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Abstract
The temporal dynamics by which linguistic information becomes available is one of the key properties to understand how language is organized in the brain. An unresolved debate between different brain language models is whether words, the building blocks of language, are activated in a sequential or parallel manner. In this study, we approached this issue from a novel perspective by directly comparing the time course of word component activation in speech production versus perception. In an overt object naming task and a passive listening task, we analyzed with mixed linear models at the single-trial level the event-related brain potentials elicited by the same lexico-semantic and phonological word knowledge in the two language modalities. Results revealed that both word components manifested simultaneously as early as 75 ms after stimulus onset in production and perception; differences between the language modalities only became apparent after 300 ms of processing. The data provide evidence for ultra-rapid parallel dynamics of language processing and are interpreted within a neural assembly framework where words recruit the same integrated cell assemblies across production and perception. These word assemblies ignite early on in parallel and only later on reverberate in a behavior-specific manner.

Biped robots are similar to human beings and have broad application prospects in the fields of family service, disaster rescue and military affairs. However, simplified models and fixed center of mass (COM) used in previous research ignore the large-scale stability control ability implied by whole-body motion. The present paper proposed a two-level controller based on a simplified model and whole-body dynamics. In high level, a model predictive control (MPC) controller is implemented to improve zero moment point (ZMP) control performance. In low level, a quadratic programming optimization method is adopted to realize trajectory tracking and stabilization with friction and joint constraints. The simulation shows that a 12-degree-of-freedom force-controlled biped robot model, adopting the method proposed in this paper, can recover from a 40 Nm disturbance when walking at 1.44 km/h without adjusting the foot placement, and can walk on an unknown 4 cm high stairs and a rotating slope with a maximum inclination of 10°. The method is also adopted to realize fast walking up to 6 km/h.

Objective We examine the spatiotemporal dynamics of neural activity and its correlates in heart rate and its variability (HR/HRV) during a fatiguing visuospatial working memory task. Background The neural and physiological drivers of fatigue are complex, coupled, and poorly understood. Investigations that combine the fidelity of neural indices and the field-readiness of physiological measures can facilitate measurements of fatigue states in operational settings. Method Sixteen healthy adults, balanced by sex, completed a 60-minute fatiguing visuospatial working memory task. Changes in task performance, subjective measures of effort and fatigue, cerebral hemodynamics, and HR/HRV were analyzed. Peak brain activation, functional and effective connections within relevant brain networks were contrasted against spectral and temporal features of HR/HRV. Results Task performance elicited increased neural activation in regions responsible for maintaining working memory capacity. With the onset of time-on-task effects, resource utilization was seen to increase beyond task-relevant networks. Over time, functional connections in the prefrontal cortex were seen to weaken, with changes in the causal relationships between key regions known to drive working memory. HR/HRV indices were seen to closely follow activity in the prefrontal cortex. Conclusion This investigation provided a window into the neurophysiological underpinnings of working memory under the time-on-task effect. HR/HRV was largely shown to mirror changes in cortical networks responsible for working memory, therefore supporting the possibility of unobtrusive state recognition under ecologically valid conditions. Applications Findings here can inform the development of a fieldable index for cognitive fatigue.

Pediatric traumatic brain injury (TBI) represents a serious public health concern. Family members are often caregivers for children with TBI, which can result in a significant strain on familial relationships. Research is needed to examine aspects of family functioning in the context of recovery post-TBI, especially in Latin America, where cultural norms may reinforce caregiving by family members, but where resources for these caregivers may be scarce. This study examined caregiver-reported family satisfaction, communication, cohesion, and flexibility at three time points in the year post-injury for 46 families of a child with TBI in comparison to healthy control families. Families experiencing pediatric TBI were recruited from a large hospital in Guadalajara, Mexico, while healthy controls were recruited from a local educational center. Results from multilevel growth curve models demonstrated that caregivers of children with a TBI reported significantly worse family functioning than controls at each assessment. Families experiencing pediatric TBI were unable to attain the level of functioning of controls during the time span studied, suggesting that these families are likely to experience long-term disruptions in family functioning. The current study highlights the need for family-level intervention programs to target functioning for families affected by pediatric TBI who are at risk for difficulties within a rehabilitation context. ; This study was supported by the Department of Veterans Affairs Office of Academic Affiliations Advanced Fellowship Program in Mental Illness Research and Treatment, the Medical Research Service of the Veterans Affairs Central Virginia Health Care System, and the Department of Veterans Affairs Mid-Atlantic Mental Illness Research, Education, and Clinical Center (MIRECC). Ramos-Usuga, D. was supported by a predoctoral fellowship from the Basque Government (PRE_2019_1_0164).

Recently introduced effective connectivity methods allow for the in-vivo investigation of large-scale functional interactions between brain regions. However, dynamic causal modeling, the most widely used technique to date, typically captures only a few predefined regions of interest. In this study, we present an alternative computational approach to infer effective connectivity within the entire connectome and show its performance on a developmental cohort with emerging language capacities. The novel approach provides new opportunities to quantify effective connectivity changes in the human brain. ; G.D. was supported by the ERC Advanced Grant DYSTRUCTURE (n. 295129), the Spanish Research Project PSI2013-42091-P and the FP7-ICT BrainScales (n. 269921). D.M. was supported by a Sir Henry Dale Fellowship of the Wellcome Trust and the Royal Society (n. 101253/Z/13/Z), a Marie Curie Integration Grant of the European Commission (n. 2012-334039), the KU Leuven Special Research Fund (grant C16/15/070), and the Research Foundation Flanders (Pegasus incoming fellowship 12G9417N to MG). MG received funding from the FWO and European Union's Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie action (grant 665501). G.D., G.H and A.D. received support from the flagship Human Brain Project (n.604102). A.D was also supported by CNRS, UNIC, the foundation "Voir et Entendre" and Idex (NeuroSaclay). A.D.F. was funded by a grant from the European Research Council (ERC-2010-AdG 20100407, NEUROSYNTAX).

Background: The proteins S100B, neuron-specific enolase (NSE), glial fibrillary acidic protein (GFAP), ubiquitin carboxy-terminal hydrolase L1 (UCH-L1), and neurofilament light (NF-L) have been serially sampled in serum of patients suffering from traumatic brain injury (TBI) in order to assess injury severity and tissue fate. We review the current literature of serum level dynamics of these proteins following TBI and used the term "effective half-life" (t₁⁄₂) in order to describe the "fall" rate in serum. Materials and methods: Through searches on EMBASE, Medline, and Scopus, we looked for articles where these proteins had been serially sampled in serum in human TBI. We excluded animal studies, studies with only one presented sample and studies without neuroradiological examinations. Results: Following screening (10,389 papers), n = 122 papers were included. The proteins S100B (n = 66) and NSE (n = 27) were the two most frequent biomarkers that were serially sampled. For S100B in severe TBI, a majority of studies indicate a t₁⁄₂ of about 24 h, even if very early sampling in these patients reveals rapid decreases (1–2 h) though possibly of non-cerebral origin. In contrast, the t₁⁄₂ for NSE is comparably longer, ranging from 48 to 72 h in severe TBI cases. The protein GFAP (n = 18) appears to have t₁⁄₂ of about 24–48 h in severe TBI. The protein UCH-L1 (n = 9) presents a ₁⁄₂ around 7 h in mild TBI and about 10 h in severe. Frequent sampling of these proteins revealed different trajectories with persisting high serum levels, or secondary peaks, in patients with unfavorable outcome or in patients developing secondary detrimental events. Finally, NF-L (n = 2) only increased in the few studies available, suggesting a serum availability of >10 days. To date, automated assays are available for S100B and NSE making them faster and more practical to use. Conclusion: Serial sampling of brain-specific proteins in serum reveals different temporal trajectories that should be acknowledged. Proteins with shorter serum availability, like S100B, may be superior to proteins such as NF-L in detection of secondary harmful events when monitoring patients with TBI. ; ET: Swedish Society of Medicine (Grant no. SLS-587221). FZ: Cambridge Commonwealth Trust Scholarship, the Royal College of Surgeons of Canada—Harry S. Morton Travelling Fellowship in Surgery, the University of Manitoba Clinician Investigator Program, R. Samuel McLaughlin Research and Education Award, the Manitoba Medical Service Foundation, and the University of Manitoba Faculty of Medicine Dean's Fellowship Fund. AB: Hungarian Brain Research Program—Grant No. KTIA_13_NAP-A- II/8. DM: National Institute for Healthcare Research (NIHR, UK) through the Acute Brain Injury and Repair theme of the Cambridge NIHR Biomedical Research Centre, an NIHR Senior Investigator Award to DM. The authors were also supported by a European Union Framework Program 7 grant (CENTER-TBI; Grant Agreement No. 602150). AH: Medical Research Council, Cambridge Biomedical Research Centre, Royal College of Surgeons of England. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Functional connectivity (FC) sheds light on the interactions between different brain regions. Besides basic research, it is clinically relevant for applications in Alzheimer's disease, schizophrenia, presurgical planning, epilepsy, and traumatic brain injury. Simulations of whole-brain mean-field computational models with realistic connectivity determined by tractography studies enable us to reproduce with accuracy aspects of average FC in the resting state.Most computational studies, however, did not address the prominent non-stationarity in resting state FC, which may result in large intra- and inter-subject variability and thus preclude an accurate individual predictability. Herewe showthat this non-stationarity reveals a rich structure, characterized by rapid transitions switching between a few discrete FC states. We also show that computational models optimized to fit timeaveraged FC do not reproduce these spontaneous state transitions and, thus, are not qualitatively superior to simplified linear stochastic models, which account for the effects of structure alone. We then demonstrate that a slight enhancement of the non-linearity of the network nodes is sufficient to broaden the repertoire of possible network behaviors, leading to modes of fluctuations, reminiscent of some of themost frequently observed Resting State Networks. Because of the noise-driven exploration of this repertoire, the dynamics of FC qualitatively change now and display non-stationary switching similar to empirical resting state recordings (Functional Connectivity Dynamics (FCD)). Thus FCD bear promise to serve as a better biomarker of resting state neural activity and of its pathologic alterations. ; The research reported herein was supported by the Brain Network Recovery Group through the James S. McDonnell Foundation and funding from the European Union Seventh Framework Programme (FP7-ICT BrainScales and Human Brain Project (grant no. 60402)). DB was supported by the Marie Curie career development fellowship FP7-IEF 330792 (DynViB) and by the Federal Ministry of Education and Research (BMBF) Germany under grant number 01GQ1005B. We thank Patrick Hagmann and his group for providing the empirical data.

This article presents a glimpse into the literary writings emanating from a community that has, at best, remained at the margins of global South Asian diasporic literary scholarship: that of the Indian diaspora in Malaysia. It begins with a brief historical overview of the Malaysian Indian community together with an overview and cartography of Malaysian Indian writings. It then develops a comparative analysis of the representation of an issue quite central to Malaysian Indian identity politics, that of caste and class, in two novels: The Return by K.S. Maniam, an established Malaysian writer, and Evening Is the Whole Day by Preeta Samarasan, the newest writer to emerge from this community. The ultimate aim of this article is to show that if one steps closer to the canvas and look deeper at the representations of the community in literary texts that contextualize and individualize the Malaysian Indian experience, then intra-ethnic heterogeneity and conflicts within the diasporic community, as well as the forms of subaltern positioning, become visible, and they insistently reveal that such a community is as heterogeneous as its global counterparts.

Introductory Remarks -- 0 What is a Generator Like? -- I. Overview -- 1 DC Potentials of the Brain -- 2 Activity of Single Neurons and Their Relationship to Normal EEG Waves and Interictal Epilepsy Potentials in Humans -- II. Psychophysiology -- 3 Determinants of CNV Amplitude -- 4 Changes of Slow Brain Potential Shifts Following Failure -- 5 Association Cortex Contributions to the Human P3 -- 6 Interactions between the DC Potential of the Brain and Slow Potential Shifts under Mental Load -- 7 The "Oddball CNV" as Indicator of Information Processing in Healthy Subjects and Patients with Panic Disorders -- 8 Lateralization of Slow Brain Potentials and Preparatory Processes -- III. Neurophysiology -- 9 The Genesis of Cortical Event-Related Potentials: Excitatory and Inhibitory Contributions -- 10 Prolonged Unstable Depression: A Modified Manifestation of Spreading Depression in Rat Hippocampus -- 11 Modulation of Glutamate Responses by Noradrenaline and GABA in Neo- and Archicortical Structures -- 12 Extracellular Changes of Aspartate, Glutamate, and Taurine in Relation to DC Changes during Complete Cerebral Ischemia and Cortical Spreading Depression -- 13 Evoked Field Potentials—Beyond Correlates of Behavior: An Approach to Determining the Neural Mechanism of Behavior -- IV. Glia and Microenvironment -- 14 Cortical Slow Potentials, Depolarization of Glial Cells, and Extracellular Potassium Concentration -- 15 Voltage- and Ligand-Gated Membrane Currents of Identified Glial Cells in the Hippocampal Slice -- 16 Contributions of Extracellular Potassium Increases to Transient Field Potentials (Review of Data) -- 17 Cornea-Negative and Cornea-Positive Slow Components of the ERG and Light-induced Extracellular Potassium Changes -- V. Biomagnetism -- 18 Magnetoencephalographic Signals and Their Registration -- 19 Neuromagnetism and Source Location -- 20 Measurement of Neuromagnetic Signals -- 21 Extracranial Slow Magnetic Field Changes during Epileptic Activity -- VI. Motor Control -- 22 DC Shifts and Event-related Potentials Associated with Workload in a Dual Task Situation -- 23 Frontomesial Activation during Spatial Bilateral Coordination: Tentative Conclusions on SMA Function -- 24 Phasic and Tonic Changes of the Mean Alpha Frequency (MAF) of the EEG during Motor Performance -- 25 Changes of CNS Activation Patterns during Motor Imagination.

IntroductionEpstein‐Barr virus (EBV) viraemia is associated with nasopharyngeal carcinoma and lymphoproliferative diseases. In HIV‐1 infection, persistent EBV viraemia is a common phenomenon. The underlying mechanism of these high EBV DNA loads has not been clarified. We studied EBV viraemia during primary HIV‐1 infection (PHI) to explore the mechanism of EBV viraemia in HIV‐1 infection.MethodsPatients with PHI, participating in Primo‐SHM study, a clinical trial with three study arms: no treatment, 24 weeks of combination antiretroviral therapy (cART) and 60 weeks of cART, were sampled longitudinally during PHI and 24 and 48 weeks thereafter. EBV DNA was assayed by PCR on stored samples of lysed whole blood.Results39 patients were tested, in 22 of whom EBV DNA was detected at one or more time points. All patients tested positive for anti‐VCA and anti‐EBNA antibodies, most patients that had EBV viraemia did not receive cART or interrupted cART. The prevalence of EBV viraemia at baseline was 29%, 18% and 33% for the untreated, 24 weeks cART and continuous cART groups. At week 48, these percentages were 38, 64 and 17 respectively (p < 0.05). Individual concentrations of EBV DNA for the three groups are shown in Figure 1.The Black lines show the individual log10 transformed EBV DNA concentrations in whole blood in patients that remained untreated (panel a), patients that were treated for 24 weeks with cART (panel b) and patients that were treated continuously with cART (Panel c).imageConclusionIntermittent EBV viraemia is highly prevalent in patients with PHI. Assuming that patients with very early HIV‐1 infection are still immunocompetent, this indicates that EBV viraemia is not caused by immunodeficiency. Antiretroviral therapy started during PHI but not later during chronic HIV infection might reduce the prevalence of EBV viraemia in HIV‐1 infection.