bluuebunny/crossref_metadata_2025_split huggingface dataset:
Microbial diversity of the glass spongeVazella pourtalesiiin response to anthropogenic activities
Authors: Busch Kathrin , Beazley Lindsay , Kenchington Ellen , Whoriskey Frederick , Slaby Beate , Hentschel Ute 
Published: May 2020

ABSTRACTEstablishment of adequate conservation areas represents a challenging but crucial task in the conservation of genetic diversity and biological variability. Anthropogenic pressures on marine ecosystems and organisms are steadily increasing. Whether and to what extent these pressures influence marine genetic biodiversity is only starting to be revealed. Using 16S rRNA gene amplicon sequencing, we analysed the microbial community structure of 33 individuals of the habitat-forming glass spongeVazella pourtalesii, as well as reference seawater, sediment, and biofilm samples. We assessed how two anthropogenic impacts, i.e. habitat destruction by trawling and artificial substrate provision (moorings made of composite plastic), correspond within situ V. pourtalesiimicrobiome variability. In addition, we evaluated the role of two bottom fishery closures in preserving sponge-associated microbial diversity on the Scotian Shelf, Canada. Our results illustrate thatV. pourtalesiisponges collected from pristine sites within fishery closures contained distinct and taxonomically largely novel microbial communities. At the trawled site we recorded significant quantitative differences in distinct microbial phyla, such as a reduction in Nitrospinae in sponges and environmental references. Individuals ofV. pourtalesiigrowing on the mooring were significantly enriched in Bacteroidetes, Verrucomicrobia and Cyanobacteria in comparison to sponge individuals growing on the natural seabed. Due to a concomitant enrichment of these taxa in the mooring biofilm, we propose that biofilms on artificial substrates may ‘prime’ sponge-associated microbial communities when small sponges settle on such substrates. These observations likely have relevant management implications when considering the increase of artificial substrates in the marine environment, e.g., marine litter, off-shore wind parks, and petroleum platforms.
Portable Take-Home System Enables Proportional Control and High-Resolution Data Logging with a Multi-Degree-of-Freedom Bionic Arm
Authors: Brinton Mark , Barcikowski Elliott , Davis Tyler , Paskett Michael , George Jacob , Clark Gregory 
Published: May 2020

AbstractThis paper describes a portable, prosthetic control system for at-home use of an advanced bionic arm. The system uses a modified Kalman filter to provide 6 degree-of-freedom, real-time, proportional control. We describe (a) how the system trains motor control algorithms for use with an advanced bionic arm, and (b) the system’s ability to record an unprecedented and comprehensive dataset of EMG, hand positions and force sensor values. Intact participants and a transradial amputee used the system to perform activities-of-daily-living, including bi-manual tasks, in the lab and at home. This technology enables at-home dexterous bionic arm use, and provides a high-temporal resolution description of daily use—essential information to determine clinical relevance and improve future research for advanced bionic arms.
Dismantling and rebuilding the trisulfide cofactor demonstrates its essential role in human sulfide quinone oxidoreductase
Authors: Landry Aaron P. , Moon Sojin , Bonanata Jenner , Cho Uhn Soo , Coitiño E. Laura , Banerjee Ruma 
Published: May 2020

AbstractSulfide quinone oxidoreductase (SQR) catalyzes the first step in sulfide clearance, coupling H2S oxidation to coenzyme Q reduction. Recent structures of human SQR revealed a sulfur atom bridging the SQR active site cysteines in a trisulfide configuration. Here, we assessed the importance of this cofactor using kinetic, crystallographic and computational modeling approaches. Cyanolysis of SQR proceeds via formation of an intense charge transfer complex that subsequently decays to eliminate thiocyanate. Cyanolysis leads to reversible loss of SQR activity, which is restored in the presence of sulfide. We captured a crystallographic intermediate in SQR that provides clues as to how the oxidized state of the cysteines is preserved. Computational modeling and MD simulations revealed an ~105-fold rate enhancement for nucleophilic addition of sulfide into the trisulfide versus a disulfide cofactor. The cysteine trisulfide in SQR is thus critical for activity and provides a significant catalytic advantage over a cysteine disulfide.
The role of the hypothalamus in cortical arousal and sleep homeostasis
Authors: Yamagata Tomoko , Kahn Martin C. , Šabanović Merima , Guillaumin Mathilde C.C. , van der Vinne Vincent , Huang Yi-Ge , McKillop Laura E. , Jagannath Aarti , Peirson Stuart N. , Mann Edward O. , Foster Russell G. , Vyazovskiy Vladyslav V. 
Published: May 2020

AbstractSleep and wakefulness are not simple homogenous all-or-none states, but instead are characterized by rich dynamics of brain activity across many temporal and spatial scales. Rapid global state transitions between waking and sleeping are believed to be controlled by hypothalamic circuits, but the contribution of the hypothalamus to within-state changes of sleep and wake “intensity” remains largely unexplored. Here we show that stimulation of inhibitory neurons in the preoptic hypothalamus does not merely trigger awakening from sleep, but the resulting awake state is also characterized by increased cortical activity. This activation is associated with a faster build-up of sleep pressure, proportional to the arousal level. These findings show that hypothalamic systems thought to exclusively control global state switching, also regulate within-state “intensity”, which we propose as a key intrinsic variable in shaping the architecture of sleep/wake states across the 24h day.
Oxidative Stress and Neuroinflammation in a Rat Model of Co-Morbid Obesity and Psychogenic Stress
Authors: Santana Jose M. Santiago , Vega-Torres Julio David , Ontiveros Angel Perla , Lee Jeong Bin , Torres Yaria Arroyo , Gonzalez Alondra Y. Cruz , Aponte Boria Esther , Zabala Ortiz Deisha , Carmona Carolina Alvarez , Figueroa Johnny D. 
Published: May 2020

AbstractBackgroundThere is growing recognition for a reciprocal, bidirectional link between anxiety disorders and obesity. Although the mechanisms linking obesity and anxiety remain speculative, this bidirectionality suggests shared pathophysiological processes. Neuroinflammation and oxidative damage are implicated in both pathological anxiety and obesity. This study investigates the relative contribution of comorbid diet-induced obesity and stress-induced anxiety to neuroinflammation and oxidative stress.MethodsThirty-six (36) male Lewis rats were divided into four groups based on diet type and stress exposure: 1) control diet unexposed (CDU) and 2) exposed (CDE), 3) Western-like high-saturated fat diet unexposed (WDU) and 4) exposed (WDE). Neurobehavioral tests were performed to assess anxiety-like behaviors. The catalytic concentrations of glutathione peroxidase and reductase were measured from plasma samples, and neuroinflammatory/oxidative stress biomarkers were measured from brain samples using Western blot. Correlations between behavioral phenotypes and biomarkers were assessed with Pearson’s correlation procedures.ResultsWe found that WDE rats exhibited markedly increased levels of glial fibrillary acidic protein (185%), catalase protein (215%), and glutathione reductase (GSR) enzymatic activity (418%) relative to CDU rats. Interestingly, the brain protein levels of glutathione peroxidase (GPx) and catalase were positively associated with body weight and behavioral indices of anxiety.ConclusionsTogether, our results support a role for neuroinflammation and oxidative stress in heightened emotional reactivity to obesogenic environments and psychogenic stress. Uncovering adaptive responses to obesogenic environments characterized by high access to high-saturated fat/high-sugar diets and toxic stress has the potential to strongly impact how we treat psychiatric disorders in at-risk populations.HighlightsPredatory odor stress heightens footshock reactivity and anxiety-like behaviors in Lewis rats.WD intake increases glutathione reductase activity in plasma.WD intake and PS exposure acted synergistically to increase the brain protein levels of catalase and the glial fibrillary acidic protein.The protein levels and activities of some redox/neuroinflammatory biomarkers are closely associated with behavioral proxies related to fear and anxiety in rats.
Coxsackievirus B3 Infection Early in Pregnancy Induces Congenital Heart Defects Through Suppression of Fetal Cardiomyocyte Proliferation
Authors: Sharma Vipul , Goessling Lisa S. , Brar Anoop K. , Joshi Chetanchandra S. , Mysorekar Indira U. , Eghtesady Pirooz 
Published: May 2020

ABSTRACTAimsCoxsackievirus B (CVB), the most common cause of viral myocarditis, targets cardiomyocytes through Coxsackie and Adenovirus Receptor, which is highly expressed in the fetal heart. We hypothesized CVB3, a well-recognized culprit for viral myocarditis, can precipitate congenital heart defects (CHD), when fetal infection occurs during critical window of gestation.Methods & ResultsWe infected C57Bl/6 pregnant mice with CVB3 during serial time points in early gestation (E5, E7, E9 and E11). We used different viral titers to examine possible dose- response relationship and assessed viral loads in various fetal organs as well as kinetics of virus passage into the fetus during gestation. Provided viral exposure occurred between E7-E9, we observed characteristic features of ventricular septal defect (33.6%), abnormal myocardial architecture resembling non-compaction (23.5%), and double outlet right ventricle (4.4%) among 209 viable fetuses examined. We observed a direct relationship between viral titers, severity and incidence of CHD, with apparent predominance among female fetuses. Infected dams remained healthy; we did not observe any maternal heart or placental injury suggestive of direct viral effects on developing heart as likely cause of CHD. We examined signaling pathways in CVB3-exposed hearts using RNAseq, KEGG enrichment analysis and immunohistochemistry. Signaling proteins of the Hippo, tight junction, transforming growth factor β1 and extracellular matrix proteins were the most highly enriched in CVB3-infected fetuses with VSD (log fold change >1.9, P<0.02). Moreover, cardiomyocyte proliferation was 50% lower in fetuses with VSD compared with uninfected controls.ConclusionPrenatal CVB3 infection can induce CHD, provided the infection occurs during a critical window. Alterations in myocardial proliferate capacity and consequent changes in cardiac architecture and trabeculation appear to account for the majority of observed phenotypes.GRAPHICAL ABSTRACT
Time course of alterations in adult spinal motoneuron properties in the SOD1(G93A) mouse model of ALS
Authors: Huh Seoan , Heckman Charles J. , Manuel Marin 
Published: May 2020

AbstractAlthough ALS is an adult-onset neurodegenerative disease, motoneuron electrical properties are already altered during embryonic development. Motoneurons must therefore exhibit a remarkable capacity for homeostatic regulation to maintain a normal motor output for most of the life of the patient. In the present paper, we demonstrate how maintaining homeostasis could come at a very high cost. We studied the excitability of spinal motoneurons from young adult SOD1(G93A) mice to end-stage. Initially homeostasis is highly successful in maintaining their overall excitability. This initial success, however, is achieved by pushing some cells far above the normal range of passive and active conductances. As the disease progresses, both passive and active conductances shrink below normal values in the surviving cells. This shrinkage may thus promote survival, implying the previously large values contribute to degeneration. These results support the hypothesis that motoneuronal homeostasis may be “hyper-vigilant” in ALS and a source of accumulating stress.Significance StatementDuring ALS, motoneurons exhibit a remarkable ability to maintain a normal motor output despite continuous alterations of their electrophysiological properties, up to the point when overt symptoms become apparent. We show that this homeostatic process can sometimes push motoneurons beyond the normal range, which may be causing long-lasting harm.
Deep learning for automated analysis of fish abundance: the benefits of training across multiple habitats
Authors: Ditria Ellen , Sievers Michael , Lopez-Marcano Sebastian , Jinks Eric L. , Connolly Rod M. 
Published: May 2020

AbstractEnvironmental monitoring guides conservation, and is thus particularly important for coastal aquatic habitats, which are heavily impacted by human activities. Underwater cameras and unmanned devices monitor aquatic wildlife, but manual processing of footage is a significant bottleneck to rapid data processing and dissemination of results. Deep learning has emerged as a solution, but its ability to accurately detect animals across habitat types and locations is largely untested for coastal environments. Here, we produce three deep learning models using an object detection framework to detect an ecologically important fish, luderick (Girella tricuspidata). Two were trained on footage from single habitats (seagrass or reef), and one on footage from both habitats. All models were subjected to tests from both habitat types. Models performed well on test data from the same habitat type (object detection measure: mAP50: 91.7 and 86.9% performance for seagrass and reef, respectively), but poorly on test sets from a different habitat type (73.3 and 58.4%, respectively). The model trained on a combination of both habitats produced the highest object detection results for both tests (92.4 and 87.8%, respectively). Performance in terms of the ability for models to correctly estimate the ecological metric, MaxN, showed similar patterns. The findings demonstrate that deep learning models extract ecologically useful information from video footage accurately and consistently, and can perform across habitat types when trained on footage from the variety of habitat types.
The Cognitive Mechanisms That Drive Social Belief Updates During Adolescence
Authors: Ma I. , Westhoff B. , van Duijvenvoorde A.C.K. 
Published: May 2020

ABSTRACTAdolescence is a key life phase for developing well-adjusted social behaviour. Belief updates about the trustworthiness of peers are essential during adolescence as social reorientation emerges and peer relationships intensify. This study maps the age-related changes of those belief updates during adolescence (n= 157, 10-24 years). We used computational modelling and an information sampling paradigm to reveal that three cognitive mechanisms contribute to age-related changes in those belief updates: prior beliefs, prior uncertainty, and uncertainty tolerance. The age-related changes in these three cognitive mechanisms result in increasingly adaptive belief updates from early to mid-adolescence when it comes to beliefs about trustworthiness. Our findings shed light on age-related changes in adaptive learning about others during adolescence.
Intrinsic connectivity of the prefrontal cortex and striato-limbic system respectively differentiate Major Depressive from Generalized Anxiety Disorder
Authors: Xu Xiaolei , Dai Jing , Chen Yuanshu , Liu Congcong , Xin Fei , Zhou Xinqi , Zhou Feng , Stamatakis Emmanuel A , Yao Shuxia , Luo Lizhu , Huang Yulan , Wang Jinyu , Zou Zhili , Vatansever Deniz , Kendrick Keith M , Zhou Bo , Becker Benjamin 
Published: May 2020

AbstractMajor Depressive Disorder (MDD) and Generalized Anxiety Disorder (GAD) are highly prevalent and debilitating disorders. The high overlap on the symptomatic and neurobiological level led to ongoing debates about their diagnostic and neurobiological uniqueness. The present study aims to identify common and disorder-specific neuropathological mechanisms and treatment targets in MDD and GAD. The present study combined categorial and dimensional disorder models with a fully data-driven intrinsic network level analysis (Intrinsic Connectivity Contrast, ICC) to resting state fMRI data acquired in 108 partn = 35 and n = 38 unmedicated patients with first-episode GAD, MDD respectively and n=35 healthy controls). Convergent evidence from categorical and dimensional analyses revealed MDD-specific decreased whole-brain connectivity profiles of the medial prefrontal and dorsolateral prefrontal cortex while GAD was specifically characterized by decreased whole-brain connectivity profiles of the putamen and decreased communication of this region with the amygdala. Together, findings from the present data-driven analysis suggest that intrinsic communication of frontal regions engaged in executive functions and emotion regulation represent depression-specific neurofunctional markers and treatment targets whereas dysregulated intrinsic communication of the striato-amygdala system engaged in reinforcement-based and emotional learning processes represent GAD-specific markers and a promising treatment target.
Transcriptional and epigenetic characterization of early striosomes identifies Foxf2 and Olig2 as factors required for development of striatal compartmentation and neuronal phenotypic differentiation
Authors: Cirnaru Maria-Daniela , Song Sicheng , Tshilenge Kizito-Tshitoko , Corwin Chuhyon , Mleczko Justyna , Aguirre Carlos Galicia , Benlhabib Houda , Bendl Jaroslav , Apontes Pasha , Fullard John F. , Muncunill Jordi Creus , Reyah Azadeh , Nik Ali M. , Carlsson Peter , Roussos Panos , Mooney Sean D. , Ellerby Lisa M. , Ehrlich Michelle E. 
Published: May 2020

AbstractThe basal ganglia, best known for processing information required for multiple aspects of movement, is also part of a network which regulates reward and cognition. The major output nucleus of the basal ganglia is the striatum, and its functions are dependent on neuronal compartmentation, including striosomes and matrix, which are selectively affected in disease. Striatal projection neurons are GABAergic medium spiny neurons (MSNs), all of which share basic molecular signatures but are subtyped by selective expression of receptors, neuropeptides, and other gene families. Neurogenesis of the striosome and matrix occurs in separate waves, but the factors regulating terminal neuronal differentiation following migration are largely unidentified. We performed RNA- and ATAC-seq on sorted murine striosome and matrix cells at postnatal day 3. Focusing on the striosomal compartment, we validated the localization and role of transcription factors and their regulator(s), previously not known to be associated with striatal development, includingIrx1, Foxf2, Olig2andStat1/2. In addition, we validated the enhancer function of a striosome-specific open chromatin region located 15Kb downstream of theOlig2gene. These data and data bases provide novel tools to dissect and manipulate the networks regulating MSN compartmentation and differentiation and thus provide new approaches to establishing MSN subtypes from human iPSCs for disease modeling and drug discovery.
Purifying selection on noncoding deletions of human regulatory elements detected using their cellular pleiotropy
Authors: Radke David W. , Sul Jae Hoon , Balick Daniel J. , Akle Sebastian ,   Alzheimer’s Disease Neuroimaging Initiative, Green Robert C. , Sunyaev Shamil R. 
Published: May 2020

Genomic deletions provide a powerful loss-of-function model in non-coding regions to assess the role of purifying selection on human noncoding genetic variation. Regulatory element function is char-acterized by non-uniform tissue/cell-type activity, necessarily linking the study of fitness consequences from regulatory variants to their corresponding cellular activity. We used deletions from the 1000 Genomes Project (1000GP) and a callset we generated from genomes of participants in the Alzheimer’s Disease Neuroimaging Initiative (ADNI) in order to examine whether purifying selection preserves noncoding sites of chromatin accessibility (DHS), histone modification (enhancer, transcribed, polycomb-repressed, heterochromatin), and topologically associated domain loops (TAD-loops). To examine this in a cellular activity-aware manner, we developed a statistical method, Pleiotropy Ratio Score (PlyRS), which calculates a correlation-adjusted count of “cellular pleiotropy” for each noncoding base-pair by analyzing shared regulatory annotations across tissues/cell-types. Comparing real deletion PlyRS values to simulations in a length-matched framework and using genomic covariates in analyses, we found that purifying selection acts to preserve both DHS and enhancer sites, as evident by both depletion of deletions overlapping these annotations and a shift in the allele frequency spectrum of overlapping deletions towards rare alleles. However, we did not find evidence of purifying selection for transcribed, polycomb-repressed, or heterochromatin sites. Additionally, we found evidence that purifying selection is acting on TAD-loop boundary integrity by preserving co-localized CTCF binding sites. Notably, at regions of DHS, enhancer, and CTCF within TAD-loop boundaries we found evidence that both sites of tissue/cell-type-specific activity and sites of cellularly pleiotropic activity are preserved by selection.Significance StatementWe used natural genomic deletions as a loss-of-function model to assess the role of purifying selection in preserving human noncoding regulatory sites. We examined this in a cellular activity-aware manner through development of a statistical method, Pleiotropy Ratio Score (PlyRS), which calculates an adjusted count of “cellular pleiotropy” for each noncoding basepair by analyzing correlations from shared regulatory annotations across tissues/cell-types. By comparing real deletion PlyRS values to simulations, we found that purifying selection acts to preserve both DHS and enhancer sites and TAD-loop boundary integrity by preserving co-localized CTCF binding sites. Notably, we found evidence at these regulatory regions that both sites of tissue/cell-type-specific activity and sites of cellularly pleiotropic activity are preserved by selection.
Color constancy based on the geometry of color distribution
Authors: Morimoto Takuma , Kusuyama Takahiro , Fukuda Kazuho , Uchikawa Keiji 
Published: May 2020

AbstractA white surface appears white under different lighting environments. This ability is referred to color constancy. The physical inputs to our visual system are dictated by the interplay between lights and surfaces, and thus for the surface color to be stably perceived, the illuminant influence needs to be discounted. To reveal our strategy to infer the illuminant color, we conducted three psychophysical experiments designed to test optimal color hypothesis: we internalize the physical color gamut under a particular illuminant and apply the prior to estimate the illuminant color. In each experiment, we presented 61 hexagons arranged without spatial gaps, where the surrounding 60 hexagons were set to have a specific shape in their color distribution. We asked participants to adjust the color of a center test field so that it appears a full-white surface placed under a test illuminant. Results and computational modeling suggested that although our proposed model is limited in accounting for estimation of illuminant intensity by human observers, it agrees fairly well with the estimates of illuminant chromaticity in most tested conditions. The accuracy of estimation generally outperformed other tested conventional color constancy models. These results support the hypothesis that our visual system can utilize the geometry of scene color distribution to achieve color constancy.