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0.420118 | 595d48f7c07d472789e01cfc0f371fb9 | Secondary adventitious budding in Hornera spp. (a) Longitudinally ground, adventitious, kenozooidal strut (top of image) budded on top of thick secondary wall of a transversely cut Hornera sp. 1 branch; abfrontal side up, strut growing perpendicular to branch surface (scanning electron microscopy). (b) Close up of arrowed region in (a). Two adventitiously budded kenozooidal chambers with flat bases corresponding to outer secondary skeletal wall arrowed. (c) Adventitious zooid buds (arrowed) on abfrontal wall of living branch of Hornera robusta. Budding took place on a cultured branch resting directly on substrate, suggesting contact‐induced budding of kenozooids. (d) Large, adventitiously budded chamber (arrow) at base of longitudinally ground kenozooidal strut, same orientation as (a) (H. robusta). (e) Secondary adventitious or possibly delayed exomural budding on outer wall of basal stem (arrows). Focus‐stacked micrograph of bleached colony. (f) Adventitious branch crown with functioning autozooids (H. robusta). Scale bars in µm | PMC10234448 | JMOR-283-783-g003.jpg |
0.475858 | 68858040bc054333ac69c0505dd8afde | Respective orientations of branch and autozooidal walls in a branch segment of Hornera sp. 1 abscised by skeletal resorption (abfrontal side up). Frontal/lateral autozooidal chambers are dimorphic. Recently budded laterals are roughly triangular. The entire surface of the endozone is composed of developmentally frontal walls. Scanning electron microscopy illuminated from below | PMC10234448 | JMOR-283-783-g004.jpg |
0.50899 | a9a7b0f397284e13be712933d0f61262 | Formation of developmentally bilaminate branches from the ancestrula stage in Hornera sp. All numbered stages are transverse slices that show morphogenetic events occurring at or near the growing tip at the respective heights (dotted lines) of the colony shown in the central image—that is, not cross‐sections of a mature branch. Lilac—ancestrula; red—adventitious periancestular zooids; green—exomurally budded lateral autozooids; blue—basal budding of frontal autozooids from budding lamina; pink—septate budding of mostly kenozooids; dark purple—secondary wall calcification (shown in central image only). Black “X,” exomural budding locus; white “X,” budding events along budding lamina | PMC10234448 | JMOR-283-783-g005.jpg |
0.453406 | faf149f0178a4eb48671447840984c19 | Schematic of a longitudinal section of a typical Hornera branch. Note that the skeleton is fully enclosed within a skeleton‐secreting epithelium. bb, brown body; F, frontal autozooid; L, lateral autozooid | PMC10234448 | JMOR-283-783-g006.jpg |
0.487187 | e775f5dd6f0f44138beac8a6e7414141 | The hornerid Calvetia osheai. (a) Colony growing on a bivalve shell; arrow indicates eruptive unilaminate branch. (b) Combined interior/exterior isosurface render of the unilaminate branch arrowed in (a), abfrontal view. Two exomurally budded “laterals” highlighted in yellow. (c) Longitudinal micro‐computed tomography slice of the same branch showing interior morphology: white arrows: exomurally budded lateral autozooids; arrowheads, apertures of “frontal” autozooids. (d) Branching pattern of autozooidal apertures, bordered by patches of zooid‐free, cancellus‐bearing wall, superimposed upon a much wider, roughly cylindrical branch of C. osheai. (e) Branch tip, exterior view, with broad region of unlocalized budding, probably containing a mixture of autozooids and kenozooids (arrowed region). (f) Hornera sp. 1. with teratological budding at branch tips, associated with local suppression of secondary calcification. Normal branch development visible at center and bottom right. Scale bars in µm | PMC10234448 | JMOR-283-783-g007.jpg |
0.507966 | b6aab68a5d7745a593220152f35d4a06 | Early colony morphology of Hornera sp. (a) Living colony of Hornera sp. of equivalent size to the micro‐computed tomography (CT)‐scanned specimen used herein to study development of autozooidal budding. Box shows approximate region scanned. (b) Exterior view of micro‐CT‐scanned basal stem and proximal part of the branch crown of Hornera sp. Webbing‐like septa at the branch axil are incipient kenozooidal chambers. (c) Interior view of same colony (back‐face isosurface render). Autozooids digitally truncated; autozooids and large chambers formed by septa are colored gold. Secondary calcification evident as a radial sequence of proximally directed kenozooids and cancelli (semitransparent purple) originating from the autozooids. Scalebar ~200 µm | PMC10234448 | JMOR-283-783-g008.jpg |
0.489588 | ef83f6e47b8d4e39b0df9cb97c13357f | Overview of hornerid skeletal morphology. (a) Scanning electron microscopy of frontal surface of a Hornera sp. 1. branch bearing autozooidal apertures with dentate peristomes; smaller openings of cancelli also visible. (b) Abfrontal branch surface from the same colony; lines of cancelli and pustulose secondary calcification extend to the branch tips. (c) Micro‐computed tomography interior/exterior reconstruction of frontal surface of Hornera sp. 1; most of the fine tubes (cancelli/kenozooids) have been removed during model processing. Autozooidal chambers (blue) are surrounded by secondarily calcified body wall (yellow). Frontal autozooids (F) bordered by frontolaterally curved lateral autozooids (L). (d) Abfrontal surface of same branch bearing only lateral autozooids (L). Scalebars: (a and b) 500 µm; (c and d) ~500 µm | PMC10234448 | JMOR-283-783-g009.jpg |
0.461916 | f5b96c4dbdd748cfbc58a690f2ceb607 | Interior reconstruction of Hornera robusta: view through the paramedial budding lamina showing the origins of frontal autozooidal chambers (partly or fully colorized for clarity); distal at left. Arrows indicate interzooidal pores at chamber origins: (a) probable aborted autozooid; (b–i) frontal autozooids. Note variability in autozooid morphology, including zooids (g–i), which originate in parallel and share proximal connections to a single frontal autozooid. Image: back‐face isosurface render through abfrontally truncated micro‐computed tomography data set | PMC10234448 | JMOR-283-783-g010.jpg |
0.446127 | 3445f5d90cd64d8682f0006eb7d55daf | Exomural budding in Hornera. (a) Conspicuous exomural budding of two autozooids (pale orange) on a secondarily formed (=lateral) branch of Hornera robusta (abfrontal view). (b) Exterior (left) and interior (right) micro‐computed tomography reconstructions of the same Hornera sp. 1 branch tip showing two newly budded lateral autozooids (*). Viewed externally, the location of zooids is obscured by secondary calcification. (c) Abfrontal view of H. robusta branch tip, arrows show newly budded kenozooids in sulci, similar to, but more proximally sited, than exomurally budded autozooids. (d) Hypostegal pore‐associated exomural budding sites of two lateral autozooids of Hornera sp. 1; distal at left; some cancellus openings outlined for clarity. (e) Sagittal semithin section of distal branch of Hornera sp. 2 showing bilaminate zooid arrangement. Lateral (L) and frontal (F) autozooids comprise two layers of separately budded chambers interfacing at paramedial budding lamina. (f) Sagittal semithin section of H. sp. 2. Circle at left indicates hypostegal pore‐associated exomural budding site of lateral autozooid; circle at right shows an interzooidal pore‐associated budding site of frontal autozooid | PMC10234448 | JMOR-283-783-g011.jpg |
0.530608 | 92580015129b49bdb61e7e4751566a29 | Schematic drawings showing two views of exomural budding and chamber development in the same Hornera branch (both drawings abfrontal side up). (a) Changes in shape and position of newly budded lateral autozooid chambers (a–c) during distal growth and intercalation with older lateral autozooids (pink); (d) paramedial budding lamina; (e) exomural budding site. Frontal zooids not shown; arrow: distal direction. (b) Longitudinal section of the yellow autozooid in (a), with secondary calcification added. Colors and labels (c–e) correspond to (a) (additional colors: dark gray; primary calcification; light gray, secondary calcification) | PMC10234448 | JMOR-283-783-g013.jpg |
0.471867 | ce46e72d930e4c0f8ce7bcecde2892cf | Transverse mid‐branch section of Hornera cf. robusta, frontal side up. On the abfrontal side the lateral autozooid chambers (L) are empty, except for residual brown bodies (B) and sparse endocystal cell cover. Away from branch tips, polypides of lateral autozooids are located only at the lateral edges of the branch in wide‐branched hornerid taxa. Note significant dimorphism of frontal and lateral autozooid diameter in this species. C, cancellus; P, pharynx; T, tentacle. Scale bar in µm | PMC10234448 | JMOR-283-783-g014.jpg |
0.426061 | 0d34dd78a8a04c00bd472a50c1d5d775 | Astogeny in Hornera spp. (a) Living ancestrula of Hornera sp., settled in the laboratory. White arrows show first‐formed walls of two frontally budded adventitious (periancestrular) autozooids on the ancestrula. Proximal footprint of each periancestrular zooid is approximately the same as a typical autozooid (a, aperture of ancestrula). (b) Semithin section of the same ancestrula shown in (a) with the anlage of the periancestrular zooid atop the newly calcified ancestrular dome (longitudinal section, position roughly corresponding to short arrows in a). (c) Scanning electron microscopy of more‐advanced ancestrula. White arrows show two periancestrular zooids partly fused with ancestrular tube (a). (d) Live colony showing two periancestrular zooids (white arrows) growing up wall of central ancestrular zooid (a). (e) Ancestrula of Hornera sp. 2 from Foveaux Strait. Daughter autozooids are fully separated from each other. (f) Multizooidal stem, with new exomurally budded lateral autozooid (asterisk). (g) Incipient branch crown; diverging zooids are connected by septa, long zooids with peristomial spines are laterals; central space where frontal autozooids will bud centripetally is appearing. (h) Young branch crown of Hornera sp. (i) Close up of circled region in (h), showing first‐formed lateral autozooids (L1–L3); the frontal zooids (F1–F4) bud upon and grow along the frontal budding lamina formed by the basal surface of the laterals. (j) Tip of mature branch of Hornera sp. Paramedial budding lamina is established (yellow arrowheads), frontals (F) and laterals (L) labeled. Note roofs of lateral autozooids alternate in size and distance from branch tip. Unlabeled scale bars, 100 µm | PMC10234448 | JMOR-283-783-g015.jpg |
0.48363 | 25d4c66fb6094453904823131a34dea6 | Micro‐computed tomography slices showing budding loci in main branches of eight hornerid species and one crisinid. Arrows show exomural budding loci of lateral autozooids; chambers of recently budded laterals are highlighted in yellow. Gracile taxa (Hornera currieae, Horneridae gen., sp. 1 & 2, and the fenestrate Hornera foliacea) each have a single medial budding locus for laterals; Hornera robusta and H. sp. 1 have multiple budding sites for laterals, and grow wider branches. Budding sites/laminae for frontal autozooids are shown in light blue. In H. currieae and Horneridae gen., sp. 1, budding sites are axial; all other hornerids have paramedial budding laminae. In Calvetia osheai the main branches have widespread, unlocalized endozonal budding (possible newly budded chambers highlighted in blue). The crisinid Mesonea buds all autozooids from a basal budding lamina. Thick secondary calcification was not present at the time of budding. Slices not shown to scale for clarity; slices edited to enhance contrast and remove nonskeletal material | PMC10234448 | JMOR-283-783-g016.jpg |
0.432854 | ca2130ecb990418ba7998bac483b4191 | Sequence of selected micro‐computed tomography transverse orthoslices upwards through the ancestrula, basal stem, and crown of a small colony of Hornera sp. Colors: blue, ancestrular zooid; green, periancestrular autozooids; yellow, exomurally budded lateral autozooids; white, frontal autozooids, kenozooids budded from the endozone and/or secondary kenozooids (outer layer). Each red arrow indicates the addition of a new exomurally budded lateral autozooid in the sequence. Sequence orthoslices (a–w) are discussed in main text | PMC10234448 | JMOR-283-783-g017.jpg |
0.443237 | f41791332a154199af805af2165afe17 | Immunohistochemical protein expression of COX-2, Ki-67 and Bcl-2. COX-2 protein expression in: A, Well-differentiated (WD) OSC; B, Moderately differentiated (MD) OSCC; C, Poorly differentiated (PD) OSCC; and D, Oral mucosa (OM). Ki-67 protein expression in: E, WD OSCC; F, MD OSCC; G, PD OSCC; and H, OM. Bcl-2 protein expression in: I, WD OSCC; J, MD OSCC; K, PD OSCC; and L, OM. (400×). | PMC10234467 | gr1_lrg.jpg |
0.467121 | 14df20233cff46f0a738c5ebe750d686 | Immunohistochemical protein expression of Bax, VEGF and CD105. Bax protein expression in: A, Well-differentiated (WD) OSCC; B, Moderately differentiated (MD) OSCC; C, Poorly differentiated (PD) OSCC; and D, Oral mucosa (OM). VEGF protein expression in: E, WD OSCC; F, MD OSCC; G, PD OSCC and H, OM. CD105 protein expression in: I, WD OSCC; J, MD OSCC; K, PD OSCC; and L, OM. (400×). | PMC10234467 | gr2_lrg.jpg |
0.428264 | 1b5405e8cb544b6399bd0d4f622a0370 | Comparison of IM (%) positive cells immunostaining for A, COX-2; B, Ki-67; C, Bcl-2; D, Bax; E, VEGF; F, CD105 in well-differentiated (WD) OSCC, Moderately differentiated (MD) OSCC, Poorly differentiated (PD) OSCC and oral mucosa (OM) (mean ± SD). (* p < 0.05, ** p < 0.01). | PMC10234467 | gr3_lrg.jpg |
0.389029 | f947b2510c1d415a8af79d80aff95a18 | Spearman's correlation test between COX-2, Ki-67, Bcl-2, Bax, VEGF and CD105 in A, Well-differentiated (WD) OSCC; B, Moderately differentiated (MD) OSCC; C, Poorly differentiated (PD) OSCC; D, oral mucosa (OM). Crossed out rho-value indicates that the correlation was not significant. | PMC10234467 | gr4_lrg.jpg |
0.448968 | f6e02f4182914b2db4eb8fcc9d82f8ad | Unfractionated and F3 bromelain exhibited cytotoxicity in colorectal cancer cells.After treatment of DLD-1, HT29, and HCT116 cell lines with unfractionated or F3 bromelain at different doses (0 to 100 μg/mL), the relative cell survival rate was determined through an SRB colorimetric assay. Unfractionated bromelain treatment (A) and F3 bromelain (B) resulted in reduced cell survival in colorectal cancer cells in a dose-dependent manner compared with the survival of the control-treated cells, which was defined as 100%. X-axis represents the concentration with Log10 (Concentration). | PMC10234570 | pone.0285970.g001.jpg |
0.450845 | f846b7ddeb094e7981c37cdc43d4f91d | Unfractionated and F3 bromelain treatment induced apoptosis in colorectal cancer cells.(A-C) The apoptotic cell population was analyzed using Annexin V-FITC/propidium iodide staining and FACS analysis in DLD-1, HCT116, and HT29 cells after being treated with unfractionated or F3 bromelain. The apoptosis cell population was indicated by the percentage of Q2+Q3. (D) Protein levels of apoptosis-related genes were determined through Western blot analysis. Cells treated with unfractionated or F3 bromelain exhibited increased levels of Bax, Bad, cleaved (c)-caspase 3, c-caspase 8, c-caspase 9, and c-PARP. All experiments were performed at least three times independently (* p < 0.05, ** p < 0.01, *** p < 0.001). | PMC10234570 | pone.0285970.g002.jpg |
0.419747 | 5f142ca335a3455490205b69fe3e8f42 | Unfractionated and F3 bromelain increased reactive oxygen species (ROS) levels and superoxide production in colorectal cancer cells.HCT116 cells were treated with unfractionated bromelain at 15 μg/mL or F3 bromelain at 15 μg/mL for 48 h. Compared with the control, unfractionated or F3 bromelain treatments significantly increased ROS and superoxide levels, which were detected using a fluorescent dye detection kit (A). Relative mRNA levels of antioxidant genes were lower after treatment with unfractionated or F3 bromelain (B) (* p < 0.05, ** p < 0.01). | PMC10234570 | pone.0285970.g003.jpg |
0.438986 | 63abae75703b42669ddddbe0aae7f222 | Unfractionated and F3 bromelain induced autophagy and lysosome formation in colorectal cancer cells.HCT116 cells were treated with unfractionated bromelain at 15 μg/mL or F3 bromelain at 15 μg/mL for 48 h, and autophagic vacuoles and autophagic flux were detected using a Cyto-ID Autophagy Detection Kit (A). Lysosome formation was detected using a Lyso-ID Green Detection Kit (B). Autophagosome and lysosome formation was increased after the treatment. Relative levels of autophagy-related proteins were obtained through Western blot analysis, and the results indicated that autophagy was induced after treatment with unfractionated or F3 bromelain (C) (* p < 0.05). | PMC10234570 | pone.0285970.g004.jpg |
0.461818 | 34831c449e814d03b293347616cc6eb4 | Blocking autophagy further enhanced unfractionated bromelain–induced or F3 bromelain–induced cytotoxicity in colorectal cancer cells.The viability of CRC cells treated with unfractionated or F3 bromelain, in the presence or absence of chloroquine (CQ), was determined through an SRB colorimetric assay (A). Cell viability was further decreased by autophagy blockage. Autophagy blockage was confirmed by accumulation of LC3-II in Western blot analysis (B) (* p < 0.05, ** p < 0.01). | PMC10234570 | pone.0285970.g005.jpg |
0.39039 | 46d6ea14263945cfb1528cbd741578b9 | Combination treatment with unfractionated or F3 bromelain further enhances chemotherapy-induced cytotoxicity in colorectal cancer.Cytotoxic effect of unfractionated bromelain at 15 μg/mL (A) as well as F3 bromelain at 15 μg/mL (B) in combination with routine chemotherapeutic agents (5-FU at 12.5 μM, irinotecan at 40μM, or oxaliplatin at 2.5 μM) was evaluated. The results showed synergistic cytotoxicity of unfractionated or F3 bromelain in combination with 5-FU, irinotecan, or oxaliplatin (* p<0.05, ** p<0.01). | PMC10234570 | pone.0285970.g006.jpg |
0.489858 | a933a251facb409d9b69350f1eefabe4 | Scree plot shows that two components had eigenvalues higher than 1 | PMC10236069 | 41155_2023_257_Fig1_HTML.jpg |
0.495582 | 7300d8001dd0431ab843ff391468f489 |
Helicobacter pylori associated chronic gastritis with lymphoid aggregates and curved rods of Helicobacter pylori carpeting the mucosal surface. A: Hematoxylin and eosin staining, × 200; B: Hematoxylin and eosin staining, × 400. | PMC10237098 | WJG-29-2950-g001.jpg |
0.416159 | eab9e5bdffdf4a31974c3be4e08ae187 |
Polymerase chain reaction amplification of cagA and vacA genotypes using 100 bp ladder. A: Lanes 1, 2, 6 cagA-negative and lanes 3, 4, 5, 7, and 8 cagA-positive; B: Lanes 1 and 3 vacA genotype s2m2 and lanes 4 and 5 vacA genotype s1m1. | PMC10237098 | WJG-29-2950-g002.jpg |
0.394216 | ffaaab60604744d78acf92482458e2ae |
Evaluation of nonstructural protein 3-transactivated protein 1 expression in carbon tetrachloride-induced hepatic fibrosis and Transforming growth factor 1 beta 1-stimulated LX-2 cells. A: Real-time quantitative polymerase chain reaction analysis of fibrosis-related genes in liver tissues (n = 6); B: Immunofluorescence staining for alpha smooth muscle actin (α-SMA); red: α-SMA (n = 3), scale bar = 20 μm; C: Immunohistochemical staining for α-SMA, scale bar = 100 μm; D: Image J analysis of immunohistochemical staining for α-SMA (n = 3); E: Immunofluorescence staining for nonstructural protein 3-transactivated protein 1 (NS3TP1); green: NS3TP1 (n = 3), scale bar = 20 μm; F: Western blot analysis of NS3TP1 in L02, LX-2, Huh7, and G2 cells; G and H: NS3TP1 was overexpressed in LX-2 cells treated with transforming growth factor 1 beta 1 (TGFβ1) for 24 h (n = 3). The data was presented as mean ± SE. aP < 0.05, bP < 0.01 vs TGFβ1 (0 ng/mL) group; cP < 0.01 vs corn oil control group. NS3TP1: Nonstructural protein 3-transactivated protein 1; TGFβ1: Transforming growth factor 1 beta 1; CCl4: Carbon tetrachloride; RT-qPCR: Real-time quantitative polymerase chain reaction; α-SMA: Alpha smooth muscle actin. | PMC10237113 | WJG-29-2798-g001.jpg |
0.412835 | 91318de93d0a4c4294e3820759c3a63d |
Influence of nonstructural protein 3-transactivated protein 1 on liver fibrosis in vitro. A: Western blot analysis of fibrosis-related genes after Nonstructural protein 3-transactivated protein 1 (NS3TP1) overexpression (n = 3); B: Real-time quantitative polymerase chain reaction (RT-qPCR) analysis of fibrosis-related genes after NS3TP1 overexpression (n = 3); C: Western blot analysis of the fibrosis-related genes after NS3TP1 interference (n = 3); D: RT-qPCR analysis of the fibrosis-related genes after NS3TP1 interference (n = 3); E and F: Cell proliferation was measured by cell counting kit-8 assays after interference or overexpression of NS3TP1 (n = 3); G and H: Western blot analysis of Bcl-2 and Bax after interference or overexpression of NS3TP1 (n = 3). The data was represented as mean ± SE. aP < 0.05, bP < 0.01 vs pcDNA-NS3TP1 group; cP < 0.05, dP < 0.01, eP < 0.001 vs siRNA-NS3TP1 group. NS3TP1: Nonstructural protein 3-transactivated protein 1; CCK-8: Cell counting kit-8; COL1A1: Type 1 collagen alpha 1 chain; COL1A2: Type 1 collagen alpha 2 chain; COL3A1: Type 3 collagen alpha 1 chain; COL4A2: Type 4 collagen alpha 2 chain. | PMC10237113 | WJG-29-2798-g002.jpg |
0.431504 | bceab4dd34374b68a1f498c40a736232 |
Promotion of nonstructural protein 3-transactivated protein 1 in hepatic fibrosis via transforming growth factor beta 1 receptor/Smad3 and NF-kB signaling pathways. A and B: The protein levels of molecules in the transforming growth factor beta 1 (TGFβ1)/Smad3 and NF-kB signaling pathways after nonstructural protein 3-transactivated protein 1 (NS3TP1) interference or overexpression in LX-2 cells were analyzed by Western blot (n = 3); C and D: Western blot analysis of the above signaling pathway molecules in LX-2 cells after Smad3-specific inhibitor or licochalcone D treatment (n = 3); E: Coimmunoprecipitation analysis between NS3TP1 and Smad3 or p65; F: Luciferase activity analysis between NS3TP1 and the TGFβ1 receptor 1 (TGFβRI) promoter (n = 3); G: Luciferase activity analysis between TGFβ1 and the NS3TP1 promoter; TGFβ1 (L: 2.5 ng/mL, M: 5 ng/mL, H: 10 ng/mL) (n = 3); H: Luciferase activity analysis between NS3TP1 and the p65 promoter (n = 3); I: Luciferase activity analysis between p65 and the NS3TP1 promoter (n = 3). The data was represented as mean ± SE. aP < 0.001 pcDNA3.1 + TGFβ1R promoter vs pGL4.10 + pcDNA3.1, bP < 0.0001 NS3TP1 + TGFβ1R promoter vs NS3TP1 + pGL4.10; cP < 0.001; NS3TP1 + TGFβ1R promoter vs pcDNA3.1 + TGFβ1R promoter; dP < 0.01 pGL4.10 + NS3TP1 promoter vs pGL4.10; eP < 0.001 pcDNA3.1 + p65 promoter vs pGL4.10 + pcDNA3.1, fP < 0.01 NS3TP1 + p65 promoter vs NS3TP1 + pGL4.10; gP < 0.01 pcDNA3.1 + NS3TP1 promoter vs pGL4.10 + pcDNA3.1, hP < 0.0001 p65 + NS3TP1 promoter vs p65 + pGL4.10; iP < 0.001 p65 + NS3TP1 promoter vs pcDNA3.1 + NS3TP1 promoter. NS3TP1: Nonstructural protein 3-transactivated protein 1; TGFβ1R: Transforming growth factor beta 1 receptor; p-smad3: Phosphorylated sekelsky mothers against decapentaplegic homolog 3; SIS3: Smad3-specific inhibitor; LD: Licochalcone D; Co-IP: Coimmunoprecipitation. | PMC10237113 | WJG-29-2798-g003.jpg |
0.409275 | 971e019c9ce943f884f6e4334fa6a7b1 |
The role of calcitriol in hepatic fibrosis. A: Western blot analysis of collagen I and α-smooth muscle actin (α-SMA) in LX-2 cells treated with different concentrations of calcitriol; B: The protein levels of collagen I and α-SMA after calcitriol treatment at various time points were analyzed by Western blot; C: Calcitriol reduced the transforming growth factor beta 1 (TGFβ1)-induced elevation of collagen I and α-SMA at the protein level (n = 3); D: Western blot analysis of the calcitriol-induced level of Bcl-2 and Bax; E and F: An Annexin V-FITC/7-AAD kit was utilized to measure cellular apoptosis by flow cytometry; G and H: LX-2 cell migration was measured using the wound-healing test at 0 h, 24 h, 48 h, and 72 h (× 100) (n = 3); I: Hematoxylin-eosin, Masson staining, Sirius red staining, and immunohistochemical staining for α-SMA in hepatic tissue, scale bar = 100 μm; J: Immunofluorescence staining for α-SMA in hepatic tissue, red: α-SMA (n = 3), scale bar = 20 μm; K and L: Protein expression of α-SMA in the hepatic tissues was evaluated by Western blot (n = 3); M: The fibrosis score was analyzed according to the Ishak scoring system (n = 6); N: Levels of alanine aminotransferase and aspartate aminotransferase in plasma for the three groups. The carbon tetrachloride (CCl4) group was contrasted with the corn oil group, while the calcitriol group was contrasted with the CCl4 group (n = 6). The data was presented as mean ± SE. aP < 0.05, bP < 0.01, cP < 0.0001 vs without calcitriol control group; dP < 0.001 CCl4 group vs corn oil control group, eP < 0.001 calcitriol group vs CCl4 group; fP < 0.01 CCl4 group vs corn oil control group, gP < 0.01 calcitriol group vs CCl4 group; hP < 0.0001 CCl4 group vs corn oil control group, iP < 0.0001 calcitriol group vs CCl4 group. ALT: Alanine aminotransferase; AST: Aspartate aminotransferase; CCl4: Carbon tetrachloride; TGFβ1: Transforming growth factor beta 1. | PMC10237113 | WJG-29-2798-g004.jpg |
0.423918 | f8c3f5bbe6144db4a9d5a5d52c8c448e |
The relationship between calcitriol and nonstructural protein 3-transactivated protein 1. A: RT-qPCR analysis of nonstructural protein 3-transactivated protein 1 (NS3TP1) in mice treated with calcitriol (n = 6); B: Immunohistochemical staining for α-smooth muscle actin (α-SMA) in hepatic tissue, scale bar = 100 μm; C: Image J analysis of immunohistochemical staining for α-SMA, (n = 3); D: Immunofluorescence staining for NS3TP1 in liver tissue, green: NS3TP1 (n = 3), scale bar = 20 μm; E and F: Western blot analysis of NS3TP1 in LX-2 cells stimulated with various concentrations of calcitriol or with 16 μmol/L calcitriol for various durations (n = 3); G: Analysis of luciferase activity between the NS3TP1 promoter and calcitriol in HepG2 cells, calcitriol (L: 8 μmol/L, M: 16 μmol/L, H: 32 μmol/L); H: Western blot analysis of the activity of both above signaling pathways in LX-2 cells treated with different concentrations of calcitriol; I: Collagen I, α-SMA, NS3TP1, and p-p65 in calcitriol-treated LX-2 cells were measured by Western blot and compared to LPS-treated cells; J: Extracellular matrix accumulation was evaluated by Western blot in LX-2 cells stimulated with calcitriol after NS3TP1 overexpression. The data was represented as mean ± SE. aP < 0.01 CCl4 group vs corn oil control group, bP < 0.01 calcitriol group vs CCl4 group; cP < 0.0001 pGL4.10-NS3TP1 promoter vs pGL4.10, dP < 0.0001 pGL4.10-NS3TP1 promoter + calcitriol (32 μmol/L) vs pGL4.10-NS3TP1 promoter. ECM: Extracellular matrix; LPS: Lipopolysaccharide; NS3TP1: Nonstructural protein 3-transactivated protein 1; TGFβ1: Transforming growth factor 1 beta 1; CCl4: Carbon tetrachloride. | PMC10237113 | WJG-29-2798-g005.jpg |
0.466183 | a6259ec3e28349cbbfd9d2f3ba4d4f55 | Data pre-processing methodology. | PMC10237406 | pone.0276150.g001.jpg |
0.433166 | b4b8149092aa43dc820ac77109c068d5 | Original tables mapping. | PMC10237406 | pone.0276150.g002.jpg |
0.614439 | 0f1c6849e8a540dea168d25b8196d420 | Creation of data set for the six experiment using data balancing and one-hot encoding techniques. | PMC10237406 | pone.0276150.g003.jpg |
0.430037 | edd05e416bce481aa74f1728ef438b66 | Design flowchart of models training and testing. | PMC10237406 | pone.0276150.g004.jpg |
0.3911 | 8fa4a9835e354eaab90463293e5dfa1c | Comparison of the best SFA models among all experiments. | PMC10237406 | pone.0276150.g005.jpg |
0.43945 | 8f9b3fa002314a309976ec8d35922627 | Comparison of the best health expert models. | PMC10237406 | pone.0276150.g006.jpg |
0.46744 | 5e3ac827999043b082c8a07068a1f37a | SVM-BDS-SFA and AdaBoost-BODS-Expert comparision. | PMC10237406 | pone.0276150.g007.jpg |
0.472289 | da69a7e8d51346f9a710d7bc7fd533f5 | Haplotype network of deltamethrin-resistant and deltamethrin-sensitive mosquitoes. Circles represent a haplotype, black dots represent the assumed intermediate haplotype and the horizontal line represents a mutation step. The size of the circle is proportional to the frequency of the haplotype | PMC10239179 | 13071_2023_5796_Fig1_HTML.jpg |
0.435245 | 3fb2591f9e5346b39cdc649a9e9b11e2 | Flowchart of the study population | PMC10239594 | 12894_2023_1259_Fig1_HTML.jpg |
0.40746 | 10e68f95810547db81f002c054a5a5ef | Discrimination and calibration plots of the cancer risk prediction model of the validation cohort. A, deciles of predicted and real incidence rates in the validation cohort, B deciles of predicted and real incidence rates in the validation cohort. Nam-D’Agostino test statistics are displayed in plots A and B | PMC10239594 | 12894_2023_1259_Fig2_HTML.jpg |
0.392755 | 72fe61dce8d844f69304b892b9d2dc42 | Nomogram for calculating the probability of developing PCa | PMC10239594 | 12894_2023_1259_Fig3_HTML.jpg |
0.426053 | 3f596b58003f4b39b7614acd03194097 | Uniform 2D platelets with segmented cores obtained by sequential growth of PCL (C6) and PHL (C7) homopolymer/block copolymer blends (1:1, wt/wt in CHCl3) from 1D PCL62-b-PDMA270 (C6) seeds colloidally dispersed in EtOH.a–f, Scheme for the formation of 2D PCL–PHL (C6–C7) block co-micelles (a), TEM image (b), AFM height image (c), STED image of BODIPY-dye-labelled platelet block co-micelles (d), height profiles of PCL–PHL block co-micelles corresponding to the numbered lines in c (e) and TEM image and SAED patterns for a PCL–PHL platelet block co-micelle (f). The PCL and PHL domains can be clearly distinguished from the TEM and AFM height images. | PMC10239731 | 41557_2023_1177_Fig1_HTML.jpg |
0.423757 | c179741f6291497fa87f652fd47b3151 | Two-dimensional platelet block co-micelles formed from four different polylactones.a–j, TEM images of PCL–POL (C6–C8) (a), PCL–PDDL (C6–C12) (b), PHL–POL (C7–C8) (c), PHL–PDDL (C7–C12) (d), POL–PCL (C8–C6) (e), POL–PHL (C8–C7) (f), POL–PDDL (C8–C12) (g), PDDL–PCL (C12–C6) (h), PDDL–PHL (C12–C7) (i) and PDDL–POL (C12–C8) (j) block co-micelles prepared by a sequential seeded growth approach in ethanol. The right-hand images of POL–PCL (C8–C6) (e) and PDDL–PCL (C12–C6) (h) are AFM height images. The different sizes of the block co-micelles obtained in each case are due to the different molecular weights of the crystallizable homopolymers and block copolymers. Scale bars = 2,000 nm. | PMC10239731 | 41557_2023_1177_Fig2_HTML.jpg |
0.449351 | ec499a46269945c4b6dd7162e31bec72 | Uniform 2D AB di- and ABA triblock segmented platelets with spatially distinct core chemistries prepared by seeded growth of P(VL-co-CL)-based blend unimer and PCL-based blend unimer using 1D PCL62-b-PDMA270 seeds.a–d, Schematic representation of the formation of triblock co-micelles from a PCL62-b-PDMA270 seed (a), TEM image (b), AFM height image (c) and corresponding height information of the lines indicated in c (d) for the triblock co-micelle. e–g, TEM and corresponding STED images of 2D platelets labelled with BODIPY dyes: diblock co-micelles of P(VL-co-CL)-PCL prepared from sequential addition of P(VL-co-CL) and PCL blend unimer into 1D PCL62-b-PDMA270 seeds (e), diblock co-micelle of PCL-P(VL-co-CL) prepared from sequential addition of PCL and P(VL-co-CL) blend unimer into 1D PCL62-b-PDMA270 seeds (f) and triblock co-micelles of PCL-P(VL-co-CL)-PCL prepared from sequential addition of PCL, P(VL-co-CL) and PCL blend unimer into 1D PCL seeds (g). The PCL region is labelled with green dye, and the P(VL-co-CL) region with blue dye. | PMC10239731 | 41557_2023_1177_Fig3_HTML.jpg |
0.473412 | 1591934d8c264b069e4e39b56f643f25 | Formation of 2D ABC triblock segmented platelets with distinct core chemistries by seeded growth.a, Scheme of uniform 2D platelet block co-micelles prepared by sequential seeded growth of P(VL-co-CL), PCL and PHL blend unimers from 1D PCL62-b-PDMA270 seeds. b–d, TEM image (b), AFM height image (c) and corresponding height profile (d) of triblock co-micelles in c. e, Corresponding STED images of BODIPY-dye-labelled 2D triblock co-micelles; P(VL-co-CL) is labelled in blue, PCL in green and PHL in red. | PMC10239731 | 41557_2023_1177_Fig4_HTML.jpg |
0.425185 | a25f5bacb0144cc0a4d2efc2360ddcbc | Time-resolved degradation for the 2D ABC triblock segmented platelets with a P(VL-co-CL)-PCL-PHL core in an aqueous 1 M KOH solution.a–d, Schematic illustration of the degradation process, where wavy grey lines represents the corona block of PDMA, and the blue, green and red colours correspond to P(VL-co-CL), PCL and PHL core components, respectively (a), the TEM morphologies (b) and corresponding AFM height images (c), and the height profiles of the lines indicated in c (labelled 1, 2, 3 and 4) (d) of the triblock co-micelles at different degradation times. | PMC10239731 | 41557_2023_1177_Fig5_HTML.jpg |
0.439403 | 87352e5ebacc4cb88b69f841c03d24b6 |
(A) Findings on bowel ultrasound (proximal descending colon). (B) Findings on colonoscopy (sigmoid colon) (C) Findings on histopathology (H/E staining, 10x magnification). | PMC10240064 | fonc-13-1149450-g001.jpg |
0.505625 | 2281f02ee536405ea6725b0f4c640cb7 |
(A) Immunohistochemistry of a colon biopsy for CD3 (10x magnification). (B) Flow cytometry of peripheral blood T cells expressing the chimeric antigen receptor (CAR) or not. The frequency of α4+β7+ cells is indicated. CAR T cells were analyzed as previously described (3). Briefly, peripheral blood mononuclear cells were isolated by density centrifugation, stained with CD19 CAR detection reagent, washed twice and stained with Biotin antibody (both Miltenyi Biotec, Bergisch-Gladbach, Germany), 7-AAD (BD Biosciences) and a standardized panel of antibodies against CD45, CD3, CD4, CD8 (all BD Biosciences, Heidelberg, Germany), α4 integrin and β7 integrin (both Biolegend). Gating strategies are depicted in the
Supplementary Figure 1
. Data were acquired on a LSRFortessa (BD Biosciences) and analyzed by Kaluza software v2.1 (Beckman Coulter, Krefeld, Germany). (C) Flow cytometry of peripheral blood (left) and lamina propria (right) T cells. The frequency of CAR+ cells is indicated. | PMC10240064 | fonc-13-1149450-g002.jpg |
0.483212 | b512e15bb06e47a084b28011418945e8 | Scheme of interconnected internal and external triggers contributing to coronary heart disease in SR-B1-/-ApoE-R61h/h mouse model. CHD is trigerred by HFC diet. Changes at the cellular and metabolic levels are primarily driven by deficiency for SR-B1 and by reduced levels of ApoE-R61. Modification in the diet further changes lipids/cholesterol metabolism and causes the accumulation of lipids/cholesterol in various cell types. Subsequently, those cells possess even more affected morphology and function, further contributing (more or less) to CHD | PMC10240136 | 10557_2023_7475_Fig1_HTML.jpg |
0.463591 | be20a21b3b274fbb98aabb35e0960627 | Coronary atherosclerosis in standard diet fed SR-B1-/-ApoE-R61h/h mice. Four exemplary atherosclerotic coronary arteries: A, B, C, and D (with atherosclerotic plaques found in septal heart regions) are shown in 4 rows. For each artery, 3 serial sections (H&E stainings on paraffin sections, first to third columns) from serial sectioning along the artery are depicted. Scale corresponds 100 μm for A–C; 10× objective magnification for D (black letter). Histological images (software-based magnification) with detailed characteristics: necrotic core/cholesterol clefts (black #), macrophages (black §), and hemorrhages (black *) are shown in the 5th row (white letter D) | PMC10240136 | 10557_2023_7475_Fig2_HTML.jpg |
0.437553 | 128e65e041064cd8bc6a3ed7aaddbbbb | HFC diet triggers myocardial infarctions. Short-axis 18F-FDG-PET images (first and third columns, scale bar: cps/ml) with corresponding Masson Goldner-stained paraffin cross sections (second and fourth columns) of the basal, mid-ventricular, and apical heart regions from 2 exemplary SR-B1-/-ApoE-R61h/h mice under standard diet (left) versus HFC diet (right). Masson Goldner stainings differentiate between viable (orange-red) and post-ischemic/fibrotic (green) myocardium. These areas are clearly matched with regional 18F-FDG uptake. Physiological 18F-FDG uptake (1st column) in standard diet fed mouse correlates with histological images (second column, orange-red heart tissue). Areas of decreased 18F-FDG uptake (third column) in HFC-fed mouse correlate with post-ischemic myocardial damage (green areas in heart sections, fourth column) observed throughout the basal (septal part), midventricular (septal part), and apical regions. The scales refer to all samples in respective column | PMC10240136 | 10557_2023_7475_Fig3_HTML.jpg |
0.473553 | 179dbd1f2c1c42e2a42c54bcc9183cab | HFC diet triggers atherosclerosis in the aorta and coronary arteries in SR-B1-/-ApoE-R61h/h mice. A Representative photo of explanted aorta. B Representative cryosection of the whole aorta stained for lipids: red-colored, oil-red counterstained with haematoxylin, scale corresponds 1 mm. Cryosections of aortic atherosclerotic lesions stained for C lipids: red colored, oil-red counterstained with haematoxylin, scale 100 μm; D macrophages: brown colored, Mac-3 staining, scale 100 μm; and E morphology: H&E staining, scale 100 μm. Yellow circles in C and D indicate multinucleated giant cells. Representative heart cryosections with F semi- and G totally (thrombosed) occluded atherosclerotic coronary arteries stained for lipids: red-colored, oil-red counterstained with haematoxylin, scale corresponds 10 μm | PMC10240136 | 10557_2023_7475_Fig4_HTML.jpg |
0.457475 | 2080a9d9ee3d45bfabcdf8c35ff0b2ce | Plaque ruptures and thrombi formation in HFC-fed SR-B1-/-ApoE-R61h/h mice. Examples of thrombi found in various myocardial regions of HFC-fed mice: in septum (A–C), lateral wall (D), and right ventricle (E). First column (A–E): heart sections (scale 1 mm) with white frames indicating the respective location of the thrombotic artery (scale 100 μm). Second to fourth columns (A1–A3 to E1–E3): 3 serial cuts of the thrombotic artery. Symbols are used to label lipid-rich core (white #), thrombus (white *), and perivascular inflammation (white §). H&E stainings were performed on paraffin sections | PMC10240136 | 10557_2023_7475_Fig5_HTML.jpg |
0.466438 | 0a65630a75b841c0b2e591b70c08dc5e | The size of atherosclerotic coronary arteries in HFC-fed SR-B1-/-ApoE-R61h/h mice. The arteries with atherosclerotic plaques and thrombi were categorized according to their size. The value of the outer equivalent diameter (OED) was derived from the measurement of outer areas of atherosclerotic arteries which were considered as the safest quantifiable areas. The value of OED determines the diameter of a circle with the same area as the measured object: Eqdia = sqrt (4 × area / π). The measurements (on H&E paraffin sections) were done for 34 low-grade stenotic (< 50% reduction of original luminal area), 36 high-grade stenotic (> 50% reduction of original luminal area), 30 randomly chosen occlusive, and 29 thrombosed arteries | PMC10240136 | 10557_2023_7475_Fig6_HTML.jpg |
0.45458 | e6b44bf9f9814e3f9ee21b3131c2f39d | 18F-FDG-PET and histological findings in HFC-fed SR-B1-/-ApoE-R61h/h mice with aspirin treatment. Short-axis 18F-FDG-PET images (first column, scale bar: cps/ml) and corresponding Masson Goldner-stained cross sections (second to fourth columns) of the basal, mid-ventricular, and apical heart regions from the exemplary mouse on HFC diet with aspirin treatment are shown. Masson Goldner stainings differentiate between viable (orange-red) and post-ischemic/fibrotic (green) myocardium. The areas of post-ischemic myocardial tissue (light green colored) correlate with decreased uptake of 18F-FDG. Detailed histological images (yellow frames in second column, third and fourth columns) either depict remodeling processes = formation of collagen-based scar (basal region: first row, green parallel collagen fibers) or post-ischemic necrotized myocardium and tissue debris (mid-ventricular region: second row and apical region: third row, green colored). The scales refer to all samples in respective column | PMC10240136 | 10557_2023_7475_Fig7_HTML.jpg |
0.433548 | 753037f8edec436889decc8329b1072c | Total-Body Contrast CT ScanAn intracardiac hypodense mass can be observed in the right atrium. CT = computed tomography; LA = left atrium; LV = left ventricle; RV = right ventricle. ∗Right atrial mass. | PMC10240270 | gr1.jpg |
0.411283 | dffc3fa9e3d74155a7874a7aa370f4c4 | 2-Dimensional Transesophageal EchocardiographyThe right atrial mass can be seen on the lateral wall of the right atrium. RA = right atrium; RV = right ventricle; TV = tricuspid valve. ∗Right atrial mass; ∗∗Thickened atrial wall. | PMC10240270 | gr2.jpg |
0.450608 | b9d92ef1acd448ca9ff88c4039272513 | Positron Emission Tomography–CT ScanSome metabolic hyperactivities can be seen in the mediastinum and the pelvis (A). Image C showing the CT scan acquisition of the cardiac mass. A hyperactive rim (red arrow) could be clearly seen in the cardiac mass (B, D). | PMC10240270 | gr3.jpg |
0.45771 | 0283ffa865d7444aaed096bec63a73e2 | Intracardiac Echocardiography GuidanceThe bioptome (white arrow) approaching the right atrial mass (black asterisk) can be seen. | PMC10240270 | gr4.jpg |
0.505441 | a246e5850b3f4fcc8515630beb136ecd | Histology Specimen From the Cardiac Biopsy(A) Azan Mallory stain. (B) Immunohistochemical expression of CD31. | PMC10240270 | gr5.jpg |
0.471984 | 79dea212ceea4325ab2ca479aa8f8805 | Surgical Resection of the Right Atrial Hemangioma(A) The right atrial hemangioma (indicated by the asterisk) is clearly distinguishable from the nonaffected heart tissue. (B) The right atrium after the resection of the hemangioma; the black box indicates the distal tip of the central line placed in the superior vena cava. (C) Reconstruction of the right atrial wall using a bovine pericardial patch. (D) The right atrial hemangioma resected. | PMC10240270 | gr6.jpg |
0.42267 | de715d1e783c4d0abed65a3e0f80fb12 | Kaplan Meier curves drawn to compare the rates of the primary outcome of “all-cause mortality” (A) and the secondary outcome of “all-cause mortality + rehospitalization for all causes” (B) in the two HFmrEF age groups. HFmrEF heart failure with mildly reduced ejection fraction | PMC10241373 | 40520_2023_2454_Fig1_HTML.jpg |
0.446754 | 2dc433747c984b4293c88178e62f4948 | Prognostic ROC curves and Kaplan–meier survival curves drawn to compare the rates of “all-cause mortality” (A1, A2) and the composite of “all-cause mortality + rehospitalization for all causes” (B1, B2) in HFmrEF patients, categorized according to EF < 45% and ≥ 45% | PMC10241373 | 40520_2023_2454_Fig2_HTML.jpg |
0.42239 | 3bee16c68f60460fbb5deecf3a5e1542 | The computed tomography (CT) images of pneumatosis cystoides intestinalis (PCI) in six dermatomyositis (DM) patients. Red arrow: pneumatosis cystoides intestinalis and free gas in the abdominal cavity. (A) PCI in case 1; (B) the disappearance of PCI in case 1. (C) PCI in case 2; (D) the reduction of PCI in case 2. (E) The prior CT without PCI in case 3; (F) PCI in case 3; (G) the disappearance of PCI in case 3. (H) The prior CT without PCI in case 4; (I) PCI in case 4. (J) The prior CT without PCI in case 5; (K) PCI in case 5; (L) the disappearance of PCI in case 5. (M) The prior CT without PCI in case 6; (N) PCI in case 6; (O) the disappearance of PCI in case 6. | PMC10242029 | fimmu-14-1194721-g001.jpg |
0.519404 | ce2775eec3d140cdbe361896799b2a9c | (A,B) student participants’ previous chronic pain and IPE experiences. Percentage of students who have or have not had prior experiences working with chronic pain patients and in what form are shown in (A). Percentage of students who have or have not worked in an IP setting are shown in (B). | PMC10242053 | fpain-04-1144666-g001.jpg |
0.444665 | 89987bb001434c3dad10737fb1ff5bf8 | (A,B) overall combined improvements on participants’ knowledge in chronic pain physiology and pain management measured with (A) RNPQ and (B) KP50 before and after the program. RNPQ, Revised neurophysiology of pain questionnaire; KP50, KnowPain50. | PMC10242053 | fpain-04-1144666-g002.jpg |
0.430643 | 89a294a4502548bc805d9f8b5d6236a2 | (A,B) overall combined improvements of participants’ perception in interprofessional teamwork abilities measured with (A) IEPS and (B) TSS scores before and after the program. IEPS, Interprofessional education perceptions scale. TSS, Team skill scale. | PMC10242053 | fpain-04-1144666-g003.jpg |
0.465655 | ae56f9e2c2f747979286c51d04a1f344 | (A–D) changes in outcome measures for each program session. Knowledge in chronic pain physiology and pain management were assessed with (A) RNPQ and (B) KP50. Interprofessional teamwork abilities were measured through (C) IEPS and (D) TSS. | PMC10242053 | fpain-04-1144666-g004.jpg |
0.473413 | 5c0bce0691ab4c27a3aac4697351efc6 | Flowchart of the app selection process. Q/A: questions and answers. | PMC10242473 | mhealth_v11i1e44838_fig1.jpg |
0.389735 | edb1ad32a4394c28acffe708c9acc1d3 | DCMRL of individuals 1, 2, and 4.(A) Intrahepatic DCMRL of individual 1 illustrating retrograde mesenteric perfusion (arrow) and pulmonary lymphatic perfusion with dilated mediastinal lymphatics (arrowhead). (B) Intranodal DCMRL of individual 1 shows retrograde into the mesentery (arrow), right renal, and dermal lymphatics (arrow), with an i.p. leak and intact thoracic duct coursing to the left venous angle (arrowhead). (C) Intrahepatic DCMRL of individual 2 shows retrograde flow into the lumbar and iliac lymphatics (arrow), splenic lymphatics (arrow), and i.p. leak (*). There is also bilateral pulmonary and mediastinal lymphatic perfusion (arrowhead) without a thoracic duct. (D) Intrahepatic and (E) intranodal DCMRL of individual 4 show a normal-appearing thoracic duct (arrowhead) with retrograde lumbar perfusion (arrow) and intraduodenal leak (arrow). Intranodal DCMRL shows dilated iliac lymphatics with retrograde dermal perfusion (scrotal and penile). | PMC10243805 | jciinsight-8-155888-g236.jpg |
0.397449 | 2e34e578f76943a99de95e5ca7831d89 | A 2D in vitro model of lymphatic dysplasia.HDLECs were stained with VE-cadherin or actin. Scale bars: 50 μm. (A) KRAS WT. (B) KRAS p.Gly12Asp. Yellow circles show extensions from cells. (C) KRAS p.Gly12Asp treated with 30 nm trametinib. (D) KRAS p.Gly12Asp treated with 1 μm binimetinib. Yellow arrows show areas where abnormal extensions remain. (E) Cell lysates from HDLECs transduced with either KRAS WT or p.Gly12Asp were analyzed with IB for pERK at T202 and Y204 or pS6 at S235/236 with actin as control. (F) Quantification of IB, pERK, or pS6 normalized to actin, normalized to WT + DMSO sample. Data were quantitated from 4 independent experiments. Bars are means; error bars are SDs. One-sided Student’s t tests were performed to calculate significance. Bin, binimetinib; Tram, trametinib. | PMC10243805 | jciinsight-8-155888-g237.jpg |
0.469792 | 024f1ab85faf462ebd4cc98a4db84023 | In vitro organoid model.(A) Lymphatic organoids were transduced with KRAS WT, KRAS p.Gly12Asp, or KRAS p.G13D and treated with DMSO (control), 1 μM binimetinib, 3 μM binimetinib, 10 μM binimetinib, or 300 nM trametinib. Scale bars: 300 μm. (B) Quantitation of sprouting data from 3 independent experiments showing cumulative sprout length per sphere (top), mean sprout length per sphere (middle), and number of sprouts per sphere (bottom). In the box and whisker plots, the center line is the median, the lower and upper boundaries of the box are the 25% and 75% quartiles, and the whiskers extend to 1.5 times the interquartile range from the 25% and 75% quartiles. Two-sided Student’s t tests were performed to calculate significance. Comparisons were made between DMSO-treated WT and both DMSO-treated mutants, as well as each DMSO-treated mutant and all the drug treatments of that mutant; P values were corrected for multiple testing with the Benjamini and Hochberg FDR method. Bin, binimetinib; Tram, trametinib. (C) IB from in vitro organoid model. Cell lysates from HDLECs transduced with either KRAS WT, p.Gly12Asp, or p.Gly13Asp were analyzed with IB for pERK at T202 and Y204 or pS6 at S235/236 with actin as control and quantified. (D) Quantification of IB from 4 separate experiments, pERK or pS6 normalized to actin, normalized to WT + DMSO sample. Bars are means; error bars are SDs. Bin, binimetinib; Tram, trametinib. | PMC10243805 | jciinsight-8-155888-g238.jpg |
0.449678 | 8d1cf7483dd84a7aa288b77f3d6025df | In vivo zebrafish larvae modeling and therapeutic screening.(A) Embryos were injected at 0-cell stage with either mrc1a:wt-hKRAS, mrc1a:hKRAS p.Gly12Asp, mrc1a:hKRAS p.Gly13Asp and tol2 transposase. Larvae at 7 dpf under light microscopy (2.5× magnification), GFP (2.5× magnification), mCherry (2.5× magnification), and confocal microscopy (20× magnification). Larvae injected with mrc1a:hKRAS p.Gly12Asp or p.Gly13Asp under light microscopy have edema around the heart and intestine (arrows). Mrc1a:wt-hKRAS have essentially normal vasculature of larvae injected with under confocal microscopy. Vasculature of larvae injected with mrc1a:hKRASp.Gly12Asp or mrc1a:hKRASp.Gly13Asp under confocal microscopy showing fusion of the thoracic duct with the cardinal vein (brackets). (B) In vivo zebrafish larvae therapeutic screening. Embryos were treated at 48 hpf and screened for edema at 5.5 dpf. (C) Fraction of larvae with edema by KRAS variant, drug, and concentration. Each dot represents a single experiment. *P < 0.05 by unpaired, 1-tailed Student’s t tests, after correction for multiple testing with the Benjamini and Hochberg FDR method. The mechanism of action for each drug can be seen in Supplemental Table 1. Due to figure legend space limitations, the number of zebrafish larvae for each experiment are in Supplemental Table 2. | PMC10243805 | jciinsight-8-155888-g239.jpg |
0.483333 | 74362288745d411595dcd3664c93e8d2 | Conceptual approach for predicting population dynamics in response to multiple stressors. Effects on population growth rate (λ) depend on the responses of individual vital rates, which can have complex responses to different stressors, and the sensitivity of λ to each of those vital rates. | PMC10243908 | plad023_fig1.jpg |
0.597751 | fa0adae00c58449d9573d4893d5fba37 | Interactions among stressors can be additive, synergistic or antagonistic. (A) The black dashed line indicates a measurement under a control treatment (grey). The light and dark blue bars and arrows represent responses to single stressors A and B, respectively (left of grey line). An additive response (red bar) occurs when the difference between the control and each stressor (C-A and C-B) is equal to their algebraic sum (indicated with the red dashed line). A synergistic interaction (purple) occurs when the combined effect of two stressors is larger than the sum of their individual effects, while an antagonistic interaction (gold) occurs when their combined effects are less than their sum. Synergistic and antagonistic interactions represent non-additive responses. The additive sum provides a null hypothesis that provides a threshold (red dashed line) for distinguishing the two types of non-additive interactions. (B) When the responses to two single stressors A and B are in the same direction, values below their sum represent antagonistic interactions (gold arrows) while values above their sum represent synergistic interactions (purple arrows). (C) However, these categories become complicated when two stressors induce opposing responses, with some studies considering any value above or below the null synergistic versus antagonistic, respectively, while others advocate for positive or negative classifications of these interactions (double-barred arrow in C, with ± indicating positive vs. negative synergy and antagonism) depending on thresholds based on the single stressor responses (blue dashed lines) (cf. Fig. 2 in Piggott et al. 2015). | PMC10243908 | plad023_fig2.jpg |
0.462813 | 863029292ae14d42bb5eddcd5af19c2f | Multiple stressors can have additive, synergistic or antagonistic interaction effects on long-term population growth rates (λ). In the case of additive interactions, the combined effects of stressor A and stressor B (medium grey arrow; width of the arrows represents combined effect size) on λ equal the sum of their individual effects (medium grey lines). If the interaction between A and B is synergistic, their combined effect on λ will be greater than their sum, exacerbating their single effects (black arrow), while if the interaction between A and B is antagonistic, their combined effects will be less than their sum (light grey arrow), negating the potential negative effects of a single stressor. | PMC10243908 | plad023_fig3.jpg |
0.451321 | 7574ba287a52442c994385b1dd591f3e | (A) Using only two levels of a stressor (points) may oversimplify the shape of a reaction norm in response to stress (dashed curve), potentially missing biologically meaningful responses to stress, whereas (B) adding even one additional level of a stressor may capture more of the underlying shape. (C) However, five points are considered a minimum to fit nonlinear response curves using a regression design (Collins et al. 2022). | PMC10243908 | plad023_fig4.jpg |
0.399061 | 2f5ce868c29546daa1b86b4499c1b825 | Study design for the entire experiment.A Selection of healthy newborn and diarrheal piglets. B Transplantation of fecal microbiota from healthy and diarrheic piglets to GF mice. C The protective effect of L. mucosae and L. reuteri on intestinal damage caused by fecal microbiota in diarrheal piglets. D The protective effect of L. mucosae on intestinal damage caused by ETEC K88. E The protective effect of EVs of L. mucosae on intestinal damage caused by ETEC K88. F In vivo elimination of macrophages in mice. | PMC10244441 | 41522_2023_403_Fig1_HTML.jpg |
0.42915 | 1d5ba090a39f4f3da0c31eed76711f57 | Gut microbiome characteristics at the species level in neonatal diarrheal piglets vs healthy piglets.A Comparison of alpha diversity (Richness, Shannon, and Simpson) of gut microbiomes at the species level between healthy and diarrheal newborn piglets. B PCoA analysis of gut microbiomes between healthy and diarrheal newborn piglets at the species level; data were analyzed using PERMANOVA. C Histogram of the species composition of the top 20 bacterial species. D Differential bacteria species between the two groups. E Key species obtained from random forest analyses. F ROC analysis was performed for the random forest model. G The top 20 KEGG pathways enriched by differential KOs. H Fecal LPS content. n = 30. Data were expressed as the means ± SEM (H) and one-way ANOVA was performed, followed by LSD’s test (H). *P < 0.05, diarrhea group vs healthy group. | PMC10244441 | 41522_2023_403_Fig2_HTML.jpg |
0.487038 | 09dde0428303499d92a927cbc7394df7 | Evaluation of growth, systemic inflammation, and gut transcriptome characteristics in H-FMT GF mice vs D-FMT GF mice.A Body weights of mice during the experimental period. B Levels of WBC, LYM, NEU, MON, LYM%, NEU%, and MON% in the blood of experimental mice. C Volcano plot of differential genes in five intestinal segments. Blue denotes genes that are significantly downregulated in the D-FMT group, and red denotes genes that are significantly upregulated in the D-FMT group. D KEGG signaling pathways enriched in five intestinal segment differential genes. The sizes of the circles represent the number of genes enriched in the pathway, and the color is related to P_adjust. n = 10 for A, B; n = 4 for C, D. Data were expressed as the means ± SEM (A, B) and one-way ANOVA was performed, followed by LSD’s test (A, B). *P < 0.05: H-FMT group vs D-FMT group. | PMC10244441 | 41522_2023_403_Fig3_HTML.jpg |
0.477077 | 6dd9d9705f3e46689409191c28387c5b | Characteristics of the gut barrier, inflammatory response, and microenvironment in H-FMT GF mice vs D-FMT GF mice.A Ileum and colon tissue sections from H-FMT and D-FMT mice: the first row of the image show H&E staining, the second row shows PAS staining, and the third row shows AB staining (scale bar, 50 μm). B The levels of IL-1β, IL-6, IL-8, TNF-α, LPS, DAO, and D-LA in the serum. C The levels of IL-1β, IL-6, IL-8, TNF-α, LPS, DAO, and D-LA in ileum tissue. D The levels of IL-1β, IL-6, IL-8, TNF-α, LPS, DAO, and D-LA in colon tissue. E Levels of ZO-1, occludin, AKT, and NF-κB proteins and p-AKT and p-NF-κB in ileum and colon. F PCoA analysis at the species levels: data were analyzed using PERMANOVA; Species composition histogram of the top 20 species; The top 20 KEGG pathways enriched in differential KOs; Microbial bubble plots of the differences between H-FMT and D-FMT groups at the species level. G PLS-DA analysis of the metabolome; The heatmap of differential metabolites. The left side of the picture is the enriched group of metabolites, and the right side is the name of the metabolite and its corresponding class. n = 10 for A–D, F, G; n = 4 for E. Data were expressed as the means ± SEM (B–D) and one-way ANOVA was performed, followed by LSD’s test (B–D). *P < 0.05: H-FMT group vs D-FMT group. | PMC10244441 | 41522_2023_403_Fig4_HTML.jpg |
0.464587 | ecaafe96b9c54641814aeeb0ded059bb | The protective effect of L. mucosae and L. reuteri on intestinal damage caused by fecal microbiota in diarrheal piglets.A Body weights of mice were determined during the experimental period. B Ileum and colon tissue sections of experimental mice: the first row of the image show H&E staining, the second row shows PAS staining, and the third row shows AB staining (scale bar, 50 μm). C Levels of WBC, LYM, NEU, MON, LYM%, NEU%, and MON% in the blood of experimental mice. D The levels of IL-1β, IL-6, IL-8, TNF-α, LPS, DAO, and D-LA in the serum. E The levels of IL-1β, IL-6, IL-8, TNF-α, LPS, DAO, and D-LA in ileum tissue. F The levels of IL-1β, IL-6, IL-8, TNF-α, LPS, DAO, and D-LA in colon tissue. G Levels of ZO-1, occludin, AKT, and NF-κB proteins and p-AKT and p-NF-κB in ileum and colon. H Principal coordinates analysis at the ASV level; Relative abundance of the bacterial composition of the fecal microbiota of GF mice at the phylum and genus level; Bubble diagram for fecal microbial differential analysis at the genus level. n = 10 for A–F and H; n = 3 for G. Data were expressed as the means ± SEM (A and C–F) and one-way ANOVA was performed, followed by LSD’s test (A and C–F). *P < 0.05. | PMC10244441 | 41522_2023_403_Fig5_HTML.jpg |
0.454414 | 114dfd4b79b84fb8a86b9fb9d6d92de1 | The protective effect of L. mucosae on intestinal damage caused by ETEC K88.A Body weights of mice were determined during the experimental period. B H&E staining in the ileum and colon tissue sections of experimental mice; The villus length, crypt length, ratio of the villus to crypt length of the ileum, and histopathological score of the colon (scale bar, 50 μm). C The levels of IL-1β, IL-6, IL-8, TNF-α, LPS, DAO, and D-LA in the serum. D The levels of IL-1β, IL-6, IL-8, TNF-α, LPS, DAO, and D-LA in ileum tissue. E The levels of IL-1β, IL-6, IL-8, TNF-α, LPS, DAO, and D-LA in colon tissue. F Levels of ZO-1, occludin, AKT, and NF-κB proteins and p-AKT and p-NF-κB in ileum and colon. G Principal coordinates analysis at the ASV level; Relative abundance of the bacterial composition of the fecal microbiota of mice at the phylum and genus level; Bubble diagram for fecal microbial differential analysis at the ASV level. n = 6 for A–E and G; n = 3 for F. Data were expressed as the means ± SEM (A–E) and one-way ANOVA was performed, followed by LSD’s test (A–E). * P < 0.05. | PMC10244441 | 41522_2023_403_Fig6_HTML.jpg |
0.433998 | 53f7b4be6ae043b094ccab0a6555d3bd | The protective effect of EVs of L. mucosae on intestinal damage caused by ETEC K88.A TEM of isolated EVs (scale bar, 200 or 100 nm). B Size distribution of EVs analyzed by NTA. C Body weights of mice during the experimental period. D H&E staining of ileum and colon tissue sections of experimental mice; Measurements of villus length, crypt length, and villus to crypt length ratios of the ileum and the histopathological scores of the colon (scale bar, 50 μm). Levels of IL-1β, IL-6, TNF-α, LPS, DAO, and D-LA in E the serum, F the ileum tissue, and G the colon tissue. H Expression of iNOS, Arg1, ZO-1, occludin, AKT, and NF-κB proteins and levels of p-AKT and p-NF-κB in ileum and colon. I Principal coordinates analysis at the ASV level; Relative abundance of the bacterial composition of the fecal microbiota of mice at the phylum and genus level; Bubble diagram for fecal microbial differential analysis at ASV level. n = 3 for A and B; n = 6 for C, E–G, and I; n = 5/6 for D; n = 3 for H. Data were expressed as the means ± SEM (C–G) and one-way ANOVA was performed, followed by LSD’s test (C–G). *P < 0.05. | PMC10244441 | 41522_2023_403_Fig7_HTML.jpg |
0.489229 | ee509a1b915a4822b9c9decfa7555ea8 | Effect of macrophage clearance on L. mucosae-derived EVs in the alleviation of ETEC K88-induced intestinal injury.A Body weights of mice over the experimental period. B H&E staining of ileum and colon tissue sections of experimental mice; Measurements of villus length, crypt length, and the villus to crypt length ratio of the ileum, and histopathological scores of the colon (scale bar, 50 μm). The levels of IL-1β, IL-6, TNF-α, LPS, DAO, and D-LA in the C serum, D ileum tissues, and E colon tissues. F Principal coordinates analysis at the ASV level; Relative abundance of the bacterial composition of the fecal microbiota of mice at the phylum and genus level; Bubble diagram for fecal microbial differential analysis at the ASV level. n = 6 for A–F. Data were expressed as the means ± SEM (A–E) and one-way ANOVA was performed, followed by LSD’s test (A–E). *P < 0.05. | PMC10244441 | 41522_2023_403_Fig8_HTML.jpg |
0.465554 | e518470ca2054cc3b8b16d1bb5a07cf4 | Schematic diagram summarizing the findings in the present study. | PMC10244441 | 41522_2023_403_Fig9_HTML.jpg |
0.402796 | 448379b3cf4a4ad59d6c7f5ffd0c4945 | Correlations between cerebrospinal fluid (CSF) and plasma concentrations of soluble biomarkers measured in the current study.Correlations are shown for the full sample, and for subgroups of participants: people with HIV and Any Depressive Symptoms (maximum sample n = 33), people with HIV and No Depressive Symptoms (maximum sample n = 92), people without HIV and with Any Depressive Symptoms (maximum sample n = 9), and people without HIV and with No Depressive Symptoms (maximum sample n = 70). For correlations in the full sample, the strength of correlations are graded across a 3-point scale selected to range from the 5th and 95th percentiles of the correlation coefficients to optimise visual comparisons: −0.6 (in deep red), 0.0 (in light yellow), and +0.6 (in deep blue). For correlations in subgroups, the grading scale was: −1.0 (in deep red), 0.0 (in light yellow), and +1.0 (in deep blue). | PMC10244452 | 41398_2023_2489_Fig1_HTML.jpg |
0.391073 | f0fbf084210848c59f23ad5d39c127df | Mediation of the association between HIV status and Any Depressive Symptoms by adjusting for each biomarker separately.Sample sizes for which data were available for each biomarker are indicated at the x axis next to each bar. The dotted line marks a 10% reduction in the odds ratio, which represents our criterion for potential mediation. | PMC10244452 | 41398_2023_2489_Fig2_HTML.jpg |
0.437469 | f2b39f05e0bb49cfb077d5921fbc8579 | The sample interview note of one of the top hypothetical candidates, Sandra Jensen. Sandra scores four to five in all the five metrics. | PMC10244719 | fpsyg-14-1166225-g001.jpg |
0.484352 | 2413a56b0ba24fd3b757e0078be4d1b9 | The sample interview note of one of the worst hypothetical candidates, John Williamson. John scores one to three in all the five metrics. | PMC10244719 | fpsyg-14-1166225-g002.jpg |
0.439114 | 15df81eb01d84e0dbfcb41065ade4d05 | Summary of the experiment procedures. | PMC10244719 | fpsyg-14-1166225-g003.jpg |
0.437465 | b8f2cf10da2f4137ac70fb5d39486dcc | Summary of the interactions
between rhenium and corroles as currently
elucidated. Inset: this work. | PMC10245377 | ic3c00632_0001.jpg |
0.413581 | 17772b5b68294c6ab0d3ea31aef1f0f5 | UV–vis
spectra of (a) ReH[TpXPC]2 and (b) putative
{Re[TpXPC]2}− (X = H,
CH3, and OCH3) anions in anhydrous
toluene. | PMC10245377 | ic3c00632_0002.jpg |
0.558273 | 3991e981f6f34b8cb339e4bc7c1b6d78 | All-electron OLYP-D3/ZORA-STO-TZ2P-optimized geometry
of ReH[TPC]2: (a) side and top views; (b) selected distances
(Å). | PMC10245377 | ic3c00632_0003.jpg |
0.428418 | a86b825871bc491596513054d93c00fb | Nonphase-shift-corrected Fourier transforms of the Re L3-edge EXAFS data for ReH[TPC]2: data (black); fit (red).
The inset shows the EXAFS comparison. | PMC10245377 | ic3c00632_0004.jpg |
0.471609 | dbf04c1175574837bc068013aa816b50 | An in vivo system for targeting CtBP isoforms to gene promoters using CRISPRi.A) The fly CtBP(L) and CtBP(S) FLAG-tagged coding sequences were fused to the C-terminus of the S. pyogenes nuclease dead Cas9 (dCas9; D10A mutation in RuvC catalytic domain and H840A mutation in HNH catalytic domain), and placed under UAS expression. FLAG-tagged dCas9 was used as a negative control. Vertical lines in dCas9 represent the inactivating mutations. B)
Drosophila melanogaster expressing three trangenes were generated for tissue-specific expression of dCas9-CtBP effectors using GAL4-UAS. Flies express dCas9-CtBP chimeras in the nubbin expression pattern (wing pouch of L3 wing discs), with ubiquitous expression of two tandem gRNAs designed to target a single gene’s promoter. Flies used in experiments express one copy of each of the three transgenes. gRNA flies were designed by Harvard TRiP (Zirin et al. 2022). | PMC10245716 | nihpp-2023.05.19.541472v1-f0001.jpg |
0.43381 | 99346a5740344422a918d0f005ec3e1c | Targeting CtBP(S) and CtBP(L) to gene promoters leads to diverse phenotypic effects.For all crosses, ~100 wings from ~50 adults were used for analysis. Black arrows indicate the TSS, and red lines indicate gRNA binding sites relative to the target gene’s TSS. A) Using a non-targeting control gRNA (QUAS), expression of one copy of dCas9-CtBP effectors leads to >50% of adult wings with a phenotype, such as supernumerary bristles. Legend is in panel D. B) Targeting the E2F2/Mpp6 bidirectional promoter leads to severe morphological defects observed only from CtBP(S) targeting, with midler effects caused by CtBP(L). gRNA positions are relative to the E2F2 TSS. C) Targeting the InR promoter leads to phenotypes similar to the QUAS non-targeting control, suggesting little or no specific effect on this promoter. D) Targeting the Acf promoter leads to mild phenotypes, some of which are also observed with dCas9 alone, at lower frequency. CtBP isoforms lead to a higher penetrance of phenotypes than dCas9. | PMC10245716 | nihpp-2023.05.19.541472v1-f0002.jpg |
0.602714 | 8c7bae03e1134125821adaee6e802c4d | CtBP(S) is a more potent repressor of Mpp6 than CtBP(L) in wing discs.A) Schematic of the E2F2/Mpp6 bidirectional promoter, with the two tandem gRNAs indicated in gray. B) Targeting dCas9-CtBP(S) led to repression of E2F2 by about 25%, similar to the effect of dCas9 alone. dCas9-CtBP(L) recruitment to the same sites did not lead to any measurable repression. C) Targeting dCas9-CtBP(S) led to significant repression of Mpp6 (~50%), and this repression is greater than effects by dCas9 alone. dCas9 alone and dCas9-CtBP(L) led to about 20–25% repression. * p<0.05, ** p<.01 | PMC10245716 | nihpp-2023.05.19.541472v1-f0003.jpg |
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