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0.488019 | 63b925e9efd442da96397a9b221affbe | Deletion of Wls in Col1a1-expressing cells protects against TBI-mediated augmentation of senescent MSCs. (A) The frequency of MSCs in BM and the number positive for (B) MitoSox, (C) C12FDG, or (D) p16INK4a in 4-week-old Wlsfl/fl and Col-Cre;Wlsfl/fl mice were analyzed by flow cytometry (n = 5). (E) The colony forming activity of BMSCs isolated from the mutants and littermate controls at 4 weeks of age was evaluated (n = 7). Four-week-old Wlsfl/fl and Col-Cre;Wlsfl/fl mice were exposed to sub-lethal TBI, and 4 weeks after TBI, (F) the frequency of BM MSCs, (G) MitoSox-, (H) C12FDG-, or (I) p16INK4a-positive MSCs, and (J) the colony forming activity of BMSCs were evaluated (n = 5 for F-I, n = 6 for J). (K) BMSCs isolated from TBI- or non-TBI-exposed Wlsfl/fl and Col-Cre;Wlsfl/fl mice were incubated in the presence and absence of DAG. After 21 days of incubation, the mineralization of these cells was evaluated by measuring the optical density at 405 nm (n = 7). (L) The proliferation rate of BMSCs isolated from TBI-exposed Wlsfl/fl and Col-Cre;Wlsfl/fl mice was monitored for 7 days by incubating them in growth medium. The p values in panels in panels A-D and F-I were calculated using unpaired non-parametric Wilcoxon t-test. The p values in panels E, J, and K were determined by unpaired Student’s t-test. | PMC10187694 | AD-14-3-919-g5.jpg |
0.395791 | 5dcb3ad77d2c46faab63d39467645274 | Deletion of Wls in Col1a1-expressing cells inhibits TBI-mediated enhancement of bone mass loss. Femoral bones (2D image) with magnified trabecular zones (3D image) in (A) non-TBI- and (B) TBI-exposed Wlsfl/fl and Col-Cre;Wlsfl/fl mice were analyzed by μCT when they were 8 weeks of age. For this experiment, the mouse groups for TBI were exposed to sub-lethal TBI when they were 4 weeks of age, and representative results exhibiting average BMD values among five different samples per group are shown. Values of (C) BMD (g/cm3), (D) Tb.Th. (mm), (E) BV (mm3), (F) Tb.N. (1/mm), (G) BV/TV (%), and (H) Po (%) were calculated based on the constructed 3D images (n = 5). Photographs showing (I) Wlsfl/fl and Col-Cre;Wlsfl/fl mice at 4 weeks of age and (J) after an additional 2 weeks of TBI. (K) The body weights (g) of the Wlsfl/fl and Col-Cre;Wlsfl/fl mice were monitored on the indicated days after TBI (n = 6). The p values in panels C-H were determined by non-parametric Wilcoxon t-test, whereas the values in panel K were by unpaired Student’s t-test. ns, not significant. | PMC10187694 | AD-14-3-919-g6.jpg |
0.402398 | f083e375a0e342608d41a2ef26dd26d3 | TBI acutely reduces the numbers of peripheral WBCs and lymphocytes but not the BM levels of Wnt ligands, and that is ameliorated by osteoblastic Wls depletion. The levels of circulating (A) WBCs, (B) lymphocytes, (C) granulocytes, (D) RBCs, and (E) platelets in the mouse groups were measured using an automated complete blood cell counter at the indicated times (h) after TBI (n = 5). (F) The BM levels of Wnt3a and Wnt5a in Wlsfl/fl and Col-Cre;Wlsfl/fl mice were evaluated by IHC when they were 4 weeks of age. Representative data from five different samples are shown. Scale bars = 100 μm. (G) The area (%) positively stained with Wnt3a or Wnt5a in the IHC assay was calculated (n = 5). (H) Levels of Wnt3a and Wnt5a mRNA in whole BM lysate were determined by qRT-PCR (n = 5). Protein levels of (I) Wnt3a and (J) Wnt5a in the whole BM lysate were determined by ELISA at the indicated times after TBI (n = 5). The p values in all panels were determined by non-parametric Wilcoxon t-test. The superscriptsa-c indicate significant differences among the groups compared with the value of non-TBI control or mutant group by ANOVA. The symbol ‘*’ in panels I and J indicate significant difference at p < 0.043 by the Wilcoxon t-test. ns, not significant. | PMC10187694 | AD-14-3-919-g7.jpg |
0.456552 | 63cf139d47d240d393c496a97daf7c56 | Schematic illustration of the roles played by osteoblastic Wls ablation in TBI-mediated alterations in the BM microenvironment, bone mass accrual, fate and functions of BM HSCs and MSCs, and survival. | PMC10187694 | AD-14-3-919-g8.jpg |
0.472399 | cc24277609dc4a68a02ce1a7afe78285 | TFEB promotes lysosomal biogenesis and autophagy. TFEB is activated upon dephosphorylation, and it is then translocated into the nucleus to enhance lysosomal biogenesis and autophagy via upregulation of multiple genes in the autophagy-lysosomal pathway, including ATG9, CTSD, CTSL, LAMP1, SQSTM1, MAPLC3B, UVRAG, etc. Autophagy cargos sequestered in autophagosomes are degraded upon the fusion of autophagosomes with lysosomes to form autolysosomes. | PMC10187700 | AD-14-3-652-g1.jpg |
0.437938 | de35495b9e324cffbb0d46e7bc2a5306 | Modification of TFEB by diverse kinases. The subcellular localization or activity of TFEB is regulated by phosphorylation, acetylation, or glucosylation. Phosphorylation of TFEB by mTORC1 at Ser122, Ser142 and Ser211, by ERK2 at Ser142, or by GSK3β at Ser134 and S138, promotes its accumulation in the cytoplasm in an inactive form. In addition, AKT- inhibited TFEB nuclear translocation is via phosphorylating Ser467. In contrast, dephosphorylation of TFEB by PP2A at Ser109 and Ser114, and dephosphorylation of TFEB by calcineurin at Ser142 and Ser211 induce the nuclear accumulation of TFEB. In addition, TFEB activities can be regulated via deacetylation and glucosylation. For example, SIRT1 deacetylates TFEB at Lys116, resulting in the upregulation of TFEB transcriptional activity. GCN5 acetylates TFEB at Lys274 and Lys279, leading to decreased TFEB transcriptional activity, while SAHA (suberoylanilide hydroxamic acid) promotes TFEB activity via acetylation of TFEB at Lys91, Lys103, and Lys430. Apart from acetylation, the glucosyltransferase activity of SetA is required for the impairment of TFEB nuclear export by glucosylation at its Ser138 site. | PMC10187700 | AD-14-3-652-g2.jpg |
0.494293 | f31f072701404d3c9107f7173fdee0a0 | TFEB-induced autophagy-lysosome pathway in AD. (A) Dysregulation of TFEB-mediated signaling in AD. Normally, TFEB is phosphorylated by mTOR and GSK3β, leading to its inactivation in the cytoplasm. In addition, GSK3β is important for promoting tau phosphorylation. In the nucleus of AD models, APOE4 is mutated, and it competitively binds to CLEAR motif to disrupt TFEB-mediated lysosomal biogenesis and autophagy. As a result, the clearance of p-tau and Aβ is disrupted due to compromised TFEB functions. (B) Activation of TFEB enhances p-tau and Aβ clearance via lysosomal biogenesis and autophagy. Activated TFEB by mTOR and GSK3β inhibitor or overexpression of TFEB promotes lysosomal biogenesis and autophagy. APOE3, rather than APOE4, does not competitively bind to CLEAR motif, leading to the normal running of TFEB-mediated autophagy. As a result, p-tau and Aβ are degraded by TFEB-mediated autophagy. | PMC10187700 | AD-14-3-652-g3.jpg |
0.504105 | 3fe9d44a3a6c4ef68b4900b2e28b64c9 | TFEB-mediated autophagy-lysosomal pathway in PD. (A) Dysfunction of TFEB-mediated lysosomal autophagy in PD. α-synuclein- sequestered TFEB in the cytoplasm. PARP1 induces the formation of PAR, leading to the formation of higher toxicity of α-synuclein. Activation of mTOR and GSK3β via phosphorylation at Y216 by elevated c-Abl in PD induces TFEB phosphorylation and thus impairs TFEB-mediated lysosome biogenesis and autophagy. These results lead to impairment of the clearance of α-synuclein via TFEB-mediated lysosomal autophagy. (B) Activation of TFEB-mediated lysosomal autophagy in PD. PARP1 inhibition induces Sirt1-mediated mTOR inactivation and subsequently TFEB dephosphorylation and activation, PARP1 inhibition also compromises TFEB nuclear export via disrupting the interaction of TFEB and CRM1. In addition, inhibition of GSK3β also promotes TFEB dephosphorylation and activation. These results lead to the induction of TFEB-mediated lysosomal autophagy, and thus accelerate α-synuclein degradation. | PMC10187700 | AD-14-3-652-g4.jpg |
0.443308 | e826deb739d140e68002d39416c0e8c1 | Known small molecules that promote TFEB nuclear translocation. TFEB can be activated through multiple pathways that are activated via different drugs. For example, melatonin, HEP14, SMK-17, STI-571, CHIR-99021, curcumin, GSK3 inhibitor III, and SB216763 induce TFEB nuclear translocation through the GSK3β-mediated pathway. Celastrol, chlorogenic acid, dynasore, fisetin, flubendazole, ibudilast, ouabain, rapamycin, temsirolimus, curcumin analog E4, PNU-282987, liraglutide, and metformin triggers TFEB nuclear translocation via mTOR signaling pathway. Exendin-4, ikarugamycin, SB202190, ML-SA5, trehalose, digoxin, sulforaphane, and alexidine induce calcium release and subsequently activate TFEB by calcineurin. In addition, aspirin induces TFEB nuclear translocation via PPARα activation. F-SLOH inhibits MAPK and activates PP2A, leading to TFEB dephosphorylation. Apart from those drugs, acacetin and curcumin C1 trigger TFEB translocation to the nucleus by mTORC1-independent pathway. | PMC10187700 | AD-14-3-652-g5.jpg |
0.419926 | 66a192b0ca3847c493a9229dd7ad48cb | The PHD-HIF oxygen-sensing system. In well oxygenated cells (schematic on the right side), PHDs hydroxylate HIFα on specific proline residues using O2 and 2-OG as co-substrates. The E3 ubiquitin ligase pVHL recognizes the hydroxylated HIFα and mediates HIFα ubiquitination and proteasomal degradation. In hypoxic cells (left side), the PHDs’ prolyl hydroxylase activity is inhibited, leading to HIFα accumulation. HIFα then dimerizes with HIF-1β and recruits CBP and p300 co-factors. The complex binds to hypoxia response element (HRE) within or near target genes to activate transcription of these genes. Abbreviations used: HIF, hypoxia-inducible factor; PHD, prolyl hydroxylase; Ub, ubiquitin; pVHL, the von Hippel-Lindau protein; 2-OG, 2-oxoglutarate. | PMC10187758 | fphar-14-1045997-g001.jpg |
0.433469 | 90781b02253d491bac05c383e2451cfe | Protective role of HIF in intestinal epithelial barrier. Activation of HIF-1 in the intestine epithelial cells induces a barrier-protective pathway by increasing the expression of barrier-protective proteins such as mucus, trefoil factor 3, CD39, CD73 and β-defensin-1 and TJ protein claudin-1. Activation of HIF-2 promotes the expression of CK and VEGF that promotes AJ and angiogenesis, respectively. Abbreviations: AJ, adhesion junction; CK, creatine kinase; TJ, tight junction; VEGF, vascular endothelial growth factor. | PMC10187758 | fphar-14-1045997-g002.jpg |
0.435405 | 9cf746ab4c1c417594c87919fb8b5b3c | Roles of HIF-1α in immune cells. HIF-1α promotes survivability and motility of macrophage, stimulates production of interferon, IL-22 and IL-10 by dentric cells, favors differentiation of Treg cells and decreases proliferation and increases death of B cells. | PMC10187758 | fphar-14-1045997-g003.jpg |
0.426328 | d0abc7e6405b4c26aeec7b5020b90ca8 | Screening flowchart of the participants. | PMC10189144 | fonc-13-1150539-g001.jpg |
0.489339 | 50812fb2465948c18750cb2f69e487b9 | The level of FR+CTC (A), CA19.9 (B), ProGRP (C), CYFRA21.1 (D), and TPS (E) in malignant and benign groups, respectively. | PMC10189144 | fonc-13-1150539-g002.jpg |
0.467615 | 90074f2f73bb465fa8cc3f97979903fa | Receiver operating characteristic (ROC) curve-single marker and prediction model. | PMC10189144 | fonc-13-1150539-g003.jpg |
0.395943 | d2ce698a2769495eb61b0e2512a71dd2 | Nomogram (A) and the result of Hosmer–Lemeshow test for the model (B). | PMC10189144 | fonc-13-1150539-g004.jpg |
0.505027 | 014cb03209cc484783fa25ecc3c92202 | Regional division of Anhui Province. | PMC10189381 | gr1.jpg |
0.450838 | 8b27ecab8c2045a0877fb827f1307f34 | Interannual variation of air pollutant concentrations in Anhui Province from 2015 to 2021. | PMC10189381 | gr2.jpg |
0.429907 | f2f6e0e816914bc988a97b46a9460a3e | Monthly variation of air pollutant concentrations in Anhui Province from 2015 to 2021. | PMC10189381 | gr3.jpg |
0.408684 | 5e568f2ef63e4eefa4bdf09c6701bdcf | Monthly calendar of major pollutants in each city from 2015 to 2021. | PMC10189381 | gr4.jpg |
0.417677 | 743ea12b51014ff89d9d5bd38e7f66b7 | Spatial distribution of the concentrations of the six pollutants from 2015 to 2021. | PMC10189381 | gr5.jpg |
0.414127 | 29a6b420b10644b3a2635c7ef8e1a2f8 | Schematic diagram of the experimental pipeline for all conditions. (A) AO-BCI condition, where participants controlled virtual finger flexions with P300-BCI. Each trial includes the presentation of visual stimuli, a period of anticipation, and the presentation of feedback in the form of a video sequence with finger movements. (B) Passive AO condition, where half of all trials included an anticipatory cross-presentation 1 s before movement onset to warn participants of the action. | PMC10192585 | fnhum-17-1180056-g001.jpg |
0.487177 | f722cb736119400884e9d028d1bc7f32 | (A) The averaged temporal dynamics of mu/beta ERD during action anticipation and observation in AAO (blue line) and AO (red line) conditions. Colored shapes with asterisks indicate significant differences. The vertical lines delimit the 2-second time intervals during which a finger movement was presented. On the right, the averaged spatial patterns corresponding to each EEG reaction are displayed. (B) Averaged evoked potentials related to action observation in two different conditions. The ERP evoked by anticipatory cross occurred before action presentation and is marked as “iCNV”. Above the topography distribution of its amplitude is shown. The first dashed line indicates the moment of anticipatory cross presentation, while the second indicates the moment of finger flexion onset. | PMC10192585 | fnhum-17-1180056-g002.jpg |
0.482469 | 58560a61a69c4b5f9ecb20f8f5cded16 | The averaged temporal dynamics of mu/beta ERD and beta ERS (bottom) during anticipation and observation of actions presented as BCI feedback. The blue line denotes observation of CORRECT actions, while the red line denotes observation of ERRONEOUS actions colored shapes with asterisks indicate significant differences. The vertical lines limit the 2 s time intervals during which the BCI feedback was presented. On the right, the averaged spatial patterns corresponding to each EEG reaction are shown. | PMC10192585 | fnhum-17-1180056-g003.jpg |
0.461381 | 009ef02550e543d4ba4733fb2cbfd033 | Example of the time-frequency dynamics of the ERD/S value obtained prior to CSP application for a participant. The data corresponds to channel “C3”. All conditions are shown: AO, passive action observation; AAO, passive action observation with action anticipation; AO-BCI, observation of actions presented as BCI feedback; AE, action execution. The spatial distribution of ERD/S for each condition is shown on the right. | PMC10192585 | fnhum-17-1180056-g004.jpg |
0.438248 | b41b597b91444458af9a6cdb7217b4e6 | (A) Significant differences from the cluster-based permutation test. On the left is the F-score map, with significant channels highlighted. The average ERPs waveform for the spatial cluster is shown on the right, with the time interval containing significant differences highlighted (p = 0.0002). The vertical line indicates the onset of the finger action. Panel (B) is a color map that depicts the temporal evolution of the amplitude of the difference ErrP (Error–Correct) at the midline and nearest electrodes. Specific ErrP components are denoted: Ne, error-related negativity; Pe, error-related positivity; Ip, interaction potential. Corresponding topographic maps are presented below. | PMC10192585 | fnhum-17-1180056-g005.jpg |
0.482447 | af4667007a3c4144b2503017a52ca40d | Identification of burn injuries associated with infant feeding items, hot water, and water heating consumer products for further review for relation to water heating during powdered infant formula preparation. | PMC10192855 | fped-11-1125112-g001.jpg |
0.436214 | a6f57cc9f72b4dda958b43156ed3b1b0 | Flowchart for Dataset 1 and 2, including input data and final data that was used as input for the method. | PMC10193118 | gr1.jpg |
0.434731 | d029df24a78c4be39b2f21c9bd1210d1 | Automatic segmentation of the olfactory bulbs in MRI scans using convolutional neural networks (CNNs). First, the center of each OB is localized. Subsequently, a region of interest (ROI) containing both olfactory bulbs is extracted and used as input for the segmentation of both olfactory bulbs to determine their volumes (figure derived from [Noothout et al., 2021], with permission). | PMC10193118 | gr2.jpg |
0.458067 | a07b5ff9a9854de6b34b76a82423d139 | Automatic segmentation of the left (orange) and right (blue) olfactory bulb in two MRI scans (rows). The first column shows a coronal slice of the image, cropped for visualization purposes. The middle column shows the automatic segmentation result, obtained with the method while the last column shows the reference segmentation (manual segmentation). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.) | PMC10193118 | gr3.jpg |
0.486172 | 394a729ab07e47a3914e418aa883effe | Automatic segmentation of the right (yellow) olfactory bulb. The left column shows the posterior coronal slice, where the cut-off needs to be made between the olfactory bulb and the olfactory nerve, cropped for visualization purposes. The middle column shows the automatic segmentation result, obtained with the method while the last column shows the reference segmentation (manual segmentation). | PMC10193118 | gr4.jpg |
0.435784 | 245540ec85074efbb3ef1e770b27de88 | Automatic segmentation of the left (orange) and right (blue) olfactory bulb in two MRI scans (rows). The first column shows an axial slice of the image, cropped for visualization purposes. The second and third column show the segmentation results, obtained with the segmentation CNN trained with only Dataset 1 and with additional training with Dataset 2, respectively, while the last column shows the reference segmentation. Dice coefficients improved from 0.64 to 0.75 (first row), and from 0.42 to 0.62 (second row) for the left olfactory bulb, while for the right olfactory bulb Dice coefficients improved from 0.74 to 0.83 (first row), and from 0.54 to 0.65 (second row). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.) | PMC10193118 | gr5.jpg |
0.494539 | 6f87a22597db4c4cb9544d205fa63ff8 | Bland-Altman plot, showing the average difference in measurements between both measurements. | PMC10193118 | gr6.jpg |
0.428551 | 6ff96f0fed204b398bc2ed0be321d04b | Schematic of CNT-ZIF-fMoS2 synthesis.
The hierarchical
composite is prepared by sequential solvothermal processes of the
porous ZIF and the flower-like MoS2 (fMoS2)
on percolated stem-like CNT networks. The core carbon networks can
deliver the charges to the system efficiently given the highly conductive
nature. The intermediate ZIF offers the ion diffusivity to the electrode
with the pore-rich conformation. The fMoS2 structures have
large surface areas for electric double layers, while the exposed
edges and sulfur vacancies facilitate faradaic reactions, thus drastically
improving the energy storage performance of the supercapacitor. | PMC10193431 | ao3c00445_0002.jpg |
0.487245 | 8a67a830dda64a9ea912718256de16c3 | SEM images of (a) CNT, (b) CNT-ZIF, and
(c) CNT-ZIF-fMoS2. We marked several points with white
arrows showing the components.
The pristine CNT film shows extremely thin tubular structures, while
the nanotubes have an average diameter of approximately 1 nm. The
ZIF-grown network shows significantly thicker tubes with a diameter
of roughly 30 nm. The flower-like structure shows many curvy MoS2 flakes. (d) Raman spectra of CNT, CNT-ZIF, and CNT-ZIF-fMoS2 and (e) spectra expanded at low wavenumbers along with the
Raman signatures of fMoS2. The spectra are plotted offset
for clarity. The samples containing CNT show G, D, RBM, and G′
Raman modes. The samples including the TMD flakes also show out-of-plane
(A1g) and in-plane (E2g1) vibration
signatures of few-layer-thick MoS2. XPS spectra of CNT-ZIF-fMoS2: (f) C 1s, (g) S 2s and Mo 3d, and (h) S 2p. The spectral
deconvolution indicates sub-binding energies of the elements. The
carbon peak shows comparable intensities of sp2 and sp3 electronic states, suggesting a successful synthesis of ZIF
crystal. The sample also exhibits clear Mo and S peaks originating
from MoS2. | PMC10193431 | ao3c00445_0003.jpg |
0.399296 | cb0edf97f1cb4416802fc82cd9216880 | Electrochemical
characterization of CNT-ZIF-fMoS2. The
measurements were carried out with cyclic voltammetry using a three-electrode
system in a 6 M KOH electrolyte solution. (a) Current–voltage
responses of the composite electrode under various scan rates of 0.5,
1, 2, 5, 10, and 20 mV/s. The area covered by the CV curve increases with the scan rate, which is a typical behavior
of a supercapacitor. (b) Specific capacitance of the electrode as
a function of scan rate, showing a maximum specific capacitance of
∼510 F/g at the lowest scan rate (0.5 mV/s). (c) GCD plots
of the ternary electrode operating under various current densities
ranging from 1.5 to 10 A/g. While discharging the device, the potential
drops slowly at a rate of −0.1 mV/s at approximately 0.05 V,
attributed to the FPC response. The device exhibits a fast discharging
behavior with a rate of −7 mV/s at ∼−0.4 V from
the EDLC process. | PMC10193431 | ao3c00445_0004.jpg |
0.394679 | 946c39c8d65c4e9bb48db259a34ab49e | Effect of electrode morphologies on the energy storage
performance.
SEM images of (a) CNT-ZIF-fMoS2, (b) CNT-ZIF-pMoS2, and (c) CNT-ZIF-eMoS2. Each composite exhibits a unique
morphology. CNT-ZIF-fMoS2 resembles an ivy plant, where
the flowers are made of MoS2, and they are weaved by the
CNT-ZIF stems. In contrast, the ternary composite bearing pMoS2 only shows stacked plates. Here, the carbon networks may
be buried under the TMD layer. Last, the electrode with the exfoliated
TMD demonstrates a MoS2 flake in the middle connected with
the carbon networks. (d) Cyclic voltammetry profiles of fMoS2, pMoS2, and eMoS2 integrated composite electrodes
at a scan rate of 5 mV/s in 6 M KOH solution. CNT-ZIF-fMoS2 generates the greatest electric current and the largest area closed
by the profile. (e) Relative contributions of EDLC and FPC mechanisms
at the scan rates of 0.5, 1, 2, and 5 mV/s. Overall, CNT-ZIF-fMoS2 (shown in blue/sky blue) demonstrates a greater contribution
of the FPC-driven energy storage than the other electrodes made of
pMoS2 (red/pink) and eMoS2 (black/gray). (f)
Plot of energy density vs power density showing the energy and power
densities at various scan rates in half-cell measurements. | PMC10193431 | ao3c00445_0005.jpg |
0.482659 | 36b9fbab500b452aabef009e78d07e9d | Research framework of policy for rare diseases in China. | PMC10196157 | fmed-10-1180550-g001.jpg |
0.401329 | cb05fdfc888140eab7080ebc2439d500 | Time distribution of China’s rare disease policies, 2009–2022. | PMC10196157 | fmed-10-1180550-g002.jpg |
0.446319 | 9778c7c4e5ea4309a6e434a2a6435164 | Network of rare disease policy-making departments in China. | PMC10196157 | fmed-10-1180550-g003.jpg |
0.418315 | 05a718e3957a45eba53f66dd5e845c0e | High-frequency word network of rare disease policies during 2009–2022 in China. | PMC10196157 | fmed-10-1180550-g004.jpg |
0.404035 | 234eef43b69744d0b3c9b6c9156e29b6 | Policy “Tools-Themes” two-dimensional distribution. | PMC10196157 | fmed-10-1180550-g005.jpg |
0.493433 | 65f6591050a941d796cec9e0738a262d | MR coronary angiography in a 7-month-old boy. (A) Noncontrast-enhanced MR coronary angiography only detects the origin of the RCA. (B) Contrast-enhanced MR coronary angiography images reveal all the coronary arteries. The image quality improves significantly. RCA, right coronary artery; AO, aorta; LMT, left main trunk; LAD, left anterior descending coronary artery; LCX, left circumflex coronary artery. | PMC10196256 | fped-11-1159347-g001.jpg |
0.45812 | 6b045fb1e77444f8b985cfdf86c659ab | MR coronary angiography in a 3-year-old boy. (A) Precontrast imaging. (B) Postcontrast imaging. Compared with noncontrast-enhanced MR coronary angiography, the three dimension reconstruction image of MR coronary angiography after applying gadolinium-DTPA reveals more coronary artery side branches (arrowhead). Maximal intensity projection images show that the signal-to-noise ratio and contrast-to-noise ratio of all the coronary arteries increase after the application of gadolinium-DTPA, but the image quality is not improved significantly. AO, aorta; LMT, left main trunk; LAD, left anterior descending coronary artery; LCX, left circumflex coronary artery; RCA, right coronary artery. | PMC10196256 | fped-11-1159347-g002.jpg |
0.487071 | 5c77ec4d9e694a569407decae6c6da14 | MR coronary angiography in a 13-year-old boy. (A) Precontrast imaging. (B) Postcontrast imaging. Despite an increase in the signal-to-noise ratio and contrast-to-noise ratio in the coronary arteries after the application of gadolinium-DTPA, contrast-enhanced MR coronary angiography neither improves the image quality significantly nor shows more side branches. AO, aorta; LMT, left main trunk; LAD, left anterior descending coronary artery; LCX, left circumflex coronary artery; RCA, right coronary artery. | PMC10196256 | fped-11-1159347-g003.jpg |
0.448694 | 4f03206a6b3b405bbec5efb861622d2e | EBICglasso model based on the domain-level (A) and the item-level (B) network analysis according to the relationships between GD, rumination and sleep quality among 1,872 participants. gd1~gd4, Gaming disorder; RE, r1~r10 = Rumination; PQSI, Sleep quality; SSQ, Subjective sleep quality; SL, Sleep latency; SD, Sleep duration; HSE, Habitual sleep efficiency; SDD, Sleep disturbance; USM, Used sleep medication; DD, Daytime dysfunction. | PMC10196354 | fpsyt-14-1108016-g001.jpg |
0.415714 | 5b11afdf1e7c45e49a9b143ae67b2f44 | Bootstrapped confidence intervals of estimated edge-weights (A) and Case-dropping bootstrap procedure for node strength (B). | PMC10196354 | fpsyt-14-1108016-g002.jpg |
0.445283 | 8e4e9e69b3b44d799e60ffe27cc57bca | The item-level Network structure according to the relationships between GD, rumination and sleep quality among 1,872 participants. gd1~gd4, Gaming disorder; r1~r10 = Rumination; SSQ, Subjective sleep quality; SL, Sleep latency; SD, Sleep duration; HSE, Habitual sleep efficiency; SDD, Sleep disturbance; USM, Used sleep medication; DD, Daytime dysfunction. Nodes identified as bridge symptoms are colored in blue. | PMC10196354 | fpsyt-14-1108016-g003.jpg |
0.621426 | 92e03c8ec77341898fdf61ff7037ca6d | HPLC identified compounds in C. sativa infusion. | PMC10196869 | gr1.jpg |
0.448477 | 4f5a30cd0fac4b3c977ea0ed8c12da0b | Molecular interactions of (A) cannabidiol with CDK6; and (B) rutin with CDK2. | PMC10196869 | gr10.jpg |
0.470101 | afbb859aeced4d899cdf03793fc4ba41 | Schematic pathway of relevant identified pathways and metabolites in the studied MCF-7 cells. THF: tetrahydrofolate; TAG: triacylglycerol; DAG: diacylglycerol; CDP-DAG: CDP- diacylglycerol; PE: phosphatidylethanolamine; PG: prostaglandin; PS: phosphatidylserine; PA: phosphatidic acid; PUFAs: polyunsaturated fatty acids; MUFAs: monounsaturated fatty acids; APS: adenosine phosphosulfate; and PAPS: phosphoadenosine phosphosulfate. | PMC10196869 | gr11.jpg |
0.374417 | efe8f53ca47f47aeb621932cf4c8f6b0 | Cytotoxic effect of C. sativa on MCF-7 cancer cells. Values = mean ± SD; n = 3. *Statistically significant to control. | PMC10196869 | gr2.jpg |
0.422677 | 641f620ad96c460a8b0ea61f7cde012b | Effect of C. sativa on glucose metabolism in MCF-7 cells. (A) Glucose metabolic pathway enrichment; (B) Heat map of LC-MS identified metabolites involved in glucose metabolism in MCF-7 cells; (C) LC-MS identified metabolites involved in glucose metabolism in MCF-7 cells; and (D) PC scores of LC-MS identified metabolites. Values = mean ± SD; n = 3. *Statistically significant to each other. CON = control; CINF = C. sativa; and Dox = doxorubicin. | PMC10196869 | gr3.jpg |
0.456553 | a5a61666ee494e1d8462abeaf96331ba | Effect of C. sativa on lipid metabolism in MCF-7 cells. (A) Lipid metabolic pathway enrichment; (B) Heat map of LC-MS identified metabolites involved in lipid metabolism in MCF-7; (C) LC-MS identified metabolites involved in lipid metabolism in MCF-7 cells; and (D) PC scores of LC-MS identified metabolites. Values = mean ± SD; n = 3. *Statistically significant to each other. CON = control; CINF = C. sativa; and Dox = doxorubicin. | PMC10196869 | gr4.jpg |
0.480121 | 1a88ff298b574a9c9f73299f4038b33f | Effect of C. sativa on amino acids metabolism in MCF-7 cells. (A) Amino acids metabolic pathway enrichment; (B) Heat map of LC-MS identified metabolites involved in amino acids metabolism in MCF-7; (C) LC-MS identified metabolites involved in amino acids metabolism in MCF-7 cells; and (D) PC scores of LC-MS identified metabolites. Values = mean ± SD; n = 3. *Statistically significant to each other. CON = control; CINF = C. sativa; and Dox = doxorubicin. | PMC10196869 | gr5.jpg |
0.409933 | db644993a6564190a213a94e56819a06 | Effect of C. sativa on vitamins metabolism in MCF-7 cells. (A) Vitamins metabolic pathway enrichment; (B) Heat map of LC-MS identified metabolites involved in vitamins metabolism in MCF-7; (C) LC-MS identified metabolites involved in vitamins metabolism in MCF-7 cells; and (D) PC scores of LC-MS identified metabolites. Values = mean ± SD; n = 3. *Statistically significant to each other. CON = control; CINF = C. sativa; and Dox = doxorubicin. | PMC10196869 | gr6.jpg |
0.431539 | 7084a1ba7148440d9d6b46db6ccb5ff5 | Effect of C. sativa on nucleotide metabolism in MCF-7 cells. (A) nucleotide metabolic pathways enrichment; (B) Heat map of LC-MS identified metabolites involved in nucleotide metabolism in MCF-7; (C) LC-MS identified metabolites involved in nucleotide metabolism in MCF-7 cells; and (D) PC scores of LC-MS identified metabolites. Values = mean ± SD; n = 3. *Statistically significant to each other. CON = control; CINF = C. sativa; and Dox = doxorubicin. | PMC10196869 | gr7.jpg |
0.424819 | 9b4f9fe17c9940a7989df9c8e19b619d | Effect of C. sativa on porphyrin and oxidative metabolisms in MCF-7 cells. (A) porphyrin and oxidative metabolic pathways enrichment; (B) Heat map of LC-MS identified metabolites involved in porphyrin and oxidative metabolisms in MCF-7; (C) LC-MS identified metabolites involved in porphyrin and oxidative metabolisms in MCF-7 cells; and (D) PC scores of LC-MS identified metabolites. Values = mean ± SD; n = 3. *Statistically significant to each other. CON = control; CINF = C. sativa; and Dox = doxorubicin. | PMC10196869 | gr8.jpg |
0.484493 | ee3486b703264e3cb9092172cdba4bd4 | Effect of C. sativa on apoptosis of MCF-7 cells. Values = mean ± SD; n = 3. **significantly different (p < 0.001) to control. | PMC10196869 | gr9.jpg |
0.453484 | 553e51731c4f4f3585de50b9540c8065 | Magnetic resonance imaging showing superficial ductal enhancement in the medial left breast (circle). | PMC10196917 | gr1.jpg |
0.457512 | 419abdcd468e47219e846d75e123228c | (A) Immediate post biopsy magnetic resonance imaging showing the clip's susceptibility artefact (white arrow) in a superficial location and the presence of blood at the biopsy site (blue arrow). (B) Craniocaudal mammogram demonstrating the clip's position away from the skin. | PMC10196917 | gr2.jpg |
0.462089 | 0085dea15da44fb38b38d66a1d07758d | Migrated clip at skin, with a thread from the patient's clothing caught at the clip. | PMC10196917 | gr3.jpg |
0.411921 | 62244005a22d4a019ffa9fd1a6b993e9 | Craniocaudal (A) and mediolateral oblique (B) mammogram and ultrasound of the left breast (C) 6 months after MRI biopsy confirming the delayed migration of clip to skin (arrow). | PMC10196917 | gr4.jpg |
0.422304 | 7f51d4c862f64ba1b8e90f27f737f05e | TCF3 germline variants in patients with pediatric B-ALL identified by targeted sequencing. (A) CONSORT diagram of COG and St. Jude patients included in this study. (B) Protein domain plot of TCF3 E12 isoform (NM_003200): Activation Domain (AD) 1 to 3 and b-HLH domain. The upper panel shows rare deleterious TCF3 E12 germline variants in patients with B-ALL, and the lower panel shows TCF3 E12 variants in the gnomAD control participants. Each dot represents 1 case. | PMC10196986 | BLOODA_ADV-2022-008563-gr1.jpg |
0.412534 | 9e916c47d3c646a6914a50a171c30694 | Functional characterization of TCF3 variants and their association with clinical features of pediatric B-ALL. (A) Relative μE5/μE2 promoter activity in luciferase reporter assay using HEK293T cells ectopically expressing TCF3–E12 WT or TCF3-E12 variants. TCF3-E47 p.E555K was included as a positive control. The results are represented as the average ± standard deviation of 6 independent experiments. (B) Characteristics of 10 patients with TCF3 germline variant compared with 3799 patients with B-ALL treated in COG P9904/5/6 and COG AALL0332 clinical trials. WBC, white blood count. | PMC10196986 | BLOODA_ADV-2022-008563-gr2.jpg |
0.52824 | 3a7eb373d6ad44e9ac32d6cf2d95a5ef | Flow diagram of participant selection. ASCVD, atherosclerotic CVD. | PMC10197088 | S0007114522002896_fig1.jpg |
0.546813 | 70472b9885cb4915a1e20c011bf684bf | Frequency of distribution of weekly fish consumption. | PMC10197088 | S0007114522002896_fig2.jpg |
0.482846 | 3de24f56100b415ca4258e7a9cd8175c | Relationship between fish consumption and aerobic exercise habits. | PMC10197088 | S0007114522002896_fig3.jpg |
0.419672 | 207d77ccaeb44a53b91484b03f128653 | Relationship between fish consumption and cigarette smoking habits. | PMC10197088 | S0007114522002896_fig4.jpg |
0.498109 | 53309e89294c4f8094ea8f5f74e02f7a | Relationship between fish consumption and sleep duration. Mean values of sleep duration were 5·86 ± 1·11 h, 5·96 ± 0·96 h, 6·05 ± 0·95 h, 6·07 ± 0·95 h, 6·15 ± 0·94 h, 6·19 ± 0·94 h and 6·09 ± 1·12 h in groups with 1, 2, 3, 4, 5, 6 or 7 instances of fish consumption per week, respectively. | PMC10197088 | S0007114522002896_fig5.jpg |
0.465373 | 5f1ea8c3008448eca476722df568755d | Relationship between fish consumption and leucocytes count. Median (IQR) leucocytes counts were 5100 (4300/6075) cells/μl, 4800 (4100/5800) cells/μl, 4700 (4000/5600) cells/μl, 4700 (3900/5700) cells/μl, 4600 (3825/5400) cells/μl, 4500 (3900/5500) cells/μl and 4400 (3700/5500) cells/μl in groups with 1, 2, 3, 4, 5, 6 or 7 instances of fish consumption per week, respectively. | PMC10197088 | S0007114522002896_fig6.jpg |
0.437305 | 87d0b18fdb204c11965513b4560bb455 | Relationship between sleep duration and leucocytes count. Median (IQR) leucocytes counts according to sleep duration category: 4800 (4200/5875) cells/μl, 4800 (4100/5700) cells/μl, 4700 (4000/5600) cells/μl, 4700 (4000/5600) cells/μl and 4800 (4000/5700) cells/μl. The leucocytes counts may be higher in both short and long sleep durations than adequate sleep duration. IQR, interquartile range. | PMC10197088 | S0007114522002896_fig7.jpg |
0.430029 | cde6f746cf964bd8933474947e1595d2 | Sequence analysis of the IM3796 and IM1634.A, module composition of IM3796, IM1634, CSase ABC I from Proteus vulgaris (GenBank accession number: P59807.2) (40), CSase ABC I from Bacteroides thetaiotaomicron (GenBank accession number: ABV21364.1) (54). The GAG lyase module is a hypothetical catalytic domain (Lys84-Pro766 in IM3796, Arg249-Pro875 in IM1634, Ala256-Pro960 in P59807.2 and Glu 238-Pro931 in ABV21364.1), and the module Lyase_8 (Arg445-Leu688 in IM3796, Arg554-Leu797 in IM1634 and Val607-Asp855 in ABV21364.1) is relatively conserved in PL8 family. The numbers in the graph represent the number of amino acids. B, multiple sequence alignment of IM3796, IM1634, and two identified CSase ABC Is from Proteus vulgaris (GenBank accession number: P59807.2) and Bacteroides thetaiotaomicron (GenBank accession number: ABV21364.1). | PMC10197112 | gr1.jpg |
0.430239 | 35176eb9963c4b1baf1b111069e6d6e9 | The substrate specificity of IM1634-T109 and IM3796-A109 toward HA and CS/DS. Ten micrograms of CS-A (A and F), CS-C (B and G), CS-E (C and H), HA (D and I), or DS (E and J) was digested by 5 μl IM1634-T109 (10 μM) (A–E) or IM3796-A109 (9 μM) (F–J) with the addition 2 μl corresponding fresh enzyme every 24 h up to 48 h. The final products were detected by gel filtration chromatography as described under “Experimental procedures.” The elution positions of the following standard oligosaccharides are indicated by arrows: 1, unsaturated dodecasaccharides; 2, unsaturated decasaccharides; 3, unsaturated octasaccharides; 4, unsaturated hexasaccharides; 5, unsaturated tetrasaccharides; 6, unsaturated disulfated disaccharides; 7, unsaturated monosulfated disaccharides; 8, unsaturated nonsulfated disaccharides. | PMC10197112 | gr10.jpg |
0.43721 | 205c0f3a4fd8438ebbd3c18215ebf8cb | Phylogenetic analysis of IM3796 and IM1634. Phylogenetic analysis of IM3796 and IM1634 was executed based on Clustal W multiple alignments with identified CSases from bacteria by using the neighbor-joining method in MEGA version 7.0.26. The numbers on the branches are the bootstrap confidence values obtained from 1000 replications. | PMC10197112 | gr2.jpg |
0.512468 | 4cf794e597834d66b5a3dc0b2ef2b1e1 | Purification of recombinant IM3796 and IM1634 by Ni2+affinity chromatography. The expression and purification of recombinant IM3796 (A) and IM1634 (B) were assessed by SDS-PAGE using 13.2% polyacrylamide gels. Lane 1, prestained protein molecular weight marker PageRuler (26616, Thermo Fisher Scientific); lane 2, lysate of cells transfected with empty plasmid (pET30a); lane 3, lysate of cells transfected with expression plasmid; lane 4, supernatant from the lysate of cells transfected with expression plasmid; and lane 5, purified recombinant IM3796 or IM1634. Molecular weight markers and their corresponding masses are also indicated. | PMC10197112 | gr3.jpg |
0.429739 | 5698ede0f5a148438f028b9a1922c001 | Biochemical characteristics of recombinant IM3796 and IM1634.A and E, effects of temperature. The enzymatic activities of IM3796 (A) and IM1634 (E) were detected using CS-C as substrates in the 50 mM NaH2PO4-Na2HPO4 buffer (pH 7.0) at various temperatures (0–70 °C). The data are shown as a percentage of the activity obtained at their corresponding optimal temperatures (100%). B and F, effects of pH. The activities of IM3796 and IM1634 toward CS-C were evaluated in buffers with pH values ranging from 5 to 10 at their optimal temperatures. Data are shown as the percentage of the activity obtained in the corresponding optimal pH. C and G, effects of chemicals. The impacts of different chemicals (5 mM) towards IM3796 and IM1634 against CS-C were assessed in their respective optimal conditions. Data are shown as the percentage of the activity that acquired in the buffer without these tested chemicals. D and H, Thermostability of IM3796 and IM1634. The enzymes were incubated at different temperatures (0–70 °C) for different time interval (0–24 h), and the residual activity against CS-C was measured in the optimal conditions of each enzyme. Data are displayed as the activities relative to that of an untreated enzyme. The error bars mean of triplicate ± SD values. | PMC10197112 | gr4.jpg |
0.45172 | c551d91c8d3143309b5190b04835a2c1 | Time-course experiments of digestion of CS-C by IM3796 and IM1634. One hundred microliter of CS-C (1 mg/ml) or CS-A (1 mg/ml) was depolymerized by 100 μl IM3796 (10 μM) (A) and 20 μl IM1634 (9 μM) (B), and a 30 μl aliquot was taken out at different time interval and analyzed by gel filtration chromatography as described under “Experimental procedures”. The elution positions of the following CS standard oligosaccharides are indicated by arrows: 1, unsaturated CS decasaccharides; 2, unsaturated CS octasaccharides; 3, unsaturated CS hexasaccharides; 4 unsaturated CS tetrasaccharides; 5, unsaturated CS disulfated disaccharides; 6, unsaturated CS monosulfated disaccharides. The peaks marked with a pentagram are salt. | PMC10197112 | gr5.jpg |
0.445562 | d6e35fffc0ac409fb302292eb18ec38d | Time-of-flight(TOF)mass spectra analysis of the monosulfated disaccharide products of IM3796and IM1634towardCS-C. The monosulfated disaccharides from the digestion of CS-C by IM3796 (A) and IM1634 (B) were individually analyzed by ESI-MS on an IT-TOF hybrid mass spectrometer in negative ion mode. | PMC10197112 | gr6.jpg |
0.403545 | fba9063ab6f14f4da9d47f2ca86ea117 | The substrate specificity of IM3796 and IM1634 toward HA and CS/DS. Ten micrograms of CS-A (A and F), CS-C (B and G), CS-E (C and H), HA (D and I), or DS (E and J) was digested by 10 μl IM3796 (10 μM) with the addition 2 μl fresh enzyme every 24 h up to 72 h (A–E), or by 2 μl IM1634 (9 μM) for 12 h (F–J). The products were detected by gel filtration chromatography as described under “Experimental procedures.” The elution positions of the following standard oligosaccharides are indicated by arrows: 1, unsaturated dodecasaccharides; 2, unsaturated decasaccharides; 3, unsaturated octasaccharides; 4, unsaturated hexasaccharides; 5, unsaturated tetrasaccharides; 6, unsaturated disulfated disaccharides; 7, unsaturated monosulfated disaccharides; 8, unsaturated nonsulfated disaccharides. | PMC10197112 | gr7.jpg |
0.387851 | 4002189f701e452d89dbeee1f401ebcf | Sequencing of tetrasaccharide products of IM3796 toward CS-C.Top panel, Isolated tetrasaccharide subfraction labeled with 2-AB; middle panel, the disaccharide composition of each tetrasaccharide subfraction; Bottom panel, the reducing-end disaccharide of each tetrasaccharide subfraction. All of the samples were analyzed on a YMC-Pack PA-G column using a linear gradient from 16 to 460 mM NaH2PO4 solution (shown by the dotted line) during a 60 min period and monitored by a fluorescence detector at excitation and emission wavelengths of 330 and 420 nm, respectively. The authentic 2-AB-derivatized unsaturated CS disaccharides were used as standards. A, ΔC-C; B, ΔC-A; C, ΔD-A; D, ΔD-C. | PMC10197112 | gr8.jpg |
0.408803 | a47d109c645f4338985ccd7e7edbf145 | The tertiary structure modeling of IM3796, IM1634, and their variants.A, the crystal structure of CSase ABC I from Proteus vulgaris. B–E, the tertiary structure modeling of IM3796, IM1634, IM1634-T109, and IM3796-A109 were carried out using SWISS-MODEL software online. | PMC10197112 | gr9.jpg |
0.455914 | 5c07e577d7a24f93961b505095b0f909 | (a) Chemical
structures of SO42–, SCN–, ClO4–, and BPh4– anions.
(b) Im χ(2) spectra of the neat D2O as
well as the D2O solution of 3.0 M NaSCN, 1.5 M NaClO4, 1.5 M NaI, 3.0 M NaCl, 0.5 M Na2SO4, and 20 mM NaBPh4 at the solution–vapor interfaces.
For clarity, the Im χ(2) spectrum for NaBPh4 was scaled by a factor of 0.2. | PMC10197129 | ja3c00517_0002.jpg |
0.380229 | caada0a66bd84adaa4502bb16f2c0fdd | (a–e)
Im χ(2) spectra at the D2O–vapor
interfaces with various salt mixtures: (a) 1.5 M NaCl
(), 1.5 M NaClO4 (), and 0.75 M NaClO4 + 0.75 M
NaCl ; (b) 1.5 M NaCl (), 1.5 M NaI (), and 0.75 M NaI + 0.75 M NaCl (); (c) 3.0 M NaCl (), 3.0 M NaSCN (), and 1.5 M NaSCN + 1.5 M NaCl (); (d) 1.0 M NaCl (), 0.5 M Na2SO4 (), and 0.25 M Na2SO4 + 0.5 M NaCl (); (e) 20 mM NaCl (), 20 mM NaBPh4 (), and 10 mM NaBPh4 + 10 mM NaCl
(). The black dotted lines represent the
fits based on eq 1. The
inset schematics depict the putative picture of interfacial ions’
distribution. | PMC10197129 | ja3c00517_0003.jpg |
0.435643 | c71c06ee071e45878ffbeb6e3d5458c8 | (a,b) HD-SFG measurement of NaBPh4 and DCl with NaCl
at the D2O–vapor interfaces: (a) 5 mM NaBPh4 + 5 mM NaCl () and 5 and 10 mM NaBPh4 ( and , respectively). (b) 1.0 M NaCl (), 1.0 M DCl (), and 0.5 M DCl + 0.5 M NaCl . The black dotted lines represent the fits
based on eq 1. | PMC10197129 | ja3c00517_0004.jpg |
0.440896 | cdecf8ded2fc47a889f0a865e9280c75 | TR-SFG time
trace signals of DCl with NaCl at the D2O–vapor
interfaces. The samples are 1.0 M NaCl, 1.0 M DCl,
and 0.5 M DCl + 0.5 M NaCl solutions. The 1.0 M NaCl sample shows
strong GHz oscillations, reduced in the presence of excess hydrated
protons. | PMC10197129 | ja3c00517_0005.jpg |
0.400864 | a345df12d0824a8f968cfc3e02211910 | (a,b)
Depth profiles of the X– concentration
(bulk concentrations: ∼2.4 M for pure NaX and ∼1.2 M
each for co-solvated NaX/NaY solutions). z = 0 represents
the position of the GDS of water. The LJ radii of X– are (a) 1. and (b) 1.05 . The boundary of the interfacial region
and bulk is defined as 5 Å below GDS. (c) Surface enrichment
of anion as a function of the solvation energy difference of X– and Y–. The surface enrichment is
defined as the relative peak concentration in the range −2.4
Å < z < 4.4 Å region for X– in mixture solutions with respect to those for pure X– in the blue dotted lines. The peak positions and concentrations
were determined based on quadratic fits. . With increasing , the surface enhancement becomes more prominent.
Note that the error bars in panels (a–c) are negligibly small
(see the Supporting Information). (d) Schematic
of the speciation of ions with the variation of LJ radii of ions. | PMC10197129 | ja3c00517_0006.jpg |
0.427137 | 9e22738586d043adbe75b2227e2fe74a | COMPACT strategy for hydrogel materials miniaturization.a, Schematic illustrations of hydrogel network of metamorphic polymers’ amorphous-crystal transition (COMPACT). COMPACT treatment includes cross-linking with both glutaraldehyde (GA) and tetraethyl orthosilicate (TEOS), acidification and mechanical stretching. b-e, Representative photographs and water contents of TEOS-GA cross-linked polyvinyl alcohol (PVA) hydrogel with COMPACT treatment (+) and GA cross-linked hydrogel without acidification and stretching (−) at the pristine state (b), desiccated state (c) and re-hydrated state (d). Grid size: 5 mm. f, Shrinking behaviors of TEOS-GA cross-linked PVA (4 wt.% TEOS) hydrogel film with acidification treatment. Film thickness is quantified as mean ± standard deviation (s.d., paired student’s t-test, ***p=0.0004). Each dot represents one individual film. g, Shrinking behaviors of COMPACT hydrogel fibers (1-4 wt.% TEOS and 200% stretching). Hydrogel fibers’ length (black) and diameter (red) are quantified as mean ± s.d. Each dot represents one independent fiber. h, Shrinking behaviors of cross-linked hydrogel cylinders. The volume of TEOS-GA cross-linked hydrogel cylinders (4 wt.% TEOS) and with acidification treatment and GA cross-linked hydrogel cylinders without acidification treatment are compared with mean ± s.d. (unpaired student's t-test, F3,3=6.084, *p=0.0161). Each dot represents one independent hydrogel cylinder. i, Fourier transform infrared (FTIR) spectroscopy of COMPACT (−) and COMPACT (+) hydrogels. j, Differential scanning calorimetry (DSC) profiles of COMPACT (−) and COMPACT (+) and their crystallinity percentages. k, Small-angle X-ray (SAXS) and wide-angle X-ray (WAXS) results of hydrogel materials in the desiccated state (mean ± s.d.). Inset: SAXS and WAXS 2D patterns. | PMC10197780 | nihpp-rs2864872v1-f0001.jpg |
0.491567 | fb81c68ee84f47f88ad913e2dc26737f | Controllable hydrogel fiber fabrication and its properties.a, A shrinking diagram of COMPACT (+) hydrogel fibers. Each dot (mean ± s.d.) represents an independent hydrogel fiber sample. The samples shaded in red areas are treated with acidification. b, Shrinking behaviors of COMPACT hydrogel fibers (4wt.% TEOS) prepared in different sizes of molds. Each dot (mean ± s.d.) represents one independent fiber (one(One-way ANOVA and Tukey's multiple comparisons test, F3,12=0.9543, n.s.: not significant. p=0.4455). c, COMPACT hydrogel fibers’ optical properties of refractive index (blue) and normalized light transmittance (red) (mean ± s.d). Inset: representative photographs of 0 wt.% TEOS and 4 wt.% TEOS hydrogel membranes. Grid size: 1 mm. d, COMPACT hydrogel fibers’ mechanical properties of elastic modulus (blue) and stretchability percentage (red). Each dot represents one independent fiber sample. One-way ANOVA and Tukey's multiple comparisons test were used to determine the statistical significance of elastic modulus: (F4,15=20.51, ****p<0.0001;) and stretchability: (F4,15=1.492, n.s. p=0.2543), respectively. e, Stability assessment of diameter reduction of COMPACT hydrogel fibers (3wt.% TEOS). Each dot (mean ± s.d.) represents one independent fiber (two-way ANOVA and Tukey's multiple comparisons tests). f, Cytotoxicity assessment of COMPACT (+) hydrogels. Hydrogel incubated media was used to culture with HEK293 cell cultures. Calcein-AM (green) was used to stain living cells and ethidium homodimer-1 (red) was used to stain dead cells. Cell death rates are presented as mean ± standard error (s.e.m., unpaired student’s t-test). | PMC10197780 | nihpp-rs2864872v1-f0002.jpg |
0.414687 | 33d3d005ddb449d3b3d1e2b9d9c4fd3a | Hydrogel optical neural probes for photometric recording with behavioral assessment.a, A schematic illustration of light transmission in a step-index hydrogel fiber. b, Schematic illustrations and representative photographs of a COMPACT core hydrogel fiber, a COMPACT core-plain-cladding hydrogel fiber, and a COMPACT core-rGO-cladding fiber. Scale: 200 μm. c, Representative photographs of blue light (480 nm) transmission from a COMPACT (−) core hydrogel fiber and a COMPACT (+) core hydrogel fiber into solutions containing Calcein fluorescent dye. d, Light attenuation coefficients of COMPACT core hydrogel fibers, COMPACT core-plain-cladding hydrogel fibers, and COMPACT core-rGO-cladding fibers (mean ± s.d., one-way ANOVA and Tukey's multiple comparisons test, F2,9=13.3, **p=0.0021). Each dot presents one independent hydrogel fiber sample. e, Experimental scheme for the viral injection, optical fiber implantation, photometric recording and social behavior tests. f, Representative images in mouse social interaction tests. g, A schematic illustration of fiber photometry recording setup with concurrent mouse social behavior tests. h, Normalized fluorescence intensity change (ΔF/F0) of GCaMP6s in the VTA from mice social interactions. Blue bars indicate social interaction time. | PMC10197780 | nihpp-rs2864872v1-f0003.jpg |
0.468629 | bfb929dc859444a48877679ad8047476 | Integrated multifunctional hydrogel neural probes.a, A Representative photograph of a carbon nanotube (CNT)-PVA hydrogel electrode as compared with a piece of human hair. Scale: 300 μm. b, A transmission electron microscopy (TEM) image of CNTs. Scale: 200 nm. c, Impedance at 1 kHz (red dots) and diameters of the electrodes (blue dots) fabricated different stretching percentages (mean ± s.d.). Each dot represents one independent hydrogel electrode. d, Impedance at 1 kHz of electrodes fabricated with different CNT concentrations (mean ± s.d.). Each dot represents one independent hydrogel electrode. e, Impedance at 1 kHz of electrodes (red dots) and diameters of the electrode (blue dots) fabricated with different sizes of molds (mean ± s.d.). Each dot represents one independent hydrogel electrode. f, Stability assessment on impedance (red dots) and diameters (blue dots) of hydrogel electrodes (mean ± s.d.). Each dot represents one independent hydrogel electrode. g, A schematic illustration of electrical recordings from mouse gastrocnemius muscles with a CNTs-PVA electrode in the presence of transdermal optical stimulation. h, Representative EMG signals recorded with CNT-PVA hydrogel electrodes upon transdermal optogenetic stimulations in Thy1::ChR2-EYFP mice (λ=473 nm, 0.5 Hz, pulse width 50 ms, 200 mW/mm2). Blue bars indicate the light illumination periods. i, Overlay plot of EMG peaks. j, A scanning electron microscopy (SEM) image at the cross-section of an integrated multifunctional neural probe containing an optical core and two CNT-PVA hydrogel electrodes. Scale: 100 μm. k-l, Photographs of a hydrogel optoelectronic device (optrode) before implantation and after implantation in a Thy1::ChR2-EYFP mouse brain. Scale: 2 mm. m, Confocal images of the expression of ChR2-EYFP in the VTA region of mouse. Scale: 50 μm. n, Representative in vivo electrophysiological signals recorded with optrodes upon optical stimulation (blue bars, λ=473 nm, 0.5 Hz, pulse width 50 ms, 10 mW/mm2). l, Amplitudes of electrophysiological signals recorded with optical stimulation on day 3, day 5, day 7, and day 14 post-implantation (λ=473 nm, 0.5 Hz, pulse width 50 ms, 10 mW/mm2, mean ± s.e.m.). | PMC10197780 | nihpp-rs2864872v1-f0004.jpg |
0.378998 | f59f467f2914414599cc09d511fd7628 | The relative expression of miR-183 and PTEN in MCF-7, MDA-MB-231, and MCF-10A cells was measured with qRT-PCR (A) Relative expression of miR-183; **p = 0.0024, ***p = 0.0009 (B) Relative expression of PTEN; ***p = 0.0008, ***p = 0.0004. Data are presented as the mean ± SD. *P < 0.05; **P < 0.01; ***P < 0.001. | PMC10199038 | 41598_2023_35059_Fig1_HTML.jpg |
0.458517 | 597dfef86f44486fae62ae8ea899413c | MiR-183 targets PTEN expression. (A) PTEN is a direct target of miR-183 demonstrated by 3UTR luciferase assay; *p = 0.0451; Wnt-7b gene 3′UTR sequence was used as off target in this experiment. (B) The transfection efficiency of miR-183 was measured by qRT-PCR 48 h after transfection **p = 0.0032, **p = 0.0012 (C) The mRNA of PTEN was measured by Real-time PCR in MCF-7 and MDA-MB-231 transfected with miR-183; *p = 0.0167, *p = 0.0200 (D) The protein expression of PTEN was measured by Western blot assay in MCF-7 and MDA-MB-231 transfected with miR-183; *p = 0.0273, *p = 0.0420. A full-length image is included in a Supplementary Information file. NC negative control. *p < 0.05; **p < 0.01; ***p < 0.001. | PMC10199038 | 41598_2023_35059_Fig2_HTML.jpg |
0.421438 | c4b46abee7774cd79c995fea7bbe58af | Overexpression of miR-183 leads to considerable enhancements in cell migration. (A) Wound healing assay; **p = 0.0084, **p = 0.0038 (B) Trans-well assay; **p = 0.0054, **p = 0.0049. *p < 0.05; **p < 0.01; ***p < 0.001. NC negative control. | PMC10199038 | 41598_2023_35059_Fig3_HTML.jpg |
0.475284 | 88dab02b6f2a496d8315e5c3be628a52 | The effect of miR-183 on cell cycle progression and cell viability in breast cancer cells. (A) Cell cycle profiles were analyzed using flowcytometry after MCF-7 and MDA-MB-231 cells transfection with miR-183; (G0/G1: **p = 0.0019, **p = 0.0026; S: **p = 0.0012, **p = 0.0074; G2/M: **p = 0.0068, **p = 0.0093). (B) Cell growth viability was measured by MTT assay 48 h after transfection; *p = 0.0395, *p = 0.0127. The un-transfected cells serve as the negative control. *p < 0.05; **p < 0.01; ***p < 0.001. NC negative control. | PMC10199038 | 41598_2023_35059_Fig4_HTML.jpg |
0.448281 | 326cb74db4f14847846199d139d4177b | Study flow. ASD, atrial septal defect; RHC, right heart catheterization; RVMW, right ventricular myocardial work | PMC10199586 | 12947_2023_306_Fig1_HTML.jpg |
0.454987 | 5530be0b4ef645a5a92c18663c76bb21 | Process for calculating right ventricular myocardial work. A Evaluating the right ventricular longitudinal strain. B Tracking the TR velocity-time integral to assess the mean gradient pressure between the right ventricle and atrium. C Identifying the event timing of the tricuspid valve and pulmonary valve. D Obtaining right ventricular myocardial work by the right ventricular pressure-strain loop | PMC10199586 | 12947_2023_306_Fig2_HTML.jpg |
0.496097 | 102d5b145ee743998eaaccb63d06309e | Receiver operating characteristic analysis of TAPSE, RV Sʹ, RV GLS, RVGWI, RVGWW, and RVGWE for predicting atrial septal defect. GLS, global longitudinal strain; RV, right ventricular; RVGCW, RV global constructive work; RVGWE, RV global work efficiency; RVGWI, RV global work index; RVGWW, RV global work waste; RV Sʹ, tissue Doppler-derived tricuspid lateral annular systolic velocity; TAPSE, tricuspid annular plane systolic excursion | PMC10199586 | 12947_2023_306_Fig3_HTML.jpg |
0.385086 | a48c7e35461445a5a1678829621fd6ab | Overview of the study design. | PMC10199945 | 41598_2023_35223_Fig1_HTML.jpg |
0.485984 | 443a56e30d1a4e30a4712af0795d2ae0 | Flow chart of patient selection. | PMC10199945 | 41598_2023_35223_Fig2_HTML.jpg |
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