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0.54824 | ae66ddad430b42718b72ad6e6db76577 | Longitudinal associations between antidepressants and WBC count. Asterisks (*) indicate associations passing multiple testing correction (<9.09 × 10−4). | PMC9892923 | cxp-2023-0009-01-4-528605_f2.jpg |
0.403164 | 5ee02535c4384de4a855f80b5c428511 | Longitudinal associations between (a) SSRI, (b) SNRI, (c) TCA, and (d) atypical use and complete blood count and creatinine laboratory values. Asterisks (*) indicate associations passing multiple testing correction (<9.09 × 10−4). | PMC9892923 | cxp-2023-0009-01-4-528605_f3.jpg |
0.462902 | 2af57ef7d60046af84c553ea4ad09261 | Longitudinal associations between antidepressant use and WBC values stratified by antidepressant indications (a) depression, (b) anxiety, and (c) chronic pain. Asterisks (*) indicate associations passing multiple testing correction (<9.09 × 10−4). | PMC9892923 | cxp-2023-0009-01-4-528605_f4.jpg |
0.483054 | 42a443f50ecf46799810e7bcc7726f2a | Schematic diagram of
the CO2 flooding apparatus. | PMC9893740 | ao2c06805_0002.jpg |
0.414332 | 3952f50e6a354c1baec2d47e21472508 | Diagenetic
minerals and several types of pores in the samples.
(A) Linear contacts of particles and intergranular pores in sample
FDK-3. (B) Kaolinite in sample FDK-2. (C) Chlorite in sample FDK-3.
(D) Mosaic shape ferrocalcite in sample FDK-5. (E) Combine pore with
irregular shape in sample FDK-2. (F) Intercrystalline pores of illite
in sample FDK-4. | PMC9893740 | ao2c06805_0003.jpg |
0.509178 | 9309d7f1990947dfa6bde1ba322f52bd | T2 distribution
of NMR in samples from
Chang 7 Member. (A–H) Samples FDK1–FDK8, respectively. | PMC9893740 | ao2c06805_0004.jpg |
0.512413 | 1b55690e4df14fc78dfce1fef82da19c | Plots of log(N(r)) versus log(T2) for two stages. (A–H)
Samples FDK1–FDK8,
respectively. | PMC9893740 | ao2c06805_0005.jpg |
0.413823 | 0b25a7ea17464239a5659865715d7acb | Relationship between
corrosion rate and ferrocalcite content. | PMC9893740 | ao2c06805_0006.jpg |
0.492161 | 38aee89cffdf43f68929476e062c7360 | Comparisons of T2 distribution curves
before and after CO2 flooding in the sample from Chang
7 Member. (A–H) Samples FDK1–FDK8, respectively. | PMC9893740 | ao2c06805_0007.jpg |
0.497694 | 304ca861c94b4f25bafb26d508b71896 | Plots of log(N(r)) versus log(T2) after CO2 flooding. (A–H)
Samples FDK1–FDK8, respectively. | PMC9893740 | ao2c06805_0008.jpg |
0.443748 | be489436ce0a4e67bfeb54813492fdaa | Comparison of pore distribution in (A) sample
FDK2 and (B) sample
FDK6. | PMC9893740 | ao2c06805_0009.jpg |
0.421565 | 6d869d2b60cd43e591bb896d52fed0f6 | Microscopic characteristics in different lithofacies
samples. (A)
Chlorite coats the particle in sample FDK3. (B) Kaolinite fill pores
in sample FDK1. (C) Intercrystalline pores connect with surrounding
pores in sample FDK6. (D) Ferrocalcite fills the pores in a large
cluster of crystals in sample FDK8. | PMC9893740 | ao2c06805_0010.jpg |
0.469451 | 1b76d600dea34e159e37abb1cb39ef65 | Mineral content before and after CO2 flooding in (A)
CL lithofacies and (B) CA lithofacies. | PMC9893740 | ao2c06805_0011.jpg |
0.408146 | 56262c48b15e46cd9e0aa9774071b5c3 | Schematic
diagrams of mineral changes after CO2 flooding
in CL and CA lithofacies. (A) Mineral distribution in CL lithofacies
before CO2 flooding. (B) Newly formed minerals fill the
pores after CO2 flooding. (C) Ferrocalcite fills the pores
in CA lithofacies before CO2 flooding. (D) Dissolution
of ferrocalcite and new flow paths after CO2 flooding. | PMC9893740 | ao2c06805_0012.jpg |
0.492741 | db2704ebed2547558fae27dec5b66435 | Best overall response (A), PFS (B), OS (C), MRD (D), and blood cell immunophenotyping results at baseline and day 1/cycle 3 (predose) (E). (A–D) Patients included in efficacy population (n = 15): Isa 10 mg/kg-VCd, n = 12; Isa 20 mg/kg-VCd, n = 3. All = all patients in the efficacy population. MRD was evaluated in patients with ≥VGPR by NGF and NGS methods at 10−5 and MRD negativity rate determined by combining both methods in the case of at least 1 method yielding negative results and the other method showing no positive result at the same time. (E) Patients included in baseline population: Isa 10 mg/kg–VCd, n = 13; Isa 20 mg/kg–VCd, n = 4 and in on-treatment population: Isa 10 mg/kg-VCd, n = 10; Isa 20 mg/kg-VCd, n = 2. Results expressed as percentage of leukocytes. C = cyclophosphamide; C3D1 = cycle 3 day 1; CR = complete response; d = dexamethasone; Isa = isatuximab; MRD = minimal residual disease; NGF = next-generation flow; NGS = next-generation sequencing; NK = natural killer; ORR = overall response rate; OS = overall survival; PFS = progression-free survival; PR = partial response; sCR = stringent CR; SD = standard deviation; T-reg = regulatory T cell; V = bortezomib; VGPR = very good partial response. | PMC9894356 | hs9-7-e829-g001.jpg |
0.437816 | 51a7454ba0b44a5cac5ecd1f24aeb506 | Study 1: Summary of Path Analyses.Note. Unstandardized path coefficients are reported. Dashed
lines represent paths that are not significant. Control variables were included
in the model, but their coefficients are not reported here. The model without
control variables provides substantively equivalent results and does not change
the interpretation of the relationships between variables (see Supplemental
Online Materials).*p < .05. **p < .01. | PMC9895284 | 10.1177_19485506221077858-fig1.jpg |
0.448241 | 6d486faa5c26439686e73959b29d522d | Study 2: Summary of Path Analyses.Note.a 1 = High Gratitude, 0 = Low Gratitude.
Unstandardized path coefficients are reported. Dashed lines represent
nonsignificant paths. Control variables were included in the model, but
their coefficients are not reported here. The model without control
variables provides substantively equivalent results and does not change
the interpretation of the relationships between variables (see
Supplemental Online Materials).*p < .05. **p < .01. | PMC9895284 | 10.1177_19485506221077858-fig2.jpg |
0.40868 | 553d88fb12ae43cfbd22cc4f777f7f9d | Molecular design and interaction between FTPA and perovskite.a Molecular structure design of FTPA, and schematic diagram of the possible phase evolution of the nucleation and crystallization of FA-based mixed anion perovskites (FA0.95MA0.05Pb(I0.95Br0.05)3) during the film-forming process with (w) or without (w/o) FTPA. In the control perovskite film, the complicated intermediate phases, MA2Pb3I8·2DMSO and δ-FAPbI3, caused two competition pathways of crystal-nucleation as shown in Eqs. (1) and (2), and finally resulted in a low crystal orientation with δ-phase and PbI2. In contrast, perovskite film with FTPA restrained the formation of the intermediate phases and formed a hydrogen-bonding polymer network in the perovskite films which induced stable and preferred orientation of α-FAPbI3. b A comparison of 1H NMR spectra of FAI, FTPA/FAI, and FTPA/FAI/ PbI2. The photos are the FAI solution and FTPA/FAI mixture. Theoretical calculation show that the hydrogen bonds F⋯HN and O⋯HN formed between FTPA and FAI have a strength of −29.37 kcal mol−1. c FTIR spectra of the FAI, FTPA/FAI, and FTPA/FAI/PbI2. d Pb 4 f XPS spectra of the perovskite films of control and with FTPA, respectively. | PMC9895431 | 41467_2023_36224_Fig1_HTML.jpg |
0.393102 | 85c7608a1c4e4faeb30b7cfb4394704f | In-situ monitoring of intermediate phase, nucleation, and crystallization process of the control and FTPA based perovskite films during spin-coating and annealing procedures.a In-situ tracking of X-ray diffraction of the perovskite films during three processes: wet perovskite film without (w/o) anti-solvent during spin-coating, wet perovskite film with (w) anti-solvent during spin-coating, and perovskite films annealed at 100 °C for various times. α and δ symbols indicated α-phase and δ-phase perovskite. b Optical microscopy images of the wet perovskite films without antisolvent during the spin-coating process. MA2Pb3I8·2DMSO film was prepared by perovskite of MAI/PbI2 (1:1 mol%) and δ-FAPbI3 was prepared by perovskite of FAI/PbI2 (1:1 mol%). c In-situ UV absorption spectra during the spin-coating process. d In-situ GIWAXS patterns during spin-coating process. e In-situ UV absorption spectra during the initial annealing process at 100 °C. f GIWAXS patterns of perovskite films after annealing 1 h. | PMC9895431 | 41467_2023_36224_Fig2_HTML.jpg |
0.457831 | 1864dbb5c4204f85addfa0a963445bdd | Morphology, carrier extraction and energy level behaviors of the control, B-FTPA and BS-FTPA perovskite films.B-FTPA is the perovskite film with FTPA in the bulk, and BS-FTPA is the film further spin-coated 2 mg mL−1 FTPA and annealed for in-situ polymerizing on the surface of the B-FTPA. a Top-view SEM images. b HR-TEM image clearly shows the polymerized FTPA surround the grain boundaries of perovskite. J-V curves of c the electron-only device (FTO/SnO2/perovskite/PCBM/Ag) and d the hole-only device (FTO/PEDOT PSS/perovskite/Spiro-OMeTAD/Au) measured by SCLC model. The J-V curves can be divided into three regions that are the Ohmic region, trap-filled limit region (TFL), and Child’s region. The electron and hole trap density (Nt) are shown in Fig. 3c, d, respectively. e Time-resolved PL spectra. f Valence-band region and photoemission cut off energy of the UPS spectra. g Energy level scheme of the devices. Conduction band minimum (EC), Valence band maximum (EV), and Fermi level (EF). | PMC9895431 | 41467_2023_36224_Fig3_HTML.jpg |
0.43941 | 7d8afcf3cc0b4b25a948ed2ea409ceab | Photovoltaic characteristics and stability of PSCs based on control, B-FTPA and BS-FTPA.a A cross-sectional SEM images showed the device architectures: FTO/SnO2/perovskite/Spiro-OMeTAD/Au for control, FTO/SnO2/B-FPTA perovskite (with FTPA 43.13 mg mL−1 in the bulk)/FTPA (2 mg mL−1)/Spiro-OMeTAD/ Au for BS-FTPA; ToF-SIMS cross-section images presented the element distribution in BS-FTPA. C12H10N- signals attributed to the diphenylamine branches of FTPA and Spiro-OMeTAD; F- signals corresponding to the Li-TFSI in Spiro-OMeTAD solution, FTPA in bulk and surface of perovskite, and FTO; the PbI3- signals corresponding to the perovskite. b
J-V curves of the champion PSCs. c IPCE spectra of the devices integrated over the AM 1.5 G (100 mW cm−2) solar spectrum. d Semilog plot of IPCE at the absorption onset for BS-FTPA based PSCs, measured using FTPS at Jsc. An Urbach energy (Eu) of 14.5 meV can be obtained from the red line, a sharp absorption edge. e Statistical device data based on 30 devices. f Device stability of unencapsulated devices under1-sun illumination at 23 ± 2 °C in a nitrogen atmosphere (ISOS-LC-1). g Device stability of unencapsulated devices held at 25 ± 5 °C and 50 ± 10% relative humidity (RH) (ISOS-D-1). h Contact angle of perovskite films, and photographs of perovskite films dipped in water, FTO/SnO2/perovskite for control and FTO/SnO2/B-FTPA/FTPA for BS-FTPA. i Device stability of unencapsulated devices under 65 ± 3 °C thermal aging (ISOS-T-1). All of the error bars in Fig. 4f, g and i represent the standard deviation for six devices. | PMC9895431 | 41467_2023_36224_Fig4_HTML.jpg |
0.449018 | 3e42a8bd4e44428386ed275c7eabbb41 | Liver structure and zonation. A Schematic diagram of hepatic lobule and zonation. B A summary of hepatic zonation and its main function. Adapted from Halpern K.B.et al. 2017 | PMC9895469 | 13619_2022_152_Fig1_HTML.jpg |
0.43474 | 4d49860cd11e46869d32fb34359c5cea | Significant host biomarker concentrations determined in colon tissue homogenates of C3H/HeOuJ mice from the EPC experiment. a Cyanocobalamin supplementation enhanced IL-12/23p40 and IL-17A cytokines of naïve mice, with a higher trend of IL-4 levels (P = 0.06) compared to control. bC. rodentium challenge led to a significant increase in IFNγ, IL-10, IL-17A, and GM-CSF in the cyanocobalamin-supplemented mice (n = 8; *P < 0.05, **P < 0.01, ***P < 0.001) | PMC9896722 | 40168_2023_1461_Fig10_HTML.jpg |
0.514985 | aba4229bf03641f093540ff2f0514e2e | Cyanocobalamin-induced dysbiosis increased the production of the p40 subunit in colon tissues of mice prior to pathogen challenge. Pre-infection levels of IL-12/23p40 in colon tissues were directly related to microbiota structure and independent of related mice genotypes. a Gene expression was significantly higher for IL12B, the p40 subunit coding gene, but not for the IL-12A (p35) gene (n = 8) in the EPC experiment. b The SURV experiment did not display the increase in IL-12/23p40 (n = 5–6), nor did c germ-free C57BL/6J mice (n = 4; *P < 0.05, **P < 0.01, ***P < 0.001). d Cyanocobalamin and methylcobalamin supplementation at 10 μg/ml and 40 μg/ml increased IL/23p40 protein levels in the colon of conventional C57BL/6J mice (n = 6; P < 0.05) compared to control | PMC9896722 | 40168_2023_1461_Fig11_HTML.jpg |
0.541171 | ac8cb108d6994de4b7096c0f46f4b96a | The impact of cyanocobalamin supplementation on survival and early onset of C. rodentium infection in C3H/HeOuJ mice. a Supplementing cyanocobalamin in drinking water increased cecal and colon levels of cobalamin by ~1000 times (n = 15; *P < 0.05, **P < 0.01). b Daily fecal enumeration of C. rodentium in the EPC experiment indicated increased colonization burden at day 2 postinfection (D2PI) and D3PI from cyanocobalamin supplementation (n = 8; #P < 0.10, * P < 0.05). c Enumeration of C. rodentium at D5PI in the ileum and cecum was more consistent with cyanocobalamin supplementation, but colonization levels were similar (n = 8). d Consistent with the more rapid colonization, the SURV experiment revealed an earlier onset of mortality, reducing mice survival over the first 10-day postinfection (n = 9; P < 0.05; Mantel-Cox test). e Colon pathology scores at D5PI in naïve and infected mice show that cyanocobalamin significantly increased mucosal and epithelial damage (*) compared to infected control mice (n = 8; P < 0.05; limit of detection (LOD)) | PMC9896722 | 40168_2023_1461_Fig1_HTML.jpg |
0.517086 | 48d9757f9e874801b5498be98c0ffe79 | Microbiota analyses of naïve and infected (inf_) mice from the EPC experiment. Principal coordinate plots of the ileum, cecum, and colon microbiota are based on the weighted and unweighted UniFrac dissimilarity metric. Distinct clustering was determined by unweighted UniFrac in the cecum and colon (Additional file 1 Table S2). Cyanocobalamin supplementation significantly reduced alpha diversity (observed and PD) in the colon (n = 7–12; P < 0.05) | PMC9896722 | 40168_2023_1461_Fig2_HTML.jpg |
0.453673 | 706c02e9ccdb46168f7604c7e8b14bb8 | DESeq2 differential analyses of microbial communities in mice from the EPC experiment. Cyanocobalamin supplementation altered the Firmicutes population throughout the GI tract. The control group had a greater abundance of Firmicutes, including Lachnospiraceae species and Clostridia vadinBB60 group bacterium in the cecum and colon a preinfection and b postinfection (n = 6–8; only ASVs with a P-value less than 0.05 were plotted; adjusted P-value was used for significance; bolded taxa represent a trend (P < 0.10); *P < 0.05, **P < 0.01, *** P < 0.001) | PMC9896722 | 40168_2023_1461_Fig3_HTML.jpg |
0.447111 | b9bc2f06f5054b45b9693aab506cb0bb | Comparison of the colonic microbial communities in naïve C3H/HeOuJ mice from the SURV and EPC experiments. a Unweighted UniFrac PCoA plot and b weighted UniFrac comparison show a similar pattern in microbial community clustering (Additional file 1 Table S2). c The changes were associated with a consistent reduction in alpha diversity (Observed and PD) regardless of experiment (n = 10–12; P < 0.05). Differential expression determined by DEseq2 analysis also showed that the Firmicutes populations (Clostridia vadinBB60 group) were impacted by cyanocobalamin in both mice harboring d SURV and e EPC gut microbiota (n = 10–12; bolded taxa represent a trend (P < 0.10; *P < 0.05, **P < 0.01, ***P < 0.001) | PMC9896722 | 40168_2023_1461_Fig4_HTML.jpg |
0.434154 | 8e6f18eefb0c406786444f35d18e4bac | Cecal microbiota analysis of the 16S rRNA gene identified by SAMSA2 metatranscriptome analysis from the EPC experiment. Distinct clustering of microbial communities in a unweighted but not b weighted UniFrac PCoA plots (Additional file 1 Table S2). c Alpha diversity as determine by Observed, Shannon, and PD metrics showed that diversity (PD only) increased postinfection for cyanocobalamin-supplemented mice compared to control (P < 0.05). Differential expression analysis using DEseq2 of microbial taxa confirmed that the Firmicutes populations were altered from cyanocobalamin supplementation in d naïve and e infected mice (n = 6–8; bolded taxa represent a trend (P < 0.10); ***P < 0.001) | PMC9896722 | 40168_2023_1461_Fig5_HTML.jpg |
0.395811 | 9588eb9d45c44c9ea5b47e0718e05a82 | DESeq2 differential expression analyses of cecal metatranscriptome from the EPC experiment. a Naïve and bC. rodentium-challenged mice (inf_) supplemented with cyanocobalamin displayed altered functional activities related to metabolism (citrate:sodium symporter) and motility (flagellin domain protein) and confirmed to be from the Lachnospiraceae family (n = 8; bolded taxa represent a trend (P < 0.10); *P < 0.05, **P < 0.01) | PMC9896722 | 40168_2023_1461_Fig6_HTML.jpg |
0.3992 | 9517b0199e984877b4d09794cd2eac45 | SEED subsystems level 3 DESeq2 analysis of the C3H/HeOuJ cecal metatranscriptome from the EPC experiment. Cyanocobalamin supplementation increased pathways related to gram-negative lipopolysaccharide assembly while decreasing genes related to the competence of gram-positive bacteria in a naïve mice but not in bC. rodentium-challenged mice (n = 8; bolded taxa represent a trend (P < 0.10); *P < 0.05) | PMC9896722 | 40168_2023_1461_Fig7_HTML.jpg |
0.435506 | 04e0ab8dafd04e0295193c91721a83c3 | DESeq2 differential expression analyses of Lachnospiraceae and Citrobacter-specific functional activity from the EPC experiment. Prior to infection, the functional activity of the Lachnospiraceae family (a) shows that cyanocobalamin treatment increased the expression of numerous genes, including fibronectin type 3 domain-containing protein and serine/threonine transport SstT. b After exposure to C. rodentium, the Lachnospiraceae family members of the inf_CNCbl40 group displayed distinct activities compared to inf_CON group. Citrobacter-specific gene expression (c) was more pronounced in the inf_CNCbl40 group than inf_CON with notable signals of increased virulence gene expression, while control mice had more family 31 glucosidase activity (n = 8; bolded taxa represent a trend (P < 0.10); *P < 0.05, **P < 0.01) | PMC9896722 | 40168_2023_1461_Fig8_HTML.jpg |
0.465803 | ab42e9e788154a09b595b922dbeaa03b | In vitro competition assay of C. rodentium and B. thetaiotaomicron under physiological relevant concentrations of cyanocobalamin. Cyanocobalamin alone was unable to directly alter C. rodentium growth or virulence. a Enumeration of C. rodentium and B. thetaiotaomicron grown in competition for 6 h anaerobically and b of C. rodentium grown alone. Expression of gene related to virulence (Ler, Tir, and EspA) did not differ between treatments when C. rodentium was grown in c competition or d alone at different concentrations of cyanocobalamin (n = 6; P < 0.05) | PMC9896722 | 40168_2023_1461_Fig9_HTML.jpg |
0.429182 | 5fd5f877deb4485e8ef6cf7cae42ee83 | SEM images of Au cube (a), Au octahedron (b), Au tetradecahedron (c), Ag NPs (d), Au NRs (e) and Au NPs (f). | PMC9897048 | d2ra07216e-f1.jpg |
0.398234 | d775797c3a4548d8bd8714e913348897 | (a)Reproducibility characterization of gold nanorod substrates for detection of 10−11 M CV; (b). relative standard deviation (RSD) at the 1619 cm−1 characteristic peak of the CV molecule. | PMC9897048 | d2ra07216e-f2.jpg |
0.436226 | df9e7320bb48440197b43e5b545c1cb5 | Principle causing the solvent to move toward the smaller gaps of the nanocapillary pumping model. In the schematic diagram of Au NRs films, 1,2 and 3 represent small gaps between nanorods. Partial enlargement of the gap between two nanorods (b) and multiple nanorods (c). r1 and r2 represent the radius of curvature at different interstices, and P1 and P2 represent the pressures generated by the liquid at different interstices. | PMC9897048 | d2ra07216e-f3.jpg |
0.522775 | 2b991b9276874263b1c403b0c3ca97f2 | SERS spectra at different concentrations. (a) GTX with concentrations ranging from 10−6 to 10−9 M. (b) NOD with concentrations ranging from 6 × 10−5 to 6 × 10−7 M. A plot of SERS intensity versus logarithmic (c) GTX, (d) NOD concentration for the band at 1609 and 1001 cm−1, respectively. | PMC9897048 | d2ra07216e-f4.jpg |
0.445172 | 621f15eb481f44b59ff375aab0eeb228 | Psychosocial risk-factor screening questions and required response flow to qualify for the study. | PMC9897276 | joem-65-e93-g001.jpg |
0.592445 | 531ecd719705450aa11fac50e1b0cbad | Participant flow, from screening to onboarding on the Wysa app. | PMC9897276 | joem-65-e93-g002.jpg |
0.429141 | 4aee0a383910485486f3f241b5e3c371 | The total number of sessions completed by all users across tools on the app. | PMC9897276 | joem-65-e93-g003.jpg |
0.432803 | 76c974e195b34341b7eb1bd876bebf99 | Strategies to reduce regulatory cells in cancer patients. Several strategies alone or combining the targeting of different biochemical pathways have been reported to modulate regulatory cells in cancer patients. Some approaches aim to reduce the frequency, function and extent of blocking mobilization, while others focus on enabling phagocytosis, polarization, or potentiating differentiation. Blue crosses indicate potentiation/increase; forbidden sign indicates blockade/reduction | PMC9898962 | 12943_2023_1714_Fig1_HTML.jpg |
0.484198 | b563df0712f74a17ba16a60287a428f9 | Effect of immunotherapy on Tregs. Several ICIs and other treatments can directly affect the number and function of regulatory T cells consequently, improving anti-tumoral function and preventing tumor growth. Some treatments act by reducing the number of Tregs (by antibody dependent cellular citotoxicity, ADCC) while others affect their suppressive activity or positively modulate the functions of CD8 T, NK cells and dendritic cells. The modulation towards pro-inflammatory cytokines and the increase in the CD4 + effector/Treg ratio are other mechanisms by which immunotherapy can potentiate the immune response within the tumor microenvironment. Created with Biorender.com | PMC9898962 | 12943_2023_1714_Fig2_HTML.jpg |
0.49133 | cf82c0c5618e49e8869c36b1e8da221b | Effect of immunotherapy on MDSCs. The figure depicts different treatments that can modulate MDSC expansion and function. The drugs affect the frequency of MDSCs, reduce MDSC suppressive activity, improve CD8 T cell function, and modulate the release of cytokines from the tumor. A combination of these therapies may have a synergistic effect that promotes better outcomes. Created with Biorender.com | PMC9898962 | 12943_2023_1714_Fig3_HTML.jpg |
0.505114 | 460689512a724b44a978f3097550f14b | Effect of immunotherapy on TAMs. The figure displays treatments that aim to prevent the expansion of TAMs, consequently enhancing the anti-tumoral effect. The drugs work by promoting apoptosis (which reduces TAM frequencies)and TAM differentiation to M1 macrophages, and by blocking TAM mobilization, infiltration and metastasis. On the other hand, there is an increase in pro-inflammatory cytokine release and a reduction in the phagocytic activity of macrophages. Also, the use of these treatments combined with chemotherapy or other ICIs may be synergistic, bursting the immune response against the tumor. Created with Biorender.com | PMC9898962 | 12943_2023_1714_Fig4_HTML.jpg |
0.509718 | f3ae83c274054b3fbdf6f5216c4fc3bd | Lunasin inhibited the viability of breast cancer cells. (a) MCF-10A cells, (b) MDA-MB-231 cells, and (c) MCF-7 cells were treated with various doses of lunasin for 24, 48, and 72 h, and the cell viability was determined by MTT assay. The values of the data are presented as the mean ± SEM from at least three independent experiments. Statistical analysis was performed by independent sample t-test; significant differences are displayed as follows: *P < 0.05 for 24 h; #P < 0.05 for 48 h; †P < 0.05 for 72 h, which indicates lunasin treatment compared to the control group. | PMC9899045 | FNR-67-8991-g001.jpg |
0.416982 | 72a456bd2fba4fac9027401ea69e1ddf | The effects of lunasin on carcinogenic-related gene expression and protein secretion in breast cancer cells. Carcinogenic-related gene expression is shown in (a) MDA-MB-231 cells and (b) MCF-7 cells treated with lunasin for 24 h, and the gene expression was measured by qPCR. The specific gene expression is shown as the fold change compared with the control group. Cytokine production is shown in (c) MDA-MB-231 cells and (d) MCF-7 cells treated with lunasin for 24 and 48 h, and the supernatants were analyzed by ELISA. The value of data is presented as mean ± SEM, and statistical analysis was done by independent sample t-test; significant differences of control displayed in *P < 0.05. | PMC9899045 | FNR-67-8991-g002.jpg |
0.46284 | af5af573c7fd4bcb878e44afe6c4bc86 | The effects of lunasin on estrogen receptor and aromatase gene expression and aromatase activity in breast cancer cells. Gene expression is shown in (a) MDA-MB-231 cells and (b) MCF-7 cells treated with lunasin for 24 h, and the gene expression was measured by qPCR. The specific gene expression is shown as the fold change compared with the control group. The aromatase activity was determined in (c) MDA-MB-231 cells and (d) MCF-7 cells treated with lunasin for 48 h. The value of data is presented as mean ± SEM, and statistical analysis was done by independent sample t-test; significant differences of control displayed in *P < 0.05. | PMC9899045 | FNR-67-8991-g003.jpg |
0.452253 | 3455e51777fd417c844dc2b8c4601c33 | The effects of β-estradiol and lunasin on cell viability in breast cancer cells. (a) MCF-10A cells, (b) MDA-MB-231 cells, and (c) MCF-7 cells were treated with various doses of β-estradiol (E2) for 24 and 48 h. Lunasin affected the viability of (d) MCF-10A cells, (e) MDA-MB-231 cells, and (f) MCF-7 cells treated with 20 nM E2 for 24 and 48 h, and the cell viability was determined by the MTT assay. The data are presented as the mean ± SEM from three independent experiments. Statistical analysis was performed by independent sample t-test; significant difference displayed in symbols: *P < 0.05, lunasin treatment versus control without E2; #P < 0.05, lunasin treatment versus control with E2. | PMC9899045 | FNR-67-8991-g004.jpg |
0.463361 | 4ff942dc2b824c99b94686c1331c41f6 | Cell vitality of breast cancer cells treated with lunasin. MDA-MB-231 and MCF-7 cells were treated with lunasin for 48 h, MCF-7 cells were treated with or without 20 nM E2 at the same time, and the cells were collected. The cell vitality was analyzed: (a) definition of histogram plots and (b) fluorescent intensity plots, (c) the proportion of MDA-MB-231 cells, and (d) the proportion of MCF-7 cells. This figure represents the analytic pattern by the NC-3000, and the experiment was performed in at least three independent experiments. | PMC9899045 | FNR-67-8991-g005.jpg |
0.407146 | e3a5b63e04084be7bb5e67d3b2421b6a | Cell apoptosis of breast cancer cells treated with lunasin. MDA-MB-231 and MCF-7 cells were treated with lunasin for 48 h, MCF-7 cells were treated with or without 20 nM E2 at the same time, and the cells were collected. Cell apoptosis was analyzed: (a) the definition of histogram plots and (b) fluorescent intensity plots, (c) the proportion of MDA-MB-231 cells, and (d) the proportion of MCF-7 cells. The figure represents the analytic pattern by the NC-3000, and the experiment was performed in at least three independent experiments. | PMC9899045 | FNR-67-8991-g006.jpg |
0.521636 | 110684eda89b4392a9da9c2b4d73c5ce | Proposed scheme of the possible mechanism by which lunasin suppresses the growth of breast cancer cells. Lunasin regulated inflammatory mediators, estrogen receptors gene expression, and aromatase activity, resulting in apoptosis induction and decreased cell viability and contributing to suppressing breast cancer progression. Abbreviations: COX-2, Cyclooxygenase-2; ER, estrogen receptor; IL, interleukin; PGE2, prostaglandin E2; VEGF, vascular endothelial growth factor. | PMC9899045 | FNR-67-8991-g007.jpg |
0.490719 | 8d28bbf28d3649e599673b9a8ee5bcc8 | Comparison of linear regression models between Vcmax estimated from full A–Ci curves against apparent photosynthetic capacity estimated by the ‘one-point method’ (Vʹcmax; Equation 2) (A), and the modified version including the temperature dependency (Vʹcmax–ρ; Equation 5) (B). The light gray line is the 1:1 relationship. | PMC9899412 | erac466f0001.jpg |
0.378464 | 164c09ae09a240728eee3814634efb34 | Residuals of maximum carboxylation rate, Vcmax, estimated from A–Ci curves estimated from apparent maximum carboxylation capacity, Vʹcmax (Equation 2) using the estimated Rday:Vcmax ratio (A), and using the temperature-dependent scaling factor (B) as a function of leaf temperature. | PMC9899412 | erac466f0002.jpg |
0.583958 | 1f0e3272c87b4f4baff7d2a047c4eb1a | The chalcogen-bonded chains in the crystal structure of ebselen 1. | PMC9899513 | c-79-00043-fig1.jpg |
0.535179 | b941c4b8ee9e410ba6f2772bcbb4d27c | The hydrogen-bonding interactions in the structure of 2-Me+ tosylate trihydrate. The undulating chain extends along the a axis. | PMC9899513 | c-79-00043-fig10.jpg |
0.583366 | f552cd6b5c904aa0814cb4c273d11ac8 | Hydrogen bonding, chalcogen bonding and π–π stacking in the structure of 2-Me+ tosylate trihydrate. | PMC9899513 | c-79-00043-fig11.jpg |
0.496522 | 7c38349a53f8457baf6f7cb8e530dbd4 | Experimentally determined electrostatic potential for compound 2 mapped onto the 0.05 a.u. isosurface. | PMC9899513 | c-79-00043-fig12.jpg |
0.525664 | fda97c8c85f8462bb6d8f404549a3bd3 | Critical points (CPs) in the vicinity of the Se atom for compound 2. (3,−1) CPs are shown in red (intramolecular) and green (intermolecular), and (3,+1) CPs are shown in blue. | PMC9899513 | c-79-00043-fig13.jpg |
0.393972 | 8e86f2a01d544fd49b19e0bf607219a5 | Electron localization function (ELF) in the plane of the ring system for compound 2. | PMC9899513 | c-79-00043-fig14.jpg |
0.422926 | 05b7db2757c54675b492b1d83103078d | ELF plotted along the N1—Se1—N2 and C1—Se1—O1 bonds for compound 2. BCPs are shown as vertical dashed lines. | PMC9899513 | c-79-00043-fig15.jpg |
0.554532 | 97a88029c514484f91fcc8ffba11d80a | Difference electron residuals from the multipole refinement of compound 2 with 0.05 e Å−3 contours. Red contours are positive, blue are negative and dashed grey are zero. | PMC9899513 | c-79-00043-fig2.jpg |
0.559737 | 10a53f58db6a4941aecda1b9d2f1cc6a | The molecular structure of compound 2, showing 50% probability displacement ellipsoids. | PMC9899513 | c-79-00043-fig3.jpg |
0.623832 | 2188dea46e004177b18c79a970624e63 | The chalcogen-bonded chains of compound 2 propagating along the ac diagonal. | PMC9899513 | c-79-00043-fig4.jpg |
0.528869 | 524604ba77bd4365a2702d3bc5a7fa8c | The N⋯Se and O⋯Se chalcogen-bonding interactions and π–π stacking interactions in the structure of compound 2. | PMC9899513 | c-79-00043-fig5.jpg |
0.501468 | f570cf5e0a6646a396fda375c3f5b589 | Partial packing diagram of compound 2, showing the three-dimensional network built up of chalcogen-bonding interactions and π–π stacking interactions, viewed parallel to the (010) plane. | PMC9899513 | c-79-00043-fig6.jpg |
0.612432 | 5bdfdf43a1a84bbdbf3c510c94563f09 | The molecular structure of 2-Me+ iodide, showing 50% probability displacement ellipsoids. | PMC9899513 | c-79-00043-fig7.jpg |
0.461878 | 3bcba1d713974961a041920b30b938c1 | The π–π stacking interactions in the structure of 2-Me+ iodide. | PMC9899513 | c-79-00043-fig8.jpg |
0.529147 | 6340ba922e614812857facfeaed33a31 | The molecular structure of 2-Me+ tosylate trihydrate, showing 50% probability displacement ellipsoids. | PMC9899513 | c-79-00043-fig9.jpg |
0.44623 | f3ec8c64a0f34d5e8669940f37485c2b | Growth curves of S. costatum
(A) and P. globosa
(B) in +P and −P groups. Error bars show the mean ± standard error (SE) of triplicate treatments. Superscripts indicate significant differences between +P group and −P group according to a two-way ANOVA with a post-hoc test (**p < 0.01, *p < 0.05). | PMC9899818 | fmicb-14-1085176-g001.jpg |
0.436982 | 1654500703d0439382d341a8a4041bb8 | Maximum photochemistry efficiency (Fv/Fm) of S. costatum
(A) and P. globosa
(B) in +P and −P groups. Error bars show the mean ± standard error (SE) of triplicate treatments. Superscripts indicate significant differences between +P group and −P group according to a two-way ANOVA with a post-hoc test (**p < 0.01, *p < 0.05). | PMC9899818 | fmicb-14-1085176-g002.jpg |
0.502269 | 3c69c8a9662d4551953a091162d2aa9f | The maximum electron transport rate ETRmax (A: S. costatum, B: P. globosa), light-harvesting efficiency alpha (C: S. costatum, D: P. globosa), and the point of light saturation Ik (E: S. costatum, F: P. globosa) in +P and −P groups. Error bars show the mean ± standard error (SE) of triplicate treatments. Superscripts indicate significant differences between +P group and −P group according to a two-way ANOVA with a post-hoc test (**p < 0.01, *p < 0.05). | PMC9899818 | fmicb-14-1085176-g003.jpg |
0.428221 | 0a31089f20e04d75b88b812e7e1f0a83 | Normalized chlorophyll a fluorescence transient of S. costatum
(A) and P. globosa
(B) in −P group for various periods of time plotted by the mean of triplicate (Error bars omitted). Differential curves of ΔVt (obtained by subtracting the curve on day 0 from the samples for various periods of time) in S. costatum
(C) and P. globosa
(D) under P-limited condition. | PMC9899818 | fmicb-14-1085176-g004.jpg |
0.380287 | 3551a03f0be1452f81ed16994054a565 | Photosynthetic parameters (relative to day 0) derived by the JIP-test of S. costatum
(A) and P. globosa
(B) under P-limited condition. φE0 = ET0/ABS = (Fv/Fm) × (1 – VJ), which is the quantum yield of electron transport to intersystem electron acceptors at t = 0; RE0/RC = (RE0/ET0) – (ET0/RC), denoting the reduction in end acceptors on the PSI electron acceptor side per RC at t = 0; RC/CS0 = φP0 × (ABS/CS0) × (VJ/M0), reflecting the amount of active PSII RCs per CS at t = 0. Error bars are mean ± standard error (SE) of triplicate treatments. Superscripts indicate significant differences between +P group and − P group according to a two-way ANOVA with a post-hoc test (**p < 0.01, *p < 0.05). | PMC9899818 | fmicb-14-1085176-g005.jpg |
0.478057 | de6684a1060a4290ac978d1c83ccabd0 | Normalized QA− reoxidation kinetic curves of S. costatum and P. globosa in +P and −P groups for various periods of time. Fluorescence decay in the absence of 3-(3,4-dichlorophenyl)-1,1-dimethylurea (DCMU) of S. costatum
(A) and P. globosa
(B). Fluorescence decay in the presence of 20 μM DCMU of S. costatum
(C) and P. globosa
(D). Each value represents the mean of the results from triplicates (Error bars omitted). | PMC9899818 | fmicb-14-1085176-g006.jpg |
0.463466 | 0fff4166f0e04b98afc858b5e9b00a33 | Proportion of PSIIX centers of S. costatum
(A) and P. globosa
(B) in +P and −P groups for various periods of time. Error bars show the mean ± standard error (SE) of triplicate treatments. Superscripts indicate significant differences between +P group and −P group according to a two-way ANOVA with a post-hoc test (**p < 0.01). | PMC9899818 | fmicb-14-1085176-g007.jpg |
0.441931 | e20f52cf866e459aa7033eccc0effad7 | Immunoblot analysis of PSII proteins and stained with Coomassie blue (CB). (A) Immunoblot analysis was performed using antibodies specific to D1. (B) Immunoblot analysis was performed using an antibody specific to PsbO. (C) Ratios of the D1 protein level of P-limited cells were semi-quantitated by the immunoblot analysis relative to that of cells on day 1, which was set to 100% for easy comparison. (D) Ratios of the PsbO protein level of P-limited cells were semi-quantitated by the immunoblot analysis relative to that of cells on day 1, which was set to 100% for easy comparison. Error bars show mean ± standard error (SE) of triplicate treatments. Superscripts indicate significant differences between day 1 and other days according to a two-way ANOVA with a post-hoc test (**p < 0.01, *p < 0.05). | PMC9899818 | fmicb-14-1085176-g008.jpg |
0.503792 | c3e2c7b087d54a0abf44973c17f99be3 | (A) Immunoblot analysis of D1 protein levels in S. costatum and P. globosa cultures treated with or without lincomycin in +P and −P groups. The blot was stained with Coomassie blue (CB). (B) Ratios of the D1 protein level of S. costatum cells semi-quantitated by the immunoblot analysis relative to that of cells on day 0, which was set to 100% for easy comparison. (C) Ratios of the D1 protein level of P. globosa cells semi-quantitated by the immunoblot analysis relative to that of cells on day 0. (D) Newly synthesized D1 protein (relative to day 0) in S. costatum in +P and −P groups. Newly synthesized D1 in PSII repair was measured as the change in the active D1 content in the absence of lincomycin (PSII repair active) minus the change in the active D1 content in the presence of lincomycin (PSII repair blocked). (E) Newly synthesized D1 protein (relative to day 0) in P. globosa in +P and −P groups. Newly synthesized D1 in PSII repair was measured as the change in the active D1 content in the absence of lincomycin (PSII repair active) minus the change in the active D1 content in the presence of lincomycin (PSII repair blocked). Error bars are mean ± SE of triplicate treatments. Superscripts indicate significant differences according to a two-way ANOVA with a post-hoc test (B,C: day 0 vs. other days; D,E: +P group vs.−P group. **p < 0.01, *p < 0.05). | PMC9899818 | fmicb-14-1085176-g009.jpg |
0.461478 | bd0fef9799d34ae9875ff3418423570e | Non-photochemical quenching (NPQ) capacity of S. costatum
(A) and P. globosa
(B) in +P and −P groups. Error bars show the mean ± standard error (SE) of triplicate treatments. Superscripts indicate significant differences between +P group and −P group according to a two-way ANOVA with a post-hoc test (*p < 0.05). | PMC9899818 | fmicb-14-1085176-g010.jpg |
0.452224 | dbcd74a96c5340e3ad1386a3db940bf8 | The photosynthetic responses of S. costatum (red line) and P. globosa (blue line) under P limitation (the thickness of the line indicates the strength of the effect). | PMC9899818 | fmicb-14-1085176-g011.jpg |
0.491391 | a0fede4f98fd4922b999e1616ee3a23a | Perioperative course of (A) bio-ADM and (B) penKid. n, number of patients; S1, prior to surgery; S2, intraoperatively at the end of cardiopulmonary bypass; S3, at ICU-admission; S4, 24 h after surgery; and S5, 48 h after surgery; bio-ADM, bioactive Adrenomedullin; penKid, proenkephalin A. | PMC9900105 | fcvm-09-1017867-g0001.jpg |
0.487439 | 11ac3bc1388f4f84a1f4a844c09f53ae | AUC/ROC analysis of intraoperative levels of penKid and EuroSCORE II alone (S2) and a combination of penKid (S2) with preoperative EuroSCORE II for the combined outcome “ICU length of stay >1 day or in-hospital death.” AUC/ROC, area under the curve/receiver operating characteristics; penKid, proenkephalin A; S2, intraoperatively at the end of cardiopulmonary bypass; EuroSCORE II, preoperative European System for Cardiac Operative Risk Evaluation Score II. | PMC9900105 | fcvm-09-1017867-g0002.jpg |
0.38816 | 253e1f05024d4c82a161987c6877668d | Association of proenkephalin A (penKid) with acute kidney injury (AKI). (A) Comparison of penKid levels in patients with/without AKI. (B) penKid levels in patients by Acute Kidney Injury Network (AKIN) class. n, number of patients; S1, prior to surgery; S2, intraoperatively at the end of cardiopulmonary bypass; S3, at ICU admission; S4, 24 h after surgery; and S5, 48 h after surgery. | PMC9900105 | fcvm-09-1017867-g0003.jpg |
0.434503 | 6cd2cdfeb6d5431ebefde991a0400bf3 | Association of bioactive Adrenomedullin (bio-ADM) and proenkephalin A (penKid) with the combined endpoint “in-hospital mortality, patients receiving mechanical ventilation support, re-intubation, post-surgery infection and wound infections” (A) bio-ADM and (B) penKid; n, number of patients; S1, prior to surgery; S2, intraoperatively at the end of cardiopulmonary bypass; S3, at ICU admission; S4, 24 h after surgery; and S5, 48 h after surgery. | PMC9900105 | fcvm-09-1017867-g0004.jpg |
0.424098 | 1c18cbb5230c4aafbb74508023e3d27c | MiSL predicts ACC1 as a metabolic dependency for mutant IDH1, but not mutant IDH2. A, Schematic showing MiSL algorithm and prediction of ACC1 (ACACA) as a potential synthetic lethal partner of mutant IDH1 across pan-cancer. CNA, copy-number alteration. B,ACC1 mRNA expression comparing mutated IDH1 and IDH2 AML vs. wild-type in The Cancer Genome Atlas based on RNA sequencing data. Differences in expression were compared with Student t test with P values as shown. C, Validation of ACC1-specific hairpins on protein expression by Western blot (left) with quantification (right). Experiment was performed 3 independent times. *, P < 0.05. RFU, relative fluorescence unit. D, ACC1-specific hairpins with mRNA quantified by TaqMan qPCR compared with nontargeting shRNA. Experiment was performed in triplicate 2 independent times; ***, P < 0.001; **, P < 0.01; Student t test. E, Knockdown of ACC1 using shRNA#1 (left) or shRNA#2 (right) in THP-1 cells expressing IDH1 R132H (mIDH1) or IDH2 R140Q (mIDH2) under dox-induced promoter in lipid-depleted media. The number of viable RFP+GFP+ double-positive cells at day 10 was enumerated relative to fluorescent counting beads. RFP tracks integrated ACC1-specific shRNA hairpin; eGFP tracks mutant protein after dox induction. This experiment was performed 3 times with a representative graph shown. Bars represent standard deviation. ***, P < 0.001; **, P < 0.01; *, P < 0.05; Student t test performed on 4 sorted biological replicates for each transduction group. F, Similar experiment using wild-type IDH cells. ACC1 was knocked down using shRNA#1 or shRNA#2 in THP-1 cells expressing IDH1 or IDH2 wild-type proteins under dox-induced promoter in lipid-depleted media. As in D, the number of viable RFP+GFP+ double-positive cells at day 10 was enumerated relative to fluorescent counting beads. RFP tracks integrated ACC1-specific shRNA hairpin; eGFP tracks wild-type protein after doxycycline induction. This experiment was performed 3 times with a representative shown. Bars represent standard deviation. NS, nonsignificant; NT, nontargeting shRNA. | PMC9900324 | 496fig1.jpg |
0.46521 | 7a078156b26a410eb92b8deea21a75ca | IDH1-mutant AML associated with decreased single-chain fatty acid metabolites. A, Principal component analysis of extracted nonpolar metabolites identified by mass spectrometry in negative ion mode from THP-1 cells cultured in low serum media following induction of mIDH1 R132H, mIDH2 R140Q, wild-type IDH1, or wild-type IDH2. B, Heat map showing differentially abundant nonpolar lipid species globally decreased in IDH1 R132H THP-1 cells (+dox) compared with IDH2 R140Q (+dox) vs. no-dox controls. C, Schematic showing metabolomics protocol for extracting nonpolar lipid species using organic solvent and derivatization of polar metabolites with O-benzylhydroxylamine and dansyl-tags from primary cell AML extracts. Putative metabolite identifications based on mass/charge ratio and retention time were determined from the Human Metabolome Database, Lipid Annotator software, and a validated in-house lipidomics fragmentation library. HMDB, Human Metabolome Database. D, Heat map showing clustering of primary AML samples based on differentially abundant metabolites (all metabolites, both polar and nonpolar). mIDH1 samples are shown in red. CB, cord blood. E, Volcano plot highlighting significant differentially abundant metabolites in healthy IDH1 wild-type CD34+ progenitors vs. mIDH1 AML. Red dashed line indicates a nonadjusted P value threshold of 0.05. F, Volcano plot highlighting significant differentially abundant metabolites in 6 × mIDH1 vs. 5 × mIDH2 AML samples. Dashed line indicates a nonadjusted P value threshold of 0.05. G, Representative examples of distinct lipid metabolites with decreased abundance in IDH1-mutant vs. IDH2-mutant AML and wild-type AML; x-axis shows metabolite abundance. Bars represent standard error of independent samples. All P values represent comparison with wild-type. LPE, lysophosphatidylethanolamine; MG, monoacylglycerolipids; NS, nonsignificant; WT, wild-type. | PMC9900324 | 496fig2.jpg |
0.435321 | a1b432c158354594baf45e431d95c5a4 | IDH1 mutation is linked to defective reductive carboxylation, increased fatty acid consumption, and decreased NADPH. A, Schematic and graph of flux studies showing the percentage of labeled M2 glycerol-3-phosphate derived from 13C[1,2] labeled glucose (2 of 6 carbons as heavy isotope) across THP-1 cells induced to express mIDH1 vs. IDH1 wild-type compared with mIDH2 vs. IDH2 wild-type. Glucose was added to media in normoxia over 13 hours. Schematic indicates M2 isotopolog of glycerol-3-phosphate de novo synthesis directly from glycolysis utilizing labeled glucose rather than the oxidative pentose phosphate pathway (M1 isotopolog). A two-tailed unpaired Student t test was used to compare differences between groups. This experiment was performed with 6 cell pellets for each sample blinded and randomized on each LC-MS run. DHAP, dihydoxyacetone phosphate; G-6-P, glucose-6-phosphate. B, Decreased reductive carboxylation of mIDH1 compared with IDH1 wild-type and mIDH2 expressed in THP-1 cells measured by the percentage of M5 citrate isotopolog obtained from U-13C5 glutamine labeling in 2% hypoxia over 16 hours, as shown in the schematic. The last bar shows mIDH1 cells cultured in the presence of 10 μmol/L ivosidenib added prior to adding a label. This experiment was performed with 6 cell pellets for each sample blinded and randomized on each LC-MS run. ****, P < 0.0001; Student t test. C, Column graph showing FC increase in acylcarnitine metabolites after induction of mIDH1 (+dox) vs. wild-type (−dox) in comparison with mIDH2 (+dox) vs. IDH2 wild-type (−dox) in THP-1 cells as measured by LC-MS. Student t test is used to compare groups. D, Column graph showing mean fatty acid β-oxidation as measured by the etomoxir (ETO)-sensitive component of oxygen consumption in pmole/min/105 cells in mIDH1 vs. IDH1 wild-type, mIDH2 and IDH2 wild-type in THP-1 cells measured on Seahorse analyzer (3 independent experiments). E, Column graph showing the percentage of b-oxidation of total oxygen consumption (etomoxir-sensitive component) in mIDH1 and mIDH2 before and after the addition of the ACC1 inhibitor 100 nmol/L ND-646. A representative experiment is shown. Statistics represent paired t test with n = 4 replicates. F, Column graph showing percentage of etomoxir-sensitive component in mIDH1 before and after the addition of 10 μmol/L ivosidenib. P = nonsignificant, Student t test, 4 replicates. G, Western blot showing phospho-AMPK (pAMPK) on threonine 172 in THP-1 cells induced with mIDH1, mIDH2, and wild-type counterparts in lipid-replete conditions. Comparison with total AMPK α isoform and Actin is shown in panels below. H, NADPH levels measured in identical 2 × 106 viable cell pellets of mIDH1, mIDH2, or wild-type primary AML blasts vs. normal CD34+ cells grown in culture for 48 hours in normoxia. Symbols indicate individual sample values. Student t test is used to compare groups. **, P < 0.01.I, Schematic summarizing mIDH1-induced mechanisms impacting lipid metabolism. Pathways involved directly in phospholipid synthesis that are perturbed by mIDH1 are shown in red. Thin arrows indicate reduced flux, and thick arrows indicate preserved or increased flux. Black arrows indicate pathways not measurably affected by mIDH1. Mechanistic causes for aberrant lipid metabolism identified in our study include (i) reduced carbon flux arising from defective reductive carboxylation by mutant IDH1 hetero/homodimers exacerbated in relative marrow hypoxia and mitochondrial stress; (ii) cumulative NADP(H) decrease by neomorphic reverse αKG to 2HG reaction; (iii) ongoing depletion of NADPH by residual reductive carboxylation of glutamine; (iv) insufficient NADPH replenishment by impaired forward reaction akin to TCA cycle; (v) increased fatty acid β-oxidation with a concomitant increase in acylcarnitines that is sensitive to ACC1 inhibition, but not ivosidenib; and (vi) decreased AMPK phosphorylation, indicating an AMPK-independent mechanism for enhanced oxidative phosphorylation of fatty acids. In contrast, the flux of glucose to produce glycerol-3-phosphate, the building block for the glycerol component of glycerolipids, is not impaired but rather is upregulated in mIDH1 compared with mIDH2, shown in black. This would suggest de novo synthesis of glycerol from glucose is not the major cause of defective lipid species in mIDH1 AML. Similarly, static levels of citric acid cycle metabolites are decreased to similar levels in both mIDH1 and mIDH2 AML, as shown in Supplementary figures. Blockade of 2HG production by ivosidenib is not sufficient for restoring defective reductive carboxylation or abrogating β-oxidation. NS, nonsignificant; WT, wild-type. | PMC9900324 | 496fig3.jpg |
0.427904 | 9038657254624cd79d6a78ba4081c44b | Lipid-free diet causes decreased growth of mIDH1 AML. A, Growth of mIDH1 vs. mIDH2 THP-1 cells in lipid-stripped serum over 10 days shown as a relative FC compared with IDH1 wild-type cells. Growth was measured using Presto-Blue cell viability. Bars represent standard deviation of 4 replicates in a representative experiment performed 3 times. B, Schematic showing change in diet to sucrose-rich lipid-free diet at 10 weeks after engraftment of human AML. C, Triglyceride levels measured in NSG mice after 6 weeks of lipid-free dietary supplementation. D–H, Human CD33+ engraftment of mIDH1 AML (D, E), mIDH2 AML (F, G), and normal CD34+ hematopoietic stem/progenitor cells (H) after 6 weeks in mice treated with lipid-free compared with normal rodent diet. Bars represent standard error. Mann–Whitney U test was used to compare engraftments with P values as shown. NS, nonsignificant. | PMC9900324 | 496fig4.jpg |
0.42905 | a80418bc4e114737bb7803acc532fa12 | ACC1 is a potential target in IDH1-mutant solid tumors. A, Growth of HT-1080 tumors over 21 days after knockdown of ACC1 measured by intravital imaging of shRNA-transduced luciferase+ cells. B,In vivo imaging of tumors from the same experiment. C, Colony assays quantified by crystal violet showing decreased colonies in mIDH1 with ACC1 knockdown compared with wild-type in lipid-replete conditions. D, Column graphs showing mean number of colonies after seeding 2,500 cells per well; bars represent standard error of the mean from 2 independent experiments. E,In vivo growth of IDH1 wild-type HT-1080 cells after CRISPR–Cas9 correction. Plots show median tumor growth after 25 days. P = nonsignificant; Mann–Whitney U test. F, Ki-67 IHC stain of explanted HT-1080 (5 tumors × 10 fields of view) after ACC1 knockdown compared with control with Student t test. Right, quantification of the Ki-67 proliferation index in tumors with ACC1 knockdown vs. control. G, Summary bar graph of 5 tumors × 10 fields of view showing increased apoptosis in ACC1 knockdown explants as measured by IHC staining of cleaved caspase-3 in explanted tumors. H, Kaplan–Meier log-rank survival curve for NSG mice transplanted with HT-1080 cells comparing ACC1 knockdown (pink) to nontargeting control (black) ± ivosidenib (ivo) treatment 25 mg/kg/day (gray, purple) or vehicle given by oral gavage for 50 days. Mice eventually succumbed by 72 days in all treatment groups due to increased tumor growth requiring euthanasia. P values represent log-rank Mantel–Cox test between groups as indicated. I, Bar graph summarizing total flux (photons per second) based on intravital imaging at day 21 for the same experiment. Student t test with indicated P values assessed statistical significance. J, Kaplan–Meier log-rank survival curve for NSG mice transplanted with HT-1080 cells and fed lipid-free vs. normal (lipid-replete) rodent diet. As in the previous experiment, mice eventually succumbed by day 70 in all treatment groups due to increased tumor growth. P values represent log-rank Mantel–Cox test between groups as indicated. kd, knockdown. K, Bar graph summarizing tumor size at 21 days after engraftment as measured by calipers. NS, nonsignificant; NT, nontargeting; WT, wild-type. | PMC9900324 | 496fig5.jpg |
0.440029 | ad3405413d24491fb2e13b6c4ba871f5 | ACC1 selective inhibitors have activity in mIDH1 cancers. A, Viability of HT-1080 mIDH1 R132C cells after exposure to 4 μmol/L TOFA for 72 hours measured by DAPI-negative cell population. B, Representative images of wild-type IDH1 reversion HT-1080 cells cultured at low density in 4% lipid-depleted serum or IDH1 R132C parental cells or IDH1 R132C treated with 10 μmol/L ivosidenib. Note that cells with IDH1 R132C mutation form ultrathin adherent elongated spindle-like cells. This morphology change was not reversed by coculture with ivosidenib. C, Measurement of 2HG in the supernatant of parental mIHD1 HT-1080 cells but undetectable in wild-type IDH1 reversion HT-1080 cells (clone #65 is shown as representative clone) after 72 hours. D, Total abundance of lysophospholipids (LPC + LPE) measured by LC-MS in mIDH1 vs. WT HT-1080 cultured in lipid-depleted media. AUP, area under the peak. E, Growth curves of mIDH1 vs. wild-type revertant HT-1080 in lipid-replete (left) vs. lipid-depleted (right) serum over 7 days. F, FC decrease in the number of live IDH1 R132C HT-1080 cells compared with IDH1 reversion wild-type HT-1080 cells after 96-hour exposure to the ACC1 inhibitor TOFA compared with DMSO vehicle. Graph shows mean of 3 independent experiments. G, Western blot showing increased phosphorylated ACC1 Serine 79 after treatment of HT-1080 wild-type cells with increasing concentration of AICAR. H, FC decrease in the number of live IDH1 R132C HT-1080 cells after 96-hour exposure to AICAR vs. H2O vehicle in comparison with IDH1 reversion wild-type HT-1080 cells under same conditions. Graph is a summary of 3 independent experiments. I and J, Primary mIDH1 AML cells isolated by flow cytometry from a patient at relapse (I) and a de novo patient (J) are sensitive to 10 μmol/L TOFA over 72 hours, but cytotoxicity is not reversed by 10 μmol/L ivosidenib. ***, P < 0.001;**, P < 0.01; *, P < 0.05. RFU, relative fluorescence unit. K, Summary of TOFA IC50 at 72 hours after in vitro treatment of mIDH1, mIDH2, and IDH wild-type primary AML blasts cultured in low serum media. P value reflects nonparametric two-tailed comparison between groups; bars represent median IC50 in μmol/L. L, Engraftment of mIDH1 AML at baseline and after 30 days of treatment with either vehicle or 50 mg/kg TOFA given by daily intraperitoneal injection. P = 0.007, paired t test, treated vs. baseline. PDx, patient-derived xenograft; WT, wild-type. | PMC9900324 | 496fig6.jpg |
0.464883 | 4b6df81810a44de69ab3a62e8b916fdb | The ACC1-selective inhibitor ND-646 can overcome venetoclax resistance. A, FC decrease in the number of live IDH1 R132C HT-1080 cells compared with IDH1 reversion wild-type (WT) HT-1080 cells after 96 hours exposure to the ACC1 inhibitor ND-646 compared with DMSO vehicle. Graph shows mean of 3 independent experiments. B, Parental IDH1 R132C HT-1080 cells were treated with increasing concentrations of the ACC1/2 inhibitor ND-646 ± 10 μmol/L ivosidenib. Cell viability was measured after 5 days in 4% lipid-stripped serum culture. This experiment was performed 3 times with a representative experiment shown. Bars represent standard deviation of technical replicates. No statistical differences were observed between ivosidenib-treated cells vs. untreated. RFU, relative fluorescence unit. C, Baseline and posttreatment bone marrow (BM) engraftment levels of human CD45+CD33+ mIDH1 AML exposed to ABT-199 50 mg/kg or ABT-199 50 mg/kg in combination with the selective ACC1 inhibitor ND-646 100 mg/kg for 7 days by oral gavage. P values represent the nonparametric Mann–Whitney U test. D, Peripheral blood (PB) engraftment levels of mIDH1 primary AML after treatment for 14 days with either vehicle, ABT-199 50 mg/kg, or ABT-199 in combination with ND-646. E, Bone marrow engraftment levels of the same experiment in D. P values represent the nonparametric Mann–Whitney U test for D and E. NS, nonsignificant; PDx, patient-derived xenograft. | PMC9900324 | 496fig7.jpg |
0.450355 | 51ab4626f1214d80a3e2710eebd6def2 | Spatio-temporal and social orientation changes along the AD continuum.Mean efficiency scores (ES) of CN (N= 16, blue), MCI (N = 23, green) and AD dementia participants (N = 12, red) for the orientation task in all domains (A), the orientation task in the domains of space and time (spatio-temporal) (B), the orientation task in person (social) (C), and the lexical control task in all domains (D). Significant CN-MCI differences were found in all domain orientation (A; P < 0.05), and space and time orientation (B; P < 0.001). Significant MCI-AD dementia and CN-AD dementia differences were found in all domains, spatio-temporal and social orientation task ES (A, B, C; P < 0.001), as well as in the lexical task (D; P < 0.05). Statistical significance was estimated using ANOVA and Tukey-Kramer post hoc test. | PMC9900945 | nihpp-2023.01.25.525587v1-f0001.jpg |
0.388254 | 9fa8394f22a048f8906184615984e58e | Changes in spatio-temporal and social orientation activity in AD.(A) Spatio-temporal and social pattens of brain activity. Results of GLM analysis exhibiting contrast maps of spatio-temporal (A1) and social (A2) orientation tasks over the lexical control task (All participants, DF=50, P<0.05 FDR corrected, cluster size > 20 voxels). (B, C) Divergent changes in spatio-temporal and social orientation activity. Spatio-temporal (B) and social (C) disorientation contrasted task-evoked activity maps across the three clinical groups: CN greater than MCI participants in spatio-temporal (B1) and social (C1) orientation (DF=38, P<0.05 FDR corrected, cluster size thresholding of 20 voxels); CN greater than AD dementia participants in spatio-temporal (B2) and social (C2) orientation (DF=34, P<0.05 FDR corrected, cluster size thresholding of 20 voxels); MCI greater than AD dementia participants in spatio-temporal (B3) and social (C3) orientation (DF=27, P<0.05 FDR corrected, cluster size thresholding of 20 voxels). | PMC9900945 | nihpp-2023.01.25.525587v1-f0002.jpg |
0.435466 | bc005076d5184a8ab794a8bdb6c69760 | Orientation-evoked activity overlaps Default Mode sub-networks differently.(A) Spatio-temporal and social activity and DMN A, B, and C overlap. Delineations of DMN sub-networks (Schaefer et. al, 2018) DMN A (dark), DMN B (medium), DMN C (light) superimposed on maps of spatio-temporal (A1) and social (A2) orientation tasks (Orientation > Lexical control; All participants, DF=50, P<0.05 FDR corrected, cluster size > 20 voxels). (B) The precent of overlap between supra-threshold task-evoked spatio-temporal (B1) and social (B2) maps and DMN subnetworks A, B, and C. Asterisks indicate significant overlap (permutation test, 10,000 iterations). (C) Spatio-temporal and social task-evoked coefficients in DMN A, B, and C ROIs. Mean GLM-derived parameter estimates for social (C2 and 3) and spatio-temporal (C1) orientation (>rest) in significantly overlapping (B) DMN subnetworks (C1 – DMN C - spatio-temporal; C2 –DMN B – social; C3 – DMN C - social) for CN (N= 16, blue), MCI (N = 23, green) and AD dementia (N = 12, red). Significant differences were found between CN and AD dementia participants in DMN A, B, and C, between MCI and AD dementia participants in DMN A and B, and between CN and MCI participants in DMN C (ANOVA and Tukey-Kramer post hoc test, P < 0.05). | PMC9900945 | nihpp-2023.01.25.525587v1-f0003.jpg |
0.420726 | 5c85f9f24b93405783586486d84803dc | Mediation models of brain activity, glucose metabolism and orientation performance.(A) Mediation analysis was used to test the hypothesis that changes in FDG-PET uptake (M) across the AD continuum alter the relations between spatio-temporal (B2) and social (B2) orientation-evoked brain activity (X) and orientation task performance (Y). (B) Spatio-temporal and social mediation and DMN A, B, and C overlap. Delineations of DMN sub-networks (Schaefer et. al, 2018) DMN A (dark), DMN B (medium), and DMN C (light) superimposed on maps of spatio-temporal (B1) and social (B2) mediation (P<0.05, FDR-corrected). (C) The precent of overlap between supra-threshold task-evoked spatio-temporal (C1) and social (C2) suprathreshold mediation maps and DMN subnetworks A, B, and C. Asterisks indicate significant overlap (permutation test, 10,000 iterations). | PMC9900945 | nihpp-2023.01.25.525587v1-f0004.jpg |
0.36937 | 5e4ef6de9c2e486a86bbe2bc971a7286 | Postpartum complications mentioned by women who gave birth in the last 12 months in Arba Minch town, Southern Ethiopia, December 2019. | PMC9901784 | pone.0281242.g001.jpg |
0.459538 | 11a695b688284bb98294fb3253d44bac | The plasma level of major elements that have relevance to endothelial function in patients with IS and HVs. (A-D) The levels of pro-inflammatory mediator TNF-α and chemoattractant SDF-1 increased in patients at different phases of ischemic stroke while no differences were observed in the levels of G-CSF and total antioxidant capacity. (E, F) Gradual decreases observed in pro-angiogenic factors, VEGF and PDGF-BB reached significance at day 90 of ischemic stroke. (G-J) Ischemic stroke differentially regulated the levels of angiogenic suppressors in that the levels of endostatin constantly increased after ischemic injury while the levels of thrombospondin-1, and thrombospondin-2 decreased. No change was observed in angiostatin levels. * < 0.05, **P < 0.01, ***P < 0.001 versus HVs (t test or Mann Whitney U test). NS: not significant compared to HVs. G-CSF, granulocyte colony-stimulating factor; HVs, healthy volunteers; IS, ischemic stroke; PDGF-BB, platelet-derived growth factor; SDF-1, stromal cell-derived factor 1; TNF-α, tumor necrosis factor-α; VEGF, vascular endothelial growth factor | PMC9902316 | 12015_2022_10439_Fig1_HTML.jpg |
0.41762 | 0c39d969383d4896b4f7f0519ad618b8 | Schematic diagram of an in
vitro model of human BBB and the effect of OEC-CM on BBB integrity and function and actin cytoskeleton organization in HBMECs and OECs. (A)
In
vitro models of human BBB consisting of astrocytes, pericytes, and HBMECs alone or mixed with OECs. (B, C) TNF-α significantly disrupted BBB integrity and function, as shown by decreases in TEER and concomitant increases in paracellular flux of sodium fluorescein, which were prevented by OEC-CM treatment. (D) Co-treatment with OEC-CM prevented the effects of TNF-α on cytoskeletal reorganization in HBMECs and OECs and decreased stress fiber formation (white arrows). (E) Quantification of stress fiber formation in both cells. Scale bar: 25 μm. *P < 0.05 versus BBB formed by HBMECs or control, #P < 0.05 versus BBB formed by HBMECs exposed to TNF-α, †P < 0.05 versus BBB formed by HBMECs exposed to TNF-α and OEC-CM, φP < 0.05 versus BBB formed by HBMECs and OECs, ψP < 0.05 versus BBB formed by HBMECs and OECs exposed to TNF-α (one-way ANOVA followed by Tukey's post-hoc analysis). BBB, blood–brain barrier; HBMECs, human brain microvascular endothelial cells; OEC-CM, outgrowth endothelial cell-derived conditioned medium; OECs, outgrowth endothelial cells; TNF-α, tumor necrosis factor-α | PMC9902316 | 12015_2022_10439_Fig2_HTML.jpg |
0.389959 | a0a0bd06703749c895b5036ea4395c4a | The effect of OEC-CM on HBMEC and OEC functional characteristics and analysis of angiogenesis-related proteins in HBMEC and OEC secretomes and OEC-CM. (A, B) OEC-CM accelerated wound closure in both HBMEC and OECs. (C-E) OEC-CM negated the impact of TNF-α on HBMEC and OEC tubule network. (F, G) Treatments with OEC-CM neutralized the inhibitory effect of TNF-α on HBMEC and OEC adhesion to fibronectin, an extracellular matrix protein. (H, I) Proteome profiling of OEC-CM along with HBMEC and OEC secretomes revealed significant variations in various pro- and anti-angiogenic factors e.g. endothelin-1, MCP-1 and endostatin in OEC-CM. Scale bars = 100 μm. *P < 0.05 versus control, #P < 0.05 versus TNF-α (one-way ANOVA followed by Tukey's post-hoc analysis). HBMECs, human brain microvascular endothelial cells; IL-8, interleukin-8; MCP-1, monocyte chemoattractant protein-1; OEC-CM, outgrowth endothelial cell-derived conditioned medium; OECs, outgrowth endothelial cells; TIMP-1, tissue inhibitors of metalloproteinase-1; TNF-α, tumor necrosis factor-α; uPA, urokinase plasminogen activator | PMC9902316 | 12015_2022_10439_Fig3_HTML.jpg |
0.426387 | 6d50c706077b48a7b8232d896f1f2a54 | Primary wintering regions of the Midcontinent population of greater white-fronted goose (Anser albifrons frontalis) in North America (excluding regions in Mexico). Transmitters were deployed during winters 2016–2018 in the Chenier Plain (Louisiana), Lower Texas Coast, and Rolling/High Plains regions. Geese that made winter movements outside of these defined regions were classified as ‘Other’ regions. Map created using Esri ArcMap (version 10.3.1; www.esri.com). | PMC9902612 | 41598_2023_28937_Fig1_HTML.jpg |
0.454489 | 66a428ab70b247a985baf8e65a20bd13 | Mean effect on habitat-specific transition probability (± 95% credible intervals; log-odds scale) to each of seven landcover types for the specific wintering region selected by 56 greater white-fronted geese during winters 2016–2017 and 2017–2018. Note varying scales of the y-axis on each panel to show increased detail due to small credible intervals. Also, effects were not estimated for transitions that were not observed; for example, no estimate is reported for transitions to corn in Chenier Plains in the upper left panel. | PMC9902612 | 41598_2023_28937_Fig2_HTML.jpg |
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