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0.413606 | 641d2b9b6cc04515aaaa346bb207cdda | The virtues of a simplified approach to biomaterials design should include considerations for the path to clinical translation (top). For instance, a new biomaterial entails a more complex path to clinical translational than repurposing an already-approved device, known by the US FDA as the 510(k) pathway. However, a simple or reductionist approach to biomaterials design does not entail a simple end-product. This is exemplified in the complex functional biomaterials that are realized from modular strategies for additive manufacturing (bottom left) or in routes to use simple biomaterials to harness complex endogenous, and often immune-linked, processes in tissue repair or disease mitigation (bottom right). | PMC9616010 | gr1.jpg |
0.458445 | 6772a2025fef468a9fded6f1cf2d4498 | Logic model for the intervention. The first contact in the different risk factor groups is shown in bold text.*Rehabilitation counsellor, customer counsellor, social counsellor or nurse, depending on local resources. | PMC9617258 | JRM-54-2723-g001.jpg |
0.604334 | 50e8a3fb91524b12bb199250b16b5873 | Imidazo[1,2-a]pyridines evaluated in in vivo preclinical toxicology studies. | PMC9618103 | tfac046f1.jpg |
0.438177 | 4e1add1c5504487d8c7cee1aa30f1f33 | Model 2 corresponding to the comparison between control and 1a-b/3a-b. A) PLS crossvalidated scores plot along with the corresponding density plots for both components derived from kernel density estimates and scaled to a maximum estimated value of 1. Color code: () control, () 1a, () 1b, () 3a, and () 3b. B) Manhattan plots of the significant variables corresponding to the renal functionality parameters. The color code is according to the difference between the estimated group means, more than (blue) or less than (red) the control, 1a, 1b, or 3a. Cutoffs: black (−log10(.05) = 1.3), green (−log10(.01) = 2.0). Key: PLS VIP, VIP from the PLS model; FEG, fractional excretion of glucose; RAU, rationalized arcsine transform. Adjusted P-values (Padj) are reported in Supplementary Table S5. | PMC9618103 | tfac046f2.jpg |
0.439752 | 218b9f13cf9742488ba696ab4bafe914 | Model 3 corresponding to the comparison between control, tween 80, and 2a-b. A) PLS crossvalidated scores plot along with the corresponding density plots for both components derived from kernel density estimates and scaled to a maximum estimated value of 1. Color code: () control, () tween 80, () 2a, and () 2b. Manhattan plots of the significant variables corresponding to the B) renal and C) hepatic functionality parameters. The color code is according to the difference between the estimated group means, more than (blue) or less than (red) the control, tween 80, or 2a. Cutoffs: black (−log10(0.05) = 1.3), green (−log10(0.01) = 2.0). Adjusted P-values (Padj) are reported in Supplementary Table S6. | PMC9618103 | tfac046f3.jpg |
0.504854 | 97a2b6059f0f4ab899685efcb79220a0 | Model 4 corresponding to the comparison between control, peanut oil and 4. A) PLS crossvalidated scores plot along with the corresponding density plots for both components derived from kernel density estimates and scaled to a maximum estimated value of 1. Color code: () control, () peanut oil, and () 4. Manhattan plots of the significant variables corresponding to the B) renal and C) hepatic functionality parameters. The color code is according to the difference between the estimated group means, more than (blue) or less than (red) the control or peanut oil. Cutoffs: black (−log10(.05) = 1.3), green (−log10(.01) = 2.0). Adjusted P-values (Padj) are reported in Supplementary Table S7. | PMC9618103 | tfac046f4.jpg |
0.431343 | eab66342eb124734be02d2a0be87f8a9 | Model 5 corresponding to the comparison between control, peanut oil, and tween 80. A) PLS crossvalidated scores plot along with the corresponding density plots for both components derived from kernel density estimates and scaled to a maximum estimated value of 1. Color code: () control, () peanut oil, and () tween 80. Manhattan plots of the significant variables corresponding to the B) renal and C) hepatic functionality parameters. The color code is according to the difference between the estimated group means, more than (blue) or less than (red) the control or peanut oil. Cutoffs: black (−log10(.05) = 1.3), green (−log10(.01) = 2.0). Adjusted P-values (Padj) are reported in Supplementary Table S8. | PMC9618103 | tfac046f5.jpg |
0.42362 | ee8e4f31e2f14f9ea99fc8562d5f0529 | PRISMA Flowchart for selection of studies included in the systematic review. | PMC9618606 | fimmu-13-997853-g001.jpg |
0.416835 | deb2d4280c1248d19d4dcf833e6129d8 | Quality assessment of the including studies base on QUADAS quality evaluation scale. | PMC9618606 | fimmu-13-997853-g002.jpg |
0.416223 | ec9ef8bb06074ed3b6eaf9cdadf68dfd | Forest plot of combined sensitivity and combined specificity and their corresponding 95% Cl. | PMC9618606 | fimmu-13-997853-g003.jpg |
0.476015 | e34fe5d5ae9c47d6a20faae2433ac7fb | Summary receiver operating characteristics curve and the 95% confidence contour and 95% prediction contour. | PMC9618606 | fimmu-13-997853-g004.jpg |
0.353464 | d24695b9f603458db5467833ab8bd636 | Sensitivity analysis of the result base on the new definition and clinical criteria for sepsis (Sepsis-s and Sepsis-3). Also showed the lower and upper 95% Cl. | PMC9618606 | fimmu-13-997853-g005.jpg |
0.473886 | bb36d76394164876ab48923e3ee8e65a | Fagan nomogram of the RDW test for diagnostic prediction of mortality in adult sepsis. | PMC9618606 | fimmu-13-997853-g006.jpg |
0.515885 | ac81fc3643a8412f8b467e2823ef033e | Deek’s funnel plot for publication bias analysis. A p value=0.52 suggested that the publication bias of this Meta-analysis was low. EES, Effective Sample Size. | PMC9618606 | fimmu-13-997853-g007.jpg |
0.412593 | ccb5a15a26c44ca59d7bebbe36871fe0 | Univariable Meta-regression and subgroup analysis of RDW for predicting of mortality in adult sepsis patients. The forest plot indicated that Test description, Prospective design and Blinded may be responded for the heterogeneity. | PMC9618606 | fimmu-13-997853-g008.jpg |
0.479783 | 46f3095df8cd4557b224a6d6e2745e31 | Structural research model. | PMC9618707 | fpsyg-13-966033-g001.jpg |
0.507102 | 6c51aca3d4a3441cb8a0f720e55cd45f | Research model of hypothesis testing. | PMC9618707 | fpsyg-13-966033-g002.jpg |
0.52019 | dba4e229a5ac4118b696bbbf2bac54c5 | A: AGT-194. The mature human PPT1 enzyme (NP_000301) was fused via a 31-amino acid linker to the carboxyl terminus of each heavy chain of the HIRMAb. Fig. 1B: SDS-Polyachrylamide gelelectrophoresis comparing AGT-194, HIRMAb and BSA. Reducing gradient SDS-PAGE gel shows the separate heavy chain (HC) and light chain (LC) of AGT-194 and the HIRMAb, in comparison to 5% BSA. AGT-194 and the HIRMAb share the same LC; the HC of AGT-194 is ∼40 kDa larger than the HC of the HIRMAb owing to fusion of the PPT1 enzyme. | PMC9618832 | gr1.jpg |
0.438793 | 805301b28ccf420288af9840bdae9410 | Biochemical characterization of AGT-194. A, schematic depiction of the fusion protein consisting of an anti-human insulin receptor antibody (AGT-1) and PPT 1, fused by a linker peptide. B, SDS-PAGE of purified AGT-194. Endotoxin content was <0.07 EU/mg and CHO host cell content 1 ppm. C, Affinity to human insulin receptor as measured by ELISA and enzymatic activity of AGT-194. | PMC9618832 | gr2.jpg |
0.453698 | 2471b582a4e244549aabdfcb53978a03 | The 36-Item Short Form Survey (SF-36).Deviations from the normal mean for different domains of the SF3–6 by using the German version before (blue columns) and after 26 months of treatment with AGT-194 (orange columns), demonstrating substantial improvement in the majority of categories (PHYFU = Physical functioning; PHYRO = Physical Role Function; EMRO = Emotional Role Function; GENHE = General Health Perception; SOFU = Social Functioning; PHYPA = Physical Pain; PSYC = Psychological Well-Being; VITA = Vitality). | PMC9618832 | gr3.jpg |
0.424209 | c9f3f064623c418d9fb1c9f1cd30b1a9 | Time course of myoclonic seizure frequency after the treatment with AGT-194. | PMC9618832 | gr4.jpg |
0.398021 | 580c2f1d8aa847febeb50bcfe45baa35 | Transverse ultrasound image through the scrotum shows a partially imaged extratesticular mass (white arrows), area of central necrosis (red arrows), right testis (yellow arrow), and partially imaged right hydrocele (blue arrow). | PMC9619145 | gr1.jpg |
0.441142 | fa7f2dd7a36c4bcaba0056f1edd2ece4 | Longitudinal (A) and transverse (B) ultrasound image through the scrotum shows an extratesticular mass (white arrows) and areas of central necrosis (red arrows). | PMC9619145 | gr2.jpg |
0.59452 | 60fd9af868824a1c8a89b3544a019ffa | H&E (10×) shows pleomorphic spindle cells with eosinophilic cytoplasm forming fascicles intersecting at right angles. | PMC9619145 | gr3.jpg |
0.539164 | 68d5b813855144e08f3b38d7653570ed | H&E (10×) showing large area of necrosis (pink geographic area). | PMC9619145 | gr4.jpg |
0.599274 | 71f697a2781942a2a015c9f9c2bc327a | H&E (40×) displaying marked cytologic atypia and frequent mitotic figures. | PMC9619145 | gr5.jpg |
0.507779 | bdeb3de40dda47ff88f6791b291d02e9 | Desmin immunostain (10×) shows the tumor is strongly and diffusely positive for desmin, and negative for myoD1 and myogenin (not shown) by immunohistochemistry, supporting their smooth muscle lineage. | PMC9619145 | gr6.jpg |
0.435989 | 7cec394d0b264729be54d92d1e693e0c | Long-axis superficial ultrasound image of the left upper arm shows a soft tissue mass (yellow arrow). | PMC9619145 | gr7.jpg |
0.460907 | 46c5a5935de54481b69aa4d271ee6799 | Axial IV contrast-enhanced CT image through the pelvis shows a soft tissue nodule in the right inguinal region compatible with lymph node metastasis (yellow arrow). | PMC9619145 | gr8.jpg |
0.432079 | 11fad70a2aa54831a3eed7778be6c2bc | Axial IV contrast-enhanced CT image through the chest shows subcentimeter pulmonary nodules in the right middle lobe and in the left lower lobe (blue arrows). | PMC9619145 | gr9.jpg |
0.430067 | d630ade6c13346eb8f0b5a39c8f2ac05 | Relative distribution of PRRSV ORF5 genes detected from 2018 to 2020 and analyzed in this study between different Clusters. | PMC9620939 | epidemiologia-03-00022-g001.jpg |
0.467354 | 09745e0e2eaf44ce845b71891c4a2c14 | Relative distribution of PRRSV ORF5 genes detected from 2018 to 2020 and analyzed in this study by admirative region between different Clusters. Each patterned circle represents a region of Japan. | PMC9620939 | epidemiologia-03-00022-g002.jpg |
0.412012 | e26d13fc61ee4066980240c9838526e2 | Homology distribution of PRRSV isolates classified in Cluster I (A,B), Cluster II (C), Cluster III (D), Cluster IV (E), and Cluster V (F) detected from 2018 to 2020. The reference strains used were Prime Pac® MLV (A) and Fostera® PRRS (B) for Cluster I, Ingelvac® PRRS MLV for Cluster II, EDRD-1 for Cluster III, Jpn5-37 for Cluster IV, and Jos1 for Cluster V. Blue, orange, and gray bars indicate 2018, 2019, and 2020, respectively. | PMC9620939 | epidemiologia-03-00022-g003.jpg |
0.507383 | 0d8a14a39b114865bfda6223847b0639 | Schematic representation of measured radial artery by ultrasound. | PMC9622370 | cad-33-648-g001.jpg |
0.510982 | 9af1c8946c8a4c2486c393ef9efee2ec | Trial profile. | PMC9622370 | cad-33-648-g002.jpg |
0.513116 | 1562d76aed9148908ccf08bc111399b5 | Comparisons of FMD across baseline, 24 and 48 h after transradial catheterization. *P < 0.05 vs. baseline; **P < 0.01 vs. baseline; ∆P < 0.05 nifedipine vs. control; ∆∆P < 0.01 nifedipine vs. control. (a) The FMD of distal RA in the cannulated arm. (b) The FMD of distal RA in the noncannulated arm. (c) The FMD of proximal RA in the cannulated arm. (d) The FMD of proximal RA in the noncannulated arm. FMD, flow-mediated dilation; RA, radial artery. | PMC9622370 | cad-33-648-g003.jpg |
0.540335 | b18ea8e278434ab1b695c00f58cfd6b7 | Comparisons of NMD across baseline, 24 and 48 h after transradial catheterization. *P < 0.05 vs. baseline; **P < 0.001 vs. baseline; △P < 0.05 nifedipine vs. control; △△P < 0.01 nifedipine vs. control. (a) The NMD of distal RA in the cannulated arm. (b) The NMD of distal RA in the noncannulated arm. (c) The NMD of proximal RA in the cannulated arm. (d) The NMD of proximal RA in the noncannulated arm. NMD, nitroglycerin-mediated dilation; RA, radial artery. | PMC9622370 | cad-33-648-g004.jpg |
0.519344 | ad221a21b59743e899f5408eca257988 | An explanation for why the estimated association between books at home and achievement is stronger in more developed countries. | PMC9623014 | fpsyg-13-1026387-g001.jpg |
0.399593 | 7089ed53a8d642ea95042c0b1984ad03 | How mean literacy scores (centered on the mean in each country) among students who reported the lowest number of books at home (0–10, dashed line) or the highest number of books at home (> 200, solid line) vary across different values of books at home as reported by parents. | PMC9623014 | fpsyg-13-1026387-g002.jpg |
0.425584 | d0affa924688496db217d5def1308f25 | Country variation in the reliability of books at home data (x-axis) and the relative predictive strength of books at home (y-axis), operationalized as the difference between the literacy-books at home correlation and the literacy-parents’ education correlation. Above the reference line at zero are 12 countries where student literacy was better predicted by books at home than by parent’s education. | PMC9623014 | fpsyg-13-1026387-g003.jpg |
0.485304 | 7a59f3c0a5114160b75ba60079537f5d | Summary: Regrouping (i.e., mixing individuals to form a new social group) is common on dairy farms. The practice is known to be stressful, but how cattle react emotionally to this stressor is still poorly understood. We studied whether heifers experience anhedonia (i.e., the reduced ability to experience pleasure) following regrouping by comparing their use of a mechanical brush before and after regrouping. Heifers reduced their use of the brush 8 h after regrouping, suggesting that they were experiencing anhedonia. This method shows promise for assessing affective states when animals are subjected to routine stressors. | PMC9623682 | fx1.jpg |
0.374029 | 6a3eb5b4e0a244ce86162ab5740e3354 | Timeline of the experimental procedure. Heifers (n = 16) were individually tested on the brush test before (3 times), during (2 times), and after regrouping (2 times). Tests were always separated by 48 h and took place at 1600 h. Regrouping took place at 0800 h with the first and second tests taking place 8 and 56 h later, respectively. Baseline was calculated using the average brush use of the 3 pre-regrouping tests. Brush tests always occurred in the same arena and away from the other pens. | PMC9623682 | gr1.jpg |
0.474404 | a7690775b4474280ad6a2e847be8727c | Change in brush use after regrouping and return to the home pen. Heifers (n = 15) were individually tested on the brush test before (3 times), during (2 times), and after regrouping (2 times). Baseline was calculated using the 3 pre-regrouping tests when animals were housed in their home pen. Percentage change was calculated for each of the post-regrouping time points. The test on d 0 was performed 8 h after regrouping and the test on d 2 was performed 56 h after regrouping. Tests on d 4 and 6 were performed 48 and 96 h after the return to the home pen, respectively. Tests were always performed 2 d apart at 1600 h. Brush tests always occurred in the same dedicated arena, away from the other pens. Boxes represent the interquartile ranges with median change; each dot is an individual point. | PMC9623682 | gr2.jpg |
0.399882 | 9b976c2614b54e7f861057aec348b9a2 | COVID-19 epidemic curve and estimates. A Shows the number of COVID-19 confirmed cases (orange bars for total cases and dark green bars for hospitalized cases). The middle panel shows the number of hospitalization cases in dark green bars. B Contains the weekly trend of the following estimations: hospitalization percentage among confirmed cases (green line), intubation percentage among hospitalized (yellow line) and hospital case fatality rate (CFR) (red line). Figures include the onset of symptoms week period from 2020-14 (April 1st, 2020) to 2022-34 (August 27th, 2022). Dotted vertical lines represent the separation of the five epidemic waves. Epidemic waves correspond to the following onset of symptoms periods: the first wave from week 2020-14 to week 2020-40 (from March 29th, 2020 to October 3rd, 2020); the second wave from week 2020-41 until week 2021-21 (from October 4th, 2020 to May 29th, 2021); the third wave from week 2021-22 to week 2021-50 (from May 30th, 2021 until December 18th, 2021); the fourth wave from week 2021-51 to 2022-17 (from December 19th, 2021 to April 30th, 2022); and fifth wave from week 2022-18 to week 2022-34 (from May 1st, 2022 until August 27th, 2022) | PMC9623964 | 12879_2022_7800_Fig1_HTML.jpg |
0.450589 | e20c207608c54c26927b1e5a1f927931 | COVID-19 estimates according to the five epidemic waves. The figure shows the following estimations with a 95% confidence interval: incidence rate among the population (orange bars), hospitalization rate among the population (dark green bars), hospitalization percentage among confirmed cases (green bars), hospital case fatality rate (red bars), mean hospital admission delay (purple bars) intubation percentage (yellow bars), and mean hospitalization days (blue bars). Epidemic waves correspond to the following onset of symptoms periods: the first wave from week 2020-14 to week 2020-40 (from March 29th, 2020 to October 3rd, 2020); the second wave from week 2020-41 until week 2021-21 (from October 4th, 2020 to May 29th, 2021); the third wave from week 2021-22 to week 2021-50 (from May 30th, 2021 until December 18th, 2021); the fourth wave from week 2021-51 to 2022-17 (from December 19th, 2021 to April 30th, 2022); and fifth wave from week 2022-18 to week 2022-34 (from May 1st, 2022 until August 27th, 2022) | PMC9623964 | 12879_2022_7800_Fig2_HTML.jpg |
0.381352 | f0d85a5024e2462c976f00e34760cefd | Severe COVID-19 outcomes according to age group. The figure shows the weekly trend of the following severe COVID-19 outcomes by age group: hospitalization percentage among confirmed cases (left panel), intubation percentage among hospitalized (middle panel) and hospital case fatality rate (right panel). Age groups are represented as follows: age below 20 years old in the green line, 20 to 39 years old in the blue line, 40 to 59 years in the orange line, and red line for the group aged 60 years old and over. Figures include the onset of symptoms from week 2020-14 to week 2022-34 (from April 1st, 2020, to August 27th, 2022). Dotted vertical lines represent the separation of the five epidemic waves. Epidemic waves correspond to the following onset of symptoms periods: the first wave from week 2020-14 to week 2020-40 (from March 29th, 2020 to October 3rd, 2020); the second wave from week 2020-41 until week 2021-21 (from October 4th, 2020 to May 29th, 2021); the third wave from week 2021-22 to week 2021-50 (from May 30th, 2021 until December 18th, 2021); the fourth wave from week 2021-51 to 2022-17 (from December 19th, 2021 to April 30th, 2022); and fifth wave from week 2022-18 to week 2022-34 (from May 1st, 2022 until August 27th, 2022) | PMC9623964 | 12879_2022_7800_Fig3_HTML.jpg |
0.485972 | 8403255da8a34ba6b2231b9c64f5cf59 | The potential transmission pathway of coronaviruses via food products and processes [35] | PMC9626693 | 42506_2022_112_Fig1_HTML.jpg |
0.516825 | 63bd7d1b08784b08a311adaadb56349c | Esterification reaction [88] | PMC9626693 | 42506_2022_112_Fig2_HTML.jpg |
0.416839 | cf8faa59d50648169b76ee5892f853a7 | Potential electrostatic interactions between basic proteins and nucleic acids (DNA and RNA) [89] | PMC9626693 | 42506_2022_112_Fig3_HTML.jpg |
0.465576 | bb685fda3d0945b292061bd3197de770 | Flowchart of cohorts. | PMC9627286 | fphar-13-1001038-g001.jpg |
0.430674 | dfce2b1d3e314fec9bd324b7cad06aa6 | Calibration plots with non-linear fit (blue line) and 95% prediction interval (light blue area). | PMC9627286 | fphar-13-1001038-g002.jpg |
0.468631 | ffe1358986d3418db7925d7d6d6d5893 | Partial dependence plots of T2D patients with high level of similarity. | PMC9627286 | fphar-13-1001038-g003.jpg |
0.389553 | a1b1aa21c832405b94d0ba6be5ba372b | The prevalence of prophylactic antibiotic use across provinces for A all delivery and B vaginal delivery: China, 2015–2016 | PMC9628083 | 12916_2022_2577_Fig1_HTML.jpg |
0.40299 | a97b351de82c46949c76faa50a896992 | The prevalence of clinician adherence to guidelines across provinces for A all delivery and B vaginal delivery: China, 2015–2016 | PMC9628083 | 12916_2022_2577_Fig2_HTML.jpg |
0.380664 | 24967d3a53ff4976a3257ee4bc1dba92 | Temperature (A, B) and weight (C, D) profiles of animals vaccinated by the scarification (A, C) or i.m. (B, D) route. Six- to eight-week-old female Balb/c mice were vaccinated with VACV strain Lister at doses of: 1 × 103 (); 1 × 104 (); 1 × 105 (); 1 × 106 (); or 1 × 107 () pfu/animal as described in Materials and Methods, or sham vaccinated with PBS(). Animals were monitored daily for temperature and weight. Percentage weight was calculated as the percentage of initial weight for each animal. Data is presented as the daily mean temperature and percentage weight for each group. Group size = 10. Data from individual mice was subjected to 2-way ANOVA to compare the two vaccination routes, and a series of ANOVAs to compare each vaccination dose with the cognate mock vaccinated group. A further 5 mice for each group were not monitored for post-vaccination weight or temperature. These additional mice were required to provide enough animals for subsequent challenge procedures. The animals not monitored for post-vaccination temperature and weight were all assigned to the 3.4 × 108 pfu challenge groups in subsequent procedures. | PMC9628712 | gr1_lrg.jpg |
0.428726 | d0b0e315073b4edfbfdecd21f25301df | ELISA of sera from vaccinated animals. Subsets (n = 5) of the animals described in Fig. 1 receiving vaccine at doses of 1 × 103 (); 1 × 104 (); 1 × 105 (); 1 × 106 (); or 1 × 107 () pfu/animal, or sham vaccinated with PBS(), were selected for blood collection for serology. Animals were sequentially bled at 7 (A), 14 (B), 21 (C), and 28 (D) days post vaccination. Sera were prepared and used as described in Material and Methods. Data is shown as means and standard deviations of the results from the 5 mice in each subset. | PMC9628712 | gr2_lrg.jpg |
0.496122 | 79b0bf877d424318b654f5f89dc7012b | Lethality of i.n. challenge in mock vaccinated controls. Control animals described in Fig. 1 were mock vaccinated with PBS by the scarification (filled symbols) or i.m. (empty symbols) routes and challenged i.n. 28 days later with VACV strain WR at 1 × 107 (, ), 1 × 108 (, ), or 3.4 × 108 (, ) pfu/animal. Surviving animals were recorded daily until 14 days post-challenge, when remaining animals were culled. Group size = 5. | PMC9628712 | gr3_lrg.jpg |
0.492719 | ce489373f0f54d5fa64c5d65976b163c | Temperature profiles of animals challenged with virulent VACV after vaccination by the scarification (A, C, E) or i.m. (B, D, F) routes. Animals described in Fig. 1 vaccinated at doses of: 1 × 103 (); 1 × 104 (); 1 × 105 (); 1 × 106 (); or 1 × 107 () pfu/animal, or sham vaccinated with PBS() were challenged i.n. 28 days after vaccination with VACV strain WR at 1 × 107 (A, B), 1 × 108 (C, D), or 3.4 × 108 (E, F) pfu/animal. Animals were monitored daily for temperature for 14 days post-challenge, after which surviving animals were culled. Data is presented as the daily mean temperature for each group. Data from individual mice was subjected to 2-way ANOVAs to compare the two vaccination routes; and separately to compare vaccination/challenge doses for each route with a randomly chosen subset of pre-challenge data from the cognate vaccination dose. Group size = 5. | PMC9628712 | gr4_lrg.jpg |
0.391332 | a539c8d9d6dc4fe3bc9326306789b21a | Weight profiles of animals challenged with virulent VACV after vaccination by the scarification (A, C, E) or i.m. (B, D, F) route. Animals described in Fig. 4 vaccinated at doses of: 1 × 103 (); 1 × 104 (); 1 × 105 (); 1 × 106 (); or 1 × 107 () pfu/animal, or sham vaccinated with PBS() and challenged i.n. with 1 × 107 (A, B), 1 × 108 (C, D), or 3.4 × 108 (E, F) pfu/animal, were monitored daily for weight for 14 days post-challenge, after which surviving animals were culled. Data is presented as the daily mean percentage weight for each group. Percentage weight was calculated as the percentage of initial weight for each animal. Data from individual mice was subjected to 2-wayANOVAs to compare the two vaccination routes; and separately to compare vaccination/challenge doses for each route with a randomly chosen subset of pre-challenge data from the cognate vaccination dose. Group size = 5. | PMC9628712 | gr5_lrg.jpg |
0.485984 | 19f150de404d47c7b4213eebd075756b | Post-challenge clinical scores of vaccinated animals. All challenged animals that received vaccine at doses of 1 × 103 (); 1 × 104 (); 1 × 105 (); 1 × 106 (); or 1 × 107 () pfu/animal, were evaluated daily for clinical signs of disease as described in Methods. The scores for each group over the entire 14 day post-challenge period were aggregated and plotted in histograms, for challenge doses of 1 × 107 (A), 1 × 108 (B), and 3.4 × 108 (C). Comparison of scarification and IM routes was by separate ANOVAs for each challenge dose, over all vaccine doses. | PMC9628712 | gr6_lrg.jpg |
0.455753 | c0c708685f994a47820c4be35b9eaa00 | Changes in bacterial count, pH, residual sugar content and total acid content during the fermentation process.A, bacterial count; B, pH value; C, residual sugar content; D, total acid content. | PMC9628816 | jmb-32-4-473-f1.jpg |
0.442721 | 588e2bfbf8b74554ae6cf9d4b3ce374e | Antioxidant activity of the extract of W. somnifera before and after fermentation.A, DPPH scavenging capacity; B, ferrous chelating activity; C, total reducing capacity; D, FRAR value. Fermented supernatant was diluted 5 times and then used to measure. F1, fermented by Lactiplantibacillus plantarun DY-1; F2, fermented by Lacticaseibacillus casei KDBLC; F3, fermented by Lactobacillus acidophilus KDB-03; F4 fermented by Limosilactobacillus fermentum KDB-08; FMIX, fermented by mixture of the above strains. Different letters indicate significant differences (p < 0.05). | PMC9628816 | jmb-32-4-473-f2.jpg |
0.435666 | 4cef968c79784d209504dbc92ea85985 | Changes of total flavonoid and total phenol content before and after the fermentation.A, TFC, total flavonoid content; B, TPC, total polyphenol content. F1, fermented by Lactiplantibacillus plantarun DY-1; F2, fermented by Lacticaseibacillus casei KDB-LC; F3, fermented by Lactobacillus acidophilus KDB-03; F4 fermented by Limosilactobacillus fermentum KDB-08; FMIX, fermented by mixture of the above strains. Different letters indicate significant differences (p < 0.05). | PMC9628816 | jmb-32-4-473-f3.jpg |
0.437999 | 21558b7d859b4b3b97e1a5fbb1a29f7c | 3D-topographic of GC-IMS analysis and gallery plot (finger-print) of volatile compounds of the fermented or unfermented samples. (A) 3D-topographic of GC-IMS analysis, the color of the signal peak represents the concentration of the substance, among which white indicates a lower concentration and red indicates a higher concentration, and the darker the color, the higher the concentration; (B) Gallery plot (finger-print) of volatile compounds, row represents the volatile composition of a sample and column represents the signal peaks of a volatile substance in different samples. UFNFSTW, W. somnifera extract with sterilized and unfermented treatment; F-NS, W. somnifera extract with sterilized and fermented by the mixture of LAB. | PMC9628816 | jmb-32-4-473-f4.jpg |
0.395694 | 59e4de3ed0b341f19896a90eed176b47 | Overview of widely targeted metabolome analysis of fermented and unfermented extracts of W. somnifera.(A) Heatmap visualization of metabolites. Red indicates high abundance, whereas low relative metabolites are shown in green. (B) PLS-DA analysis of metabolites. (C) Volcano plot of metabolites. (D) Heatmap of DAMs. (E) Category and number of DAMs. | PMC9628816 | jmb-32-4-473-f5.jpg |
0.41548 | b05c7cd442684209825edc13682ad511 | The top 10 regulated DAMs and KEGG enrichment pathway of DAMs.(A) Top 10 regulated DAMs. Red bars indicate upregulated DAMs. Blue bars indicate downregulated DAMs. (B) KEGG enrichment pathway of DAMs. The arrows highlight the significant enrichment metabolism pathways. | PMC9628816 | jmb-32-4-473-f6.jpg |
0.421912 | 28603972d9eb4c0b80f79e3630169ac3 | Trial sequences for all experiments (images not to scale), Experiments 2–5 had identical timings and responses (see Table 1 for a summary of experimental methods) | PMC9630199 | 13414_2022_2560_Fig1_HTML.jpg |
0.629508 | 82afa6b6a138420cae3255c106d3b562 | Bar charts (95% confidence interval error bars; asterisks indicate one-sample t-tests, μ = 0.5, * p < .05, ** p < .01) of proportions of early (< 250 ms) and late (> 250 ms) first saccades to distractors (D) and targets (T), averaged across participants. In the ‘ignore’ instructions condition of Experiment 1 (top row, left) first saccades were fast and there was an early bias toward distractors (AWB effect), under typical search instructions (‘find’, top row, middle), a target bias was observed in both early and late saccades. In Experiment 2 under ignore instructions (top row, right), the introduction of the pre-search stimulus (PSS) extinguished this early bias. Experiment 3 produced similar results to Experiment 2 in displays with one (middle row, left) and three (middle row, right) distractors. No effect of PSS category congruency was observed in Experiment 4 (bottom row, left and middle). In Experiment 5, with a simple colour PSS (bottom row, right), an early target bias was observed as in Experiment 1 under ignore instructions | PMC9630199 | 13414_2022_2560_Fig2_HTML.jpg |
0.565276 | b7bb65f5844c47708a4d7f8d4c1b1220 | Moving-average frequency of first saccades made to targets and distractors in Experiments 1–3, calculated over onset latencies for all first saccades. The top two plots show data from the ‘ignore’ and ‘find’ instruction conditions from Experiment 1 where no pre-search stimulus (PSS) was present. The middle plot shows data from Experiment 2 where ignore instructions and a PSS were used. The bottom two plots show data from Experiment 3, which replicated the conditions of Experiment 2 but with one and three distractor displays. The vertical dashed line indicates the 250-ms onset latency cutoff used to categorise early and late first saccades | PMC9630199 | 13414_2022_2560_Fig3_HTML.jpg |
0.540562 | 9ad2930c11e44ec299a6c552b0dce5e6 | Moving-average frequency of first saccades made to targets and distractors in Experiments 4 and 5, calculated over onset latencies for all first saccades. The top and middle rows show data from Experiment 4, which included pre-search stimuli (PSS), which were either congruent or incongruent with the distractor category. The bottom row shows data from Experiment 5, where a simple colour PSS was used | PMC9630199 | 13414_2022_2560_Fig4_HTML.jpg |
0.508316 | d753a20851124a51aa4fcdf5a6282b7f | Algorithm to diagnose and manage the fungal co-infections in COVID-19 patients | PMC9630809 | 40588_2022_184_Fig1_HTML.jpg |
0.39799 | 659d8533112f474ea601377a8e4a1713 | Estimated proportions and 95% confidence intervals of SVA-seropositive breeding farms by state, region, and national estimate. | PMC9631314 | fvets-09-1011975-g0001.jpg |
0.503429 | ec657eb8bf994060a51d2f27b7126470 | Box and whisker plot of the number of SVA IFA-positive samples by pig farm type in the U.S. | PMC9631314 | fvets-09-1011975-g0002.jpg |
0.397526 | fcdf8e01173048f1bc1e3cced6ab1950 | Estimated proportions and 95% confidence intervals of SVA-seropositive growing-pig farms, by state, region, and national estimate. | PMC9631314 | fvets-09-1011975-g0003.jpg |
0.443029 | 0b6c5211626e4e35ab9cda3ffb674c86 | Effects of venetoclax in DHL cells. (A-C) Trypan blue exclusion test of cell viability in CARNAVAL (A), WILL-2 (B), and Oci-Ly7 (C) cells treated with increasing concentrations of venetoclax (VEN) for up to 48 hours. Technical triplicates were counted per experiment. Graphs show results of 3 independent experiments (n = 3, SD). (D-F) Annexin V staining measured by flow cytometry in CARNAVAL (D), WILL-2 (E), and Oci-Ly7 (F) cells subjected to escalating concentrations of 1 nM to 1 µM VEN and DMSO for 12 hours. (G-I) Protein expression of Bcl-2 and apoptotic markers Caspase 3, 7, 9, cPARP, and total levels analyzed by Western blot in CARNAVAL (G), WILL-2 (H), and Oci-Ly7 (I) cells after treatment with VEN for 12 hours with concentrations as indicated. Tubulin served as a loading control. Quantification of Western blot was done with ImageJ. Intensities were calculated relative to tubulin and normalized to DMSO solvent control. N/A, not analyzable. | PMC9631674 | advancesADV2022007364f1.jpg |
0.490465 | 3fc44913428b47248ae93877f4cc6f7c | ADCP in Bcl-2–expressing DHL cell lines and PDX samples on combination of VEN and therapeutic antibodies. Percentages of cells phagocytosed by human macrophages with VEN/antibody combinations compared with VEN or antibody (RTX, DARA, CD19-DE) alone. (A) CARNAVAL cells after treatment with 1 nM VEN for 12 hours, RTX, and the control antibody CTX. (B) WILL-2 cells treated with 1 nM VEN for 12 hours, DARA, and the control antibody RTX. (C) Oci-Ly7 cells after treatment with 1 nM VEN for 12 hours, RTX, and the control antibody CTX. (D) ADCP in BL PDX sample subjected to 1 nM VEN for 12 hours, RTX, and the control antibody CTX. (E) t(17;19)-positive BCP-ALL PDX sample treated with 1 nM VEN for 12 hours, CD19-DE, and the control antibody HER2-DE (a version of trastuzumab containing the same modification in the Fc part of the antibody as CD19-DE). DMSO, solvent control; w/o, no antibody. Phagocytosis was determined as the percentage of macrophages with completely ingested carboxyfluorescein succinimidyl ester green–positive cells by counting in total 100 macrophages by at least 3 independent observers. Each dot represents an independent experiment with different human donors. Data are presented as mean ± standard error of the mean (SEM) from independent experiments with 5 healthy blood donors. Statistical analysis: ns, not significant; *P < .05; **P < .005; Mann-Whitney test. All antibodies used in vitro were applied to a final concentration of 10 µg/mL. | PMC9631674 | advancesADV2022007364f2.jpg |
0.520066 | 7c03759af95a4d7891fbe4fc08502923 | Combination of VEN and antibodies in xenograft mice in vivo. (A) Experimental scheme: CARNAVAL cells or t(17;19) BCP-ALL PDX were injected IV into NSG mice. VEN (100 mg/kg per day) was given daily via oral gavage. Therapeutic antibodies (1 mg/kg) were applied weekly via the intraperitoneal route. (B) CARNAVAL cells were injected into NSG mice and left untreated (control), treated with 100 mg/kg per day VEN, 1 mg/kg per week RTX, or the combination (combi) of both. (C) One t(17;19)-positive BCP-ALL PDX sample was injected into NSG mice and either left untreated (control), treated with 100 mg/kg per day VEN, 1 mg/kg per week CD19-DE, or the combination (combi) of both. (D) NSG mice were injected with CARNAVAL cells. Animals were left untreated (control), treated with RTX (1 mg/kg per week intraperitoneal), VEN (100 mg/kg per day oral gavage), or the combination (VEN+RTX). For macrophage depletion, mice received weekly injection of LC (100 µL/wk intraperitoneally, i.p.). Survival was analyzed using the Kaplan-Meier method and log-rank statistics. P < .05 was considered statistically significant. n, animals per group. | PMC9631674 | advancesADV2022007364f3.jpg |
0.405881 | e3d2f7eaccac4ef5a8168e2698351a63 | Apoptosis independence in VEN-induced phagocytosis. (A) CARNAVAL cells were pretreated with increasing concentrations of the pan caspase inhibitor Z-VAD-FMK for 1 hour before being subjected to 1 µM VEN for 12 hours. Protein levels of cPARP were analyzed by Western blot. (B) Percentages of cells phagocytosed by human macrophages with VEN/antibody combinations compared with VEN, the pan-caspase inhibitor Z-VAD-FMK (Z-VAD) for 1 hour, RTX, or combination of VEN and Z-VAD-FMK (combi). CARNAVAL cells were treated with 50 µM Z-VAD-FMK for 1 hour or/and 1 nM VEN for 12 hours. (C) WILL-2 cells were pretreated with increasing concentrations of the pan caspase inhibitor Z-VAD-FMK/1 hour before subjected to 1 µM VEN for 12 hour. Protein expression of cPARP was analyzed by Western blot. (D) In vitro phagocytosis assays with human macrophages in WILL-2 cells treated with 1 nM VEN for 12 hours or/and 50 µM Z-VAD-FMK for 1 hour alone, the combination (combi), DARA, and the control antibody RTX. Phagocytosis was analyzed as described above. Data are presented as mean ± SEM from independent experiments with 4 healthy blood donors. Tubulin served as a loading control. | PMC9631674 | advancesADV2022007364f4.jpg |
0.476136 | 62a06deab36f48adabfafe9bddc54e13 | VEN-mediated phagocytosis in Bax/Bak-deficient DHL cell lines. (A) Protein levels of Bax and Bak in CARNAVAL and WILL-2 Bax/Bak ko cells and control cells (Cas9) analyzed by Western blot. (B) Examination of cPARP and cCaspase 3 in CARNAVAL and WILL-2 Bax/Bak ko cells control cells (Cas9) subjected to 1 nM or 1 µM VEN for 12 hours. (C) ADCP in CARNAVAL deficient for Bax/Bak or control cells (Cas9) after treatment with 1 nM VEN for 12 hours, RTX, and the control antibody CTX. (D) ADCP in WILL-2 lacking Bax/Bak or control cells (Cas9) treated with 1 nM VEN for 12 hours, DARA, and the control antibody RTX. Data are presented as mean ± SEM from independent experiments with 5 healthy blood donors. Statistical analysis: *P < .05; **P < .005; Mann-Whitney test. All antibodies used in vitro were applied to a final concentration of 10 µg/mL. Tubulin served as a loading control. | PMC9631674 | advancesADV2022007364f5.jpg |
0.50185 | 7f01c73039a14c338361aea6ffcb7e84 | X-ray
molecular structure of bisphosphonylallene 2d, showing
thermal displacement ellipsoids at the 30% probability
level. | PMC9631903 | ao2c04619_0002.jpg |
0.538945 | a16f9df36856430dada5565fb679fb97 | X-ray molecular structures of 4f (left) and 4j (right), showing thermal displacement
ellipsoids at the
30% probability level. | PMC9631903 | ao2c04619_0003.jpg |
0.405791 | 567638bd90b24a53a8d3235ff823d073 | Percentage
growth inhibition ± standard error of the mean
(72 h treatment with 10–5 M in 2000 A2058 melanoma
cells). | PMC9631903 | ao2c04619_0004.jpg |
0.35775 | 5356d6fb38554eeb91f6713e7c31e673 | Microphotography of A2058
melanoma cells after 72 h growth in the
control cell culture medium containing 1% DMSO (control) or the cell
culture medium containing 10–5 M molecule (4n, 3′f, or 3″h). | PMC9631903 | ao2c04619_0005.jpg |
0.46689 | 54d6e8c2fdcd4d8a88165ccf56bb0866 | An example sentence for the input and output in BioNER | PMC9632084 | 12859_2022_4994_Fig1_HTML.jpg |
0.426809 | 89f38e78f3b7499ab98fc330ade38319 | A constituency parse tree example | PMC9632084 | 12859_2022_4994_Fig2_HTML.jpg |
0.500259 | 1435a074e66443f28905ec87d8cad9ac | The architecture of the proposed single-task model for BioNER (the context features and syntactic labels of the 7th word “congenital” in the example sentence are extracted from the results processed by the NLP toolkit) | PMC9632084 | 12859_2022_4994_Fig3_HTML.jpg |
0.452566 | 91dd6db2c0f64de3aac6a93c77fb6ea9 | An example of syntactic feature extraction | PMC9632084 | 12859_2022_4994_Fig4_HTML.jpg |
0.490547 | 6b158a52dcd6469eba49a821c2914789 | The architecture of the proposed multi-task learning model for BioNER | PMC9632084 | 12859_2022_4994_Fig5_HTML.jpg |
0.459128 | f8bb7867512142099ff2f2e16c0c3cd3 | Impact of different sizes of dimension \documentclass[12pt]{minimal}
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0.416333 | 8187436b78ec45e0a66df4afc9c94674 | Flowchart of sample selection for the study, the TLGS study | PMC9632145 | 12933_2022_1665_Fig1_HTML.jpg |
0.463004 | d09f5da7498742308534b5da5cfbec7f | Association of change in MetS status with the risk of CVD, Tehran Lipid and Glucose Study. HR: hazard ratio; MetS: metabolic syndrome; CVD: cardiovascular disease; HR was estimated using COX regression model adjusted for age, smoking status, physical activity level, education, marital status, family history of CVD, body mass index | PMC9632145 | 12933_2022_1665_Fig6_HTML.jpg |
0.484003 | d55f7466746045a9ad4cb687aaa79fd9 | Association of change in MetS status with the risk of CHD, Tehran Lipid and Glucose Study. HR: hazard ratio; MetS: metabolic syndrome; CHD: Coronary heart disease; HR was estimated using COX regression model adjusted for age, smoking status, physical activity level, education, marital status, family history of CVD, body mass index | PMC9632145 | 12933_2022_1665_Fig7_HTML.jpg |
0.416237 | ac7dffb12aad4c54be2e828b214e3022 | Remote sensing archaeology (RSA)(A) The development of remote sensing platforms.(B) The electromagnetic spectrum and approximate scale of the wavelength for RSA.(C) The schematic diagram of combing remote sensing networks (includes airborne and spaceborne sensing, proximal sensing, in situ sensing, and laboratory instrumental measurement and observation) with emerging cutting-edge technologies (AI, BD, CI, DT) for archaeological applications over the next century. | PMC9634031 | gr1.jpg |
0.369853 | 2a098b1b7eca4c5581f696467e8c53f7 | PRISMA flow diagram. | PMC9634150 | gr1.jpg |
0.375085 | 6f4abbf6808a4e31ae8f2d1d33426d19 | Survival curves according to treatment approaches: event-free survival (A), overall survival (B). Survival curves according to Ann Arbor stage: event-free survival (C), overall survival (D). Survival curves according to proposed TNM staging: event-free survival (E), overall survival (F). Used with permission from Wolters Kluwer Health Inc. | PMC9634150 | gr2.jpg |
0.444011 | 782f3bd3c33b4fc3abceebee9dccac90 | Inhibition of CDC7 (DDK) induces a delay in mitotic onset. Ewing sarcoma cells (A673 and TC32) as well as the non-Ewing osteosarcoma cell line U2OS were treated with either 0.1% DMSO, or 10 μmol/L nocodazole with increasing concentrations of TAK-931 (100 nmol/L, 300 nmol/L, and 1 μmol/L) for 24 hours. Cells were fixed and stained for pHH3 and pHH3+ cells were measured via FACS. A, Representative dot plots showing pHH3+ TC32 and U2OS cells upon nocodazole and TAK-931 treatment. B, Quantification of above-described experiment (n = 3 biological replicates, two-way ANOVA, *, P < 0.05; ****, P < 0.0001). C, A673 and TC32 cells were as described in A, protein lysates were collected, and Western blot analysis was performed for the specified proteins (Vinculin is used as a loading control). D, U2OS, A673 and TC32 cells were treated as described in A. Cells were then fixed and stained for DNA with propidium iodide and cell cycle was analyzed via FACS (n = 2 biological replicates). | PMC9635308 | crc-22-0130_fig1.jpg |
0.40341 | 88bed0bed8a44699a33989243d566f9b | WEE1 activity is required for pCDK1 and mitotic entry delay upon DDK inhibition in Ewing cells. A, Simple schematic depicting WEE1’s role in the inhibition of mitotic onset. B and C, Cells were treated with 300 nmol/L TAK-931, 1 μmol/L MK1775 or combination for 24 hours. Cells were then fixed, and DNA was stained using PI. DNA content was analyzed via FACS. B, Representative histograms show a TAK-931 induced accumulation of cells during the cell cycle that is partially abrogated with the addition of MK1775 to TAK-931 (black gates). C, Quantification of DDKi-induced cell-cycle accumulation. Black gates from B were used to determine the proportion of these cells (n ≥ 3 biological replicates, one-way ANOVA, **, P < 0.005; ***, P < 0.001; ****, P < 0.0001). D, A673 and TC32 cells were treated with 300 nmol/L TAK-931 or 1 μmol/L MK1775 or the combination for 24 hours. Cell lysates were collected, and a Western blot analysis was performed for the specified proteins. Vinculin was used as the loading control. E, Cells were treated as described in B and C. Total DNA content was analyzed via FACS and cell-cycle distribution was determined (2N DNA content = G1, 4N DNA content = G2–M, >2N–<4N DNA content = S; n = 2 biological replicates). F, Cells were treated with 10 μmol/L nocodazole, 300 nmol/L TAK-931 with or without increasing concentrations of MK1775 (100 nmol/L, 500 nmol/L, and 1 μmol/L) for 24 hours. Cells were fixed and stained for pHH3 and analyzed via FACS (n = 3 biological replicates, two-way ANOVA, *, P > 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001). G, Cells were treated as described in F. Whole-cell lysates were collected, and Western blot analysis was performed for the specified proteins. Vinculin was used as a loading control. | PMC9635308 | crc-22-0130_fig2.jpg |
0.409046 | 8f36bb6620d045dfb6d91b7bbf8409d9 | Combined inhibition of WEE1 and DDK induces premature mitotic entry, mitotic progression abnormalities and mitotic catastrophe in Ewing cells. A–C, Cells were treated with 300 nmol/L TAK-931, 1 μmol/L MK1775 or combination for 24 hours. Cells were then fixed and stained for DNA content (PI) and pHH3 and analyzed via FACS. Premature mitotic cells were identified as cells that stained positive for pHH3 that contain <4N DNA content (top left quadrant). A, Representative dot plots. B, Quantification of percentage of premature mitotic cells as a proportion of total mitotic cells [(premature mitotic cells/total mitotic cells) * 100%] (n = 3 biological replicates, two-way ANOVA, ****, P < 0.0001). C, Quantification of total mitotic cells (pHH3+ cells; n = 3 biological replicates, two-way ANOVA, ****, P < 0.0001). D, A673 cells were treated with 300 nmol/L TAK-931, 1 μmol/L MK1775 or combination for 24 hours. DNA was stained using DAPI and abnormal anaphase events were quantified (n = 2 biological replicates, ≥50 anaphase events analyzed per condition, per replicate). E, A673 cells were treated as described in D. Total DNA was stained using DAPI and micronucleated cells were quantified (n = 3 biological replicates, ≥ 100 cells were analyzed per condition, per replicate, one-way ANOVA, ****, P < 0.0001). | PMC9635308 | crc-22-0130_fig3.jpg |
0.406067 | aceb31597d2741ceb8586ce8f89dab89 | DDK and WEE1 inhibitors synergistically reduce Ewing sarcoma cell viability. A and B, Cells were treated with 300 nmol/L TAK-931, 1 μmol/L MK1775 or combination for 48 hours. Cells were then stained for live or dead with PI and apoptosis with Annexin-V. A, Representative dot plots. B, Quantification of dead or apoptotic cells of the above-described experiment (n ≥ 3 biological replicates, one-way ANOVA, *, P > 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001). C, A673 and TC32 cells were treated as described in A. Whole-cell lysates were collected, and Western blot analysis was performed for the following proteins. GAPDH was used as a loading control. D, Cells were treated with increasing combinations of TAK-931 (1–0.0625 μmol/L) and MK1775 (5–0.125 μmol/L) for 72 hours and cell viability was assessed. C, Representative cell viability grid. Orange represents areas of high viability while blue represents areas of low viability. Representative results of four biological replicates. E, Cell viability results from D were used to calculate CI values with the CompuSyn software (referenced in text). CI < 1 = synergistic, CI of 1 = additive, CI > 1 = antagonistic. Fraction affected is calculated by subtracting the cell viability from 1 (100% cell viability would have a fraction affected of 0, while 0% cell viability would have a fraction affected of 1). Red line represents slope of the data. A negative slope indicates that, as the fraction affected becomes larger, the CI values approach. This means that the combinations that display the highest level of synergy also display the highest level of cell killing; this is desirable. Representative results of four biological replicates. F, Average CI values from E (n = 4 biological replicates; TC32 = 2 biological replicates). | PMC9635308 | crc-22-0130_fig4.jpg |
0.471623 | 84d07b02ca854daaa50861a550d2f5dd | Apoptotic induction of TAK-931 + MK1775 requires mitotic entry or progression. A, Schematic representing the targets of the various drugs used in this experiment. Black arrow depicts the findings from Fig. 2—TAK-931 activates WEE1. B, Cells were treated with 10 μmol/L nocodazole in combination with increasing concentrations of RO-3306. Cells were then fixed and stained for DNA content and pHH3 (n = 2 biological replicates). C, Cells were treated with 300 nmol/L TAK-931 in combination with 1 μmol/L MK1775 with or without 10 μmol/L RO-3306 or 10 μmol/L nocodazole for 24 hours. Whole-cell lysates were collected, and Western blot analysis was performed for the specified proteins. GAPDH was used a loading control. D, Cells were treated as described in C. Cells were then stained for live or dead with PI and apoptosis with Annexin-V. Quantification of dead or apoptotic cells is shown. Relative dead or apoptotic cells were calculated on the basis of the level of dead or apoptotic of cells that were not given the T + M combination (e.g., T + M + RO-3306 is relative to RO-3306 alone; n = 3 biological replicates, two-way ANOVA, *, P < 0.05; ****, P < 0.0001). | PMC9635308 | crc-22-0130_fig5.jpg |
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