dedup-isc-ft-v107-score
float64 0.3
1
| uid
stringlengths 32
32
| text
stringlengths 1
17.9k
| paper_id
stringlengths 8
11
| original_image_filename
stringlengths 7
69
|
|---|---|---|---|---|
0.391333 | 5d4474c291904214bc4c3a71c7a83860 | The trend of posts on Mpox and Mpox plus Two-Spirit, Lesbian, Gay, Bisexual, Transgender, Queer and/or Questioning, Intersex, Asexual (2SLGBTQIAP+) keywords and the number of Mpox cases. LGBTQ: Lesbian, Gay, Bisexual, Transgender, Queer. | PMC10186192 | jmir_v25i1e45108_fig1.jpg |
0.443793 | c96048c30c2243eab6465f97b73efcdc | (A) Relative number and (B) sentiment intensity of posts gathered with Mpox and LGBTQ keywords for each polarity for English, Spanish, and French posts. LGBTQ: Lesbian, Gay, Bisexual, Transgender, Queer. | PMC10186192 | jmir_v25i1e45108_fig2.jpg |
0.433885 | 5fb182c09ca648aaa158da9c01b61446 | (A) Sentiment polarity and (B) sentiment intensity on different topics. CDC: Centers for Disease Control and Prevention; LGBTQ: Lesbian, Gay, Bisexual, Transgender, Queer; WHO: World Health Organization. | PMC10186192 | jmir_v25i1e45108_fig3.jpg |
0.530347 | dbb7585aad624692aa2fdf6a5cb33cb2 | (A) Distribution of sentiment scores on different topics and ANOVA test. (B) Recognizing topics with lower sentiment scores with Dunn test. CDC: Centers for Disease Control and Prevention; LGBTQ: Lesbian, Gay, Bisexual, Transgender, Queer; WHO: World Health Organization. | PMC10186192 | jmir_v25i1e45108_fig4.jpg |
0.442014 | 1f597097db144c619a6a1d3f1b090104 | Visualization of geotagged tweets on Mpox and Mpox plus LGBTQ keywords. LGBTQ: Lesbian, Gay, Bisexual, Transgender, Queer. | PMC10186192 | jmir_v25i1e45108_fig5.jpg |
0.438616 | 5eea0efd0fea4522b6b26100add02cd1 | Tweets belonging to each topic for Mpox and the Two-Spirit, Lesbian, Gay, Bisexual, Transgender, Queer and/or Questioning, Intersex, Asexual (2SLGBTQIAP+) community in different countries. CDC: Centers for Disease Control and Prevention; LGBTQ: Lesbian, Gay, Bisexual, Transgender, Queer; WHO: World Health Organization. | PMC10186192 | jmir_v25i1e45108_fig6.jpg |
0.44724 | 13affa80b1a8456998b27c191dca5a2a | (A) Sentiment polarity in different countries. (B) Distribution of sentiment scores across different countries and Mann-Whitney U test. LGBTQ: Lesbian, Gay, Bisexual, Transgender, Queer; UK: United Kingdom; US: United States. | PMC10186192 | jmir_v25i1e45108_fig7.jpg |
0.452669 | 2b303f52a37a489d967e00a849fcc06a | Change from baseline through week 14 in A ASQoL, B ASAS HI, and C SF-36 PCS (MMRM). *Nominal P value ≤ 0.05; **nominal P value ≤ 0.01; ***nominal P value ≤ 0.001. aSignificant after multiplicity adjustment. MMRM analysis included treatment, visit, and treatment-by-visit interaction as fixed factors and baseline value as covariate. Stratification factor hsCRP level (≤ ULN vs. > ULN) was also included in the model. ASAS HI Assessment of SpondyloArthritis international Society Health Index, ASQoL Ankylosing Spondylitis Quality of Life, CI confidence interval, hsCRP high-sensitivity C-reactive protein, MMRM mixed-effect model for repeated measures, PBO placebo, PCS Physical Component Summary, SF-36 36-Item Short Form Health Survey, ULN upper limit of normal, UPA upadacitinib | PMC10186301 | 40744_2023_550_Fig1_HTML.jpg |
0.44936 | 24cd8fcf5bad4b1eb6e3b1493b3f5724 | Mean change (95% CI) from baseline in WPAI at week 14. *Nominal P value ≤ 0.05; **nominal P value ≤ 0.01. aIncludes patients currently employed. Within-group mean and 95% CI and between-group mean, 95% CI, and nominal P value for each visit are based on analysis of covariance model including treatment and main stratification factors MRI and screening hsCRP status (MRI + /hsCRP > ULN, MRI + /hsCRP ≤ ULN, and MRI–/hsCRP > ULN) as fixed factors and baseline value as covariate for all WPAI domains. CI confidence interval, hsCRP high-sensitivity C-reactive protein, MRI magnetic resonance imaging, PBO placebo, ULN upper limit of normal, UPA upadacitinib, WPAI Work Productivity and Activity Impairment | PMC10186301 | 40744_2023_550_Fig2_HTML.jpg |
0.402797 | e5146a9896bf4fa8aa452b70e1405561 | Proportion of patients reporting improvements ≥ MCID and NNTs in PROs at week 14 (NRI-MI). **Nominal P ≤ 0.01 and ***nominal P ≤ 0.001 versus placebo. NRI-MI is non-responder imputation (NRI) incorporating multiple imputation (MI) to handle missing data due to COVID-19. MCID definitions: ≥ 3 points decrease (ASAS HI and ASQoL) and ≥ 2.5-point increase (SF-36 PCS). ASAS HI Assessment of SpondyloArthritis international Society Health Index, ASQoL Ankylosing Spondylitis Quality of Life, MCID minimal clinically important difference, NNT number needed to treat, PBO placebo, PCS Physical Component Summary, PRO patient-reported outcome, SF-36 36-Item Short Form Health Survey, UPA upadacitinib | PMC10186301 | 40744_2023_550_Fig3_HTML.jpg |
0.456304 | dd4bb416431f48638592566f0090fb78 | Cumulative probability of change from baseline to week 104 in SI joint total sacroiliitis score. Groups are presented as randomized (patients who switched to standard of care or from placebo to active treatment are analyzed according to the original treatment assignment at randomization). Green, yellow, and red lines represent the change from baseline in total sacroiliitis score of 0.46 (SDC), 1, and 2, respectively. SDC, smallest detectable change; SI, sacroiliac | PMC10186767 | 13075_2023_3051_Fig1_HTML.jpg |
0.410713 | e5886ac069e54d258add61a9c17af568 | Cumulative probability of change from baseline to week 104 in mSASSS total score. Groups are presented as randomized (patients who switched to standard of care or from placebo to active treatment are analyzed according to the original treatment assignment at randomization). Green, yellow, and red lines represent the change from baseline in total mSASSS score of 0.76 (SDC), 2, and 5, respectively. SDC, smallest detectable change; mSASSS, modified Stoke Ankylosing Spondylitis Spine Score | PMC10186767 | 13075_2023_3051_Fig2_HTML.jpg |
0.385567 | 4489785f9f484308b1f2442057e16726 | The mean change in SI joint bone marrow edema score by MRI in the overall population and in patients with baseline score > 2 through week 104. Data presented are as observed. The secukinumab group includes patients who continued on secukinumab to week 104. The placebo group includes only patients randomized to placebo who remained on placebo to week 52. At each time point, only patients with a value at both baseline and that time point are included. MRI, magnetic resonance imaging; n, number of evaluable patients; SI, sacroiliac | PMC10186767 | 13075_2023_3051_Fig3_HTML.jpg |
0.414302 | 221462522ffa4de482a474cc57564fdd | Cryo-EM structures of the S. cerevisiae Pol α.a) Domain architecture of the four subunits of the holoenzyme. The red asterisk indicates the polymerase activity in the catalytic NTD of Pol1 which is referred to as Pol1-core. The yellow asterisk indicates the primase activity in Pri1. b) A sketch of Pol α RNA primer and DNA primer synthesis steps. c-g) Six cryo-EM maps of Pol α in different states of catalysis: Pol α in the absence of T/P exists in the Apo state (conformers I and II), c), Pol α–T (T refers to template DNA) is in the primer initiation state (d), Pol α–T/P8 (T/P8 refers to the 8-nt RNA primer annealed to the template) is in the RNA synthesis state (e), Pol α–T/P10 (T/P10 refers to the 10-nt RNA primer annealed to the template) is in the post RNA hand-off state (f), and Pol α–T/P15 (T/P15 refers to the 10-nt RNA and 5-nt DNA chimeric 15-mer primer annealed to the template) is in the DNA elongation state. | PMC10187153 | nihpp-2023.05.03.539257v1-f0001.jpg |
0.443903 | 57b8271e19c644998b1457b8cf8e020f | Atomic models of Pol α in the apo and primer initiation states.a-c) Two conformations of the apo state of Pol α-primase. a) Front cartoon view of superimposed Pol α-primase apo state conformers I and II. Conformer I is in color and II is in grey. b) Enlarged view of the interaction between Pol1-core, Pri2-CTD, and Pol12/Pol1-CTD platform, the catalytic site of Pol1 is indicated by the red asterisk. c) Comparison of Pri1 between apo conf I and II. Pri1-NTD binds to different domains of Pol1: Pri1-NTD binds to the Pol1 palm in apo conf I but to the N-term of Pol1-core in apo conf II. d) Side cartoon view of superimposed Pol α-primase in Apo conf II and primer initiation state. Pol1-core is dissociated from the Pol12/Pol1-CTD platform. e) Comparison of Pol1-core between apo conf II and primer initiation state: Pol1-core rotates 69° downwards towards the primase. The inset shows representative 2D averages in the initiation state, showing the partially flexible Pol1-core and the Pri1 movement. f) Comparison of Pri2-CTD between apo conf II and primer initiation state. Pri2-CTD shifts 22 Å and rotates 92°. | PMC10187153 | nihpp-2023.05.03.539257v1-f0002.jpg |
0.410973 | 4144b944937f4b5a932b0d32e0f4c0d2 | Atomic model of Pol α–T/P8 in the RNA synthesis state.A) Front cartoon view of Pol α–T/P8. Inserted at lower left is a typical 2D class average showing the domain arrangement and the partially flexible Pol1-core. B) Top view of Pol α–T/P8 with Pol12 and Pol1-CTD removed for clarity. C-f) Comparison of yeast Pol α-primase among c) apo (conf II), d-e) primer initiation state, and f) RNA priming state, and the published human Pol α-primase (PDB ID 8D0K). The left and middle columns show the side and top views of Pri1 and Pri2-CTD interacting with ssDNA and RNA/DNA. The right column shows a cartoon model of Pri1 and Pri2-CTD collaborating to load template DNA and synthesize an RNA primer. | PMC10187153 | nihpp-2023.05.03.539257v1-f0003.jpg |
0.478322 | 9e0f58f1e15f4cb69d7587092e50ce45 | Atomic model of Pol α–T/P10 in the post RNA hand-off state.a) Front cartoon view of Pol α–T/P10 in the post RNA hand-off state. Insert at lower left is a typical 2D class average. The lower right panel shows an enlarged view of the interface between Pol1-core and RNA/DNA. The thumb and palm subdomains bind the RNA primer nt 2–9, and the thumb is flush with P5. b) Comparison of Pol1-core in the RNA synthesis state (Pol α–T/P8, grey) and primer hand-off state (Pol α-T/P10, color). Pol1-core rotates 60° to bind the RNA/DNA duplex. Lower left panel shows the change of Pol1-core in the post RNA hand-off state will occupy the space of Pri1. Lower right panel shows the N-term of Pol1-core may interact with Pri1-NTD as seen in Apo conf II. c) Changes from post RNA hand-off state to DNA elongation state. Pol1-core captures the RNA/DNA while Pri1 dissociates from template DNA. d) Cartoon model showing RNA primer hand-off from the primase (Pri1) to the polymerase (Pol1-core). | PMC10187153 | nihpp-2023.05.03.539257v1-f0004.jpg |
0.412602 | d4b1754931994b0eb6c57a413b03ab9e | Atomic model of Pol α–T/P15 in the DNA elongation state.a) Front cartoon view of Pol α–T/P15. Three insets show detailed contacts between Pol1-core and T/P. Inserted at lower left is a typical 2D class average showing the largely flexible Pri1. b) Schematic diagram of the interactions of Pol α’s thumb and palm subdomains with the T/P. c) Comparison of RNA priming state, post-RNA hand-off state, and DNA elongation state. The structures are aligned based on Pri2-CTD. The Pol1-core thumb touches the bottom of the RNA/DNA duplex in the RNA synthesis state. The Pol1-core thumb and palm subdomains fit the first minor groove and interact with the RNA primer (P1-P10 region) in the post-RNA hand-off state. In the DNA elongation state, the thumb and palm subdomains of Pol1-core fit the second minor groove and interact with primer strands nt 1–2 and 9–14, as well as the template strand nt 9–14. d) Sketch of DNA polymerase loading and DNA primer elongation. | PMC10187153 | nihpp-2023.05.03.539257v1-f0005.jpg |
0.478874 | 21d83848ce1c4ad680975014f0713679 | Model for hybrid RNA-DNA primer synthesis by the yeast Pol α.1) Pol α fluctuates between apo conformers I & II in the absence of a DNA template, with the Pol1-core catalytic site being blocked by the Pol1-CTD/Pol12 platform and Pri2-CTD and Pri1 moving about. 2) In the primer initiation state, Pol α engages a template DNA. Pol1-core dissociates from the platform. Pri2-CTD directs the template DNA to the primase active site in Pri1. 3) In the RNA synthesis state, Pri1 synthesizes the RNA primer on the DNA template. The RNA/DNA hybrid duplex displaces Pri2-CTD from Pri1, allowing Pol1-core to engage the growing T/P. 4) In the RNA primer hand-off state, Pol1-core captures the 3’-end of the RNA primer and expels Pri1 from template DNA. This completes the RNA primer hand-off from Pri1 to Pol1-core. 5,6) In the DNA elongation state, Pol1-core spirals around the RNA/DNA duplex to synthesize the DNA primer. | PMC10187153 | nihpp-2023.05.03.539257v1-f0006.jpg |
0.434785 | 560f05f3648141fdb123e0b18b7f9036 | Association between anti-spike IgG levels and protection from new SARS-CoV-2 infection using the most recent antibody measurement obtained 21–59 days before the current assessment.a Mean protection against any new infection in the Omicron BA.4/5 epoch. b Mean protection against infection with a moderate to high viral load (Ct value <30) in the Omicron BA.4/5 epoch. c Mean protection against infection with self-reported symptoms in the Omicron BA.4/5 epoch. The 95% CIs are calculated by prediction ± 1.96 × standard error of the prediction. Five groups are investigated: vaccinated participants without evidence of prior infection, vaccinated participants with a most recent Pre-Alpha or Alpha infection, vaccinated participants with a most recent Delta infection, vaccinated participants with a most recent Omicron BA.1 infection and vaccinated participants with a most recent Omicron BA.2 infection. Participants with 1 (629 assessments, 0.3%), 2 (7657 assessments, 3.7%), 3 (171,650 assessments, 83.9%) or 4 (24,753 assessments, 12.1%) vaccinations were grouped together. Protection is defined as relative protection against baseline protection from 16 BAU/mL in those vaccinated without infection, which is the threshold for vaccine non-responders. In a–c, antibody measurements were plotted after the first percentile overall in each previous infection group (16, 80, 100, 140 and 200 BAU/mL, respectively). The distribution and number of the most recent anti-spike IgG measurements for the four population groups are shown in d–h. Results remained similar, restricting to those who had only one prior infection (84,034 assessments, 90%). | PMC10187514 | 41467_2023_38275_Fig1_HTML.jpg |
0.639081 | f6b7902bdb8541dda461cedfbebee885 | Posterior predicted trajectories of mean anti-spike IgG levels (95% CrI) from second vaccination through third/booster vaccination or infection using Bayesian linear mixed interval-censored models.Time 0 indicates the earliest of the date each participant received their third/booster vaccination or their first breakthrough infection. For each group, two separate models were fitted: (1) piecewise model on antibody decline after the second vaccination and subsequent increase after third/booster vaccination or infection; (2) antibody decline 42 days after the third/booster vaccination or infection. The shaded area between 14- and 42-days post-third/booster vaccination or infection represents different timepoints individuals reach peak antibody levels. Models are adjusted for age, sex, ethnicity, time from second vaccination to booster/infection, long-term health conditions and healthcare role. Plotted at the reference categories (female, white ethnicity, 6 months between second vaccination and booster/infection, not reporting a long-term health condition, not working in healthcare). Line types indicate the primary vaccine course. Line colours indicate the booster type or infection. Lines prior to the booster/infection, i.e. before t = 0, are included to allow comparison of antibody declines prior to and following booster/infection. The ChAdOx1-BNT162b2 (red dotted line) and ChAdOx1-mRNA-1273 (blue dotted line) are overlapped before time 0. Plots are separated by age (30 y only estimated for those who had BNT162b2 as primary and were boosted by mRNA-1273 or infection due to low numbers in other groups). Predicted values are plotted on a log scale. Black dashed lines indicate the correlation for 67% protection against the Delta variant (100 BAU/mL) and the threshold of IgG positivity (23 BAU/mL). | PMC10187514 | 41467_2023_38275_Fig2_HTML.jpg |
0.426283 | 836e38383e7a4e0f96509208e1400c83 | Comparisons of antibody levels 42 days post-third/booster vaccination or infection, half-lives, and days from third/booster vaccination or infection to reaching antibody levels associated with 67% protection by primary vaccine course, third/booster vaccination or infection and age.a Comparisons of antibody levels 42 days post-third/booster vaccination or infection. b Comparisons of half-lives after third/booster vaccination or infection. c Comparisons of days from third/booster vaccination or infection to reaching antibody levels associated with 67% protection. Median values with 95% credible intervals are plotted. 95% credible interval in panel c are calculated from posterior simulations from the GAM model estimating correlates of protection and posterior predictions from the Bayesian linear mixed models estimating antibody levels. Predictions are on specific ages (30, 40, 55 and 70 years). 30 y is not plotted for ChAdOx1 primary course because the majority of participants receiving the ChAdOx1 primary course are >40 y. Numbers are shown in Supplementary Table 3. Plotted at the reference categories (female, white ethnicity, 6 months between second vaccination and booster/infection, not reporting a long-term health condition and not working in healthcare). | PMC10187514 | 41467_2023_38275_Fig3_HTML.jpg |
0.429006 | a5c40915b9c14b3eb37a0be32205a10b | Posterior predicted trajectories of mean anti-spike IgG levels (95%CrI) from third/booster vaccination or infection.a By age. b By the time from second vaccination to third/booster vaccination or infection. For each group, two separate models are fitted: (1) piecewise model on antibody decline after the second vaccination and subsequent increase after third/booster vaccination or infection; (2) antibody decline 42 days after the third/booster vaccination or infection. The shaded area between 14- and 42-days post-third/booster vaccination or infection represents different timepoints individuals reach peak antibody levels. Models are adjusted for age, sex, ethnicity, time from second vaccination to booster/infection, long-term health conditions and healthcare role. Plotted at the reference categories (female, white ethnicity, time from second vaccination to booster/infection 6 months, not reporting a long-term health condition, not working in healthcare). Plots are separated by primary vaccine courses and booster types or infection. Predicted values are plotted on a log scale. Black dashed lines indicate the correlation for 67% protection against the Delta variant (100 BAU/mL) and the threshold of IgG positivity (23 BAU/mL). | PMC10187514 | 41467_2023_38275_Fig4_HTML.jpg |
0.50241 | d1a3f7659c77456397a3feefd62bb2c6 | Proportion of participants above the anti-spike IgG antibody threshold level associated with 67% protection by time from third/booster vaccination or infection.The numbers of participants in each panel are [numbers in brackets represent <40, 40–55, 55–70 and >70 years]: ChAdOx1-Infection: n = 4214 [537, 2167, 1216, 294]; ChAdOx1-BNT162b2: n = 41,152 [1295, 8826, 19,232, 11,799]; ChAdOx1-mRNA-1273: n = 14,748 [738, 5341, 7859, 810]; BNT162b2-Infection: n = 1857 [956, 438, 313, 150]; BNT162b2-BNT162b2: n = 24,749 [2447, 3613, 8955, 9734]; BNT162b2-mRNA-1273: n = 4403 [1791, 889, 1,409, 314]. ‘< 40-year’ group is not plotted for ChAdOx1 primary course because the vast majority of those receiving ChAdOx1 were 40 years of age or older. Median values with 95% credible intervals are plotted. | PMC10187514 | 41467_2023_38275_Fig5_HTML.jpg |
0.454697 | 66b5250209884793827f83ddaf47aa82 | Median protection level by calendar time.Estimations were based on assumptions that participants did not receive another vaccination and were not infected after their third/booster vaccination or breakthrough infection. The numbers of participants in each panel are [numbers in brackets represent <40, 40–55, 55–70 and >70 years]: ChAdOx1-Infection: n = 4214 [537, 2167, 1216, 294]; ChAdOx1-BNT162b2: n = 41,152 [1295, 8826, 19,232, 11,799]; ChAdOx1-mRNA-1273: n = 14,748 [738, 5341, 7859, 810]; BNT162b2-Infection: n = 1857 [956, 438, 313, 150]; BNT162b2-BNT162b2: n = 24,749 [2447, 3613, 8955, 9734]; BNT162b2-mRNA-1273: n = 4,403 [1791, 889, 1409, 314]. The ‘<40-year’ group is not plotted for ChAdOx1 primary course because the vast majority of those receiving ChAdOx1 were 40 years of age or older. A 95% credible interval is calculated from posterior simulations from the GAM model estimating correlates of protection and posterior predictions from the Bayesian linear mixed models estimating antibody levels. | PMC10187514 | 41467_2023_38275_Fig6_HTML.jpg |
0.460267 | cdb2da0864c540e8b4fdf16b70526a9b | Structure of S-F and S-D.Streptothricins share streptolidine and carbamoylated gulosamine sugar moieties. They are distinguished by differing numbers of β-lysines attached end-to-end through amide bonds to the ε-amino groups. Nourseothricin is the natural product mixture of several streptothricins, predominantly S-F (1 β-lysine) and S-D (3 β-lysines). Acetylation of the β-amino group blocks activity and is the major known mechanism of antimicrobial resistance to streptothricins. S-D, streptothricin D; S-F, streptothricin-F. | PMC10187937 | pbio.3002091.g001.jpg |
0.462296 | e892359287444fd48cf1063ed08f36f5 | Rapid bactericidal activity against the Klebsiella pneumoniae Nevada strain.(A) Nourseothricin MIC 0.25 μM. (B) S-F MIC 1 μM. Data are available in S1 Data. MIC, minimal inhibitory concentration; S-F, streptothricin-F. | PMC10187937 | pbio.3002091.g002.jpg |
0.481179 | 53bcf09be38347108f96c9ac12d9369e | Inhibition of prokaryotic and eukaryotic translation.(A) Inhibition of prokaryotic in vitro translation using coupled in vitro transcription–translation extracts with readout from a nanoluciferase reporter. (B) Inhibition of eukaryotic in vitro translation using coupled in vitro transcription–translation extracts with readout from a nanoluciferase reporter. S-F, S-D, NTC, APR, and TET data represent mean and standard deviation from 3 independent experiments. Data are available in S3 Data. APR, apramycin; NTC, nourseothricin; S-D, streptothricin D; S-F, streptothricin-F; TET, tetracycline. | PMC10187937 | pbio.3002091.g003.jpg |
0.460169 | 5a6e91ade3b6450ab35ee4270878382a | Cytotoxicity of streptothricins against mammalian cell lines.J774 macrophages and LLC-PK-1 renal epithelial cells were treated with 2-fold doubling dilutions of nourseothricin, S-D, and S-F for up to 5 days in the presence of SYTOX-Green. SYTOX-Green is a cell membrane-impermeant nucleic acid binding dye that fluoresces on binding to nuclear DNA. It therefore provides a real-time readout of eukaryotic cell membrane permeabilization associated with cell death that can be continuously monitored through fluorescence measurements. Cytotoxicity was minimal to absent after a single day incubation but increased on subsequent days. Nourseothricin and S-D effects were essentially indistinguishable. S-F toxicity was only observed at molar concentration at least 10-fold greater than S-D beginning at 32 μM, significantly above MIC ranges observed in activity spectrum analysis. Each data point represents mean and standard deviation for assays performed in quadruplicate. Data are available in S4 Data. MIC, minimal inhibitory concentration; S-D, streptothricin D; S-F, streptothricin-F. | PMC10187937 | pbio.3002091.g004.jpg |
0.508833 | 27247248192a42c8af381e700a4ce672 | Delayed nephrotoxicity occurs at >10-fold higher doses of S-F than nourseothricin.(A) S-F dosing at 100 mg/kg without obvious histological abnormality in kidney. (B) Nourseothricin dosing at 10 mg/kg showing cellular necrosis and nuclear degeneration of proximal convoluted tubule epithelial cells (arrowheads). Glomeruli and distal tubules were spared. Tissue was harvested 3 days after dosing. Size bar = 20 μM. | PMC10187937 | pbio.3002091.g005.jpg |
0.408968 | 07117e6ac18d4f6fa21ca6c34f86dd41 | Murine thigh infection model.S-F demonstrated substantial therapeutic effect against pandrug-resistant Klebsiella pneumoniae Nevada AR-0636 at doses without observable or minimal toxicity. Dotted line is assay limit of detection. Data points for 5 mice per condition are shown. * designates significant difference from untreated controls using Kruskall–Wallis nonparametric test. Data are available in S5 Data. | PMC10187937 | pbio.3002091.g006.jpg |
0.421902 | 18410bea53134fe399adf29e949ca004 | S-F and S-D binding sites in the ribosome.(A, B) Location of the S-F and S-D binding sites in the A. baumannii 70S ribosome with P-site tRNA, respectively. (C, D) Hydrogen-bonding interactions between the streptolidine moieties of S-F and S-D and C1054 of the 16S rRNA, respectively (E, F) Electrostatic interactions of the S-F and S-D 12-carbamoylated gulosamine moiety with A1196, respectively. (G, H) Electrostatic interactions between β-amino of the β-lysine and the O2’ atoms of C1054 and U1052. Throughout the figure, the 50S is blue, 30S is yellow, S-F is gray sticks, S-D is green sticks, and highlighted residues are cyan. The cryo-EM densities corresponding to the 2 terminal β-lysine moieties of S-D were very weak, indicating that these 2 lysine moieties are flexible. We therefore did not include these 2 terminal β-lysine moieties in panels D, F, and H. cryo-EM, cryo-electron microscopy; S-D, streptothricin D; S-F, streptothricin-F. | PMC10187937 | pbio.3002091.g007.jpg |
0.446778 | fb6456da23d6468196f4e5c775c01896 | (A) Clinical image of multiple itchy erythematous genital lesions covered with delicate scale in a 38-year old man (iPhone 6 camera). (B) Polarized dermatoscopy of one of the genital lesions showing a “delta-wing jet with a contrail sign”; a triangular structure is better seen in the box. (Dermlite DL5 paired with iPhone 6). (C) UV dermatoscopy of the same lesion highlights the bright-blue fluorescence of the burrow, but also visualizes the bright-green fluorescence generated by the female mite’s body (better seen in the box) (Dermlite DL5 paired with iPhone 6). | PMC10188151 | dp1302a135g001.jpg |
0.503669 | 37f650c8a0b0435fafc1010adb5c3536 | (A) Presence of bluish indurated plaque of right arm. (B) Diffuse proliferation of spindle cells in a storiform pattern. Some cells contain abundant melanin. (H&E x4). | PMC10188180 | dp1302a117g001.jpg |
0.489988 | 87803e38af784a42a73b7131c6804515 | (A,B) Diffuse white-bluish pigmentation associated to white streaks (black square). Arborizing vessels are present over the entire lesion and are not focused (white square). At periphery, a pigmented network is evident (black arrow). In some part of the lesion this network appears linearly stretched (black circle). | PMC10188180 | dp1302a117g002.jpg |
0.490711 | d0de170352d54945adc214e76f150247 | Schematic presentation of this study.Illustration of using COFs as adsorbents to selectively reduce indole intake to delay the progression of chronic kidney disease. | PMC10188479 | 41467_2023_38427_Fig1_HTML.jpg |
0.41033 | bf5388ef8b2a41d983de42c28b205965 | Characterization of NKCOFs.a Chemical structures of the COFs. b FT-IR spectra of NKCOF-12 and corresponding monomers: TFB (purple), TMT (blue), NKCOF-12 (red). c PXRD patterns of NKCOF-12: measured patterns (red), simulated pattern (black). d Nitrogen adsorption and desorption isotherms of NKCOF-12. The inset shows the pore size distribution profile of NKCOF-12. e SEM image of NKCOF-12 (scale bar = 300 μm, inset: magnified field of view, scale bar = 10 μm). This experiment was independently repeated three times. f Histogram of particle size distribution calculated from SEM image. g PXRD patterns of NKCOF-12 after treatment with simulated gastric fluid (SGF) and simulated intestinal fluid (SIF). | PMC10188479 | 41467_2023_38427_Fig2_HTML.jpg |
0.452628 | 3b4006bc79654997bf3eef6277c8c390 | Adsorption experiment of NKCOF-12.a Measurement of indole adsorption capacities of olefin-linked COFs (0.5 mg mL−1) and AST-120 materials as a function of time. b Adsorption kinetic quasi-second-order fitting plots for indole adsorption. c Freundlich model fitting plots for indole adsorption isotherms. d Cumulative release rates of olefin-linked COFs and AST-120 materials. a, d Data were presented as the mean ± SD (n = 3). | PMC10188479 | 41467_2023_38427_Fig3_HTML.jpg |
0.529942 | 5a96a8176b74455bb728e739e62a2a5b | Selective adsorption of NKCOF-12 toward indole.a Affinity of NKCOF-12 for indole in a single solution system. b Selective removal rate of adsorbents for indole in a multicomponent mixture system within 15 min. c Selective removal rate of adsorbents for indole in a multicomponent mixture system within 1 h. d Zeta potentials of NKCOF-12 and different compounds. e FT-IR spectra of indole (blue), NKCOF-12 (green), and their composite (red). f Water contact angle of NKCOF-12. a–c Data were presented as the mean ± SD (n = 3). (IND indole, IAA indole-3-acetic acid, Trp tryptophan, KYNA kynurenic acid). | PMC10188479 | 41467_2023_38427_Fig4_HTML.jpg |
0.452072 | 675ed35d8f66424b8b17a82042be3145 | Molecular size of each compound.a IND. b IAA. c Trp. d KYNA. (IND indole, IAA indole-3-acetic acid, Trp tryptophan, KYNA kynurenic acid). | PMC10188479 | 41467_2023_38427_Fig5_HTML.jpg |
0.39696 | 5f06065e2fb34958a6f3ac42ec2e75f9 | In vitro cytocompatibility and cellular uptake of NKCOF-12.a Cell viability of Caco-2 cells after 24 h incubation with different concentrations of NKCOF-12. Data were presented as the mean ± SD (n = 6). b Confocal images of Caco-2 cells recorded after co-incubation with NKCOF-12 for 24 h. Scale bar = 20 μm. This experiment was independently repeated three times. | PMC10188479 | 41467_2023_38427_Fig6_HTML.jpg |
0.518218 | 118492904aea413fa72d0818e60c3cd2 | Therapeutic effect of NKCOF-12 on CKD mice.a Kidney weight index of mice in different groups (n = 6). b Serum Cr level of mice in different groups (n = 6). c Serum BUN levels of mice in different groups (n = 6). d Serum IS level of mice after drug intervention for 8 weeks (n = 6). e Collagen fiber area percentage of kidney measured by Masson staining (n = 3). a Data were represented as the mean ± SD. b, c Data presented as box-and-whisker plots, whiskers represent minima and maxima. * P < 0.05, **P < 0.01, ***P < 0.001, ns: no significance. Statistics were calculated by one-way ANOVA followed by Tukey’s post-test. Exact P values are given in the Supporting Information file. | PMC10188479 | 41467_2023_38427_Fig7_HTML.jpg |
0.433483 | f4e8d37052d64ea291d04505f572fea6 | Histopathological staining.a Micrographs of H&E-stained kidney slices from mice of different groups. b Micrographs of H&E-stained liver slices from mice of different groups. c Micrographs of H&E-stained intestine slices from mice of different groups. d Micrographs of Masson trichrome-stained kidney slices from mice of different groups. Scale bar = 50 μm. Each experiment was independently repeated three times. | PMC10188479 | 41467_2023_38427_Fig8_HTML.jpg |
0.446671 | 9574f51f14994d80be6126d22c47144d | Neuronal pathogenic detection and cellular signaling pathways. Do ion channels incur specificity? The pathogenic sensing capability of sensory neurons is exemplified by the multitude of pathogenic detection receptors (51–79). These receptors appear to be linked spatially and by protein kinase stimulation/phosphorylation of downstream ion channels. *However, as indicated by the diamond, what forces direct the specific trafficking of protein kinases to specific phosphorylation sites on downstream ion channels? And, to which specific ion channel/set of ion channels? | PMC10189129 | fimmu-14-1184000-g001.jpg |
0.443301 | 2351030b233649c7a9402ca817c3f988 | Sensory innervation of barrier tissues. The innervation of tissues by sensory neurons and the parasympathetic and sympathetic arms of the autonomic nervous system affords constant patrol of mammalian systems. In addition, the enteric nervous system has a layered system of innervation within the gut. These systems allow constant detection and also the possibility of dual stimulation should multiple neurons in different locations/tissues be stimulation. Can parallel and concurrent sensory neuron pathogenic stimulation increase signaling magnitude? The potential for this case has been examined previously (43, 103). | PMC10189129 | fimmu-14-1184000-g002.jpg |
0.38965 | aa2d7c2a0217496d8d4e3c9652f4661d | Graphical abstract of study design and workflow. The panel illustrates the schematic of experimental design and workflow used in this study. Normal rectosigmoid colon biopsies were collected from 18 LS participants [placebo N=6, low dose (LD, 220 mg) N=6, high dose (HD, 440 mg) N=6]. Participants (N=18) provided a pre- and post-exposure biopsy samples (N=36 samples) for tissue micro array (TMA), which was used for image mass cytometry (IMC) and analysis. This figure was generated using BioRender.com. | PMC10189148 | fimmu-14-1162669-g001.jpg |
0.444387 | b0fc4ffe6dea4c2ca29a1d7628a0852f | Immune mass cytometry isolated discrete immune cell populations following tissue segmentation. (A) Fluorescent image of tissue section stained for epithelial and immune cell markers. Upper left: red for CD19, blue for CD3, green for Ru101; Upper right: red for epithelial, green for lymphoid tissue; Bottom left: red for Na/K ATPase, blue for CK, green for Ru101; Bottom right shows Ru101; (B) Tissue section slides stained with multiplex metal-labeled antibody markers. Panel shows the representative image of IMC from an individual sample. Segmentation was performed to demarcate epithelium (cytokeratin, CK) from stroma. Metal-labeled antibody markers are listed in
Table 1
. | PMC10189148 | fimmu-14-1162669-g002.jpg |
0.385297 | a70072e0374345dda190514fc3de2c07 | Chemopreventive naproxen increases activation of cytotoxic T-lymphocytes in the mucosa. (A) Data-driven analysis of the cell population within the mucosa. Change in cell ratio in those immune cell types for the naproxen and placebo groups that showed statistically significant changes. Solid line denotes median and dashed line denotes quartiles. P-values from paired Wilcoxon test from left to right: P=0.032, P=0.048, P=0.0047, P=0.052 (*, P-value<0.05; **, P-value<0.01); (B) Dot-plot graph shows the expression level of stained makers for the four cell types with statistically significant changes between naproxen and placebo groups. The color gradient represents the mean expression level of the corresponding marker in the population. Markers are grouped into categories based on cell type; Red boxes indicate expression markers of highlighted in the text; (C) High-resolution IMC image of Ki67+ (red), CD8a+ (blue), and Ru101 (green) in a LS mucosal sample. The white arrows indicate double-positive CD8+/Ki67+ cells in the colonic mucosa. | PMC10189148 | fimmu-14-1162669-g003.jpg |
0.474445 | dcf9523923444bcd98606fa806a6e881 | Biplots of the principal component analysis (PCA) from the mean values of all vegetables in the present study, with (A, B) showing the PCA analyzed from the mean values of the proximate data (ash, carbohydrates, energy, fats, fiber and protein) of all vegetables, (A) showing the plot between PC1 (41.09%) and PC2 (29.53%), and (B) showing the plot between PC1 (41.09%) and PC3 (17.44%). The PCA (C, D) was analyzed from the mean values of the minerals (calcium, iron, magnesium, potassium, phosphorus, sodium and zinc) and vitamin C of all vegetables, while (C) shows the plot between PC1 (34.43%) and PC2 (23.61%), and (D) shows the plot between PC1 (34.43%) and PC3 (14.88%). Abbreviations – Ac: A. cepa; Af: A. fistulosum; Al: Al. galangal; As: A. sativum; Br: B. rotunda; Cm: C. mangga; Ca: Ca. annuum; Ci: Ci. hystrix; Co: Co. sativum; Cy: Cy. citratus; Ef: E. foetidum; Mc: M. cordifolia; Oa: O. africanum; Ob: O. basilicum; Og: O. gratissimum; Pt: P. tetragonolobus; Sm: So. melongena; Sp: S. pennata; St: So. torvum; Zo: Z. officinale; 1 from source 1; 2 from source 2. | PMC10189170 | gr1.jpg |
0.395269 | 94155d86e0ee4219b5bd37babc9e7faa | The biplots of principal component analysis (PCA) from mean values of carotenoids (capsanthin, lutein, zeaxanthin, β-cryptoxanthin, α-carotene, β-carotene and total carotenoids) of all vegetables. Abbreviations; Ac: A. cepa; Af: A. fistulosum; Al: Al. galangal; As: A. sativum; Br: B. rotunda; Cm: C. mangga; Ca: Ca. annuum; Ci: Ci. hystrix; Co: Co. sativum; Cy: Cy. citratus; Ef: E. foetidum; Mc: M. cordifolia; Oa: O. africanum; Ob: O. basilicum; Og: O. gratissimum; Pt: P. tetragonolobus; Sm: So. melongena; Sp: S. pennata; St: So. torvum; Zo: Z. officinale; 1 from source 1; 2 from source 2. | PMC10189170 | gr2.jpg |
0.478934 | c34ba843ab604ddaac6b7651ca5b6097 | The dendrogram of hierarchical cluster analysis (HCA) derived from the mean data of the proximate data (ash, carbohydrates, energy, fats, fiber and protein), minerals and vitamin C (calcium, iron, magnesium, potassium, phosphorus, sodium, vitamin c and zinc) and carotenoids (capsanthin, lutein, zeaxanthin, β-cryptoxanthin, α-carotene, β-carotene and total carotenoids) of all vegetables. Abbreviations; Ac: A. cepa; Af: A. fistulosum; Al: Al. galangal; As: A. sativum; Br: B. rotunda; Cm: C. mangga; Ca: Ca. annuum; Ci: Ci. hystrix; Co: Co. sativum; Cy: Cy. citratus; Ef: E. foetidum; Mc: M. cordifolia; Oa: O. africanum; Ob: O. basilicum; Og: O. gratissimum; Pt: P. tetragonolobus; Sm: So. melongena; Sp: S. pennata; St: So. torvum; Zo: Z. officinale; 1 from source 1; 2 from source 2. | PMC10189170 | gr3.jpg |
0.438534 | f1a019620b9e465dae2d3264f037695f | The abdominal Magnetic Resonance Imaging confirmed the presence of a 11 × 9 cm-sized right adrenal tumor with hyposignal on T1 and hypersignal on T2. | PMC10189252 | gr1.jpg |
0.429532 | cded01f817264951a660bf18532b60f6 | Activin A is associated with OA through ACVR2B. a) Heatmap of Gdf5, Gdf8, Gdf11, and activin A expression in cartilage from human OA patients, SRT/ort OA mice, and DMM‐operated mice, and in IL‐1β treated human chondrocytes. b,c) Images of Alcian blue or Safranin‐O staining and activin A immunostaining in human OA cartilage and DMM‐operated mouse cartilage (b,c; left, n = 10), with immunostaining intensity (b,c; right). d) The indicated molecules were determined by qRT‐PCR analysis of mouse primary chondrocytes treated with 200 ng mL−1 of Gdf5, 8, 11, or activin A. e) GSEA of OA signature genes in chondrocytes infected with Ad‐C or Ad‐activin A. f) Western blot images of the indicated molecules after chondrocytes were treated with recombinant activin A (left), infected with Ad‐activin A (middle), or treated with the indicated concentrations of activin A siRNA (right). g) Mmp3, Mmp13, and Cox‐2 expression levels after knockdown of ACVR2A, ACVR2B, or BMPR2 in activin A‐treated chondrocytes. Tidemarks are indicated by yellow dotted lines (c). Values are presented as means ± SD, and were assessed using two‐tailed t‐test (b,c) or one‐way ANOVA with Bonferroni's post‐hoc test (d,g). **p < 0.01; ***p < 0.001. | PMC10190289 | ADVS-10-2205161-g001.jpg |
0.456906 | 8fa1fd9512284f9183dc6b75a7d16a4d | Trapping activin receptor IIB (ACVR2B) ligands attenuates OA and metabolic OA pathogeneses. a,b) Sham‐ or DMM‐operated WT mice were IA injected with PBS as a vehicle or sACVR2B‐Fc (10 µg in a total volume of 10 µL) to block interactions between ACVR2B and its ligands, and sacrificed at 10 weeks after the surgery (n = 10). a) Schematic of the experimental procedure used for vehicle or sACVR2B‐Fc knee‐joint injection prior to DMM surgery. b) Representative Safranin‐O staining images of joint sections (left) and scoring of OARSI grade (right). c,d) HFD‐fed sham‐ or DMM‐operated WT mice were sacrificed at the indicated days after surgery (n = 5). c) Schematic showing the experimental procedure for a vehicle or sACVR2B‐Fc knee‐joint injection in HFD‐fed mice induced with DMM surgery. d) Representative Safranin‐O staining images of cartilage sections (left) and scoring of OARSI grade (right). Tidemarks are indicated by yellow dotted lines (b,d). Values are presented as means ± SD and were assessed using the Kruskal‐Wallis test followed by Mann‐Whitney U test (b,d; right). *p < 0.05; **p < 0.01; ***p < 0.001, ns; not significant. Scale bar: 100 µm. | PMC10190289 | ADVS-10-2205161-g002.jpg |
0.488085 | 64d9f4fd9cf4474cbb571982d0154c31 | Upregulation of ACVR2B in OA cartilage is necessary for OA pathogenesis. a) Schematic summary of screening for novel pathogenic receptors. b) DMM‐operated mice were sacrificed at the indicated weeks after surgery (n = 5). Safranin‐O staining images of cartilage sections (upper left), scoring of OARSI grade (upper right), and immunostaining image density analysis (lower). c) Upregulation of ACVR2B in human OA cartilage (n = 10). Images show Alcian blue and immunostaining of ACVR2B in human OA cartilage (left) and analysis of immunostaining intensities (right). d,e) Primary‐culture mouse articular chondrocytes were treated with ACVR2B siRNA (n = 4). Shown are (d) Western blot images of the indicated molecules, along with (e) collagenase activity (left) and PGE2 production (right). f,g) DMM‐operated WT mice were IA injected with Ad‐ACVR2B shRNA (Ad‐shA) in the joint tissues. Shown are a schematic of the experimental procedures used for Ad‐ACVR2B shRNA injection (f, upper left), Safranin‐O staining images of joint sections (n = 10) (f, upper right), scoring of OARSI grade (f, right), and IHC intensity analysis (g). Yellow dotted lines indicate tidemarks (b,f). Values are presented as means ± SD, and were assessed using two‐tailed t‐test (c; right), one‐way ANOVA with Bonferroni's post‐hoc test (b, e, g), and Kruskal‐Wallis test followed by Mann‐Whitney U test (f). **p < 0.01; ***p < 0.001, ns; not significant. Scale bar: 100 µm. Ad‐shC, control shRNA adenovirus. Ad‐shA, ACVR2B shRNA adenovirus. | PMC10190289 | ADVS-10-2205161-g004.jpg |
0.430221 | 9b57d5acfc4a463c94be0dbf0335de60 | Activin A is a critical catabolic regulator of OA pathogenesis. a) Schematic illustration of the strategy used to concentrate conditioned media from chondrocytes of WT and activin A Tg mice (left), along with Western blot images (middle) and relative protein intensity levels (right) of the indicated molecules. The culture medium from Wt and activin A Tg chondrocytes were collected for 24 h, concentrated it to 10×, and applied the indicated volumes (in µL) of the concentrate to normal chondrocytes. (n = 5). b) Cartilage destruction in 18 month old WT (n = 5) and activin A Tg (n = 9) mice was determined by Safranin‐O staining (left) and OARSI scoring (right). c) Safranin‐O staining images of joint sections (left) and scoring of OARSI grade (right) (n = 10). d) 3D µCT images (left; n = 5) and stacked‐bar plot showing the trabecular bone thickness distribution of the indicated samples (right). e) The elastic modulus of cartilage, as measured by bioindentation (n = 5). f) Safranin‐O staining images of joint sections (left) and scoring of OARSI grade (right) (n = 10). g) Representative 3D µCT images (left; n = 5) and stacked‐bar plot showing the trabecular bone thickness distribution of the indicated samples (right). h) The elastic modulus of cartilage, as measured by bioindentation (n = 5). Tidemarks are indicated by yellow dotted lines (b,c,f). Values are presented as means ± SD and were assessed using one‐way ANOVA with Bonferroni's post‐hoc test (a), two‐tailed t‐test (b), or Kruskal‐Wallis test followed by Mann‐Whitney U test (c,e,f,h). **p < 0.01; ***p < 0.001. Scale bar: 100 µm. | PMC10190289 | ADVS-10-2205161-g005.jpg |
0.476662 | 2cf23e25d6e340fc96b50318a6f16f00 | ACVR1B and AP‐1 are required to complete the ACVR2B assembly and thereby accelerate OA. a,b) Chondrocytes were treated with rActivin A (200 ng mL−1) in the absence or presence of 100 × 10−9
m of control siRNA (C‐si) or 50 × 10−9
m to 100 × 10−9
m of siRNA against type I receptors (ACVR1A, ACVR1B, ACVR1C, BMPR1A, or BMPR1B; n = 5). a) Relative mRNA levels of the indicated molecules, as assessed by qRT‐PCR analysis. b) Representative Western blot images (upper) and relative protein intensity levels (lower) of p‐Smad2/3 in type I receptor‐knockdown chondrocytes treated with rActivin A. c) Computational docking models for ACVR2B (cyan), ACVR1B (pink), and NOX4 (olive) (upper). Purple: ACVR1B transmembrane domain. Green: NOX4 binding sites (lower). d) Interaction of endogenous ACVR2B and ACVR1B heterodimers with endogenous Nox4 in IL‐1β‐treated or Ad‐activin A‐infected chondrocytes (n = 3). e) Profiling of activin A‐ or Nox4‐induced transcription factors. List of the highest‐ and lowest‐expressed transcription factors in Ad‐activin A‐ or Ad‐Nox4‐infected chondrocytes. Ad‐C‐infected chondrocytes were used as controls. f) Chondrocytes were infected with Ad‐C, Ad‐activin A, or Ad‐Nox4 in the presence of 20 × 10−6
m of T5224 for 24 h. Representative qRT‐PCR analysis results for the indicated molecules (n = 8). Values are presented as means ± SD and were assessed using one‐way ANOVA with Bonferroni's post‐hoc test (a,b,f) and two‐tailed t‐test (e). *p < 0.05; **p < 0.01; ***p < 0.001, ns; not significant. | PMC10190289 | ADVS-10-2205161-g006.jpg |
0.413833 | 00dbd0f862304405b8d830673b80e872 | Nox4 is a critical downstream catabolic mediator of the activin A‐ACVR2B axis in OA pathogenesis. a) GSEA (upper) and heatmap of ROS‐related genes (lower) altered following Ad‐activin A infection in chondrocytes. b) Intracellular ROS levels in postnatal chondrocytes of activin A Tg (red line) and WT littermate (black line) mice. c) Intracellular ROS levels in chondrocytes infected with 800 MOI of Ad‐C (black line), Ad‐activin A (blue line), or Ad‐Nox4 (red line). d) Intracellular ROS levels of chondrocytes infected with Ad‐C (orange line) or Ad‐activin A (blue line) in the presence of diphenyleneiodonium (green line) or Nox4 siRNA (yellow line). Quantification of ROS fluorescence intensity (b,c,d; right; n = 5). e–g) DMM‐operated activin A Tg:Nox4 KO mice were analyzed. Shown are Safranin‐O staining images of joint sections (e; n = 10), the elastic modulus of cartilage determined by bioindentation (f; n = 5), 3D µCT images (g; left), and the trabecular bone thickness distribution (g; right; n = 5). h) Computational docking models for ACVR2B (cyan) and NOX4 (olive). Pink: ACVR2B transmembrane domain. Green: NOX4 binding sites (lower). i) Chondrocytes were transfected with WT ACVR2B or muACVR2B. Cell lysates were subjected to immunoprecipitation (IP) with FLAG (n = 3). Yellow dotted lines indicate tidemarks (e). Values are presented as mean ± SD and were analyzed using two‐tailed t‐test (b), one‐way ANOVA with Bonferroni's post‐hoc test (c,d), or Kruskal‐Wallis test followed by Mann‐Whitney U test (e,f). **p < 0.01; ***p < 0.001. Scale bar: 100 µm. | PMC10190289 | ADVS-10-2205161-g007.jpg |
0.454453 | 3e969f107d244c0ca7657d83d2064b12 | Chronic low‐dose Cd exposure results in malignant lesions in the mouse lung and malignant transformation of bronchial epithelial cells. A) Representative H&E staining of lung lesions in untreated and Cd‐treated mice after 45 weeks. Scale bar = 100 µM. B) Concentration of Cd in mouse serum. n (Control) = 10, n (Cd) = 10. C) Immunohistochemical analysis of Aldh1a1 and Sox2 expression levels in the lung tissue of untreated and Cd‐treated mice. Scale bar = 100 µM. D) Expression levels of Aldh1a1 and Sox2 in the lung tissue of untreated and Cd‐treated mice were assessed by Western blot analysis. n (Control) = 10, n (Cd) = 10. E) Relative levels of proliferation of BEAS‐2B (above) and 16HBE (below) Cd‐transformed cells were determined using the CCK8 assay. F) The Transwell assay was used to determine levels of migration in Cd‐transformed cells. G) The Transwell assay was used to assess levels of invasion in Cd‐transformed cells. H) Sphere formation with unanchored growth of Cd‐transformed cells. I–K) The tumor volumes and weights of Cd‐induced tumors in a nude mouse xenograft model. *p < 0.05, **p < 0.01, ***p < 0.001. | PMC10190647 | ADVS-10-2206896-g002.jpg |
0.406379 | e4e5629b8c494d86bbbf6de63c3b02ec | Expression and function of circCIMT in a Cd‐induced model of malignant transformation. A) Concentration of Cd in human urine. n (normal) = 19, n (cancer) = 14. B) circCIMT expression in human normal and cancer lung tissues. n (normal) = 19, n (cancer) = 14. C,D) q‐PCR was used to determine circCIMT expression levels in the lung tissue (C) and blood (D) of untreated and Cd‐treated mice. n (Control) = 10, n (Cd) = 10. E) Correlation between circCIMT (2−ΔCT) levels and Cd concentration in mouse blood. F,G) circCIMT expression levels were examined in Cd‐transformed BEAS‐2B (F) and 16HBE (G) cells. H,I) The CCK8 assay was used to examine the effects of circCIMT knockdown and overexpression on the proliferative abilities of Cd‐transformed BEAS‐2B cells. J,K) The Transwell assay was used to determine the effects of circCIMT knockdown (J) and overexpression (K) on the migration of Cd‐transformed BEAS‐2B cells. L,M) The Transwell assay was used to determine the effects of circCIMT knockdown (L) and overexpression (M) on the invasive abilities of Cd‐transformed BEAS‐2B cells. *p < 0.05, **p < 0.01, ***p < 0.001. | PMC10190647 | ADVS-10-2206896-g003.jpg |
0.422605 | d3bac59cb3c74308ada97b37bdeafb03 | Simultaneous knockdown of circCIMT and APEX1 promotes expression of tumor‐associated genes and malignant transformation of cells. A) KEGG scatter plot of CSC‐like pathway gene sets in si‐circCIMT‐ versus si‐NC‐treated cells. B) Pik3cb, Myc, Cdkn1a, and Smad3 mRNA expression levels in human lung tissue. n (normal) = 19, n (cancer) = 14. C–F) Pik3cb, Myc, Cdkn1a, and Smad3 mRNA expression levels were detected in chronic Cd‐treated cells simultaneously treated with si‐circCIMT and si‐APEX1. G) The EdU assay was used to assess cell proliferation levels in chronic Cd‐exposed cells simultaneously treated with si‐circCIMT and si‐APEX1. H) Anchorage‐independent cell growth ability was measured in 16HBE cells continuously exposed to Cd for 25 weeks. I–K) Tumor volumes and weights in nude mice injected with knockdown of both circCIMT and APEX1 cells and exposed to Cd. n (NC) = 6, n (circCIMT sh) = 6, n (circCIMT sh+APEX1 sh) = 6. *p < 0.05, **p < 0.01, ***p < 0.001 | PMC10190647 | ADVS-10-2206896-g004.jpg |
0.421338 | aff59e72c52c4f31966cf0c98c2b625f | circCIMT‐interference inhibits the expression of nuclear base excision repair (BER) complex proteins after Cd exposure. A–C) Western blot analysis of γ‐H2AX, APEX1, XRCC1, PARP1, and LIG3 protein expression levels in Cd‐exposed cells following treatment with circCIMT#2‐ and circCIMT‐overexpression vectors. D–F) Western blot analysis of APEX1, XRCC1, PARP1, and LIG3 protein expression levels in Cd‐treated cells after circCIMT knockdown. G) Co‐localization and expression of APEX1, XRCC1, PARP1, and LIG3 were detected in circCIMT‐silenced cells exposed to Cd by immunofluorescence staining. Scale bar = 5 µM. H) Nuclear/cytoplasmic circCIMT levels were analyzed in control and Cd‐treated cells. I) Western blot analysis of the nuclear/cytoplasmic protein levels of APEX1, XRCC1, PARP1, and LIG3 in Cd‐exposed cells following circCIMT knockdown. *p< 0.05, **p < 0.01, ***p < 0.001. | PMC10190647 | ADVS-10-2206896-g005.jpg |
0.479776 | 12f0fa4f57ed4ced80093a2da35cad35 | circCIMT interacts with APEX1 to suppress DNA damage. A) Mass spectrometry analysis of APEX1 on the circCIMT RNA pull‐down assay samples. B) The interaction between circCIMT and APEX1 was confirmed by western blot analysis of the circCIMT pull‐down samples. C) The RIP assay using an anti‐APEX1 antibody was used to confirm that circCIMT and APEX1 interacted with each other. D) APEX1 expression in the lung tissue of untreated and Cd‐treated mice was assessed by western blot analysis. n (Control) = 10, n (Cd) = 10. E) Correlation between APEX1 (APEX1/Tubulin) and circCIMT (2−ΔCT) in mouse lung tissue. F) γ‐H2AX levels in si‐APEX1‐treated BEAS‐2B and 16HBE cells were assessed by western blot analysis. G) γ‐H2AX levels in APEX1‐overexpressing BEAS‐2B and 16HBE cells were examined by western blot analysis. H) Western blot analysis of APEX1 protein expression levels in 16HBE cells after simultaneous knockdown of circCIMT and APEX1. I) The number of γ‐H2AX foci was detected by immunofluorescence staining after circCIMT and APEX1 co‐interference. Scale bar = 5 µM. *p < 0.05, **p < 0.01, ***p < 0.001. | PMC10190647 | ADVS-10-2206896-g006.jpg |
0.423841 | f660810ec96f4be2a9ccd25232526de0 | circCIMT suppresses Cd‐induced DNA damage. A) γ‐H2AX foci levels were detected in BEAS‐2B and 16HBE cells exposed to different concentrations of Cd by immunofluorescence staining. Scale bar = 5 µM. B) γ‐H2AX expression levels were assessed in BEAS‐2B and 16HBE cells exposed to different concentrations of Cd by western blot analysis. C) The comet assay was used to measure DNA damage levels in Cd‐treated BEAS‐2B and 16HBE cells. D) γ‐H2AX expression levels were measured in the lung tissue of untreated and Cd‐treated mice by western blotting. n (Control) = 10, n (Cd) = 10. E) Relative 8‐OHdG expression levels were detected in the serum from untreated and Cd‐treated mice. n (Control) = 10, n (Cd) = 10. F,G) The effects of circCIMT knockdown (F) and overexpression (G) on γ‐H2AX levels in untreated and Cd‐treated BEAS‐2B and 16HBE cells were examined by western blot analysis. H) The comet assay was used to measure DNA damage levels in Cd‐treated BEAS‐2B and 16HBE cells following circCIMT knockdown and overexpression. *p < 0.05, **p < 0.01, ***p < 0.001. | PMC10190647 | ADVS-10-2206896-g007.jpg |
0.421203 | d1206be5a7d641eb93bef0876697fcf0 |
(A) Identified signals that contribute the most to the outgoing or incoming signaling of individual cell groups. (B) PPI analysis of ICD signaling pathway genes. (C) Outgoing communication patterns of secreting cells. (D) Incoming communication patterns of target cells. | PMC10191229 | fimmu-14-1087978-g001.jpg |
0.410331 | 758cab50699246c5bf038fd0d5b42f9c |
(A) Endothelial cells release ligands that act on myeloid cells (macrophages, monocytes and dendritic cells) and T cells (CD4 T/NK cells and cytotoxic T cells). (B) Fibroblasts release ligands that act on myeloid cells and T cells. (C) VSMCs release ligands that act on myeloid cells and T cells. (D) Cytotoxic T cells release ligands that act on nonimmune cells (fibroblasts, VSMCs, endothelial cells). (E) CD4 T/NK cells release ligands that act on nonimmune cells. (F) Mature dendritic cells release ligands that act on nonimmune cells. (G) Monocytes release ligands that act on nonimmune cells. (H) Macrophages release ligands that act on nonimmune cells. | PMC10191229 | fimmu-14-1087978-g002.jpg |
0.416484 | 75c5155961de436cbbf20a92f60858d0 | Data processing and defining cell types. (A, B) Harmony package sample batch effect elimination and PCA dimensionality reduction. (C) t-SNE dimensionality reduction. (D) The t-SNE results were divided into 10 cell populations using marker genes. (E–T) Sixty clusters defined using marker genes. | PMC10191229 | fimmu-14-1087978-g003.jpg |
0.375494 | eca7ca0f0ef940e593f342856380ea05 |
(A–L) Sixty clusters defined using marker genes. (M) The expression of cell type marker genes is shown in the dot plot. (N–O) Proportion of various types of cells in each sample. | PMC10191229 | fimmu-14-1087978-g004.jpg |
0.42134 | 5f575db4263c4dec825fb26820402f18 |
(A) ICD marker gene heatmap in ten cell types. (B) GSEA for differentially expressed genes between different cell types. (C) GO analysis of the differentially expressed genes between the endothelial and VSMC clusters. (D) KEGG analysis of the differentially expressed genes between the endothelial and VSMC clusters. | PMC10191229 | fimmu-14-1087978-g005.jpg |
0.486534 | 1129342eef1c467c90e889ab0fe04019 | Ferric maltol mechanism of action. Fe2+ = ferrous iron; Fe3+ = ferric iron. | PMC10191551 | pg9-2-e090-g001.jpg |
0.386614 | 87794e0e7b854177b88c53f291776db0 | Response–time profiles for (A) mean serum iron (g/mL) and (B) mean TSAT (%) by ferric maltol dose on day 1 (left panels) and day 10 (right panels) in the intention-to-treat population. b.d. = twice daily; TSAT = transferrin saturation. | PMC10191551 | pg9-2-e090-g002.jpg |
0.49215 | 08a55c951dd345fb92addb3baa424b0f | Measurement of skin-to-the anterior wall of rectus sheath distance using the tip of the Veress needle in neutral position (a); in manuel elevation (b) and during fascial elevation (c). | PMC10191715 | FVVinObGyn-14-171-g001.jpg |
0.482798 | 583d53b50e3e496198f734272cadeb63 | Illustration of the measurement methods used in this study: (1) in neutral position, (2)during manual elevation and(3) during fascia elevation by a forceps. | PMC10191715 | FVVinObGyn-14-171-g002.jpg |
0.402513 | a48d1c545e9a403e86e3801be1999844 | Nomogram for predicting 3-year overall survival. BMI, body mass index; CMT, adjuvant chemotherapy. | PMC10191766 | ogs-22262f1.jpg |
0.418016 | cc32961100cc410bb3b36c9a72f63e2f | Calibration curves of the nomogram. Solid line represents the actual nomogram; gray line represents the ideal agreement between the actual and predicted probabilities of 3-year overall survival; vertical bars represent 95% confidence interval; dots correspond to apparent predictive accuracy; and crosses mark the bootstrap-corrected estimates. | PMC10191766 | ogs-22262f2.jpg |
0.432111 | 24ae5883ba93497ea163c164850885d6 | Illustration of a symmetrical bifactor model. The circle labelled ‘G’ is the general factor and the circles labelled ‘S’ are specific factors. Squares represent indicators (e.g., items of an assessment measure). Arrows represent the correlation between a factor and one of its indicators. In a symmetrical bifactor model, every indicator loads on the general factor and on one specific factor. The factors are set to be orthogonal (i.e., uncorrelated), thereby completely partitioning the systematic variance into components due to the general and specific factors. | PMC10192445 | 41598_2023_35017_Fig1_HTML.jpg |
0.499229 | 23c41a57097c4161b734316ec3d94718 | Path diagram of the confirmatory symmetrical bifactor (A) and unidimensional models (B) of the HADS (n = 874). Factor loadings considered at least adequate (absolute λ ≥ 0.32) are shown in boldface. Significant factor loadings are indicated with an asterisk. All factor loadings were significant (all ps ≤ 0.001) except for the loadings of Items 7 and 11 on the specific anxiety factor (ps > 0.05). ANX anxiety subscale item, DEP depression subscale item. | PMC10192445 | 41598_2023_35017_Fig2_HTML.jpg |
0.439984 | f5a6d02de64a4b368806b4ed3b7464c9 | Box plots showing the distributions of HADS total (A), anxiety subscale (B), and depression subscale scores (C) between four psychiatric diagnostic groups (total n = 184). Dots represent the HADS scores of individual participants. Group means were compared using Tukey’s honest significant difference, with p-values adjusted for multiple comparisons. HADS Hospital Anxiety and Depression Scale, SCID Structured Clinical Interview for DSM-IV Axis I Disorders. NO DX no SCID diagnosis of any Axis I disorder (n = 108). ANX ONLY SCID diagnosis of one or more anxiety disorders but no depressive disorder (n = 19). DEP ONLY SCID diagnosis of a depressive disorder but no anxiety disorder (n = 23). COMORBID = SCID diagnoses of both one or more anxiety disorders and a depressive disorder (n = 34). *Adjusted p < 0.05, **adjusted p < 0.01, ***adjusted p < 0.001, ****adjusted p < 0.0001, ns non-significant (adjusted p ≥ 0.05). | PMC10192445 | 41598_2023_35017_Fig3_HTML.jpg |
0.453868 | cf8a3fffbf294155a4edd68934764a48 | Model for the analysis of the relationships between recognition at work, health-related quality of life, depression, anxiety and job satisfaction. QOL, quality of life. | PMC10193074 | bmjopen-2021-051933f01.jpg |
0.469407 | 010c89ed23f047b9a8aa6c1d80be5107 | Representation of the path analysis model with GOF. Solid line represents the relationship between variables with β coefficient standardised. Dotted line represents the path with an inverse relationship. GOF: CFI=0.98, TLI=0.96, RMSEA=0.039, SRMR=0.036. *Path with statistically significant relationship (p<0.05). CFI, comparative fit index; GOF, goodness of fit; QOL, quality of life; RMSEA, root mean square error of approximation; SRMR, standardised root mean square; TLI, Tucker-Lewis index. | PMC10193074 | bmjopen-2021-051933f02.jpg |
0.447112 | 9ce7b8b29dd14cb6b2ddd9ebd9ec86f8 | Outline of the Snakemake RenSeq workflows. SMRT-RenSeq (green) assembles RenSeq HiFi reads and produces assembly and NLR summary statistics. AgRenSeq (red) takes a metadata file of diversity panel reads and can use the output of SMRT-RenSeq as a reference for k-mer mapping. It outputs highly associated contigs and NLR loci as well as k-mer scoring plots and mapping of contigs to a reference genome. dRenSeq (blue) can use a list of NLRs of interest or the output from AgRenSeq to calculate read coverage | PMC10193785 | 12859_2023_5335_Fig1_HTML.jpg |
0.426188 | 21c3bfdbed7e4085b477648fb2c59368 | Output plots produced by the Ag-RenSeq snakemake workflow. A Dot plot of the analysed contigs in the Ag-RenSeq workflow. Each contig in the assembly is arranged on the x-axis, with k-mers plotted on the y-axis. The size of the dot represents the number of k-mers. Contigs with k-mers above a threshold association score of 26 are highlighted in red. B A plot of NLRs by chromosomal location based on the DM reference assembly. The grey bars represent the number of NLRs per 1000 kb. The red dot represents the location of contigs scored as positive by the association genetics following a BLAST analysis | PMC10193785 | 12859_2023_5335_Fig2_HTML.jpg |
0.471159 | 47812458bd8d48cba4ff094ea7f5c624 | Diglyphusdifasciatus sp. nov. 1 female holotype, habitus, dorsal view 2 male paratype, habitus, dorsal view. | PMC10193845 | zookeys-1148-065_article-98853__-g001.jpg |
0.424268 | 7a7ca9db7f514f6fb1187b8c2a549143 | Diglyphus spp. 3–7D.difasciatus sp. nov. 3 female paratype, habitus, lateral view 4 female paratype, antenna, lateral view 5 male paratype, head, lateral view 6 male paratype, mesosoma, dorsal view 7 female holotype, left fore and hind wings, dorsal view 8D.bimaculatus Zhu, LaSalle & Huang, female, left fore and hind wings, dorsal view. | PMC10193845 | zookeys-1148-065_article-98853__-g002.jpg |
0.444767 | 3b3414ae03b04beda90d1e4ee85476d3 | Diglyphusbimaculatus9 female habitus, lateral view 10 male habitus, dorsal view. | PMC10193845 | zookeys-1148-065_article-98853__-g003.jpg |
0.540195 | 897d2dff0a274eebb436f1f2409fb2bb | Collection sites of Diglyphusdifasciatus sp. nov. in China from 2016 to 2022. | PMC10193845 | zookeys-1148-065_article-98853__-g004.jpg |
0.411498 | 4d79e7b169324e868f939631a210acb4 | Phylogenetic tree of the three Diglyphus species based on the COI gene. The phylogenetic tree was constructed using the maximum likelihood method based on the Neighbor-Joining model. Accession numbers submitted to GenBank are shown next to each haplotype, and bootstrap support values (≥ 75%) are shown next to the branches. | PMC10193845 | zookeys-1148-065_article-98853__-g005.jpg |
0.452045 | 8430919c9ace4d5fabffd7a769a5bc7a | Family Sharing Chatbot (FSC).A. Opening the FSC landing pageCAPTION: This figure displays the first page that probands see immediately after clicking on their link to open the FSC. This page provides introductory material prior to starting the chatbot conversation.B. Starting the FSC conversationCAPTION: This figure displays the chatbot conversation that probands can engage with in the FSC. The response options at the bottom of the screen are pre-populated for probands to select.C. Sharing from the FSCCAPTION: This figure displays the sharing module at the end of the FSC that probands can utilize to send a CC link to at-risk relatives. The sharing options include email, text message, Facebook messenger, or copied link. | PMC10194298 | gr1.jpg |
0.451969 | bdaa0017da104e2bb364899c96e3e3ec | One Month Chatbot (OMC).A. Opening the OMC landing pageCAPTION: This figure displays the first page that probands see immediately after clicking on their link to open the OMC. This page provides introductory material prior to starting the chatbot conversation.B. Starting the OMC conversationCAPTION: This figure displays the chatbot conversation that probands can engage with in the OMC. The response options at the bottom of the screen are pre-populated for probands to select.C. Nudging to share in the OMCCAPTION: This figure displays the messaging at the end of the OMC that encourages probands to send a CC link to at-risk relatives. | PMC10194298 | gr2.jpg |
0.410505 | 21dc0df421894ca084bf5ff8f29f5fbe | Workflow diagram.CAPTION: This figure displays chatbot workflow for the IMPACT-FH study. All probands were offered a genetic counseling visit and verbally introduced to the family sharing strategies, including the chatbots, during return of their FH result. Probands who did not opt out of receiving chatbots were sent an initial FSC invite and two reminders, regardless of whether or not they started the FSC. Probands who did not opt out of receiving chatbots and did not complete a genetic counseling visit received an initial OMC invite and up to two reminders. Separately, the study team attempted to follow up with each proband one month after return of their FH result for the purpose of discussing their family sharing preferences. | PMC10194298 | gr3.jpg |
0.377721 | d56e1422b8da414d92cef55d5f74f618 | Frequencies of Family Sharing Chatbot (FSC) Utilization by Digital Communication PreferenceEHR: Electronic Health RecordFSC: Family Sharing ChatbotCC: Cascade Chatbot. | PMC10194298 | gr4.jpg |
0.443877 | b95f4e73c2ea4d5ab800f361a6eebbc9 | Answers of the patients values and preferences (in %). | PMC10194409 | gr1.jpg |
0.424633 | 336f50cd37ce4f2584c37740da77b309 | Answers of the patients preference of treatment (in %). | PMC10194409 | gr2.jpg |
0.417157 | 53c13ce1ad57458a825806d749451c3d | Flow diagram of literature search and study selection. | PMC10194801 | medi-102-e33791-g001.jpg |
0.396458 | 04814af15e98441db8a14c625647bda9 | Association between admission antibody TPOAb levels and selenium supplementation after (A) 3 months or (B) 6 months. CI = confidence interval, TPOAb = thyroid peroxidase antibodies, WMD = weighted mean difference. | PMC10194801 | medi-102-e33791-g002.jpg |
0.432136 | b5159bab73c24930ba60272e1c1be37d | Association between admission antibody TgAb levels and selenium supplementation after 3 months (A) or 6 months (B). CI = confidence interval, TgAb = thyroglobulin antibodies, WMD = weighted mean difference. | PMC10194801 | medi-102-e33791-g003.jpg |
0.429878 | 0c981e26b8dd44a1ad2e6680e6ccc606 | Meta-regression analysis assessing the impact TPOAb on WMD. TPOAb = thyroid peroxidase antibodies, WMD = weighted mean difference. | PMC10194801 | medi-102-e33791-g004.jpg |
0.427168 | 9152928600b247bab7070febb3d70618 | Meta-regression analysis assessing the impact TgAb on WMD. TgAb = thyroglobulin antibodies, WMD = weighted mean difference. | PMC10194801 | medi-102-e33791-g005.jpg |
0.375609 | d4fc52267561416eb009fe3e231a0f68 | Summary of study population selection for each outcome, diabetes eye care service use in New Zealand, 2006–2019. | PMC10194990 | pone.0285904.g001.jpg |
0.460819 | 3f4efcb3ede5428ba279177618acd1ea | Rate of biennial screening by District Health Board (DHB) in New Zealand 2006–2019.Note: Incomplete data for six District Health Boards (DHBs) (Bay of Plenty, Hawke’s Bay, Lakes, Hutt Valley, Wairarapa, and Midcentral) meant these DHBs were omitted from analysis; the values displayed are unadjusted rates. | PMC10194990 | pone.0285904.g002.jpg |
Subsets and Splits
No community queries yet
The top public SQL queries from the community will appear here once available.