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| 1 | 0 | Effect of CsA on ΔΨm loss of Sf9 cells treated with AZA and CPT. (a) ΔΨm loss induced by AZA and AZA+ CsA -treatments at 3 h, 6 h, 9 h, 12 h, 18 h and 24 h, respectively. (b) ΔΨm loss induced by CPT and CPT+ CsA-treatments at 2 h, 3 h, 6 h, 9 h, 12 h and 18 h, respectively. Results represent means ±S.E (n = 4). Different asterisks above the S.E bars represent statistically significant difference (*p<0.05, **p<0.01), when the data were analyzed by ANOVA followed by DMRT. | ||
| 2 | 1 | Cotranslational folding in WT, uL23 delta-loop, and uL24 delta-loop ribosomes. (A) Δf profiles (Δf = f(50 μM Zn2+) – f(50 μM TPEN)) for ADR1a constructs translated in the PURE system supplemented with in-house purified WT (gray), uL23 Δloop (red), and uL24 Δloop (blue) E. coil ribosomes. (B) f profiles for spectrin R16 constructs translated in the PURE system supplemented with in-house purified WT (gray), uL23 Δloop (red), and uL24 Δloop (blue) E. coli ribosomes. (C) f profiles for titin I27 constructs translated in the PURE system supplemented with in-house purified WT (gray), uL23 Δloop (red), and uL24 Δloop (blue) E. coli ribosomes. Error bars in panels a-c show SEM values calculated from at least three independent experiments. Dashed lines indicate L and L values, c.f., Table 1. f profiles for non-folding mutants of R16 and I27 are found in (Nilsson et al., 2017; Tian et al., 2018). (D) Simulated f profiles (full lines) for ADR1a, spectrin R16, and titin I27 obtained with WT (gray), uL23 Δloop (red), and uL24 Δloop (blue) ribosomes. The corresponding experimental f profiles from panels a-c are shown as dashed lines. The simulated ADR1a f profile marked by X’s was obtained with a uL23 Δloop(70-72) ribosome model. Simulated f profiles for ADR1a with uL24 Δloop ribosomes, and for R16 and I27 with uL23 Δloop ribosomes, are essentially identical to the corresponding profiles obtained with WT ribosomes, and are shown in Figure 3—figure supplement 10. | ||
| 3 | 2 | Association of axillary volume coverage with breast volume and body mass index by simple linear regression. | ||
| 4 | 3 | exist | Clusters of cells constrained by ECM exist in the intact adult epicardium. Immunofluorescent staining (IMF) for podoplanin (Pdpn; green) in the intact adult epicardium identifies clusters of cells within basement membrane (white arrowheads; a–c). Clusters in the epicardium (white arrowheads) are encapsulated by ECM as indicated by IMF for fibronectin (Fn; green; d). Inset box in d is shown at higher magnification in e, and CD29 (β1-integrin; f). IMF for CD44 and CD45 revealed the clusters were a heterogeneous population of mesenchymal (CD44; g) and HCs (CD45; h). The clusters resided in close proximity to coronary vessels (i,j) as confirmed by immunostaining on a Tie2Cre;R26R-tdTomato background (k). cv, coronary vessel; ep, epicardium; my, myocardium. Scale bars, 40 μm (a); 20 μm (b–e); 10 μm (f–k). | |
| 5 | 4 | optimize | Optimized molecular structure of (a) the isolated alizarin dye, (b) the alizarin-(TiO) complex. The red, green, black, and grey beads represent oxygen, titanium, carbon, and hydrogen atoms, respectively. | |
| 6 | 5 | express | EPS15 and EPS15L1 are expressed during erythropoiesis and they are absent in Tie2+ cells from cDKO mice. (A) Methylene blue–stained blood smears of adult WT mice, 7 d after injection with PBS or PHZ. Note numerous blue dye–retaining reticulocytes in the blood smear from PHZ-treated mice. Bar, 10 μm. (B) FACS analysis with anti-TfR/CD71 and thiazole orange to analyze the maturation status of RBCs from WT mice at 0, 7, 10, and 16 d after PHZ injection. (C) Western blotting of blood lysates at 7, 10, and 16 d after treatment with PHZ. Equal amounts of lysates, corresponding to 7 μl of whole blood, were loaded and probed for the indicated proteins. (D) Western blotting of brain (Br), liver (Li), and spleen (Sp) lysates from adult WT and cDKO mice. Twenty micrograms of each lysate was loaded. (E) Iron, transferrin, and ferritin levels in the serum of adult WT and cDKO mice. Three animals of each phenotype were analyzed. **P < 0.01 versus WT. Note that the iron levels were increased in the serum of cDKO mice, indicating that iron absorption was not defective. (F) Perls’ Prussian blue staining of the liver and spleen of adult WT and cDKO mice. Iron deposition is in blue. Arrows point to increased erythropoiesis in the spleen of cDKO mice. Bar, 50 μm. Note that, despite increased serum iron, we did not detect tissue iron overload in the spleen or liver of cDKO mice. In contrast, other murine models of microcytic hypochromic anemia, such as the hematopoietic-specific KO for Stat5a/b, present iron overload in the liver (Zhu et al, 2008). A possible explanation might be that cDKO displayed increased secondary erythropoiesis, particularly in the spleen (this panel), which actively remove iron excess. Consistent with the absence of tissue iron overload, other iron metabolism proteins (transferrin and ferritin) were not altered in cDKO mice (panel E), indicating that a certain balance in iron metabolism in cDKO mice has still been preserved and/or re-established. (G) Molecular phylogenesis of the EPS15 family. Protein sequences were retrieved from the NCBI or the Joint Genome Institute (http://genome.jgi.doe.gov/) databases. Sequences were aligned with ClustalW, and the evolutionary history was inferred by using the maximum likelihood method based on the JTT matrix–based model (Jones et al, 1992). The tree is drawn to scale, with branch lengths measured in the number of substitutions per site. All positions containing gaps and missing data were eliminated. Alignment and evolutionary analyses were conducted in MEGA7 (Kumar et al, 2016). Protein accession numbers are shown. | |
| 7 | 6 | Effects of SAA1 on insulin signaling pathway in cultured granulosa cells. A, B Concentration dependent effect of SAA1 (0, 0.01, 0.1 and 1 μg/ml for 24 h) on PTEN expression (n = 4). ** P < 0.01 compared with ctr (0) and # P < 0.05 compared with SAA1 (0.01 μg/ml). C, D Effect of prior treatment with SAA1 (1 μg/ml for 24 h) on Akt phosphorylation induced by insulin (100 nM for 15 min) (n = 4). *** P < 0.001 compared with control-insulin, ## P < 0.01 vs. SAA1-insulin, && P < 0.01 vs. control+insulin. E, F Dose-dependent effect of SAA1 (0, 0.01, 0.1 and 1 μg/ml for 24 h) on total GLUT4 expression (n = 4). G, H Effect of prior treatment with SAA1 (1 μg/ml for 24 h) on GLUT4 translocation (from cytoplasm to membrane) induced by insulin (100 nM for 30 min) (n = 3). * P < 0.05 compared with control. I Effect of prior treatment with SAA1 (1 μg/ml for 24 h) on glucose uptake induced by insulin (100 nM for 30 min) (n = 4). ** P < 0.01 compared with control-insulin, ## P < 0.01 compared with control+insulin. All values are the mean ± SEM | ||
| 8 | 7 | mHTT- and S506X-related changes in the abundance of YFP-EAAT2 binders. (A) Injected vectors. (B) Animal groups. (C) Scheme of immunoprecipitation experiment. (D) List of EAAT2 bands to be detected in the Western blots (WB) from the beads preparation (this figure) or lysates (Figure 3). (E,F) Western blot samples prepared from the beads YFP-immunoprecipitate. Note dimer bands and shift of the EAAT2-S506X band (YEX, boxed). (G) Similar amounts of mYFP immunoreactivity (YE or YEX bands) pulled down in the three animal test groups. (H) Heat-map plot illustrating the mHTT-related differences between WT:EAAT2 and HET:EAAT2. The signal from each animal was normalized to the mYFP median intensity value in a histogram constructed from all samples. The inter-group intensities were compared by a two-tailed t-test. The asterisks next to the listed genes denote the significance level of the difference. The proteins are listed with their gene names and sorted according to their abundance in WT:EAAT2. (I,J) Plot illustrating the recovery potential of significant EAAT2 binders. The LFQ intensity difference denotes the log2 difference between the compared groups. Compared were WT:EAAT2 vs. HET:EAAT2 (empty bars with black asterisks) and HET:EAAT2-S506X vs. HET:EAAT2 (filled bars with green asterisks). The dashed bars indicate the corresponding WT levels. An up-regulation is shown as upward bar, a down-regulation as downward bar. *p < 0.05, **p < 0.01, ***p < 0.001. | ||
| 9 | 8 | The effect of incubation temperature on extracellular (A+C) and intracellular (B+D) Isoleucine concentration. The concentration of isoleucine in media (A,C) and lysed cells (B,D) for CHOK1 (A+B) and CHOS (C+D) is plotted as percentage of the maximum of each metabolite recorded within the data set. Shift in culture temperatures is denoted by the wide dashed line, and recovered temperature with the short dashed line. Legend: • 37 °C, ■ 27 °C shift, ▲ 10 °C shift, □ 27 °C recover, △ 10 °C recover. | ||
| 10 | 9 | perform | Flipping of a button was performed under direct arthroscopic visualization. | |
| 11 | 10 | Prevalence of (a) T-2 metabolites and (b) T-2-3-Glc and its phase I metabolites in 300 human urine samples. Although HT-2 was assessed through a targeted methodology, it was introduced in this section as a major T-2 metabolite. | ||
| 12 | 11 | Cardiovascular disease incidence and mortality rate according to types of disability: A) Cardiovascular disease incidence. B) Cardiovascular mortality. | ||
| 13 | 12 | Intrahepatic macrophages are responsible for increased apoptosis of WT but not Cd24−/− mouse livers and for suppression of HCC development. To deplete liver macrophages, 13-day-old mice were injected i.p. with 70 μL of liposomal clodronate or control at 48 h before 15 μg/g DEN administration. a F4/80 staining for liver macrophages following injection of control liposomes and clodronate liposomes into WT and Cd24−/− mice. Scale bar = 100 μm. b mRNA levels of F4/80-encoding Emr1 were analyzed by RT-PCR. c Liver sections were analyzed by TUNEL assay. Scale bar = 100 μm. d Average numbers of TUNEL-positive cells in a high-power field of a fluroscerent microscope. At least 10 fields from different section were counted. Control liposomes: n = 8; Clodronate liposomes: n = 12. Representative data from one of two experiments are shown. The data were analyzed by Student’s t-test. (e–i Depletion of macrophage at the time of DEN induction increases the incidence of HCC. Liver macrophages in 13-day-old WT mice were depleted by injection i.p. with 70 µl of clodronate or control liposomes twice within 5 days. 48 h after the first injection of liposomes, mice were treated with 15 µg/g DEN. Mice in both groups were kept for 5 additional months, after which they were killed and analyzed to determine tumor load and morphology. (e Histology analyses revealed significant difference in neoplastic transformation of adenomas from control liposome-treated (top panels) or clodronate-treated macrophage-depleted mice (bottom panels). The left panels show 10 × images, whereas the right panels show high-power images. Note enlarged and pleomorphic nuclei in the adenoma from the macrophage-depleted mice. f Tumor incidences (diameter ≥1.0 mm), g liver to body weight ratios, h tumor numbers, and i maximal tumor sizes are shown. Control liposomes: n = 15; Clodronate liposomes: n = 8. Data from two pooled independent experiments are shown. j–n WT mice were injected with 15 μg/g DEN at 15-day of ages. After 5 months, 200 μL of a 1:1 PBS-diluted liposomes were injected via the tail vein once every 5 days for a total of three times. All mice were killed 1 month after the last injection. (j) Histology analyses revealed significant difference in neoplastic transformation of adenomas from control liposome-treated (top panels) or clodronate-treated macrophage-depleted mice (bottom panels). The left panels show 10 × images, whereas the right panels show high-power images. Note: more heterogenous, enlarged, and pleomorphic nuclei as well as mitosis (red arrow) in adenoma from the macrophage-depleted but not control liposome-treated mice. (k) Tumor incidences (diameter ≥1.0 mm), l tumor numbers, m maximal tumor sizes, and n total tumor volumes were shown. Control liposomes: n = 11; Clodronate liposomes: n = 8. The data were analyzed by Student’s t-test | ||
| 14 | 13 | EBSD grain orientation map of the irradiated Nd2Zr2O7 sample utilizing the cif generated from neutron diffraction assigned to the undamaged part of the sample, direction of He2+ ions are from the bottom of the image. The white rectangle indicates the area where the high-resolution EBSD was taken in Figure 6, and the top left inset shows pole figure orientation. The plot to the left is the SRIM simulation and is provided as a comparison for penetration depth of the He2+ ions. | ||
| 15 | 14 | Forest plot for the meta-analysis of serum S100B levels before vs. after neuroleptic/antipsychotic treatment in longitudinal studies. Hedges’ g was used as an estimate of effect size under a random effects model. Effect sizes are shown for each treatment duration separately as well as the overall effect of treatment regardless of duration. CI, confidence interval. | ||
| 16 | 15 | represent | deviation | Mean SRMRND based on samples drawn from population factor models with model error for q = 3 with p = 15 and q = 6 with p = 30 for the MFA-model, MFA-scores, PCA-scores, and SPFA-scores; λ = initial population loadings; λ = maximal population loadings; the error bars represent standard deviations. |
| 17 | 16 | The muscle strength of 3 groups among before, immediately after, and at 24 hr, 48 hr, and 72 hr after exercise. p < 0.05, Group CC versus Group Y or Group CON. | ||
| 18 | 17 | Flow diagram of the study selection process | ||
| 19 | 18 | Graphical representation of Cov-I-Vac and Cov-II-Vac. All the available ORFs were subjected to epitope mapping and shortlisted epitopes were used to design Cov-I-Vac. Furthermore, beta defensin adjuvant was added at N-terminus to design Cov-II-Vac. Cov-I-vac and Cov-II-vac have CTL as well as HTL epitopes to incite cell mediated as well as humoral immunity. | ||
| 20 | 19 | 7 MHz transducer. The silhouette of midbrain is marked with a colored line. Substantia nigra (*) and brainstem raphe (arrow) can be identified. | ||
| 21 | 20 | Lateral radiograph and computed tomography images of the thoracolumbar spine showing outgrowth in the 12th thoracic vertebra. | ||
| 22 | 21 | make | Characteristics that have made the NGF Conference series unique. | |
| 23 | 22 | assay | RuBisCo activase (Rca) activity assay in contrasting wheat cultivars at different stages of growth and development under control (C) and heat stress (HS) conditions. (A) HD2985 (C and HS), (B) HD2329 (C and HS), (C) Halna (C and HS), (D) PBW621 (C and HS); samples collected from pollination, milky-ripe and mealy-ripe stages were used for the activity assay; C −22 ± 3°, heat stress −42°C for 2 h; NaH14CO3 (20 mM, specific activity 50 mCi mmol−1, BARC, Mumbai) was used for the labeling; different letters above each bar indicate a significant difference (p < 0.05) between the treatments (one-way ANOVA); vertical bars indicate SE (n = 3). | |
| 24 | 23 | Image segmentation and reference coordinate system. (a) Three-dimensional rendering and typical sagittal section of a reconstructed and realigned calcaneus bone at 5 μm resolution. The cutting plane (red dashed lines) demarcates the analyzed region. (b) Cropped bone with a close up on the insertion site. The cross-sections considered for the tuberosity analysis are highlighted in purple. The anatomical landmarks to identify the tuberosity in the sagittal plane are also illustrated, together with the cutting orientation (dashed lines) used for the segmentation of the tuberosity. (c) Representation of the spherical coordinate system with the azimuthal (ϕ) and polar (θ) angles used to define the orientation of microstructural features. (d) Illustration of the cubic volumes of interest defined for the spatially resolved analysis of the trabecular network (the analyzed trabecular compartment is highlighted in yellow). Cubes were displaced along two directions: cranio-caudal (orange arrow) and dorso-plantar (blue arrow). Scale bars: 500 µm. | ||
| 25 | 24 | Illustration of the calorimetry testing fixture. The setup is designed to prevent ice formation on the probe surface during a freeze and allows for assessment of temperature change of water during a given freeze run. Time and temperature data are then utilized to calculate the cooling power of a given cryoprobe. | ||
| 26 | 25 | inhibit | replication | MD inhibited viral replication and the expression levels of HSV-1 proteins even after HSV-1 entry. a Schematic view. b L929 cells were infected with HSV-1 and washed twice with PBS at the indicated time points. Then cells were cultured with fresh medium added with MD (3.0 μM) for additional 18 h. Then the cell survival rate was determined by measuring ATP levels. HeLa (c) and L929 (d) was infected with HSV-1 for 2 h, then the cells were washed twice with PBS and cultured in viral free medium containing DMSO or MD (3.0 μM) for additional 6 h. The expression levels of viral proteins were measured by western blot analysis. The viral titers in HeLa cells (e) were measured by plaque forming assay |
| 27 | 26 | promote | activation | Dlg5 depletion promotes JNK and p38 activation. A: LLc-PK1 cells were stimulated with 4 ng/ml TGF-β and incubated for the indicated periods. Cells were then lysed and immunoblotted using the indicated antibodies. B, C, D, E: LLc-PK1 cells were transfected with Dlg5 siRNA (KD) or control siRNA and incubated for two days. Cell lysates were then immunoblotted using the indicated antibodies, and the results were quantitated. The values represent the mean ± S.E. from at least three independent experiments. Dlg5 depletion promoted JNK and p38 activation but not Smad2/3 activation. |
| 28 | 27 | Percentage cercarial shedding from heat-pulsed resistant BS-90 snails that were either treated (+GA), or untreated (−GA) prior to S. mansoni exposure. Note that the snails that were not treated with GA but heat- pulsed and exposed began to shed cercariae at 4 weeks PE (with 70% shedding parasites at 9 weeks PE). In contrast, note that the heat -pulsed- GA-treated - infected snails remained negative for the entire 9 weeks duration of the experiment. | ||
| 29 | 28 | Conventional calpains in vascular ECs influence amino acid composition in liver of HFD-fed mice. Mice were fed an HFD for 18 weeks. A, BCAA levels in fatty liver in the HFD-fed endothelial/hematopoietic-specific Capns1-targeted mice. Amino acids were quantified by HPLC analysis (fl/fl: n = 5; cKO: n = 5). B, BCAA content in fatty liver in HFD-fed EC/hematopoietic-specific Capns1-targeted mice. BCAA was measured by biochemical assay (fl/fl: n = 6; cKO: n = 6). C, plasma BCAA levels in the HFD-fed endothelial/hematopoietic-specific Capns1-targeted mice (fl/fl: n = 12; cKO: n = 12). D, BCAA content in liver from HFD-fed EC/hematopoietic-specific CAST tg mice (cont: n = 9; cTg: n = 10). E, BCAA content in fatty liver from the HFD-fed chimeric CAST cTg mice (cont→WT: n = 10; cTg→WT: n = 10). F, amino acid release from isolated liver ECs. Cells were stimulated with high glucose concentrations at 25 mmol/l (fl/fl: n = 4; cKO: n = 4). G, amino acid release from isolated liver bone marrow–derived macrophages. Cells were stimulated with high glucose concentrations of 25 mmol/l (fl/fl: n = 4; cKO: n = 4). Statistical analysis was performed using two-tailed Student’s t test (A, B, and D) and two-way ANOVA with Bonferroni post hoc test (F). ∗p < 0.05, ∗∗p < 0.01. BCAA, branched-chain amino acid; cKO, conditional KO; EC, endothelial cell; HFD, high-fat diet. | ||
| 30 | 29 | Cross-sections of ommatidia in the dorsal rim area (DRA). (a) The cross-section of an ommatidium of the desert ant Cataglypis with a dumb-bell shape and fused rhabdom. The microvilli of photoreceptor cells R1 and R5 are orthogonally to the remaining photoreceptor cells (figure adapted and modified from [58]). (b) Cross-section of a dung beetle ommatidium with a heart shape and fused rhabdom, microvilli R1 orthogonally with other photoreceptor cells (adaptation from [15]). (c) Cross-section of a honeybee ommatidium with rectangular shape and fused rhabdom. (d) Cross section of a fly with open rhabdom (adaptation from [44]) figure ©Zainalum. | ||
| 31 | 30 | fuse | Synthesis of azulene-fused TTFs 70a and 70b by the condensation reaction. | |
| 32 | 31 | complete | AP and lateral radiograph when lengthening was completed (panels a and b) and 6 weeks later (panels c and d) (nail group: pair 3). | |
| 33 | 32 | analyze | Western blot analysis of synaptic proteins in the prefrontal cortex of TERT-tg mice (A) Postsynaptic protein levels including NR1, NR2A, NR2B, GluR1 and GluR2 in the PFC of 4 weeks old FVB mice and TERT transgenic mice were analyzed by Western blot. (B) Also, the pre-synaptic proteins including vGluT1 and GAD, and somatic proteins including Tuj-1 and β-actin in the PFC of FVB mice and TERT transgenic mice were analyzed. All data are expressed as the mean ± SEM. One male, and one female mouse was chosen from each of 4 litters for a total of 4 mice per group. **p<0.01, ***p<0.001 vs. FVB male group; ##p<0.01, ###p<0.001 vs. TERT transgenic female group, as revealed by Bonferroni’s posthoc comparisons following two-way ANOVA | |
| 34 | 33 | EPT task paradigm. (A) Each participant was asked to passively view 2 runs of 6 blocks of meaningful pictures (i.e., positive [Pos], negative [Neg] and neutral [Neu]) and 6 blocks of masked images (i.e., positive [MPos], negative [MNeg] and neutral [MNeu]) during scanning. (B) Each block consisted of 8 trials of image presentation (3.5 s) and blank screen (0.25 s).Two of the trials is presented in this figure. The pictures for the 3.5 s image presentation shown here are for illustration and are different from those used in the formal study. | ||
| 35 | 34 | promote | differentiation | IOX2-mediated inhibition of PHD2 promotes differentiation of articular chondrocytes. Primary articular chondrocytes were cultured with 20 μM PHD2 inhibitor IOX2 or vehicle (DMSO) for 72 hours and expression of markers were measured by Real time RT-PCR. (A) mRNA expression of cell proliferation marker p57Kip2 and cyclin D1. (B) mRNA expression of SZ progenitor marker tenascin C and clusterin. (C) mRNA expression of chondrocyte marker Col2 and chondrocyte hypertrophy marker Col10. (D) mRNA expression of HIF-1α targets, vascularization marker Vegf, Epo, and glycolysis marker Glut1 and Pgk1. *P < 0.05, **P < 0.01, n = 4/group. Data were normalized to controls and presented as the mean ± SEM. |
| 36 | 35 | reduce | ability | Substitution of some amino acid residues in the Gm structure reduces the cytotoxic ability, but did not modify the cell death mechanism. B16 cells were stimulated by Gm and analogues for 24 h. (A) Cytotoxic activities of Gm and its analogues were quantified by the MTT reduction test. (B) Cell death type identification caused by Gm was evaluated using annexin-V and 7-AAD assay by flow cytometry using the IC50 values. (C-H) Apoptosis (Z-VAD) and necroptosis (necrostatin) inhibitors were unable to reduce cell death induced by Gm and analogues. Cells were incubated with inhibitors for 1 h before to stimulation with the peptides (IC50 values for each peptide was used) and the viability was assessed by the MTT. Results are the means ± SEM of three independent experiments preformed in duplicate. |
| 37 | 36 | represent | Autoradiograph showing cleavage activity of DR36 against full length cyclin B5 mRNA in the presence (RnH) and absence (C) of RNase H. Other control lanes represent full-length cyclin B5 mRNA incubated for 2 hr at 37°C in the presence or absence of RNase H. RNase H mapping reaction contained ∼25 fmol 32P-end-labelled transcript, 10 mM MgCl2, 50 mM KCl, 50 mM Tris-HCl pH 7.4, 1 mM DTT, 0.5 U RNase H, 0.5 U RNase inhibitor (Promega) and 100pmol of DNAzyme) in a total volume of 10 μl. The reactions were incubated at 30°C for 1hr and terminated by addition of 10 μl of formamide gel loading dye buffer. A 5 μl aliquot was analysed on a 8% (w/v) denaturing polyacrylamide gel. | |
| 38 | 37 | The expression levels of miRNA-21 in Sca-1+ CSCs after transfection in blank, negative control, miRNA-21 mimic, and miRNA-21 inhibitor groups (* – the miRNA-21 mimic group was compared with the other 3 groups, P<0.05). The miRNA-21 mimic group had a higher expression level of miRNA-21 than other groups. | ||
| 39 | 38 | (A) Stress-strain curve of sample A, B, and C; (B) Burst pressure of sample A, B, and C. | ||
| 40 | 39 | Effects of CLP gene mutations on bacterial biofilm formation (A) and colony morphology (B). (A) Spectrophotometric quantification of biofilms formed by Pseudomonas sp. 11K1 and CLP mutants. Mean values of three replicates are given, and error bars indicate standard error. Visual representation of biofilm formation by Pseudomonas sp. 11K1 and CLP mutants on tubes is shown. Biofilms were stained with Crystal Violet. (B) Colony morphology detected on PDA plates. A 5 μL sample of overnight culture of WT 11K1 or mutant strains was spot-inoculated in the center of a PDA plate and incubated for 48 h at 28°C. Δbam, brasmycin gene cluster deletion mutant; Δbap, braspeptin gene cluster deletion mutant; Δbaa, brasamide gene cluster deletion mutant; ΔbamΔbap, brasmycin and braspeptin double gene cluster deletion mutant; ΔbamΔbaa, brasmycin and brasamide double gene cluster deletion mutant; ΔbapΔbaa, braspeptin and brasamide double gene cluster deletion mutant; ΔbamΔbapΔbaa, brasmycin, braspeptin, and brasamide triple gene cluster deletion mutant. | ||
| 41 | 40 | center | Delineation of a VOI centered on the left hippocampus of a healthy control for single-voxel spectroscopy (see Fig. 3; courtesy Dr. Lukas Scheef, Dept. of Radiology, University Bonn) | |
| 42 | 41 | Purpose of SHG loans, SHGs with and without CIFs. | ||
| 43 | 42 | (Left) a therapy garden not being used during most of the day in NH3. (Middle) residents in geriatric chairs passively sitting in the sun in NH5. (Right) a resident in a wheelchair looking outside through the window in NH5. | ||
| 44 | 43 | Disposition of subjects. | ||
| 45 | 44 | Nepmucin/CD300LG expression is apparently absent from immunologically privileged sites. Frozen sections of the indicated tissues were incubated with an anti-nepmucin mAb or anti-CD31 mAb, followed by HRP-conjugated anti-rat IgG. The reaction was then developed with DAB substrate. Arrows indicate blood vessels in the brain. No nepmucin expression was observed in these tissues. Scale bars, 100 µm. | ||
| 46 | 45 | confer | modulation | Notch signaling confers epithelial-intrinsic modulations of organoid growth and differentiation. (A) Representative brightfield pictures of cardia organoids of pL2.Dclk1, pL2.Dclk1.N2fl and pL2.Dclk1.N2IC mice, respectively; scale bars = 100 µm. (B) Organoid survival and size showed significantly increased in organoids from pL2.Dclk1.N2IC mice (measurements n = 6 pL2.Dclk1, n = 5 pL2.Dclk1.N2fl, n = 4 pL2.Dclk1.N2IC, Kruskal–Wallis test, pL2.Dclk1 vs. pL2.Dclk1.N2IC p = 0.028), organoid size (2d, measurements n = 47 pL2.Dclk1, n = 15 pL2.Dclk1.N2fl, n = 19 pL2.Dclk1.N2IC; 4d n = 39 pL2.Dclk1, n = 53 pL2.Dclk1.N2fl, n = 12 pL2.Dclk1.N2IC; 7d n = 29 pL2.Dclk1, n = 20 pL2.Dclk1.N2fl, n = 17 pL2.Dclk1.N2IC; ordinary two-way ANOVA, pL2.Dclk1 vs. pL2.Dclk1.N2IC p = 0.001, pL2.Dclk1.N2fl vs. pL2.Dclk1.N2IC p = 0.007), while organoid wall thickness significantly increased in organoids from pL2.Dclk1.N2fl mice (2d, measurements n = 47 pL2.Dclk1, n = 15 pL2.Dclk1.N2fl, n = 19 pL2.Dclk1.N2IC; 4d n = 39 pL2.Dclk1, n = 48 pL2.Dclk1.N2fl, n = 12 pL2.Dclk1.N2IC; 7d n = 30 pL2.Dclk1, n = 23 pL2.Dclk1.N2fl, n = 18 pL2.Dclk1.N2IC; ordinary two-way ANOVA, pL2.Dclk1 vs. pL2.Dclk1.N2fl p = 0.0011). (C) Representative brightfield pictures of pL2.Dclk1 cardia organoids undergoing the indicated treatments; scale bars = 100 µm. Organoid size was significantly reduced following treatment with DAPT (3d measurements n = 44 pL2.Dclk1, n = 38 pL2.Dclk1 DMSO, n = 19 pL2.Dclk1 DAPT, ordinary two-way ANOVA, pL2.Dclk1 vs. pL2.Dclk1 DAPT p = 0.041, pL2.Dclk1 DMSO vs. pL2.Dclk1 DAPT p = 0.015; 6d n = 98 pL2.Dclk1, n = 22 pL2.Dclk1 DMSO, n = 17 pL2.Dclk1 DAPT, ordinary two-way ANOVA, pL2.Dclk1 vs. pL2.Dclk1 DAPT p = 0.0005, pL2.Dclk1 DMSO vs. pL2.Dclk1 DAPT p = 0.0031); error bars indicate SEM. |
| 47 | 46 | protect | structure | Stimulation treatment protects cortical structure in aged rats. A, Representative coronal sections from an untreated (left) and a treated rat (right) with TTC assay for infarct. Red staining indicates healthy tissue; lack of staining indicates ischemic infarct. Arrows point toward MCA blood supply territory. Scale bar = 5 mm. B, Box-and-whisker plot of infarct volume (mm3), with individual subjects plotted for untreated (green) aged subjects and treated (gold) aged groups. |
| 48 | 47 | Probe 7 and its reaction with GSH or Cys (n = 1)/Hcy (n = 2). | ||
| 49 | 48 | Symptomatology of wheat cultivar Chuanmai42 (CM42) inoculated with CYR32 and V26. A-C represent different day-after inoculation with Pst. CK, un-inoculated wheat leaves. | ||
| 50 | 49 | A photo captured from the height of 100 m AGL (a); a zoomed ground target (b). | ||
| 51 | 50 | Schematic of the various CCR7 N-terminal peptides used in this study. CCR7 peptides correspond to the sequence of the mature CCR7 N-terminus. Those peptides including residue 24 have a C24A mutation to prevent oxidative peptide dimer formation. Tyrosine posttranslational modifications are as indicated. | ||
| 52 | 51 | KEGG analysis of DMGs in Angus (left side) and Nellore (right side) in challenge and recovery periods. Peak hight is proportial to the number of differentially methylated genes, color to p value. Negative values indicate hypo-methylation, positive values hyper-methylation during heat stress. | ||
| 53 | 52 | Treatment of s.c. PC3-PSCA macrotumors with different activities of 211At-A11. Tumor volumes (a) and mouse weights (b) are shown as mean ± SEM. ***p < 0.001, *p < 0.05 | ||
| 54 | 53 | CA3 is necessary for normal place field responses in CA1. a) Two example CA1 place fields in CON rats. Top: Rat position as a function of time during linear track traversals (thin line), overlaid with spiking activity only in the running direction depicted by the arrow. Spikes in light OFF and light ON conditions are shown as black and green dots, respectively. Bottom: The average place fields calculated from above lap-by-lap spiking activities. b) All non-repetitive CON place fields sorted by their peak firing position during light OFF condition on the linear track. Each row depicts the color map of same place field in light OFF (left) and light ON (right) conditions. Each field is normalized by its maximum peak firing rate across OFF and ON conditions and the order of fields is similar between the two light conditions. c-d) Two example CA1 place field (c) and all non-repetitive sorted fields from EXP rats (d) as described in a-b. e-g) Place field features in light ON vs. light OFF conditions. Values are presented as mean ± s.e.m. e) Peak firing rate (CON: OFF: 7.97 ± 0.62 Hz and ON: 7.95 ± 0.55, two-tailed signed rank test, n = 157 fields, z(156) = −1.1, p = 0.3; EXP: OFF: 6.63 ± 0.43 and ON: 4.70 ± 0.40, two-tailed signed rank test, n = 236 fields, z(235) = 5.8, p = 10−8). f) Place field size (CON: OFF: 51.40 ± 1.95 cm and ON: 51.01 ± 1.98, two-tailed paired t-test, n = 157 fields, F(156) = 0.06, p = 0.80; EXP: OFF: 57.58 ± 2.17 and 39.97 ± 2.23; two-tailed signed rank test, n = 236 fields, z(235) = 6.8, p = 2×10−11). g) COM (CON: OFF: 65.81 ± 2.02 cm and 65.81 ± 2.03, two-tailed paired t-test, n = 156 fields, F(155) = 0.00, p = 1; EXP: OFF: 62.89 ± 1.54 and ON: 63.27 ± 1.81, two-tailed signed rank test, n = 207 fields, z(206) = −0.1, p = 0.9). h-l) the CDF of place field features in CON and EXP rats. h) The CDF of the absolute value of the lap-by-lap stability modulation of original and firing-matched (FM) place fields (Original: two-tailed rank sum test, n1 = 156 and n2 = 207 fields, z(362) = −3.9, p = 2×10−4; FM: two-tailed rank sum test, n1 = 156 and n2 = 207 fields, z(362) = −2.5, p = 0.013; EXP original vs EXP FM: two-tailed signed rank test, n = 207 fields, z(206) = 4.2, p = 5×10−5). i) The CDF of the absolute value of the amount of peak firing rate modulation (Original: two-tailed rank sum test, n1 = 156 and n2 = 207 fields, z(362) = −6.7, p = 3×10−11; FM: two-tailed rank sum test, n1 = 156 and n2 = 207 fields, z(362) = −2.1, p = 0.036). j) The CDF of the absolute value of the amount of field size modulation (Original: two-tailed rank sum test, n1 = 156 and n2 = 207 fields, z(362) = −5.1, p = 5×10−7; FM: two-tailed rank sum test, z(362) = −3.4, p = 7×10−4; EXP original vs EXP FM: two-tailed signed rank test, n = 207 fields, z(206) = 3.2, z(362) = −3.0, p = 0.0015). k) The CDF of the absolute value of the amount of COM shift (Original: two-tailed rank sum test, n1 = 156 and n2 = 207 fields, p = 0.0025; FM: two-tailed rank sum test, n1 = 156 and n2 = 207 fields, z(362) = −3.3, p = 0.001; EXP original vs EXP FM: two-tailed signed rank test, n = 207 fields, p = 0.3). l) The CDF of the spatial correlation (Original: two-tailed rank-sum test, n1 = 156 and n2 = 207 fields, z(362) = 5.0, p = 10−6; EXP original vs EXP FM: two-tailed signed rank test, n = 207 fields, z(206) = 2.7, p = 0.008). | ||
| 55 | 54 | image | movement | Simultaneous video imaging colonic wall movements with electrical recordings made from two independent sites along the smooth muscle. a shows a photomicrograph of the isolated colon and location of two independent extracellular recording electrodes, separated by 30 mm, where one electrode is located in the proximal/mid colon, the other in the distal colon. b Spatio-temporal map with superimposed simultaneous electrical recordings from the mid colon. The white band shows the propagating contraction associated with propulsion of fluid. c Superimposed electrical recordings from the proximal and distal colon. d Wavelet coherence of electrical activities between electrical recordings from electrode 1 (proximal colon) and electrode 2 (distal colon). The yellow band shown from ~6 to 17 s shows ~2 Hz peak coherence. e The relative time alignment between electrical recordings shown in panel c are presented. There is a small temporal difference between EJPs until ~17 s where the time difference increases and the propulsive wavefront passes. fi shows an expanded period represented by the black bar from panel c–e, where the close temporal synchronization between recordings EJPs is shown. fii, shows two different periods of recordings (represented by the two black bars) take from panel fi. The recording on the left hand side shows close synchronicity between EJPs, while the right hand panel recording in fii shows EJPs are phase shifted slightly by ~100–200 ms. |
| 56 | 55 | Calibration method. (a) Schematic diagram of the calibration process. (b) A representative of calibration results for the 10X MO. (c) A representative of calibration results for the 40X MO. | ||
| 57 | 56 | FT-IR spectra of the (a) Fe3O4, (b) Fe3O4@SiO2@KCC-1, (c) Fe3O4@SiO2@KCC-1@MPTMS, and (d) Fe3O4@SiO2@KCC-1@MPTMS@CuII nanosystems. | ||
| 58 | 57 | Means on MMSE. MEMTOTAL, MSDR sample; MEMTOT2, sample of HSM. | ||
| 59 | 58 | Increases in motor performance after motor practice (MP), somatosensory electrical stimulation (SES), and MP + SES in the intervention (open bars) and non-intervention (filled bars). Motor performance was computed as a reduction in template-matching errors. Performance improved more after MP and MP + SES in the right hand compared to SES. Asterisk, significant Time main effect (p < 0.05, open and filled bars, respectively, pooled, not graphed); dagger, significant Group by Time interaction (p < 0.05). Vertical bars denote +1SD | ||
| 60 | 59 | indicate | A plot indicates that the viruses become steady. | |
| 61 | 60 | Sex differences in the intensity (i.e., pathogen load), prevalence (i.e., proportion of population with disease), incidence (i.e., new cases of disease), and severity (i.e., hospitalization or progression of disease state) of disease following microbial infections in humans. | ||
| 62 | 61 | range | 3.5–5 | Annual cryo-EM model depositions now outnumber X-ray model depositions in the resolution range 3.5–5 Å. |
| 63 | 62 | Schematic diagrams for the mechanism of the cardiac-specific miR-1 overexpression-induced decline in synaptic vesicle exocytosis. Overexpressed miR-1 in the hearts of Tg and MI mice were secreted into the extracellular space carried by exosomes. Exosomes entered the blood and were transported into the brain through blood circulation. After exosomes enter the brain, they were accepted by neurons and inhibited the expression of SNAP-25 by binding with the target in the 3’UTR of the Snap25 gene. The inhibition of SNAP-25 results in the impairment of vesicle exocytosis through impeding SNARE-complex formation | ||
| 64 | 63 | Olive PAP correlation with the different pollutants and meteorological parameters | ||
| 65 | 64 | Mandibular denture after capturing the titanium cylinder and distal bar. | ||
| 66 | 65 | The examples of brain MRI slices in different datasets. (a) BT-4C, (b) BT-3C, (c) BT-2C. | ||
| 67 | 66 | Per capita all-cause mortality in India by month, 2019 to 2021, based on 13 states and two union territories, as described in the Methods section. This figure appears in color at www.ajtmh.org. | ||
| 68 | 67 | Source localization on aligned peaks of rivalry amplitude time course. (A) Schematic of the SSVEP amplitudes used to find the time point of peak in competition measured as the maximum of difference between SSVEPs after the button press (t = 0). This time point was used in source localization. (B) The difference in the two competing SSVEPs was localized on a standard brain for the green (top) and red grating percept (bottom) during binocular rivalry. Subjects (n = 5) with clear counterphase amplitude modulation during either stimulus rivalry or binocular rivalry were selected for source localization. SSVEP signals were phase-aligned and then localized to a standard brain with standard electrode positions common for all subjects. Right panel shows the same source localization procedure but for stimulus rivalry. | ||
| 69 | 68 | Immunolocalization of Ubx (FP6.87 antibody) in honeybee white-eyed pupale hind legs. A-C: Ubx is expressed in the tibia and basitarsi of workers. There is a region in the tibia (which may be the future corbicula) that does not express Ubx. D-I: In the basitarsus and distal portion of the tibia (arrowhead) in workers, there are double nuclei that do not express Ubx, arranged in a similar pattern as that of the bristles in the adult hind leg. J-L: In the hind legs of queen white-eyed pupae, Ubx is expressed only in the basitarsi. In blue: DAPI; in red: Ubx; Btar: basitarsi; Tb: tibia. Original scale bars of confocal system. | ||
| 70 | 69 | Four tiers of the fingerprint and timing-based snooping (FATS) attack. | ||
| 71 | 70 | Kaplan-Meier estimates of overall survival according to the mRNA expression levels of (a) RRM2, (b) TS, (c) ERCC1, (d) p53R2, (e) TUBB3, (f) BRCA1, and (g) RRM1 in the overall population. | ||
| 72 | 71 | Correlations wheels showing significant correlations between elements within an experiment. A–B are taken from Ghandilyan 2009, [26], Figure 5. C is taken from Ghandilyan 2009, [27], Table 2. D–H taken from Buescher et al. [24] Figure 1. Only significant correlations (p<0.001 and R2>0.32) are displayed on each wheel. Positive correlations are denoted by solid lines, negative correlations are denoted by dashed lines. Thick lines indicate R2>0.5, thin lines indicate 0.32<R2<0.5. Ions not measured in a given experiment are colored in grey. | ||
| 73 | 72 | Bee swarm plots of the changing rate of indices and segmented volumes following shunt surgery compared to those at baseline magnetic resonance imaging. Graph A shows the distribution and mean value of the relative changes in the following indices; Evans index (brown), z-Evans index (green), callosal angle (red), brain per ventricle ratio (BVR) at the anterior commissure (AC) level (purple) and BVR at the posterior commissure (PC) level (blue), and convexity subarachnoid space (SAS) per ventricle ratio (CVR; orange). Graph B shows the distribution and mean value of the relative volume changes in the brain parenchyma (brown), total ventricles (red), and total SAS (blue). Graph C shows the distribution and mean value of the relative volume changes in the convexity part of SAS (blue), Sylvian fissure and basal cistern (red), and SAS in the posterior fossa (brown). | ||
| 74 | 73 | decrease | level | Dasatinib decreases p53 basal expression levels in primary CLL lymphocytes expressing wild type p53. Dasatinib and chlorambucil IC50s were significantly different between CLL lymphocytes expressing wild type TP53 or del 17 (*P = 0.012). The bars represent the median values and 95% confidence intervals (CI 95%). (A). The lymphocytes of 11 CLL lymphocyte patients were treated for 24 h with vehicle (dimethyl sulphoxide), dasatinib 100 nmol/l or the IC50 concentration as shown in Table I. Protein extracts were obtained as described before and 50 μg of proteins for each sample were resolved by sodium dodecyl sulphate poyacrylamide gel electrophoresis. p53 and p21 protein levels were assessed by Western blot using specific antibodies (Amrein ). The signals obtained in TP53 wild type lymphocytes (B) were analysed using National Institutes of Health -Scion image and normalized to actin, p53 or p21 levels (y-axis) and are expressed as the percentage of vehicle treated lymphocytes (control) value ([OD value/control OD value]x 100) vis à vis the treatments indicated in the x-axis; * and ** indicates significance P = 0·003 and P = 0·004 respectively (C). Dasatinib-induced changes in p53 levels and p21 signal were not detected in protein extracts from del 17p13·1 CLL lymphocytes (D). Dasatinib IC50s correlate with the percentage of residual p53 protein levels (in respect to vehicle treated lymphocytes) after dasatinib treatment, r = 0·82, P = 0·02 (E). Two-sided tests with α-value of 0·05 were used. Correlations between the data were assessed using the Spearman test. All tests were performed using SigmaStat software. |
| 75 | 74 | add | yield | (A) Site-specific yield of and fragments from CAD (42 eV laboratory frame collision energy) of (M+4H)4+ ions of RNA 1 electrosprayed from solutions at pH 6.8 and 3.0, (B) added yields for sites 1–2 (blue), 3–5 (gray), 6–8 (purple) and 9–14 (black) and (C) added yields for sites 1–2 (blue) and 6–8 (purple) divided by the added yields from sites 3–5 and 9–14 versus solution pH. |
| 76 | 75 | The different structural configurations of quaterpyridyl ligand and modes of coordination to metal ion. | ||
| 77 | 76 | The ROC curve of Model 4 and Model 5 in training and testing sets. | ||
| 78 | 77 | compute | Computed tomography scan (coronal view) of patient with congenital peritoneal encapsulation. | |
| 79 | 78 | Transcription factor-mediated regulatory network. Heatmap (A) and volcano plot (B) showing differentially expressed transcription factors (TFs). (C) Regulatory network based on clinically relevant TFs and IRGs. | ||
| 80 | 79 | Photographs and SEM images of GCA from different GO:oPAN mass ratios: (a,b) GCA12, (c,d) GCA22, (e,f) GCA42, (g,h) GCA14, (i,j) GCA24, and (k,l) GCA44. | ||
| 81 | 80 | Medical management and clinical outcomes for patients with ≥ 10 pp decrease in LVEF to an absolute value < 50% in FLAURA and AURA3. *Events being marked not resolved is because of the event not having had resolution marked in the database by the time of the data cutoff. †Final LVEF measurements were not available for five patients. LVEF, left ventricular ejection fraction; pp, point percentage. | ||
| 82 | 81 | Data acquisition location map of Tianningsi Tower. | ||
| 83 | 82 | Analysis results of actual damaged specimens. | ||
| 84 | 83 | indicate | lesion | (A, B, C, D) Arrows indicate the flat elevated mucosal lesion in the interposed colon, located at the anastomosis site and measuring 12 mm (A). Another flat elevated lesion located 4 cm proximal to the anastomosis site, measuring 20 mm is indicated with arrow heads (B). These polyps were removed by snare polypectomy after the submucosal injection of saline (C, D). |
| 85 | 84 | Effects of menadione and acetaldehyde on NAD(P)H oxidation in permeabilized yeast cell suspension. Black and white bars show oxidation rate of NADH and NADPH, respectively. Non, M and A mean non-addition, the addition of menadione and acetaldehyde, respectively. M+A means the addition of acetaldehyde after 1 min-incubation with menadione. A+M means the addition of menadione after 1 min-incubation with acetaldehyde. Each bar represents the mean of three different determinations, and the standard deviation was less than 6% of the mean. | ||
| 86 | 85 | SERS of biomolecules (β-lactoglobulin and glucose) on the PCNA substrate. a Measured Raman spectra of β-lactoglobulin molecules on the silicon, PCNA, and commercial metal substrates. The Raman signal intensity of β-lactoglobulin molecules on the PCNA substrate is 10 times higher than that on the metal substrate. b SERS maps of β-lactoglobulin on the PCNA substrate, showing high surface homogeneity in enhancement factor at two characteristic Raman shifts of the molecule on both large and small scales with a step size of 1 and 0.1 µm, respectively. c Histograms of the enhancement factors on the large and small scales. d Measured Raman spectra of glucose molecules on the silicon and PCNA substrates. e Time-to-time consistency of the PCNA substrate in the Raman spectrum of glucose. Small hour-to-hour fluctuations in the Raman spectrum indicate high reproducibility and biocompatibility. | ||
| 87 | 86 | reduce | secretion | ATO and sulforaphane combination treatment effectively reduces protein secretion. Clones of KMS-11 and ARP-1 cells stably expressing Gluc were treated with 1 μM ATO, 3 μM sulforaphane or in combination for 24 h. After treatment, Gluc secretion was assessed by measuring luciferase activity in the media. Percent secreted Gluc is determined by the following equation: (RLU of treated cells/RLU ratio of the untreated, DMSO control cells) × 100. *P<0.05. All experiments were performed in triplicate and error bars were calculated using SEM. NT, no treatment; A, ATO; S, sulforaphane. |
| 88 | 87 | Comparison of the FTIR spectra between the M4 and the urethane acrylic (UA4). | ||
| 89 | 88 | Effect of CTHRC1 gain/loss of function on EOC cell malignant phenotype A. Down-regulation and up-regulation of CTHRC1 by CTHRC1-siRNA and pcDNA3.1-CTHRC1, respectively. Data are means ± SD of 3 independent experiments (**p < 0.01). B. 48 h after transfection, cells were seeded in the null-adhesion condition (day 0). At days 2–3, an adhesion index (%) was calculated as [n cells grown in adhesion/(n cells grown in adhesion + n cells grown in suspension) × 100%]. CTHRC1 significantly inhibited EOC cell adhesion (*p < 0.05). C. Transwell assay showed that cell invasiveness was diminished by CTHRC1-siRNA treatment, and enhanced by pcDNA3.1-CTHRC1 treatment (*p < 0.05). D. Transfected EOC cells were also tested for the ability to form colonies in soft agar: 7 days after seeding in soft agar, transfected cell samples were analyzed by light microscopy and the size/number of colonies was evaluated, considering percentage fractions. E. Cell viability was tested by MTT assay: cell viability was impaired by CTHRC1-siRNA treatment (the upper), and elevated by pcDNA3.1-CTHRC1 treatment (the lower). Data are from three separate experiments (*p < 0.05). | ||
| 90 | 89 | (A) The diversity of morphological traits of panicles in Kam fragrant glutinous rice. (B) The diversity of morphological traits of spikelets and seeds in Kam fragrant glutinous rice. No. 96–99 are the control varieties, in which 97 and 98 are glutinous japonica, 96 and 99 are non-glutinous indica. | ||
| 91 | 90 | mediate | Defect in UPS-mediated MEF2-degradation in the most aggressive LMS cell line. A) Immunoblot analysis of HDAC4, SKP2 and MEF2 family members in LMS cells. Cells were treated for 8 hours with 2.5μM of the UPS inhibitor MG132. RACK1 was used as loading control. B) Immunoblot analysis of MEF2D isoforms in LMS cells engineered to express the dominant negative version of SKP2 (DN). RACK1 was used as loading control. C) Immunoblot analysis of MEF2D in LMS cells engineered to express an inducible version of SKP2 fused to ER as indicated. SKP2 was induced for 30 hours with 0.5μM 4-OHT. RACK1 was used as loading control and the nuclear relocalization of SKP2 after 4-OHT treatment was scored by immunofluorescence. D) Cellular lysates obtained in SK-LMS-1 cells expressing the DN mutant of SKP2 were immunoprecipitated using anti-MEF2Dα1 antibody and immunoblotted with the indicated antibodies. Immunoblots with total lysates (input) are also included. E) Cellular lysates obtained in SK-UT-1 cells expressing the DN mutant of SKP2 were immunoprecipitated using anti-MEF2Dα1 isoform and immunoblotted with the indicated antibodies. Immunoblots with total lysates (input) using the indicated antibodies are also included. | |
| 92 | 91 | Patient grouping process (dendrogram) | ||
| 93 | 92 | Cross-linking of LTGS geopolymeric reaction. | ||
| 94 | 93 | General strategy for the carbon quantum dot’s (CQD’s) preparation and application. | ||
| 95 | 94 | Baseline volumes of each method for (a) whole brain, (b) lateral ventricles, (c) left hippocampus and (d) right hippocampus for all groups. Red squares indicate the AD patient group and blue circles indicate the control group for each technique. | ||
| 96 | 95 | All-atom simulations of FL-ATP. (A) 10 snapshots of the three long atomistic MD simulations of FL-ATP DnaK bound to the DnaJ JD. Green: NBD, magenta: linker, brown SBD, red/cyan/purple: JD for the three trajectories. For ease of visualization, only helices II and III of the JD are depicted. (B) Distributions of the distances of the three coevolving contacts and the D35-R167 contact. The distance distributions for the three cases follow the color scheme of panel A (red/cyan/purple). Shaded areas are the sum of the distributions for each case. See (Figure 4—figure supplement 4) for traces of the trajectories. DOI: http://dx.doi.org/10.7554/eLife.23471.012 | ||
| 97 | 96 | Significant premorbid personality and biomarker interaction effect on cognitive functioning. Dispersion diagram plot depicting the fit of a model with predicted cognitive performance score (ordinate axis) and an interaction between biomarker concentrations (abscissa axis) and premorbid personality. Lines, predicted centred values of premorbid personality traits. Left: with low neuroticism (N), greater ptau-181/Aβ1–42 concentrations predict lower CDR SoB scores, and thus better cognitive functioning. With relatively small ptau-181/Aβ1–42 value, the interaction effect is inversed. Middle: interaction between high agreeableness (A) level and high ptau-181/Aβ1–42 value predicts higher CDR SoB score, and thus lower cognitive functioning. Effect is inversed with relatively small ptau-181/Aβ1–42 concentrations. Right: at low conscientiousness (C) level, greater ptau-181/Aβ1–42 concentrations predict poorer cognitive performance (high CDR SoB score). With high C, smaller ptau-181/Aβ1–42 ratios predict better cognitive functioning (low CDR SoB score). CDR SoB Res residuals of clinical dementia rating Sum of Boxes score, Aβ amyloid beta, ptau phosphorylated tau | ||
| 98 | 97 | absorbance | Calculated solar absorbance α and solar selectivity α/ε for LaB6 samples and comparison with HfB2, ZrB2 and SiC. | |
| 99 | 98 | relate | Factors related to the use of assistive technology by people with intellectual disabilities. | |
| 100 | 99 | Nonprompt and prompt D meson [31, 62], and charged hadron [58, 60] vs. centrality (top), and vs. (bottom). For the top plot, the average values correspond to events flatly distributed across centrality |