green line (A–D) indicates the % mass loss in samples. | PMC9416187 | pharmaceutics-14-01711-g006.jpg |
0.521232 | ed5e8bc63de74d0cbacc2ab70d0b1212 | FT-IR spectra of β–sitosterol (A); Chitosan (B); Sodium alginate (C); and β–sito–Alg/Ch/NPs (D). | PMC9416187 | pharmaceutics-14-01711-g007.jpg |
0.495794 | 9730a10a2cee457e9d56a43f299042a6 | X–rd study of β–sitosterol (a); Chitosan (b); Sodium alginate (c); and β–sito–Alg/Ch/NPs (d). | PMC9416187 | pharmaceutics-14-01711-g008.jpg |
0.484617 | 6b21e5cc818c41f6b7e281c3e075122b | % Cumulative drug release from β–sito–Alg/Ch/NPs in comparison with β–sito–suspension in pH 7.4 (A); pH 5.5 (B); the sampling interval was 0, 8, 16, 32, 64, 48, 80, and 96 h, respectively. | PMC9416187 | pharmaceutics-14-01711-g009.jpg |
0.435826 | 1f2c3ac80d6b452d809f811313d1ba6e | The ex vivo intestinal permeation experiment expresses flux of β–sito from β–sito–Alg/Ch/NPs and β–sito–suspension. Data expressed as mean ± SD in triplicate (n = 3) level of significance (** p ≤ 0.01). | PMC9416187 | pharmaceutics-14-01711-g010.jpg |
0.433995 | bce2815b60624b77bd2823ee95841cd0 | Cell viability (% control) after treatment with β–sito–Alg/Ch/NPs and β–sito–suspension at a dose ranges 10–50 µM effectively regressed the breast cancer cell line after an incubation time of 24 h (A) and 48 h (B). Data expressed as mean ± SD in triplicate (n = 3). Results estimated statistically using one way ANOVA and Tukey’s multiple comparisons test (* p < 0.05), (** p < 0.01), ns-not significant (p > 0.05) when β–sito–Alg/Ch/NPs compared with β–sito–suspension. | PMC9416187 | pharmaceutics-14-01711-g011.jpg |
0.41691 | bedccd7b38544bc997724f7e51944afa | The comparative radical scavenging activity by DPPH assay of β–sito–Alg/Ch/NPs,β–sito–suspension and control (Alg/Ch/NPs) (A). Statistical significance “*” indicates significant * p < 0.05, “**” highly significant ** p < 0.01 value, and “***” extremely significant *** p < 0.001 when compared with β–sito–suspension. Comparative pharmacokinetic profile of β–sito–Alg/Ch/NPs and β–sito–suspension (B). Data expressed as mean ± SD in triplicate (n = 3). | PMC9416187 | pharmaceutics-14-01711-g012.jpg |
0.453416 | 9a6b0cd29ff844269c59ff9a15f2a20c | Stability assessment of β–sito–Alg/Ch/NPs for a period of three months at room temperature (25 ± 2 °C) shows alteration in particle size, PDI, % entrapment efficiency, and % drug loading (A); and zeta potential (B). Stability of the formulation illustrated that insignificant (p > 0.05) changes in the parameters under study at the designated condition. | PMC9416187 | pharmaceutics-14-01711-g013.jpg |
0.466044 | 515eb1de27ef4ca3ae7317286d983aeb | Key collaborators for inspiring COVID-19 vaccine confidence in African American and Latino communities. | PMC9416715 | vaccines-10-01319-g001.jpg |
0.38843 | c1f041b2e01148aead1dc4a994665d42 | KCl stimulation increases the expression of HSP90a and the co-chaperone endoplasmin in murine brain endothelial cells. bEnd.3 mouse endothelial cells cultured in the presence of astrocyte-conditioned media were treated with 60 mM KCl or aCSF for 5 min. The KCl pulse (60 mM) mimicked the conditions during cortical spreading depression. aCSF was used as vehicle control. The cells were then lysed in lysis buffer and subjected to proteomic analysis. The graphs show proteomic spectral counts for HSP70 isoforms (A), HSP90 isoforms (B), and HSP90 co-chaperones (C) detected by unlabeled proteomic approaches. (A) No significant differences were observed in the expression of HSP70 isoforms between KCl vs. aCSF-treated cells. (B) The KCl pulse significantly increased the expression of HSP90a, but not HSP90b compared to aCSF control. (C) Significant increase in the expression of endoplasmin was detected in KCl-treated cells, compared to aCSF ones, but there was no significant difference in the expression of CDC37 between KCl and aCSF-treated cells. ns = non-significant, * p < 0.05, ** p < 0.01, as assessed by two-way ANOVA, Sidak–Holms corrected t-test. Values are mean ± SEM (n = 4). Circles and squares indicate individual subjects. | PMC9416719 | pharmaceutics-14-01665-g001.jpg |
0.427734 | a6a247a7b0384a069960f78e99bc7333 | Selective inhibition of HSP90 with 17-AAG mitigated the loss of barrier integrity caused by the KCl pulse in vitro. bEnd.3 cells were cultured on transwell inserts in the presence of astrocyte-conditioned media on the abluminal side. The cells were treated with either 17-AAG (1µM) or vehicle (1% DMSO in media) 24 h before the KCl pulse. On the day of the experiment, the media on the abluminal side were changed to media containing 60 mM KCl (KCl pulse). Media containing aCSF were utilized as vehicle control. The medium was changed to a fresh one after 5 min KCl pulse. TEER measured before any treatment served as baseline. TEER was also assessed right before the KCl pulse (0 min), right after the KCl pulse (5 min), then 10, 20, 30, 60, 120, and 180 min after KCl/aCSF treatment. (A) Setup of the probe in transwell plates for measurement. (B) TEER values were significantly reduced after the KCl pulse (5 min, 60 mM) as compared to aCSF controls on the monolayer of bEnd.3 cells, suggesting loss of barrier integrity (KCl vs. aCSF: *** p < 0.001, **** p < 0.0001, as tested by one-way ANOVA with Tukey’s post-test). Twenty-four hour preincubation with 17-AAG (1 µM) attenuated the KCl-induced changes in TEER values (KCl + 17-AAG vs. KCl + vehicle: ^^^ p < 0.001, assessed by one-way ANOVA, Tukey’s post-test). Values were calculated as measured TEER—insert blank TEER avg and are reported as mean ± SD (n = 3 in triplicate). | PMC9416719 | pharmaceutics-14-01665-g002.jpg |
0.457119 | 49824fed1bad43cca3ce68ab3c857da1 | Selective inhibition of HSP90 with 17-AAG reduced the elevated sucrose movement caused by the KCl pulse across the monolayer of bEnD.3 cells. bEnd.3 cells were cultured in transwell inserts with astrocyte-conditioned media. The treatment was set as in the TEER experiments, 24 h pretreatment of 17-AAG (1 μM) or vehicle (1% DMSO in media), followed by KCl pulse (60 mM, 5 min). 14C-sucrose was added to the luminal side when KCl or aCSF was applied on the abluminal side. Samples were collected from the abluminal side after the 5 min KCl pulse (0–5 min) and 30 min after the KCl pulse (6–30 min) to detect radioactivity. (A) Setup of transwell paracellular leak model. (B) The amount of 14C-sucrose detected in the abluminal chamber was significantly increased after 5 min KCl exposure compared to aCSF controls, indicating reduced barrier integrity (KCl vs. aCSF at 5 min: ^^^ p < 0.001, as tested by one-way ANOVA with Tukey’s post-test). Treatment with the HSP90 inhibitor 17-AAG (1 μM, 24 h) prevented sucrose movement across the monolayer in KCl-treated cells, but it did not influence sucrose permeability in aCSF-treated cells (KCl + 17-AAG vs. KCl + vehicle: *** p < 0.001, assessed one-way ANOVA with Tukey’s post-test). (C) No significant difference among any groups was observed after 30 min. Values are normalized to percent of vehicle ± SEM (n = 4, dotted line). | PMC9416719 | pharmaceutics-14-01665-g003.jpg |
0.439346 | 3b8708b98cc94134977c55c4b4d67cdb | 17-AAG reduced cortical spreading depression-associated blood–brain barrier leak in vivo. Dural cannulation was performed on female Sprague Dawley rats. After recovery, they were injected with 17-AAG (0.5 nmol) or vehicle (1% DMSO in saline) via dural cannula 24 h before CSD induction. CSD was induced by injection of KCl (1 M) through dural cannula. In situ brain perfusion was performed 90 min after the cortical injection of KCl. (A) Timeline of treatment, cortical injection, and perfusion. (B) 14C-sucrose uptake was measured in whole cortex and presented as the brain to plasma ratio (RBr) after 10 min brain perfusion. Dural application of 17-AAG (0.5 nmol) 24 h before cortical injections significantly reduced 14C-sucrose uptake in cortex as compared to vehicle control, suggesting that HSP90 inhibition could prevent KCl-caused BBB leak. (KCl + 17-AAG vs. KCl + vehicle: * p < 0.05, assessed unpaired t-test.) Dotted line represents the 14C-surose uptake measured in aCSF-treated animals. (C) No statistically significant difference was observed in sucrose uptake in the brainstem (p = 0.17). Values are mean ± SEM (n = 6–11). Circles and squares indicate individual subjects. | PMC9416719 | pharmaceutics-14-01665-g004.jpg |
0.436187 | 89816ac5e8f04b569b46d9b2dacb725a | 17-AAG increased the expression of claudin 5 in cortex and PAG after induction of CSD. Female Sprague Dawley rats underwent dural cannulation surgery. After recovery, 17-AAG (0.5 nmol) or vehicle (1%DMSO in saline) were injected via dural cannula 24 h before cortical KCl injection. Cortex and PAG tissue were harvested 90 min after CSD induction and subjected to Western immunoblotting. Representative images of cortex (A) and PAG (B) samples showing the expression of claudin 5 and α-tubulin, as loading control. Pretreatment of 17-AAG increased the expression of claudin 5 in cortex (A) and PAG (B) samples as compared to vehicle control. All data in panel A represent the % of vehicle-treated relative expression ± SEM (n = 4 in each group), whereas in panel B, all data represent the % of vehicle-aCSF pretreated controls’ relative expression ± SEM (n = 4/condition). * p < 0.05 as assessed by unpaired t-test. Circles and squares indicate individual subjects. | PMC9416719 | pharmaceutics-14-01665-g005.jpg |
0.465575 | 00dff80cd3834a21991b9d44d3e01f61 | Summary of findings. Inhibition of HSP90 using 17-AAG improves blood–brain barrier integrity. Our results revealed that preincubation with 17-AAG mitigated the reduction of TEER values caused by the KCl pulse on the monolayer of bEnd.3 cells. The increased uptake of 14C-sucrose across the same endothelial monolayer induced by the KCl pulse was significantly attenuated after preincubation with the same HSP90 inhibitor. Pre-exposure to 17-AAG significantly reduced the transient BBB leak after CSD induced by cortical KCl injection as determined by in situ brain perfusion in female rats. The pharmacological blockade of HSP90 increased the detection of claudin 5 in cortex and PAG, which can play a part in the effect of HSP90 inhibition to protect BBB integrity. | PMC9416719 | pharmaceutics-14-01665-g006.jpg |
0.36366 | b3596b6e0db24ad681a49fa328a2f5a7 | (a) TEM image, (b) HAADF-STEM image, (c) atomic-resolution HAADF-STEM image, and (d) XRD pattern of Rh/WO3−x-2 hybrid nanowires prepared using the standard procedure by adding 6 mg of the Rh precursor. | PMC9416929 | c9na00424f-f1.jpg |
0.403399 | b084ff9079e54610a3799e8a9b31b075 | XPS spectra of (a) Rh 3d orbitals for Rh/C, Rh + WO3−x, and Rh/WO3−x-2 catalysts and (b) W 4f orbitals for WO3−x nanowires, Rh + WO3−x, and Rh/WO3−x-2 catalysts. | PMC9416929 | c9na00424f-f2.jpg |
0.441772 | 1c964e0e253b421092c9b4f5cab8a52f | Plots of time versus volume of hydrogen generated from the catalytic hydrolysis of AB over different catalysts including Rh/WO3−x, Rh + WO3−x, Rh/C, and WO3−x nanowires (a) in the dark and (b) under visible light irradiation at a reaction temperature of 298 K. Their corresponding TOF values achieved (c) in the dark and (d) under visible light irradiation. | PMC9416929 | c9na00424f-f3.jpg |
0.394958 | 51b0d8abf1e544b1bc97fc5fb30de1e8 | Plots of time versus volume of hydrogen generated from the hydrolysis of AB catalyzed by Rh/WO3−x for five cycles. | PMC9416929 | c9na00424f-f4.jpg |
0.465672 | 57ef8a3caf5740a4b7485be8e2cd7e4c | (a) Molecular structures of (1) KU and (2) p-MBA ligands. (b) Atomic structure of Au102–KU complex, with deprotonated p-MBA ligands. Colour coding (orange) KU atoms (yellow) Au (cyan) p-MBA C (white) H (red) O. (c) Absorption spectra of Au102 and KU in water solution in comparison with the emission spectrum of KU with λex = 500 nm. (d) Relative intensity of KU emission as function of [Au102]/[KU] concentration ratio in basic conditions (pH = 10, black dots) and after acidification of the solution (pH = 2, red and blue dots). (e) Image of dried PAGE gel in ambient room lighting and under UV light (λ = 254) for different Au102 : Ku ratios in comparison with two Au102 references. (f) Relative intensity of KU emission with respect to the initial fluorescence of the Au102–KU mixture with different concentrations plotted as a function of increasing ionic strength. | PMC9417352 | d1na00368b-f1.jpg |
0.405455 | e85f5df65d7d4eafa3805f971215b1d8 | (a) Proposed molecular structure of Au102–KU hybrid (3). (b) (Left) Image of PAGE run of Au102–KU hybrid synthesis product with Au102 reference. (Right) Normalized grayscale intensity cross-section of the Au102 reference (black) and Au102–KU hybrid (red) PAGE lanes. (c) TEM image of Au102–KU hybrid sample, scale = 20 nm. (Inset) Close-up of cluster, scale = 2 nm. (d) (Inset) Full absorption spectrum of Au102–KU-hybrid in comparison to Au102 spectrum in basic (pH = 10) water solution. (Main panel) Difference spectrum of Au102–KU-hybrid and Au102 (black), absorption spectrum of KU in water (green), and excitation spectrum of Au102–KU-hybrid (pH = 4.1) with detection at λ = 600 nm (red). (e) Normalized fluorescence intensity pH-dependence for Au102–KU-hybrid (red points) and aqueous KU solution (blue points). Red curve: Result of least squares fitting with using eqn (1) (for parameters, see text, direction of pH change from basic to acidic). Black curve: Ligand protonation behavior of Au102(p-MBA)44 Au102(p-MBA)44 from ref. 31. | PMC9417352 | d1na00368b-f2.jpg |
0.425015 | 5f19abb7ed604321bd4b91ad8fd4204d | (Left panel) Time-resolved fluorescence data for Au102–KU hybrid at different pH values. Thick solid lines are deconvolution fits with two exponential functions (see ESI11†) to the experimental data points. Inset shows expanded view of the early time dynamics for the different pH values. (Right panel) Fitted parameters from different pH decay curves in comparison with KU dye. | PMC9417352 | d1na00368b-f3.jpg |
0.399783 | dc9836f63a2d47a18098eb6d754e9a4c | Confocal fluorescence microscopy images of HeLa cells treated with the cluster–dye hybrid (pH sensor) or the dye only for details of image analysis, see ESI12.† The hybrid was internalized for 10 min in the cells, quickly washed and then treated with internalization medium without the hybrid for 15 min, 2 h or overnight at 37 °C (upper row). As a control, HeLa cells were treated with the KU dye only (10 min internalization followed by further 40 min without the dye). pH dependence of the fluorescence was tested in a live-cell sample after overnight loading of Au102–KU hybrid and then adding bafilomycin A1 for 3 min. Bars, 20 μm. | PMC9417352 | d1na00368b-f4.jpg |
0.412075 | ac28c5a9f5b84bd2af2d21764aeb2b5a | Schematic synthesis procedure of F,Ti:Fe2O3 nanorods via the two-step co-doping process of in situ F-doping and ex situ external Ti-doping. | PMC9418710 | d2na00029f-f1.jpg |
0.415139 | 2f76744dfe2b42b1a1c875160a8b071e | SEM (top view (a) and cross-sectional (b)), TEM (c), HRTEM (d), HAADF (e), and elemental mapping images of Fe (f), O (g), Ti (h), F (i), and Sn (j) of F,Ti:Fe2O3 nanorods. | PMC9418710 | d2na00029f-f2.jpg |
0.415059 | c97696b3378649979e4e9f7608ef9614 | XRD patterns (a), Raman spectra (b), light absorption spectra (c) and Tauc plots (d) of Fe2O3, F:Fe2O3, Ti:Fe2O3, and F,Ti:Fe2O3 photoanodes. | PMC9418710 | d2na00029f-f3.jpg |
0.454118 | 7bf4a5ae3e1d41319dc6adb08875a4c4 | Fe 2p and O 1s XPS spectra of F:Fe2O3 (a) and (b), Ti:Fe2O3 (c) and (d) and F,Ti:Fe2O3 (e) and (f). The coloured peaks in (a), (c), and (e) denote the Fe3+ satellite peak. Core-level O 1s XPS spectra in (b), (d), and (f) show the Fe–O bond, oxygen vacancy, and surface hydroxyl group peaks, respectively, from low to high binding energies. | PMC9418710 | d2na00029f-f4.jpg |
0.371908 | 86d02470e6914b26a33160a98f8bcb13 | Comparison of single-step (in situ or ex situ) and two-step (in situ followed by ex situ) co-doping of F and Ti into hematite to fabricate the F,Ti:Fe2O3 photoanode. (a) J–V curves of water oxidation (without H2O2). (b) J–V curves of H2O2 oxidation. The PEC water oxidation was performed under 1 sun irradiation (100 mW cm−2) in 1 M NaOH electrolyte. | PMC9418710 | d2na00029f-f5.jpg |
0.477185 | 0b1f4d9e3fc2493c9d22d95f178a4e2c |
J–V curves with (dashed) and without (solid) the H2O2 hole scavenger in electrolyte (a), Nyquist plots (b), Mott–Schottky plots (c), IPCE (d), ηsurf (e) and ηbulk (f) of F:Fe2O3, Ti:Fe2O3, and F,Ti:Fe2O3. The PEC water oxidation was performed under 1 sun irradiation (100 mW cm−2) in 1 M NaOH electrolyte. | PMC9418710 | d2na00029f-f6.jpg |
0.446253 | 0d601926e6ea4212a848117bae205e87 | Characteristics of the vortex fluidic device (VFD) and moulded fluid flow. (a) Confined mode of operation of the VFD with the expected oscillation in film thickness which also prevails in (b) the continuous flow mode where liquids are injected as droplets into the rapidly rotating tube. (c) Expected fluid flow and film thickness at 90° and 0° degree tilt angles (θ). (d) (i) Shear stress induced fullerene C60 crystallisation resulting in spicules or rods, (ii) anti-solvent crystallisation at the glass–liquid interface, leading to cones, (iii) BSA and glutaraldehyde polymerization in moulding high shear and low shear flow, (iv) as for (iii) for the nucleation and growth of a metal organic framework (MOF5), (v) shear stress melting elemental bismuth, and (vi) shear stress ‘molecular drilling’ of holes on polysulfone with their signature retained at the glass–polymer interface post positional shift of the double-helical fluid flow. (e) Possible representation of the fluid flow behaviour for the spinning top and double-helical flow from Faraday waves into spicular flow. (f) Double-helical fluid flow with a reduction in helical pitch (P) for increasing rotational speed, ω, for the same thickness of the film, di,j, with preservation of ωP. (g) Diagrammatic representation of change in film thickness in a type γ liquid which is dominated by double-helical flow across the rotational landscape, and the reduction in film thickness and associated Faraday waves driving the formation of linear arrays of double-helical flows orientated parallel to the rotation axis of the tube. | PMC9419266 | d1na00195g-f1.jpg |
0.46194 | 34d3372a98e94a9cba94cb87056c0488 | Mixing and thermal response, and film thickness. (a) and (b) Thermal response and mixing times, and change in average film thickness versus ω for water in a 20 mm OD quartz tube (17.5 mm ID) and 10 mm tube (8.5 mm ID) respectively, with all data points measured in triplicates. Mixing time (red) corresponds to the time taken for a drop of water containing a small amount of dye added at the bottom of the tube rotating at a specific speed to uniformly mix in half way up the preformed film generated from 2 mL of water. The temperature (black) was measured midway along the tube using an IR camera, for residual water present in the tube, being equivalent to the continuous flow mode of operation of the VFD (water along the complete length of the tube), with the average film thickness (blue) determined at θ = 45° for a specific speed from the mass of residual water also equivalent to the continuous flow mode of operation of the VFD, converted to a volume of liquid spread uniformly on the inner wall of the tube. (c) Thermal response for water in the tube, retaining the maximum amount of water at each speed, for varying tilt angles, θ, using a 20 mm OD tube. (d) Mixing time (s) for 2 mL of liquid in the 20 mm OD tube for change in θ and ω. (e–h) Thermal response (black), mixing times (red) and film thickness (blue) versus ω for toluene (small film thickness at high speed arises from solvent evaporation under high shear in the liquid), DMF, a 3 : 1 mixture of ethanol and water, and a 1 : 1 mixture of DMF and o-xylene in 20 mm OD tubes, respectively. Temperatures were recorded at the mid-point along the tube to minimise any heating from the bearings. Recording change in temperature starts at high ω relative to ω for recording mixing times, a consequence of requiring extra liquid in the tube when mimicking continuous flow processing, and this requires higher ω to generate a vortex to the bottom of the tube. Three separate thermal response plots are provided for (g) because of fluctuations from one temperature run to another, whereas for all other plots (a–f and h), a single plot of the average of three runs are provided. (i) Summary of the different fluid flows, and flow regimes characterised by the relative contributions from the spinning top Coriolis (FC) and Faraday wave (FFW) induced flows, supported by computational fluid dynamics (CFD) simulations conducted using OpenFoam v1806, as detailed in the ESI Section 11.† (j) Images of water in a 10 mm tube at different rotational speeds, captured from 5k frames per s (Movie S2†). (k) Photographs of partitioned mixing of an aqueous dye in water into 2 mL of water in a 10 mm OD tube rotating at 2k rpm where the vortex is not developed to the bottom of the tube (Movie S1†). Additional information is provided in the ESI file†). | PMC9419266 | d1na00195g-f2.jpg |
0.432154 | dfa700bd73314407b71b2a62ad3c75ec | Manipulating graphene oxide. Processing GO in a 20 mm OD tube (17.5 cm ID) at θ 45°, 0.2 mg mL−1 in DMF, flow rate 0.45 mL min−1, result in (i) scrolls at 4k rpm, (ii) crumbling into globular particles at 5k rpm, and (iii) no perturbation at 8k rpm, with the ability to cycle between the three forms of GO by changing the rotational speed akin to another form, with transformation of the GO into ca. 100 nm spheroidal particles at 5.5k rpm (transition from spicular to double-helical flow at the dynamic equilibrium). | PMC9419266 | d1na00195g-f3.jpg |
0.393384 | 8d67554f65ca4021b81a44a9900f9715 | Moulding nano-carbon and polymer material. (a) Shear stress induced crystallisation and self-assembly of C60 in toluene (0.1 mg mL−1, θ 45°), affording (i) spicules (flow rate 0.1 mL min−1) and (ii) rods (flow rate 1.0 mL min−1), and (iii) mixtures of spicules and rods (flow rate 0.5 mL min−1), at 4, 7, and 6k rpm, corresponding to spicular flow, transitioning from spicular to double-helical flow and helical flow respectively. (b) Micromixing a 1 : 1 solution of o-xylene solution of C60 (0.1 mg mL−1, flow rate 0.1 mL min−1) and DMF (0.1 mL min−1) in a VFD, θ 45°, 20 mm OD tube, affording (i) regular and (ii) irregular cones in a 20 mm OD tube, and (iii) and (iv) sharper pitch cones with extended arms in a 10 mm OD tube. (v) Cones attached to the wall of the glass tube in the VFD, post VFD processing in a 10 mm OD tube. (c) (i and ii) Signature of the pattern of the double-helical flows formed at the interface of the glass tube and a thin film of polysulfone (ca. 5 μm) formed in toluene at 20 °C, θ = 45°, 7k rpm rotational speed, along the length of the tube, with the arrow representing the rotational direction of the axis of the tube. | PMC9419266 | d1na00195g-f4.jpg |
0.401704 | cb0bc07edc884c0eb56376e6622c5060 | Moulding elemental bismuth. (a) SEM image of an as received particle of elemental bismuth, with (b–f) as SEM images of material formed after confined mode processing of the material in (a) in 1 mL isopropyl alcohol (IPA) with the 20 mm diameter quartz tube tilted at θ = 45° and spun at 8k rpm for 20 min under nitrogen, at room temperature; the image in (f) appears to be the reverse side of the crater (that was attached to the surface of the tube), and shows rods mattered together. (g) One possible mechanism for the formation of the resulting craters and rods. | PMC9419266 | d1na00195g-f5.jpg |
0.414492 | 06f355b8e5cd45c2bc129d7d2883e798 | Moulding polymer growth. (a) Schematic of the formation of porous spheroidal particles of cross linked BSA with glutaraldehyde formed in the VFD under confined mode BSA in aqueous 10 mM PBS of pH 7.4 (1 mg mL−1) to ethanol ratio 1 : 3 (300 : 900 μL) and 15 μL of glutaraldehyde, using (b) 0.5 mL of combined solution in a 10 mm OD tube for 1 min at 3k, 5k and 7k rpm (i–iii) respectively, and 1 mL of combined solution for a 20 mm OD tube, for 1 min at 3k, 5k and 7k rpm (iv–vi) respectively, reporting SEM images and derived particle size distributions from 100 randomly chosen spheres. | PMC9419266 | d1na00195g-f6.jpg |
0.459859 | f528612b39fb4a559624c96e45ce280e | Moulding metal organic frameworks. (a) Schematic of the synthesis of MOF5 where terephthalic acid (63.3 mg) and triethylamine (106.3 μL) were dissolved in 4.9 mL of DMF and Zn(OAc)2·2H2O (169.9 mg) was dissolved in 5 mL of DMF. For a typical VFD experiment, 556 μL of zinc solution was added to 444 μL terephthalic acid solution followed by 20 mm VFD processing for 30 min at 110 °C. (b and c) SEM and AFM images respectively for MOF5 formed at 110 °C for 30 min at 4k rpm. (d) Variation in morphology of the particles formed under the same processing as a function of rotational speed (i–vi), 3k, 4k, 5k, 5.5k, 6k and 7k rpm, respectively, for the confined mode of operation of the VFD for 30 min, showing SEM images and particle size plots, determined by randomly counting 100 particles. | PMC9419266 | d1na00195g-f7.jpg |
0.440089 | 09f5539b422049d3b05f9e7a12cd16bc | Design and production of EETI-II-C16 (CKP-C16). (A) Design of EETI-II-C16 (CKP-C16). The lipid tag was added through an N-terminal lysine onto EETI-II. (B) The process of EETI-II-C16 (CKP-C16) production. EETI-II-C16 (CKP-C16) and EETI-II (CKP) can be produced with high purity. LC-MS verifies the identity and purity of (C) EETI-II-C16 (CKP-C16) and (D) EETI-II (CKP). Analytical RP-HPLC shows EETI-II-C16 (CKP-C16) is more hydrophobic than EETI-II (CKP) (indicated by the longer retention time of EETI-II-C16) with the addition of the fatty acid tag. | PMC9419673 | d1na00218j-f1.jpg |
0.47093 | fde0ac1f5ff94797be552c5dfe950953 | Assembly and analysis of CKP loaded NLPs (NLP-CKP). (A) Schematic of CKP-NLP assembly. (B) SEC chromatogram of CKP-NLP. Dotted lines show the fraction that were pooled for further analysis. (C) RP-HPLC chromatogram of the CKP-NLP using ELSD detector. Three peaks were observed corresponding to ApoE422k, CKP and DOPC as indicated by the cartoon. (D) SEC-MALS analysis of MW. Red line is the MW across the CKP-NLP peak (left axis). The IR signal is shown on the right axis. (E) SEC-MALS analysis of Rh. Red line is this Rh across the CKP-NLP peak (left axis). The IR signal is shown on the left axis. | PMC9419673 | d1na00218j-f2.jpg |
0.481654 | d75dfd71d8904134823c5ecb2cffa05a | Effect of CKP loading on NLP size, composition and CKP activity. (A) SEC chromatogram of CKP-NLPs assembled at increasing CKP-C16 mol%. (B) Average Rh analysis across the CKP-NLP SEC peak as a function of CKP mol% in the CKP-NLP assembly. (C) HPLC quantification of number of CKP molecules per NLP after purification as a function of the number of CKP molecules per NLP that was included in the self-assembly reaction. Assemblies were analyzed in duplicate. (D) CKP activity assay for CKP-NLPs containing different levels of CKP incorporation (0–63 CKP/NLP). Assays were performed in triplicate. | PMC9419673 | d1na00218j-f3.jpg |
0.480983 | 33fe342e42cc423ba9d91e6d021a79dc | Effect of CKP loading on NLP stability. (A) SEC chromatograms of NLPs at different times after storage at 37 °C in 50% serum. NLPs were labeled with AF488 and the absorbance in the SEC trace was monitored at A495 to limit background signal from the biological matrix. (B) Normalized peak areas of CKP-NLPs as a function of time when incubated at 37 °C in 50% serum. | PMC9419673 | d1na00218j-f4.jpg |
0.423465 | e4786bf5f8404ee38f2fcd994828e564 | Assembly and characterization of Fab–CKP-NLP conjugate. (A) Schematic of the strategy for generating Fab–CKP-NLP conjugates. The CKP-NLPS are assembled with a reactive DSPE-PEG-Mal lipid and the assembled CKP-NLP are conjugated to Fab via a free cysteine. (B) SEC chromatogram of the Fab–CKP-NLP conjugate after conjugation is complete. Three peaks are observed corresponding to the Fab–CKP-BLP conjugate, Fab dimer and unconjugated Fab. (C) HPLC chromatogram of the SEC purified Fab–CKP-NLP conjugate. All components of the Fab–CKP-NLP were detected as indicated by the cartoon. (D) SEC-MALS analysis of the MW (left panel) and Rh (right panel) across the Fab–CKP-NLP conjugate peak. | PMC9419673 | d1na00218j-f5.jpg |
0.498267 | 3dbe0affa4d44d62a18c1c0247186d77 | Fab loading and stability of Fab–CKP-NLPs. (A) SEC chromatograms of Fab–CKP-NLP conjugates generated at different Fab to CKP-NLP ratios (0–150) during the conjugation step. Three peaks are observed corresponding to the Fab–CKP-BLP conjugate, Fab dimer and unconjugated Fab. (B) HPLC analysis of the number of Fabs per NLP in the purified Fab–CKP-NLP conjugate as a function of the Fab ratio in the reaction for both low CKP-NLP and high CKP-NLP. (C). The Rh of the Fab–CKP-NLP as a function of Fab loading for both low CKP-NLP and high CKP-NLP. (D) CKP activity assay for the Fab–CKP-NLP as a function of Fab loading for both low CKP-NLP and high CKP-NLP. Assays were performed in triplicate (E) normalized peak areas of CKP-NLP and Fab–CKP-NLP as a function of time when incubated at 37 °C in 50% serum. | PMC9419673 | d1na00218j-f6.jpg |
0.436283 | 769065cac2854e6e85279937e05ff946 | Diagram illustrating the method used to measure the thickness of total soft tissue, paraspinal muscle and subcutaneous layer at the level of L5 through sagittal view on T2-weighted MRI. | PMC9420975 | fsurg-09-966197-g001.jpg |
0.46568 | 51627c0fda4a4d14bc0c647b29f40c33 | Representative images of Sesbania rostrata inoculated with ORS571 or uninoculated group as a control at different salt concentrations for 20 days. (A) Growth condition of the aboveground part. (B) Growth condition of the underground part. | PMC9423025 | fpls-13-926850-g001.jpg |
0.598901 | 3303628284c543cd8808515ec16d46c3 | Effects of inoculation with ORS571 on the biomass of Sesbania rostrata under different salt concentrations. The plant height (A), DW underground (B), FW above ground (C), DW above ground (D) were measured. Different lower-case letters in each column shape indicate a significant difference at p < 0.05 by statistical analysis. Error bars indicate standard deviations from four parallel replicates. | PMC9423025 | fpls-13-926850-g002.jpg |
0.464311 | 1cb6e63f9b3445b09f40d152cef7cc96 | Chlorophyll content in leaf samples and nodule number inoculated with ORS571 or not under different salt concentrations. (A) The chlorophyll content of the inoculated group under salt stress was significantly higher than that of the uninoculated group. (B)The number of nodules formed by ORS571 was detected and decreased with increasing salt concentration. Different lower-case letters in each column shape indicate a significant difference at p < 0.05 by statistical analysis. Error bars indicate standard deviations from four parallel replicates. | PMC9423025 | fpls-13-926850-g003.jpg |
0.661146 | 79fe3a414bf849629273109a2f39763c | Effects of exogenous addition of GABA on the biomass aboveground/underground and plant height of Sesbania rostrata under different salt concentrations. The plant height (A), DW underground (B), FW above ground (C), and DW above ground (D) were measured. Different lower-case letters in each column shape indicate a significant difference at p < 0.05 by statistical analysis. Error bars indicate standard deviations from four parallel replicates. | PMC9423025 | fpls-13-926850-g004.jpg |
0.420452 | 23229e3ea3c249b7846779c0d49ab194 | Chlorophyll content of Sesbania rostrata under NaCl stress with or without GABA. The chlorophyll content of GABA treatment was significantly higher than that of the control under salt stress. Different lower-case letters in each column shape indicate a significant difference at p < 0.05 by statistical analysis. Error bars indicate standard deviations from four parallel replicates. | PMC9423025 | fpls-13-926850-g005.jpg |
0.651624 | 17ec331236ac4a00824a8deb9dcc7941 | Effects of exogenous addition of GABA on the biomass aboveground/underground and plant height of ORS571-Sesbania rostrata symbiotic system under different salt concentrations. The plant height (A), DW underground (B), FW above ground (C), and DW above ground (D) were measured. Different lower-case letters in each column shape indicate a significant difference at p < 0.05 by statistical analysis. Error bars indicate standard deviations from four parallel replicates. | PMC9423025 | fpls-13-926850-g006.jpg |
0.424633 | f66341bb31c74dc8af0748eb36d6a6ef | Chlorophyll content of Sesbania rostrata inoculated with ORS571 under NaCl stress with or without GABA. The chlorophyll content of GABA treatment was significantly higher than that of the control under salt stress. Different lower-case letters in each column shape indicate significant difference at p < 0.05 by statistical analysis. Error bars indicate standard deviations from four parallel replicates. | PMC9423025 | fpls-13-926850-g007.jpg |
0.409028 | 0026415d6b754e9eb7b3965ba369a522 | Coronary angiogram showing multiple stenosis on the right coronary artery
and the evidence of aortic wall dissection after stenting (A & B,
arrow). Axial thoracic computed tomography view showing the type A
aortic dissection progressing to the descending aorta (C & D,
arrows). | PMC9423804 | rbccv-37-04-0595-g01.jpg |
0.446059 | f008bd5d729a4f479b9cb615d63c8817 | Coronary angiogram with rapid onset and extension of ascending aorta
dissection (A & B, arrow) confirmed at an urgent computed tomography
scan (C & D, arrows). | PMC9423804 | rbccv-37-04-0595-g02.jpg |
0.40333 | f107bb33241240d890af65738c2bf8eb | Intraoperative picture. Note the extensive intimal flap within the
ascending aorta just above the right coronary ostium towards the
non-coronary sinus (arrow). | PMC9423804 | rbccv-37-04-0595-g03.jpg |
0.396977 | bae9e52c255245d0874566a257216350 | Fluoroscopy of the aortic dissection of case #1. | PMC9423804 | rbccv-37-04-0595-g04.jpg |
0.379012 | 585804ff7dfb4581aab2842aefee8ff6 | Fluoroscopy of the aortic dissection of case #2. | PMC9423804 | rbccv-37-04-0595-g05.jpg |
0.400729 | 3c571aa155b34f5f8d493f11622f1727 | Fluoroscopy of the aortic dissection of case #3. | PMC9423804 | rbccv-37-04-0595-g06.jpg |
0.414937 | 19d4a6fba8f94390abed1d014db64c2d | Axial contrast-enhanced computed tomography images. Hepatosplenomegaly and ascites (a) were observed on computed tomography (CT) three days before transfer to our hospital. Contrast-enhanced CT revealed consolidation in the lower lobe of the left lung (b) and multiple lymphadenopathies (c; arrow) at day 7 in our hospital. Many subcutaneous abscesses were observed in the CT images at approximately day 140 (d; arrow). | PMC9424072 | 1349-7235-61-2377-g001.jpg |
0.446337 | 75d4707efe8e4fa3874b2f054e8f5b00 | The patient’s clinical course. After he was transferred to our hospital, the prednisolone (PSL) dose was gradually tapered. He was temporarily transferred to the previous hospital until the NTM species were identified (days 53-139). With the identification of M. kansasii, we re-transferred him to our hospital and started treatment with rifampicin (RFP), clarithromycin (CAM), and ethambutol (EB) on day 140. Since his general condition temporarily worsened, we added isoniazid (INH) to the treatment regimen. From day 163, we administered 200 mg/day of intravenous hydrocortisone for 3 days because of suspected adrenal insufficiency, followed by an increase in the oral PSL dose to 20 mg/day to suppress anti-interferon (IFN)-γ autoantibody production. We also added intravenous immunoglobulin for the treatment of disseminated nontuberculous mycobacterial infection (DNTM) on days 160-162. On day 260, the patient was discharged with a successfully tapered PSL dose. | PMC9424072 | 1349-7235-61-2377-g002.jpg |
0.432998 | 50663461a6504bd992109964e131aca2 | Multiple subcutaneous abscesses. Many subcutaneous masses were observed on the right anterior chest (a), right back (b), and right neck (c) at approximately day 140. Puncture of the subcutaneous mass on the right back revealed the presence of purulent fluid (d). | PMC9424072 | 1349-7235-61-2377-g003.jpg |
0.491421 | e7016cb543284dda9de6c0765ce8c360 | Osteolytic changes in the second middle phalanx of the right hand. On comparing hand X-ray images obtained on days 26 (a) and 182 (b), a diffuse reduction in bone density was noted. Osteolytic changes were observed in the second middle phalanx of the right hand, and the second finger was shortened (arrow). | PMC9424072 | 1349-7235-61-2377-g004.jpg |
0.440275 | 2df050ddebcb4c32a0015fdb33e4cd69 | Preoperative computed tomography angiography (CTA) in coronal (A), sagittal (B), transversal (C), and reconstruction (D) views. Asterisk indicates mediastinal and pleural hematoma. The posterior side of the aneurysm is irregular and suggestive of rupture (arrow). The diameters were as follows: proximal landing zone, 24 mm; aneurysm, 50 mm; coarctation, 14 mm; distal landing zone, 35 mm. | PMC9424345 | gr1.jpg |
0.383054 | f923c46ab9f74f9ab9a10d2c7b00cd25 | Radiograph at completion depicting deployed thoracic endovascular aortic repair (TEVAR; Gore cTAG, 26 × 100 mm, 34 × 200 mm, and 37 × 150 mm) in tortuous and coarctated aorta. Asterisk indicates 9F apical sheet and transapical through-and-through wire. | PMC9424345 | gr2.jpg |
0.41816 | df713085461d42da856a453909e68360 | Three-dimensional reconstruction of postoperative computed tomography (CT) scan illustrating adequate thoracic endovascular aortic repair (TEVAR) positioning in tortuous aorta, including aortic coarctation. A, Anteroposterior view. B, Left anterior oblique view. C, Left lateral view. D, Left posterior oblique view. E, Extra view, focused on aortic coarctation. | PMC9424345 | gr3.jpg |
0.454192 | de969d445e154337a2531c01ec783ee7 | Prurigo simplex. Tiny excoriated papules on the flank of case 4, treated with methotrexate 10 mg/week. | PMC9425620 | ActaDV-101-9-235-g001.jpg |
0.444247 | 486bde2a192541b59dc7d9644782079b | Prurigo simplex. Erythematous papules and papulo-vesicles on the upper arm of case 5 before systemic treatment. | PMC9425620 | ActaDV-101-9-235-g002.jpg |
0.409965 | 688e448dbc744cccb23a9b8c259b294e | Selection process for subjects in the TraumAR database (non-eligible records have a white background. | PMC9425960 | jpha-13-22-2138-g001.jpg |
0.463939 | 45fba03309f44816a54b2a6abec3ce83 | Occurrence of deaths according to referral times. | PMC9425960 | jpha-13-22-2138-g002.jpg |
0.420191 | bca9a48719994b5a842a92ac0c1aac95 | Ptf1a enhancer deletion in mice causes pancreatic hypoplasia and diabetes(A) Human PTF1A locus and ECR Browser conservation tracks. Sequences with >70% similarity over 100 bp in pairwise alignments are identified by horizontal pink lines on top of each track. The location of the mouse Ptf1aenhP deletion is shown below.(B and C) (B) Body weight and (C) pancreas weight (expressed as percentage of body weight) in 6- to 11-week-old mice (n = 22 each genotype, Student’s t test p values).(D) Ad libitum glycemia of male mice after weaning (n = 22 each genotype).(E) Basal and post-fed plasma insulin from 7-week-old male mice (n = 7 each genotype) after an overnight fast. (D) and (E) show means ± SEM. Student’s t test. ∗∗∗p ≤ 0.0001, ∗∗∗∗p ≤ 0.00001. See also Figure S1. | PMC9426562 | gr1.jpg |
0.404637 | 387297fc16dd4fb981761c30741ab6d8 | Ptf1aenhP controls Ptf1a expression in mouse multipotent pancreatic progenitors(A) HE staining of pancreas from adult control and Ptf1aenhΔ/enhΔ mice.(B) PTF1A immunofluorescence was preserved in acinar cells from adult Ptf1aenhΔ/enhΔ pancreas.(C) 3D reconstructions of E11.5 pancreatic buds from in toto immunofluorescence stainings for PTF1A (green), PDX1 (red), and glucagon (GCG, blue). See also Video S1.(D) PTF1A (green) was depleted in dorsal pancreas from E11.5 Ptf1aenhΔ/enhΔ embryos. PDX1 (red) and NKX6.1 (blue) were co-stained to label MPCs.(E) PTF1A expression in sagittal sections from control and mutant E12.5 neural tube, hypothalamus, cerebellum, and retinal cells. See also Figure S1. | PMC9426562 | gr2.jpg |
0.43304 | 70793864aa4a41b58002bf0611371677 | Modeling PTF1A enhancer mutations in human MPCs(A) qRT-PCR of human MPCs for pancreatic progenitor markers (n = 7–13 independent differentiation experiments per genotype, using 6 PTF1AenhΔ/enhΔ clones—3 lines with 127 bp and 3 lines with 321-bp deletions, see Figure S2B—and 4 PTF1A+/+ control lines. Graphs show means ± SEM. Mann-Whitney ∗p ≤ 0.05, ∗∗p ≤ 0.01, ∗∗∗p ≤ 0.001).(B) Quantification of FACS data for PDX1+ NKX6-1+ stage-4 in vitro derived MPCs (n = 8–10 independent differentiation experiments per genotype; ns, not significant).(C) Immunofluorescence of human MPCs (stage 4) shows absence of PTF1A in PTF1AenhΔ/enhΔ lines, without changes in NKX6-1. See also Figure S2. | PMC9426562 | gr3.jpg |
0.406535 | 5d9a1c0de38d480ea602115adb2d88f0 | PTF1A regulates an evolutionary conserved program in MPCs(A) Differential analysis of H3K27ac at active regulatory regions in human PTF1AenhΔ/enhΔ MPCs. Regions bound by PTF1A in MPCs are highlighted in pink.(B) Top HOMER de novo motifs of regions bound by PTF1A in MPCs.(C and D) (C) Uniform Manifold Approximation and Projection (UMAP) plots of scATAC and (D) metacell 2D projection of scRNA-seq from E10.5 Ptf1aenhΔ/enhΔ and Ptf1a+/+ pancreatic buds. Both identified cells compatible with MPCs and glucagon-expressing cells (Alpha). Cells are colored by cell type (left) or genotype (right).(E) Functional enrichment of 244 genes showing PTF1A-binding or loss of H3K27ac in human mutant cells and differential accessibility or mRNA expression in mouse mutants.(F) Selected PTF1A-regulated genes in human and mouse MPCs. Mesenchymal cells (mesen) are shown as controls. Dot sizes represent adjusted p values, and color shade fold-change in mutant samples.(G–J) Examples of loci showing altered chromatin at PTF1A-bound regions in human mutant cells, and altered chromatin in orthologous or syntenic regions in mouse mutant E10.5 MPCs. Shown are genes involved in endocrinogenesis (NKX2-2, ST18), Notch signaling (HEY1), and cell adhesion (KIRREL2-NPHS1). Mouse tracks show aggregated MPC single-cell chromatin accessibility. See also Figures S3 and S4 and Tables S1, S2, S3, S4, and S5. | PMC9426562 | gr4.jpg |
0.40161 | be8eb9e58b404b03a4d61dd1cfc8853a | PTF1A in MPCs primes endocrine differentiation of mouse bipotent trunk progenitors(A) E12.5-15.5 pancreas showing NKX6-1 (red) in “trunk” bipotent duct-endocrine progenitors, and PTF1A (green) in peripheral pro-acinar cells. White empty arrows point to NKX6-1 negative poorly differentiated trunk cells in Ptf1aenhΔ/enhΔ pancreas. White solid arrowheads depict PTF1A-positive tip cells in Ptf1aenhΔ/enhΔ pancreas.(B) NEUROG3+ endocrine progenitors (red) are severely reduced in E13.5 Ptf1aenhΔ/enhΔ pancreas (see also Figure S5J).(C and D) Insulin (INS), glucagon (GCG), and somatostatin (SOM) immunofluorescence of neonatal (P1) and E18.5 pancreas showed reduced endocrine cells. A representative section from P1 is shown in (C), whereas (D) shows quantifications of the relative pancreas area occupied by each endocrine cell type in E18.5 (n = 6/genotype; ∗∗p ≤ 0.01, ∗∗∗Welch’s t-test p ≤ 0.0001).(E) qRT-PCR of endocrine markers in human hPSC-derived beta-like cells (n = 6–8 independent differentiations/genotype, using 6 PTF1AenhΔ/enhΔ and 4 PTF1A+/+ control lines). Error bars represent mean ± SEM. Mann-Whitney test, ∗∗p < 0.01.(F and G) (F) Flow cytometry for C-peptide expressing beta-like cells in differentiated control and mutant S7 stem cell islets (Mann-Whitney test, ∗∗p < 0.01), and (G) representative FACS plots (n = 6 independent differentiations/genotype).(H) Schematic summarizing the differentiation phenotype in Ptf1aenhΔ/enhΔ pancreas. See also Figure S5. | PMC9426562 | gr5.jpg |
0.472002 | a843c2fa578c41858a822d4ad3cecac1 | PTF1A in MPCs triggers sequential chromatin changes in Neurog3(A) scATAC UMAP plots of E13.5 Ptf1aenhΔ/enhΔ and Ptf1a+/+ pancreas identifies NEUROG3+ endocrine progenitors, pro-acinar progenitors, trunk bipotent progenitors, and mutant-specific trunk null cells. Nuclei are colored by cell type (left) or genotype (right).(B–E) Pseudo-bulk scATAC-seq profiles from E13.5 Ptf1a+/+ and Ptf1aenhΔ/enhΔ trunk and trunk null cells. Regions downregulated in trunk null cells (log2-fold-change < −0.5, binomial test FDR < 0.1) are highlighted in yellow. (B) Depicts Hnf1b and Sox9 loci and (C–E) show reduced accessibility in Ptf1aenhΔ/enhΔ trunk null cells at indicated sites of endocrine regulatory loci. Profiles in NEUROG3+ cells are shown for comparison. In (E), E13.5 Ptf1a+/+ trunk progenitors exhibit an active chromatin state at Neurog3 that is similar to NEUROG3+ progenitors, whereas this is abrogated in Ptf1aenhΔ/enhΔ trunk null cells and is altered at several sites in other Ptf1aenhΔ/enhΔ trunk cells.(F) Proposed model illustrating sequential steps triggered by PTF1AenhP activation of PTF1A. PTF1A binds and remodels chromatin at pro-endocrine gene loci in MPCs. Active chromatin states are maintained at endocrine genes such as NEUROG3 in bipotent progenitor trunk cells, enabling full activation of NEUROG3 in endocrine-committed progenitors. PTF1AenhP deletion prevents this process, causing reduced endocrine differentiation. See also Figure S6. | PMC9426562 | gr6.jpg |
0.411796 | d429012dbfe24ef69ee622b60e3cf0d9 | PTF1AenhP creates an active enhancer cluster in mouse and human MPCs(A) Regulatory landscape of the human PTF1A locus in PTF1A+/+ and PTF1AenhΔ/enhΔ MPCs. Six H3K27ac-enriched putative enhancers and the PTF1A promoter, most of which show strong mediator (MED1) binding, are shaded in gray. All show absent activity in PTF1AenhΔ/enhΔ MPCs (q < 0.05). ChIP-seq tracks show a MACS2 −log10 p values.(B) scATAC-seq profiles for MPCs from Ptf1a+/+ and Ptf1aenhΔ/enhΔ E10.5 pancreatic buds showed chromatin accessibility at Ptf1a and E1-E6 regions orthologous to human enhancers, highlighted in gray. All showed loss in Ptf1aenhΔ/enhΔ cells (q < 0.1, log2FC < −0.5). Conservation tracks show multiple alignments between 100 vertebrate species.(C and D) H3K27ac at the PTF1A locus in 2 hPSC-derived pancreatic progenitor datasets (Alvarez-Dominguez et al., 2020; Geusz et al., 2021). Both used a protocol that generates two stages of early pancreatic progenitors: PP1 PDX1+ cells that do not express MPC markers such as NKX6-1, PP2 PDX1+, and NKX6.1+ cells that are comparable with stage 4 MPCs from the current study. In both datasets, H3K27ac enrichment at PTF1AenhP preceded that of all other enhancers.(E) Summary model illustrating how PTF1AenhP precedes and activates the enhancer cluster in the PTF1A locus. See also Figure S7. | PMC9426562 | gr7.jpg |
0.434012 | 10657aa2533e4d18b4caa37a49aaef4f | Estimated numbers of unrecruited ALS cases in individual Ohio counties. | PMC9428141 | 41598_2022_18944_Fig1_HTML.jpg |
0.467251 | bc17e9d9072a4b80ac4482df149beb98 | The incidence rate of ALS in Ohio. (a) Before including the estimated unrecruited cases; (b) after including the estimated unrecruited cases. | PMC9428141 | 41598_2022_18944_Fig2_HTML.jpg |
0.444833 | f65ffa9e3b464d1ba8d3c52b81751076 | Sites are invited to participate in the Ohio ALS Registry. Participating sites are institutions and neurologists that have contributed cases to the Registry; Declining sites are those that have not. | PMC9428141 | 41598_2022_18944_Fig3_HTML.jpg |
0.40361 | d8cc45e8f69d43a5937e66fe50ed9a47 | Plots of the ranked ALS incidence and the difference and ratio between two consecutive values. All plots are for the counties with non-zero incidence rates in Ohio. | PMC9428141 | 41598_2022_18944_Fig4_HTML.jpg |
0.43092 | d4291d76b020461c876f11a4bf3e7a4c | Spatial smoothing for adjusting the statistically estimated case counts in hotspot and cold spot areas. | PMC9428141 | 41598_2022_18944_Fig5_HTML.jpg |
0.425927 | d32064605fd24cc99549fc225145b33d | Schematic diagram of ncRNA biogenesis and action patterns. (A) Pri-miRNA is transcribed by RNA polymerasel II from genomic loci and further processed into pre-miRNA by microprocessor complex. Subsequently, pre-miRNA is exported to the cytoplasm and further processed into double-stranded miRNA via the Dicer/TRBP/PACT complex. Next, with the help of Ago/GW182, the double-stranded miRNA is processed into mature miRNA, which directly binds to the 3’-UTR of target mRNA, and then facilitates its degradation. (B) LncRNA transcribed by RNA polymerase II is exported to the cytoplasm. Subsequently, lncRNA exerts its biological role by acting as sponges of miRNAs, RBPs, and TFs. (C) CircRNA is mainly derived from precursor mRNAs via back-splicing reaction, by which the single strand of circRNA forms a covalently closed-loop structure. CircRNA plays crucial roles in cellular processes by serving as sponges of miRNAs, RBPs, and TFs. | PMC9428469 | fonc-12-951864-g001.jpg |
0.427961 | ecfc398e6aac43f2aa0b759d7d4762d8 | Classical mechanisms of ncRNAs in cancer drug resistance. The dysregulation of ncRNAs contributes to the development of cancer drug resistance by modulating multiple cellular processes of cancer cells, such as drug efflux, cell apoptosis, autophagy, and EMT as well as the acquisition of CSC characteristics. | PMC9428469 | fonc-12-951864-g002.jpg |
0.449246 | dcd6ce08f92b41c2a70f75080a1f72ef | Clinical implications of ncRNAs in cancer drug resistance. NcRNAs are enriched in tissue, blood, and urine samples from cancer patients with drug resistance. The expression profiles of ncRNAs are mapped using high-throughput sequencing technologies. Next, the differentially expressed ncRNAs are screened and identified by bioinformatics analysis. Subsequently, the mechanisms of ncRNAs in cancer drug resistance are elucidated using cell and animal models. The aberrantly expressed ncRNAs that possessed great potential as biomarkers and/or therapeutic targets are identified. Finally, cancer patients, particularly those with drug resistance, receive the individualized precision treatment strategies. | PMC9428469 | fonc-12-951864-g003.jpg |
0.490785 | d1b2b6db31464152bdc4f70d6719ed6a | Geographical and temporal distribution of the 35 Y. pseudotuberculosis isolated in France in2020. (A) Map of France with the departments. Size of the circle depends on the number of isolates. Colors of the circles depends on the isolates’ lineages. (B) Number of strains per month. Colors of the squares depends on the isolates’ lineages. | PMC9431522 | spectrum.01145-22-f001.jpg |
0.413907 | 8cf32cf3e6f946cc870a7a5b368f041f | Minimum spanning tree obtained using the allelic profiles of the cgMLST (1,921 genes) on the 35 Y. pseudotuberculosis isolates in France in 2020. The branch lengths are based on a logarithmic scale. Numbers close to the branches reveals the alleles differences. Colors of the circles depends on the isolates’ lineages. Pie charts identifies several isolates with the same allelic profile. | PMC9431522 | spectrum.01145-22-f002.jpg |
0.451052 | 3aa5686209584a1bb01d6fe108fcbc4b | Minimum spanning tree reconstructed on the 39 Y. pseudotuberculosis belonging to the lineage 16 isolated in France,1969 to 2020. (A) MST cgMLST-based (B) MST SNP-based. The branch lengths are based on a linear scale. Numbers close to the branches reveals the alleles differences (A) or SNP differences (B). Colors of the circles depends on the isolates’ lineages. Pie charts identifies several isolates with the same allelic profile (3.A.) or same SNP profile (3.B.). | PMC9431522 | spectrum.01145-22-f003.jpg |
0.516136 | d48a7e0f26314eacbc7660d184ede976 | Ciprofloxacin-mediated stimulation of pyocin expression in ΔxerC strains is RecA independent. (A) Representative growth curves (OD600) and luminescence traces (P07990-lux) of wild-type PA14 (MTC2280) and ΔrecA (MTC2302) strains treated (gray) or not (black) with 0.03 μg/mL ciprofloxacin (Cipro). Note that the y axis scales on the luminescence graphs vary. Light gray shading surrounding the traces indicates standard deviation from three technical replicates. Time is indicated in hours. (B) Representative growth curves and luminescence traces as in panel A, but for ΔxerC (MTC2297) and ΔxerC ΔrecA (MTC2301) strains. (C and D) OD-normalized luminescence traces of the indicated strains from panels A and B, respectively. | PMC9431673 | spectrum.01167-22-f001.jpg |
0.470961 | 02f4b1ca58af4e2d8291baf5f6dad77b | Mitomycin C-mediated stimulation of pyocin expression in ΔxerC strains is RecA independent. (A) Representative growth curves (OD600) and luminescence traces (P07990-lux) of wild-type PA14 (MTC2280) and ΔrecA (MTC2302) strains treated (gray) or not (black) with 0.1 μg/mL mitomycin C (MMC). Note that the y axis scales on the luminescence graphs vary. Light gray shading surrounding the traces indicates standard deviation from three technical replicates. Time is indicated in hours. (B) Representative growth curves and luminescence traces as in panel A, but for ΔxerC (MTC2297) and ΔxerC ΔrecA (MTC2301) strains. (C and D) OD-normalized luminescence traces of the indicated strains from panels A and B, respectively. | PMC9431673 | spectrum.01167-22-f002.jpg |
0.476703 | f3aee5d3f9f643f28d738afb5974660b | Mitomycin C-mediated stimulation of pyocin expression in wild-type and ΔxerC strains requires PrtN. (A) Representative growth curves (OD600) and luminescence traces (P07990-lux) of wild-type PA14 (MTC2280) and ΔprtN (MTC2303) strains treated (gray) or not (black) with 0.1 μg/mL mitomycin C (MMC). Note that the y axis scales on the luminescence graphs vary. Light gray shading surrounding the traces indicates standard deviation from three technical replicates. Time is indicated in hours. (B) Representative growth curves and luminescence traces as in panel A, but for ΔxerC (MTC2297) and ΔxerC ΔprtN (MTC2298) strains. (C and D) OD-normalized luminescence traces of the indicated strains from panels A and B, respectively. | PMC9431673 | spectrum.01167-22-f003.jpg |
0.398483 | 26b615e1272d4d569555538f8ed102bd | Single-cell analysis of pyocin expression in ciprofloxacin-induced strains. Representative phase-contrast and GFP fluorescence (P07990-gfp) micrographs are shown in each panel above distributions of mean GFP fluorescence in individual cells of the indicated strains. As in our previous work, cells above a cutoff of 1.2× (gray dashed line) background fluorescence (black dashed line) were considered GFP positive. In each panel, untreated cells are compared to the same strain treated with 0.03 μg/mL ciprofloxacin for 135 min. All micrographs are sized and scaled identically. (A) PA14 (MTC2277). (B) ΔrecA strain (MTC2448). (C) ΔxerC strain (MTC2252). (D) ΔxerC ΔrecA strain (MTC2291). Percentages and average fluorescence (× background) of GFP-positive cells are indicated. A larger number of cells was analyzed in strains expected to have a lower proportion of GFP positivity to improve detection of rare GFP-positive cells. | PMC9431673 | spectrum.01167-22-f004.jpg |
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