id
stringlengths
36
36
status
stringclasses
2 values
inserted_at
timestamp[us]date
2025-04-29 14:36:04
2025-04-29 14:36:04
updated_at
timestamp[us]date
2025-04-29 14:36:04
2025-05-27 14:00:52
_server_id
stringlengths
36
36
text
stringlengths
0
14k
links
stringlengths
4
1.19k
span_label.responses
listlengths
1
1
span_label.responses.users
listlengths
1
1
span_label.responses.status
listlengths
1
1
assess_ner.responses
listlengths
1
1
assess_ner.responses.users
listlengths
1
1
assess_ner.responses.status
listlengths
1
1
assess_nel.responses
listlengths
1
1
assess_nel.responses.users
listlengths
1
1
assess_nel.responses.status
listlengths
1
1
comments.responses
listlengths
1
1
comments.responses.users
listlengths
1
1
comments.responses.status
listlengths
1
1
span_label.suggestion
listlengths
0
69
span_label.suggestion.agent
null
span_label.suggestion.score
null
4643ee17-dd2c-487f-9287-e084fdd4fe2e
pending
2025-04-29T14:36:04.699556
2025-04-29T14:36:04.699556
3aee57ee-8960-45f6-94a8-99b048f5a64f
AbstractNatural competence for transformation is a primary mode of horizontal gene transfer (HGT). Competent bacteria are able to absorb free DNA from their surroundings and exchange this DNA against pieces of their own genome when sufficiently homologous. And while it is known that transformation contributes to evolution and pathogen emergence in bacteria, there are still questions regarding the general prevalence of non-degraded DNA with sufficient coding capacity. In this context, we previously showed that the naturally competent bacteriumVibrio choleraeuses its type VI secretion system (T6SS) to actively acquire DNA from non-kin neighbors under chitin-colonizing conditions. We therefore sought to further explore the role of the T6SS in acquiring DNA, the condition of the DNA released through T6SS-mediated killing versus passive cell lysis, and the extent of the transfers that occur due to these conditions. To do this, we herein measured the frequency and the extent of genetic exchanges in bacterial co-cultures on competence-inducing chitin under various DNA-acquisition conditions. We show that competentV. choleraestrains acquire DNA fragments with an average and maximum length exceeding 50 kbp and 150 kbp, respectively, and that the T6SS is of prime importance for such HGT events. Collectively, our data support the notion that the environmental lifestyle ofV. choleraefosters HGT and that the coding capacity of the exchanged genetic material is sufficient to significantly accelerate bacterial evolution.Significance StatementDNA shuffled from one organism to another in an inheritable manner is a common feature of prokaryotes. It is a significant mechanism by which bacteria acquire new phenotypes, for example by first absorbing foreign DNA and then recombining it into their genome. In this study, we show the remarkable extent of the exchanged genetic material, frequently exceeding 150 genes in a seemingly single transfer event, inVibrio cholerae. We also show that to best preserve its length and quality, bacteria mainly acquire this DNA by killing adjacent, healthy neighbors then immediately absorbing the released DNA before it can be degraded. These new insights into this prey-killing DNA acquisition process shed light on how bacterial species evolve in the wild.
None
[ [] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[]
null
null
5923f8c4-9490-4f29-99bd-cc76b565720a
pending
2025-04-29T14:36:04.699562
2025-04-29T14:36:04.699562
14c1a257-f7eb-4801-9b1a-225d422cfbe4
The T6SS fosters horizontal co-transfer events encompassing two selective markers To compare the absorption of T6SS-mediated prey-derived DNA as opposed to environmental DNA (released through, for example, random lysis), we first scored the transformability of T6SS-positive (wild-type [WT] predator) and T6SS-negative (acceptor) V. cholerae strains, which would allow us to directly measure the contribution of the T6SS on gene uptake.These two strains were co-cultured with non-kin prey (donor) bacteria that were all derived from the environmental isolate Sa5Y (Keymer et al., 2007;Miller et al., 2007;Borgeaud et al., 2015;Matthey et al., 2018) and contained two antibiotic resistance genes in their genomes: 1) An aph cassette (Kan R ), which was integrated in the vipA gene on the small chromosome (chr 2); and 2) a cat cassette (Cm R ), which was inserted at variable distances from the aph cassette on the same chromosome or, alternatively, on the large chromosome (chr 1).As shown in Figure 1, the WT predator strain efficiently absorbed and integrated the prey-released resistance cassettes (aph or cat), while the transformation efficiency for the T6SS-defective acceptor strain was significantly reduced (by 97.8% and 99.2% for aph and cat, respectively) (Figure 1A).Moreover, comparable frequencies were observed for both selective markers, suggesting that their acquisition does not significantly affect the strains' fitness under nonselective conditions.We tested whether these transfer events were indeed competence-mediated and not based on other modes of HGT using a strain with a competence-related DNA import deficiency in that it lacked the competence protein ComEA that reels external DNA into the periplasm (Seitz et al., 2014).This comEA-minus strain was never transformed under these predator-prey coculture conditions, confirming that the gene transfer did depend entirely on natural competence. Next, we scored the frequencies of transformants that had adopted resistance against both antibiotics, which would show the possibility of two transformation events or the transfer of a large piece of DNA (indicated by the distance between the two genes on the same chromosome).These transformations occurred, as expected, at lower rates compared to single-resistant clones and were mostly below the limit of detection for the T6SS-minus acceptor strain (Figure 1B).Interestingly, we observed a gradual decrease in the frequencies the further the two resistance genes were apart from each other on the same chromosome, while a sharp drop occurred in the number of recovered transformants when the two resistance genes were carried on the two separate prey chromosomes (Figure 1B).While the latter scenario unambiguously requires at least two separate DNA-uptake events, the former, in which the resistance markers are carried in cis, could reflect a mix between single and multiple DNA absorption and integration events.When purified genomic DNA was instead provided as the transforming material to simplify the experiment and provide measurable results for all conditions, the in cis double-resistance acquisition efficiencies reached a comparable range to the in trans efficiencies when the two resistance genes were separated by at least 100 kbp.This suggested that the more efficient transformations of less than 100 kbp likely often occurred through a single acquisition (Figure 1C).Furthermore, the WT predator and T6SS-minus acceptor behaved similarly when purified DNA was provided, which makes sense as the need for active DNA release through neighbor predation was eliminated.Based on these data and the fact that the double-acquisition rates for the T6SS-minus acceptor strain were mostly below the detection limit in the prey scenario (Figure 1B), we hypothesized that neighbor predation might foster the transfer of long DNA stretches, which frequently exceeded 50 kbp and therefore carry significant coding capacity.Moreover, the significantly lower double-acquisition rates when both cassettes are located in trans (e.g., on two different chromosomes) for the co-culturing conditions compared to the supplementation of purified gDNA (Figure 1-figure supplement 1) led us speculate that long DNA stretches might be released from the killed prey thereby saturating the system against uptake of additional fragments.
None
[ [] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[]
null
null
a1ebcba6-ea6d-4bfc-a69b-09c6f38ffa25
completed
2025-04-29T14:36:04.699569
2025-05-27T14:00:46.015469
81d03f73-0cf3-4b33-9ee4-0d81d1e27d8f
Cell-cell communication in the brain is controlled by multiple mechanisms, including proteolysis. Membrane-bound proteases generate signaling molecules from membrane-bound precursor proteins and control the length and function of cell surface membrane proteins. These proteases belong to different families, including members of the "a disintegrin and metalloprotease" (ADAM), the beta-site amyloid precursor protein cleaving enzymes (BACE), membrane-type matrix metalloproteases (MT-MMP) and rhomboids. Some of these proteases, in particular ADAM10 and BACE1 have been shown to be essential not only for the correct development of the mammalian brain, but also for myelination and maintaining neuronal connections in the adult nervous system. Additionally, these proteases are considered as drug targets for brain diseases, including Alzheimer's disease (AD), schizophrenia and cancer. Despite their biomedical relevance, the molecular functions of these proteases in the brain have not been explored in much detail, as little was known about their substrates. This has changed with the recent development of novel proteomic methods which allow to identify substrates of membrane-bound proteases from cultured cells, primary neurons and other primary brain cells and even in vivo from minute amounts of mouse cerebrospinal fluid (CSF). This review summarizes the recent advances and highlights the strengths of the individual proteomic methods. Finally, using the example of the Alzheimer-related proteases BACE1, ADAM10 and γ-secretase, as well as ADAM17 and signal peptide peptidase like 3 (SPPL3), we illustrate how substrate identification with novel methods is instrumental in elucidating broad physiological functions of these proteases in the brain and other organs.
<li> <b>brain:</b> brain (UBERONParcellation)<li> <b>cerebrospinal fluid:</b> Other (UBERONParcellation)<li> <b>mammalian:</b> Other (species)<li> <b>proteomic:</b> Other (technique)<li> <b>in vivo:</b> inVivo (preparationType)
[ [ { "end": 36, "label": "UBERONParcellation", "start": 31 }, { "end": 651, "label": "UBERONParcellation", "start": 646 }, { "end": 814, "label": "UBERONParcellation", "start": 809 }, { "end": 978, "label": "UBERONParcellation", "start": 973 }, { "end": 1257, "label": "UBERONParcellation", "start": 1252 }, { "end": 1756, "label": "UBERONParcellation", "start": 1751 }, { "end": 1329, "label": "UBERONParcellation", "start": 1310 }, { "end": 645, "label": "species", "start": 636 }, { "end": 1125, "label": "technique", "start": 1116 }, { "end": 1436, "label": "technique", "start": 1427 }, { "end": 1280, "label": "preparationType", "start": 1273 }, { "end": 742, "label": "UBERONParcellation", "start": 728 }, { "end": 1309, "label": "species", "start": 1304 }, { "end": 1334, "label": "UBERONParcellation", "start": 1331 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "nervous system: Other (UBERONParcellation)\nmouse: musMusculus (species)\n\r\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 36, "label": "UBERONParcellation", "start": 31 }, { "end": 651, "label": "UBERONParcellation", "start": 646 }, { "end": 814, "label": "UBERONParcellation", "start": 809 }, { "end": 978, "label": "UBERONParcellation", "start": 973 }, { "end": 1257, "label": "UBERONParcellation", "start": 1252 }, { "end": 1756, "label": "UBERONParcellation", "start": 1751 }, { "end": 1329, "label": "UBERONParcellation", "start": 1310 }, { "end": 645, "label": "species", "start": 636 }, { "end": 1125, "label": "technique", "start": 1116 }, { "end": 1436, "label": "technique", "start": 1427 }, { "end": 1280, "label": "preparationType", "start": 1273 } ]
null
null
1ef9db9c-b29e-42f7-8c25-2258adae2418
completed
2025-04-29T14:36:04.699575
2025-05-27T14:00:46.117245
530ba6dd-d04e-4259-9964-627ae911cd13
The metalloprotease ADAM17 is a homolog of ADAM10.When activated, it can act as an additional α-secretase and may reduce Aβ levels (Caccamo et al., 2006).ADAM17 is also known as TNF-α converting enzyme (TACE) and was the first sheddase to be identified, as the enzyme responsible for releasing the soluble ectodomain of TNF (Moss et al., 1997).ADAM17 plays a crucial role in cellcell communication, being able to release not only TNF, but also several other transmembrane proteins, including cytokines, adhesion molecules, receptors and growth factors.ADAM17deficient mice display several abnormalities at birth, including open eyes and skin defects, that phenocopy mice lacking EGF receptor or a number of its ligands, which are known substrates of ADAM17 (Blobel, 2005).Most ADAM17 substrates have been identified through candidate approaches (Qian et al., 2016).Proteomics has not been extensively used to uncover ADAM17 substrates.However, a few secretome analyses have been performed which searched for transmembrane proteins undergoing shedding in response to specific stimuli, such as lipopolysaccharide (LPS) and 12-O-tetradecanoylphorbol 13-acetate/Phorbol 12-myristate 13-acetate (TPA/PMA), which are known to also activate ADAM17.One study identified a number of transmembrane proteins, such as CSF1R and Sema4D, that are shed by metalloproteinases in response to LPS or TPA in macrophage-like cells (Shirakabe et al., 2014).In order to investigate proteomic changes induced by LPS in macrophages, one study used a method similar to SPECS (Eichelbaum and Krijgsveld, 2014), whereas another group performed secretome analysis from a small number of cells cultured without serum (Meissner and Mann, 2014).Together with a list of known substrates of ADAM17, these studies identified a number of proteins that can also potentially be cleaved by ADAM17.However, these proteins were not validated as ADAM17 substrates so far.Another study specifically investigated changes in the secretome of ADAM17 -/-mouse embryonic fibroblasts (MEFs) by using SILAC or label-free based approaches (Kawahara et al., 2014).Label free secretome analysis identified 179 proteins, which were significantly down-regulated in ADAM17-deficient MEF cell supernatants.Transmembrane proteins, including TNFR2 and syndecan-4, were strongly reduced in the secretome of ADAM17 -/-MEFs, suggesting that they are ADAM17 substrates.Furthermore, a proteomic study of ADAM17deficient epidermis was performed which showed pronounced changes in a number of proteins involved in barrier formation, including transglutaminases, involucrin, filaggrin and filaggrin-2 (Tholen et al., 2016). Functions of ADAM17 in the brain have been little explored so far and no proteomic study has as yet been done to address this issue specifically.Yet, the role of ADAM17 in inflammation suggests that ADAM17 is also involved in various neuroinflammatory conditions.γ-Secretase γ-secretase has been a major drug target in AD in the past.It is a protease complex that cleaves transmembrane type 1 proteins within or close to their transmembrane domain.While γ-secretase only directly sheds the ectodomain of a single, naturally short substrate (Laurent et al., 2015), it typically requires shedding of its substrates in order to cleave them within the transmembrane domain.In 2008, a proteomic study was performed to identify γ-secretase substrates in HeLa cells (Hemming et al., 2008).Therefore, cells were differentially labeled with the SILAC method and treated with the γ-secretase inhibitor DAPT or DMSO as a control.Since γ-secretase cleavage usually requires previous shedding by other proteases (Struhl and Adachi, 2000), such as BACE1 or ADAM10, substrates are commonly identified by an accumulation of the CTF upon γ-secretase inhibition.Hence, SDS-PAGE of membrane fractions was applied for proteomic γ-secretase substrate profiling to separate CTFs from full-length proteins (Hemming et al., 2008).The gels were cut into 10 slices and in-gel digestion was performed with trypsin.Relative quantification between DAPT and DMSO was done separately for each fraction.CTFs with a DAPT/DMSO intensity ratio larger than 1.86 were considered as enriched.Overall, CTFs of 13 proteins, among them APP and APLP2 showed enrichment for DAPT treatment.Very likely, this approach missed to identify more γ-secretase substrates as CTFs of proteins with a short cytoplasmic domain are hard to quantify.Additionally, low molecular weight peptides and proteins offer just few tryptic peptides and are often lost during washing steps of the in-gel digestion protocol (Klein et al., 2007;Müller et al., 2010).
<li> <b>brain:</b> brain (UBERONParcellation)<li> <b>macrophages:</b> Other (species)
[ [ { "end": 2690, "label": "UBERONParcellation", "start": 2685 }, { "end": 572, "label": "species", "start": 568 }, { "end": 670, "label": "species", "start": 666 }, { "end": 2013, "label": "species", "start": 2008 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "mice: musMusculus (species)\nmouse: musMusculus (species)\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 2690, "label": "UBERONParcellation", "start": 2685 }, { "end": 1507, "label": "species", "start": 1496 } ]
null
null
8cd4bbe1-231c-4300-b594-26c6a36c3abc
pending
2025-04-29T14:36:04.699581
2025-04-29T14:36:04.699581
f686455a-5c75-462f-8d1d-6f7354c2e05a
AbstractThe introduction of mild cognitive impairment (MCI) as a diagnostic category adds to the challenges of diagnosing Alzheimer’s Disease (AD). No single marker has been proven to accurately categorize patients into their respective diagnostic groups. Thus, previous studies have attempted to develop fused predictors of AD and MCI. These studies have two main limitations. Most do not simultaneously consider all diagnostic categories and provide suboptimal fused representations using the same set of modalities for prediction of all classes. In this work, we present a combined framework, cascaded multiview canonical correlation (CaMCCo), for fusion and cascaded classification that incorporates all diagnostic categories and optimizes classification by selectively combining a subset of modalities at each level of the cascade. CaMCCo is evaluated on a data cohort comprising 149 patients for whom neurophysiological, neuroimaging, proteomic and genomic data were available. Results suggest that fusion of select modalities for each classification task outperforms (mean AUC = 0.92) fusion of all modalities (mean AUC = 0.54) and individual modalities (mean AUC = 0.90, 0.53, 0.71, 0.73, 0.62, 0.68). In addition, CaMCCo outperforms all other multi-class classification methods for MCI prediction (PPV: 0.80 vs. 0.67, 0.63).
None
[ [] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ "\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[]
null
null
2743b16a-f4d4-43fe-ac39-e8ee4f934d1f
completed
2025-04-29T14:36:04.699587
2025-05-27T14:00:46.207536
d0e5b7c9-0bf1-49c7-a75c-058d32e724a9
Performance measures used to evaluate each classification task include: accuracy (ACC), balanced accuracy (BACC) 37 , area under the receiver operating characteristic curve (AUC) 38 , sensitivity (SEN), specificity (SPE) and positive predictive value (PPV).The definitions and descriptions of each of these metrics are provided in Table 8 in the Appendix.CaMCCO Model.Class groupings and modalities selected for fusion at each level of the cascaded classification design employed by CaMCCo (Fig. 1) was determined experimentally on the training set.One-vs-all (AD vs. all, MCI vs. all, HC vs. all) classifiers were constructed and evaluated independently for each considered modality.The task that most consistently resulted in the highest AUC across all modalities served as the first level of the cascade so as to reduce error propagation.Among AD, MCI and HC, the remaining classes were assigned to the second level of the cascade. For every classification task within the cascade, each modality was ranked based on the AUC it achieved across iterations and cross validation folds within the training set.The n highest performing modalities were fused via sMVCCA, where n was varied from 2 to 6 (total number of considered modalities).The n modalities, which in combination, provided the highest training AUC were selected. Comparative Strategies.CaMCCo represents a framework () composed of multiple modules corresponding to modality selection (), multimodal data fusion ( ), and multiclass classification ().Accordingly, the comparative strategies against which we evaluate CaMCCo involve systematically replacing the method used for one or more of these modules with an alternative strategy.Table 5 lists the notation for each of these strategies and provides a short description. Single Modality and Multimodality Approaches.Each modality was evaluated using a single modality framework ( MRI ,  PET , CSF  , PP  , APOE  ,  ADAS ) consisting of cascaded classification ( CAS ) to ensure fair comparison with CaMCCo.In addition, we compared classification performance of CaMCCo with that of a cascaded classification model where all modalities were fused at each level of the cascade ( ALL ). Principal Component Analysis for Data Fusion.Principal Component Analysis (PCA) is a dimensionality reduction method which projects input data onto an alternate subspace defined by orthogonal basis vectors which capture the direction of variance in the data.Consider a high dimensional, concatenated multimodal data matrix where K refers to the number of modalities, n refers to the number of subjects, and M k refers to the number of features in modality k.
<li> <b>MRI:</b> magneticResonanceImaging (technique)<li> <b>PET:</b> positronEmissionTomography (technique)
[ [ { "end": 1904, "label": "technique", "start": 1901 }, { "end": 1912, "label": "technique", "start": 1909 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 1904, "label": "technique", "start": 1901 }, { "end": 1912, "label": "technique", "start": 1909 } ]
null
null
6c5e1d56-6b1e-4ce7-b135-1e5cd1fc546a
completed
2025-04-29T14:36:04.699594
2025-05-27T14:00:46.360524
cd8a8750-c968-4f61-9881-96b1ace0b718
AbstractThis study examines the electrical properties of isolated brain microtubules (MTs), which are long hollow cylinders assembled from αβ-tubulin dimers that form cytoskeletal structures engaged in several functions. MTs are implicated in sensory functions in cilia and flagella and cellular activities that range from cell motility, vesicular traffic, and neuronal processes to cell division in the centrosomes and centrioles. We determined the electrical properties of the MTs with the loose patch clamp technique in either the presence or absence of the MT stabilizer Paclitaxel. We observed electrical oscillations at different holding potentials that responded accordingly in amplitude and polarity. At zero mV in symmetrical ionic conditions, a single MT radiated an electrical power of 10–17 W. The spectral analysis of the time records disclosed a single fundamental peak at 39 Hz in the Paclitaxel-stabilized MTs. However, a richer oscillatory response and two mean conductances were observed in the non-Paclitaxel MTs. The findings evidence that the brain MTs are electrical oscillators that behave as "ionic-based" transistors to generate, propagate, and amplify electrical signals.
<li> <b>brain:</b> brain (UBERONParcellation)<li> <b>microtubules:</b> Other (UBERONParcellation)<li> <b>patch clamp:</b> patchClamp (technique)
[ [ { "end": 71, "label": "UBERONParcellation", "start": 66 }, { "end": 1069, "label": "UBERONParcellation", "start": 1064 }, { "end": 509, "label": "technique", "start": 498 }, { "end": 367, "label": "UBERONParcellation", "start": 361 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "neuron: Other (UBERONParcellation)" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 71, "label": "UBERONParcellation", "start": 66 }, { "end": 1069, "label": "UBERONParcellation", "start": 1064 }, { "end": 84, "label": "UBERONParcellation", "start": 72 }, { "end": 509, "label": "technique", "start": 498 } ]
null
null
aa61c877-9951-431d-bd1c-0ab3c5dc0325
completed
2025-04-29T14:36:04.699600
2025-05-27T14:00:46.857919
28240665-97f6-4642-b7a0-de32dcce186f
with brain MT bundles 8 , in contrast to the high seal resistances usually obtained with MT sheets 7,8 .Isolated MTs formed in the absence of Paclitaxel were initially voltage-clamped at zero mV, showing no electrical activity in any successful experiments (n = 14).However, under these conditions, the variance of the current at 0 mV was statistically different from that of the pipette in solution (solution vs. MT-attached: 1.17 ± 0.15 pA 2 , n = 6, vs. 2.27 ± 0.49 pA 2 , n = 6, p = 0.04) that was concomitant with the presence of oscillatory peak frequencies (Fig. 1C).MTs displayed spontaneous, self-sustained electrical oscillations in 69% of cases (20/29) in direct response to the magnitude and polarity of the electrical stimulus (Figs. 1D and2A).The most prominent frequency peaks Currents elicited by different holding potentials obtained with the pipette in solution before (Red) and after (Black) attachment to an isolated MT.Bottom.Frequency spectra at 0 mV for the pipette in solution (Black) and after MT apposition (Red).Please, note that notch filtering was applied to eliminate contaminating line frequencies at 50 and 100 Hz. (D) Electrical recordings from an isolated MT at different holding potentials (± 100 mV) as indicated.Expanded tracings on the Right show electrical oscillations of regions numbered "1" through "5".Applied voltages represented the driving potentials at the patch clamp amplifier. with the simplest oscillations observed were at 43-47 Hz and 90 Hz at negative holding potentials.At positive holding potential, only 43-47 Hz was observed, at least at the beginning of the experiments.These oscillations showed monoperiodic limit cycles, as shown in the three-dimensional phase portrait (Fig. 2B).At zero mV, only the 50 Hz line interference frequency was present.Current-to-voltage relationship and frequencies of non-Paclitaxel stabilized isolated microtubules.The mean oscillatory currents were linear concerning the corrected holding potential (Fig. 4A,B), showing at least two different "high" and "low" conductances of 103.0 ± 3.5 nS (n = 3) and 11.3 ± 1.2 nS (n = 4), respectively.Freedman et al. 12 calculated single MT current-voltage relationships from a cation conductance circuit model with a conductance in the order of 10 nS.Three-dimensional phase-space portraits showing monoperiodic limit cycles were observed for both conductance levels (Fig. 4C). Fundamental frequencies were seen at approximately 7, 13, 28, 39, 47, 90, 140, and 147 Hz (Fig. 5).However, not all the frequencies were prominent in experiments with low and high conductance.The 13 and 147 Hz were observed only in the high conductance experiments, while the 140 Hz was noticeable in the low conductance experiments. A richer oscillatory behavior was observed when the same holding potential was applied for several minutes (Fig. 6).In these instances, the oscillation patterns observed were variable in the time with low frequencies periods alternating with high frequencies periods, making evident a more coherent activity at different fundamental frequencies (Fig. 6) for positive and negative potentials, respectively.
<li> <b>brain:</b> brain (UBERONParcellation)<li> <b>patch clamp:</b> patchClamp (technique)
[ [ { "end": 10, "label": "UBERONParcellation", "start": 5 }, { "end": 1415, "label": "technique", "start": 1404 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 10, "label": "UBERONParcellation", "start": 5 }, { "end": 1415, "label": "technique", "start": 1404 } ]
null
null
71a313fe-561d-4c3e-8a6d-39df1bdb915b
completed
2025-04-29T14:36:04.699607
2025-05-27T14:00:46.949744
f6ecfc90-edc3-44ff-b74c-06e431c481aa
AbstractBackgroundChromosome 17q21.31 contains a common inversion polymorphism of approximately 900 kb in populations with European ancestry. Two divergentMAPThaplotypes, H1 and H2 are described with distinct linkage disequilibrium patterns across the region reflecting the inversion status at this locus. TheMAPTH1 haplotype has been associated with progressive supranuclear palsy, corticobasal degeneration, Parkinson’s disease and Alzheimer’s disease, while the H2 is linked to recurrent deletion events associated with the 17q21.31 microdeletion syndrome, a disease characterized by developmental delay and learning disability.ResultsIn this study, we investigate the effect of the inversion on the expression of genes in the 17q21.31 region. We find the expression of several genes in and at the borders of the inversion to be affected; specific either to whole blood or different regions of the human brain. The H1 haplotype was found to be associated with an increased expression ofLRRC37A4,PLEKH1MandMAPT. In contrast, a decreased expression ofMGC57346,LRRC37AandCRHR1was associated with H1.ConclusionsStudies thus far have focused on the expression ofMAPTin the inversion region. However, our results show that the inversion status affects expression of other genes in the 17q21.31 region as well. Given the link between the inversion status and different neurological diseases, these genes may also be involved in disease pathology, possibly in a tissue-specific manner.
<li> <b>brain:</b> brain (UBERONParcellation)
[ [ { "end": 912, "label": "UBERONParcellation", "start": 907 }, { "end": 906, "label": "species", "start": 901 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "human: homoSapiens (species)" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 912, "label": "UBERONParcellation", "start": 907 } ]
null
null
839799d1-a64d-444e-bc96-7db92d85ca89
completed
2025-04-29T14:36:04.699613
2025-05-27T14:00:47.054146
7bb7711f-260d-4798-aaf1-66daeafbdd64
AbstractExpression profiling has identified four consensus molecular subtypes (CMS1-4) in colorectal cancer (CRC). The receptor tyrosine kinase KIT has been associated with the most aggressive subtype, CMS4. However, it is unclear whether, and how, KIT contributes to the aggressive features of CMS4 CRC. Here, we employed genome-editing technologies in patient-derived organoids (PDOs) to study KIT function in CRC in vitro and in vivo. CRISPR-Cas9-mediated deletion of the KIT gene caused a partial mesenchymal-to-epithelial phenotype switch and a strong reduction of intra-tumor stromal content. Vice versa, overexpression of KIT caused a partial epithelial-to-mesenchymal phenotype switch, a strong increase of intra-tumor stromal content, and high expression of TGFβ1. Surprisingly, the levels of phosphorylated SMAD2 were significantly lower in KIT-expressing versus KIT-deficient tumor cells. In vitro analyses showed that TGFβ signaling in PDOs limits their regenerative capacity. Overexpression of KIT prevented tumor-suppressive TGFβ signaling, while KIT deletion sensitized PDOs to TGFβ-mediated growth inhibition. Mechanistically, we found that KIT expression caused a strong reduction in the expression of SMAD2, a central mediator of canonical TGFβ signaling. We propose that KIT induces a pro-fibrotic tumor microenvironment by stimulating TGFβ expression, and protects the tumor cells from tumor-suppressive TGFβ signaling by inhibiting SMAD2 expression.
<li> <b>in vitro:</b> inVitro (preparationType)<li> <b>in vivo:</b> inVivo (preparationType)
[ [ { "end": 424, "label": "preparationType", "start": 416 }, { "end": 436, "label": "preparationType", "start": 429 }, { "end": 908, "label": "preparationType", "start": 900 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 424, "label": "preparationType", "start": 416 }, { "end": 436, "label": "preparationType", "start": 429 } ]
null
null
82a21f41-bb5b-4a53-bd61-1d66ff5bf2d2
completed
2025-04-29T14:36:04.699619
2025-05-27T14:00:47.164332
f5701433-2c67-452d-9e61-87fc7f221c73
IntroductionMotor Imagery (MI) is a powerful tool to stimulate sensorimotor brain areas and is currently used in motor rehabilitation after a stroke. The aim of our study was to evaluate whether an illusion of movement induced by visuo-proprioceptive immersion (VPI) including tendon vibration (TV) and Virtual moving hand (VR) combined with MI tasks could be more efficient than VPI alone or MI alone on cortical excitability assessed using Electroencephalography (EEG).MethodsWe recorded EEG signals in 20 healthy participants in 3 different conditions: MI tasks involving their non-dominant wrist (MI condition); VPI condition; and VPI with MI tasks (combined condition). Each condition lasted 3 minutes, and was repeated 3 times in randomized order. Our main judgment criterion was the Event-Related De-synchronization (ERD) threshold in sensori-motor areas in each condition in the brain motor area.ResultsThe combined condition induced a greater change in the ERD percentage than the MI condition alone, but no significant difference was found between the combined and the VPI condition (p = 0.07) and between the VPI and MI condition (p = 0.20).ConclusionThis study demonstrated the interest of using a visuo-proprioceptive immersion with MI rather than MI alone in order to increase excitability in motor areas of the brain. Further studies could test this hypothesis among patients with stroke to provide new perspectives for motor rehabilitation in this population.
<li> <b>brain:</b> brain (UBERONParcellation)<li> <b>sensorimotor brain areas:</b> Other (UBERONParcellation)<li> <b>Electroencephalography:</b> electroencephalography (technique)<li> <b>EEG:</b> electroencephalography (technique)<li> <b>motor area:</b> primaryMotorCortex (UBERONParcellation)
[ [ { "end": 892, "label": "UBERONParcellation", "start": 887 }, { "end": 1331, "label": "UBERONParcellation", "start": 1326 }, { "end": 87, "label": "UBERONParcellation", "start": 63 }, { "end": 464, "label": "technique", "start": 442 }, { "end": 469, "label": "technique", "start": 466 }, { "end": 493, "label": "technique", "start": 490 }, { "end": 903, "label": "UBERONParcellation", "start": 893 }, { "end": 1318, "label": "UBERONParcellation", "start": 1307 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "\r\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 81, "label": "UBERONParcellation", "start": 76 }, { "end": 892, "label": "UBERONParcellation", "start": 887 }, { "end": 1331, "label": "UBERONParcellation", "start": 1326 }, { "end": 87, "label": "UBERONParcellation", "start": 63 }, { "end": 464, "label": "technique", "start": 442 }, { "end": 469, "label": "technique", "start": 466 }, { "end": 493, "label": "technique", "start": 490 }, { "end": 903, "label": "UBERONParcellation", "start": 893 } ]
null
null
196801d0-cf47-40d4-9243-088fe579fa86
completed
2025-04-29T14:36:04.699626
2025-05-27T14:00:47.264044
62607236-a548-4891-886d-0c8c88ed82a2
In the context of theories of embodied cognition, motor imagery (MI) is said to involve fundamentally the same neuronal circuit as the execution of complex voluntary acts (e.g.Decety, 1996;Jeannerod, 1995;Jeannerod and Decety, 1995;Jeannerod and Frak, 1999).In the case of hand movements like finger tapping, this circuit involves, among other brain structures, the region corresponding to the arm and hand representation in the primary motor (M1) and somatosensory (S1) cortex of the contralateral hemisphere, the premotor cortex (Witt et al., 2008) and, in the case of self-initiated actions, the supplementary motor area (SMA) (Nachev et al., 2008).The suggestion that imagined actions are likely to involve the same circuit as actually executed (and observed) ones is based on the notion that a motor image is the conscious representation of a non-executed action (Jeannerod, 1994;Jeannerod, 1995). There is ample evidence that imagined actions bear the same temporal regularities and the same responsiveness to physical laws as their overt counterparts (Anquetil and Jeannerod, 2007;Decety et al., 1989;Sirigu et al., 1995) and that real and imagined hand movements share partially overlapping neuronal networks (Ehrsson et al., 2003;Gerardin et al., 2000;Lotze et al., 1999;Nair et al., 2003;Porro et al., 2000;Roth et al., 1996;Sharma et al., 2008). However, despite the general consensus regarding regional overlap between imagery and sensory processing, there is disagreement concerning the set of areas that support the generation of mental motor representations and, more so, when subjects have to form these representations adopting different perspectives (Hetu et al., 2013).An important area whose involvement in motor imagery has been repeatedly debated is the primary motor cortex (M1) (Dechent et al., 2004;Guillot et al., 2012;Hetu et al., 2013). There are several factors that can account for the discrepancies concerning the set of areas activated during motor imagery and the activation of M1 in particular (Dechent et al., 2004;Hetu et al., 2013;Lotze and Halsband, 2006).It has been suggested that the lack of agreement among studies could be due to the inadequate sensitivity of the neuroimaging methods to capture small or transient activations (e.g.Dechent et al., 2004;Hetu et al., 2013).Specifically, that the whole brain analysis that is used in many studies, may be inadequate to capture such activations and a regions of interest (ROI) approach may be a more sensitive method (Hetu et al., 2013); or, as it has been suggested that the usually employed general linear model has limitations which may be surpassed using multivariate models (e.g.Norman et al., 2006;Peelen and Downing, 2007;Sauvage et al., 2011).A second reason for the diversity of the results could be the type of action that subjects are imagining.For example, imagery of simple movements may or may not recruit different neuronal populations than imagery of complex motor acts (e.g.Gerardin et al., 2000) as could imagining novel versus skilled, overlearned movements (e.g.Lacourse et al., 2005). Another, quite plausible reason for the discrepancies in the literature, may be the strategy employed during performance of the task.Imagining an action can involve visual, kinesthetic or both imagery strategies (e.g.Guillot et al., 2009;Madan and Singhal, 2012). One may engage predominantly in "external visual imagery" meaning that one imagines someone else performing the imagined action (Callow and Hardy, 2004;Fourkas et al., 2006;Lorey et al., 2009;Moran, 2009;Ramsey et al., 2010) which coincides with what others call imagery from the third person perspective (e.g.Jackson et al., 2006;Holmes and Calmels, 2008;Guillot et al., 2009).Alternatively one may engage instead in "internal visual imagery" involving imagining oneself performing the action.However, as many investigators have commented (e.g.Ruby and Decety, 2001;Callow and Hardy, 2004;Lorey et al., 2009;Jiang et al., 2015), this form of strategy may confound visual and kinesthetic imagery.More explicitly, when people resort to such a strategy they may imagine the sensation one experiences during performance of an act (kinesthetic imagery) or visualize themselves performing this act as being the spectators of their own actions (visual imagery). Consequently, instructions to the subjects to either visualize themselves performing the act or to use kinesthetic imagery and imagine themselves moving in the appropriate way (e.g.Jiang et al., 2015) are essential to avoid complicating interpretation of the neuroimaging data. Reviewing the relevant literature one can find many examples that demonstrate how different strategies applied by subjects may introduce ambiguity in the interpretation of the results.For example, Leonardo et al. (1995) used a simple finger-to-thumb opposition movement and asked their participants to imagine themselves performing this action.This study does not clarify the strategy the participants used and the general statement (i.e. "…imagine themselves performing…") does not allow us to appraise their finding of activation of the contralateral sensorimotor cortex.Similarly, Lotze et al. (1999) found M1 activation when they asked their participants to imagine forming a fist without explicitly reporting the imagery strategy that was used.Later studies too, in which the motor imagery modality was not specified, also replicated the finding of M1 activation (e.g.Diers et al., 2010).On the other hand, other studies where it was also not specified whether the participants adopted the kinesthetic or visual strategy during the internal imagery, did not report activation of M1 in the imagery condition.In one such study, the researchers used simple and complex flexion/extension finger movements and asked the participants to imagine performing these movements (Gerardin et al., 2000). Equally puzzling results are also observed in studies where the modality of imagery is specified.For example, Porro et al. (1996) reported increased activation in M1 during mental representation of sequential finger movements, when the instructions for motor imagery were "to imagine using the right hand to perform movements and feeling the sensations associated with finger-tapping", therefore urging the participants to employ both visual and kinesthetic imagery.Furthermore, studies in which participants used only kinesthetic imagery (e.g.Guillot et al., 2008;Zhang et al., 2011) do find activation of M1, perhaps pointing to the direction that kinesthetic rather than visual imagery is essential for recruiting M1.However, the same data indicate that M1 recruitment may depend on the different imagery capabilities of the participants and not on the specific type of imagery (Guillot et al., 2008).On the other hand, there is accumulated evidence that M1 is not recruited either in the visual or in the kinesthetic imagery (e.g.Stephan et al., 1995;Hanakawa et al., 2008;Guillot et al., 2009;Fleming et al., 2010;Chang et al., 2011;Szameitat et al., 2012).Moreover, whether kinesthetic or visual imagery is adopted depends on how well subjects may have already developed their internal motor representations (e.g.Olsson et al., 2008). Therefore, a major challenge in imaging the circuits that mediate imagining motor acts is the choice of the appropriate experimental design as well as the specification of the kind of mental imagery subjects are to engage in during scanning, given the many and varied imagination strategies people are able to adopt. The aforementioned studies are few examples in the vast literature on motor imagery which indicate that we have yet to reach a solid conclusion regarding the network that is consistently activated during motor imagery, and whether this network involves M1, in particular.In fact, a recent metanalysis of 122 motor imagery experiments (from 75 papers) reports that only 22 of them mention activation of M1 and 100 do not (Hetu et al., 2013). To minimize such confounds and maximize the use of either kinesthetic imagery while subjects imagined themselves performing an act or visual imagery when asked to imagine someone else performing the act, we trained our subjects in these two strategies using concrete examples of an act they had first to actually perform and actually observe during an execution and observation condition.Specifically, to reduce the uncertainty associated with the strategy used during motor imagery tasks, it was necessary to provide individuals with concrete examples of precisely what is to be imagined.Accordingly, we trained a group of participants to perform finger tapping movements and then to imagine performing the same movements (kinesthetic imagery).Moreover, we instructed them to observe the same videotaped action performed by someone else and immediately afterwards to imagine what they had just observed (visual imagery).This way, by specifying the strategies that individuals adopt in performing tasks, one could probably identify the cortical regions that are differentially activated in the two modalities, and the possible contribution of the primary motor cortex in each case.
<li> <b>primary motor:</b> primaryMotorCortex (UBERONParcellation)<li> <b>somatosensory:</b> somatosensoryCortex (UBERONParcellation)<li> <b>premotor cortex:</b> premotorCortex (UBERONParcellation)<li> <b>supplementary motor area:</b> Other (UBERONParcellation)<li> <b>primary motor cortex:</b> primaryMotorCortex (UBERONParcellation)<li> <b>M1:</b> primaryMotorCortex (UBERONParcellation)<li> <b>S1:</b> primarySomatosensoryCortex (UBERONParcellation)<li> <b>contralateral hemisphere:</b> cerebralHemisphere (UBERONParcellation)<li> <b>regions of interest:</b> Other (UBERONParcellation)
[ [ { "end": 442, "label": "UBERONParcellation", "start": 429 }, { "end": 465, "label": "UBERONParcellation", "start": 452 }, { "end": 530, "label": "UBERONParcellation", "start": 515 }, { "end": 623, "label": "UBERONParcellation", "start": 599 }, { "end": 1796, "label": "UBERONParcellation", "start": 1776 }, { "end": 9156, "label": "UBERONParcellation", "start": 9136 }, { "end": 446, "label": "UBERONParcellation", "start": 444 }, { "end": 1800, "label": "UBERONParcellation", "start": 1798 }, { "end": 2013, "label": "UBERONParcellation", "start": 2011 }, { "end": 5206, "label": "UBERONParcellation", "start": 5204 }, { "end": 5450, "label": "UBERONParcellation", "start": 5448 }, { "end": 5680, "label": "UBERONParcellation", "start": 5678 }, { "end": 6055, "label": "UBERONParcellation", "start": 6053 }, { "end": 6499, "label": "UBERONParcellation", "start": 6497 }, { "end": 6609, "label": "UBERONParcellation", "start": 6607 }, { "end": 6649, "label": "UBERONParcellation", "start": 6647 }, { "end": 6850, "label": "UBERONParcellation", "start": 6848 }, { "end": 7803, "label": "UBERONParcellation", "start": 7801 }, { "end": 7952, "label": "UBERONParcellation", "start": 7950 }, { "end": 469, "label": "UBERONParcellation", "start": 467 }, { "end": 509, "label": "UBERONParcellation", "start": 485 }, { "end": 628, "label": "UBERONParcellation", "start": 625 }, { "end": 2349, "label": "UBERONParcellation", "start": 2344 }, { "end": 9033, "label": "UBERONParcellation", "start": 9025 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "SMA: supplementary motor cortex (UBERONParcellation)\nbrain: Other (UBERONParcellation)\ncortical: Other (UBERONParcellation)\n\r\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 442, "label": "UBERONParcellation", "start": 429 }, { "end": 1789, "label": "UBERONParcellation", "start": 1776 }, { "end": 9149, "label": "UBERONParcellation", "start": 9136 }, { "end": 465, "label": "UBERONParcellation", "start": 452 }, { "end": 530, "label": "UBERONParcellation", "start": 515 }, { "end": 623, "label": "UBERONParcellation", "start": 599 }, { "end": 1796, "label": "UBERONParcellation", "start": 1776 }, { "end": 9156, "label": "UBERONParcellation", "start": 9136 }, { "end": 446, "label": "UBERONParcellation", "start": 444 }, { "end": 1800, "label": "UBERONParcellation", "start": 1798 }, { "end": 2013, "label": "UBERONParcellation", "start": 2011 }, { "end": 5206, "label": "UBERONParcellation", "start": 5204 }, { "end": 5450, "label": "UBERONParcellation", "start": 5448 }, { "end": 5680, "label": "UBERONParcellation", "start": 5678 }, { "end": 6055, "label": "UBERONParcellation", "start": 6053 }, { "end": 6499, "label": "UBERONParcellation", "start": 6497 }, { "end": 6609, "label": "UBERONParcellation", "start": 6607 }, { "end": 6649, "label": "UBERONParcellation", "start": 6647 }, { "end": 6850, "label": "UBERONParcellation", "start": 6848 }, { "end": 7803, "label": "UBERONParcellation", "start": 7801 }, { "end": 7952, "label": "UBERONParcellation", "start": 7950 }, { "end": 469, "label": "UBERONParcellation", "start": 467 }, { "end": 509, "label": "UBERONParcellation", "start": 485 }, { "end": 2460, "label": "UBERONParcellation", "start": 2441 } ]
null
null
06bc4f45-ef33-4d14-b1e7-224a66341a97
completed
2025-04-29T14:36:04.699632
2025-05-27T14:00:47.372076
eb33a603-2404-4e49-bfb6-f84829047029
This collection offers an insightful overview about some recent advancements in identifying neuronal targets, circuits, and potential pharmacological treatments to combat sleep-related disorders. Poor sleep increases the risk of developing a wide range of disorders, from neurological to metabolic, that compromise the health of the effected individuals. Developing effective and specific treatments for sleep disorders represent a real challenge, mainly due to the difficulty in finding drugs that show a selective action on defined targets without causing unwanted side effects. Therefore, controlling the symptoms of the sleep-related disorders, with highly selective drugs, is an important goal for this field. In this issue of Frontiers in Neuroscience-section: Sleep and Circadian Rhythms -the contributing authors described novel circuits and mechanisms involved in sleep disorders. Our special issue comprises articles that aim to fill the gaps in our understanding of the regulation of sleep, addressing both well-known and novel mechanisms through which new targets for pharmacological intervention could be identified. A particular focus regards the intriguing link between sleep deprivation (SD), inflammation and neuro-inflammation (Figure1). The review by Gall and Shuboni-Mulligan looks at the phenomenon of masking, arguing that masking is a separate factor which contributes to the patterns of behavior, not simply as something that obscures endogenous circadian rhythms. The authors review evidence of various exogenous stimuli that can act as masking agents, demonstrating their ability to interact with homeostatic and circadian systems, and discuss the neural circuitry involved. There is the potential for masking agents to be used therapeutically to improve abnormal and maladaptive sleep behaviors resulting from primary sleep disorders and/or sleep disruptions that are secondary to other illnesses. Using masking stimuli themselves, or pharmacological approaches targeting the neural circuitry through which masking occurs could be a valuable approach in treating disordered sleep. In a similar vein, the review by Potter and Burgess explores the Frontiers in Neuroscience frontiersin.org
<li> <b>sleep:</b> Other (UBERONParcellation)
[ [] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Incorrect" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Incorrect" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 176, "label": "UBERONParcellation", "start": 171 }, { "end": 206, "label": "UBERONParcellation", "start": 201 }, { "end": 409, "label": "UBERONParcellation", "start": 404 }, { "end": 629, "label": "UBERONParcellation", "start": 624 }, { "end": 878, "label": "UBERONParcellation", "start": 873 }, { "end": 1000, "label": "UBERONParcellation", "start": 995 }, { "end": 1190, "label": "UBERONParcellation", "start": 1185 }, { "end": 1811, "label": "UBERONParcellation", "start": 1806 }, { "end": 1850, "label": "UBERONParcellation", "start": 1845 }, { "end": 1873, "label": "UBERONParcellation", "start": 1868 }, { "end": 2106, "label": "UBERONParcellation", "start": 2101 } ]
null
null
9b560999-79c5-4b1e-9c08-ac5c9d7522a9
completed
2025-04-29T14:36:04.699638
2025-05-27T14:00:47.494630
727fef3a-c023-4a97-b64d-b743c9937821
A schematic representation describing the major findings that the contributing articles provided to our special issue and that highlight the novel targets and potential pharmacological treatments to treat sleep and circadian disorders (created with BioRender.com). history and promise of the melanin concentrating hormone (MCH) system as a target for treating sleep disorders.MCH containing neurons project throughout the brain and have been implicated in a number of important physiological processes, including regulation of REM sleep.This makes it a potentially attractive target for drugs aimed at disorders of REM sleep, such as narcolepsy.As the review details, MCH also affects consummatory behavior and there were several attempts to develop MCH-based drugs or derivatives for obesity, but these have proven to be difficult to bring to market.However, given the extent of basic science demonstrating the power of MCH to influence sleep, this remains a viable target for development of new tools to treat sleep disorders. It has been extensively demonstrated that getting low-quality or little sleep can be detrimental for memory performance and, at the same time, it can be a significant factor for the development of anxiety and depression-related behaviors.Interestingly, it has also been reported that SD causes alterations of immune function and that neuroinflammation, as consequence of sleep disturbances, could play an important role in worsening cognition or in inducing rapid mood changes.In this respect, the work published by Ugalde-Muñiz et al. described the neuroprotective role of dopamine (DA) and the activation of DA receptor 2 (DRD2) that is involved in the reduction of inflammation caused by SD.In mice, REM sleep deprivation (RSD) increased proinflammatory cytokines (TNFα and IL-1β) in the hippocampus and serum and was sufficient to induce inflammation.In general, SD causes memory impairments and immunological alterations by increasing the levels of TNFα, IL-1β, and IL-6.In this study, an emerging role of DA in modulating the immune response was described.Agonism at the level of DRD2 by quinpirole reduced inflammation caused by RSD and also recovered spatial memory impairments in RSD mice.At the same time, RSD mice showed inflammation within the hippocampus suggesting that DRD2 could be a potential target for treating memory deficits induced by RSD.However, DRD2 activation per se does not improve the mnemonic capabilities.Quinpirole also prevented a depressive-like behavior caused by RSD.This neuropathological status, as well as the anhedonia behavior observed in RSD mice, is indeed characterized by high levels of IL-1β, IL-6, and TNFα, as a consequence of the inflammatory state triggered by SD. Finally, a new chemical compound was tested to potentially treat inflammation caused by sleep disturbances.In the work of Hua et al., the effect of Lonicerae Japonicae flos (LJF) was explored.The LJF extracts are able to reduce and downregulate the production of inflammatory cytokines.Among the components of LJF extracts, chlorogenic acid and luteolin are linked to the increase of sleep time and reduction of sleep latency.Very little is known about the mechanisms by which LJF can regulate sleep homeostasis.The aim of this study was to understand the action of LJF on sleep-wake cycle under normal conditions, in SD, and with lipopolysaccharide (LPS) treatment, which induces inflammation in animals.As previously discussed in the work of Ugalde-Muñiz et al., SD is associated with the increase of inflammatory cytokines such as IL-6 and TNFα.Under basal conditions, LJF increases the time spent in non-REM sleep and reduced wakefulness.Moreover, LJF helped sleep recovery after acute SD.In another set of experiments, the authors found that LJF promoted REM sleep after injections of LPS in mice.Another effect observed was the capability of LJF to decrease the levels of proinflammatory cytokines in both blood serum and brain tissues in mice treated with LPS.The authors concluded that LJF inhibits microglial activation in hippocampus and in medial prefrontal cortex to reduce the inflammation.This study highlights the potential of LJF, as a new compound, to be used in clinics for the treatment of neuroinflammatory conditions linked to SD.
<li> <b>brain:</b> brain (UBERONParcellation)<li> <b>REM sleep:</b> Other (UBERONParcellation)<li> <b>hippocampus:</b> hippocampalFormation (UBERONParcellation)<li> <b>mice:</b> musMusculus (species)<li> <b>hippocampus:</b> hippocampalFormation (UBERONParcellation)<li> <b>medial prefrontal cortex:</b> Other (UBERONParcellation)
[ [ { "end": 427, "label": "UBERONParcellation", "start": 422 }, { "end": 3977, "label": "UBERONParcellation", "start": 3972 }, { "end": 1831, "label": "UBERONParcellation", "start": 1820 }, { "end": 2296, "label": "UBERONParcellation", "start": 2285 }, { "end": 4087, "label": "UBERONParcellation", "start": 4076 }, { "end": 1730, "label": "species", "start": 1726 }, { "end": 2226, "label": "species", "start": 2222 }, { "end": 2253, "label": "species", "start": 2249 }, { "end": 2617, "label": "species", "start": 2613 }, { "end": 3845, "label": "species", "start": 3841 }, { "end": 3993, "label": "species", "start": 3989 }, { "end": 4119, "label": "UBERONParcellation", "start": 4102 }, { "end": 398, "label": "UBERONParcellation", "start": 391 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "neuron: Other (UBERONParcellation)\r\nprefrontal cortex: prefrontalCortex (UBERONParcellation)\r\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 427, "label": "UBERONParcellation", "start": 422 }, { "end": 3977, "label": "UBERONParcellation", "start": 3972 }, { "end": 536, "label": "UBERONParcellation", "start": 527 }, { "end": 624, "label": "UBERONParcellation", "start": 615 }, { "end": 1741, "label": "UBERONParcellation", "start": 1732 }, { "end": 3661, "label": "UBERONParcellation", "start": 3652 }, { "end": 3813, "label": "UBERONParcellation", "start": 3804 }, { "end": 1831, "label": "UBERONParcellation", "start": 1820 }, { "end": 2296, "label": "UBERONParcellation", "start": 2285 }, { "end": 4087, "label": "UBERONParcellation", "start": 4076 }, { "end": 1730, "label": "species", "start": 1726 }, { "end": 2226, "label": "species", "start": 2222 }, { "end": 2253, "label": "species", "start": 2249 }, { "end": 2617, "label": "species", "start": 2613 }, { "end": 3845, "label": "species", "start": 3841 }, { "end": 3993, "label": "species", "start": 3989 }, { "end": 1831, "label": "UBERONParcellation", "start": 1820 }, { "end": 2296, "label": "UBERONParcellation", "start": 2285 }, { "end": 4087, "label": "UBERONParcellation", "start": 4076 }, { "end": 4119, "label": "UBERONParcellation", "start": 4095 } ]
null
null
0cff4942-92fd-4170-8739-376fcfdf2ef1
completed
2025-04-29T14:36:04.699644
2025-05-27T14:00:47.592913
11cf5a83-da46-47f5-af87-933000d7b75b
The longitudinal relationship between central plastic changes and clinical presentations of peripheral hearing impairment remains unknown. Previously, we reported a unique plastic pattern of "healthy-side dominance" in acute unilateral idiopathic sudden sensorineural hearing loss (ISSNHL). This study aimed to explore whether such hemispheric asymmetry bears any prognostic relevance to ISSNHL along the disease course. Using magnetoencephalography (MEG), inter-hemispheric differences in peak dipole amplitude and latency of N100m to monaural tones were evaluated in 21 controls and 21 ISSNHL patients at two stages: initial and fixed stage (1 month later). Dynamics/Prognostication of hemispheric asymmetry were assessed by the interplay between hearing level/hearing gain and ipsilateral/contralateral ratio (I/C) of N100m latency and amplitude. Healthy-side dominance of N100m amplitude was observed in ISSNHL initially. The pattern changed with disease process. There is a strong correlation between the hearing level at the fixed stage and initial I/C(amplitude) on affected-ear stimulation in ISSNHL. The optimal cut-off value with the best prognostication effect for the hearing improvement at the fixed stage was an initial I/C(latency) on affected-ear stimulation of 1.34 (between subgroups of complete and partial recovery) and an initial I/C(latency) on healthy-ear stimulation of 0.76 (between subgroups of partial and no recovery), respectively. This study suggested that a dynamic process of central auditory plasticity can be induced by peripheral lesions. The hemispheric asymmetry at the initial stage bears an excellent prognostic potential for the treatment outcomes and hearing level at the fixed stage in ISSNHL. Our study demonstrated that such brain signature of central auditory plasticity in terms of both N100m latency and amplitude at defined time can serve as a prognostication predictor for ISSNHL. Further studies are needed to explore the long-term temporal scenario of auditory hemispheric asymmetry and to get better psychoacoustic correlates of pathological hemispheric asymmetry in ISSNHL.
<li> <b>brain:</b> brain (UBERONParcellation)<li> <b>magnetoencephalography:</b> magnetoencephalography (technique)<li> <b>MEG:</b> magnetoencephalography (technique)
[ [ { "end": 1774, "label": "UBERONParcellation", "start": 1769 }, { "end": 449, "label": "technique", "start": 427 }, { "end": 454, "label": "technique", "start": 451 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "\n\r\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 1774, "label": "UBERONParcellation", "start": 1769 }, { "end": 449, "label": "technique", "start": 427 }, { "end": 454, "label": "technique", "start": 451 } ]
null
null
7bf0e178-1182-4f09-b038-c87998a0d9e8
pending
2025-04-29T14:36:04.699651
2025-04-29T14:36:04.699651
6a4676b7-f6c5-4903-aa32-7550b87e5aa8
About half of patients achieved hearing improvement (Table 1).Within-group differences of I/C among prognostic subgroups (i.e., complete, partial, and no recovery) evaluated using Kruskal-Wallis revealed statistical significance in three of them (Table 4 and5): initial I/C as on healthy-ear stimulation (p = 0.046), initial I/C ls on healthy-ear stimulation (p = 0.027), and initial I/C ls on affectedear stimulation (p = 0.02).Mann-Whitney U test furthermore showed that the differences existed between subgroups of complete and partial recovery (p = 0.037 for I/C as on healthy-ear stimulation, the smaller the ratio, the better recovery; p = 0.036 for I/C ls on healthy-ear stimulation, the larger the ratio, the better recovery; p = 0.014 for I/C ls on affected-ear stimulation, the smaller the ratio, the better recovery), as well as those of partial and no recovery (p = 0.027 for I/C as on healthy-ear stimulation, the larger the ratio, the better recovery; p = 0.02 for I/C ls on healthy-ear stimulation, the smaller the ratio, the better recovery; p = 0.026 for I/C ls on affected-ear stimulation, the larger the ratio, the better recovery), but not of complete and no recovery (p = 0.63 for I/C as on healthy-ear stimulation; p = 0.28 for I/C ls on healthy-ear stimulation; p = 0.25 for I/C ls on affected-ear stimulation).The ROC curves in turn showed the best prediction effect of I/C for the hearing improvement at fixed stage: between subgroups of complete and partial recovery, the optimal cut-off value was an initial I/C ls on affected-ear stimulation at 1.34 (area under curve 1, sensitivity 100%, specificity 100%); between subgroups of partial and no recovery, the optimal cut-off value was an initial I/C ls on healthy-ear stimulation at 0.76 (area under curve 0.87, sensitivity 80%, specificity 100%; the smaller the ratio, the better recovery, Figure 2A). When ipsilateral/contralateral ratio were correlated to hearing levels, no significant correlation was revealed except for that between the initial I/C a on affected-ear stimulation and the hearing level at the fixed stage (r = 0.58, p = 0.006; the smaller the ratio, the lower the hearing level; Figure 2B) in ISSNHL.There was no correlation between hearing gain and ipsilateral/ contralateral ratio at various stages.
None
[ [] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[]
null
null
2e9a241a-ea2c-4cd4-a464-02ebd1e2454a
completed
2025-04-29T14:36:04.699657
2025-05-27T14:00:47.690825
fa00d50f-4568-4a7d-951c-755f10bdc8d4
Parkinson's disease (PD) is characterized by motor symptoms with depression. We evaluated the influence of dopaminergic depletion on hippocampal neurogenesis process to explore mechanisms of depression production. Five consecutive days of 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) injection in mice (MPTP-mice) reduced dopaminergic fibers in hippocampal dentate gyrus (DG). MPTP-mice exhibited depressive-like behaviors later for 2-3 weeks. BrdU was injected 4 h after last-injection of MPTP. BrdU-positive (BrdU+) cells in dorsal (d-DG) and ventral (v-DG) DG were examined on day 1 (D1), 7 (D7), 14 (D14) and 21 (D21) after BrdU injection. Fewer D7-, D14- and D21-BrdU+ cells or BrdU+/NeuN+ cells, but not D1-BrdU+ cells, were found in v-DG of MPTP-mice than in controls. However, the number of BrdU+ cells in d-DG did not differ between the both. Loss of doublecortin-positive (DCX+) cells was observed in v-DG of MPTP-mice. Protein kinase A (PKA) and Ca2+/cAMP-response element binding protein (CREB) phosphorylation were reduced in v-DG of MPTP-mice, which were reversed by D1-like receptor (D1R) agonist SKF38393, but not D2R agonist quinpirole. The treatment of MPTP-mice with SKF38393 on days 2-7 after BrdU-injection reduced the loss of D7- and D21-BrdU+ cells in v-DG and improved the depressive-like behaviors; these changes were sensitive to PKA inhibitor H89. Moreover, the v-DG injection of SKF38393 in MPTP-mice could reduce the loss of D21-BrdU+ cells and relieve the depressive-like behaviors. In control mice, the blockade of D1R by SCH23390 caused the reduction of D21-BrdU+ cells in v-DG and the depressive-like behaviors. Our results indicate that MPTP-reduced dopaminergic depletion impairs the D1R-mediated early survival of newborn neurons in v-DG, producing depressive-like behaviors.
<li> <b>hippocampal:</b> hippocampalFormation (UBERONParcellation)<li> <b>dentate gyrus:</b> dentateGyrusOfHippocampalFormation (UBERONParcellation)<li> <b>dorsal:</b> Other (UBERONParcellation)<li> <b>ventral:</b> Other (UBERONParcellation)<li> <b>mice:</b> musMusculus (species)
[ [ { "end": 144, "label": "UBERONParcellation", "start": 133 }, { "end": 308, "label": "species", "start": 304 }, { "end": 319, "label": "species", "start": 315 }, { "end": 393, "label": "species", "start": 389 }, { "end": 764, "label": "species", "start": 760 }, { "end": 935, "label": "species", "start": 931 }, { "end": 1063, "label": "species", "start": 1059 }, { "end": 1187, "label": "species", "start": 1183 }, { "end": 1435, "label": "species", "start": 1431 }, { "end": 1535, "label": "species", "start": 1531 }, { "end": 377, "label": "UBERONParcellation", "start": 352 }, { "end": 381, "label": "UBERONParcellation", "start": 379 }, { "end": 546, "label": "UBERONParcellation", "start": 544 }, { "end": 565, "label": "UBERONParcellation", "start": 563 }, { "end": 569, "label": "UBERONParcellation", "start": 567 }, { "end": 825, "label": "UBERONParcellation", "start": 823 }, { "end": 922, "label": "UBERONParcellation", "start": 920 }, { "end": 1050, "label": "UBERONParcellation", "start": 1048 }, { "end": 1286, "label": "UBERONParcellation", "start": 1284 }, { "end": 1400, "label": "UBERONParcellation", "start": 1398 }, { "end": 1616, "label": "UBERONParcellation", "start": 1614 }, { "end": 1780, "label": "UBERONParcellation", "start": 1778 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "DG: dentateGyrusOfHippocampalFormation (UBERONParcellation)\n\r\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 144, "label": "UBERONParcellation", "start": 133 }, { "end": 363, "label": "UBERONParcellation", "start": 352 }, { "end": 377, "label": "UBERONParcellation", "start": 364 }, { "end": 540, "label": "UBERONParcellation", "start": 534 }, { "end": 559, "label": "UBERONParcellation", "start": 552 }, { "end": 308, "label": "species", "start": 304 }, { "end": 319, "label": "species", "start": 315 }, { "end": 393, "label": "species", "start": 389 }, { "end": 764, "label": "species", "start": 760 }, { "end": 935, "label": "species", "start": 931 }, { "end": 1063, "label": "species", "start": 1059 }, { "end": 1187, "label": "species", "start": 1183 }, { "end": 1435, "label": "species", "start": 1431 }, { "end": 1535, "label": "species", "start": 1531 } ]
null
null
656fb11a-f42a-4fb4-82b1-a34c77dda5e7
completed
2025-04-29T14:36:04.699663
2025-05-27T14:00:47.783576
2438e8de-15b8-48de-89e6-eb3893d008c6
Abstract The term rhombencephalitis refers to inflammatory diseases affecting the hindbrain (brainstem and cerebellum). Rhombencephalitis has a wide variety of etiologies, including infections, autoimmune diseases, and paraneoplastic syndromes. Infection with bacteria of the genus Listeria is the most common cause of rhombencephalitis. Primary rhombencephalitis caused by infection with Listeria spp. occurs in healthy young adults. It usually has a biphasic time course with a flu-like syndrome, followed by brainstem dysfunction; 75% of patients have cerebrospinal fluid pleocytosis, and nearly 100% have an abnormal brain magnetic resonance imaging scan. However, other possible causes of rhombencephalitis must be borne in mind. In addition to the clinical aspects, the patterns seen in magnetic resonance imaging can be helpful in defining the possible cause. Some of the reported causes of rhombencephalitis are potentially severe and life threatening; therefore, an accurate initial diagnostic approach is important to establishing a proper early treatment regimen. This pictorial essay reviews the various causes of rhombencephalitis and the corresponding magnetic resonance imaging findings, by describing illustrative confirmed cases.
<li> <b>hindbrain:</b> hindbrain (UBERONParcellation)<li> <b>brainstem:</b> brainstem (UBERONParcellation)<li> <b>cerebellum:</b> cerebellum (UBERONParcellation)<li> <b>cerebrospinal fluid:</b> Other (UBERONParcellation)<li> <b>brain:</b> brain (UBERONParcellation)<li> <b>magnetic resonance imaging:</b> magneticResonanceImaging (technique)
[ [ { "end": 91, "label": "UBERONParcellation", "start": 82 }, { "end": 102, "label": "UBERONParcellation", "start": 93 }, { "end": 520, "label": "UBERONParcellation", "start": 511 }, { "end": 117, "label": "UBERONParcellation", "start": 107 }, { "end": 574, "label": "UBERONParcellation", "start": 555 }, { "end": 626, "label": "UBERONParcellation", "start": 621 }, { "end": 653, "label": "technique", "start": 627 }, { "end": 819, "label": "technique", "start": 793 }, { "end": 1192, "label": "technique", "start": 1166 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "\r\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 91, "label": "UBERONParcellation", "start": 82 }, { "end": 102, "label": "UBERONParcellation", "start": 93 }, { "end": 520, "label": "UBERONParcellation", "start": 511 }, { "end": 117, "label": "UBERONParcellation", "start": 107 }, { "end": 574, "label": "UBERONParcellation", "start": 555 }, { "end": 626, "label": "UBERONParcellation", "start": 621 }, { "end": 653, "label": "technique", "start": 627 }, { "end": 819, "label": "technique", "start": 793 }, { "end": 1192, "label": "technique", "start": 1166 } ]
null
null
0e9035f7-d186-4694-bf92-595579f26aff
pending
2025-04-29T14:36:04.699669
2025-04-29T14:36:04.699669
a2f55097-a325-46b2-a119-82adb07e3a06
The most common presentation of paracoccidioidomycosis is the presence of rounded or multiloculated lesions,
None
[ [] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[]
null
null
2ab5e13b-5c6e-4a91-a40e-9dc688a28ec6
completed
2025-04-29T14:36:04.699675
2025-05-27T14:00:47.917072
8d66680f-7e37-4089-9a73-029873b48efa
Intensive cognitive-behavioral therapy (CBT) can effectively reduce symptoms in obsessive-compulsive disorder (OCD). However, many relapse after treatment. Few studies have investigated biological markers predictive of follow-up clinical status. The objective was to determine if brain network connectivity patterns prior to intensive CBT predict worsening of clinical symptoms during follow-up.We acquired resting-state functional magnetic resonance imaging data from 17 adults with OCD prior to and following 4 weeks of intensive CBT. Functional connectivity data were analyzed to yield graph-theory metrics. We examined the relationship between pre-treatment connectome properties and OCD clinical symptoms before and after treatment and during a 12-month follow-up period.Mean OCD symptom decrease was 40.4 ± 16.4% pre- to post-treatment (64.7% responded; 58.8% remitted), but 35.3% experienced clinically significant worsening during follow-up. From pre- to post-treatment, small-worldness and clustering coefficient significantly increased. Decreases in modularity correlated with decreases in OCD symptoms. Higher pre-treatment small-world connectivity was significantly associated with worsening of OCD symptoms during the follow-up period. Psychometric and neurocognitive measures pre- and post-treatment were not significant predictors.This is the first graph-theory connectivity study of the effects of CBT in OCD, and the first to test associations with follow-up clinical status. Results show functional network efficiency as a biomarker of CBT response and relapse in OCD. CBT increases network efficiency as it alleviates symptoms in most patients, but those entering therapy with already high network efficiency are at greater risk of relapse. Results have potential clinical implications for treatment selection.
<li> <b>brain:</b> brain (UBERONParcellation)<li> <b>functional magnetic resonance imaging:</b> functionalMagneticResonanceImaging (technique)
[ [ { "end": 285, "label": "UBERONParcellation", "start": 280 }, { "end": 458, "label": "technique", "start": 421 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 285, "label": "UBERONParcellation", "start": 280 }, { "end": 458, "label": "technique", "start": 421 } ]
null
null
f6120458-33d0-49cc-a63f-6c5a54f5f204
completed
2025-04-29T14:36:04.699681
2025-05-27T14:00:48.024654
68af5045-08e2-44fe-949f-033f4469195a
Follow-up data were available for all 17 participants.Mean duration of follow-up was 7 ± 4.53 months.Four participants received medication only in the follow-up period, eight were treated with CBT only, two with medications and CBT, and three received no treatment (Table 1). All 17 participants completed treatment.Mean YBOCS scores decreased 40.4 ± 16.4% from pre-to post-treatment [t(16) = 10.00,P < 0.0001] (Table 2).Eleven (64.7%) were responders and 10 (58.8%) achieved remission. There was a mean increase in YBOCS from post-treatment to follow-up of 13.98 ± 50.91%.Six (35.3%) experienced clinically significant worsening of symptoms during follow-up consisting of ≥5 points worsening on YBOCS (53).
<li> <b>CBT:</b> Other (technique)
[ [] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Incorrect" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Incorrect" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 196, "label": "technique", "start": 193 }, { "end": 231, "label": "technique", "start": 228 } ]
null
null
e71876a8-1ee1-4f4d-ace9-483add7528d7
pending
2025-04-29T14:36:04.699688
2025-04-29T14:36:04.699688
7f8e1462-5d20-41d6-b441-b3aff6f622ed
Deep learning has been widely used for inferring robust grasps. Although human-labeled RGB-D datasets were initially used to learn grasp configurations, preparation of this kind of large dataset is expensive. To address this problem, images were generated by a physical simulator, and a physically inspired model (e.g., a contact model between a suction vacuum cup and object) was used as a grasp quality evaluation metric to annotate the synthesized images. However, this kind of contact model is complicated and requires parameter identification by experiments to ensure real world performance. In addition, previous studies have not considered manipulator reachability such as when a grasp configuration with high grasp quality is unable to reach the target due to collisions or the physical limitations of the robot. In this study, we propose an intuitive geometric analytic-based grasp quality evaluation metric. We further incorporate a reachability evaluation metric. We annotate the pixel-wise grasp quality and reachability by the proposed evaluation metric on synthesized images in a simulator to train an auto-encoder–decoder called suction graspability U-Net++ (SG-U-Net++). Experiment results show that our intuitive grasp quality evaluation metric is competitive with a physically-inspired metric. Learning the reachability helps to reduce motion planning computation time by removing obviously unreachable candidates. The system achieves an overall picking speed of 560 PPH (pieces per hour).
None
[ [] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[]
null
null
fe00de87-accf-4715-8ec6-954f144e1d3c
pending
2025-04-29T14:36:04.699694
2025-04-29T14:36:04.699694
792fb383-af42-46c9-b360-090f39f62b62
Eppner [19] firstly detected objects and then pushed objects from top or side until suction was achieved.Hernandez et al. [11] firstly recognized objects and estimated their 6D poses [20], [21].They then generated suction candidates on the 3D model of the item based on primitive shapes.Those candidates were finally scored based on geometric and dynamic constraints.Zeng et al. [1] used a neural network trained on a human-labeled dataset to predict grasping affordance map from the RGB-D input and chose the suction point with max affordance value.Morrison et al. [12] firstly obtained semantic segmentation of the scenes and scored the suctions using heuristics like distance from boundary and object curvature.Mahler et al. [10] designed a network to score a suction candidate with the depth image centered at the suction point and suction pose information as input.Correa et al. [22] further proposed a toppling strategy to expose access to robust suction points and increase the suction reliability.Shao et al. [9] proposed an online self-supervised learning method by predicting suction and getting results from a simulated environment.
None
[ [] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[]
null
null
57567688-2ec4-4522-a89d-72ef462373ef
completed
2025-04-29T14:36:04.699700
2025-05-27T14:00:48.169584
253679a2-607b-42a1-b54a-2e1f2a157084
Impaired orienting to social stimuli is one of the core early symptoms of autism spectrum disorder (ASD). However, in contrast to faces, name processing has rarely been studied in individuals with ASD. Here, we investigated brain activity and functional connectivity associated with recognition of names in the high-functioning ASD group and in the control group.EEG was recorded in 15 young males with ASD and 15 matched one-to-one control individuals. EEG data were analyzed with the event-related potential (ERP), event-related desynchronization and event-related synchronization (ERD/S), as well as coherence and direct transfer function (DTF) methods. Four categories of names were presented visually: one's own, close-other's, famous, and unknown.Differences between the ASD and control groups were found for ERP, coherence, and DTF. In individuals with ASD, P300 (a positive ERP component) to own-name and to a close-other's name were similar whereas in control participants, P300 to own-name was enhanced when compared to all other names. Analysis of coherence and DTF revealed disruption of fronto-posterior task-related connectivity in individuals with ASD within the beta range frequencies. Moreover, DTF indicated the directionality of those impaired connections-they were going from parieto-occipital to frontal regions. DTF also showed inter-group differences in short-range connectivity: weaker connections within the frontal region and stronger connections within the occipital region in the ASD group in comparison to the control group.Our findings suggest a lack of the self-preference effect and impaired functioning of the attentional network during recognition of visually presented names in individuals with ASD.
<li> <b>brain:</b> brain (UBERONParcellation)<li> <b>EEG:</b> electroencephalography (technique)<li> <b>event-related potential:</b> Other (technique)<li> <b>ERP:</b> Other (technique)
[ [ { "end": 229, "label": "UBERONParcellation", "start": 224 }, { "end": 366, "label": "technique", "start": 363 }, { "end": 457, "label": "technique", "start": 454 }, { "end": 397, "label": "biologicalSex", "start": 392 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "male: male (biologicalSex)" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 229, "label": "UBERONParcellation", "start": 224 }, { "end": 366, "label": "technique", "start": 363 }, { "end": 457, "label": "technique", "start": 454 }, { "end": 509, "label": "technique", "start": 486 }, { "end": 514, "label": "technique", "start": 511 }, { "end": 818, "label": "technique", "start": 815 }, { "end": 885, "label": "technique", "start": 882 } ]
null
null
91e98db8-1db6-474c-8a09-b13b3f182e0a
completed
2025-04-29T14:36:04.699706
2025-05-27T14:00:48.258300
1408af82-a6be-4d92-a97b-ea035691468b
The ERP analysis was performed using the BrainVisionA-nalyzer® software (Brain Products, Gilching, Germany).Preprocessing steps were analogous to those used in our previous study on name detection in ASD [29] since we aimed to compare the current and the previous P300 findings.First, EEG data were re-referenced to the averaged earlobes and then Butterworth zero phase filters were implemented: high-pass -0.1 Hz, 12 dB/oct, low-pass -30 Hz, 12 dB/oct, and notch filter -50 Hz.Correction of ocular artifacts was then performed using the Independent Component Analysis -ICA [72].After the decomposition of each data set into maximally statistically independent components, the components representing eye blinks were rejected based on the visual inspection of the component map [73].Ocular-artifactfree EEG data were obtained by back-projecting the remaining ICA components after they were multiplied using the reduced component-mixing matrix.Next, the EEG was segmented to obtain epochs extending from 200 ms before to 1000 ms after the stimulus onset (baseline correction from -200 to 0 ms).In the automatic artifact rejection, the maximum permitted voltage step per sampling point was 50 μV.In turn, the maximum permitted absolute difference between two values in the segment was 200 μV.The minimum and maximum permitted amplitudes were -200 and 200 μV, respectively, and the lowest permitted activity difference in the 100 ms interval was 0.5 μV. ERPs for own, close-other's, famous, and unknown names were computed for correct trials only.ERPs for the unknown category were computed only for one of the unknown names per subject, randomly chosen from the set of all three unknown names.This was done to have similar number of trials for different experimental conditions, thus to avoid problems with different signal-to-noise ratios in different experimental conditions (the higher the number of trials/repetitions, the higher the signal-to-noise ratio).Since we had three unfamiliar names (each presented 50 times, resulting in 150 trials in the unfamiliar condition) and one self-name (50 repetitions), one close-other's name (50 repetitions), and one famous name (50 repetitions), for each participant one unfamiliar name (50 repetitions) was selected for further analyses. The mean number of segments used to compute ERPs (in ASD and control groups, respectively) was as follows: own name -48, 48, close other's name -49, 47, famous name -47, 47, and unknown name -48, 48.We did not find any significant differences in the number of epochs used to compute ERPs between name categories or between groups.Trials were averaged individually for each electrode site, for each participant, and for each stimulus condition. For each experimental condition, P300 amplitude was calculated as the mean of values at each time point within the 400-550 ms time window (i.e., the mean amplitude method).This method is less affected by the possibly low signal-to-noise ratio than the peak amplitude method [74].Mean amplitudes of P300 were analyzed at CPz that is the typically selected electrode location for the analysis of P300 (e.g., [12,29,75]). ERD/S, coherence as a function of time, and DTF ERD/S reflects relative changes of the EEG spectral power recorded after the stimulus onset in comparison to a reference period registered before the stimulus presentation [59].Quantification of ERD/S was performed in time and frequency domains and was based on a method similar to the event-related spectral perturbation (ERPS) proposed by Makeig [76]. Coherence is a measure of synchronization between two signals based mainly on phase consistency.Coherence indicates the level of synchronization in activity between different neural populations, where high coherence reflects greater functional integration due to either corticocortical or cortical-subcortical-cortical connections [60].In order to obtain its time course, we estimated coherence in a way similar to event-related coherence [77].This is a method for the analysis of coherence between electrodes as a function of time (see Additional file 1 for the detailed description), and it generates coherence values for the entire time-frequency spectrum, allowing the analysis of coherence related to particular events in time, such as the presentation of visual stimuli. DTF, in turn, measures causal interactions in the frequency domain between two EEG channels, with respect to connections between all other available channels.DTF enables estimation of a strength and direction of activity flow from one location to another [61,62].DTF is defined within the framework of the Mulivariate Autoregressive Model -MVAR [61].In comparison to coherence, a great advantage of the MVAR approach is that it accounts for the whole multivariate set of signals, so the analysis is not performed separately for every pair of signals (which is the case for coherence), thus eliminating the problem of a presence of common sources in the set of signals [78].Detailed description of ERD/S, coherence, and DTF calculations is provided in Additional file 1. The EEG data preprocessing was as follows.EEG data were re-referenced to the averaged earlobes and then down-sampled to 250 Hz.Next, the signals were segmented into trials with respect to the onset of the fixation point.Trials with amplitudes exceeding ±125 μV were removed from further analysis.Accepted trials were passed to a third-order Butterworth bandpass filter in the frequency range of 3.0-32 Hz. Then EEG signals were decomposed by means of ICA [72], implemented into EEGLab using extended Infomax.All components identified as a source of eye movements or muscle artifacts were removed, and then the remaining ICA components were used to reconstruct the signal in the original electrode space.Next, a 1500ms segment was extracted from each trial in each experimental condition, with respect to the onset of the blank screen epoch that followed the presentation of the fixation point.In the case of DTF, the second step of artifact rejection was omitted because ICA disturbs the fitting of the MVAR model to EEG data [79]. The reasons are as follows.The MVAR model assumes that the amplitude of signal at a given channel and time sample can be described as a linear combination of previous samples derived from itself or from other channels with an added unpredictable random component (noise).According to this model, all channels of the multivariate signal may be more or less correlated but they are linearly independent.The procedure of the artifact rejection performed by ICA consists of three major steps: (i) decomposition of the original signal by ICA; (ii) removal the ICA components identified as sources of artifacts; and (iii) reconstruction of EEG signal from the remaining ICA components.As one can see, the steps (ii) and (iii) lead to removal from each channel of initial signal the same activity recognized as undesirable distribution.Thus, steps (ii) and (iii) make the channels of reconstructed, artifacts-free multivariate signal linearly dependent.However, the condition of the linear independence of the channels must be absolutely satisfied if he MVAR model has to be fitted to data. The number of EEG channels that could be used for estimation of the MVAR model was restricted by the number of available samples.In our study, the amount of the measured EEG data allowed the MVAR model to be fitted for up to 17 electrodes.Thus, 17 electrodes from the 62 available sensors were selected within our two regions of interest: frontal (F7, F5, F3, F1, FZ, F2, F4, F6, and F8) and parieto-occipital (P7, PO7, O1, OZ, O2, PO8, P8, and Iz).The criteria for selection were as follows: (i) electrodes had to be evenly distributed within each region of interest; (ii) in the case of the frontal region, they had to be at some distance away from the most anterior electrode sites that are typically strongly influenced by eye-movements artifacts (in the case of DTF calculations, ICA-based artifact rejection had to be omitted); and (iii) the number of electrodes located within the left and right hemisphere had be the same (we had no hypothesis regarding lateralization).ERD/S, coherence, and DTF were calculated for the same set of electrodes. ERD/S was analyzed at each of the 17 electrodes in the following frequency ranges (within the theta, alpha, and beta bands, respectively): 4-8 Hz in 100-250 ms time window, 10-13 Hz in 350-800 ms time window and 13-18 Hz in 100-250 ms time window.Selection of time windows and frequency ranges was guided by results of ERD/S collapsed across groups and conditions (see Additional file 2, Figure A1) [80]. Coherence was statistically analyzed for selected pairs of electrodes.In order to avoid the double-dipping problem [81], such selection has to be orthogonal to potential differences between groups or experimental conditions.To this end, we (i) collapsed the EEG signal across the two groups (ASD, controls) and across the four name categories (self, close-other's, famous, and unknown); (ii) noticed that local (i.e., within-region) effects were very weak whereas between-regions effects (i.e., long-range connections) were clearly visible (see Additional file 2, Figure A2); (ii) calculated the average coherence values for the theta, alpha, and beta bands based on all posterioranterior pairs of electrodes; and finally, (iii) selected pairs of electrodes in which the coherence values were higher than the average calculated for a given frequency band. In this way, we selected 13, 11, and 21 pairs of electrodes for the analyses of coherence in the theta, alpha, and beta bands, respectively, and the following statistical analyses were run only on these pairs of electrodes.Our selection procedure is independent from our main analysis; the selection was based on the collapsed data from both groups and all conditions, whereas the analysis compared the groups/ conditions between each other.Thus, without introducing any bias [81], we could limit the number of electrodes pairs in our analysis and lower the risk of type II error due to the correction for multiple comparisons. Selection of time windows and frequency ranges was also based on coherence results collapsed across groups and conditions (see Additional file 2, Figure A2) [80].Coherence was analyzed in the following frequency ranges (within the theta, alpha, and beta bands, respectively): 4-8 Hz in 250-650 ms time window, 10-13 Hz in 500-800 ms time window, and 21-28 Hz in 250-750 ms time window. DTFs were calculated for three subsequent time windows: 0-200, 200-400, and 400-600 ms.DTF calculations were restricted to frequencies within the beta band: low (13-18 Hz) and high (18-30 Hz) as moderate and long-distance cortical connections are based mainly on beta oscillations [82,83].This is also consistent with the evidence pointing to the role of beta oscillations in attentional processes in the visual domain [44,[84][85][86][87]. Selection of connections for statistical analyses was based on a procedure that was orthogonal to potential group differences [81] and was done on the basis of the DTF averaged for the control and ASD groups (see Additional file 2, Figures A3, A4, andA5).Similarly to the selection procedure used for the coherence, connections with DTF values higher than the average were further statistically compared in the two groups.The number of connections was 56, 64, and 45, for the 0-200, 200-400, and 400-600 ms time-window, respectively.
<li> <b>ERP:</b> Other (technique)<li> <b>EEG:</b> electroencephalography (technique)<li> <b>ERD/S:</b> Other (technique)<li> <b>DTF:</b> Other (technique)<li> <b>frontal:</b> frontalLobe (UBERONParcellation)<li> <b>parieto-occipital:</b> Other (UBERONParcellation)
[ [ { "end": 288, "label": "technique", "start": 285 }, { "end": 806, "label": "technique", "start": 803 }, { "end": 956, "label": "technique", "start": 953 }, { "end": 3235, "label": "technique", "start": 3232 }, { "end": 4406, "label": "technique", "start": 4403 }, { "end": 5101, "label": "technique", "start": 5098 }, { "end": 5139, "label": "technique", "start": 5136 }, { "end": 5508, "label": "technique", "start": 5505 }, { "end": 6114, "label": "technique", "start": 6111 }, { "end": 6763, "label": "technique", "start": 6760 }, { "end": 7227, "label": "technique", "start": 7224 }, { "end": 7383, "label": "technique", "start": 7380 }, { "end": 8928, "label": "technique", "start": 8925 }, { "end": 7556, "label": "UBERONParcellation", "start": 7549 }, { "end": 7810, "label": "UBERONParcellation", "start": 7803 }, { "end": 7619, "label": "UBERONParcellation", "start": 7602 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "\r\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 7, "label": "technique", "start": 4 }, { "end": 288, "label": "technique", "start": 285 }, { "end": 806, "label": "technique", "start": 803 }, { "end": 956, "label": "technique", "start": 953 }, { "end": 3235, "label": "technique", "start": 3232 }, { "end": 4406, "label": "technique", "start": 4403 }, { "end": 5101, "label": "technique", "start": 5098 }, { "end": 5139, "label": "technique", "start": 5136 }, { "end": 5508, "label": "technique", "start": 5505 }, { "end": 6114, "label": "technique", "start": 6111 }, { "end": 6763, "label": "technique", "start": 6760 }, { "end": 7227, "label": "technique", "start": 7224 }, { "end": 7383, "label": "technique", "start": 7380 }, { "end": 8928, "label": "technique", "start": 8925 }, { "end": 3150, "label": "technique", "start": 3145 }, { "end": 3198, "label": "technique", "start": 3193 }, { "end": 3393, "label": "technique", "start": 3388 }, { "end": 5026, "label": "technique", "start": 5021 }, { "end": 8193, "label": "technique", "start": 8188 }, { "end": 8267, "label": "technique", "start": 8262 }, { "end": 8586, "label": "technique", "start": 8581 }, { "end": 3192, "label": "technique", "start": 3189 }, { "end": 4327, "label": "technique", "start": 4324 }, { "end": 4485, "label": "technique", "start": 4482 }, { "end": 4590, "label": "technique", "start": 4587 }, { "end": 5046, "label": "technique", "start": 5043 }, { "end": 6005, "label": "technique", "start": 6002 }, { "end": 7980, "label": "technique", "start": 7977 }, { "end": 8213, "label": "technique", "start": 8210 }, { "end": 10627, "label": "technique", "start": 10624 }, { "end": 11145, "label": "technique", "start": 11142 }, { "end": 11314, "label": "technique", "start": 11311 }, { "end": 7556, "label": "UBERONParcellation", "start": 7549 }, { "end": 7810, "label": "UBERONParcellation", "start": 7803 }, { "end": 7619, "label": "UBERONParcellation", "start": 7602 } ]
null
null
d79fd466-74d9-4f6d-b530-dc09d5dc51dd
completed
2025-04-29T14:36:04.699712
2025-05-27T14:00:48.357756
cead24b1-175c-4274-80e6-3146a2e3ef0a
Moderate physical activity improves various cognitive functions, particularly when it is applied simultaneously to the cognitive task. In two psychoneuroendocrinological within-subject experiments, we investigated whether very low-intensity motor activity, i.e. walking, during foreign-language vocabulary encoding improves subsequent recall compared to encoding during physical rest. Furthermore, we examined the kinetics of brain-derived neurotrophic factor (BDNF) in serum and salivary cortisol. Previous research has associated both substances with memory performance.In both experiments, subjects performed better when they were motorically active during encoding compared to being sedentary. BDNF in serum was unrelated to memory performance. In contrast we found a positive correlation between salivary cortisol concentration and the number of correctly recalled items. In summary, even very light physical activity during encoding is beneficial for subsequent recall.
<li> <b>brain-derived neurotrophic factor:</b> Other (technique)<li> <b>BDNF:</b> Other (technique)<li> <b>serum:</b> Other (UBERONParcellation)
[ [] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Incorrect" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Incorrect" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 459, "label": "technique", "start": 426 }, { "end": 465, "label": "technique", "start": 461 }, { "end": 702, "label": "technique", "start": 698 }, { "end": 475, "label": "UBERONParcellation", "start": 470 }, { "end": 711, "label": "UBERONParcellation", "start": 706 } ]
null
null
c40f3845-bba9-4fd9-a34c-38e6d6aded8a
completed
2025-04-29T14:36:04.699718
2025-05-27T14:00:48.485665
9c0366ce-8a25-4baa-8dc6-819cd93de10c
Subjects were first screened in a pre-experimental evaluation session.After this session participants were asked to come to our laboratory for two experimental learning sessions.The experimental procedure was identical for experiment 1 and 2. The only difference was that we collected blood samples for BNDF analysis in experiment 1 and saliva samples for cortisol analysis in experiment 2.
<li> <b>BNDF:</b> Other (technique)
[ [] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Incorrect" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Incorrect" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 307, "label": "technique", "start": 303 } ]
null
null
0b15b828-44d6-4b60-a7f2-42968ea1db5d
completed
2025-04-29T14:36:04.699725
2025-05-27T14:00:48.575501
e156cac1-d754-4ad5-add9-f92e2d6c9af2
It has been suggested that changes in some event-related potential (ERP) parameters associated with controlled processing of stimuli could be used as biomarkers of amnestic mild cognitive impairment (aMCI). However, data regarding the suitability of ERP components associated with automatic and involuntary processing of stimuli for this purpose are not conclusive. In the present study, we studied the Mismatch Negativity (MMN) component, a correlate of the automatic detection of changes in the acoustic environment, in healthy adults and adults with aMCI (age range: 50-87 years). An auditory-visual attention-distraction task, in two evaluations separated by an interval of between 18 and 24 months, was used. In both evaluations, the MMN amplitude was significantly smaller in the aMCI adults than in the control adults. In the first evaluation, such differences were observed for the subgroup of adults between 50 and 64 years of age, but not for the subgroup of 65 years and over. In the aMCI adults, the MMN amplitude was significantly smaller in the second evaluation than in the first evaluation, but no significant changes were observed in the control adult group. The MMN amplitude was found to be a sensitive and specific biomarker of aMCI, in both the first and second evaluation.
<li> <b>event-related potential:</b> Other (technique)<li> <b>ERP:</b> Other (technique)<li> <b>Mismatch Negativity:</b> Other (technique)<li> <b>MMN:</b> Other (technique)<li> <b>adults:</b> homoSapiens (species)
[ [] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Incorrect" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Incorrect" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 66, "label": "technique", "start": 43 }, { "end": 71, "label": "technique", "start": 68 }, { "end": 253, "label": "technique", "start": 250 }, { "end": 422, "label": "technique", "start": 403 }, { "end": 427, "label": "technique", "start": 424 }, { "end": 742, "label": "technique", "start": 739 }, { "end": 1015, "label": "technique", "start": 1012 }, { "end": 1183, "label": "technique", "start": 1180 }, { "end": 536, "label": "species", "start": 530 }, { "end": 547, "label": "species", "start": 541 }, { "end": 797, "label": "species", "start": 791 }, { "end": 824, "label": "species", "start": 818 }, { "end": 908, "label": "species", "start": 902 }, { "end": 1006, "label": "species", "start": 1000 } ]
null
null
d143ad27-b2cb-4d96-af24-bea674f24a47
pending
2025-04-29T14:36:04.699731
2025-04-29T14:36:04.699731
9b5bac34-41e4-42cf-8938-0613d4e84e80
ABSTRACT Staff training has been cited as an effective intervention to reduce behavioral and psychiatric symptoms of dementia (BPSD) in nursing home residents. However, the reproducibility of interventions can be a barrier to their dissemination. A systematic review of controlled clinical trials on the effectiveness of staff training for reducing BPSD, published between 1990 and 2013 on the EMBASE, PUBMED, LILACS, PSYCHINFO and CINAHL databases, was carried out to evaluate the reproducibility of these interventions by 3 independent raters. The presence of sufficient description of the intervention in each trial to allow its reproduction elsewhere was evaluated. Descriptive analyses were carried out. Despite reference to a detailed procedures manual in the majority of trials, these manuals were not easily accessible, limiting the replication of studies. The professional expertise requirement for training implementation was not clearly described, although most studies involved trainers with moderate to extensive expertise, further limiting training reproducibility.
None
[ [] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[]
null
null
b400036d-e610-4845-b99b-c806e4e42b50
pending
2025-04-29T14:36:04.699737
2025-04-29T14:36:04.699737
6492b277-6397-401e-8234-05fe0e37cbe9
B ehavioral and psychiatric symptoms of dementia (BPSD) are highly frequent particularly at moderate to severe stages. 1 These symptoms are very distressing and represent one of the leading causes of institutionalization of demented subjects. 2][10] A new study using an intervention that has already been applied will only prove feasible if sufficient information about the original procedures is provided in previous studies.It is important to ascertain whether interventions were described in such a way that makes them amenable to replication.Therefore, the aim of this study was to evaluate the provision of welldescribed operationalization of staff training programs and the presence of guidelines that ensure their reproducibility in future studies.
None
[ [] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[]
null
null
7a5de404-3490-4e3b-9ad0-8edb277bda29
completed
2025-04-29T14:36:04.699743
2025-05-27T14:00:48.733536
6738b47a-e989-47da-b2db-694bacacc487
AbstractIndividuals with autism are reported to integrate information from visual and auditory channels in an idiosyncratic way. Multisensory integration (MSI) of simple, non-social stimuli (i.e., flashes and beeps) was evaluated in adolescents and adults with (n = 20) and without autism (n = 19) using a reaction time (RT) paradigm using audio, visual, and audiovisual stimuli. For each participant, the race model analysis compares the RTs on the audiovisual condition to a bound value computed from the unimodal RTs that reflects the effect of redundancy. If the actual audiovisual RTs are significantly faster than this bound, the race model is violated, indicating evidence of MSI. Our results show that the race model violation occurred only for the typically-developing (TD) group. While the TD group shows evidence of MSI, the autism group does not. These results suggest that multisensory integration of simple information, void of social content or complexity, is altered in autism. Individuals with autism may not benefit from the advantage conferred by multisensory stimulation to the same extent as TD individuals. Altered MSI for simple, non-social information may have cascading effects on more complex perceptual processes related to language and behaviour in autism.
<li> <b>autism:</b> homoSapiens (species)<li> <b>adolescents:</b> homoSapiens (species)<li> <b>adults:</b> homoSapiens (species)
[ [] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Incorrect" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Incorrect" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 31, "label": "species", "start": 25 }, { "end": 288, "label": "species", "start": 282 }, { "end": 842, "label": "species", "start": 836 }, { "end": 992, "label": "species", "start": 986 }, { "end": 1017, "label": "species", "start": 1011 }, { "end": 1283, "label": "species", "start": 1277 }, { "end": 244, "label": "species", "start": 233 }, { "end": 255, "label": "species", "start": 249 } ]
null
null
38e357d9-90bd-4ff6-a636-af9963c125f5
completed
2025-04-29T14:36:04.699749
2025-05-27T14:00:48.841456
ec087229-cf94-4935-9aad-60167e0314c6
Individuals with autism are reported to integrate information from visual and auditory channels in an idiosyncratic way.Multisensory integration (MSI) of simple, non-social stimuli (i.e., flashes and beeps) was evaluated in adolescents and adults with (n = 20) and without autism (n = 19) using a reaction time (RT) paradigm using audio, visual, and audiovisual stimuli.For each participant, the race model analysis compares the RTs on the audiovisual condition to a bound value computed from the unimodal RTs that reflects the effect of redundancy.If the actual audiovisual RTs are significantly faster than this bound, the race model is violated, indicating evidence of MSI.Our results show that the race model violation occurred only for the typically-developing (TD) group.While the TD group shows evidence of MSI, the autism group does not.These results suggest that multisensory integration of simple information, void of social content or complexity, is altered in autism.Individuals with autism may not benefit from the advantage conferred by multisensory stimulation to the same extent as TD individuals.Altered MSI for simple, non-social information may have cascading effects on more complex perceptual processes related to language and behaviour in autism. Individuals with autism often avoid certain sensory stimuli (e.g., withdrawing from specific noises like the sound of a vacuum cleaner, avoiding certain textures or smells) and/or seek out sensory experiences through stimulatory behaviours (e.g., peering, echoing, tapping surfaces) 1,2 .The prevalence of sensory issues in autism is thought to vary between 69 and 95%, which confirms that sensory abnormalities are a concern for the vast majority of individuals with autism 3 .Furthermore, sensory issues have been shown to occur across development in autism 3,4 , as well as across sensory modalities 1 .Atypical reactivity to sensory input is now included among the DSM-5 symptoms for Autism Spectrum Disorder 5 .Autism Spectrum Disorder will continue to be referred to as "autism" throughout the text. In light of the significance of sensory processing abnormalities, it has been suggested that these may actually contribute to some of the core social and behavioural characteristics of autism 6,7 .If sensory processing was altered, there would be a subsequent effect on higher-order processes.For instance, disruption in basic visual or auditory processing may contribute to deficits found at the higher level, such as socio-communicative functioning 7 .In fact, studies have demonstrated a relationship between sensory processing issues and social responsiveness 8 , communicative impairments and maladaptive behaviours 9 , as well as behavioural/emotional problems 10,11 . The study of unimodal integration (e.g., integrating multiple visual stimuli into a whole) can be helpful to better understand different unisensory experiences.However, multisensory integration (MSI) may be a more ecological construct in that it better reflects naturalistic sensory experiences given that most of the situations that are encountered involve stimulation of more than one sensory modality at a time 12,13 .Multisensory integration is the process by which information from multiple sensory modalities are integrated into a whole 14,15 .The main advantage of MSI is that it allows to process incoming information more quickly and effectively 15 .In fact, the advantage conferred by MSI, referred to as multisensory facilitation, goes beyond what would be expected due to the effect of sensory redundancy 16 . Various cognitive theories have hypothesized that there may exist altered sensory integration in autism, and that this alteration may be at the root of many diagnostic features of autism [17][18][19] .Deficits in sensory integration would potentially lead to a disjointed, confusing, and overwhelming perception of the physical surroundings 20 .Sensory aversion and sensory seeking behaviours in autism, as well as social withdrawal, and communication difficulties may then be partially explained as an effort to cope with the overload of information. As the wide-ranging implications of MSI alterations in autism have become more apparent, studies using a variety of different paradigms to evaluate this area of functioning have emerged.Some such approaches have included complex stimuli and task demands, like the ability to integrate audiovisual information to process emotional expressions 21 , the speech-in-noise paradigm 22,23 , and the McGurk effect task [24][25][26][27][28][29][30] .Other researchers have investigated the issue using more simple approaches using non-social stimuli, such as the flash-beep illusion task [31][32][33][34] , and visual search tasks 35,36 . The simple reaction time (RT) task has been frequently used to investigate the ability to integrate basic auditory and visual information in clinical populations (e.g., Schizophrenia 37,38 ; Developmental Dyslexia 39 ; Parkinson's Disease 40 ) and non-clinical populations 41,42 .During the audiovisual version of the RT task, participants are exposed to 3 conditions: (1) visual only, (2) auditory only, and (3) audiovisual multisensory presentation.The expectation is that typical multisensory function would lead to a facilitatory effect (i.e., significantly faster reaction time) during the audiovisual condition relative to the two unimodal conditions. Despite the fact that the RT paradigm is arguably the simplest and most straightforward approach to investigate multisensory facilitation, only one study to date has used it to evaluate MSI in children and adolescents (7-16 years old) with autism using simple, non-social audiovisual stimuli 43 .While the typically-developing comparison group showed evidence for multisensory facilitation, in autism, both the younger (ages 7-10) and older (ages 11-16) age groups did not.Given the need to evaluate MSI using simple, non-social stimuli in order to better conceptualize this area of functioning in autism, and the fact that this basic task has never been completed with an older autistic population, the current study aims to fill the gaps in the literature, and help to better define MSI functioning in autism.
<li> <b>adolescents:</b> homoSapiens (species)<li> <b>adults:</b> homoSapiens (species)
[ [] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Incorrect" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Incorrect" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 235, "label": "species", "start": 224 }, { "end": 5629, "label": "species", "start": 5618 }, { "end": 246, "label": "species", "start": 240 } ]
null
null
0021772e-4885-40bf-90a7-b66788f1536b
completed
2025-04-29T14:36:04.699755
2025-05-27T14:00:48.941898
96a30464-1924-4cb0-acf1-bf7b188c961c
Preoperative evaluation of nipple-areola complex (NAC) tumour involvement is crucial to select patients candidates for nipple-sparing mastectomy. Our aim was to validate a previously developed automated method able to compute the three-dimensional (3D) tumour-to-NAC distance (the most predictive parameter of nipple involvement), using magnetic resonance imaging (MRI) datasets acquired with a scanner and protocol different from those of the development phase.We performed a retrospective analysis of 77 patients submitted to total mastectomy and preoperatively studied with MRI. The new method consisted of automated segmentation of both NAC and tumour and subsequent computation of the 3D distance between them; standard manual two-dimensional segmentation was independently performed. Paraffin-embedded section examination of the removed NAC was performed to identify the neoplastic involvement. The ability of both methods to discriminate between patients with and without NAC involvement was compared using receiver operating characteristic (ROC) analysis.The 3D tumour-to-NAC distance was correctly computed for 72/77 patients (93.5%); tumour and NAC segmentation method failed in two and three cases, respectively. The diagnostic performance of the 3D automated method at best cut-off values was consistently better than that of the 2D manual method (sensitivity 78.3%, specificity 71.4%, positive predictive value 87.5%, negative predictive value 56.3%, and AUC 0.77 versus 73.9%, 61.2%, 47.2%, 83.3%, and 0.72, respectively), even if the difference did not reach statistical significance (p = 0.431).The introduction of the 3D automated method in a clinical setting could improve the diagnostic performance in the preoperative assessment of NAC tumour involvement.
<li> <b>magnetic resonance imaging:</b> magneticResonanceImaging (technique)<li> <b>MRI:</b> magneticResonanceImaging (technique)
[ [ { "end": 363, "label": "technique", "start": 337 }, { "end": 368, "label": "technique", "start": 365 }, { "end": 580, "label": "technique", "start": 577 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 363, "label": "technique", "start": 337 }, { "end": 368, "label": "technique", "start": 365 }, { "end": 580, "label": "technique", "start": 577 } ]
null
null
ebd20c31-361d-4eff-ad8f-ce3bf9cf265c
completed
2025-04-29T14:36:04.699761
2025-05-27T14:00:49.037871
b5c02b9c-dbab-44d9-ac2a-8833987b8930
Preoperative MRI has been shown to have a crucial role in the assessment of breast cancer patients potentially eligible for NSM.Compared to mammography, which is a 2D imaging modality, breast MRI provides a 3D evaluation of the whole breast, thus reducing the loss of spatial information about tumour extent and location.For that reason, MRI has been considered as the method of choice to preoperatively predict occult nipple involvement [20,21]. To facilitate surgical planning and to standardise the use of tumour-to-NAC distance as the main predictor of nipple infiltration by tumour, Giannini et al. [16] recently developed an automated method to compute the 3D tumour-to-NAC distance, which overcomes the performance of manual 2D methods in predicting NAC involvement.However, this method was developed and validated using images acquired with the same MRI scanner and having the same acquisition protocol.When developing automated methods, this could represent a strong bias, since images strongly differ between scanners and imaging protocols. In the current study, we validated this algorithm using an external dataset of images acquired in a different centre, using a different MRI scanner and acquisition protocol from that used in the development phase.The performance reached by this method with this external dataset (sensitivity 78%, specificity 72%) demonstrated that this 3D automated method could represent a reliable method to preoperatively compute tumour-to-NAC distance, improving the management of patients candidate for NSM.The algorithm had a failure rate of only 5% because of the failure of the nipple (two cases) or tumour (two cases) segmentation. The automated system presented in this study may show many advantages.First, the 3D tumour-to-NAC measurements were more reliable than the 2D measurements calculated using MIP images.In fact, when a measurement is carried out on the axial/sagittal projection, the information along the z-/y-axes is lost, with the consequent chance that the lesion and the nipple appear closer, as lying on the same x-/y-axis.Actually, the lesion and nipple are often more distant, as they are seated in different slices of MRI volume.In fact, the distance calculated by the automated algorithm was greater than that manually calculated in 55/72 cases (76%).In a recent study [21], the issue of three-dimensional "real" distance has been discussed.However, in that case, the measurements were done in a completely manual way, by computing four distinct distances in each case, using digital images on flat-screen liquid-crystal display monitors.This is a time-consuming task, which is difficult to apply in clinical practice.In addition, this study [21] did not make a comparison with the standard methods. Interestingly, no fully automated methods for the nipple segmentation on MRI are available yet.The nipples often differ in form and intensity of the signal in different patients; in addition, the nipple is not always perfectly located at the centre of the T2-weighted image and, when inverted, cannot always be distinguished from glandular tissue.In our experience, 92% of the nipples were properly segmented by the algorithm.Taken for granted that the tumour-to-NAC distance is up to date the most useful parameter for the preoperative assessment when NSM is under consideration, the main issue is to define the best cut-off value capable of predicting NAC involvement.In this regard, the literature is inhomogeneous.Some authors propose 10 mm as the ideal cut-off [13], while others recommend 20 mm [22,23].In a recent study, a distance of 5 mm was suggested [14]. In the present series, the 3D automated method improved the diagnostic performance when compared to 2D manual measurement, even though not significantly.In particular, the best compromise between sensitivity and specificity for each method was reached using the cut-off of 30 mm for the automated method and of 21 mm for the manual method.This difference is consistent with the increase by 11.5 mm in the average tumour-to-NAC distance when processed by the automated method versus the manual one and with the previously mentioned greater distance in 76% of cases as compared to the manual measurement. As shown in Table 2, specificity and PPV of the automated method overcome those of the manual method at all the cut-off values.Sensitivity and NPV are instead higher only for the best cut-off (30 mm) since the automated method is not able to clearly identify NAC-negative patients at smaller distances.All the patients with tumour-to-NAC automated distance ≤ 5 mm and ≤ 10 mm showed tumour involvement of the nipple at the final pathology, confirming the high specificity of the automated method.This performance is higher compared to the manual measurement, which showed 96% and 86% specificity at these thresholds.However, the sensitivity at ≤ 5 and ≤ 10 mm was very low: only 9% and 26% of the patients with tumour involvement of the nipple were positive when tested with the automated method at these cut-off values, respectively. Since the aim of the assessment before surgery is to propose NSM to all patients who may potentially preserve the nipple (i.e.patients without NAC tumour involvement at pathology), specificity and PPV are the most useful preliminary parameters to know.As a high specificity is related to a low sensitivity, many patients with NAC involvement (i.e.patients with NAC tumour involvement at pathology) will still be candidates for NSM. By choosing the cut-off at ≤ 10 mm, the high specificity (100%) allows to exclude all the patients who certainly will not be able to keep the nipple, while the low sensitivity (26%) causes the inclusion in the selection for NSM of most patients (74%) with NAC involvement.However, the current protocol for the NSM mandates the intraoperative histological examination of the retroareolar tissue, which shows a good negative predictive ability.In such cases, the surgery may be converted to SSM at the same surgical time. The data obtained from our study are similar to those we have previously obtained with the same 3D methods on images obtained on a different equipment, as shown in Table 3, as expected from an automated not operatorsensitive and therefore more reliable algorithm.The main difference is between the value of the 3D best cutoff considered in the previous and in the present study, 21 mm and 30 mm, respectively.This is an important issue that deserves further investigation.A prospective series taking into account the breast volume as well as the use of a standardised MRI protocol for the acquisition of T2-weighted and DCE images may help overcoming the gap. Limitations of our study are mainly related to its retrospective design.Our series covers a period of almost 6 years, during which there have been technological advances that, although modest, could have influenced the signal to noise ratio and the image quality, changing the segmentation capabilities (especially for the nipples) of the automated algorithm, as shown in Fig. 6.The incomplete segmentation of the NAC causes the automated distance to be computed between the edge of the lesion and the front part of the nipple, rather than between the edge of the lesion and the base of NAC.Moreover, the correct localisation of the nipple could be difficult in some cases, such as malposition or introflexion, and need the supervision of a technician with specialised experience in breast MRI.The implementation of this step is definitely needed to maximise the accuracy of the algorithm.Secondly, choosing the cut-off at ≤ 10 mm, the sensitivity of the automated method remains low and many positive cases will be overlooked.It is, therefore, necessary to perform the frozen examination of subareolar tissue during surgery, which is currently considered the safest method to predict nipple involvement. In conclusion, our study suggests that breast MRI is a promising method for the preoperative assessment of patients candidate for NSM by predicting the occult involvement of the NAC.Our novel 3D automated method seems to improve the results obtained with the 2D manual distance measurement also being validated on an independent external dataset.A cutoff value of ≤ 10 mm provided great accuracy as all the patients with a tumour-to-NAC distance ≤ 10 mm require the removal of the nipple.If integrated into clinical practice, this method could be useful to reduce the variability in selecting patients who may have the nipple preserved.
<li> <b>MRI:</b> magneticResonanceImaging (technique)
[ [ { "end": 16, "label": "technique", "start": 13 }, { "end": 195, "label": "technique", "start": 192 }, { "end": 341, "label": "technique", "start": 338 }, { "end": 861, "label": "technique", "start": 858 }, { "end": 1190, "label": "technique", "start": 1187 }, { "end": 2186, "label": "technique", "start": 2183 }, { "end": 2842, "label": "technique", "start": 2839 }, { "end": 6595, "label": "technique", "start": 6592 }, { "end": 7477, "label": "technique", "start": 7474 }, { "end": 7938, "label": "technique", "start": 7935 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 16, "label": "technique", "start": 13 }, { "end": 195, "label": "technique", "start": 192 }, { "end": 341, "label": "technique", "start": 338 }, { "end": 861, "label": "technique", "start": 858 }, { "end": 1190, "label": "technique", "start": 1187 }, { "end": 2186, "label": "technique", "start": 2183 }, { "end": 2842, "label": "technique", "start": 2839 }, { "end": 6595, "label": "technique", "start": 6592 }, { "end": 7477, "label": "technique", "start": 7474 }, { "end": 7938, "label": "technique", "start": 7935 } ]
null
null
762a9ed8-6bb2-41a4-adc6-1f971308c554
completed
2025-04-29T14:36:04.699767
2025-05-27T14:00:49.175980
96990ae9-d963-452c-a23e-48396ea7b03c
AbstractNeuroinflammation is initiated in response to ischemic stroke, generally with the hallmarks of microglial activation and collateral brain injury contributed by robust inflammatory effects. Triggering receptor expressed on myeloid cells (TREM)-1, an amplifier of the innate immune response, is a critical regulator of inflammation. This study identified that microglial TREM-1 expression was upregulated following cerebral ischemic injury. After pharmacologic inhibition of TREM-1 with synthetic peptide LP17, ischemia-induced infarction and neuronal injury were substantially alleviated. Moreover, blockade of TREM-1 can potentiate cellular proliferation and synaptic plasticity in hippocampus, resulting in long-term functional improvement. Microglial M1 polarization and neutrophil recruitment were remarkably abrogated as mRNA levels of M1 markers, chemokines, and protein levels of myeloperoxidase and intracellular adhesion molecule-1 (ICAM-1) were decreased by LP17. Mechanistically, both in vivo and in vitro, we delineated that TREM-1 can activate downstream pro-inflammatory pathways, CARD9/NF-κB, and NLRP3/caspase-1, through interacting with spleen tyrosine kinase (SYK). In addition, TREM-1-induced SYK initiation was responsible for microglial pyroptosis by elevating levels of gasdermin D (GSDMD), N-terminal fragment of GSDMD (GSDMD-N), and forming GSDMD pores, which can facilitate the release of intracellular inflammatory factors, in microglia. In summary, microglial TREM-1 receptor yielded post-stroke neuroinflammatory damage via associating with SYK.
<li> <b>brain:</b> brain (UBERONParcellation)<li> <b>microglial:</b> Other (species)<li> <b>hippocampus:</b> hippocampalFormation (UBERONParcellation)<li> <b>microglia:</b> Other (species)<li> <b>in vivo:</b> inVivo (preparationType)<li> <b>in vitro:</b> inVitro (preparationType)
[ [ { "end": 145, "label": "UBERONParcellation", "start": 140 }, { "end": 701, "label": "UBERONParcellation", "start": 690 }, { "end": 1010, "label": "preparationType", "start": 1003 }, { "end": 1023, "label": "preparationType", "start": 1015 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "\r\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 145, "label": "UBERONParcellation", "start": 140 }, { "end": 113, "label": "species", "start": 103 }, { "end": 376, "label": "species", "start": 366 }, { "end": 1264, "label": "species", "start": 1254 }, { "end": 1493, "label": "species", "start": 1483 }, { "end": 701, "label": "UBERONParcellation", "start": 690 }, { "end": 1469, "label": "species", "start": 1460 }, { "end": 1010, "label": "preparationType", "start": 1003 }, { "end": 1023, "label": "preparationType", "start": 1015 } ]
null
null
6f9fe4f8-58f2-4739-89ad-c05a323e8485
completed
2025-04-29T14:36:04.699774
2025-05-27T14:00:49.278633
ec5c1b22-41ea-46e3-9f47-6f0ad1d50e43
Degenerated neurons were detected by FJC (Millipore, USA) as previously described 29 .Frozen sections were sequentially immersed in 1% NaOH/80% ethanol solution, 70% ethanol, and 0.06% potassium permanganate solution.The slides were then stained with 0.0001% FJC working solution.
<li> <b>neurons:</b> Other (species)
[ [ { "end": 19, "label": "UBERONParcellation", "start": 12 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Incorrect" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "neuron: Other (UBERONParcellation)" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 19, "label": "species", "start": 12 } ]
null
null
79584fe5-c389-4b4b-a555-4f854012abeb
pending
2025-04-29T14:36:04.699780
2025-04-29T14:36:04.699780
2abc5215-a90f-4c09-922d-deadbbde1152
None
[ [] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[]
null
null
9d4c654a-3191-4109-af58-1d2d465dc16a
completed
2025-04-29T14:36:04.699786
2025-05-27T14:00:49.379530
c46ed666-fbcc-4171-8517-791ff46da54e
The reports below describe the application of the neural technology in marketing research in combination with: fNRI, lie detection, advertisement research, fake rating behavior in e-commerce and stereotypes activated by media.
<li> <b>neural:</b> Other (species)<li> <b>fNRI:</b> Other (technique)
[ [] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Incorrect" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Incorrect" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 56, "label": "species", "start": 50 }, { "end": 115, "label": "technique", "start": 111 } ]
null
null
1cf790e0-5a73-43eb-92a6-96480a8cf830
completed
2025-04-29T14:36:04.699792
2025-05-27T14:00:49.470136
b5ebdfe4-6f4d-4d71-ab82-b0062ffa5f8c
Transcranial direct current stimulation (tDCS) is a non-invasive method to modulate cortical excitability in humans. Here, we examined the effects of anodal tDCS on suprahyoid motor evoked potentials (MEP) when applied over the hemisphere with stronger and weaker suprahyoid/submental projections, respectively, while study participants performed a swallowing task. Thirty healthy volunteers were invited to two experimental sessions and randomly assigned to one of two different groups. While in the first group stimulation was targeted over the hemisphere with stronger suprahyoid projections, the second group received stimulation over the weaker suprahyoid projections. tDCS was applied either as anodal or sham stimulation in a random cross-over design. Suprahyoid MEPs were assessed immediately before intervention, as well as 5, 30, 60, and 90 min after discontinuation of stimulation from both the stimulated and non-stimulated contralateral hemisphere. We found that anodal tDCS (a-tDCS) had long-lasting effects on suprahyoid MEPs on the stimulated side in both groups (tDCS targeting the stronger projections: F (1,14) = 96.2, p < 0.001; tDCS targeting the weaker projections: F (1,14) = 37.45, p < 0.001). While MEPs did not increase when elicited from the non-targeted hemisphere after stimulation of the stronger projections (F (1,14) = 0.69, p = 0.42), we found increased MEPs elicited from the non-targeted hemisphere after stimulating the weaker projections (at time points 30-90 min) (F (1,14) = 18.26, p = 0.001). We conclude that anodal tDCS has differential effects on suprahyoid MEPs elicited from the targeted and non-targeted hemisphere depending on the site of stimulation. This finding may be important for the application of a-tDCS in patients with dysphagia, for example after stroke.
<li> <b>Transcranial direct current stimulation:</b> Other (technique)<li> <b>tDCS:</b> Other (technique)<li> <b>cortical:</b> cerebralCortex (UBERONParcellation)<li> <b>humans:</b> homoSapiens (species)<li> <b>suprahyoid:</b> Other (UBERONParcellation)<li> <b>motor evoked potentials:</b> Other (technique)<li> <b>MEP:</b> Other (technique)<li> <b>hemisphere:</b> cerebralHemisphere (UBERONParcellation)<li> <b>a-tDCS:</b> Other (technique)<li> <b>stroke:</b> Other (species)
[ [ { "end": 39, "label": "technique", "start": 0 }, { "end": 45, "label": "technique", "start": 41 }, { "end": 161, "label": "technique", "start": 157 }, { "end": 678, "label": "technique", "start": 674 }, { "end": 987, "label": "technique", "start": 983 }, { "end": 995, "label": "technique", "start": 991 }, { "end": 1084, "label": "technique", "start": 1080 }, { "end": 1153, "label": "technique", "start": 1149 }, { "end": 1561, "label": "technique", "start": 1557 }, { "end": 1758, "label": "technique", "start": 1754 }, { "end": 115, "label": "species", "start": 109 }, { "end": 238, "label": "UBERONParcellation", "start": 228 }, { "end": 557, "label": "UBERONParcellation", "start": 547 }, { "end": 960, "label": "UBERONParcellation", "start": 950 }, { "end": 1292, "label": "UBERONParcellation", "start": 1282 }, { "end": 1433, "label": "UBERONParcellation", "start": 1423 }, { "end": 1660, "label": "UBERONParcellation", "start": 1650 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "\r\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 39, "label": "technique", "start": 0 }, { "end": 45, "label": "technique", "start": 41 }, { "end": 161, "label": "technique", "start": 157 }, { "end": 678, "label": "technique", "start": 674 }, { "end": 987, "label": "technique", "start": 983 }, { "end": 995, "label": "technique", "start": 991 }, { "end": 1084, "label": "technique", "start": 1080 }, { "end": 1153, "label": "technique", "start": 1149 }, { "end": 1561, "label": "technique", "start": 1557 }, { "end": 1758, "label": "technique", "start": 1754 }, { "end": 92, "label": "UBERONParcellation", "start": 84 }, { "end": 115, "label": "species", "start": 109 }, { "end": 175, "label": "UBERONParcellation", "start": 165 }, { "end": 274, "label": "UBERONParcellation", "start": 264 }, { "end": 582, "label": "UBERONParcellation", "start": 572 }, { "end": 660, "label": "UBERONParcellation", "start": 650 }, { "end": 1035, "label": "UBERONParcellation", "start": 1025 }, { "end": 1600, "label": "UBERONParcellation", "start": 1590 }, { "end": 199, "label": "technique", "start": 176 }, { "end": 204, "label": "technique", "start": 201 }, { "end": 238, "label": "UBERONParcellation", "start": 228 }, { "end": 557, "label": "UBERONParcellation", "start": 547 }, { "end": 960, "label": "UBERONParcellation", "start": 950 }, { "end": 1292, "label": "UBERONParcellation", "start": 1282 }, { "end": 1433, "label": "UBERONParcellation", "start": 1423 }, { "end": 1660, "label": "UBERONParcellation", "start": 1650 }, { "end": 995, "label": "technique", "start": 989 }, { "end": 1758, "label": "technique", "start": 1752 }, { "end": 1811, "label": "species", "start": 1805 } ]
null
null
8ba716f3-4c7a-498f-8deb-8b89f0a2d2c5
completed
2025-04-29T14:36:04.699798
2025-05-27T14:00:49.551553
0944a171-0c36-46ce-9a2d-ecfef7f163d6
A total of 37 healthy adult volunteers were initially recruited.Since no discernible suprahyoid/submental MEPs were induced in the alternative hemispheres of six subjects, they were excluded.The 31 remaining subjects were randomly divided into two experimental groups and assessed using the Edinburgh Handedness Inventory (Oldfield, 1971).One volunteer was intolerant to TMS.Therefore, 15 adults (eight men and seven women, 13 right-handed, mean ± standard deviation (SD) age: 29 ± 10 years, age range: 21-51 years) participated in the first experiment.Another 15 adults (six men and nine women, 14 right-handed, mean age: 26 ± 9 years, age range: 20-49 years) were included in the second experiment.No subject had any previous swallowing problems, had a history of neurological diseases, was pregnant, had a metal in the head or eyes, or used medication affecting the central nervous system. Informed consent was obtained from all the subjects.The investigation was approved by the local ethics committee and conducted in compliance with the Declaration of Helsinki.
<li> <b>suprahyoid/submental:</b> Other (UBERONParcellation)<li> <b>MEPs:</b> Other (technique)<li> <b>hemispheres:</b> cerebralHemisphere (UBERONParcellation)<li> <b>TMS:</b> Other (technique)<li> <b>adults:</b> homoSapiens (species)<li> <b>men:</b> male (biologicalSex)<li> <b>women:</b> female (biologicalSex)
[ [ { "end": 154, "label": "UBERONParcellation", "start": 143 }, { "end": 374, "label": "technique", "start": 371 }, { "end": 406, "label": "biologicalSex", "start": 403 }, { "end": 579, "label": "biologicalSex", "start": 576 }, { "end": 422, "label": "biologicalSex", "start": 417 }, { "end": 594, "label": "biologicalSex", "start": 589 }, { "end": 891, "label": "UBERONParcellation", "start": 869 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "\rcentral nervous system : Other (UBERONParcellation)\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 105, "label": "UBERONParcellation", "start": 85 }, { "end": 110, "label": "technique", "start": 106 }, { "end": 154, "label": "UBERONParcellation", "start": 143 }, { "end": 374, "label": "technique", "start": 371 }, { "end": 395, "label": "species", "start": 389 }, { "end": 570, "label": "species", "start": 564 }, { "end": 406, "label": "biologicalSex", "start": 403 }, { "end": 579, "label": "biologicalSex", "start": 576 }, { "end": 422, "label": "biologicalSex", "start": 417 }, { "end": 594, "label": "biologicalSex", "start": 589 } ]
null
null
fca3e75b-6833-4f75-8580-c84ead06d973
completed
2025-04-29T14:36:04.699804
2025-05-27T14:00:49.679642
286557c7-d803-43bb-b078-6171f781c998
Nanoparticle (NP)-assisted procedures including laser tissue soldering (LTS) offer advantages compared to conventional microsuturing, especially in the brain. In this study, effects of polymer-coated silica NPs used in LTS were investigated in human brain endothelial cells (ECs) and blood-brain barrier models. In the co-culture setting with ECs and pericytes, only the cell type directly exposed to NPs displayed a time-dependent internalization. No transfer of NPs between the two cell types was observed. Cell viability was decreased relatively to NP exposure duration and concentration. Protein expression of the nuclear factor ĸ-light-chain-enhancer of activated B cells and various endothelial adhesion molecules indicated no initiation of inflammation or activation of ECs after NP exposure. Differentiation of CD34+ ECs into brain-like ECs co-cultured with pericytes, blood-brain barrier (BBB) characteristics were obtained. The established endothelial layer reduced the passage of integrity tracer molecules. NP exposure did not result in alterations of junctional proteins, BBB formation or its integrity. In a 3-dimensional setup with an endothelial tube formation and tight junctions, barrier formation was not disrupted by the NPs and NPs do not seem to cross the blood-brain barrier. Our findings suggest that these polymer-coated silica NPs do not damage the BBB.
<li> <b>brain endothelial cells:</b> brainEndothelium (UBERONParcellation)<li> <b>blood-brain barrier:</b> bloodBrainBarrier (UBERONParcellation)
[ [ { "end": 303, "label": "UBERONParcellation", "start": 284 }, { "end": 896, "label": "UBERONParcellation", "start": 877 }, { "end": 1297, "label": "UBERONParcellation", "start": 1278 }, { "end": 157, "label": "UBERONParcellation", "start": 152 }, { "end": 267, "label": "UBERONParcellation", "start": 250 }, { "end": 901, "label": "UBERONParcellation", "start": 898 }, { "end": 1088, "label": "UBERONParcellation", "start": 1085 }, { "end": 1378, "label": "UBERONParcellation", "start": 1375 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "brain: Other (UBERONParcellation)\nbrain endothelial: brainEndothelium (UBERONParcellation)\nBBB: bloodBrainBarrier (UBERONParcellation)\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 273, "label": "UBERONParcellation", "start": 250 }, { "end": 303, "label": "UBERONParcellation", "start": 284 }, { "end": 896, "label": "UBERONParcellation", "start": 877 }, { "end": 1297, "label": "UBERONParcellation", "start": 1278 } ]
null
null
2d526e81-0e2d-4e10-a5c1-99a4508ae043
pending
2025-04-29T14:36:04.699810
2025-04-29T14:36:04.699810
436d7192-a318-419a-8d9b-55114cda3150
Interested persons may request access to datasets that are under embargo, restricted or closed access.Such requests will be forwarded to the contact person that was designated when the dataset was submitted.The contact person can then grant or deny access.Submitters can specify terms of access by means of a Data Transfer Agreement (DTA).
None
[ [] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[]
null
null
1b5d4cba-9609-466e-b0a4-fa1817f1ae7b
completed
2025-04-29T14:36:04.699816
2025-05-27T14:00:49.773882
db3befef-c044-4c79-8aec-e033489586cf
Dynamic vision requires both stability of the current perceptual representation and sensitivity to the accumulation of sensory evidence over time. Here we study the electrophysiological signatures of this intricate balance between temporal segregation and integration in vision. Within a forward masking paradigm with short and long stimulus onset asynchronies (SOA), we manipulated the temporal overlap of the visual persistence of two successive transients. Human observers enumerated the items presented in the second target display as a measure of the informational capacity read-out from this partly temporally integrated visual percept. We observed higher β-power immediately before mask display onset in incorrect trials, in which enumeration failed due to stronger integration of mask and target visual information. This effect was timescale specific, distinguishing between segregation and integration of visual transients that were distant in time (long SOA). Conversely, for short SOA trials, mask onset evoked a stronger visual response when mask and targets were correctly segregated in time. Examination of the target-related response profile revealed the importance of an evoked α-phase reset for the segregation of those rapid visual transients. Investigating this precise mapping of the temporal relationships of visual signals onto electrophysiological responses highlights how the stream of visual information is carved up into discrete temporal windows that mediate between segregated and integrated percepts. Fragmenting the stream of visual information provides a means to stabilize perceptual events within one instant in time.
None
[ [ { "end": 465, "label": "species", "start": 460 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "human: homoSapiens (species)" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[]
null
null
ca9605bc-3962-4893-97fe-776a30307ec2
completed
2025-04-29T14:36:04.699822
2025-05-27T14:00:49.878228
7a22cf65-3e66-444c-9195-8dd235567fcb
Electrophysiological activity was recorded with an on-line sampling rate of 1000 Hz using a whole-head MEG with 102 magnetometers and 204 planar gradiometers (Neuromag306 system; Elekta) in a magnetically shielded room.This system consists of 102 sensor locations each containing a triplet of one magnetometer and two gradiometers.In particular, gradiometer information is sensitive to sources close to the sensor location, i.e., neural generators at the cortical surface.To localize the head position of the subject within the MEG helmet, a subject-specific headframe coordinate reference was defined before the experimental runs.The cardinal points of the head (nasion and left and right pre-auricular points), the location of five head-position indicator (HPI) coils, and a minimum of 200 other head-shape samples were digitized for motion tracking (3Space Fastrack; Polhemus) at the start of each session.The subject's head position relative to the HPI coils and the MEG sensors was estimated before each experimental run to ensure that no large movements occurred during the data-acquisition procedure.
<li> <b>MEG:</b> magnetoencephalography (technique)
[ [ { "end": 106, "label": "technique", "start": 103 }, { "end": 531, "label": "technique", "start": 528 }, { "end": 974, "label": "technique", "start": 971 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 106, "label": "technique", "start": 103 }, { "end": 531, "label": "technique", "start": 528 }, { "end": 974, "label": "technique", "start": 971 } ]
null
null
a1e57f89-8a22-47f1-9e68-faf9bb57bd1e
completed
2025-04-29T14:36:04.699839
2025-05-27T14:00:49.969873
e8f5a6e5-a21b-4452-aa02-3f0e56e0d3b8
AbstractTranslating noisy sensory signals to perceptual decisions is critical for successful interactions in complex environments. Learning is known to improve perceptual judgments by filtering external noise and task-irrelevant information. Yet, little is known about the brain mechanisms that mediate learning-dependent suppression. Here, we employ ultra-high field magnetic resonance spectroscopy of GABA to test whether suppressive processing in decision-related and visual areas facilitates perceptual judgments during training. We demonstrate that parietal GABA relates to suppression of task-irrelevant information, while learning-dependent changes in visual GABA relate to enhanced performance in target detection and feature discrimination tasks. Combining GABA measurements with functional brain connectivity demonstrates that training on a target detection task involves local connectivity and disinhibition of visual cortex, while training on a feature discrimination task involves inter-cortical interactions that relate to suppressive visual processing. Our findings provide evidence that learning optimizes perceptual decisions through suppressive interactions in decision-related networks.
<li> <b>magnetic resonance spectroscopy:</b> magneticResonanceSpectroscopy (technique)<li> <b>visual cortex:</b> visualCortex (UBERONParcellation)
[ [ { "end": 935, "label": "UBERONParcellation", "start": 922 }, { "end": 399, "label": "technique", "start": 351 }, { "end": 278, "label": "UBERONParcellation", "start": 273 }, { "end": 805, "label": "UBERONParcellation", "start": 800 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "brain: Other (UBERONParcellation)\nultra-high field magnetic resonance spectroscopy: ultraHighFieldMagneticResonanceSpectroscopy (technique)" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 399, "label": "technique", "start": 368 }, { "end": 935, "label": "UBERONParcellation", "start": 922 } ]
null
null
2ab539ad-c62c-4f52-aab9-6ee235ee1bec
completed
2025-04-29T14:36:04.699846
2025-05-27T14:00:50.059525
1f629589-75ff-446e-a6fb-f535184e1d34
aking successful decisions entails extracting meaningful information from multiple sources in the environment that are inherently noisy and ambiguous.Experience and training have been shown to play a key role in optimizing perceptual decisions [1][2][3] by filtering external noise (e.g., when detecting targets in cluttered scenes) and retuning task-relevant feature templates (e.g., when discriminating highly similar objects) [4][5][6] .Previous functional magnetic resonance imaging (fMRI) studies have demonstrated learning-dependent changes in functional brain activity due to training on perceptual tasks that involve detecting targets in clutter or discriminating fine feature differences (for reviews 7,8 ).However, fMRI does not allow us to distinguish excitatory from inhibitory mechanisms of experiencedependent plasticity, as BOLD reflects aggregate activity from both excitatory and inhibitory signals across large neural populations 9 .Thus, the inhibitory brain plasticity mechanisms that support our ability to improve our perceptual decisions by learning to suppress noisy and task-irrelevant information through training remain largely unknown. To investigate inhibitory mechanisms of learning-dependent plasticity, we employed magnetic resonance spectroscopy (MRS) that has only recently made it possible to measure γ-aminobutyric acid (GABA), the primary inhibitory neurotransmitter in the brain.Previous animal studies have linked decreased GABAergic activity to learning and synaptic plasticity in primary motor cortex 10,11 .In accordance with these findings, human MRS studies have shown that GABA levels in the primary motor cortex decrease following interventions that facilitate cortical reorganisation 12 and motor training 13,14 .In the visual cortex, human MRS studies have shown that GABA levels relate positively to performance in perceptual tasks [15][16][17] .Further, decrease in visual GABA has been shown to relate to homeostatic plasticity 18 .Here, we took advantage of the high spectral resolution afforded by ultra-high field (7T) MRS to reliably resolve GABA 19,20 and take fast and reliable repeated measurements of functional GABA during training.This allowed us to test changes in GABA during training (i.e., while the participants were trained on a task), extending beyond standard correlational approaches that relate single measurements of GABA at baseline (i.e., when participants are at rest) to behavior.Further, we tested whether changes in GABAergic inhibition during task-specific training relate to improvement in perceptual decisions. To probe the brain mechanisms that support learning by suppressing noisy and irrelevant signals, we employed two learning tasks that have been shown to rely either on noise filtering or feature template retuning: (1) a signal-in-noise task that involves extracting a target masked by noise, (2) a feature differences task that involves judging fine differences 21 .Recent computational investigations 22,23 and animal studies propose dissociable roles for inhibition in learning to interpret noisy sensory signals vs. tuning fine feature processing.Based on this work, we hypothesized that distinct GABAergic inhibition mechanisms are involved in task-dependent learning and plasticity.Specifically, we reasoned that decreased GABAergic inhibition during training would relate to improved ability to detect targets in clutter, as changes in GABAergic inhibition have been linked to neural gain, (i.e., changes in information transmission between neurons 24 or the slope of the neural input-output relationship 25 ).In contrast, we reasoned that increased GABAergic inhibition would relate to improved performance in fine feature discrimination, as increased GABAergic inhibition has been linked to enhanced orientation selectivity in visual cortex 16,[26][27][28] . Further, previous neuroimaging and neurophysiology studies have implicated distinct functional roles for the visual and posterior parietal cortex (PPC) in sensory processing vs. perceptual decision making, respectively 29,30 .To test the role of inhibitory processing in learning for both visual and parietal cortex, we implemented an imaging protocol that measured GABA in two voxels (one in occipito-temporal (OCT), one in PPC) in alternating order and allowed us to track changes in GABA in both areas during training.Interestingly, previous studies have proposed that perceptual learning is implemented by top-down influences from decision-related areas that re-weight processing in sensory areas 30,31 .To test whether learning involves local processing within visual cortex or suppressive interactions between decision-related and sensory areas, we combined GABA measurements in occipito-temporal and posterior parietal cortex with functional brain connectivity, as measured by resting-state fMRI.In particular, we tested the hypothesis that learning is implemented by local inhibitory processing in visual cortex that is gated by functional interactions between sensory and decisionrelated areas.Specifically, we tested whether learning-dependent changes in visual cortex GABA relate to functional connectivity between visual and posterior parietal cortex. Our results reveal distinct GABAergic inhibition mechanisms in a cortical network that is known to be involved in perceptual decisions.In particular, increased parietal GABA with training suggests suppression of task-irrelevant information.In contrast, changes in occipito-temporal GABA with training relate to enhanced target detection and discriminability, suggesting learning-dependent changes in the processing of task-relevant features.Further, analysis of functional brain connectivity at rest reveals interactions within this network that relate to GABA changes and behavioral improvement during training.Learning to detect targets from clutter is implemented by local connectivity and disinhibition of the visual cortex.In contrast, learning feature differences is implemented by interactions between parietal and visual areas that relate to increased GABAergic inhibition in visual cortex.Our results provide evidence that learning improves perceptual decisions through suppressive interactions within decision-related circuits in the human brain.
<li> <b>magnetic resonance spectroscopy (MRS):</b> magneticResonanceSpectroscopy (technique)<li> <b>magnetic resonance imaging (fMRI):</b> functionalMagneticResonanceImaging (technique)<li> <b>primary motor cortex:</b> primaryMotorCortex (UBERONParcellation)<li> <b>visual cortex:</b> visualCortex (UBERONParcellation)<li> <b>posterior parietal cortex (PPC):</b> parietalCortex (UBERONParcellation)<li> <b>occipito-temporal (OCT):</b> temporalCortex (UBERONParcellation)<li> <b>posterior parietal cortex:</b> parietalCortex (UBERONParcellation)
[ [ { "end": 1541, "label": "UBERONParcellation", "start": 1521 }, { "end": 1657, "label": "UBERONParcellation", "start": 1637 }, { "end": 1780, "label": "UBERONParcellation", "start": 1767 }, { "end": 3839, "label": "UBERONParcellation", "start": 3826 }, { "end": 4637, "label": "UBERONParcellation", "start": 4624 }, { "end": 4977, "label": "UBERONParcellation", "start": 4964 }, { "end": 5136, "label": "UBERONParcellation", "start": 5123 }, { "end": 5949, "label": "UBERONParcellation", "start": 5936 }, { "end": 6119, "label": "UBERONParcellation", "start": 6106 }, { "end": 4790, "label": "UBERONParcellation", "start": 4765 }, { "end": 5220, "label": "UBERONParcellation", "start": 5195 }, { "end": 486, "label": "technique", "start": 449 }, { "end": 492, "label": "technique", "start": 488 }, { "end": 566, "label": "UBERONParcellation", "start": 561 }, { "end": 729, "label": "technique", "start": 725 }, { "end": 1278, "label": "technique", "start": 1247 }, { "end": 1283, "label": "technique", "start": 1280 }, { "end": 1416, "label": "UBERONParcellation", "start": 1411 }, { "end": 1593, "label": "technique", "start": 1590 }, { "end": 1791, "label": "technique", "start": 1788 }, { "end": 1589, "label": "species", "start": 1584 }, { "end": 1787, "label": "species", "start": 1782 }, { "end": 2076, "label": "technique", "start": 2051 }, { "end": 2610, "label": "UBERONParcellation", "start": 2605 }, { "end": 4003, "label": "UBERONParcellation", "start": 3978 }, { "end": 4008, "label": "UBERONParcellation", "start": 4005 }, { "end": 4173, "label": "UBERONParcellation", "start": 4158 }, { "end": 4286, "label": "UBERONParcellation", "start": 4283 }, { "end": 4812, "label": "UBERONParcellation", "start": 4807 }, { "end": 4860, "label": "technique", "start": 4856 }, { "end": 5700, "label": "UBERONParcellation", "start": 5695 }, { "end": 6277, "label": "UBERONParcellation", "start": 6272 }, { "end": 6271, "label": "species", "start": 6266 }, { "end": 977, "label": "UBERONParcellation", "start": 972 }, { "end": 3544, "label": "UBERONParcellation", "start": 3538 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "\rfunctional magnetic resonance imaging: functionalMagneticResonanceImaging (technique)\nfMRI: functionalMagneticResonanceImaging (technique)\nbrain: Other (UBERONParcellation)\nMRS: magneticResonanceSpectroscopy (technique)\nhuman: homoSapiens (species)\nultra-high field (7T) MRS: ultraHighFieldMagneticResonanceSpectroscopy (technique)\nneuron: Other (UBERONParcellation)\nposterior parietal cortex: posteriorParietalCortex (UBERONParcellation)\nPPC: posteriorParietalCortex (UBERONParcellation)\n\rparietal cortex: parietalCortex (UBERONParcellation)\n\r\r\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 1284, "label": "technique", "start": 1247 }, { "end": 493, "label": "technique", "start": 460 }, { "end": 1541, "label": "UBERONParcellation", "start": 1521 }, { "end": 1657, "label": "UBERONParcellation", "start": 1637 }, { "end": 1780, "label": "UBERONParcellation", "start": 1767 }, { "end": 3839, "label": "UBERONParcellation", "start": 3826 }, { "end": 4637, "label": "UBERONParcellation", "start": 4624 }, { "end": 4977, "label": "UBERONParcellation", "start": 4964 }, { "end": 5136, "label": "UBERONParcellation", "start": 5123 }, { "end": 5949, "label": "UBERONParcellation", "start": 5936 }, { "end": 6119, "label": "UBERONParcellation", "start": 6106 }, { "end": 4009, "label": "UBERONParcellation", "start": 3978 }, { "end": 4274, "label": "UBERONParcellation", "start": 4251 }, { "end": 4003, "label": "UBERONParcellation", "start": 3978 }, { "end": 4790, "label": "UBERONParcellation", "start": 4765 }, { "end": 5220, "label": "UBERONParcellation", "start": 5195 } ]
null
null
1680d2f8-308a-40dc-b5a9-0cf6a9704ff2
completed
2025-04-29T14:36:04.699852
2025-05-27T14:00:50.153875
4496e2f7-5877-4309-b980-0e42f976c486
Idiopathic epilepsy is the most common neurological disease in dogs. Similar to humans, dogs with epilepsy often experience behavioural comorbidities such as increased fear, anxiety, and aggression, as reported by their caregivers. Investigations of behaviour in canine epilepsy have yet to untangle interictal and pre and postictal behaviours, prodromal changes, and seizure-precipitating factors. Under-recognition of absence and focal seizures further complicates these assessments. These complex behavioural presentations in combination with caring for an epileptic animal have a significant negative impact on the dog’s and caregiver’s quality of life. Despite the growing recognition of behavioural comorbidities and their impact on quality of life in dogs with epilepsy, few objective research methods for classifying and quantifying canine behaviour exist. This narrative review examines the strengths, limitations, and granularity of three tools used in the investigation of canine behaviour and epilepsy; questionnaires, electroencephalography, and actigraphy. It suggests that a prospective combination of these three tools has the potential to offer improvements to the objective classification and quantification of canine behaviour in epilepsy.
<li> <b>dogs:</b> Other (species)<li> <b>electroencephalography:</b> electroencephalography (technique)
[ [ { "end": 67, "label": "species", "start": 63 }, { "end": 92, "label": "species", "start": 88 }, { "end": 762, "label": "species", "start": 758 }, { "end": 1053, "label": "technique", "start": 1031 }, { "end": 1069, "label": "technique", "start": 1059 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "actigraphy: Other (technique)\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 67, "label": "species", "start": 63 }, { "end": 92, "label": "species", "start": 88 }, { "end": 762, "label": "species", "start": 758 }, { "end": 1053, "label": "technique", "start": 1031 } ]
null
null
dece4c38-d6bb-40cf-8d23-8fe4b50b4f37
completed
2025-04-29T14:36:04.699858
2025-05-27T14:00:50.242500
5258bff6-59f5-43b4-a52d-d9d22f86918d
Questionnaires, EEG, and actigraphy have all successfully contributed to the understanding of seizures and behavioural contexts in canine epilepsy.Although useful, each of these tools has limitations that hinder researchers' ability to capture an accurate, complete, and objective picture of behavioural comorbidities in canine epilepsy.Questionnaires have provided researchers with behavioural changes caregivers have reported in their epileptic dogs from pre-to postdiagnosis, as well as prodromal changes in behaviour leading up to a seizure.Thus, questionnaires allow researchers to investigate changes in seizure characteristics and behaviour granularly and broadly across time depending on their research goals.The main limitation of the behavioural data collected from these questionnaires is that it comprises caregiver-reported, subjective accounts of behaviour.Retrospective accounts are prone to recall bias, as they recount behavioural and seizure contexts from the distant past (months to years).Ideally, capturing and quantifying behaviour objectively and in real-time or prospectively in addition to caregiver-reported questionnaires would provide the most accurate behaviour data for canine epilepsy studies.EEG remains the gold standard for seizure detection and classification in canine epilepsy, as it is the only way to definitively confirm seizure activity directly (ictal discharges), or indirectly (interictal epileptogenic discharges).The use of vEEG could be a useful tool for investigating behavioural changes in epileptic dogs on a more granular scale, such as pre-and post-seizure, but is limited to the length of the recording and may pose a privacy concern for some caregivers.Unfortunately, most research utilizing EEG in dogs thus far has only collected data on sedated subjects and therefore has not been able to collect accurate behavioural data in a home environment.The use of vEEG in awake and behaving dogs could allow researchers to visualize behaviours as they occur and establish a temporal relationship between these behaviours and ictal events.Although actigraphy has had mixed results in terms of seizure classification, it has been successful in classifying behavioural states in dogs and can be useful as an objective behavioural assessment method to supplement owner reports.Additionally, behaviour can be examined over relatively long periods of time (weeks to months) due to improved battery function of devices in recent years.Future research could investigate these behavioural states in different canine populations (i.e., diseased) to determine whether there are consistent behavioural differences between groups for further development of diagnostic and treatment monitoring tools.
<li> <b>EEG:</b> electroencephalography (technique)<li> <b>vEEG:</b> electroencephalography (technique)<li> <b>dogs:</b> Other (species)
[ [ { "end": 19, "label": "technique", "start": 16 }, { "end": 1227, "label": "technique", "start": 1224 }, { "end": 1749, "label": "technique", "start": 1746 }, { "end": 451, "label": "species", "start": 447 }, { "end": 1553, "label": "species", "start": 1549 }, { "end": 1757, "label": "species", "start": 1753 }, { "end": 1944, "label": "species", "start": 1940 }, { "end": 2229, "label": "species", "start": 2225 }, { "end": 1474, "label": "technique", "start": 1470 }, { "end": 1917, "label": "technique", "start": 1913 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 19, "label": "technique", "start": 16 }, { "end": 1227, "label": "technique", "start": 1224 }, { "end": 1749, "label": "technique", "start": 1746 }, { "end": 1474, "label": "technique", "start": 1470 }, { "end": 1917, "label": "technique", "start": 1913 }, { "end": 451, "label": "species", "start": 447 }, { "end": 1553, "label": "species", "start": 1549 }, { "end": 1757, "label": "species", "start": 1753 }, { "end": 1944, "label": "species", "start": 1940 }, { "end": 2229, "label": "species", "start": 2225 } ]
null
null
22df4eed-51f3-4f5d-964e-6bb39b04e3d5
completed
2025-04-29T14:36:04.699864
2025-05-27T14:00:50.342128
f48790fd-6c8b-4593-a1b0-5a9ef622a46c
This article aims at presenting a scale that, through the analysis of MRI images, clearly charts the various degenerative stages of the cervical spine and establishes its biological age. We have created this scale by summing together various scores linked to a selection of parameters according to which MRI images are analyzed.We examined 423 cervical spine MRI scans, belonging to patients who had been admitted to the Medical Imaging Service of the Military Hospital of Rome between January 2010 and July 2011. We selected 6 parameters for the analysis of the MRI scans of the cervical spine: (1) the degeneration of the intervertebral discs, (2) the degeneration of the yellow ligaments, (3) the degeneration of the vertebral bodies, (4) the possible presence of spondylolistheses, (5) the presence or absence of foraminal stenosis, and (6) the diameter of the spinal canal. We assigned to each parameter a score system based on a graduated scale. The cervical spine physiological age can be determined by summing up the scores obtained for each parameter.We submitted the data obtained from the study to a statistical enquiry. The results of the enquiry confirmed the suitability of the parameters selected for the evaluation of the aging process of the cervical spine.The effectiveness of the various treatments for cervical spine degenerative disorders is influenced by the overall anatomical conditions of the cervical spine. Up until now there has been no objective criterion for the evaluation of these anatomical conditions. We believe that this scale will be a useful tool to homogenize retrospective studies and to correctly set up prospective studies on the degenerative conditions of the cervical spine and relative treatments.
<li> <b>MRI:</b> magneticResonanceImaging (technique)
[ [ { "end": 73, "label": "technique", "start": 70 }, { "end": 307, "label": "technique", "start": 304 }, { "end": 362, "label": "technique", "start": 359 }, { "end": 566, "label": "technique", "start": 563 }, { "end": 150, "label": "UBERONParcellation", "start": 136 }, { "end": 358, "label": "UBERONParcellation", "start": 344 }, { "end": 594, "label": "UBERONParcellation", "start": 580 }, { "end": 644, "label": "UBERONParcellation", "start": 624 }, { "end": 970, "label": "UBERONParcellation", "start": 956 }, { "end": 1273, "label": "UBERONParcellation", "start": 1259 }, { "end": 1336, "label": "UBERONParcellation", "start": 1322 }, { "end": 1432, "label": "UBERONParcellation", "start": 1418 }, { "end": 1717, "label": "UBERONParcellation", "start": 1703 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "cervical spine: Other (UBERONParcellation)\nintervertebral discs: Other (UBERONParcellation)\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 73, "label": "technique", "start": 70 }, { "end": 307, "label": "technique", "start": 304 }, { "end": 362, "label": "technique", "start": 359 }, { "end": 566, "label": "technique", "start": 563 } ]
null
null
15b2d7d9-0577-41e1-aa59-7bdaeb76aa25
pending
2025-04-29T14:36:04.699872
2025-04-29T14:36:04.699872
cc283922-771b-434c-80c2-ae9c0b061c4b
Total Scores between 25 and correlation with the chronological age of the sample subjects (p \ 0.01). We then submitted the sample to a Factor analysis (Table 4): a single statistical factor (Fig. 2) was able to determine, in our sample, 56.26 % of variance in the scores obtained using the scale.We hypothesized this factor to be aging.
None
[ [] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[]
null
null
3e14b09c-050a-4097-8e6a-3202ecde23c5
completed
2025-04-29T14:36:04.699879
2025-05-27T14:00:50.447953
5281afa1-400d-4ea3-94ac-20cec31ff0f6
Glioma, is a representative type of intracranial tumor among adults, usually has a weak prognosis and limited treatment options. Traditional therapies, including surgery, chemotherapy, and radiotherapy, have had little impact on patient survival time. Immunotherapies designed to target the programmed cell death protein 1 (PD-1)/programmed death ligand 1 (PD-L1) signaling pathway have successfully treated various human cancers, informing the development of similar therapies for glioma. However, anti-PD-L1 response rates remain limited in glioma patients. Thus, exploring novel checkpoints targeting additional immunomodulatory pathways for activating durable antitumor immune responses and improving glioma outcomes is needed. Researchers have identified other B7 family checkpoint molecules, including PD-L2, B7-H2, B7-H3, B7-H4, and B7-H6. The current review article evaluates the expression of all 10 reported members of the B7 family in human glioma using The Cancer Genome Atlas (TCGA) and the Genotype-Tissue Expression (GTEx) data, as well as summarizes studies evaluating the clinical meanings and functions of B7 family molecules in gliomas. B7 family checkpoints may contribute to different immunotherapeutic management options for glioma patients.
<li> <b>human:</b> homoSapiens (species)
[ [ { "end": 421, "label": "species", "start": 416 }, { "end": 951, "label": "species", "start": 946 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 421, "label": "species", "start": 416 }, { "end": 951, "label": "species", "start": 946 } ]
null
null
f33db50c-6409-4cae-92aa-d102b7155e15
completed
2025-04-29T14:36:04.699885
2025-05-27T14:00:50.559270
d425d8bb-58ff-4b62-b1d4-f0ee2360d5dc
PD-L2, also called CD273, is a receptor for PD-1.Like PD-L1, PD-L2 contains IgV-like and IgC-like extracellular domains and exists on multiple immune, endothelial, and tumor cells (42).Less is known about how PD-L2 is regulated than PD-L1.Fu et al. showed that GATA-binding factor 2 (GATA2) was capable of promoting the expressions of PD-L1 and PD-L2 (43).GATA2, encoding a zinc finger transcription factor required for normal hematopoiesis, is located on chromosome 3q21.2(44).This transcription factor can increase the expressions of PD-L1 and PD-L2, which is needed for PD-L2 expression.Li et al. found that HOXC10, a which belonged to the homeobox genes (HOX) gene family, could considerably affect the physiological processes of mammalia.This gene is upregulated in glioma and promotes the expression of PD-L2, and other genes related to tumor immunosuppression (45).HOXC10 binds directly to PD-L2 promoter regions.De Waele et al. reported that poly (I:C) (Toll-like receptor 3 agonist, TLR-3) stimulates the expressions of PD-L1 and PD-L2 through TLR3-TICAM1 signaling (46).Figure 2 displays the regulatory action of PD-L2 expression.Like PD-L1, PD-L2 crucially modulates T cell activation, proliferation, and immune escape by human tumors (47).In glioma patients, PD-L2 expression could report worse clinical outcomes (43).Thus, targeting PD-L2 signaling may serve as a potential substitute therapy for glioma. 4 Clinical meanings and functions of B7-H3 in gliomas B7 homolog 3 (B7-H3), also named CD276, refers to a 316 amino acid long type I transmembrane protein (48).In 2001, researchers first clone it from a cDNA library from the dendritic cells (DCs) (49).The human B7-H3 gene can be observed on chromosome 15 (48).While B7-H3 mRNA presents an ubiquitous expression in various tissues and cells, B7-H3 protein can only be found in resting fibroblasts, osteoblasts, activated T lymphocytes, endothelial cells, NK cells, and APC ( 10).The expression of B7-H3 were assessed by immunohistochemistry and western-blot in human GBM and benign brain tissue, including 2IgB7-H3 and 4IgB7-H3 two isoforms (50,51).Despite the presence of 2IgB7-H3 in benign brain tissue, 4IgB7-H3 showed certain expression in GBM.2IgB7-H3 had a higher expression in rGBM tissue, more resistant to apoptosis under the mediation of temozolomide (9).A separate study found that 2IgB7-H3 mRNA presented expression in glioma tissues but was weak or undetectable in benign brain tissues.Meanwhile, 4IgB7-H3 mRNA could be found in benign brain and in glioma tissues (Table 3) (52). Glioma patients with isocitrate dehydrogenase (IDH) wildtype or a higher tumor grade express more B7-H3 (53).Studies also show that microRNA-29 family members can negatively regulate B7-H3 in glioma tissue.B7-H3 is positively correlated with TLR signaling (53).This protein is present in many kinds of cancers, including glioma, and is relevant to tumor aggressiveness and reports poor prognosis (54,55).According to Zhong et al., elevated B7-H3 expression exerted an obviously positive impact on the proliferation and invasion of glioma cells both in vitro and in vivo, that leads to weak clinical prognosis (56).Elevated B7-H3 levels results in the activation of the JAK2/ STAT3 prosurvival signaling pathway, that contributes to tumor growth, meanwhile inducing EMT in cancer cells.In addition, B7-H3 induces tumor cell EMT processes by downregulating ecadherin and upregulating MMP-2/-9 expression.The STAT3 inhibitor, NAP, can remarkably suppress the glioma growth and invasion and could thus be a potential strategy for treating glioma.MMP-2 (main) degrades the extracellular matrix and induces cell migration from the primary tumor to the surrounding environment.Exosomes are membrane vesicles that were released by cancer cells that promote cancer cell growth and increase tumor swelling, invasion, and migration (57) Recently, Ciprut et al. showed that angio-associated migratory cell protein (AAPP) was a binding partner of B7-H3 and that B7-H3-induced immunosuppression could be blocked by targeting AAPP (58).Kanchan et al. found that CD276 is an oncogenic target of miR-1253.MiR-1253 transfection downregulates CD276 expression.However, tumor cell migration and invasion are substantially reduced when CD276 is silent (59).Figure 3 displays the regulatory actions of B7-H3 expression. Functionally, B7-H3 promotes tumor-immune escape and confers a more aggressive phenotype to multiple tumor cell types (60).The B7-H3 checkpoint can promisingly serve for cancer The function and regulatory mechanisms of B7-H3 in gliomas.immunotherapy as a novel target.According to studies, using a monoclonal antibody to target B7-H3 can safely and effectively serve for treating stage IV childhood neuroblastoma (61).MGA271, an anti-tumor-associated B7-H3 monoclonal antibody, inhibits the growth of glioma cells through ADCC, thereby increasing the anti-tumor response (62).Meanwhile, 8H9 acts as a murine IgG1 mAb targeting B7-H3 (63, 64), which, based on the immunostaining, presents a broad response in human solid tumors, such as embryonal tumors and carcinomas (63).This mAb exhibits a good tumor uptake in xenograft models of both sarcoma and brain tumors (65).Chimeric antigen receptor (CAR) T cells have become an useful immunotherapeutic approach in cancer treatment (66).CAR essentially constitutes CAR-T, relying on which T cells can recognize tumor antigens without needing HLA, and recognize a larger number of wide target antigens compared with natural TCR (67).As CAR-T cells has enjoyed a successful application to treating hematological malignancies, using CAR-T cell therapy for solid tumor is gaining more and more attentions (68).Many clinical trials are conducted in several countries including the US, China and Europe, and with the trail progress and outcome being strictly detected.To date, some preclinical and clinical studies regarding the CAR-T immunotherapy specific to gliomas have achieved good results (69-71).Tang et al. constructed B7-H3-specific CAR-T cells and evaluated it antitumor activities in primary glioma cells and GBM cell lines, as well as found that the CAR-T group of orthotropic GBM model has significantly longer survival time than that of control group (72).According to the study by Nehama et al. in 2019, B7-H3specific CAR-T cells release effector cytokines like IL-2 and IFN-g, meanwhile controlling the growth of neurospheres and human GBM cell lines (73).In consistent with Tang et al's report, compared with control T cells, B7-H3 CAR-T group significantly prolonged the survival of treated mice.B7-H3specific CAR-T has promising antitumor activities in immunecompetent animal models and patient-derived orthotopic xenograft.Dual CAR-T target antigens improve variation of antigens and the heterogeneity in treating solid tumors and showed enhanced antitumor effects (74).Accordingly, B7-H3 is likely to be a promising CAR-T target for GBM.Table 2 lists the ongoing clinical trial results.These findings confirm B7-H3 CAR-T as an useful and safe immunotherapeutic agent for tumors.
<li> <b>brain:</b> brain (UBERONParcellation)<li> <b>immunohistochemistry:</b> immunohistochemistry (technique)
[ [ { "end": 2055, "label": "UBERONParcellation", "start": 2050 }, { "end": 2165, "label": "UBERONParcellation", "start": 2160 }, { "end": 2458, "label": "UBERONParcellation", "start": 2453 }, { "end": 2522, "label": "UBERONParcellation", "start": 2517 }, { "end": 5215, "label": "UBERONParcellation", "start": 5210 }, { "end": 2008, "label": "technique", "start": 1988 }, { "end": 1238, "label": "species", "start": 1233 }, { "end": 1679, "label": "species", "start": 1674 }, { "end": 2034, "label": "species", "start": 2029 }, { "end": 3118, "label": "preparationType", "start": 3110 }, { "end": 3130, "label": "preparationType", "start": 3123 }, { "end": 6613, "label": "species", "start": 6609 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "human: homoSapiens (species)\nin vitro: inVitro (preparationType)\nin vivo: inVivo (preparationType)\nmice: musMusculus (species)\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 2055, "label": "UBERONParcellation", "start": 2050 }, { "end": 2165, "label": "UBERONParcellation", "start": 2160 }, { "end": 2458, "label": "UBERONParcellation", "start": 2453 }, { "end": 2522, "label": "UBERONParcellation", "start": 2517 }, { "end": 5215, "label": "UBERONParcellation", "start": 5210 }, { "end": 2008, "label": "technique", "start": 1988 } ]
null
null
8a2a95a6-a87d-4f57-b76b-ddf1dca9431e
pending
2025-04-29T14:36:04.699893
2025-04-29T14:36:04.699893
ed931b1e-8a92-4092-aabd-0dd228112aef
BACKGROUND AND PURPOSE: To assess the impact of a stroke unit (SU) on acute phase treatment when compared to a conventional general ward treatment (GW). METHOD: Seventy-four patients with acute stroke were randomized between a SU and conventional general ward (GW). We compared both groups regarding the length of hospital stay, lethality and functional and clinical status within 6 months, using the Scandinavian scale and Barthel index. RESULTS: Thirty-five and thirty-nine patients were allocated at SU and GW, respectively. Lethality on the 10th day at SU and GW achieved 8.5% and 12.8% respectively (p= 0.41), whereas 30-days mortality rates achieved 14.2% and 28.2% (p= 0.24), 17.4% and 28.7% on the 3rd month (p= 0.39), and 25.7% and 30.7% on the 6th month (p= 0.41). Thirty-day survival curve achieved 1.8 log rank (p= 0.17), with a trend for lower lethality in the SU. In order to save one death in 6 months in SU, NNT (the number need to treat) was 20; to get one more home independent patient NNT was 15. No significant difference was found between the length of hospital stay and morbidity. CONCLUSION: No significant benefit was found in SU patients compared to GW group. However,an evident benefit in absolute numbers was observed in lethality, survival curve and NNT in thirty days period after stroke. Further collaborative studies or incresead number of patients are required to define the role of SU.
None
[ [] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[]
null
null
994a3e0c-557e-42b4-a8ed-a9ece37b6d9b
pending
2025-04-29T14:36:04.699899
2025-04-29T14:36:04.699899
53ee85b2-2b56-46e4-807c-e4070fe0865b
Outcome differences are shown with odds ratio and relative risk with CI (confidence interval) of 95%.BI's and SSS's scores differences have been analyzed through the Mann-Whitney test.Qui-square test was used for categorical variables and t-test for continuous variables.Kaplan-Meyer's actuarial curve has been used to assess the survival curve.Statistical analysis was performed in the Statistical Package for Social Sciences (SPSS 8.0 computer program) 18 .
None
[ [] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[]
null
null
96f4b128-2f7f-4e00-920b-fe7c4af701e9
completed
2025-04-29T14:36:04.699906
2025-05-27T14:00:50.678408
a1905661-3598-44e2-990c-cfb34e87b778
Sleep electroencephalogram (EEG) brain oscillations in the low-frequency range show local signs of homeostatic regulation after learning. Such increases and decreases of slow wave activity are limited to the cortical regions involved in specific task performance during wakefulness. Here, we test the hypothesis that reorganization of motor cortex produced by long-term potentiation (LTP) affects EEG activity of this brain area during subsequent sleep.By pairing median nerve stimulation with transcranial magnetic stimulation over the contralateral motor cortex, one can potentiate the motor output, which is presumed to reflect plasticity of the neural circuitry. This paired associative stimulation increases M1 cortical excitability at interstimulus intervals of 25 ms. We compared the scalp distribution of sleep EEG power following paired associative stimulation at 25 ms to that following a control paradigm with 50 ms intervals. It is shown that the experimental manipulation by paired associative stimulation at 25 ms induces a 48% increase in amplitude of motor evoked potentials. This LTP-like potentiation, induced during waking, affects delta and theta EEG power in both REM and non-REM sleep, measured during the following night. Slow-wave activity increases in some frontal and prefrontal derivations and decreases at sites neighboring and contralateral to the stimulated motor cortex. The magnitude of increased amplitudes of motor evoked potentials by the paired associative stimulation at 25 ms predicts enhancements of slow-wave activity in prefrontal regions.An LTP-like paradigm, presumably inducing increased synaptic strength, leads to changes in local sleep regulation, as indexed by EEG slow-wave activity. Enhancement and depression of slow-wave activity are interpreted in terms of a simultaneous activation of both excitatory and inhibitory circuits consequent to the paired associative stimulation at 25 ms.
<li> <b>Sleep electroencephalogram (EEG):</b> electroencephalography (technique)<li> <b>motor cortex:</b> primaryMotorCortex (UBERONParcellation)<li> <b>transcranial magnetic stimulation:</b> Other (technique)<li> <b>M1 cortical:</b> primaryMotorCortex (UBERONParcellation)<li> <b>motor cortex:</b> primaryMotorCortex (UBERONParcellation)<li> <b>prefrontal regions:</b> prefrontalCortex (UBERONParcellation)
[ [ { "end": 347, "label": "UBERONParcellation", "start": 335 }, { "end": 563, "label": "UBERONParcellation", "start": 551 }, { "end": 1400, "label": "UBERONParcellation", "start": 1388 }, { "end": 527, "label": "technique", "start": 494 }, { "end": 724, "label": "UBERONParcellation", "start": 713 }, { "end": 1579, "label": "UBERONParcellation", "start": 1561 }, { "end": 26, "label": "technique", "start": 6 }, { "end": 31, "label": "technique", "start": 28 }, { "end": 400, "label": "technique", "start": 397 }, { "end": 423, "label": "UBERONParcellation", "start": 418 }, { "end": 822, "label": "technique", "start": 819 }, { "end": 1170, "label": "technique", "start": 1167 }, { "end": 1712, "label": "technique", "start": 1709 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "EEG: electroencephalography (technique)\nbrain: Other (UBERONParcellation)\r\r\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 32, "label": "technique", "start": 0 }, { "end": 347, "label": "UBERONParcellation", "start": 335 }, { "end": 563, "label": "UBERONParcellation", "start": 551 }, { "end": 1400, "label": "UBERONParcellation", "start": 1388 }, { "end": 527, "label": "technique", "start": 494 }, { "end": 724, "label": "UBERONParcellation", "start": 713 }, { "end": 347, "label": "UBERONParcellation", "start": 335 }, { "end": 563, "label": "UBERONParcellation", "start": 551 }, { "end": 1400, "label": "UBERONParcellation", "start": 1388 }, { "end": 1579, "label": "UBERONParcellation", "start": 1561 } ]
null
null
db5ad32b-ec2a-4b71-bf5f-07f2ac991964
completed
2025-04-29T14:36:04.699912
2025-05-27T14:00:50.780473
792c98a2-ad6f-4602-a241-3c51c57670ee
AbstractThe processing steps that lead up to a decision, i.e., the transformation of sensory evidence into motor output, are not fully understood. Here, we combine stereoEEG recordings from the human cortex, with single-lead and time-resolved decoding, using a wide range of temporal frequencies, to characterize decision processing during a rule-switching task. Our data reveal the contribution of rostral inferior parietal lobule (IPL) regions, in particular PFt, and the parietal opercular regions in decision processing and demonstrate that the network representing the decision is common to both task rules. We reconstruct the sequence in which regions engage in decision processing on single trials, thereby providing a detailed picture of the network dynamics involved in decision-making. The reconstructed timeline suggests that the supramarginal gyrus in IPL links decision regions in prefrontal cortex with premotor regions, where the motor plan for the response is elaborated.
<li> <b>stereoEEG:</b> stereoelectroencephalography (technique)<li> <b>human cortex:</b> cerebralCortex (UBERONParcellation)<li> <b>inferior parietal lobule (IPL):</b> inferiorParietalCortex (UBERONParcellation)<li> <b>PFt:</b> Other (UBERONParcellation)<li> <b>supramarginal gyrus:</b> supramarginalGyrus (UBERONParcellation)<li> <b>prefrontal cortex:</b> prefrontalCortex (UBERONParcellation)<li> <b>premotor regions:</b> premotorCortex (UBERONParcellation)
[ [ { "end": 173, "label": "technique", "start": 164 }, { "end": 437, "label": "UBERONParcellation", "start": 407 }, { "end": 860, "label": "UBERONParcellation", "start": 841 }, { "end": 911, "label": "UBERONParcellation", "start": 894 }, { "end": 933, "label": "UBERONParcellation", "start": 917 }, { "end": 206, "label": "UBERONParcellation", "start": 200 }, { "end": 199, "label": "species", "start": 194 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "human: homoSapiens (species) \ncortex: Other (UBERONParcellation)\r\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 173, "label": "technique", "start": 164 }, { "end": 206, "label": "UBERONParcellation", "start": 194 }, { "end": 437, "label": "UBERONParcellation", "start": 407 }, { "end": 464, "label": "UBERONParcellation", "start": 461 }, { "end": 860, "label": "UBERONParcellation", "start": 841 }, { "end": 911, "label": "UBERONParcellation", "start": 894 }, { "end": 933, "label": "UBERONParcellation", "start": 917 } ]
null
null
5f695170-746e-4d9b-a44e-3708e23c95a9
completed
2025-04-29T14:36:04.699918
2025-05-27T14:00:50.874646
ed39125d-a77f-4527-bdcd-bc627b6470f6
What is the functional role of the newly identified parietal PF and OP areas in the decisionmaking process?To shed light on this, we analyzed the precise timing of the responses in the information-carrying areas.As response times can be biased when using a classifier performance metric across trials, for example, in areas sensitive to trial-to-trial variations in difficulty level, we instead identified response timings in single trials.To this end, we obtained a decoding performance trace for each trial individually, by retraining the LDA classifiers using a leave-one-out cross-validation approach for all the previously identified left/right decoding leads (see "Methods" section for details).The leave-one-out classifier provided us with a decision value (D-value, see "Methods" section), a proxy for the certainty with that the time point in the trial could be decoded by a classifier trained on the same time point from all other trials.For each trial, we then identified the time point at which the classifier performance started to increase toward the highest Fig. 3 Decisions for color and orientation rules invoke similar responses in the same brain regions.The left panels show the average classifier performance traces (± standard deviation, numbers of data points included are given in the right panels) for classifiers trained on only color rule trials (orange), only orientation rule trials (green), and the average of ten subsampled trial sets that included both color and orientation rules, and match the trial count of one rule (gray).All brain regions that showed significant left/right decoding based on all trials are included here.For all regions with three or more decoding leads for both the color and orientation only classifiers, a cluster-based permutation test was performed to compare decoding performance of color and orientation over time.None of the clusters survived FDR correction.The right panels show the number of leads that show significant decoding for each of the classifiers.For the subsampled classifier bars show the mean, and error bars indicate the standard deviation across ten repetitions (raw data can be found in Supplementary Table 5).Horizontal bars indicate a one-sided Wilcoxon rank test of the difference between the number of leads for color and orientation rule compared to pairs of randomly subsampled classifiers (α = 0.05; FDR corrected); ns is not significant.The total number of leads per brain area can be found in Supplementary Fig. 3b. performance peak (Fig. 4a left).This provided us with a distribution of trial-specific onset times for each lead. We then obtained onset time differences for all pairs of identified brain areas, using two different strategies.In the first approach (Fig. 4a), we combined the onset distributions of all leads in one brain area and computed the average onset for this area.We then computed the time difference matrix by comparing onsets of all pairs of brain areas.Averaging within a brain area provides a more stable estimate of the onset and has the advantage that the difference matrix is complete, but note that a difference is computed even if a pair of areas is not represented in the recordings from a single patient.To account for this, we used a second approach (Fig. 4a), where we computed the time difference between each trial individually for every pair of leads recorded simultaneously.We then collapsed the onset time differences within brain areas and averaged across subjects.Note that the resulting time difference matrix is incomplete when pairs of brain areas were not recorded in any of the subjects. To aid interpretation of the time difference matrices, we projected them back onto a timeline using a simplified multidimensional scaling (MDS) approach.This approach can only produce a relative timeline and not the "absolute" time before the response, as the absolute time-to-response is subtracted out in the pairwise comparisons.We therefore translated the timelines to the onset of motor cortex (BA4), as a proxy for response onset.We validated each timeline with a bootstrapping procedure, leaving out the results from one lead from each bootstrap (leading to 86 bootstraps per method).The resulting timelines and their bootstrapping results for the average onset and trial-bytrial approaches are shown in Fig. 4b,c, respectively.Both approaches identified early decoding onsets for area PFt and dorsal premotor area, together with dorsolateral prefrontal dlPFC for the trial-by-trial method, with all three areas having a response onset well before motor cortex.Though the exact timing differed slightly between methods, onsets in PMm, PFcm, OP1, and OP3 roughly coincided with BA4 response onset in all leads in each area of interest, after which the differences of the average onsets is determined ('average of onsets'), or the differences in onset of pairs of leads are compared for each trial, after which the differences are averaged within the areas of interest ('trial by trial').Both methods thus resulted in a difference matrix between all areas of interest, which was then ordered on a linear time axis using a multidimensional scaling approach.For power traces (not shown in this example), onset analyses were computed for each frequency independently and time difference distributions were combined across frequencies; b-e temporal ordering results of the average of onsets approach (b, d) and the trial-by-trial approach (c, e) for single-trial classifiers (b, c) and spectra (d, e).Connected filled circles indicate the onset of each area relative to the onset of area BA4 (gray), with blue areas starting before BA4 and yellow areas appearing after BA4.Small dots represent bootstrapping results, with each bootstrap leaving out the data from one recording lead (N = 86).The classifier onset distributions of all leads can be found in Supplementary Fig. 12 and time difference matrices for all four methods are given in Supplementary Fig. 13. both.Sensory areas BA3a and S1 were last to classify the response, together with area PFop. As the classifier performance is based on a wavelet decomposition using frequencies between 5 and 152 Hz, the time differences between areas can be confounded by differences in frequency content, with lower frequencies leading to broader responses and hence earlier onsets.To exclude this possibility, we performed the analysis described for the classifier performance on the contra-/ipsilateral power contrast traces for each frequency (see Fig. 2b for the average contrasts).To capture the potentially biphasic power response that we described earlier for PF and OP leads, we detected both increases and decreases in power contrast.By only averaging across frequencies after relative times have been computed, any influence of wavelet width is removed.Though the single-frequency single-trial analysis is much more variable and lacks the multivariate information used by the classifier, we still obtained timelines qualitatively similar to those obtained from the single-trial classifiers (Fig. 4d,e). Consensus confirms early role for dlPFC, PMd, and PFt.To test the consistency and reliability of the timelines, we integrated the four methods into a single timeline.Due to differences in scale of the time axes, the timelines will have different weights when computing a standard average.We therefore opted for a nonparametric approach, by identifying the rank order for each bootstrap for every method and collapsing the rank distributions across methods (Fig. 5a).We then computed a rank clustering score for each area (see "Methods" section) and compared this to 500 randomly generated datasets.All identified brain areas showed significant clustering (p < 0.002), except for the collection of TL leads (p > 0.998), which is therefore excluded from Fig. 5. Both the integrated rank (Fig. 5a) and the average onset across methods (Fig. 5b) paint a picture of early involvement in decision-making by areas PFt, dlPFC, and PMd, with these areas responding, on average, ~12 ms before area BA4.The response onset of BA4 coincided with the onset of PFcm, OP1, and OP3.Areas PFop and PMm showed late responses, together with sensory areas BA3a/S1, with the onset of S1 responses following ~25 ms after the onset of BA4.The late responding BA3a/S1 areas also stand out due to their high decoding performance (Supplementary Fig. 4).This suggests that for decision regions, there is little or no evidence that earlier onset is coupled to the highest decoding performance (Supplementary Fig. 14).Areas are ordered by their average rank; b average onset time of activation (color coded), relative to onset of area BA4, for all areas with significant consistency between methods.Each dot is located at the center of mass of all recording leads that contributed and the size of the circle represents the number of recording leads; c schematic of information flow suggested by the results in Figs. 3, and a and b: stimulus information and rule information all converge onto a shared decision process, consisting of an early (dlPFC, PFt, and PMd) and a late phase (PFcm, OP1, and OP3).See "Discussion" section for a detailed description. Patient 6 did not perform the task well, yet this had negligible impact on the results, as demonstrated by extremely high correlations for rank (Spearman; rho = 0.991; p < 0.0001) and timing (Pearson; rho = 0.994; p < 0.0001) between the full dataset and a reduced dataset without their data (Supplementary Fig. 15a). The majority (567/663) of tested leads were located outside the epileptogenic zone (EZ), yet 16 of the 95 left/right classifier leads were located in the EZ.Inclusion of the latter leads in the results is unlikely to influence the left/right classification results.Indeed, the fraction of leads with significant classification performance did not differ inside and outside of the EZ (Fisher's exact test; p = 0.528 for the left/right classifier; p = 0.556 for the baseline classifier).When computed without the EZ channels (Supplementary Fig. 15b), the integrated timeline produced similar results to the full dataset, leading to high correlations between the datasets for the rank conjunction (Spearman correlation; rho = 0.861; p = 0.0003) and onset times (Pearson; rho = 0.839; p = 0.0007).
<li> <b>parietal PF:</b> parietalCortex (UBERONParcellation)<li> <b>OP areas:</b> Other (UBERONParcellation)<li> <b>PFt:</b> Other (UBERONParcellation)<li> <b>dlPFC:</b> dorsolateralPrefrontalCortex (UBERONParcellation)<li> <b>PMd:</b> premotorCortex (UBERONParcellation)<li> <b>BA4:</b> primaryMotorCortex (UBERONParcellation)<li> <b>PFcm:</b> Other (UBERONParcellation)<li> <b>OP1:</b> Other (UBERONParcellation)<li> <b>OP3:</b> Other (UBERONParcellation)<li> <b>PMm:</b> Other (UBERONParcellation)<li> <b>BA3a:</b> Other (UBERONParcellation)<li> <b>S1:</b> primarySomatosensoryCortex (UBERONParcellation)<li> <b>PFop:</b> Other (UBERONParcellation)<li> <b>TL:</b> temporalLobe (UBERONParcellation)
[ [ { "end": 63, "label": "UBERONParcellation", "start": 52 }, { "end": 76, "label": "UBERONParcellation", "start": 68 }, { "end": 4421, "label": "UBERONParcellation", "start": 4418 }, { "end": 7138, "label": "UBERONParcellation", "start": 7135 }, { "end": 7995, "label": "UBERONParcellation", "start": 7992 }, { "end": 9108, "label": "UBERONParcellation", "start": 9105 }, { "end": 4491, "label": "UBERONParcellation", "start": 4486 }, { "end": 7124, "label": "UBERONParcellation", "start": 7119 }, { "end": 8002, "label": "UBERONParcellation", "start": 7997 }, { "end": 9103, "label": "UBERONParcellation", "start": 9098 }, { "end": 7129, "label": "UBERONParcellation", "start": 7126 }, { "end": 8011, "label": "UBERONParcellation", "start": 8008 }, { "end": 9117, "label": "UBERONParcellation", "start": 9114 }, { "end": 4028, "label": "UBERONParcellation", "start": 4025 }, { "end": 4712, "label": "UBERONParcellation", "start": 4709 }, { "end": 5617, "label": "UBERONParcellation", "start": 5614 }, { "end": 5661, "label": "UBERONParcellation", "start": 5658 }, { "end": 5698, "label": "UBERONParcellation", "start": 5695 }, { "end": 8076, "label": "UBERONParcellation", "start": 8073 }, { "end": 8102, "label": "UBERONParcellation", "start": 8099 }, { "end": 8299, "label": "UBERONParcellation", "start": 8296 }, { "end": 8693, "label": "UBERONParcellation", "start": 8690 }, { "end": 4671, "label": "UBERONParcellation", "start": 4667 }, { "end": 8135, "label": "UBERONParcellation", "start": 8131 }, { "end": 9141, "label": "UBERONParcellation", "start": 9137 }, { "end": 4676, "label": "UBERONParcellation", "start": 4673 }, { "end": 8140, "label": "UBERONParcellation", "start": 8137 }, { "end": 9146, "label": "UBERONParcellation", "start": 9143 }, { "end": 4685, "label": "UBERONParcellation", "start": 4682 }, { "end": 8149, "label": "UBERONParcellation", "start": 8146 }, { "end": 9155, "label": "UBERONParcellation", "start": 9152 }, { "end": 4665, "label": "UBERONParcellation", "start": 4662 }, { "end": 8168, "label": "UBERONParcellation", "start": 8165 }, { "end": 6012, "label": "UBERONParcellation", "start": 6008 }, { "end": 8224, "label": "UBERONParcellation", "start": 8220 }, { "end": 8324, "label": "UBERONParcellation", "start": 8320 }, { "end": 6019, "label": "UBERONParcellation", "start": 6017 }, { "end": 8227, "label": "UBERONParcellation", "start": 8225 }, { "end": 8249, "label": "UBERONParcellation", "start": 8247 }, { "end": 8327, "label": "UBERONParcellation", "start": 8325 }, { "end": 6079, "label": "UBERONParcellation", "start": 6075 }, { "end": 8160, "label": "UBERONParcellation", "start": 8156 }, { "end": 7784, "label": "UBERONParcellation", "start": 7782 }, { "end": 1164, "label": "UBERONParcellation", "start": 1159 }, { "end": 1567, "label": "UBERONParcellation", "start": 1562 }, { "end": 2460, "label": "UBERONParcellation", "start": 2455 }, { "end": 2692, "label": "UBERONParcellation", "start": 2687 }, { "end": 2825, "label": "UBERONParcellation", "start": 2820 }, { "end": 2961, "label": "UBERONParcellation", "start": 2956 }, { "end": 2992, "label": "UBERONParcellation", "start": 2987 }, { "end": 3460, "label": "UBERONParcellation", "start": 3455 }, { "end": 3576, "label": "UBERONParcellation", "start": 3571 }, { "end": 4023, "label": "UBERONParcellation", "start": 4011 }, { "end": 4446, "label": "UBERONParcellation", "start": 4433 }, { "end": 4592, "label": "UBERONParcellation", "start": 4580 }, { "end": 7703, "label": "UBERONParcellation", "start": 7698 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "brain: Other (UBERONParcellation)\nmotor cortex: primaryMotorCortex (UBERONParcellation)\npremotor area: premotorCortex (UBERONParcellation)\n\r\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 63, "label": "UBERONParcellation", "start": 52 }, { "end": 76, "label": "UBERONParcellation", "start": 68 }, { "end": 4421, "label": "UBERONParcellation", "start": 4418 }, { "end": 7138, "label": "UBERONParcellation", "start": 7135 }, { "end": 7995, "label": "UBERONParcellation", "start": 7992 }, { "end": 9108, "label": "UBERONParcellation", "start": 9105 }, { "end": 4491, "label": "UBERONParcellation", "start": 4486 }, { "end": 7124, "label": "UBERONParcellation", "start": 7119 }, { "end": 8002, "label": "UBERONParcellation", "start": 7997 }, { "end": 9103, "label": "UBERONParcellation", "start": 9098 }, { "end": 7129, "label": "UBERONParcellation", "start": 7126 }, { "end": 8011, "label": "UBERONParcellation", "start": 8008 }, { "end": 9117, "label": "UBERONParcellation", "start": 9114 }, { "end": 4028, "label": "UBERONParcellation", "start": 4025 }, { "end": 4712, "label": "UBERONParcellation", "start": 4709 }, { "end": 5617, "label": "UBERONParcellation", "start": 5614 }, { "end": 5661, "label": "UBERONParcellation", "start": 5658 }, { "end": 5698, "label": "UBERONParcellation", "start": 5695 }, { "end": 8076, "label": "UBERONParcellation", "start": 8073 }, { "end": 8102, "label": "UBERONParcellation", "start": 8099 }, { "end": 8299, "label": "UBERONParcellation", "start": 8296 }, { "end": 8693, "label": "UBERONParcellation", "start": 8690 }, { "end": 4671, "label": "UBERONParcellation", "start": 4667 }, { "end": 8135, "label": "UBERONParcellation", "start": 8131 }, { "end": 9141, "label": "UBERONParcellation", "start": 9137 }, { "end": 4676, "label": "UBERONParcellation", "start": 4673 }, { "end": 8140, "label": "UBERONParcellation", "start": 8137 }, { "end": 9146, "label": "UBERONParcellation", "start": 9143 }, { "end": 4685, "label": "UBERONParcellation", "start": 4682 }, { "end": 8149, "label": "UBERONParcellation", "start": 8146 }, { "end": 9155, "label": "UBERONParcellation", "start": 9152 }, { "end": 4665, "label": "UBERONParcellation", "start": 4662 }, { "end": 8168, "label": "UBERONParcellation", "start": 8165 }, { "end": 6012, "label": "UBERONParcellation", "start": 6008 }, { "end": 8224, "label": "UBERONParcellation", "start": 8220 }, { "end": 8324, "label": "UBERONParcellation", "start": 8320 }, { "end": 6019, "label": "UBERONParcellation", "start": 6017 }, { "end": 8227, "label": "UBERONParcellation", "start": 8225 }, { "end": 8249, "label": "UBERONParcellation", "start": 8247 }, { "end": 8327, "label": "UBERONParcellation", "start": 8325 }, { "end": 6079, "label": "UBERONParcellation", "start": 6075 }, { "end": 8160, "label": "UBERONParcellation", "start": 8156 }, { "end": 7784, "label": "UBERONParcellation", "start": 7782 } ]
null
null
1122248f-d607-4b42-b62d-d6cd6214e84b
pending
2025-04-29T14:36:04.699924
2025-04-29T14:36:04.699924
ac04d1b8-e7b1-4542-a244-fda248c490ae
Abstract Background Medications currently recommended for the treatment of Obsessive-Compulsive Disorder (OCD) usually decrease the severity of the symptoms by 20–30%; however, 40–60% of OCD patients do not achieve a satisfactory response. Our main objective was to investigate the effectiveness of memantine, a non-competitive N-Methyl-D-aspartate (NMDA) receptor antagonist, as an adjunct therapy to sertraline, a selective serotonin reuptake inhibitor (SSRI), to improve severity of symptoms and executive function among patients with obsessive-compulsive disorder. Methods Seventy patients with OCD according to the Diagnostic and Statistical Manual of Mental Disorders (DSM–5) criteria, and a Yale-Brown obsessive compulsive scale (Y-BOCS) score of more than 21 were recruited to the study. They received sertraline (100 mg daily initially followed by 200 mg daily after week 4) and either memantine (10 mg twice daily) or placebo in a placebo controlled, double-blinded, parallel-group, clinical trial of 12 weeks. The primary outcome was OCD symptoms measured by the Y-BOCS. Moreover, executive function of participants was measured by the Wisconsin Card Sorting Test (WCST). Results The total score, and obsession and compulsion subscales of Y-BOCS significantly dropped in both groups with no significant difference between the two groups. However, memantine group showed a greater response in the number of completed categories subscale of the WCST (p value<0.001). We did not observe any major adverse effects in any of the groups. Conclusion Memantine has an acceptable safety and tolerability in patients with OCD and might have a positive effect on their executive function. Nevertheless, the current results don`t support the efficacy of memantine as an adjunctive agent to sertraline for symptoms in patients with OCD. Trial registration The trial was registered at the Iranian Registry of Clinical Trials on 04/10/2019 (www.irct.ir; IRCT ID: IRCT20170123032145N4).
None
[ [] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[]
null
null
f55cecf2-16dd-4794-9a5b-547e1ad23f13
pending
2025-04-29T14:36:04.699930
2025-04-29T14:36:04.699930
e454eac2-f7b8-4769-aad3-7e67fccc45ee
The baseline Y-BOCS total score's difference was not significant between the groups (MD (95% CI) = -2.23(-5.07-0.61),p-value=0.12,Table 1).Total Y-BOCS score changes from baseline in memantine group at fourth and 12 th week of the study was MD (95% CI)
None
[ [] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[]
null
null
d3f92770-e8bf-46dc-8b61-f312471e0c30
completed
2025-04-29T14:36:04.699936
2025-05-27T14:00:51.009465
a91293a4-56c7-4504-99fb-bbf3da37e4a4
BackgroundStroke is a common cause of acquired disability on a global scale. Patients with motor dysfunction after a stroke have a reduced quality of life and suffer from an economic burden. Scalp acupuncture has been proven to be an effective treatment for motor recovery after a stroke. However, the neural mechanism of scalp acupuncture for motor function recovery remains to be researched. This study aimed to investigate functional connectivity (FC) changes in region of interest (ROI) and other brain regions to interpret the neural mechanism of scalp acupuncture.MethodsTwenty-one patients were included and randomly divided into patient control (PCs) and scalp acupuncture (SAs) groups with left hemiplegia due to ischemic stroke, and we also selected 20 matched healthy controls (HCs). The PCs were treated with conventional Western medicine, while the SAs were treated with scalp acupuncture (acupuncture at the right anterior oblique line of vertex temporal). All subjects received whole-brain resting-state functional magnetic resonance imaging (rs-fMRI) scan before treatment, and the patients received a second scan after 14 days of treatment. We use the National Institutes of Health Stroke Scale (NIHSS) scores and the analyses of resting-state functional connectivity (RSFC) as the observational indicators.ResultsThe contralateral and ipsilateral cortex of hemiplegic patients with cerebral infarction were associated with an abnormal increase and decrease in basal internode function. An abnormal increase in functional connectivity mainly exists in the ipsilateral hemisphere between the cortex and basal ganglia and reduces the abnormal functional connectivity in the cortex and contralateral basal ganglia. Increased RSFC was observed in the bilateral BA6 area and bilateral basal ganglia and the connectivity between bilateral basal ganglia nuclei improved. However, the RSFC of the conventional treatment group only improved in the unilateral basal ganglia and contralateral BA6 area. The RSFC in the left middle frontal gyrus, superior temporal gyrus, precuneus, and other healthy brain regions were enhanced in SAs after treatment.ConclusionThe changes in functional connectivity between the cerebral cortex and basal ganglia in patients with cerebral infarction showed a weakening of the bilateral hemispheres and the enhancement of the connections between the hemispheres. Scalp acupuncture has the function of bidirectional regulation, which makes the unbalanced abnormal brain function state restore balance.
<li> <b>resting-state functional magnetic resonance imaging (rs-fMRI):</b> functionalMagneticResonanceImaging (technique)<li> <b>bilateral BA6 area:</b> premotorCortex (UBERONParcellation)<li> <b>bilateral basal ganglia:</b> basalGanglion (UBERONParcellation)<li> <b>contralateral BA6 area:</b> premotorCortex (UBERONParcellation)<li> <b>left middle frontal gyrus:</b> middleFrontalGyrus (UBERONParcellation)<li> <b>superior temporal gyrus:</b> superiorTemporalGyrus (UBERONParcellation)<li> <b>precuneus:</b> precuneusCortex (UBERONParcellation)<li> <b>cortex:</b> cerebralCortex (UBERONParcellation)<li> <b>cerebral cortex:</b> cerebralCortex (UBERONParcellation)
[ [ { "end": 2075, "label": "UBERONParcellation", "start": 2052 }, { "end": 2086, "label": "UBERONParcellation", "start": 2077 }, { "end": 1371, "label": "UBERONParcellation", "start": 1365 }, { "end": 1614, "label": "UBERONParcellation", "start": 1608 }, { "end": 1695, "label": "UBERONParcellation", "start": 1689 }, { "end": 2233, "label": "UBERONParcellation", "start": 2218 }, { "end": 506, "label": "UBERONParcellation", "start": 501 }, { "end": 1056, "label": "technique", "start": 1019 }, { "end": 1632, "label": "UBERONParcellation", "start": 1619 }, { "end": 1727, "label": "UBERONParcellation", "start": 1714 }, { "end": 1810, "label": "UBERONParcellation", "start": 1797 }, { "end": 1863, "label": "UBERONParcellation", "start": 1850 }, { "end": 1980, "label": "UBERONParcellation", "start": 1967 }, { "end": 2050, "label": "UBERONParcellation", "start": 2030 }, { "end": 2111, "label": "UBERONParcellation", "start": 2106 }, { "end": 2251, "label": "UBERONParcellation", "start": 2238 }, { "end": 2506, "label": "UBERONParcellation", "start": 2501 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "brain: Other (UBERONParcellation)\nfunctional magnetic resonance imaging: functionalMagneticResonanceImaging (technique)\ncortex: Other (UBERONParcellation)\nbasal ganglia: collectionOfBasalGanglia (UBERONParcellation)\n\r\r\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 1066, "label": "technique", "start": 1005 }, { "end": 1782, "label": "UBERONParcellation", "start": 1764 }, { "end": 1810, "label": "UBERONParcellation", "start": 1787 }, { "end": 1863, "label": "UBERONParcellation", "start": 1840 }, { "end": 2007, "label": "UBERONParcellation", "start": 1985 }, { "end": 2050, "label": "UBERONParcellation", "start": 2025 }, { "end": 2075, "label": "UBERONParcellation", "start": 2052 }, { "end": 2086, "label": "UBERONParcellation", "start": 2077 }, { "end": 1371, "label": "UBERONParcellation", "start": 1365 }, { "end": 1614, "label": "UBERONParcellation", "start": 1608 }, { "end": 1695, "label": "UBERONParcellation", "start": 1689 }, { "end": 2233, "label": "UBERONParcellation", "start": 2227 }, { "end": 2233, "label": "UBERONParcellation", "start": 2218 } ]
null
null
cfb7d4bd-14e4-48d0-9541-1821c2be1033
completed
2025-04-29T14:36:04.699942
2025-05-27T14:00:51.148187
e1585ff8-8ddd-4288-b8e7-3f2c4ba700a8
Brain tumors (gliomas) contain large populations of infiltrating macrophages and recruited microglia, which in experimental murine glioma models promote tumor formation and progression. Among the barriers to understanding the contributions of these stromal elements to high-grade glioma (glioblastoma; GBM) biology is the relative paucity of tools to characterize infiltrating macrophages and resident microglia. In this study, we leveraged multiple RNA analysis platforms to identify new monocyte markers relevant to GBM patient outcome.High-confidence lists of mouse resident microglia- and bone marrow-derived macrophage-specific transcripts were generated using converging RNA-seq and microarray technologies and validated using qRT-PCR and flow cytometry. Expression of select cell surface markers was analyzed in brain-infiltrating macrophages and resident microglia in an induced GBM mouse model, while allogeneic bone marrow transplantation was performed to trace the origins of infiltrating and resident macrophages. Glioma tissue microarrays were examined by immunohistochemistry, and the Gene Expression Omnibus (GEO) database was queried to determine the prognostic value of identified microglia biomarkers in human GBM.We generated a unique catalog of differentially-expressed bone marrow-derived monocyte and resident microglia transcripts, and demonstrated that brain-infiltrating macrophages acquire F11R expression in GBM and following bone-marrow transplantation. Moreover, mononuclear cell F11R expression positively correlates with human high-grade glioma and additionally serves as a biomarker for GBM patient survival, regardless of GBM molecular subtype.These studies establish F11R as a novel monocyte prognostic marker for GBM critical for defining a subpopulation of stromal cells for future potential therapeutic intervention.
<li> <b>Brain:</b> brain (UBERONParcellation)<li> <b>microglia:</b> Other (UBERONParcellation)<li> <b>mouse:</b> musMusculus (species)<li> <b>RNA-seq:</b> RNASequencing (technique)<li> <b>microarray:</b> Other (technique)<li> <b>qRT-PCR:</b> Other (technique)<li> <b>flow cytometry:</b> Other (technique)<li> <b>immunohistochemistry:</b> immunohistochemistry (technique)<li> <b>human:</b> homoSapiens (species)
[ [ { "end": 5, "label": "UBERONParcellation", "start": 0 }, { "end": 568, "label": "species", "start": 563 }, { "end": 896, "label": "species", "start": 891 }, { "end": 684, "label": "technique", "start": 677 }, { "end": 699, "label": "technique", "start": 689 }, { "end": 740, "label": "technique", "start": 733 }, { "end": 759, "label": "technique", "start": 745 }, { "end": 1089, "label": "technique", "start": 1069 }, { "end": 1227, "label": "species", "start": 1222 }, { "end": 1557, "label": "species", "start": 1552 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "\r\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 5, "label": "UBERONParcellation", "start": 0 }, { "end": 100, "label": "UBERONParcellation", "start": 91 }, { "end": 411, "label": "UBERONParcellation", "start": 402 }, { "end": 587, "label": "UBERONParcellation", "start": 578 }, { "end": 872, "label": "UBERONParcellation", "start": 863 }, { "end": 1207, "label": "UBERONParcellation", "start": 1198 }, { "end": 1341, "label": "UBERONParcellation", "start": 1332 }, { "end": 568, "label": "species", "start": 563 }, { "end": 896, "label": "species", "start": 891 }, { "end": 684, "label": "technique", "start": 677 }, { "end": 699, "label": "technique", "start": 689 }, { "end": 740, "label": "technique", "start": 733 }, { "end": 759, "label": "technique", "start": 745 }, { "end": 1089, "label": "technique", "start": 1069 }, { "end": 1227, "label": "species", "start": 1222 }, { "end": 1557, "label": "species", "start": 1552 } ]
null
null
06c4f5be-92d4-4269-ab21-3fe2f6b971bd
completed
2025-04-29T14:36:04.699948
2025-05-27T14:00:51.242069
d3b31357-42c9-4789-8032-2bcef0b21a86
Abstract Background Inflammatory bowel disease (IBD) is widespread and rapidly rising in developing countries. It remains a significant issue in Western culture with a prevalence of more than 0.3%. Symptom control has been the only focus of treatment before the discovery that many individuals with IBD continue to have disease activity even in the absence of clinical symptoms. Therefore, treatment goals now include establishing clinical remission, steroid-free remission, and mucosal healing, which may eventually be complemented by transmural healing in cross-sectional imaging modalities. Magnetic resonance enterography (MRE), computed tomography enterography, and small-bowel ultrasound are now reliable methods for staging intramural lesions and extramural consequences in CD and for determining disease activity and severity. Recently literature suggests the incorporation of (MRE) for periodic reevaluation of IBD patients, as it offers small-bowel, colonic, and extra-enteric assessment as well as monitors the response to the anti-inflammatory therapy. The purpose of the current study was to compare MRE with ileo-colonoscopy findings in the diagnosis of IBD features, specifically Crohn's disease, and ulcerative colitis, as well as in the detection of disease exacerbation (Activity). Results This study used MRE and ileo-colonoscopy to assess chronic inflammatory bowel disease patients; the patient population (n = 30) was made up of (14/30, 46.7%) females and (16/30, 53.3%) males, with a mean age of 32 ± SD 13 years. MRE alone detected lymphadenopathy in 73.3% of patients, and mural thickening with a mean of 4.1 ± SD 5.1 mm. It has detected mucosal enhancement with 80% sensitivity and 60% specificity. However, it was unable to detect mucosal erosions or ulceration. Conclusions MRE is sensitive, inexpensive, noninvasive, and radiation-free for inflammatory bowel disease detection, with 86.7% diagnostic accuracy for affected areas. Unlike ileo-colonoscopy, it could examine the entire small intestine, precisely measure the affected loop, and detect activity signs such as mural thickening and lymphadenopathy. Only ileo-colonoscopy could detect mucosal degradation and superficial ulcers. IBD treatment protocols should incorporate MRE for small-bowel, colonic, and extra-enteric assessment, monitoring of disease activity, and anti-inflammatory therapy response.
<li> <b>Magnetic resonance enterography (MRE):</b> magneticResonanceImaging (technique)<li> <b>computed tomography enterography:</b> computerTomography (technique)<li> <b>small-bowel ultrasound:</b> Other (technique)<li> <b>ileo-colonoscopy:</b> Other (technique)
[ [ { "end": 631, "label": "technique", "start": 594 }, { "end": 665, "label": "technique", "start": 633 }, { "end": 693, "label": "technique", "start": 671 }, { "end": 1138, "label": "technique", "start": 1122 }, { "end": 1349, "label": "technique", "start": 1333 }, { "end": 1983, "label": "technique", "start": 1967 }, { "end": 2160, "label": "technique", "start": 2144 }, { "end": 1474, "label": "biologicalSex", "start": 1467 }, { "end": 1499, "label": "biologicalSex", "start": 1494 }, { "end": 1328, "label": "technique", "start": 1325 }, { "end": 1807, "label": "technique", "start": 1804 }, { "end": 2264, "label": "technique", "start": 2261 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "females: female (biologicalSex)\nmales: male (biologicalSex)\n\r\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 631, "label": "technique", "start": 594 }, { "end": 665, "label": "technique", "start": 633 }, { "end": 693, "label": "technique", "start": 671 }, { "end": 1138, "label": "technique", "start": 1122 }, { "end": 1349, "label": "technique", "start": 1333 }, { "end": 1983, "label": "technique", "start": 1967 }, { "end": 2160, "label": "technique", "start": 2144 } ]
null
null
53e2fc83-016d-44f9-a07e-aca67205180f
pending
2025-04-29T14:36:04.699954
2025-04-29T14:36:04.699954
a7d6704e-ee93-40e6-a5fd-255d20e0b5b1
An expert gastroenterologist has documented the symptoms, physical, and laboratory findings of the patients as part of their assessment in the IBD clinic.
None
[ [] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[]
null
null
bd33218f-2f08-4983-95e8-3a3e8e7eb20c
pending
2025-04-29T14:36:04.699961
2025-04-29T14:36:04.699961
de6c55fe-c0b2-411b-a0e1-60a9c6e6e02f
Neuron, 103 (1)
None
[ [ { "end": 6, "label": "UBERONParcellation", "start": 0 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ "neuron: Other (UBERONParcellation)" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[]
null
null
16061219-77ec-496d-985e-3aa0d7d45f1b
completed
2025-04-29T14:36:04.699967
2025-05-27T14:00:51.350918
6528a652-4e01-4df1-b4d7-5fe85f108165
Six to twelve week-old mice of either sex were anaesthetized with pentobarbital (160 mg kg À1 , i.p.) before transcardiac perfusion with 20 mL of ice-cold ACSF followed by 100 mL of 4% ice-cold paraformaldehyde (in 0.1 M sodium phosphate buffer, pH 7.4).Spinal cords tissue was post-fixated for 2 h with 4% paraformaldehyde on ice, cryoprotected in 25% sucrose solution (in 0.1 M sodium phosphate buffer) overnight at 4 C, embedded in NEG50 frozen section medium (Richard-Allen Scientific) and stored at À80 C until use.The spinal cords were cut into 30 mm cryosections using Hyrax C60 cryostat (Carl Zeiss) and mounted onto Superfrost Plus microscope slides (Thermo Fisher Scientific).Spinal cord section were incubated at 4 C overnight in a primary antibody solution (PBS, 0.3% Triton X-100, 10% normal donkey serum) containing combinations of the following antibodies: rabbit anti-GFP (1:1000), guinea pig anti-Lmx1b (1:10,000), goat anti-Pax2 (1:200), goat anti-tdTomato (1:1000), guinea pig anti-vGluT2 (1:1000).Three washing steps of 5 min each in PBS were performed before incubating spinal cord sections with secondary antibodies (1:800) for 1h at room temperature in PBS supplemented with 0.3% Triton X-100.For details on the antibodies, see Key Resources Table .Immunostaining of synaptic contacts between GRP and GRPR neurons was performed on 40 mm thick free floating sections (cutting was performed using Hyrax KS 34 microtome, Carl Zeiss) and the sections were pretreated 3 times for 10 min with 50% ethanol (in ddH 2 O), washed two-times for 10 min in PBS and incubated with primary antibodies for 3 days.Images were taken with a LSM 710 or LSM 800 with Airyscan confocal microscopes (Carl Zeiss) controlled with ZEN 2011 (black edition) or ZEN 2.3 (blue edition) software, respectively, and using, respectively, an EC Plan-Neofluar 40x/1.30oil-immersion objective or a Plan-Apochromat 40x/1.4Oil DIC M27 oil-immersion objective.Z stack images of 8 optical sections and 1.5 mm step size were used for the analysis of fluorescence colocalization and to create maximum intensity projections images, whereas Z stack images of 32 optical sections and 0.2 mm step size were used for the analysis of synaptic contacts.Images were processed using ImageJ software.For quantification, 3 or 5 animals and three sections per animal were analyzed.Cell counting was performed using the ImageJ Cell Counter plug-in. To correlate the firing patterns with either an excitatory or an inhibitory phenotype Grpr::eGFP neurons were filled during whole-cell recording with a K + -gluconate based internal solution containing biocytin (1.5 mg/ml).Slices were transferred to a 4% paraformaldehyde fixative solution and incubated for 1 h at 4 C. Afterward they were cryo-protected overnight in 20% sucrose in PB before embedding and freezing in NEG50 for sectioning.Embedded sections were re-sectioned at 25mm and mounted on Superfrost Plus microscope slides.Antibody incubation with goat anti-Pax2 and rabbit anti-Tlx3 was carried out as described above.Streptavidin-488 conjugate was applied together with the secondary antibodies at a 1:500 dilution. In situ hybridization Spinal cords used for in situ hybridization were dissected from 6 -10 week-old mice of either sex in ice-cold ACSF and immediately frozen in 1.5 mL Eppendorf tubes immersed in liquid nitrogen.Tissue was cut into 20 mm cryosections, mounted onto Superfrost Plus microscope slides (Thermo Fisher Scientific) and hybridized following RNAscope Assay guidelines (Advanced Cell Diagnostics, Newark, CA, USA), using probes designed for RNAscope Fluorescent Multiplex in situ hybridization listed in the Key Resources Table .Fiber optic cannula implantation Six to eight week-old male Grp-ChR2 (Grp::cre;Ai32 double transgenic) mice were implanted with fiber optic cannulas as was described previously (Bonin et al., 2016;Christensen et al., 2016).Control experiments were performed in Grp::cre -;Ai32 mice.Ceramic ferrules measuring ⌀ 1.25 mm (Thorlabs) were mounted with appropriate multimode optical fiber and trimmed < 1 mm at the edges.Mice were anesthetized with 2 -5% isofluorane and maintained on a motorized stereotactic frame until end of surgical procedure in 1 -2% isofluorane anesthesia.The fur over the back of the mice was shaved and an incision was made on the skin to expose the vertebral column.Incisions were made on the muscles lateral to the tendons spanning either sides of the T13 vertebral disc.The vertebral column was clamped with spinal adaptors and the T13 vertebral disc was exposed.The tissues covering the spinous and transverse processes of the disc were removed using forceps, and a hole was drilled on the caudal-transverse process approximately 2 mm from the midline to expose the L4 -L5 spinal cord segment.A rubber aspirator was used to dry the vertebral disc.Collagen strips (Lyostypt, B. Braun) were used to minimize bleeding.Small amounts of base-coat (One Coat 7 Universal, Coltene) were carefully applied to the cannula's concave end and around the drilled hole on the spinous process as well as the rostro-caudal transverse processes.The coating was cured with UV light to provide a steady base for adherence.The fiber-optic cannula was inserted into the drilled hole.A layer of dental cement (Synergy D6 Flow, Coltene) was applied around the cannula over the base-coat, cured with UV-light for 20 s, and upon hardening, a second layer of dental cement was applied and cured to firmly secure the cannula to the vertebral disc.The muscles around the vertebral column were then sutured using absorbable sutures (Safil 5-0, B. Braun) and the skin was sutured with non-absorbable sutures (Dafilon 6-0, B. Braun).The mice were allowed to recover on a heat pad.Behavior experiments started 48 h after surgery.
<li> <b>mice:</b> musMusculus (species)<li> <b>either sex:</b> notDetectable (biologicalSex)<li> <b>transcardiac perfusion:</b> transcardialPerfusionTechnique (technique)<li> <b>Immunostaining:</b> immunohistochemistry (technique)<li> <b>confocal microscopes:</b> confocalMicroscopy (technique)<li> <b>in situ hybridization:</b> inSituHybridisation (technique)<li> <b>whole-cell recording:</b> wholeCellPatchClamp (technique)<li> <b>Fiber optic cannula implantation:</b> implantSurgery (technique)<li> <b>spinal cord:</b> Other (UBERONParcellation)
[ [ { "end": 27, "label": "species", "start": 23 }, { "end": 3250, "label": "species", "start": 3246 }, { "end": 3791, "label": "species", "start": 3787 }, { "end": 3965, "label": "species", "start": 3961 }, { "end": 4292, "label": "species", "start": 4288 }, { "end": 5718, "label": "species", "start": 5714 }, { "end": 131, "label": "technique", "start": 109 }, { "end": 1698, "label": "technique", "start": 1678 }, { "end": 3210, "label": "technique", "start": 3189 }, { "end": 3648, "label": "technique", "start": 3627 }, { "end": 2561, "label": "technique", "start": 2541 }, { "end": 1102, "label": "UBERONParcellation", "start": 1091 }, { "end": 4793, "label": "UBERONParcellation", "start": 4782 }, { "end": 697, "label": "UBERONParcellation", "start": 686 }, { "end": 759, "label": "technique", "start": 743 }, { "end": 1138, "label": "technique", "start": 1117 }, { "end": 3397, "label": "technique", "start": 3385 }, { "end": 3716, "label": "technique", "start": 3704 }, { "end": 4104, "label": "species", "start": 4100 }, { "end": 4498, "label": "UBERONParcellation", "start": 4482 }, { "end": 5567, "label": "UBERONParcellation", "start": 5551 }, { "end": 1608, "label": "technique", "start": 1590 }, { "end": 266, "label": "UBERONParcellation", "start": 254 }, { "end": 536, "label": "UBERONParcellation", "start": 524 }, { "end": 1336, "label": "UBERONParcellation", "start": 1329 }, { "end": 3179, "label": "UBERONParcellation", "start": 3167 }, { "end": 3166, "label": "technique", "start": 3145 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "primary antibody: primaryAntibodyStaining (technique)\nsecondary antibodies: secondaryAntibodyStaining (technique)\nneuron: Other (UBERONParcellation)\nprimary antibodies: primaryAntibodyStaining (technique)\ncryosections: cryosectioning (technique)\nvertebral column: Other (UBERONParcellation)\r\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 27, "label": "species", "start": 23 }, { "end": 3250, "label": "species", "start": 3246 }, { "end": 3791, "label": "species", "start": 3787 }, { "end": 3965, "label": "species", "start": 3961 }, { "end": 4292, "label": "species", "start": 4288 }, { "end": 5718, "label": "species", "start": 5714 }, { "end": 41, "label": "biologicalSex", "start": 31 }, { "end": 3264, "label": "biologicalSex", "start": 3254 }, { "end": 131, "label": "technique", "start": 109 }, { "end": 1286, "label": "technique", "start": 1272 }, { "end": 1698, "label": "technique", "start": 1678 }, { "end": 3210, "label": "technique", "start": 3189 }, { "end": 3648, "label": "technique", "start": 3627 }, { "end": 2561, "label": "technique", "start": 2541 }, { "end": 3716, "label": "technique", "start": 3684 }, { "end": 1102, "label": "UBERONParcellation", "start": 1091 }, { "end": 4793, "label": "UBERONParcellation", "start": 4782 } ]
null
null
f2e8ab65-1316-4451-b24b-9b12008c27c1
completed
2025-04-29T14:36:04.699973
2025-05-27T14:00:51.572157
f605cc87-afde-48d9-a1ea-daa32c2e72f8
The Inventory D&eacute;j&agrave; Vu Experiences Assessment (IDEA) is the only screening instrument proposed to evaluate D&eacute;j&agrave; vu (DV) experience. Here we intended to validate the Italian version of IDEA (I-IDEA) and at the same time to investigate the incidence and subjective qualities of DV phenomenon in Italian healthy adult individuals on basis of an Italian multicentre observational study. In this study we report normative data on the I-IDEA, collected on a sample of 542 Italian healthy subjects aging between 18 to 70 years (average age 40, range 18-70) with a formal educational from 1-19 years. From September 2013 to March 2016 were recruited 542 healthy volunteers from ten outpatient neurological clinics in ItalyAll participants (i.e family members of neurological patients enrolled, medicine&rsquo;s student, physicians) had no neurological or psychiatric illness and they gave informed consent to participate in the study. All subjects enrolled had self-administered the questionnaire and they are able to complete I-IDEA test without any support. In total 396 (73%) of the 542 healthy controls had DV phenomenon. The frequency of DV was inversely related to age as well as to derealisation, jamais vu, precognitive dreams, depersonalization, paranormal activity, remembering dreams, travel frequency and daydreams (all P&lt;0.012). The Italian version of IDEA maintains good properties in Italian version, thus confirming that this instrument is reliable for detecting and characterising the DV phenomenon.
<li> <b>Italian healthy adult individuals:</b> homoSapiens (species)
[ [] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Incorrect" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Incorrect" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 353, "label": "species", "start": 320 } ]
null
null
5e5081ed-9a79-40c8-95eb-8d491d2323a2
pending
2025-04-29T14:36:04.699979
2025-04-29T14:36:04.699979
11401e94-4566-4350-b746-6aeb97c62919
Interrelationships among IDEA items are given in Table 3.As reported in Table 3, precognitive dreams were most correlated of Déjà vu (rho = 0.296, p < 0.001), followed by derealization (rho = 0.248, p < 0.0001) and daydreams (rho = 0.24, p < 0.001).The remaining intercorrelations among the various IDEA items ranged from 0.005 (Derealization versus Remembering dreams) to 0.344 (Derealization versus Depersonalization) (p values ranging from <0.001 to 0.915).The strength of interrelationships among the IDEA items in our study were all of a similar degree to those observed in Adachi's study.Data are Sperman rank correlation (rho) and p values.In parenthesis, the rho coefficient between each pair of items as reported in the Adachi's study [6] is also given.
None
[ [] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[]
null
null
2341247c-6d53-4b37-98ab-9482e548701f
completed
2025-04-29T14:36:04.699985
2025-05-27T14:00:51.796223
5c0b8830-aa3e-40fb-a2c2-3dc394a90914
This study compared 30 older musicians and 30 age-matched non-musicians to investigate the association between lifelong musical instrument training and age-related cognitive decline and brain atrophy (musicians: mean age 70.8 years, musical experience 52.7 years; non-musicians: mean age 71.4 years, no or less than 3 years of musical experience). Although previous research has demonstrated that young musicians have larger gray matter volume (GMV) in the auditory-motor cortices and cerebellum than non-musicians, little is known about older musicians. Music imagery in young musicians is also known to share a neural underpinning [the supramarginal gyrus (SMG) and cerebellum] with music performance. Thus, we hypothesized that older musicians would show superiority to non-musicians in some of the abovementioned brain regions. Behavioral performance, GMV, and brain activity, including functional connectivity (FC) during melodic working memory (MWM) tasks, were evaluated in both groups. Behaviorally, musicians exhibited a much higher tapping speed than non-musicians, and tapping speed was correlated with executive function in musicians. Structural analyses revealed larger GMVs in both sides of the cerebellum of musicians, and importantly, this was maintained until very old age. Task-related FC analyses revealed that musicians possessed greater cerebellar-hippocampal FC, which was correlated with tapping speed. Furthermore, musicians showed higher activation in the SMG during MWM tasks; this was correlated with earlier commencement of instrumental training. These results indicate advantages or heightened coupling in brain regions associated with music performance and imagery in musicians. We suggest that lifelong instrumental training highly predicts the structural maintenance of the cerebellum and related cognitive maintenance in old age.
<li> <b>gray matter volume (GMV):</b> brainGrayMatter (UBERONParcellation)<li> <b>cerebellum:</b> cerebellum (UBERONParcellation)<li> <b>supramarginal gyrus (SMG):</b> supramarginalGyrus (UBERONParcellation)<li> <b>cerebellum:</b> cerebellum (UBERONParcellation)<li> <b>GMV:</b> brainGrayMatter (UBERONParcellation)<li> <b>cerebellum:</b> cerebellum (UBERONParcellation)<li> <b>SMG:</b> supramarginalGyrus (UBERONParcellation)<li> <b>cerebellum:</b> cerebellum (UBERONParcellation)
[ [ { "end": 495, "label": "UBERONParcellation", "start": 485 }, { "end": 678, "label": "UBERONParcellation", "start": 668 }, { "end": 1219, "label": "UBERONParcellation", "start": 1209 }, { "end": 1816, "label": "UBERONParcellation", "start": 1806 }, { "end": 663, "label": "UBERONParcellation", "start": 638 }, { "end": 1484, "label": "UBERONParcellation", "start": 1481 }, { "end": 191, "label": "UBERONParcellation", "start": 186 }, { "end": 436, "label": "UBERONParcellation", "start": 425 }, { "end": 822, "label": "UBERONParcellation", "start": 817 }, { "end": 870, "label": "UBERONParcellation", "start": 865 }, { "end": 1368, "label": "UBERONParcellation", "start": 1358 }, { "end": 1380, "label": "UBERONParcellation", "start": 1369 }, { "end": 1640, "label": "UBERONParcellation", "start": 1635 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "gray matter: brainGrayMatter (UBERONParcellation)\r\nbrain: Other (UBERONParcellation)\r\ncerebellar: cerebellum (UBERONParcellation)\r\nhippocampal: Other (UBERONParcellation)\nsupramarginal gyrus (SMG): supramarginalGyrus (UBERONParcellation)--> this is not on openMINDS, but on UBERON\n\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 449, "label": "UBERONParcellation", "start": 425 }, { "end": 495, "label": "UBERONParcellation", "start": 485 }, { "end": 678, "label": "UBERONParcellation", "start": 668 }, { "end": 1219, "label": "UBERONParcellation", "start": 1209 }, { "end": 1816, "label": "UBERONParcellation", "start": 1806 }, { "end": 663, "label": "UBERONParcellation", "start": 638 }, { "end": 495, "label": "UBERONParcellation", "start": 485 }, { "end": 678, "label": "UBERONParcellation", "start": 668 }, { "end": 1219, "label": "UBERONParcellation", "start": 1209 }, { "end": 1816, "label": "UBERONParcellation", "start": 1806 }, { "end": 448, "label": "UBERONParcellation", "start": 445 }, { "end": 859, "label": "UBERONParcellation", "start": 856 }, { "end": 495, "label": "UBERONParcellation", "start": 485 }, { "end": 678, "label": "UBERONParcellation", "start": 668 }, { "end": 1219, "label": "UBERONParcellation", "start": 1209 }, { "end": 1816, "label": "UBERONParcellation", "start": 1806 }, { "end": 662, "label": "UBERONParcellation", "start": 659 }, { "end": 1484, "label": "UBERONParcellation", "start": 1481 }, { "end": 495, "label": "UBERONParcellation", "start": 485 }, { "end": 678, "label": "UBERONParcellation", "start": 668 }, { "end": 1219, "label": "UBERONParcellation", "start": 1209 }, { "end": 1816, "label": "UBERONParcellation", "start": 1806 } ]
null
null
bff50e49-34c5-46b1-b7df-33b86f72cfec
completed
2025-04-29T14:36:04.699991
2025-05-27T14:00:51.891277
b64b67f5-64df-4532-83ea-a582315b84db
Structural analyses revealed larger GMVs in both sides of the cerebellum in musicians compared to non-musicians.Therefore, we used ROIs in both sides of the cerebellum as the seed for the FC analyses of the task-related fMRI data.The group differences in FC are shown in Figure 4A and listed in Supplementary Table 3.Compared to non-musicians, musicians had enhanced FC between the left cerebellum and the right hippocampus.In addition, we investigated the correlation between cerebellar-hippocampal FC and behavioral functions (Figure 4B).The task-related cerebellar-hippocampal FC and left tapping speed were significantly correlated in musicians (ρ = 0.42, P = 0.039).This Spearman's ρ was higher in absolute value than the adjusted significance level threshold |ρ| = 0.36 obtained in the permutation test.By contrast, non-musicians did not show such a correlation (ρ = -0.23,P = 0.284). These results indicate that in musicians, enhancement of the cerebellar-hippocampal FC in MWM processing is linked to a higher tapping speed.
<li> <b>cerebellum:</b> cerebellum (UBERONParcellation)<li> <b>cerebellum:</b> cerebellum (UBERONParcellation)<li> <b>hippocampus:</b> hippocampalFormation (UBERONParcellation)
[ [ { "end": 72, "label": "UBERONParcellation", "start": 62 }, { "end": 167, "label": "UBERONParcellation", "start": 157 }, { "end": 397, "label": "UBERONParcellation", "start": 387 }, { "end": 423, "label": "UBERONParcellation", "start": 412 }, { "end": 224, "label": "technique", "start": 220 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "fMRI: functionalMagneticResonanceImaging (technique)" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 72, "label": "UBERONParcellation", "start": 62 }, { "end": 167, "label": "UBERONParcellation", "start": 157 }, { "end": 397, "label": "UBERONParcellation", "start": 387 }, { "end": 72, "label": "UBERONParcellation", "start": 62 }, { "end": 167, "label": "UBERONParcellation", "start": 157 }, { "end": 397, "label": "UBERONParcellation", "start": 387 }, { "end": 423, "label": "UBERONParcellation", "start": 412 } ]
null
null
51c072fc-8c9c-4643-affd-14f154aaa696
pending
2025-04-29T14:36:04.699997
2025-04-29T14:36:04.699997
9dd8ae14-e119-4e28-a3cf-80a25055933d
Une étude a été réalisée sur 2 175 personnes âgées de 3,2 à 22,04 ans diagnostiquées avec un trouble d'hyperactivité avec déficit de l'attention (TDAH) et prélevées dans 89 endroits distincts à travers les États-Unis dans des cliniques satellites avec des pratiques communes et une formation et un équipement communs du personnel. L'objectif était de déterminer l'efficacité d'un programme de formation basé sur l'hémisphère pour réduire les réflexes primitifs conservés (RPR) existants et d'examiner la relation avec la fonction motrice par moteur basé sur le métronome, DL et tâches cognitives mesurées par des sous-tests du Wechsler Wide Range Achievement Test. Après un programme de 12 semaines, les RPR ont été significativement réduits, ainsi que les performances sur toutes les mesures motrices et cognitives significativement augmentées. La compréhension orale a montré des augmentations significatives entre le pré et le post-test de 7% (W = 1213000 ; df = 2094 ; p < 0,0001) et la résolution de problèmes mathématiques a révélé une augmentation significative de 5% (W = 1331500 ; df = 2091 ; p < 0,0001) associée à une réduction significative des réflexes primitifs. L'étude a conclu que l'incorporation d'une programmation hémisphérique relativement simple dans le système éducatif mondial pourrait augmenter relativement peu coûteux les performances académiques, cognitives et motrices.
<li> <b>personnes âgées de 3,2 à 22,04 ans:</b> homoSapiens (species)
[ [] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ { "end": 69, "label": "species", "start": 35 } ]
null
null
3180bfa4-1770-4a74-b253-d29147edebb1
completed
2025-04-29T14:36:04.700003
2025-05-27T14:00:51.982109
c89816e8-ac26-46c0-898e-8510c52ea68d
Primitive reflexes are adaptive reactions in the neonate and diminish as the brain and nervous system mature.Most of these reflexes can be present in normal individuals, even in young adults.The snouting reflex has been found in 13% of those between 40 and 57 years and between 22 and 33% in those above 60 years and above; the palmomental reflex between 6 and 27% of those between 20 and 50 years of age and in those above 60 years, between 28 and 60% (6,7).Even the sucking reflex, which for some investigators (7) "invariably indicates frontal lobe disease, " has been reported to be found in more than 6% of normal individuals aged between 73 and 93 years (7). Therefore, the frequency of these retained primitive reflexes (RPRs) is varied, and there exists disagreement about their pathological impact and significance, and even on their increased incidence related to the aging process.The only RPRs consistently recognized as being markers of neurological disease or disorders are the grasp reflex and extensor plantar responses (Babinski sign).These differences may be explained by methodological and theoretical disagreements between investigators.For example, some investigators think that a positive sucking reflex involves only the muscles associated with lip contraction, while other investigators think that a sucking reflex necessitates supplementary pharyngeal and lingual sucking movements. Differences between investigators may also exist in associating variables influencing the prevalence of RPRs such as the lack of quantified and standardized protocols, heterogeneity of diseases of the patient groups studied, or stimulation strength and subject's emotional state (8), which can impact on the extent and persistence of responses.Konicarova and Bob (9) examined the notion that RPRs may be related to indicators of Attention Deficit Hyperactivity Disorder (ADHD) and found that the persisting reflexes were linked to the condition.They hypothesized that the symptoms of ADHD in children between 8 and 11 years.may reflect a compensatory strategy for delayed neurological maturation.They went on to conclude (10,11) that the symptoms found in those with ADHD are the result of functional integrative deficiencies between brain regions that result in developmental balance and coordination deficits.Bilbilaj et al. (12) supported the earlier findings of (9) when they measured eight primitive reflexes that included: sucking, asymmetric tonic, rooting, Moro handheld, Galant, tonic lateral and symmetrical tonic reflexes.Reflexes were measured by methods earlier described by Blythe (13).Bilbilaj et al. found that children with difficulties in learning, including those with ADHD, demonstrated a significantly higher level of RPRs compared with controls.The investigators suggested research to find mechanisms to better suppress these retained reflexes earlier in the developmental cycle when these reflexes persisted beyond a child's biological age. Niklasson et al. (14) offered support for the notion that developmental delays are highly associated with RPRs.These investigators compared healthy children's sensorimotor maturity to those with developmental coordination disorder (DCD), including those with ADHD, who had completed treatment with sensorimotor therapy.The children in the DCD group completed a therapeutic regimen consisting of stereotypical fetal and infant movements, vestibular, tactile, and auditory stimulation, and assorted gross motor skill exercises.The results showed that normals fared significantly better on all sensorimotor tests as compared to the untreated children in the DCD group.Results demonstrated, no significant differences between normal and treated DCD participants, indicating that RPRs relate to developmental delays that are amenable to relatively simple and easily implemented intervention perceptual-motor remedial strategies.
<li> <b>brain:</b> brain (UBERONParcellation)<li> <b>frontal lobe:</b> frontalLobe (UBERONParcellation)
[ [ { "end": 82, "label": "UBERONParcellation", "start": 77 }, { "end": 2247, "label": "UBERONParcellation", "start": 2242 }, { "end": 551, "label": "UBERONParcellation", "start": 539 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 82, "label": "UBERONParcellation", "start": 77 }, { "end": 2247, "label": "UBERONParcellation", "start": 2242 }, { "end": 551, "label": "UBERONParcellation", "start": 539 } ]
null
null
c14afa24-d3c4-4a84-833a-22b420b8c634
completed
2025-04-29T14:36:04.700010
2025-05-27T14:00:52.066700
7f2127f0-706a-4e37-85ab-6280fbb1825d
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) caused the recent global COVID-19 outbreak, which led to a public health emergency. Entry of SARS-CoV-2 into human cells is dependent on the SARS-CoV receptor, angiotensin converting enzyme 2 (ACE2) receptor, and cathepsin. Cathepsin degrades the spike protein (S protein), which results in the entry of viral nucleic acid into the human host cell.We explored the susceptibility of the central nervous system (CNS) to SARS-CoV-2 infection using single-cell transcriptome analysis of glioblastoma.The results showed that ACE2 expression is relatively high in endothelial cells (ECs), bone marrow mesenchymal stem cells (BMSCs), and neural precursor cells (NPCs). Cathepsin B (Cat B) and cathepsin (Cat L) were also strongly expressed in various cell clusters within the glioblastoma microenvironment. Immunofluorescence staining of glioma and normal brain tissue chips further confirmed that ACE2 expression co-localized with CD31, CD73, and nestin, which confirmed the susceptibility to SARS-CoV-2 of nervous system cells, including ECs, BMSCs, and NPCs, from clinical specimens.These findings reveal the mechanism of SARS-CoV-2 neural invasion and suggest that special attention should be paid to SARS-CoV-2-infected patients with neural symptoms, especially those who suffered a glioma.
<li> <b>central nervous system (CNS):</b> Other (UBERONParcellation)<li> <b>single-cell transcriptome analysis:</b> singleCellRNASequencing (technique)<li> <b>endothelial cells (ECs):</b> Other (UBERONParcellation)<li> <b>neural precursor cells (NPCs):</b> Other (UBERONParcellation)<li> <b>Immunofluorescence staining:</b> immunohistochemistry (technique)<li> <b>brain:</b> brain (UBERONParcellation)<li> <b>nervous system:</b> Other (UBERONParcellation)<li> <b>human:</b> homoSapiens (species)
[ [ { "end": 475, "label": "UBERONParcellation", "start": 447 }, { "end": 540, "label": "technique", "start": 506 }, { "end": 642, "label": "UBERONParcellation", "start": 619 }, { "end": 888, "label": "technique", "start": 861 }, { "end": 915, "label": "UBERONParcellation", "start": 910 }, { "end": 1076, "label": "UBERONParcellation", "start": 1062 }, { "end": 175, "label": "species", "start": 170 }, { "end": 398, "label": "species", "start": 393 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "\r\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 475, "label": "UBERONParcellation", "start": 447 }, { "end": 540, "label": "technique", "start": 506 }, { "end": 642, "label": "UBERONParcellation", "start": 619 }, { "end": 721, "label": "UBERONParcellation", "start": 692 }, { "end": 888, "label": "technique", "start": 861 }, { "end": 915, "label": "UBERONParcellation", "start": 910 }, { "end": 469, "label": "UBERONParcellation", "start": 455 }, { "end": 1076, "label": "UBERONParcellation", "start": 1062 }, { "end": 175, "label": "species", "start": 170 }, { "end": 398, "label": "species", "start": 393 } ]
null
null
2e5b5a17-e9a1-4a84-b125-9dee5776bfec
completed
2025-04-29T14:36:04.700016
2025-05-27T14:00:52.199080
2648e44e-0c5f-499e-b7bb-21f2cfe4c55e
ABSTRACTNeurophysiological studies in humans and non-human primates have revealed movement representations in both the contralateral and ipsilateral hemisphere. Inspired by clinical observations, we ask if this bilateral representation differs for the left and right hemispheres. Electrocorticography (ECoG) was recorded in human participants during an instructed-delay reaching task, with movements produced with either the contralateral or ipsilateral arm. Using a cross-validated kinematic encoding model, we found stronger bilateral encoding in the left hemisphere, an effect that was present during preparation and was amplified during execution. Consistent with this asymmetry, we also observed better across-arm generalization in the left hemisphere, indicating similar neural representations for right and left arm movements. Notably, these left hemisphere electrodes were centered over premotor and parietal regions. The more extensive bilateral encoding in the left hemisphere adds a new perspective to the pervasive neuropsychological finding that the left hemisphere plays a dominant role in praxis.
<li> <b>humans:</b> homoSapiens (species)<li> <b>non-human primates:</b> Other (species)<li> <b>Electrocorticography (ECoG):</b> electrocorticography (technique)<li> <b>human:</b> homoSapiens (species)<li> <b>left hemisphere:</b> cerebralHemisphere (UBERONParcellation)<li> <b>premotor:</b> premotorCortex (UBERONParcellation)<li> <b>parietal regions:</b> parietalCortex (UBERONParcellation)<li> <b>left hemisphere:</b> cerebralHemisphere (UBERONParcellation)
[ [ { "end": 44, "label": "species", "start": 38 }, { "end": 67, "label": "species", "start": 49 }, { "end": 307, "label": "technique", "start": 280 }, { "end": 329, "label": "species", "start": 324 }, { "end": 568, "label": "UBERONParcellation", "start": 553 }, { "end": 756, "label": "UBERONParcellation", "start": 741 }, { "end": 864, "label": "UBERONParcellation", "start": 849 }, { "end": 986, "label": "UBERONParcellation", "start": 971 }, { "end": 1078, "label": "UBERONParcellation", "start": 1063 }, { "end": 903, "label": "UBERONParcellation", "start": 895 }, { "end": 924, "label": "UBERONParcellation", "start": 908 }, { "end": 278, "label": "UBERONParcellation", "start": 261 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "right hemisphere: cerebralHemisphere (UBERONParcellation)\r\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 44, "label": "species", "start": 38 }, { "end": 67, "label": "species", "start": 49 }, { "end": 307, "label": "technique", "start": 280 }, { "end": 58, "label": "species", "start": 53 }, { "end": 329, "label": "species", "start": 324 }, { "end": 568, "label": "UBERONParcellation", "start": 553 }, { "end": 756, "label": "UBERONParcellation", "start": 741 }, { "end": 864, "label": "UBERONParcellation", "start": 849 }, { "end": 986, "label": "UBERONParcellation", "start": 971 }, { "end": 1078, "label": "UBERONParcellation", "start": 1063 }, { "end": 903, "label": "UBERONParcellation", "start": 895 }, { "end": 924, "label": "UBERONParcellation", "start": 908 }, { "end": 568, "label": "UBERONParcellation", "start": 553 }, { "end": 756, "label": "UBERONParcellation", "start": 741 }, { "end": 864, "label": "UBERONParcellation", "start": 849 }, { "end": 986, "label": "UBERONParcellation", "start": 971 }, { "end": 1078, "label": "UBERONParcellation", "start": 1063 } ]
null
null
df813eea-ce3f-456c-a39d-52195797aa44
completed
2025-04-29T14:36:04.700022
2025-05-27T14:00:52.283924
d0dabdbc-0dfc-4826-8997-40aa148240a1
In the final analysis, we examined how the kinematic features of the movements contribute to the encoding model used to predict HFA.Each of the four kinematic features includes 400 time lags and thus 400 weights that contribute to the model.To obtain a metric of the relative contribution of the features, we calculated the total contribution of each feature and normalized these values by dividing by the total contribution of the four features.The calculation was done for each patient separately and then averaged, with error bars representing the standard deviation across patients (Figure 6A).The relative contribution of the four kinematic features was similar for contralateral and ipsilateral reaches.We next examined the temporal profile of the weights (Figure 6B) and found that this was also similar for the two conditions, although the average weights for ipsilateral reaches are substantially lower, consistent with the observation of lower performance metrics for ipsilateral reaches across all predictive electrodes (Figure 2-figure supplement 2). As can be seen in Figure 6A, speed and position, kinematic features which are associated with timing and movement initiation make a strong contribution to the encoding model (relative contribution: contra = 68%, ipsi = 63%).This is in contrast with the smaller contribution of theta and phi, features which provide information about movement direction (relative contribution: contra = 32%, ipsi = 37%).This result is similar to that observed in single-unit and population activity recorded in premotor and motor cortex of nonhuman primates.Kaufman et al., 2016 observed that the largest response component was associated with movement timing/initiation rather than features such as movement direction.Similarly, this direction-independent signal occurs twice during sequential movements (Zimnik and Churchland, 2021); in our data, speed has two prominent peaks, one occurring before the reach and the second occurring before the return movement.We were surprised to see the markedly differential weighting for the vertical (theta) and horizontal (phi) directional features.We assume this is likely idiosyncratic to the layout of our targets. We also examined the correspondence between HFA and the kinematic features as a function of whether electrodes generalize well or poorly (Figure 7).For electrodes that generalize well, position most closely corresponds to HFA for both contralateral and ipsilateral movements.The maximum cross-correlation for contralateral and ipsilateral movements was found at a lag of 200 and 150 ms, respectively, with HFA leading hand position.For electrodes that generalize poorly, the kinematic feature that most closely corresponds to HFA for both contralateral and ipsilateral movements is speed.For these electrodes, the maximum cross-correlation for contralateral and ipsilateral movements were both at a lag of 200 ms, with HFA again leading the kinematic feature.Although the ipsilateral HFA signals are considerably lower in amplitude, the pattern between HFA and speed is quite similar for both ipsilateral and contralateral movements.The fact that the neural activity from electrodes that generalize poorly (primarily located over M1) correlates well with speed provides additional evidence that a strong component of the HFA ECoG signal is related to timing and movement initiation (Kaufman et al., 2016).
<li> <b>M1:</b> primaryMotorCortex (UBERONParcellation)<li> <b>premotor:</b> premotorCortex (UBERONParcellation)<li> <b>motor cortex:</b> primaryMotorCortex (UBERONParcellation)<li> <b>ECoG:</b> electrocorticography (technique)
[ [ { "end": 3237, "label": "UBERONParcellation", "start": 3235 }, { "end": 1564, "label": "UBERONParcellation", "start": 1556 }, { "end": 1581, "label": "UBERONParcellation", "start": 1569 }, { "end": 3334, "label": "technique", "start": 3330 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "\r\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 3237, "label": "UBERONParcellation", "start": 3235 }, { "end": 1564, "label": "UBERONParcellation", "start": 1556 }, { "end": 1581, "label": "UBERONParcellation", "start": 1569 }, { "end": 3334, "label": "technique", "start": 3330 } ]
null
null
37a23cc8-e835-415a-8d7c-ac185e41f9ee
completed
2025-04-29T14:36:04.700028
2025-05-27T14:00:52.391388
bb39f46d-0fbd-447a-92d7-4f3585a10fd4
Abstract Background To evaluate the effect of statin use on osteoarthritis (OA) incidence/progression using magnetic resonance imaging (MRI) in a population-based cohort with predominantly pre-radiographic knee OA. Methods A cohort aged 40–79 years with knee pain was recruited using random population sampling and followed for 7 years. Baseline exclusions were inflammatory arthritis, recent knee surgery/injury, and inability to undergo MRI. At baseline, current statin use was ascertained. Baseline and follow-up MRIs were read semi-quantitatively for cartilage damage (grade 0–4, 0/1 collapsed, 6 regions), osteophytes (grade 0–3, 8 regions), bone marrow lesions (BML) (grade 0–3, 6 regions) and effusion (grade 0–3). The primary outcome was cartilage damage incidence/progression, while secondary outcomes were incidence/progression of osteophytes, BML, and effusion, each defined as an increase by ≥1 grade at any region. To ensure population representative samples, sample weights were used. Logistic regression was used to assess the association of statin use at baseline with incidence/progression of MRI outcomes. Analyses were adjusted for sex, age, BMI, and multiple comorbidities requiring statin therapy. Results Of 255 participants evaluated at baseline, 122 completed the 7-year follow-up. Statin use was not significantly associated with progression of cartilage damage (OR 0.82; 95% CI 0.17, 4.06), osteophytes (OR 3.48; 95% CI 0.40, 30.31), BML (OR 0.61; 95% CI 0.12, 3.02), or effusion (OR 2.38; 95% CI 0.42, 13.63), after adjusting for confounders. Conclusion In this population-based cohort of predominantly pre-radiographic knee OA, statins did not affect MRI incidence/progression of cartilage damage, BML, osteophytes or effusion. Therefore, statin use does not appear to affect people with pre-radiographic stages of knee OA.
<li> <b>magnetic resonance imaging (MRI):</b> magneticResonanceImaging (technique)
[ [ { "end": 140, "label": "technique", "start": 108 }, { "end": 1685, "label": "technique", "start": 1682 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "MRI : magneticResonanceImaging (technique)" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 140, "label": "technique", "start": 108 } ]
null
null
4573f3cf-b06d-42e5-a0a3-edfdc7ddebaa
pending
2025-04-29T14:36:04.700034
2025-04-29T14:36:04.700034
8d549a82-3ce6-4c8c-84f5-711d3e83e3a2
The baseline descriptive characteristics were summarized using frequencies or means +/standard deviation (SD) in Table 1.Logistic regression models were developed to evaluate the association between statin use and incidence/progression of cartilage damage, osteophytes, BML and effusion.The analysis was adjusted for age, sex, and BMI.We also adjusted for hypertension, dyslipidemia, cardiovascular disease, cerebrovascular disease, and diabetes since these comorbidities are frequently associated with statin use.To adjust for these comorbidities, we combined all these variables into a propensity score.Since our cohort had few participants with cardiovascular disease and cerebrovascular disease, these two comorbidities were treated as a single variable.Because the distribution of KL grade differed significantly between the statin and non-statin users, we performed a sensitivity analysis adjusting for KL grade in addition to the above variables. All analyses were performed on SAS v9.4 (SAS institute, Cary, North Carolina). To ensure our results were population-representative, we used a sample weight for the baseline sample according to the proportion of the population sampled for a given age and sex cell compared to proportion of the sample that the given cell made up.The weight of the cell was scaled to sum to the baseline sample size (255).In this study, only 122 participants remained from the original sample of 255.To ensure our results remained population-representative, a sample weight was developed for the current sample size by taking the ratio of the baseline sample proportion in a given age-sex cell over the current sample proportion in that cell, multiplied by the baseline sample weight.The sample weight was scaled to sum to the follow-up sample size (122).All analyses in the present study were weighted with the current sample weight.The discussion of sample weights can be found in Sayre et al. [16]. To ensure our results were not altered by our small sample size we carried out a second sensitivity analysis where we used the data from the 3 year follow up and a separate set of data that was collected between the 3 year follow up to the 7 year follow up.The second data set used the 3 year follow up data as a baseline and compared it to the progression results at the 7 year follow up.With this sensitivity analysis we effectively nearly doubled our sample size to 230 participants.We ran the analysis twice with two different definitions.In the first definition, we ran the sensitivity analysis assuming no non-statin users started a statin during the follow up period, therefore the two data sets had the same number of statin users.In the second definition, we assumed that all the participants who developed dyslipidemia at 3 year follow up were treated with a statin from the 3 year follow up to the 7 year follow up, which would increase the number of statin users in the second data set and in our study.Note that these alternative definitions were necessary because statin use data was not collected at 3 years.In the sensitivity analysis, we adjusted for sex, age, BMI, and our propensity score recomputed using the new statin definition.
None
[ [] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[]
null
null
d5f819eb-5373-4c12-b045-6ddd0274147d
completed
2025-04-29T14:36:04.700040
2025-05-27T14:00:52.503887
e60e9b3e-31c4-47fa-a458-8bd5f7c6629b
IntroductionThe post-COVID-19 condition (PCC) is characterized by debilitating persistent symptoms, including symptoms suggesting neurological aberrations such as concentration difficulties, impaired memory, pain, and sleep disturbances. The underlying mechanisms remain elusive. This study aimed to investigate brain injury biomarkers, neurocognitive test performance, and self-reported neurological and neuropsychological symptoms in young people with PCC.MethodsA total of 404 non-hospitalized adolescents and young adults aged 12–25 years who tested positive for SARS-CoV-2, along with 105 matched SARS-CoV-2 negative individuals, were prospectively enrolled and followed-up for 6 months (Clinical Trials ID: NCT04686734). All participants underwent comprehensive assessment encompassing clinical examinations, questionnaires, neurocognitive testing and blood sampling. Serum samples were immunoassayed for the brain injury biomarkers neurofilament light chain (Nfl) and glial fibrillary acidic protein (GFAp). At 6 months, cross-sectional analyses of serum Nfl/GFAp, neurocognitive test results and symptom scores were performed across groups based on adherence to PCC criteria as well as initial SARS-CoV-2 test results. Also, associations between Nfl/GFAp, neurocognitive test results, and symptom scores were explored.ResultsA total of 381 SARS-CoV-2 positive and 85 SARS-CoV-2 negative were included in the final analysis at 6 months, of whom 48% and 47%, respectively, adhered to the PCC criteria. Serum levels of Nfl and GFAp were almost equal across groups and did not differ from reference values in healthy populations. Also, neurocognitive test results were not different across groups, whereas symptom scores were significantly higher in patients fulfilling PCC criteria (independent of initial SARS-CoV-2 status). No significant associations between Nfl/GFAp, neurocognitive test results, and symptom scores were found.ConclusionNormal brain injury biomarkers and neurocognitive performance 6 months after mild COVID-19 implies that the persistent symptoms associated with PCC are not concurrent with ongoing central nervous system damage or permanent disruption of cognitive functions. This finding contradicts the notion of neuroinflammation as a likely explanation for the persistent symptoms.
<li> <b>brain:</b> brain (UBERONParcellation)<li> <b>central nervous system:</b> Other (UBERONParcellation)
[ [ { "end": 317, "label": "UBERONParcellation", "start": 312 }, { "end": 920, "label": "UBERONParcellation", "start": 915 }, { "end": 1958, "label": "UBERONParcellation", "start": 1953 }, { "end": 2148, "label": "UBERONParcellation", "start": 2126 }, { "end": 906, "label": "technique", "start": 893 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "immunoassay: Other (technique)" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 317, "label": "UBERONParcellation", "start": 312 }, { "end": 920, "label": "UBERONParcellation", "start": 915 }, { "end": 1958, "label": "UBERONParcellation", "start": 1953 }, { "end": 2148, "label": "UBERONParcellation", "start": 2126 } ]
null
null
a1119047-00f0-43ef-90e2-16f79cc0e08e
completed
2025-04-29T14:36:04.700046
2025-05-27T14:00:52.593723
a57037cd-e95a-44a9-85ab-b9c1512f80f8
5'-deoxy-5'-methylthioadenosine (MTA) is an endogenous compound produced through the metabolism of polyamines. The therapeutic potential of MTA has been assayed mainly in liver diseases and, more recently, in animal models of multiple sclerosis. The aim of this study was to determine the neuroprotective effect of this molecule in vitro and to assess whether MTA can cross the blood brain barrier (BBB) in order to also analyze its potential neuroprotective efficacy in vivo.Neuroprotection was assessed in vitro using models of excitotoxicity in primary neurons, mixed astrocyte-neuron and primary oligodendrocyte cultures. The capacity of MTA to cross the BBB was measured in an artificial membrane assay and using an in vitro cell model. Finally, in vivo tests were performed in models of hypoxic brain damage, Parkinson's disease and epilepsy.MTA displays a wide array of neuroprotective activities against different insults in vitro. While the data from the two complementary approaches adopted indicate that MTA is likely to cross the BBB, the in vivo data showed that MTA may provide therapeutic benefits in specific circumstances. Whereas MTA reduced the neuronal cell death in pilocarpine-induced status epilepticus and the size of the lesion in global but not focal ischemic brain damage, it was ineffective in preserving dopaminergic neurons of the substantia nigra in the 1-methyl-4-phenyl-1,2,3,6-tetrahydro-pyridine (MPTP)-mice model. However, in this model of Parkinson's disease the combined administration of MTA and an A2A adenosine receptor antagonist did produce significant neuroprotection in this brain region.MTA may potentially offer therapeutic neuroprotection.
<li> <b>in vitro:</b> inVitro (preparationType)<li> <b>blood brain barrier (BBB):</b> bloodBrainBarrier (UBERONParcellation)<li> <b>in vivo:</b> inVivo (preparationType)<li> <b>BBB:</b> bloodBrainBarrier (UBERONParcellation)<li> <b>in vitro:</b> inVitro (preparationType)<li> <b>in vivo:</b> inVivo (preparationType)<li> <b>substantia nigra:</b> substantiaNigra (UBERONParcellation)
[ [ { "end": 337, "label": "preparationType", "start": 329 }, { "end": 513, "label": "preparationType", "start": 505 }, { "end": 729, "label": "preparationType", "start": 721 }, { "end": 938, "label": "preparationType", "start": 930 }, { "end": 475, "label": "preparationType", "start": 468 }, { "end": 758, "label": "preparationType", "start": 751 }, { "end": 1058, "label": "preparationType", "start": 1051 }, { "end": 402, "label": "UBERONParcellation", "start": 399 }, { "end": 662, "label": "UBERONParcellation", "start": 659 }, { "end": 1045, "label": "UBERONParcellation", "start": 1042 }, { "end": 1377, "label": "UBERONParcellation", "start": 1361 }, { "end": 397, "label": "UBERONParcellation", "start": 378 }, { "end": 1625, "label": "UBERONParcellation", "start": 1620 }, { "end": 563, "label": "UBERONParcellation", "start": 556 }, { "end": 1353, "label": "UBERONParcellation", "start": 1346 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "neuron: Other (UBERONParcellation)\nbrain: Other (UBERONParcellation)\r\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 337, "label": "preparationType", "start": 329 }, { "end": 513, "label": "preparationType", "start": 505 }, { "end": 729, "label": "preparationType", "start": 721 }, { "end": 938, "label": "preparationType", "start": 930 }, { "end": 403, "label": "UBERONParcellation", "start": 378 }, { "end": 475, "label": "preparationType", "start": 468 }, { "end": 758, "label": "preparationType", "start": 751 }, { "end": 1058, "label": "preparationType", "start": 1051 }, { "end": 402, "label": "UBERONParcellation", "start": 399 }, { "end": 662, "label": "UBERONParcellation", "start": 659 }, { "end": 1045, "label": "UBERONParcellation", "start": 1042 }, { "end": 337, "label": "preparationType", "start": 329 }, { "end": 513, "label": "preparationType", "start": 505 }, { "end": 729, "label": "preparationType", "start": 721 }, { "end": 938, "label": "preparationType", "start": 930 }, { "end": 475, "label": "preparationType", "start": 468 }, { "end": 758, "label": "preparationType", "start": 751 }, { "end": 1058, "label": "preparationType", "start": 1051 }, { "end": 1377, "label": "UBERONParcellation", "start": 1361 } ]
null
null
fc9d9789-176c-4fbd-b19b-52468606c2f2
completed
2025-04-29T14:36:04.700052
2025-05-27T14:00:52.683238
a43613b5-2a8d-40ee-ac9a-56aeac616b0b
A in vitro cell model of BBB permeability was established using a co-culture of bovine-brain endothelial cells (BBECs) and newborn rat astrocytes.The cells were first cultured in 24-well (Transwell R ) permeable supports with a surface area of 0.33 cm 2 and a pore size of 0.4 mm (Corning), the upper surface of which was coated with collagen type IV and fibronectin.The inserts were then placed upside down in a large petri dish, and 40 mL of a suspension (containing approximately 45,000 astrocytes) was placed on the bottom of each filter.The petri dish was incubated at 37uC for 1 h, and 40 mL of fresh DMEM+S was added to the bottom of each filter every 15 min.The inserts were then transferred back to the plate and incubated at 37uC in 5% CO 2 for 3 d.Then, 2 h before seeding the BBECs, the medium was replaced by DMEM+S supplemented with 125 mg/mL heparin and 2 h later, the cells were seeded onto the inserts (45,000 cells per filter).The plate was incubated at 37uC in 5% CO 2 for 3 more days, after which the medium was replaced by DMEM+S supplemented with cyclic adenosine monophosphate (cAMP) and RO-20-1724, and kept at 37uC in 5% CO 2 .On day 8 of the coculture, the transendothelial electrical resistance (TEER) was measured to determine whether the system was ready for transport studies.To validate the maturity of the model, permeability assays with lucifer yellow (LY) were performed in parallel as a marker of the integrity of the in vitro barrier.During the permeability assay, the samples were co-incubated with LY (20 mM) to assess the integrity of the cellular monolayer during the assay.
<li> <b>in vitro:</b> inVitro (preparationType)<li> <b>BBB:</b> bloodBrainBarrier (UBERONParcellation)<li> <b>bovine-brain endothelial cells (BBECs):</b> brainEndothelium (UBERONParcellation)<li> <b>rat:</b> rattusNorvegicus (species)<li> <b>astrocytes:</b> Other (UBERONParcellation)
[ [ { "end": 10, "label": "preparationType", "start": 2 }, { "end": 1461, "label": "preparationType", "start": 1453 }, { "end": 28, "label": "UBERONParcellation", "start": 25 }, { "end": 134, "label": "species", "start": 131 }, { "end": 145, "label": "UBERONParcellation", "start": 135 }, { "end": 500, "label": "UBERONParcellation", "start": 490 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "\r\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 10, "label": "preparationType", "start": 2 }, { "end": 1461, "label": "preparationType", "start": 1453 }, { "end": 28, "label": "UBERONParcellation", "start": 25 }, { "end": 118, "label": "UBERONParcellation", "start": 80 }, { "end": 134, "label": "species", "start": 131 }, { "end": 145, "label": "UBERONParcellation", "start": 135 }, { "end": 500, "label": "UBERONParcellation", "start": 490 } ]
null
null
0e9629eb-4f3b-42d0-adac-aaacd1045808
completed
2025-04-29T14:36:04.700059
2025-05-27T14:00:52.774997
27bdb366-21ec-4d57-9c28-be2ba9025875
The auditory pathways coursing through the brainstem are organized bilaterally in mirror image about the midline and at several levels the two sides are interconnected. One of the most prominent points of interconnection is the commissure of the inferior colliculus (CoIC). Anatomical studies have revealed that these fibers make reciprocal connections which follow the tonotopic organization of the inferior colliculus (IC), and that the commissure contains both excitatory and, albeit fewer, inhibitory fibers. The role of these connections in sound processing is largely unknown. Here we describe a method to address this question in the anaesthetized guinea pig. We used a cryoloop placed on one IC to produce reversible deactivation while recording electrophysiological responses to sounds in both ICs. We recorded single units, multi-unit clusters and local field potentials (LFPs) before, during and after cooling. The degree and spread of cooling was measured with a thermocouple placed in the IC and other auditory structures. Cooling sufficient to eliminate firing was restricted to the IC contacted by the cryoloop. The temperature of other auditory brainstem structures, including the contralateral IC and the cochlea were minimally affected. Cooling below 20°C reduced or eliminated the firing of action potentials in frequency laminae at depths corresponding to characteristic frequencies up to ~8 kHz. Modulation of neural activity also occurred in the un-cooled IC with changes in single unit firing and LFPs. Components of LFPs signaling lemniscal afferent input to the IC showed little change in amplitude or latency with cooling, whereas the later components, which likely reflect inter- and intra-collicular processing, showed marked changes in form and amplitude. We conclude that the cryoloop is an effective method of selectively deactivating one IC in guinea pig, and demonstrate that auditory processing in the IC is strongly influenced by the other.
<li> <b>brainstem:</b> brainstem (UBERONParcellation)<li> <b>commissure of the inferior colliculus (CoIC):</b> commissureOfInferiorColliculus (UBERONParcellation)<li> <b>inferior colliculus (IC):</b> inferiorColliculus (UBERONParcellation)<li> <b>anaesthetized guinea pig:</b> Other (species)<li> <b>IC:</b> inferiorColliculus (UBERONParcellation)<li> <b>ICs:</b> inferiorColliculus (UBERONParcellation)<li> <b>single units:</b> singleElectrodeExtracellularElectrophysiology (technique)<li> <b>multi-unit clusters:</b> multiElectrodeExtracellularElectrophysiology (technique)<li> <b>local field potentials (LFPs):</b> Other (technique)<li> <b>IC:</b> inferiorColliculus (UBERONParcellation)<li> <b>auditory brainstem:</b> brainstem (UBERONParcellation)<li> <b>contralateral IC:</b> inferiorColliculus (UBERONParcellation)<li> <b>cochlea:</b> Other (UBERONParcellation)<li> <b>IC:</b> inferiorColliculus (UBERONParcellation)<li> <b>un-cooled IC:</b> inferiorColliculus (UBERONParcellation)<li> <b>IC:</b> inferiorColliculus (UBERONParcellation)<li> <b>IC:</b> inferiorColliculus (UBERONParcellation)<li> <b>guinea pig:</b> Other (species)<li> <b>IC:</b> inferiorColliculus (UBERONParcellation)
[ [ { "end": 52, "label": "UBERONParcellation", "start": 43 }, { "end": 1170, "label": "UBERONParcellation", "start": 1161 }, { "end": 424, "label": "UBERONParcellation", "start": 400 }, { "end": 423, "label": "UBERONParcellation", "start": 421 }, { "end": 702, "label": "UBERONParcellation", "start": 700 }, { "end": 1004, "label": "UBERONParcellation", "start": 1002 }, { "end": 1099, "label": "UBERONParcellation", "start": 1097 }, { "end": 1213, "label": "UBERONParcellation", "start": 1211 }, { "end": 1480, "label": "UBERONParcellation", "start": 1478 }, { "end": 1589, "label": "UBERONParcellation", "start": 1587 }, { "end": 1872, "label": "UBERONParcellation", "start": 1870 }, { "end": 1938, "label": "UBERONParcellation", "start": 1936 }, { "end": 1229, "label": "UBERONParcellation", "start": 1222 }, { "end": 665, "label": "species", "start": 655 }, { "end": 1886, "label": "species", "start": 1876 }, { "end": 265, "label": "UBERONParcellation", "start": 228 }, { "end": 271, "label": "UBERONParcellation", "start": 267 }, { "end": 806, "label": "UBERONParcellation", "start": 803 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "CoIC: commissureOfInferiorColliculus (UBERONParcellation)" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 52, "label": "UBERONParcellation", "start": 43 }, { "end": 1170, "label": "UBERONParcellation", "start": 1161 }, { "end": 272, "label": "UBERONParcellation", "start": 228 }, { "end": 424, "label": "UBERONParcellation", "start": 400 }, { "end": 665, "label": "species", "start": 641 }, { "end": 423, "label": "UBERONParcellation", "start": 421 }, { "end": 702, "label": "UBERONParcellation", "start": 700 }, { "end": 1004, "label": "UBERONParcellation", "start": 1002 }, { "end": 1099, "label": "UBERONParcellation", "start": 1097 }, { "end": 1213, "label": "UBERONParcellation", "start": 1211 }, { "end": 1480, "label": "UBERONParcellation", "start": 1478 }, { "end": 1589, "label": "UBERONParcellation", "start": 1587 }, { "end": 1872, "label": "UBERONParcellation", "start": 1870 }, { "end": 1938, "label": "UBERONParcellation", "start": 1936 }, { "end": 806, "label": "UBERONParcellation", "start": 803 }, { "end": 832, "label": "technique", "start": 820 }, { "end": 853, "label": "technique", "start": 834 }, { "end": 887, "label": "technique", "start": 858 }, { "end": 423, "label": "UBERONParcellation", "start": 421 }, { "end": 702, "label": "UBERONParcellation", "start": 700 }, { "end": 1004, "label": "UBERONParcellation", "start": 1002 }, { "end": 1099, "label": "UBERONParcellation", "start": 1097 }, { "end": 1213, "label": "UBERONParcellation", "start": 1211 }, { "end": 1480, "label": "UBERONParcellation", "start": 1478 }, { "end": 1589, "label": "UBERONParcellation", "start": 1587 }, { "end": 1872, "label": "UBERONParcellation", "start": 1870 }, { "end": 1938, "label": "UBERONParcellation", "start": 1936 }, { "end": 1170, "label": "UBERONParcellation", "start": 1152 }, { "end": 1213, "label": "UBERONParcellation", "start": 1197 }, { "end": 1229, "label": "UBERONParcellation", "start": 1222 }, { "end": 423, "label": "UBERONParcellation", "start": 421 }, { "end": 702, "label": "UBERONParcellation", "start": 700 }, { "end": 1004, "label": "UBERONParcellation", "start": 1002 }, { "end": 1099, "label": "UBERONParcellation", "start": 1097 }, { "end": 1213, "label": "UBERONParcellation", "start": 1211 }, { "end": 1480, "label": "UBERONParcellation", "start": 1478 }, { "end": 1589, "label": "UBERONParcellation", "start": 1587 }, { "end": 1872, "label": "UBERONParcellation", "start": 1870 }, { "end": 1938, "label": "UBERONParcellation", "start": 1936 }, { "end": 1480, "label": "UBERONParcellation", "start": 1468 }, { "end": 423, "label": "UBERONParcellation", "start": 421 }, { "end": 702, "label": "UBERONParcellation", "start": 700 }, { "end": 1004, "label": "UBERONParcellation", "start": 1002 }, { "end": 1099, "label": "UBERONParcellation", "start": 1097 }, { "end": 1213, "label": "UBERONParcellation", "start": 1211 }, { "end": 1480, "label": "UBERONParcellation", "start": 1478 }, { "end": 1589, "label": "UBERONParcellation", "start": 1587 }, { "end": 1872, "label": "UBERONParcellation", "start": 1870 }, { "end": 1938, "label": "UBERONParcellation", "start": 1936 }, { "end": 423, "label": "UBERONParcellation", "start": 421 }, { "end": 702, "label": "UBERONParcellation", "start": 700 }, { "end": 1004, "label": "UBERONParcellation", "start": 1002 }, { "end": 1099, "label": "UBERONParcellation", "start": 1097 }, { "end": 1213, "label": "UBERONParcellation", "start": 1211 }, { "end": 1480, "label": "UBERONParcellation", "start": 1478 }, { "end": 1589, "label": "UBERONParcellation", "start": 1587 }, { "end": 1872, "label": "UBERONParcellation", "start": 1870 }, { "end": 1938, "label": "UBERONParcellation", "start": 1936 }, { "end": 665, "label": "species", "start": 655 }, { "end": 1886, "label": "species", "start": 1876 }, { "end": 423, "label": "UBERONParcellation", "start": 421 }, { "end": 702, "label": "UBERONParcellation", "start": 700 }, { "end": 1004, "label": "UBERONParcellation", "start": 1002 }, { "end": 1099, "label": "UBERONParcellation", "start": 1097 }, { "end": 1213, "label": "UBERONParcellation", "start": 1211 }, { "end": 1480, "label": "UBERONParcellation", "start": 1478 }, { "end": 1589, "label": "UBERONParcellation", "start": 1587 }, { "end": 1872, "label": "UBERONParcellation", "start": 1870 }, { "end": 1938, "label": "UBERONParcellation", "start": 1936 } ]
null
null
4cc7bcfa-ed48-42cd-bd85-887341f9137f
completed
2025-04-29T14:36:04.700065
2025-05-27T14:00:52.866887
afc8e482-34fb-47ad-9982-650baf2151f8
After establishing the effects of cooling on neural activity in the IC, the second aim of this paper is to demonstrate its viability as a means of studying the influence of the IC on neural processing by its contralateral counterpart.Here we present examples of data in the form of single unit activity and LFPs showing the effects of cooling in the contralateral IC. Figure 9A shows the PSTH of a single unit, which under control conditions (black) had a chopper response with three clearly identifiable peaks indicating a regular firing interval of ∼22 ms.This is confirmed by the single narrow peak centered on 22 ms in the interspike interval histogram (ISIH, Figure 9B).When the contralateral IC was cooled, the PSTH (blue) showed an overall reduction in the number of spikes per stimulus, as well as a notable increase in the latency to the first peak, a reduction in the number of peaks from three to two, and less regular firing exemplified by the lower and broader peaks in the PSTH.This is confirmed by the shift in the peak of the ISIH to a longer interval (∼44 ms) and the reduction in regularity is indicated by the lower height and broader width of the peak.When cooling was stopped, and the IC returned to near control temperature, the changes seen with cooling were reversed (gray). In the second example illustrated in Figure 10, the effect of cooling is demonstrated under two different stimulus conditions: monaural contralateral stimulation (Figure 10A) and binaural diotic stimulation (Figure 10B).Under control conditions the unit fired fewer spikes with binaural stimulation indicating that it had an excitatory-inhibitory (EI) type response (black).In both conditions cooling the IC increased the firing rate (blue).The increase in firing rate was greater for contralateral stimulation, but the relative increase under both conditions was about the same.When the IC rewarmed, the changes observed with cooling were reversed (gray), but this was more complete for the case where stimuli were presented to the contralateral ear. Figure 10C shows examples of the action potential waveforms for this unit, color coded as for the PSTHs.The shape, size, and time course of the waveform remained the same in control, cool, and recovery conditions.The absence of any change in the action potentials makes it unlikely that the changes observed in the firing rate of the unit are attributable to temperature change in the recorded IC (Volgushev et al., 2000b;Cao and Oertel, 2005). Figure 11 summarizes the changes in firing rate for a population of single units in the IC contralateral to cooling in response to repeated stimulation with a tone at their CF.Cooling led to an increase or decrease in firing rate in different neurons, and although the degree of change varied considerably between units in some cases it was substantial. In addition to recording single unit activity, we assessed the impact of cooling the contralateral IC on the LFP. Figure 12 shows examples of LFPs recorded from the IC before, during and after cooling of the contralateral IC under three stimulus conditions, contralateral, and ipsilateral monaural stimulation (Figures 12A,B, respectively) and diotic stimulation (Figure 12C).In the case of contralateral and binaural stimulation there was a pronounced upward-going component with a post-stimulus latency of ∼6 ms that corresponds to the afferent volley of activity to the IC followed by a biphasic waveform that returned to baseline at ∼30 ms.The afferent volley was less pronounced in the case of the response to ipsilateral stimulation.When the contralateral IC was cooled the magnitude and latency of the afferent volley was unchanged, but there were clear changes in the later potentials.The form and extent of the changes varied between the different stimulus conditions.In the case of contralateral stimulation the largest change occurred in the first negative-going potential whereas with diotic stimulation the largest difference between cool and control was in the positive-going potential at ∼17 ms.With ipsilateral stimulation the single broad positive waveform was delayed, diminished in height and became broader.
<li> <b>IC:</b> inferiorColliculus (UBERONParcellation)<li> <b>contralateral IC:</b> inferiorColliculus (UBERONParcellation)<li> <b>single unit activity:</b> singleElectrodeExtracellularElectrophysiology (technique)
[ [ { "end": 70, "label": "UBERONParcellation", "start": 68 }, { "end": 179, "label": "UBERONParcellation", "start": 177 }, { "end": 366, "label": "UBERONParcellation", "start": 364 }, { "end": 700, "label": "UBERONParcellation", "start": 698 }, { "end": 1208, "label": "UBERONParcellation", "start": 1206 }, { "end": 1706, "label": "UBERONParcellation", "start": 1704 }, { "end": 1889, "label": "UBERONParcellation", "start": 1887 }, { "end": 2447, "label": "UBERONParcellation", "start": 2445 }, { "end": 2586, "label": "UBERONParcellation", "start": 2584 }, { "end": 2951, "label": "UBERONParcellation", "start": 2949 }, { "end": 3017, "label": "UBERONParcellation", "start": 3015 }, { "end": 3074, "label": "UBERONParcellation", "start": 3072 }, { "end": 3425, "label": "UBERONParcellation", "start": 3423 }, { "end": 3614, "label": "UBERONParcellation", "start": 3612 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Partially correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "\n\r\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 70, "label": "UBERONParcellation", "start": 68 }, { "end": 179, "label": "UBERONParcellation", "start": 177 }, { "end": 366, "label": "UBERONParcellation", "start": 364 }, { "end": 700, "label": "UBERONParcellation", "start": 698 }, { "end": 1208, "label": "UBERONParcellation", "start": 1206 }, { "end": 1706, "label": "UBERONParcellation", "start": 1704 }, { "end": 1889, "label": "UBERONParcellation", "start": 1887 }, { "end": 2447, "label": "UBERONParcellation", "start": 2445 }, { "end": 2586, "label": "UBERONParcellation", "start": 2584 }, { "end": 2951, "label": "UBERONParcellation", "start": 2949 }, { "end": 3017, "label": "UBERONParcellation", "start": 3015 }, { "end": 3074, "label": "UBERONParcellation", "start": 3072 }, { "end": 3425, "label": "UBERONParcellation", "start": 3423 }, { "end": 3614, "label": "UBERONParcellation", "start": 3612 }, { "end": 366, "label": "UBERONParcellation", "start": 350 }, { "end": 700, "label": "UBERONParcellation", "start": 684 }, { "end": 2951, "label": "UBERONParcellation", "start": 2935 }, { "end": 3074, "label": "UBERONParcellation", "start": 3058 }, { "end": 3614, "label": "UBERONParcellation", "start": 3598 }, { "end": 302, "label": "technique", "start": 282 }, { "end": 2895, "label": "technique", "start": 2875 } ]
null
null
4492081e-7e53-4ae3-96b5-12bf696082b1
completed
2025-04-29T14:36:04.700071
2025-05-27T14:00:53.084898
5ebcdd66-3192-4d40-98ec-236b32a92cce
Background and Purpose: Whether patients with both lobar and deep cerebral microbleeds (mixed CMB) have advanced cerebral amyloid angiopathy (CAA), hypertensive angiopathy (HA) or both is uncertain. To get insight into the underlying small vessel disease (SVD) associated with mixed CMB, we explored its association with cortical superficial siderosis (cSS), a key marker of CAA and other MRI markers of SVD in patients with intracerebral hemorrhage (ICH). Methods: Of 425 consecutive patients with acute ICH who had received brain MRIs, 260 had ≥1 CMB and were included in the analysis. They were categorized as strictly lobar CMB (suggesting CAA), strictly deep CMB (suggesting HA) or mixed CMB. Clinical and imaging characteristics were compared (1) between the three CMB groups and (2) within mixed CMB patients according to the symptomatic ICH location. Results: Overall, 111 (26%) patients had mixed CMB. Compared to strictly lobar CMB (n = 111) and strictly deep CMB (n = 38), patients with mixed CMB had a more severe burden of lacune, white matter hyperintensities and CMB. cSS was observed in 24.3% of patients with mixed CMB compared to 44.1% in strictly lobar CMB and 10.5% in strictly deep CMB (p < 0.0001). Among patients with mixed CMB, 44 (39.6%) had a lobar symptomatic ICH and 67 (60.4%) had a non-lobar ICH. Patients with non-lobar ICH were more likely to have hypertension, whereas those with lobar ICH were more likely to have cSS and chronic lobar ICH and had higher ratio lobar CMB count/total CMB count. Conclusions: Mixed CMB is frequently encountered in patients with ICH and appears as a heterogeneous group, suggesting that both CAA and HA may be contributing to mixed CMB. Neuroimaging markers including ICH location, cSS, and CMB distribution may indicate the predominant underlying vasculopathy, with potential prognostic implications.
<li> <b>brain MRIs:</b> magneticResonanceImaging (technique)<li> <b>white matter:</b> brainWhiteMatter (UBERONParcellation)
[ [ { "end": 1056, "label": "UBERONParcellation", "start": 1044 }, { "end": 329, "label": "UBERONParcellation", "start": 321 }, { "end": 531, "label": "UBERONParcellation", "start": 526 }, { "end": 536, "label": "technique", "start": 532 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Incorrect" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "cortical: Other (UBERONParcellation)\nbrain: Other (UBERONParcellation)\nMRI: magneticResonanceImaging (technique)\r\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 536, "label": "technique", "start": 526 }, { "end": 1056, "label": "UBERONParcellation", "start": 1044 } ]
null
null
bafd8d89-f3c0-44ec-a076-e55fe965cd13
pending
2025-04-29T14:36:04.700077
2025-04-29T14:36:04.700077
5ef0d0ab-7428-4ffb-9193-d1c0dd4b6c10
Compared to patients with strictly deep CMB, patients with mixed CMB were older but had similar prevalence of hypertension and diabetes.Patients with mixed CMB were more likely to have a symptomatic lobar ICH than those with strictly deep CMB and had a more severe burden of lacunes, CMB, and WMH.Prevalence of cSS did not differ between the two groups.A multivariable model shows that compared to strictly deep CMBs, the pattern of mixed CMB was associated with symptomatic lobar ICH (OR 4.68, 95%, CI 1.27-21.68,p = 0.03) and higher CMB count (OR 11.69, 95% CI 5.43-29.62,p < 0.0001).
None
[ [] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[ null ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "discarded" ]
[]
null
null
11dc1eb4-96c0-414b-8177-053ac63f2fd4
completed
2025-04-29T14:36:04.700084
2025-05-27T14:00:53.246370
a0e7d3d9-bc9b-49c7-8c46-3a05c3518689
Entropy as an estimate of complexity of the electroencephalogram is an effective parameter for monitoring the depth of anesthesia (DOA) during surgery. Multiscale entropy (MSE) is useful to evaluate the complexity of signals over different time scales. However, the limitation of the length of processed signal is a problem due to observing the variation of sample entropy (SE) on different scales. In this study, the adaptive resampling procedure is employed to replace the process of coarse-graining in MSE. According to the analysis of various signals and practical EEG signals, it is feasible to calculate the SE from the adaptive resampled signals, and it has the highly similar results with the original MSE at small scales. The distribution of the MSE of EEG during the whole surgery based on adaptive resampling process is able to show the detailed variation of SE in small scales and complexity of EEG, which could help anesthesiologists evaluate the status of patients.
<li> <b>electroencephalogram:</b> electroencephalography (technique)<li> <b>EEG:</b> electroencephalography (technique)
[ [ { "end": 64, "label": "technique", "start": 44 }, { "end": 572, "label": "technique", "start": 569 }, { "end": 765, "label": "technique", "start": 762 }, { "end": 910, "label": "technique", "start": 907 } ] ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "Correct" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ "\n" ]
[ "3c769fcb-8d37-41a2-b5e3-943a2a1090ab" ]
[ "submitted" ]
[ { "end": 64, "label": "technique", "start": 44 }, { "end": 572, "label": "technique", "start": 569 }, { "end": 765, "label": "technique", "start": 762 }, { "end": 910, "label": "technique", "start": 907 } ]
null
null