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0.432863
22c89ffe33cf4f3188de80d436c28e22
The number of research articles published annually since 1970.
PMC9495082
animals-12-02321-g002.jpg
0.446167
843407cd651e496c8db42dbb069d3869
The number of manuscripts from the top ten of the 4739 institutions involved in Artemia research.
PMC9495082
animals-12-02321-g003.jpg
0.405515
87c5c63a44654a2aba71ba8c14129410
The primary or secondary sources (journals) utilized for the Artemia-related study literature search and scientometric analysis.
PMC9495082
animals-12-02321-g004.jpg
0.404127
ff7a89a587a5463f92b7a10d600ed8a3
Total manuscripts per nation for Artemia research. The darkest shade of purple reflects the greatest number of total publications, while lighter hues imply a moderate amount to fewer publications.
PMC9495082
animals-12-02321-g005.jpg
0.429989
ce9879441de547409290543a8d9e8c82
Network of authors’ co-citations, with a bigger writing format of an author’s name indicating a more cited author (more frequently referred to) in the research; the large node indicates a high number of citations (red ring), based on the WOSCC database only.
PMC9495082
animals-12-02321-g006.jpg
0.402469
06d37292828f4fbba1c53694f8372a53
The network of journal co-citations. A journal’s name size scales with its centrality score.
PMC9495082
animals-12-02321-g007.jpg
0.410885
79b833c8bfe24e73881dad6b15c7d624
The network of the document co-citation analysis exclusively shows articles with centrality scores greater of more than 0.1.
PMC9495082
animals-12-02321-g008.jpg
0.379079
5c4b0dae813f442e8f3ef028a55be72e
Summary of the identified top 10 document cluster lifetimes (solid lines). Cluster labels were generated from CiteSpace.
PMC9495082
animals-12-02321-g009.jpg
0.426118
1ebcc398a98740cab2447d248bb9dc6a
The phylogenetic tree (a) and principal component analysis (b) of Yunling goat (YR) and Nubian goat (NBY) were inferred from the RAD-seq dataset. (The blue and red colors represent Yunling goats and Nubian goats, respectively.).
PMC9495202
animals-12-02401-g001.jpg
0.494433
fd5ceece1f554343a05a93cad8bb1526
The population structure of Yunling goat and Nubian goat ranges from K = 2 to K = 3. (Different colors are used to distinguish different components of population structure.)
PMC9495202
animals-12-02401-g002.jpg
0.417773
f7500c8bdd984d47b5b9b80019c59d28
Genome-wide distribution of FST and π (Pi) of Yunling goats vs. Nubian goats. (Different colors are used to distinguish the corresponding part of different chromosomes.)
PMC9495202
animals-12-02401-g003.jpg
0.430653
c74aa1ca48f74493aa5655c4eeefa2c2
Intercropping altered multiple rhizosphere functions. “ns,” p > 0.05; “*,” p < 0.05; “**,” p < 0.01; “***,” p < 0.001; MZ, monoculture Zea mays; IZ, intercropping Zea mays; MS, monoculture Sophora davidii; IZ, intercropping Sophora davidii. (A) Intercropping altered the organic carbon (OC), (B) intercropping altered the microbial biomass carbon content (MBC), (C) intercropping altered the β-glucosidase activity (βG), (D) intercropping altered the water content (WC), (E) intercropping altered the ammoniacal nitrogen content (NH4_N), (F) intercropping altered the nitrate nitrogen content (NO3_N), (G) intercropping altered the microbial biomass nitrogen content (MBN), (H) intercropping altered the N-cetylglucosaminidase activity (NAG), (I) intercropping altered Nitrogenase activity, (J) intercropping altered the Leucine aminopeptidase activity (LAP), (K) intercropping altered the Nitric oxide synthetase activity (NOS), (L) intercropping altered the Glutamine synthetase activity (GS), (M) intercropping altered the total phosphorus content (TP), (N) intercropping altered the available phosphorus content (AP), and (O) intercropping altered the acid phosphatase activity (ACP).
PMC9495442
fpls-13-985574-g001.jpg
0.467668
32eadc0e238045cc95e0cf47c599c20d
(A) Principal component analysis of multiple rhizosphere functions and in the different groups, showing overall intuitive distribution of multiple functions and aboveground net primary productivity, and the contribution of each function to this distribution. (B–E) Relationships among individual rhizosphere functions and aboveground net primary productivity (ANPP). MZ, monoculture Zea mays; IZ, intercropping Zea mays; MS, monoculture Sophora davidii; IZ, intercropping Sophora davidii.
PMC9495442
fpls-13-985574-g002.jpg
0.467689
4b701d0ceb684dfd9b86a78edefcfa2a
(A–D) Boxplots indicating that the trade-off intensity of functions changed with the number of paired functions. (E–H) Difference of the trade-off intensity between groups at the number of paired functions (Wilcoxon test at α = 0.05). MZ, monoculture Zea mays; IZ, intercropping Zea mays; MS, monoculture Sophora davidii; IZ, intercropping Sophora davidii.
PMC9495442
fpls-13-985574-g003.jpg
0.395988
fde3d910706c4b0ca5efad67227d0c86
Intercropping altered rhizosphere C, N, P circling multifunctionality (CCMF, NCMF, and PCMF), average rhizosphere ecosystem multifunctionality (AEMF) and aboveground net primary productivity (ANPP). “ns,” p > 0.05; “*,” p < 0.05; “**,” p < 0.01; MZ, monoculture Zea mays; IZ, intercropping Zea mays; MS, monoculture Sophora davidii; IZ, intercropping Sophora davidii.
PMC9495442
fpls-13-985574-g004.jpg
0.410714
22f3e76cb9984bda96d867eaaa5050ee
Non-metric multidimensional scaling (NMDS) ordinations based on Bray–Curtis distance matrices of taxonomy (A,B) and functions (C,D) of bacterial (A,C) and fungal (B,D) subcommunities for all samples (n = 20). A stress <0.1 indicated that the result of NMDS is reliable. ANPP, aboveground net primary productivity; MZ, monoculture Zea mays; IZ, intercropping Zea mays; MS, monoculture Sophora davidii; IZ, intercropping Sophora davidii. R and p were reported by ANOSIM.
PMC9495442
fpls-13-985574-g005.jpg
0.449713
89236f1b17784bdd95f8bf84afebdaa0
Heatmap showing the intensity of the selected species (or functions) or the diversity indices impacting rhizosphere functions and aboveground net primary productivity (ANPP). The intensity was indicated by r of Mantel test. The selected species (or functions) were the intersection of species or functions that significantly differed among the groups (MZ, IZ, MS, and IS) and were significantly correlated with system function (C/N/P-circling multifunctionality, AEMF, and ANPP, respectively). Only the significant intensity was showed. Hierarchical cluster analysis showed the clusters of factors. CCMF, carbon-circling multifunctionality; NCMF, nitrogen-circling multifunctionality; PCMF, phosphorus-circling multifunctionality; AEMF, average ecosystem multifunctionality.
PMC9495442
fpls-13-985574-g006.jpg
0.413362
9cfb6b42bf32443585c47c458c93ef32
Overview of early, intermediate and late approaches for integrating multimodal data. (a) The early approach combines multiple datasets into an intermediate representation, from which predictive models can be inferred. (b) The intermediate approach jointly models the multiple datasets and their elements through an intermediate representation. (c) The late approach first builds local model(s) for each individual modality, which are then integrated into the final predictive model
PMC9495448
vbac065f1.jpg
0.417986
a70e3f23d3124847a4544ba873d55d79
Overview of the EI framework for multimodal data. In the implementation of EI tested in this work, we used 10 standard binary classification algorithms, such as SVM, RF and LR, as implemented in Weka (Frank et al., 2005), to derive sets of local predictive models 1, 2, … ,N from the data modalities 1, 2, … ,N. We then applied the stacking and ensemble selection methods to these local models to generate the EI models. These models generated prediction scores for the entities and multimodal data of interest that were evaluated to assess their performance. Finally, we used our novel interpretation method to identify the features that contributed the most substantially to the best-performing EI model’s predictions
PMC9495448
vbac065f2.jpg
0.471739
df78d81cfc634240a035cfd807f1c4ca
The distributions of the performances of the PFP approaches tested in this work. This performance was measured in terms of the Fmax score for each of the 2139 GO terms. For EI and the individual modalities, the score for the best-performing heterogeneous ensemble method for each GO term is shown here. For the Mashup and deepNF early integration methods, the score of the best local modeling algorithm for each term is shown.
PMC9495448
vbac065f3.jpg
0.547073
0ac10ad11a9b4ed39fad05c208a43521
Distribution of the performances (Fmax scores) of EI, deepNF and Mashup for GO terms at varying depths and information content levels. The depth and information content values of the 2139 GO terms included in this experiment were calculated using the GOATOOLS package (version 1.0.3) (Klopfenstein et al., 2018). (a) Distribution of performances across GO terms stratified by their depths in the respective ontologies. (b) Distribution of performances across GO terms stratified by their information content. The information content bins on the x-axis were created to include an equal number (20%) of GO terms included in the PFP experiments
PMC9495448
vbac065f4.jpg
0.429331
95efe3b2344c403781404210626d292b
The distribution of Fmax values of various ensemble models and XGBoost for predicting mortality from COVID-19 over a patient’s hospitalization. The performance distributions of EI and the heterogeneous ensembles derived from the individual EHR data modalities are shown as box-and-whisker plots. Each plot includes 11 ensemble models built using mean aggregation, CES and nine stacking algorithms. The numbers in parentheses next to the names on the x-axis indicate the number of features in the corresponding modality. The dotted horizontal line indicates the performance of the XGBoost model trained after concatenating the feature vectors in each individual modality
PMC9495448
vbac065f5.jpg
0.441481
882cd236b7134b68b769742ba03ca3fd
Precision-recall curves of representative models from EI, individual EHR modalities and XGBoost for predicting COVID-19 mortality. The values in parentheses show the Fmax value of each of these models, and the cross marker on each curve indicates the precision and recall at which the corresponding Fmax was obtained
PMC9495448
vbac065f6.jpg
0.48834
6454cd14187b4b5fb88d577b703c6d96
Eukaryotic mRNA undergoes several steps of processing in the nucleolus, such as 7-methylguanosine (m7G) at the 5′ and poly A-tail in the 3′-end. Ribosomes are recruited by mRNA through coordinated multiple processes. Two protein complexes, eukaryote translation initiation factor (eIF4F), which comprises eIF4E (cap-binding protein), eIF4G (scaffold protein), and eIF4A (RNA helicase), and the ternary complex, which includes eIF2-GTP and initiation tRNA (Met-tRNAiMet), have pivotal roles in translation initiation. The mRNA circularization occurs in the interaction of eIF4G with poly A-tail binding protein (PABP). The eIF4F complex displays a secondary structure in the 5′ untranslated region (5′UTR) of mRNA. The mTOR complex 1 controls the initiation of translation through the ternary complex and eIF4F complex. Moreover, the interaction of eIF4B with eIF4A increases the helicase activity of the latter.
PMC9495564
biomedicines-10-02088-g001.jpg
0.455397
ad93eb08ebc74b2ab1cc36f289ab34b3
Inhibition of eukaryotic rRNA processing in different steps. The rRNA processing scheme presented here from 35S pre-rRNA to the mature rRNA (18S, 5.8S, and 25S) is complemented with different inhibitors and their potentially targeted ribosomal maturation.
PMC9495564
biomedicines-10-02088-g002.jpg
0.463427
55a363920c43425cbaa9e076cd28c6ba
Overview of protein synthesis in bacteria and inhibition by different antibiotics. First step: initiation of protein synthesis assisted by initiation factors (IF1, 2, 3), location of the start codon in mRNA, and connection of the initiation tRNA in the peptidyl (P) site. During translation elongation, EF-Tu-delivered aminoacyl-tRNA are selected and then accommodated in the aminoacyl tRNA. The antibiotic (green highlighted)- and macrolide-inhibition of peptide bond formation depends on the structure of the nascent protein. During translocation, the A site-bound peptidyl-tRNA moves into the P site, and the tRNA with a free 3′ end is relocated into the exit E site. When the ribosome encounters a stop codon, it enters the termination phase. During this phase, the completed protein is released with the help of termination factors (RF1 or RF2 and RF3). The last step is the recycling phase, when the combination of ribosome recycling factor (RRF) and EF-G splits the ribosome into its subunits.
PMC9495564
biomedicines-10-02088-g003.jpg
0.377168
3b46572926c7450587eb41081c7f0b48
Representative images of Amazona aestiva after data augmentation. The green boxes in the images represent the ground-truth bounding boxes. (A) Initial image, (B) Horizontal flipped image, (C) Rotated image, (D) Zoomed-in image, (E) Zoomed-out image, and (F) Translated image. Photo credit: Mauro Halpern.
PMC9495850
biology-11-01303-g001.jpg
0.410444
6fe234180308480ba9e005591c941bd4
Single Shot MultiBox Detector model architecture with different convolution neural network (CNN) backbone networks for the classification of the 26 Amazon parrot species.
PMC9495850
biology-11-01303-g002.jpg
0.387834
3edbd3db79b3406ebbdc34faf8577a82
Representative images of four cases of model prediction results. The green and yellow boxes on the images represent ground-truth and prediction bounding boxes, respectively. The values in the yellow boxes are confidence scores provided by the models, indicating the probability of the prediction being correct. (A) Image of Amazona aestiva, one prediction bounding box was predicted and classified correctly; (B) Image of A. aestiva, multiple prediction bounding boxes were predicted and classified correctly; (C) Image of Amazona vittata, one prediction bounding box was predicted and classified incorrectly; (D) Image of Amazona albifrons, multiple prediction bounding boxes were predicted and classified incorrectly. Photo credit: (A) Charles J. Sharp, (B) Bernard Dupont, (C) Tom MacKenzie, and (D) Charlottesville.
PMC9495850
biology-11-01303-g003.jpg
0.463157
8c3fd6ad7d2e484492bb4c8f17214cd2
Representative images of the top five results for incorrect classification using the DenseNet121 model. Images on the left and right represent the true and predicted results, respectively. (A) Amazona vittata (left) was predicted to be Amazona tucumana (right). (B) Amazona barbadensis (left) was predicted to be Amazona oratrix (right). (C) Amazona mercenarius (left) was predicted to be Amazona auropalliata (right). (D) Amazona auropalliata (left) was predicted to be Amazona ochrocephala (right). (E) Amazona finschi (left) was predicted to be Amazona viridigenalis (right). Photo credits: (A) Tom MacKenzie (left), Carlos Urdiales (right); (B) Emőke Dénes (left), David J. Stang (right); (C) Félix Uribe (left), Andrew Gwozdziewycz (right); (D) Andrew Gwozdziewycz (left), MAClarke21 (right); and (E) Cédric Allier (left), Roger Moore (right).
PMC9495850
biology-11-01303-g004.jpg
0.44809
7d453e89cacd4026b2f391d11b08b6dd
(a) Unit structure of MCWM (a 3D-view drawing); (b) macroscopic and microscopic photographs of a PET mesh; (c) side views of a schematic drawing and a microscopic photograph of an MCWM unit structure; (d) configuration of the reading unit (i.e., the THz-TDS system) for a MCWM sensing device. L1–L3: plastic lenses; M1–M4: metal mirrors; PCA: photoconductive antenna.
PMC9496153
biosensors-12-00669-g001.jpg
0.487706
3201130d919d431a8a5d4ed61876b5ba
(a) Experimental and simulated transmittance spectra of 249 μm W MCWM; schematic diagrams of the characterized spectral (b) dip and (c) peak wavelengths relating to Aunit and Λ of the MCWM, respectively.
PMC9496153
biosensors-12-00669-g002.jpg
0.406039
f65221c56b164bf58a8373a35565e9e6
Simulated (a–d) X–Z lateral modal profiles and (e,f) Z-axial electric field distributions of 90 and 249 μm W MCWMs at the first-order spectral dips and peaks.
PMC9496153
biosensors-12-00669-g003.jpg
0.526273
44bd5c4430ba420f8737ac91d1277b1b
Normalized transmittance of a 249 μm W MCWM loaded with different weight densities of PAA membranes for thickness detection experiment.
PMC9496153
biosensors-12-00669-g004.jpg
0.471101
eea9d71ffe0748fdb7b2b71377dab8dc
(a) Normalized transmittance of a 90 μm W MCWM loaded with different weight densities of PAA membranes for thickness detection experiment; (b) calculated transmittance of a 90 μm W MCWM with different filling ratios of PAA membranes; (c) relationship between spectral shift and PAA molecular density for the first spectral dips and peaks of 90 and 249 μm W MCWMs; (d) calculated spectral dip shifts at the first-order resonance for the 90 and 249 μm W MCWMs.
PMC9496153
biosensors-12-00669-g005.jpg
0.493674
06cca04d811b44c882524f7c1bc8dbb8
Simulated Z-axial E-field integrals of 90 and 249 μm W MCWMs at the first-order spectral dips and peaks.
PMC9496153
biosensors-12-00669-g006.jpg
0.448315
7810274a1879430f8d6ddedcf0f17a0b
(a) Measured transmittance curves of a 90 μm W MCWM loaded with lactose-doped PAA membranes for refractive index detection experiment. The measured Δf values of the 90 μm W MCWM at the first spectral dip for (b) the measured thicknesses ΔZ, (c) refractive indices, and (d) optical path lengths of different lactose-doped PAA membranes.
PMC9496153
biosensors-12-00669-g007.jpg
0.390616
207cd1e6039b4320936048db1f0cf113
Measured transmission spectral curves of 90 μm W MCWM for sensing various amounts of (a) salt grains and (b) PE sphere particles.
PMC9496153
biosensors-12-00669-g008.jpg
0.462311
e9b1e465da344d4088cc36273cd7db09
Measured Δf values of 90 μm W MCWM at the first spectral dip for depositing different kinds and amounts of analytes.
PMC9496153
biosensors-12-00669-g009.jpg
0.443826
d7a087a4719b4206a09d320737345344
Study design, electrode montage, and atlas or MRI-planned electrode coordinates. (A) Study design. Following TBI, rats were divided into either the EEG or MRI cohort. The rats of the EEG cohort were implanted with electrodes after fully righting themselves following induction of TBI. The rats were followed up immediately afterward with 1 month video-EEG and then for 1 week monthly until the 6th post-TBI month. The rats of the MRI cohort were magnetic resonance-imaged at 5 months post-TBI and T2-wt images were used to calculate the coordinates of the intracerebral electrodes implanted at 6 months post-TBI. Both cohorts were continuously monitored with video-EEG for 30 days at 7 months post-TBI to diagnose epilepsy. At the end of the 7-month follow-up period, all rats were euthanized and the brains processed for histological identification of the location of the intracerebral electrodes. (B) Electrode montage used in the study. Four epidural screw electrodes (C3, C4, O1 and O2), 3 intracerebral bipolar wire electrodes (anterior cortical Cx1, posterior cortical Cx2, and hippocampal HC), a ground (Gr) and reference (Ref) electrode. (C) Atlas plates demonstrating the planned coordinates used in the EEG cohort to implant the anterior cortical, hippocampal, and posterior cortical electrodes. The black dot refers to the upper tip and the red dot to the lower tip of the bipolar electrode (1 mm apart). Reprinted/adapted with permission from [25]. 2007, Elsevier Inc. (D) MRI T2-wt images of rat 1139 demonstrating the planned-MRI coordinates of the intracerebral anterior cortical, hippocampal, and posterior cortical electrodes. The anteroposterior (AP) coordinate was determined by aligning the MR images with the atlas [25]. The mediolateral (ML) and dorsoventral (DV) coordinates were determined using ImageJ software (version 1.47v, Wayne Rasband and contributors, National Institute of Health, USA).
PMC9496327
biomedicines-10-02295-g001.jpg
0.378673
77b9fc84cdd64dc088029d5e7876e246
Anterior intracortical electrode—schematic representations of the atlas, histological, and MRI-guided coordinates in each rat of the EEG and MRI cohorts. (A) Anteroposterior (AP) coordinate. In the EEG cohort (electrode operation right after injury), the fixed atlas-based target AP coordinate of −1.72 mm from the bregma was applied to implant the electrodes (orange dots). In the MRI cohort (electrode operation 5 months after injury), the target AP coordinate was individually determined using the 5-month in vivo T2-weighted MR images. The target coordinate fluctuated depending on the extent of the TBI (traumatic brain injury)-induced lesion. Note the anterior shift (y-axis) in the histologically verified “true” AP coordinate (blue dots) relative to the target coordinate (orange dots) in both cohorts. The deviations were comparable between the sham and TBI animals (p > 0.05). Animal numbers are shown on the x-axis. (B) Mediolateral (ML) coordinate. In the EEG cohort, the fixed atlas-based target ML coordinate at 4 mm lateral to midline was targeted. In the MRI cohort, the target ML coordinate was individually determined using the 5-month in vivo MRI. Note a small deviation of the histologically verified “true” ML coordinate from the target coordinate in both cohorts. (C) Dorsoventral (DV) coordinate. In both cohorts, the lower tip of the bipolar electrode was aimed to layer V in the selected AP and ML coordinates (see above). Electrode tips were located in the cortex in 83% (36/43) of the EEG cohort and 77% (24/31) of the MRI cohort. Importantly, even though the lower tip in the remaining cases went down into the external capsule or corpus callosum, the upper tip of the bipolar electrode, being 1 mm higher in the EEG and 0.5 mm in the MRI cohort, was still recording in the cortex. The percentages of electrode locations in the sham-operated and TBI animals are shown on the right side of the panel. (D) Dot plots of the AP and ML shift in the histological AP and ML coordinate, and % of electrode in the targeted layer V (number of cases in brackets). Note posterior and medial shift of some cases from the target (vertical dashed line). y-axis represents distance from target coordinate (Y = 0) or % of cases in targeted area. Abbreviations: cavity, cortical lesion cavity; cc, corpus callosum; cg, cingulum; S, subiculum; ec, external capsule; HC, hippocampus; and V, ventricle.
PMC9496327
biomedicines-10-02295-g002.jpg
0.437291
9db0547fecb54a67a914b117340ca12f
(A–F) Electrode tracts. Histological images from the coronal thionine-stained sections of 6 rats, showing the tracts of the bipolar intracortical electrodes and location of the lower electrode tip (filled arrowhead). Roman numerals indicate the cortical layers. In panels (A,B) the electrode tip is located in layer V of the perilesional cortex. Note the electrode track-related lesion on the surface of the brain in panel (A) (open filled arrow). In panel (A), the electrode tip is within 500 µm from the edge of the TBI-induced lesion cavity (asterisk). In panel (C), the electrode tip is in the external capsule (ec). In panel (D) the electrode tip is within the cortical lesion, close to the angular bundle. Open arrow points to the electrode path associated neurodegeneration. In panel (E), the electrode tip is close to the edge of the lesion cavity (asterisk). In panel (F), the electrode tip is within the angular bundle (closed arrowhead). The open arrowhead points to the location of the upper electrode in layer IV (open arrow). The dark staining indicates iron deposits (arrowheads) adjacent to the electrode path. Scale bar = 500 µm.
PMC9496327
biomedicines-10-02295-g003.jpg
0.44926
031bbdab318f43819b21ef76e9078749
Location of the lower tip of the anterior and posterior intracortical electrodes on atlas plates and unfolded cortical maps. (A) In the EEG cohort (upper panel), the dorsoventral (DV) location of at least 1 of the tips of all anterior bipolar electrodes (atlas plate: bregma −1.4 mm) was within the primary somatosensory cortex (S1) and that of the posterior electrode (lower panel; atlas plate: bregma −6.8 mm) was within the visual cortex. Each dot represents 1 bipolar electrode. (B) An unfolded map (UFM) showing the location of electrode tracks in the EEG cohort as seen from the surface of the brain. The intersection of the electrode path with cortical layer V was used as reference. The UFMs confirmed the location of the anterior electrode paths in the S1 and posterior electrode paths in the visual cortex. (C) Atlas plate showing the DV locations of the anterior (upper panel) and posterior (lower panel) intracortical electrodes in the MRI cohort. As in the EEG cohort, the anterior electrode was in S1 and the posterior electrode was in the visual cortex. (D) A UFM showing the location of electrode tracks in the MRI cohort as seen from the surface of the brain. All electrode tracks were within S1 or the visual cortex. Note that in the MRI cohort, we used the 5-month in vivo MRI to adjust the electrode coordinates to target the perilesional cortex and to avoid lesion cavities, underlying brain areas, or ventricles. As expected, this resulted in a more heterogeneous distribution of electrode paths than in the EEG cohort with atlas-based fixed coordinates. Atlas plates and UFMs were generated using the Paxinos rat brain atlas (6th edition).
PMC9496327
biomedicines-10-02295-g004.jpg
0.445155
e052f60d86204b0a9f88807cc1d77967
Posterior intracortical electrode—schematic representations of the atlas-based, histological, and MRI-guided coordinates in each rat of the EEG and MRI cohorts. (A) Anteroposterior (AP) coordinate. In the EEG cohort (n = 47, electrode operation right after injury), the fixed atlas-based target AP coordinate of −7.56 mm from the bregma was applied to implant the electrodes (orange dots). In the MRI cohort (n = 40, electrode operation at 5 months postinjury), the target AP coordinate was individually determined using the in vivo 5-month T2-weighted MR images. The target coordinate fluctuated depending on the TBI (traumatic brain injury)-induced lesion extent. Note a mild anterior shift (y-axis) in the histologically verified “true” AP coordinate (blue dots) relative to the target coordinate (orange dots) in both cohorts. In general, the anterior shift was less than that in a case of the anterior intra-cortical electrode (compare to Figure 1). Animal numbers are shown on the x-axis. (B) Mediolateral (ML) coordinate. In the EEG cohort (n = 47), the fixed atlas-based ML coordinate at 4 mm lateral to midline was targeted. In the MRI cohort (n = 40), the target ML coordinate was individually determined using the 5-month MRI. Note almost a negligible deviation of the histologically verified “true” ML coordinate from the atlas-based (EEG cohort) or MRI-guided (MRI cohort) coordinates. (C) Dorsoventral (DV) coordinate. In both cohorts, the lower tip of the bipolar electrode was targeted to layer V in the selected AP and ML coordinates (see above). In the EEG cohort, 46% (18/39), and in the MRI cohort, 66% (19/29) of the electrode tips in injured animals were in the cortex. Importantly, even though the lower tip in the remaining cases went down into the external capsule or corpus callosum, the upper tip of the bipolar electrode, being 1 mm higher in the EEG and 0.5 mm in the MRI cohort, was still recording in the cortex in 79% (31/39) of the rats in the EEG cohort and in 72% (21/29) in the MRI cohort. In 5 rats (3 sham, 2 TBI) in the EEG cohort and 10 rats (4 sham, 6 TBI) in the MRI cohort, the electrode was recording hippocampal rather than cortical activity, which affected the interpretation of the EEG data. The percentages of electrode locations in the sham-operated and TBI animals are shown on the right side of the panel. (D) Dot plots of the AP and ML shift in the histological AP and ML coordinate, and % of electrode in the targeted layer V (number of cases in brackets). Note posterior shift of some TBI cases from the target (Y = 0). The y-axis represents distance from target coordinate (Y = 0) or % of cases in targeted area. Note that in 4 animals in the EEG cohort and 2 in the MRI cohort, the DV location of the electrode tip could not be reliably determined in histological sections. Abbreviations: cavity, cortical lesion cavity; cc, corpus callosum; cg, cingulum; dcw, deep cerebral white matter; ec, external capsule; fmj, forceps major corpus callosum; HC, hippocampus; S, subiculum; V, ventricle.
PMC9496327
biomedicines-10-02295-g005.jpg
0.447962
6c162777e5bd4f9fba088d0b0d7daffc
Histological confirmation of the success of MRI-guided electrode placement. Left panel (A–C): Anterior intracortical electrode MRI-planned coordinate, histological confirmation, and “virtual” electrode. Right panel: Posterior intracortical electrode MRI-panned coordinate histological confirmation, and “virtual” electrode. (A) T2-weighted MRI and (B) histological images showing the MRI-guided (insert) and histology-confirmed “true” location of the anterior intracortical electrode in rat 1139. The anteroposterior (AP) coordinate was estimated by aligning the magnetic resonance images with the rat brain atlas [25]. The mediolateral (ML) and dorsoventral (DV) coordinates (inserts in (A,D)) were determined using ImageJ software (version 1.47v, Wayne Rasband and contributors, National Institute of Health, USA). Note that in this case, the confirmed AP location was about 1.8 mm more rostral than the planned location (−1.20 mm vs. −2.96). Lesion area is denoted in black-dashed-line circle. (C) A “virtual” location of the electrode tip (black line) if the electrode had been implanted to the targeted atlas-based coordinate (−1.75 mm from bregma, 4 mm from midline, 1.8 mm from the surface of the brain). (D) MRI-guided (insert) AP, ML and DV coordinates and (E) histology-confirmed “true” location of the posterior intracortical electrode tip in rat 1139. The black-dashed-line circle denotes the lesion area. Note that the confirmed AP location was approximately 1.4 mm more rostral than the planned location (−3.96 vs. −5.36). Thus, even though both the anterior and posterior intracortical electrodes were more rostral than planned, their tips were recording EEG signals in the perilesional cortex. (F) A “virtual” electrode (black line) at the atlas-based coordinates would have ended up in the lesion cavity. Scale bar in (A,D) = 1 mm, and in (B,C,E,F) = 2 mm.
PMC9496327
biomedicines-10-02295-g006.jpg
0.397675
be94c6d538f240ae8ebb971214fc3e4e
Hippocampal electrode—schematic representations of the atlas-based, histological, and MRI-guided coordinates in each rat of the EEG and MRI cohorts. (A) Anteroposterior (AP) coordinate. In the EEG cohort (electrode operation right after injury), the fixed atlas-based target AP coordinate of −3 mm from the bregma was applied to implant the electrodes (orange dots). In the MRI cohort (electrode operation 5 months after injury), the target AP coordinate was individually determined using the 5-month in vivo T2-weighted MR images. The target coordinate fluctuated, depending on the TBI-induced hippocampal structural abnormality. Note the anterior shift (y-axis) in the histologically verified “true” AP coordinate (blue dots) relative to the aimed target coordinate (orange dots) in both cohorts. Note the great variability in the anterior shift from animal to animal, particularly in the MRI cohort. Animal numbers are shown on the x-axis. (B) Mediolateral (ML) coordinate. In the EEG cohort, the fixed atlas-based target ML coordinate at 1.4 mm lateral to midline was targeted. In the MRI cohort, the target ML coordinate was individually determined using the 5-month MRI. Note only a very small deviation of the histologically defined “true” ML coordinate from the atlas-based (EEG cohort) or MRI-guided (MRI cohort) coordinates. (C) Dorsoventral (DV) coordinate. In both cohorts, the lower tip of the bipolar electrode was aimed at the hilus in the selected AP and ML coordinates (see above). In the EEG cohort, most of the tips were recording in the hippocampus proper or the dentate gyrus. In the EEG cohort, in only 19% (8/43) of TBI cases, the tip was either in fimbria, ventricle, or went through the septal hippocampus to the dorsal thalamus or to an unidentified location. In the MRI cohort, in only 14% (6/31) of TBI cases, the tip was outside the hippocampus or the dentate gyrus. The percentages of electrode locations in the sham-operated and TBI animals are shown on the right side of the panel. (D) Dot plots of the AP and ML shift in the histological AP and ML coordinate, and % of electrodes in the targeted dentate gyrus (number of cases in brackets). Note posterior shift of some cases from the target (vertical dashed line). The y-axis represents distance from target coordinate (Y = 0) or % of cases in targeted area. Abbreviations: alv, alveus; CA1, CA1 subfield of the hippocampus; CA3, CA3 (CA3b, CA3c) subfield of the hippocampus; gcl, granule cell layer (s-gcl, suprapyramidal blade, i-gcl, infrapyramidal blade); hf, hippocampal fissure; l-m, stratum lacunosum moleculare of CA1; mol, molecular layer of the dentate gyrus; V, ventricle.
PMC9496327
biomedicines-10-02295-g007.jpg
0.434313
34ac12e744f94e789703e306b13d92e7
Anteroposterior and mediolateral shrinkage of the brain. In vivo magnetic resonance 3D multigradient echo (MGRE) images acquired at 5 months after TBI were used to estimate cortical shrinkage in the MRI cohort. (A1–A4) coronal, sagittal (ipsilateral and contralateral) and horizontal MGRE images of a sham rat (A1) and TBI rats (A2–A4). Anteroposterior (AP) cortical shrinkage was estimated by measuring the distance between the rostral and caudal cortical surface (double-headed arrows) in the sagittal slice at 4 mm from the midline both ipsilaterally (orange) and contralaterally (white). Note the change in the shape of the ipsilateral cortex (sagittal images) in TBI rats, indicating the TBI-induced cortical atrophy (see also turquoise arrows in (A3,A4)). Mediolateral (ML) shrinkage was assessed by measuring the distance between the midline and the lateral edge of the cortex (turquoise double headed arrow) in a horizontal slice at 1.7 mm below the pial surface at AP level −1.56 (corresponding to the targeted location of the anterior intracortical electrode tip). (B) A dot plot showing the ipsilateral (orange) and contralateral (blue) cortical AP lengths (y-axis) in the sham and TBI groups (x-axis). Note that both the ipsilateral and contralateral cortical AP lengths were reduced in TBI rats compared with sham-operated animals. Also, in the TBI group, the cortical AP length was shorter ipsilaterally than contralaterally. (C) A paired dot plot showing that the ipsilateral vs. contralateral shrinkage in each rat. The greater the ipsilateral shrinkage, the greater the contralateral shrinkage in the TBI compared with sham group. Arrows point to the 3 cases illustrated in panels (A1–A4). (D) A dot plot showing the ipsilateral and contralateral cortical ML lengths in sham-operated and TBI rats. Note that both the ipsilateral and contralateral cortical ML lengths were reduced in TBI rats compared with sham-operated animals. Also, in the TBI group, the cortical ML length was shorter ipsilaterally than contralaterally. Statistical significance: *** p < 0.001 compared with the contralateral hemisphere (Wilcoxon signed-rank test); ### p < 0.001, # p < 0.05 compared with the sham group (Mann–Whitney U test).
PMC9496327
biomedicines-10-02295-g008.jpg
0.450381
1735ffae7e154d70b431e62ac661b112
(A–C) Electrode tracts. Histological images from the coronal thionine-stained sections of 3 rats, showing the tracts of the bipolar intracortical electrodes and locations of the lower electrode tip (filled arrowhead). The target of the lower tip was the hilus. In panel (A), the electrode tip is in the suprapyramidal blade of the granule cell layer. In panel (B), the tip went through the dentate gyrus down to the dorsal thalamus. In panel (C), the tip is in the infrapyramidal blade of the granule cell layer. Note the electrode-path associated lesion in CA1 (open arrow). (D1–D3) Coronal, sagittal and horizontal in vivo magnetic resonance 3D multigradient echo (MGRE) images of the ipsilateral and contralateral hippocampus were used to assess hippocampal shrinkage after traumatic brain injury (TBI). (D1–D3) Hippocampal distortion and shrinkage. Panel (D1): A sham-operated experimental control (1107). Panels (D2,D3): Two rats with TBI (1028, 1144). The anteroposterior (AP) shift of the hippocampus was assessed by measuring the distance from the rostral edge of the frontal cortex to the rostral edge of the hippocampus at 1.4 mm from the midline in the horizontal slice 2.8 mm below the surface of the brain (left hemisphere: orange double-headed arrow; right hemisphere: white double-headed arrow). Mediolateral (ML) shrinkage was assessed by measuring the distance from the brain midline to the lateral edge of the hippocampus in the same horizontal plane (2.8 mm below the surface of the brain, turquoise double-headed arrow) in a slice sampled at AP level −2.8 mm, corresponding to the AP level of the atlas-based target coordinate. In both TBI rats (D2,D3), the distance from the frontal pole to the rostral edge of the hippocampus was longer than that in the sham-operated animal, indicating retraction of the septal hippocampus caudally. The ML length in TBI rats (D2,D3) was shorter than that in the sham-operated animal (D1), indicating a shift toward midline. (E) A dot plot showing the ipsilateral (orange) and contralateral (blue) anteroposterior lengths (y-axis) in the sham and TBI groups (x-axis). Note that both the ipsilateral and contralateral cortical AP lengths were increased in TBI rats compared with sham-operated animals. Also, in the TBI group, the cortical AP length was greater ipsilaterally than contralaterally. (F) A paired dot plot showing the ipsilateral vs. contralateral backward “movement” in each rat. The greater the ipsilateral “movement”, the greater the contralateral “movement”. Arrows point to the 3 cases illustrated in panels (D1–D3). (G) A dot plot showing the ipsilateral and contralateral hippocampal ML lengths in sham-operated and TBI rats. Note that both the ipsilateral and contralateral cortical ML lengths were reduced in TBI rats compared with sham-operated animals. Also, in the TBI group, the ML length was shorter ipsilaterally than contralaterally. Statistical significance: ##, p < 0.05; ###, p < 0.001 as compared to the sham group (Mann–Whitney U test); *** p < 0.001 compared with the contralateral hemisphere (Wilcoxon signed-rank test). Scale bar in (A–C) = 500 µm.
PMC9496327
biomedicines-10-02295-g009.jpg
0.433751
4e2a4a1d9589419ca7ec8b5a310e38d0
Location of electrode tip at 5 months postinjury without prior MRI analysis. Photomicrographs of thionine-stained coronal brain sections of 4 animals; (A) #1019, (B) #1139, (C) #1158 and (D) #1036 in the MRI cohort with electrode implantations at 5 months after TBI. Left panels: MRI-guided placement of the posterior cortical electrode. Note that all electrodes are within the perilesional cortex. Right panels: The location of the electrode tip (arrow), if the electrode was implanted according to the targeted atlas-based coordinates (−7.56 mm from bregma, 4 mm from midline, 1.8 mm from the surface of the brain). Note that in all rats except 1019, the electrode tip ended in the lesion cavity. Table 2 summarizes the locations for all cases. Scale bar = 2 mm.
PMC9496327
biomedicines-10-02295-g010.jpg
0.45722
c9d2582410394057af15fb860351051a
Distance of the intracortical electrodes from the edge of the cortical lesion cavity. (A) An unfolded cortical map of a rat 1064, showing the cytoarchitectonic distribution of the cortical lesion (blue outline) and the location of the anterior (brown filled circle in the S1BF) and posterior (yellow filled circle in the V2L) intracortical electrodes. Note that the lesion had progressed laterally and caudally. Consequently, the posterior electrode was closer to the lesion cavity edge than the anterior electrode. (B) A scatter plot showing the cortical lesion area in the EEG and MRI cohorts (each dot represents 1 rat). The lesion area was comparable between cohorts (p > 0.05). (C) In the EEG cohort, the distance from the electrode tip to the lesion cavity edge (layer V intersection was used as reference) was similar between the anterior and posterior intracortical electrodes (p > 0.05). (D) In the MRI cohort, the distance from the anterior intracortical electrode tip to the cavity edge was slightly greater than that from the EEG cohort (p < 0.05). (E) In the EEG cohort, the larger the lesion, the closer the posterior electrode tip to the lesion cavity edge (p < 0.001). (F) In the MRI cohort, the larger the lesion, the closer the posterior electrode tip to the cavity edge (p < 0.001). Abbreviations: S1BF, primary somatosensory barrel field; V2L, secondary visual cortex lateral area. Statistical significance: #, p < 0.05 compared with the EEG cohort (Mann–Whitney U test).
PMC9496327
biomedicines-10-02295-g011.jpg
0.39603
e8b7d6bc5a80487e8c2eaf79e90aceb1
Moyamoya disease with a peripheral hemorrhagic aneurysm. (A) Preoperative CT revealed periventricular and ventricular hemorrhage. (B) Left internal carotid arteriography revealed smoky vascular hyperplasia with a false aneurysm at the end of the lenticulostriate artery. (C) The parent vessels were too tortuous and slender for super-selection. A Marathon microcatheter was located at the beginning of the parent artery. (D) Glubran was used to block the parent artery with satisfactory diffusion to the distal aneurysm cavity. (E) After the embolization, the aneurysm and parent artery disappeared on arteriography. (F) Postoperative CT revealed that the position of the glue coincided with the location of a brain hemorrhage.
PMC9496767
brainsci-12-01264-g001.jpg
0.446739
b2584112cc9e4b9cb43392e7ebca3de9
AVM with peripheral hemorrhagic aneurysm. (A) Preoperative CT revealed hemorrhage in the corpus callosum’s ventricle and splenium (B) DSA demonstration of the splenium of the corpus callosum AVM supplied by the right posterior cerebral artery branches and the branches of the right anterior cerebral artery, accompanied by a blood flow related aneurysm. (C) Super selection and positioning of the microcatheter through the left vertebral artery, preparing for the embolization. (D) Embolization of the AVM and accompanied aneurysm with Onyx. (E) Arteriography after embolization revealing the complete embolization of the AVM and the aneurysm. (F) CT scan before discharge, revealing adequate treatment.
PMC9496767
brainsci-12-01264-g002.jpg
0.436267
13b3190bd6cf49c4b9f927e07412b0ea
Task Structures: (a) Emotional Self-Other Morph Neurofeedback Task (ESOM-NF) entailed participants recalling positive autobiographical memory to the cue of their own smiling face for 40 s and attempting to increase the green bar (the amygdala-hippocampal complex), viewing another’s face and counting backward for 24 s, rating their mood for 4 s after feedback or count backward blocks, and resting for 12 s. (b) Emotional Self-Other Morph-Query (ESOM-Q) was administered before (ESOM-Pre) and after (ESOM-Post) the neurofeedback task (ESOM_NF). Participants recognized faces as either their own or as different face via button press.
PMC9496932
brainsci-12-01128-g001.jpg
0.414877
4f22fd33b2b942e1b4a79af08c799599
Brain activity associated with symptom change during neurofeedback (feedback vs. count—backwards) in depressed youth, n = 34: (a) Changes in brain activity during neurofeedback vs. counting backward associated with decreased rumination; (b) Changes in brain activity during neurofeedback vs. count—backwards associated with decreased depression.
PMC9496932
brainsci-12-01128-g002.jpg
0.455053
84d6b07a8f064082beac21afc9299306
Brain activity during self-processing associated with symptom change in depressed youth, n = 34: Changes in activity during ESOM-Q Post vs. ESOM-Q Pre were associated with change in depression score.
PMC9496932
brainsci-12-01128-g003.jpg
0.392864
981501abd4f94b9e86b1d884e6672b17
Strategies aimed at generation of bone fide β-cell for replacement therapy in diabetes. Abbreviations: human embryonic stem cells (hESC); mesenchymal stem cells (MSCs); induced pluripotent stem cells (iPSC). Figure was created with BioRender http://www.biorender.com.
PMC9496933
cells-11-02813-g001.jpg
0.439705
60c7c2b387ec4b9490de2f2dfcc84696
Trans-differentiation paths of differentiated pancreatic cells into functional β cells. Abbreviations: Aristaless related homeobox (ARX); DNA (cytosine-5)-methyltransferase 1 (DNMT1); Epidermal growth factor (EGF); Insulin promoter factor 1 (PDX1); Leukemia inhibitory factor (LIF); MAF BZIP Transcription Factor A (MAFA); Neurogenin-3 (NGN3); Neurogenic differentiation 1 (NEUROD1); the paired/homeodomain transcription factor (PAX4); Preadipocyte factor 1 (Pref1); TNF-like weak inducer of apoptosis, TNFSF12 (TWEAK); γ-Aminobutyric acid (GABA). Figure was created with BioRender http://www.biorender.com.
PMC9496933
cells-11-02813-g002.jpg
0.443636
69ca8e83c3974eb1b931bb713245200b
Extra pancreatic cell sources for generation of de novo β-cells. Abbreviations: Chromatin remodeling medium(CRM); Forkhead Box O1 (FOXO1); Glucagon-like peptide-1 (GLP1); Insulin Gene Enhancer Protein (ISL1); Insulin promoter factor 1 (PDX1); MAF BZIP Transcription Factor A (MAFA); MAF BZIP Transcription Factor B (MAFB); Neurogenin-3 (NGN3); Neurogenic differentiation 1 (NEUROD1); Homeobox protein Nkx2.2 (Nkx2.2); Homeobox protein Nkx6.1 (Nkx6.1); the paired/homeodomain transcription factor (PAX4); Paired box domain 6 (PAX6); TGFβ-induced factor homeobox 2 (TGIF2); 5-AZA 5-azacytidine. Combination of four small molecules (RA (Retinoic acid), A83-01 (a TGF-β receptor inhibitor), LDE225 (a hedgehog pathway inhibitor), and 2-phospho-L-ascorbic acid (pVc), and selective G9a and GLP inhibitor of histone methyltransferase (Bix-01294)) are small molecules that enhance generation of pancreatic progenitor-like cells. Figure was created with BioRender http://www.biorender.com.
PMC9496933
cells-11-02813-g003.jpg
0.468621
7df383ff56b54721a4a7405f5a066e8b
Flow Chart Indicating Each Phase of the Research Process. MES: Modified Enlight Suite.
PMC9497647
formative_v6i8e36912_fig1.jpg
0.551521
c7dbbc2619d948c8b9586fdf9017fb97
Banding patterns for PCR-SSCP analysis of a fragment of intron 1 (A) and a fragment containing exon 17 (B) of DGAT1. The homozygous genotypes and some heterozygous genotypes for each region are shown.
PMC9498694
genes-13-01670-g001.jpg
0.455668
903daaf547784917a6c63a824338f0be
Nucleotide sequence comparisons of the ovine DGAT1 variants. Three variants in intron 1 (a) and three variants in exon 17 (b) were detected. Only the nucleotides in the variable region are shown. Nucleotides with high levels of homology are colored, with black indicating 100% homology and blue indicating ≥50%. Positions of nucleotide differences are indicated.
PMC9498694
genes-13-01670-g002.jpg
0.541511
e67e65338247448fae9635acc6f43a9a
Synaptic plasticity in the CA1 hippocampal subfield of trained and sedentary mice. (a) Percentage population spike (PS) amplitude as a function of time after high-frequency stimulation (HFS), applied at time t = 15 (arrow), is shown in CTRLs (black line, n = 8 from N = 5), in B-trained (red line, n = 6 from N = 5), and in C-trained (green line, n = 7 from N = 5) mice slices. The insert shows representative recordings obtained from slices of each experimental group. The first curve in each group refers to the basal synaptic transmission and it was recorded prior to the HFS application, whereas the other curves represent the PS measured at 15, immediately after HF, and 65 min after HFS. (b) The PS amplitude values at min 5 (black bar), at min 15 (red bar), and at min 65 (green bar) from the HFS are shown for each experimental group. Bars in the plot are means ± SEM of values obtained from different slices. Note that a significant statistical difference was reported between trained and control groups at min 15 (CTRLs vs. B-trained, **** p < 0.0001; CTRLs vs. C-trained, ** p < 0.01; B-trained vs. C-trained, **** p < 0.0001; F = 19.92) and at min 65 (CTRLs vs. B-trained, * p < 0.05; CTRLs vs. C-trained, ** p < 0.01; B-trained vs. C-trained, **** p < 0.0001; F = 9.518).
PMC9498983
ijms-23-10388-g001.jpg
0.432026
d43787ac32a546819d2faf554ef1ddf5
Haematoxylin and eosin (H&E)-stained sections of cerebellar and hippocampal tissues from the different experimental groups. (a) Cerebellar tissue of both CTRL groups: molecular cell layer with small, scattered basket cells and stellate cells; large pyriform cells in the Purkinje cell layer with open-faced vesicular nuclei, eosinophilic cytoplasm and prominent Nissl’s granules; granular cell layer with small, highly stained cells. (b) Cerebellar tissue of the B-trained group: smaller Purkinje cells with deeply stained nuclei and eosinophilic cytoplasm. (c) Cerebellar tissue of the C-trained group: larger Purkinje cells with open-faced nuclei. (d) Hippocampal tissue of both CTRL groups: pyramidal neurons (black arrow) of uniform size and arrangement, with rounded central vesicular nucleus and prominent nucleolus. Presence of many glial cells (yellow arrow) between the neuronal processes in the molecular layer is evident. (e) Hippocampal tissue of the B-trained group: reduced pyramidal neurons with hyperchromatic nuclei and some areas without neurons (asterisks). (f) Hippocampal tissue of the C-trained group: numerous and very crowded pyramidal neurons (black arrow), basophilic cytoplasm, well-formed Nissl’s granules, and vesicular nuclei. (g) The number of Purkinje cells in the cerebellar tissue is shown for each experimental group (CTRLs vs. B-trained, **** p < 0.0001; B-trained vs. C-trained, **** p < 0.0001; F = 111.0). (h) The number of pyramidal neurons in the hippocampal CA1 region is shown for each experimental group (CTRLs vs. B-trained, **** p < 0.0001; B-trained vs. C-trained, **** p < 0.0001; F = 32.34). M: molecular cell layer; P: Purkinje cell layer; G: granular cell layer; W: medulla formed by white matter fibers. 20× images, scale bar represents 50 μm.
PMC9498983
ijms-23-10388-g002.jpg
0.470086
44fd9aa97baa4f23b14e4063d4cab3b9
Brain-derived neurotrophic factor (BDNF) and fibronectin type III domain-containing protein 5 (FNDC5) expression analysis in cerebellar and hippocampal tissues of trained and sedentary mice by immunohistochemistry. (a–c) Arrows indicate representative BDNF-positive cells in the cerebellum. (d) The highest number of BDNF-positive cells was found in the cerebellum of the C-trained group (**** p < 0.0001; F = 209.7). (e–g) Arrows indicate representative FNDC5-positive cells in the cerebellum. (h) The highest number of FNDC5-positive cells was found in the cerebellum of the C-trained group (**** p < 0.0001; F = 353.2). (i–k) Arrows indicate representative BDNF-positive cells in the hippocampus. (l) The highest number of BDNF-positive cells was found in the hippocampus of the C-trained group (**** p < 0.0001; F = 198.1). (m–o) Arrows indicate representative FNDC5-positive cells in the hippocampus. (p) The highest number of FNDC5-positive cells was found in the hippocampus of the C-trained group (**** p < 0.0001; F = 413.3). 20× images, scale bar represents 50 μm.
PMC9498983
ijms-23-10388-g003.jpg
0.430822
afe2385e71ed4f7fb4cd2991d3e3b7bb
Hematoxylin and eosin (H&E)-stained sections of muscle and bone tissues from the different experimental groups. (a–c) Polygonal and multinucleated skeletal muscle fibers and peripheral nuclei were evident in the muscle tissue of each experimental group. A complete organization of the fibers into fascicles was observed in the C-trained group. (g) The muscle fiber diameter is shown for each experimental group (**** p < 0.0001; F = 114.8). (d–f) Thicker and more voluminous trabecular bones were observed in the C-trained group. (h) The bone volume (BV/TV) is shown for each experimental group (**** p < 0.0001; F = 180.7). (i) The trabecular thickness (Tb.Th) is shown for each experimental group (**** p < 0.0001; F = 189.4). (j) The trabecular separations (Tb.S) is shown for each experimental group (**** p < 0.0001; F = 160.4). For 20× images, scale bar represents 50 μm.
PMC9498983
ijms-23-10388-g004.jpg
0.398743
60673e3f18d844c8aee356cddef95730
Myostatin, collagen I (COL-1) and fibronectin type III domain-containing protein 5 (FNDC5) expression analysis in muscle and bone tissues of trained and sedentary mice by immunohistochemistry. (a–c) Black arrows indicate representative myostatin-positive cells in the muscle tissue. (d) The highest number of myostatin-positive cells was found in the muscle of the CTRLs group (**** p < 0.0001; F = 334.9). (e–g) Black arrows indicate representative FNDC5-positive cells in the muscle tissue. (h) The highest number of FNDC5-positive cells was found in the muscle of the C-trained group (**** p < 0.0001; F = 249.3). (i–k) White arrows indicate representative COL-1-positive cells in the bone tissue. (l) The highest number of COL-1-positive cells was found in the bone of the C-trained group (**** p < 0.0001; F = 354.9). (m–o) White arrows indicate representative FNDC5-positive cells in the bone tissue. (p) The highest number of FNDC5-positive cells was found in the bone of the C-trained group (**** p < 0.0001; F = 307.0). For 20× images, scale bar represents 50 μm.
PMC9498983
ijms-23-10388-g005.jpg
0.481719
cd10ea065ca44c96971a4d4b160e39c4
Intubation rate. Forest plot of comparisons between APP and UC.
PMC9499134
gr1_lrg.jpg
0.531387
2de3c8631ffe4022be5ad4ca49ece689
Mortality. Forest plot of comparisons between APP and UC.
PMC9499134
gr2_lrg.jpg
0.45409
192f97900c5e4c1fa11d649a88f2d2c6
Macrographs of samples after adhesion strength measurement. a Pristine PDA and chitosan; (b) linked-PDA and chitosan
PMC9499904
10856_2022_6688_Fig10_HTML.jpg
0.587575
86bcedcadaf04685b12b05b405b984cf
The schematic diagram of the molecular structure of glutaraldehyde linked-PDA-chitosan coating
PMC9499904
10856_2022_6688_Fig11_HTML.jpg
0.430911
ae93c2fad85547cc82f0deee1a390a64
Coating steps
PMC9499904
10856_2022_6688_Fig1_HTML.jpg
0.49194
60e445012c214430a7b0ab9bab1221d6
Surveys of linked silane XPS outmost layer and O1s, C1s, and N1s binding energy levels
PMC9499904
10856_2022_6688_Fig2_HTML.jpg
0.483343
de933fbc254d4e429b43e410b8fd71a8
Binding energies of (a) O1s, (c) N1s, (e) C1s on the pristine-PDA surface and (b) O1s, (d) N1s, (f) C1s on the linked-PDA
PMC9499904
10856_2022_6688_Fig3_HTML.jpg
0.49815
d86282c5d5f84f9b9d8038e3a1af3e16
XPS surveys of linked (red line) and pristine (black line) PDA outmost layers
PMC9499904
10856_2022_6688_Fig4_HTML.jpg
0.423691
fb27d273721349b1bd440073f51a86a5
Binding energies of secondary amine (R-NH-R) and primary amine (R-NH2) bonds of chitosan film applied on the glutaraldehyde linked-PDA films
PMC9499904
10856_2022_6688_Fig5_HTML.jpg
0.441417
5e85a4ac1a9d497f808bc9dc8cb914f9
Layer by layer binding energies of the linked-PDA surface. Numbers represent the etching levels 0–7 which equal to 0, 10, 20, 30, 60, 80, and 120 s
PMC9499904
10856_2022_6688_Fig6_HTML.jpg
0.514825
9cdd3fc67dc24fae878d5cb009acecde
Binding energies of (a, b) O 1s, (c, d) C 1s (e, f) N 1s on the linked-PDA surface from (left) EL1 and (right) EL2
PMC9499904
10856_2022_6688_Fig7_HTML.jpg
0.424978
116c866a6ccd49aba536265c648b8ad1
a Contact angles and (b) surface properties of pristine PDA, linked-PDA and linked silane
PMC9499904
10856_2022_6688_Fig8_HTML.jpg
0.44323
2baa4543686442f6a0820f6449c3f6df
Adhesion strengths chitosan coatings on various interstitial layers coated (black and blue), linked (red) bare (green) Ni-free stainless steel
PMC9499904
10856_2022_6688_Fig9_HTML.jpg
0.443135
5f339fdc11bf407eada3bb61fb8634e8
Graphical abstract
PMC9499904
10856_2022_6688_Figa_HTML.jpg
0.46978
000b20575c224376b3b0901f49c8b400
Classification and molecular functions of circRNAs. The top of the figure shows that circRNAs are divided into 4 categories: (a) exonic circRNAs (ecircRNAs), (b) exon–intron circRNAs (EIciRNAs), (c) intronic circRNAs (ciRNAs), and (d) tRNA intronic circular RNAs (tricRNAs). The bottom of the figure shows four potential functions of circRNAs: (e) microRNA (miRNA) sponging: some circRNAs serve as efficient miRNA sponges, regulating the activity of miRNA target genes; (f) binding to proteins: circRNAs affect protein function directly; (g,h) regulation: some circRNAs regulate transcription and encode peptides or proteins if they have internal ribosome entry sites (IRESs).
PMC9500598
ijms-23-10443-g001.jpg
0.440502
46d9cd3a54c04c99a03164abf3e0775b
Signal transduction through seven age−related signaling pathways. (a) IIS signaling pathway; (b) PI3K−AKT signaling pathway; (c) mTOR signaling pathway; (d) AMPK signaling pathway; (e) FOXO signaling pathway; (f) p53 signaling pathway; (g) NF−κB signaling pathway. The blue squares indicate the core factors in each pathway, while the gray squares indicate the upstream or downstream targets.
PMC9500598
ijms-23-10443-g002.jpg
0.451874
a3c0952366824bff873e64127fa80d31
An overview of circRNAs involved in the regulation of age-related signaling pathways. CircRNA/miRNA indicates circRNAs that act as miRNA sponges, circRNA/protein indicates circRNAs that directly bind to proteins, and circRNA/mRNA indicates circRNAs that regulate the transcription of mRNA.
PMC9500598
ijms-23-10443-g003.jpg
0.438615
18207fe6a1764c958eb1b7e6400bf273
Molecular docking diagram of ALA with 5-LO, HRH1, CBG, mAChR M1, mAChR M3, PDE4 B, and PGD2. 5-LO, 5-lipoxygenase; HRH1, histamine H1 receptor; CBG, corticosteroid-binding globulin; mAChR M1, M1 muscarinic acetylcholine receptor; mAChR M3, M3 muscarinic acetylcholine receptor; PDE4B, phosphodiesterase 4B; PGD2, prostaglandin D2.
PMC9501164
molecules-27-05893-g001.jpg
0.432148
b28f7d8190744d3caecba211fb89338b
Effect of ALA on OVA-induced AR in mice. The numbers of sneezing (A) and rubbing actions (B) of mice were counted for 30 min immediately after the last intranasal challenge. (C) The level of OVA-sIgE in serum were measured by enzyme-linked immunosorbent assay (ELISA). The HE (D) and PAS (E) staining were used to observe the histopathological changes in nasal mucosa samples of mice. Between-group comparisons were performed using one-way ANOVA coupled with LSD t-test (equal variances assumed) or Tamhane’s T2 test (equal variances not assumed). Data are expressed as mean ± SD; n = 10; * p < 0.05, ** p < 0.01 versus AR model. Dex, dexamethasone; ALA-L, low dose of α-linolenic acid; ALA-H, high dose of α-linolenic acid.
PMC9501164
molecules-27-05893-g002.jpg
0.556732
109dc1431152452a86af9049c5a23953
Effect of ALA on the mRNA expression levels of IL-6 (A), IL-1β (B), IFN-γ (C), and IL-4 (D) in the nasal mucosa of AR mice. Between-group comparisons were performed using one-way ANOVA coupled with LSD t-test (equal variances assumed) or Tamhane’s T2 test (equal variances not assumed). Data are expressed as mean ± SD; n = 4; ** p < 0.01 versus AR model. Dex, dexamethasone; ALA-L, low dose of α-linolenic acid; ALA-H, high dose of α-linolenic acid.
PMC9501164
molecules-27-05893-g003.jpg
0.420431
b844bf1ca0b74b4c8543a8f0e4716e5f
Effect of ALA on the percentages of CD3+CD4+IFN-γ+ Th1 and CD3+CD4+IL-4+ Th2 cells in the spleen of AR mice. Representative dot plots of CD3+CD4+IFN-γ+ Th1 (in the upper left quadrant) and CD3+CD4+IL-4+ Th2 cells (in the lower right quadrant) (A), and the percentages of CD3+CD4+IFN-γ+ Th1 cells (B) and Th2 cells (C) in the SMCs separated from the spleen samples are analyzed via flow cytometry. Between-group comparisons were performed using one-way ANOVA coupled with LSD t-test (equal variances assumed) or Tamhane’s T2 test (equal variances not assumed). Data are expressed as mean ± SD; n = 3; * p < 0.05, ** p < 0.01 versus AR model. Dex, dexamethasone; ALA-L, low dose of α-linolenic acid; ALA-H, high dose of α-linolenic acid.
PMC9501164
molecules-27-05893-g004.jpg
0.551929
7e56ddcb639546f3a83fa457bb5e5a6a
Effect of ALA on the mRNA expression levels of T-bet (A), GATA3 (B), STAT1 (C), and STAT6 (D) in the nasal mucosa in AR mice. Between-group comparisons were performed using one-way ANOVA coupled with LSD t-test (equal variances assumed) or Tamhane’s T2 test (equal variances not assumed). Data are expressed as mean ± SD; n = 4; * p < 0.05, ** p < 0.01 versus AR model. Dex, dexamethasone; ALA-L, low dose of α-linolenic acid; ALA-H, high dose of α-linolenic acid.
PMC9501164
molecules-27-05893-g005.jpg
0.418531
bcf6a70fdc1a4063a23e088b34001978
Flow chart of the OVA-induced AR model and ALA administration.
PMC9501164
molecules-27-05893-g006.jpg
0.499155
160b5bbd7d7e4880bf5b89757fe76803
Type and number of pathogens of which chickens were seropositive.
PMC9501380
vetsci-09-00503-g001.jpg
0.420914
fc992900bc1b41b28d8bbccc69672a28
Illustrative interictal EEG of patient #4, showing right posterior temporal spikes (traces #7, 8 at 1 and 5 s on double banana montage).
PMC9501736
hrp-0095-0286-g01.jpg
0.470549
f05abbf310674a869551936e5296d5f6
Performance evaluation of RF model with different classification thresholds, based on test set prediction. The test set consists of 314 instances of which 98 active.
PMC9502400
ijms-23-10653-g001.jpg
0.43914
35920658dff44a01a5fd38ed5c800134
Analysis of the MD simulations of the different Cdk5-CPD1 (A) and Cdk5-CPD4 (B) complexes.
PMC9502400
ijms-23-10653-g002.jpg
0.509991
674fa80180c245cbbe64c7dcaceb25b7
Minimized average structures of CPD1 (orange) in complex with Cdk5. The two different binding modes represented by (A) cluster 1 and (B) cluster 2 are shown. The protein residues surrounding the ligand, constituting the binding site, are shown as grey sticks, whereas hydrogen bonds are shown as black dashed lines.
PMC9502400
ijms-23-10653-g003.jpg
0.519223
a111cd8e983d45509e027907abeedcbe
Minimized average structures of CPD4 (green) in complex with Cdk5. The protein residues surrounding the ligand, constituting the binding site, are shown as grey sticks, whereas hydrogen bonds are shown as black dashed lines.
PMC9502400
ijms-23-10653-g004.jpg
0.421712
6289ece591b34923a60f95974143bef6
Workflow of the strategy adopted.
PMC9503099
pharmaceutics-14-01818-g001.jpg
0.392269
18042937bd6a48c7940fbd294366b618
Validation of docking technique and parameters via the redocking approach against the co-crystal structure of PBP2a from S. aureus (3ZFZ). (a) the superimposition showed that the top-five phenolics (chroman-4-one (green), epicatechin gallate (purple), epigallocatechin 4-benzylthioether (brown), propan-2-one (pink), silicristin (black) and amoxicillin (blue)) could achieve the same orientation with the native inhibitor (red) of 3ZFZ with a low RMSD value of <1. (b,c) showed the superimposition of silicristin (phenolic with the highest docking score) and amoxicillin (antibiotic with the highest docking score) with the native inhibitor of 3ZFZ, displaying the amino acid at the active site (located 60 Å away from the allosteric site) and the active site gatekeeper residue (Tyr 446) [16].
PMC9503099
pharmaceutics-14-01818-g002.jpg
0.423196
eb05669b1af74fa9a49c5097f4938cbf
(a) Superimposition at the allosteric site of the co-crystal structure of PBP2a from S. aureus (3ZFZ), demonstrating the capability of the top-five phenolics (chroman-4-one (green), epicatechin gallate (purple), epigallocatechin 4-benzylthioether (brown), propan-2-one (pink), silicristin (black) and amoxicillin (blue)) to achieve the same orientation with the native inhibitor of 3ZFZ (red) with a low RMSD value of <1. (b,c) showed the superimposition of epicatechin gallate (phenolic with the highest docking score) and amoxicillin (antibiotic with the highest docking score) with the native inhibitor of 3ZFZ, displaying the amino acid at the allosteric site of PBP2a of S. aureus (located 60 Å away from the active site) [16].
PMC9503099
pharmaceutics-14-01818-g003.jpg
0.479387
4262fe2d98b143d98df89fb81b8d3790
Molecular fingerprinting of the top-twenty phenolics. Compounds of the same colour and cluster were more similar than compounds of different colours and clusters. The top-twenty compounds were structurally different from the antibiotics which had the same colour (Green). Phenolics with similarity scores of zero and belonging to the same clusters were conformers, and in selecting the top five (highlighted in red colour), the conformer with the highest binding affinity that did not violate the Lipinski violation was selected among the top five. While avoiding the top-five phenolics that were conformers of each another, one common moiety that the top-five-ranked compounds had was resorcinol. Two (ZINC38337968 and ZINC03978503) of the top-five phenolics had a pyrogallol structure and from the cluster chart, these two compounds appeared to be the most similar among the top-five compounds. Only one (ZINC03978503) of the top-five phenolics had the catechol group. The top-five compounds all had a synthetic score of less than five.
PMC9503099
pharmaceutics-14-01818-g004.jpg
0.423029
90833c0af4724618beb5a18f01c3da92
Comparative root-mean-squared deviation (RMSD) plots of alpha-carbon, the top-five phenolics, and amoxicillin against the active site of PBP2a of S. aureus over a 120 ns MD simulation period.
PMC9503099
pharmaceutics-14-01818-g005.jpg