bluuebunny/crossref_metadata_2025_split huggingface dataset:
An open-access dataset of naturalistic viewing using simultaneous EEG-fMRI
Authors: Telesford Qawi K , Gonzalez-Moreira Eduardo , Xu Ting , Tian Yiwen , Colcombe Stanley , Cloud Jessica , Russ Brian Edward , Falchier Arnaud , Nentwich Maximilian , Madsen Jens , Parra Lucas , Schroeder Charles , Milham Michael , Franco Alexandre Rosa 
Published: November 2022

AbstractIn this work, we present a dataset that combines functional magnetic imaging (fMRI) and electroencephalography (EEG) to use as a resource for understanding human brain function in these two imaging modalities. The dataset can also be used for optimizing preprocessing methods for simultaneously collected imaging data. The dataset includes simultaneously collected recordings from 22 individuals (ages: 23-51) across various visual and naturalistic stimuli. In addition, physiological, eye tracking, electrocardiography, and cognitive and behavioral data were collected along with this neuroimaging data. Visual tasks include a flickering checkerboard collected outside and inside the MRI scanner (EEG-only) and simultaneous EEG-fMRI recordings. Simultaneous recordings include rest, the visual paradigm Inscapes, and several short video movies representing naturalistic stimuli. Raw and preprocessed data are openly available to download. We present this dataset as part of an effort to provide open-access data to increase the opportunity for discoveries and understanding of the human brain and evaluate the correlation between electrical brain activity and blood oxygen level-dependent (BOLD) signals.
Activity-regulated gene expression across cell types of the mouse hippocampus
Authors: Nelson Erik D. , Maynard Kristen R. , Nicholas Kyndall R. , Tran Matthew N. , Divecha Heena R. , Collado-Torres Leonardo , Hicks Stephanie C. , Martinowich Keri 
Published: November 2022

AbstractActivity-regulated gene (ARG) expression patterns in the hippocampus (HPC) regulate synaptic plasticity, learning, and memory, and are linked to both risk and treatment response for many neuropsychiatric disorders. The HPC contains discrete classes of neurons with specialized functions, but cell type-specific activity-regulated transcriptional programs are not well characterized. Here, we used single-nucleus RNA-sequencing (snRNA-seq) in a mouse model of acute electroconvulsive seizures (ECS) to identify cell type-specific molecular signatures associated with induced activity in HPC neurons. We used unsupervised clustering anda priorimarker genes to computationally annotate 15,990 high-quality HPC neuronal nuclei fromN=4 mice across all major HPC subregions and neuron types. Activity-induced transcriptomic responses were divergent across neuron populations, with dentate granule cells being particularly responsive to activity. Differential expression analysis identified both upregulated and downregulated cell type-specific gene sets in neurons following ECS. Within these gene sets, we identified enrichment of pathways associated with varying biological processes such as synapse organization, cellular signaling, and transcriptional regulation. Finally, we used matrix factorization to reveal continuous gene expression patterns differentially associated with cell type, ECS, and biological processes. This work provides a rich resource for interrogating activity-regulated transcriptional responses in HPC neurons at single-nuclei resolution in the context of ECS, which can provide biological insight into the roles of defined neuronal subtypes in HPC function.
Lipid bicelles in the study of biomembrane characteristics
Authors: Pöhnl Matthias , Kluge Christoph , Böckmann Rainer A. 
Published: November 2022

AbstractSimulations of lipid membranes typically make use of periodic boundary conditions to mimic macroscopically sized membranes and allow for comparison to experiments performed e.g. on planar lipid membranes or on unilamellar lipid vesicles. However, the lateral periodicity partly suppresses membrane fluctuations or membrane remodeling, processes that are of particular importance in the study of asymmetric membranes – i.e. membranes with integral or associated proteins and/or asymmetric lipid compositions.Here, we devised a simple albeit powerful lipid bicelle model system that (i) displays similar structural, dynamical and mechanical properties compared to infinite periodic lipid membrane systems, and allows (ii) for the study of asymmetric lipid bilayer systems, and (iii) the unperturbed formation of local spontaneous curvature induced by lipids or proteins in coarse-grained and all-atom molecular dynamics simulations. In addition, the system is characterized by largely unbiased thermal fluctuations as opposed to standard bilayer systems. Application of the bicelle system for an asymmetric lipid composition resembling the plasma membrane reveals that the cholesterol density for a tension-free plasma membrane with a vanishing spontaneous curvature is larger by 28% within the extracellular leaflet compared to the cytosolic leaflet.Graphical TOC Entry
Platelet pannexin-1 channels modulate inflammation during abdominal aortic aneurysm formation
Authors: Metz Lisa Maria , Feige Tobias , de Biasi Larissa , Ehrenberg Agnes , Mulorz Joscha , Toska Laura Mara , Reusswig Friedrich , Quast Christine , Gerdes Norbert , Kelm Malte , Schelzig Hubert , Elvers Margitta 
Published: November 2022

AbstractAbdominal aortic aneurysm (AAA) is a common disease and highly lethal if untreated. The progressive dilatation of the abdominal aorta is accompanied by degradation and remodeling of the vessel wall due to chronic inflammation. Pannexins represent anion-selective channels and play a crucial role in non-vesicular ATP release to amplify paracrine signaling in cells. Thus, pannexins are involved in many (patho-) physiological processes. Recently, Panx1 channels were identified to be significantly involved in AAA formation through endothelial derived Panx1 regulated inflammation and aortic remodeling. In platelets, Panx1 becomes activated following activation of glycoprotein (GP)VI. Since platelets play a role in cardiovascular diseases including AAA, we analyzed the contribution of platelet Panx1 in the progression of AAA. We detected enhanced Panx1 plasma levels in AAA patients. In experimental AAA using the pancreatic porcine elastase (PPE) mouse model, a major contribution of platelet Panx1 channels in platelet activation, pro-coagulant activity of platelets and platelet-mediated inflammation has been detected. In detail, platelets are important for the migration of neutrophils into the aortic wall induced by direct cell interaction and by activation of endothelial cells. Decreased platelet activation and inflammation did not affect ECM remodeling or wall thickness in platelet-specific Panx1 knock-out mice following PPE surgery. Thus, aortic diameter expansion at different time points after elastase infusion of the aortic wall was unaltered in platelet-specific Panx1 deficient mice suggesting that the modulation of inflammation alone does not affect AAA formation and progression. In conclusion, our data strongly supports the role of platelets in inflammatory responses in AAA via Panx1 channels and adds important knowledge about the significance of platelets in AAA pathology important for the establishment of an anti-platelet therapy for AAA patients.
Model-free decision making resists improved instructions and is enhanced by stimulus-response associations
Authors: Luna Raúl , Vadillo Miguel A. , Luque David 
Published: November 2022

AbstractHuman behaviour may be thought of as supported by two different computational-learning mechanisms, model-free and model-based respectively. In model-free strategies, stimulus-response associations are strengthened when actions are followed by a reward and weakened otherwise. In model-based learning, previous to selecting an action, the current values of the different possible actions are computed based on a detailed model of the environment. Previous research with the two-stage task suggests that participants’ behaviour usually shows a mixture of both strategies. But, interestingly, a recent study by da Silva and Hare (2020) found that participants primarily deploy model-based behaviour when they are given detailed instructions about the structure of the task. In the present study, we reproduce this essential experiment. Our results confirm that improved instructions give rise to a stronger model-based component. Crucially, we also found a significant effect of reward that became stronger under conditions that favoured the development of strong stimulus-response associations. This suggests that the effect of reward, often taken as indicator of a model-free component, is related to stimulus-response learning.
Completing the TRB family: newly characterized members show ancient evolutionary origins and distinct localization, yet similar interactions
Authors: Kusová Alžbeta , Steinbachová Lenka , Přerovská Tereza , Drábková Lenka Záveská , Paleček Jan , Khan Ahmed , Rigóová Gabriela , Gadiou Zuzana , Jourdain Claire , Stricker Tino , Schubert Daniel , Honys David , Schrumpfová Petra Procházková 
Published: November 2022

AbstractTelomere repeat binding proteins (TRBs) belong to a family of proteins possessing a Myb-like domain which binds to telomeric repeats. Three members of this family (TRB1, TRB2, TRB3) fromArabidopsis thalianahave already been described as associated with terminal telomeric repeats (telomeres) or short interstitial telomeric repeats in gene promoters (telo-boxes). They are also known to interact with several protein complexes: telomerase, Polycomb repressive complex 2 (PRC2) E(z) subunits and the PEAT complex (PWOs-EPCRs-ARIDs-TRBs). Here we characterize two novel members of the TRB family (TRB4 and TRB5). Our wide phylogenetic analyses have shown that TRB proteins evolved in the plant kingdom after the transition to a terrestrial habitat in Streptophyta, and consequently TRBs diversified in seed plants. TRB4-5 share common TRB motifs while differing in several others and seem to have an earlier phylogenetic origin than TRB1-3. Their common Myb-like domains bind long arrays of telomeric repeats in vitro, and we have determined the minimal recognition motif of all TRBs as onetelo-box. Our data indicate that despite the distinct localization patterns of TRB1-3 and TRB4-5 in situ, all members of TRB family mutually interact and also bind to telomerase/PRC2/PEAT complexes. Additionally, we have detected novel interactions between TRB4-5 and EMF2 and VRN2, which are Su(z)12 subunits of PRC2.
Oxidative stress-induced MMP- and γ-secretase-dependent VE-cadherin processing is modulated by the proteasome and BMP9/10
Authors: Ivaldo Caterina , Passalacqua Mario , Furfaro Anna Lisa , d’Abramo Cristina , Ruiz Santiago , Chatterjee Prodyot K. , Metz Christine N. , Nitti Mariapaola , Marambaud Philippe 
Published: November 2022

AbstractClassical cadherins, including vascular endothelial (VE)-cadherin, are targeted by matrix metalloproteinases (MMPs) and γ-secretase during adherens junction (AJ) disassembly, a mechanism that might have relevance for endothelial cell (EC) integrity and vascular homeostasis. Here, we show that oxidative stress triggered by H2O2exposure induced efficient VE-cadherin proteolysis by MMPs and γ-secretase in human umbilical endothelial cells (HUVECs). The cytoplasmic domain of VE-cadherin produced by γ-secretase, VE-Cad/CTF2 - a fragment that has eluded identification so far - could readily be detected after H2O2treatment. VE-Cad/CTF2, released into the cytosol, was tightly regulated by proteasomal degradation and was sequentially produced from an ADAM10/17-generated C-terminal fragment, VE-Cad/CTF1. Interestingly, BMP9 and BMP10, two circulating ligands critically involved in vascular maintenance, significantly reduced VE-Cad/CTF2 levels during H2O2challenge, as well as mitigated H2O2-mediated actin cytoskeleton disassembly during VE-cadherin processing. Notably, BMP9/10 pretreatments efficiently reduced apoptosis induced by H2O2, favoring endothelial cell recovery. Thus, oxidative stress is a trigger of MMP- and γ-secretase-mediated endoproteolysis of VE-cadherin and AJ disassembly from the cytoskeleton in ECs, a mechanism that is negatively controlled by the EC quiescence factors, BMP9 and BMP10.
The RNA Binding proteome of axonal mRNAs in sympathetic neurons
Authors: Luisier Raphaëlle , Andreassi Catia , Riccio Antonella 
Published: November 2022

ABSTRACTBackgroundNeurons are morphologically complex cells that rely on the compartmentalization of protein expression to develop and maintain their cytoarchitecture. Targeting of RNA transcripts to axons is one of the mechanisms that allows rapid local translation of proteins in response to extracellular signals. 3’ untranslated regions (UTRs) of mRNA are non-coding sequences that play a critical role in determining transcript localisation and translation by interacting with specific RNA binding proteins (RBPs). However, how 3’UTRs contribute to mRNA metabolism and the nature of RBP complexes responsible for these functions remain elusive.ResultsWe performed 3’ end sequencing of RNA isolated from axons and cell bodies of sympathetic neurons exposed to either Nerve Growth factor (NGF) or Neurotrophin 3 (NT3). NGF and NT3 are growth factors essential for sympathetic neuron development that act through distinct signalling mechanisms. Whereas NT3 is thought to act only locally, NGF signals back from axons to the cell bodies. We discovered that both NGF and NT3 affect transcription and alternative polyadenylation and induce the localisation of specific 3’UTR isoforms to axons. The finding that many transcripts with short 3’UTR were detected only in axons suggest that these may undergo local post-transcriptional remodelling. The integration of our data with CLIP-sequencing data revealed that long 3’UTR isoforms associate with RBP complexes in the nucleus, and once in axons, regulate cytoplasmic 3’ UTR isoform cleavage into shorter isoform.ConclusionsOur findings shed new light on the complex interplay between nuclear polyadenylation, mRNA localisation and local 3’UTR remodelling in developing neurons.Graphical abstract
Gamma-Protocadherins regulate filopodia self-recognition and dynamics to drive dendrite self-avoidance
Authors: Ing-Esteves Samantha , Lefebvre Julie L. 
Published: November 2022

SUMMARYNeurons form cell type-specific morphologies that are shaped by molecular cues and their cellular events governing dendrite growth. One growth rule is distributing dendrites uniformly within a neuron’s territory by avoiding sibling or ‘self’ branches. In mammalian neurons, dendrite self-avoidance is regulated by the clustered Protocadherins (cPcdhs), a large family of recognition molecules. Genetic and molecular studies suggest that the cPcdhs mediate homophilic recognition and repulsion between self-dendrites but this model has not been tested through direct investigation of self-avoidance during development. Here we performed live imaging and 4D quantifications of dendrite morphogenesis to define the cPcdh-dependent mechanisms of self-avoidance. We focused on the mouse retinal starburst amacrine cell (SAC), which requires the gamma-Pcdhs (Pcdhgs) and self/non-self recognition to establish a stereotypic radial morphology while permitting dendritic interactions with neighboring SACs. Through morphogenesis, SACs extend a transient population of dynamic filopodia that fill the growing arbor and contact nearby self-dendrites. Compared to non-self-contacting filopodia, self-contacting events have longer lifetimes and a subset persists as filopodia bridges. In the absence of thePcdhgs, non-self-contacting filopodia dynamics are unaffected but self-contact-induced retractions are significantly diminished. Filopodia bridges accumulate, leading to the bundling of dendritic processes and disruption to the arbor shape. By tracking dendrite self-avoidance in real-time, our findings demonstrate that the γ-Pcdhs selectively mediate contact-induced retractions upon filopodia self-recognition. Our results also illustrate how self-avoidance shapes the stochastic and space-filling behaviors of filopodia for robust dendritic pattern formation in mammalian neurons.HIGHLIGHTSDendrite self-avoidance proceeds through interstitial filopodia and contact-induced retractions between sibling processes.Self-contacting filopodia exhibit longer lifetimes and a subset of contacts persist.Pcdhgs selectively regulate self-contact-induced retractions.Loss ofPcdhgsand filopodia self-avoidance disrupts dendritic arbor shape.
The Neural Correlates of Arousal: The Ventral Posterolateral Nucleus-Global Transient Co-Activation
Authors: Han Junrong , Xie Qiuyou , Wu Xuehai , Huang Zirui , Tanabe Sean , Fogel Stuart , Hudetz Anthony G. , Wu Hang , Northoff Georg , Mao Ying , He Sheng , Qin Pengmin 
Published: November 2022

AbstractArousal and awareness are two components of consciousness whose the neural mechanisms remain unclear. Spontaneous increases of global (brain-wide) blood-oxygenation-level-dependent (BOLD) signal has been found to be sensitive to changes in arousal. By contrasting BOLD datasets with altered arousal levels, we found that the activation of ventral posterolateral nucleus (VPL) decreased during transient increase in the global signal (top 17% data) in low arousal and awareness states (non-rapid eye movement sleep and anesthesia) as compared to wakefulness, and even in eye-closed (compared with eyes-open) in healthy awake-states, while this activation remained unchanged in patients with unresponsive wakefulness syndrome characterized by high arousal without awareness. These results demonstrate that co-activation of the VPL and global activity is critical to arousal, but not to awareness.One-Sentence SummaryThe VPL nucleus-global brain transient co-activation is related to physiological arousal but not to perceptual awareness.
Hepatic WDR23 proteostasis mediates insulin clearance by regulating insulin-degrading enzyme
Authors: Duangjan Chatrawee , Arpawong Thalida Em , Spatola Brett N. , Curran Sean P. 
Published: November 2022

ABSTRACTClearance of circulating insulin is critical for metabolic homeostasis. In the liver, insulin is degraded by the activity of the insulin-degrading enzyme (IDE). Here we establish a hepatic regulatory axis for IDE through WDR23-proteostasis.Wdr23KOmice have increased IDE expression, reduced circulating insulin, and defective insulin responses. Genetically engineered human cell models lackingWDR23also increase IDE expression and display dysregulated phosphorylation of insulin signaling cascade proteins, IRS-1, AKT2, MAPK, FoxO, and mTOR, similar to cells treated with insulin, which can be mitigated by chemical inhibition of IDE. Mechanistically, the cytoprotective transcription factor NRF2, a direct target of WDR23-Cul4 proteostasis, mediates the enhanced transcriptional expression of IDE whenWDR23is ablated. Moreover, an analysis of human genetic variation inWDR23across a large naturally aging human cohort in the US Health and Retirement Study reveals a significant association ofWDR23with altered hemoglobin A1C (HbA1c) levels in older adults, supporting the use ofWDR23as new molecular determinant of metabolic health in humans.
Gasdermin D is the only Gasdermin that provides non-redundant protection against acuteSalmonellagut infection
Authors: Fattinger Stefan A. , Maurer Luca , Geiser Petra , Enz Ursina , Ganguillet Suwannee , Gül Ersin , Kroon Sanne , Demarco Benjamin , Furter Markus , Barthel Manja , Pelczar Pawel , Shao Feng , Broz Petr , Sellin Mikael E. , Hardt Wolf-Dietrich 
Published: November 2022

ABSTRACTGasdermins (GSDMs) share a common functional domain structure and are best known for their capacity to form membrane pores. These pores are hallmarks of a specific form of cell death called pyroptosis and mediate the secretion of pro-inflammatory cytokines such as interleukin 1β (IL1β) and interleukin 18 (IL18). Thereby, Gasdermins have been implicated in various immune responses against cancer and infectious diseases such as acuteSalmonellaTyphimurium (S.Tm) gut infection. However, to date, we lack a comprehensive functional assessment of the different Gasdermins (GSDMA-E) duringS.Tm infectionin vivo. Here, we have performed littermate-controlled oralS.Tm infections to investigate the impact of all murine Gasdermins. While GSDMA, -C and -E appear dispensable, we show that GSDMD (i) restrictsS.Tm loads in the gut tissue and systemic organs, (ii) controls gut inflammation kinetics, and (iii) prevents epithelium disruption by 72h of the infection. Full protection requires GSDMD expression by both bone-marrow-derived lamina propria cells and intestinal epithelial cells (IECs).In vivoexperiments, 3D- and 2D-enteroid infections further show that infected IEC extrusion proceeds also without GSDMD, but that GSDMD controls the permeabilization and morphology of the extruding cells and affects extrusion kinetics. As such, this work identifies a non-redundant multipronged role of GSDMD in mucosal tissue defence against a common enteric pathogen.HIGHLIGHTSGasdermin D restrictsSalmonellaTyphimurium (S.Tm) translocation across the gut tissue, controls gut inflammation kinetics, and prevents epithelium disruption by 72h of the infection.Gasdermins A, C and E appear dispensable for protection against acuteS.Tm gut infection.Gasdermin D in bone-marrow-derived lamina propria cells and intestinal epithelial cells complement each other to suppress gut tissueS.Tm loads.Gasdermin D is not required for extrusion of infected intestinal epithelial cells but drives their permeabilization and affects qualitative features of the extrusion process.
A multi-layer mean-field model for the cerebellar cortex: design, validation, and prediction
Authors: Lorenzi Roberta M. , Geminiani Alice , Zerlaut Yann , Destexhe Alain , Gandini Wheeler-Kingshott Claudia A.M. , Palesi Fulvia , Casellato Claudia , D’Angelo Egidio 
Published: November 2022

AbstractMean-field (MF) models can be used to summarize in a few statistical parameters the salient properties of an inter-wired neuronal network incorporating different types of neurons and synapses along with their topological organization. MF are crucial to efficiently implement the modules of large-scale brain models maintaining the specificity of local microcircuits. While MFs have been generated for the isocortex, they are still missing for other parts of the brain. Here we have designed and simulated a multi-layer MF of the cerebellar network (including Granule Cells, Golgi Cells, Molecular Layer Interneurons, and Purkinje Cells) and validated it against experimental data and the corresponding spiking neural network (SNN) microcircuit model. The cerebellar MF was built using a system of equations, where properties of neuronal populations and topological parameters are embedded in inter-dependent transfer functions. The model time constant was optimised using local field potentials recorded experimentally from acute mouse cerebellar slices as a template. The MF satisfactorily reproduced the average dynamics of the different neuronal populations in response to various input patterns and predicted the modulation of Purkinje Cells firing depending on cortical plasticity, which drives learning in associative tasks, and the level of feedforward inhibition. The cerebellar MF provides a computationally efficient tool that will allow to investigate the causal relationship between microscopic neuronal properties and ensemble brain activity in virtual brain models addressing both physiological and pathological conditions.