rudyvdbrink/CitationDatabase huggingface dataset:
Seizures elevate gliovascular unit Ca2+ and cause sustained vasoconstriction.
JCI insight, 2020

Seizures can result in a severe hypoperfusion/hypoxic attack that causes postictal memory and behavioral impairments. However, neither postictal changes to microvasculature nor Ca2+ changes in key cell types controlling blood perfusion have been visualized in vivo, leaving essential components of the underlying cellular mechanisms unclear. Here, we use 2-photon microvascular and Ca2+ imaging in awake mice to show that seizures result in a robust vasoconstriction of cortical penetrating arterioles, which temporally mirrors the prolonged postictal hypoxia. The vascular effect was dependent on cyclooxygenase 2, as pretreatment with ibuprofen prevented postictal vasoconstriction. Moreover, seizures caused a rapid elevation in astrocyte endfoot Ca2+ that was confined to the seizure period, and vascular smooth muscle cells displayed a significant increase in Ca2+ both during and following seizures, lasting up to 75 minutes. Our data show enduring postictal vasoconstriction and temporal activities of 2 cell types within the neurovascular unit that are associated with seizure-induced hypoperfusion/hypoxia. These findings support prevention of this event may be a novel and tractable treatment strategy in patients with epilepsy who experience extended postseizure impairments.
Impact of Topiramate on Rat Phrenic Nerve-Hemidiaphragm Preparations.
Noro psikiyatri arsivi, 2017

Topiramate has a negative modulatory effect on voltage-gated ion channels involved in neuromuscular junction transmission. To investigate the potential impact of topiramate on muscle contraction, phrenic nerve-hemidiaphragm preparations were used as a neuromuscular junction model.
Insulin-like growth factor 2 (IGF2) protects against Huntington's disease through the extracellular disposal of protein aggregates.
Acta neuropathologica, 2020

Impaired neuronal proteostasis is a salient feature of many neurodegenerative diseases, highlighting alterations in the function of the endoplasmic reticulum (ER). We previously reported that targeting the transcription factor XBP1, a key mediator of the ER stress response, delays disease progression and reduces protein aggregation in various models of neurodegeneration. To identify disease modifier genes that may explain the neuroprotective effects of XBP1 deficiency, we performed gene expression profiling of brain cortex and striatum of these animals and uncovered insulin-like growth factor 2 (Igf2) as the major upregulated gene. Here, we studied the impact of IGF2 signaling on protein aggregation in models of Huntington's disease (HD) as proof of concept. Cell culture studies revealed that IGF2 treatment decreases the load of intracellular aggregates of mutant huntingtin and a polyglutamine peptide. These results were validated using induced pluripotent stem cells (iPSC)-derived medium spiny neurons from HD patients and spinocerebellar ataxia cases. The reduction in the levels of mutant huntingtin was associated with a decrease in the half-life of the intracellular protein. The decrease in the levels of abnormal protein aggregation triggered by IGF2 was independent of the activity of autophagy and the proteasome pathways, the two main routes for mutant huntingtin clearance. Conversely, IGF2 signaling enhanced the secretion of soluble mutant huntingtin species through exosomes and microvesicles involving changes in actin dynamics. Administration of IGF2 into the brain of HD mice using gene therapy led to a significant decrease in the levels of mutant huntingtin in three different animal models. Moreover, analysis of human postmortem brain tissue and blood samples from HD patients showed a reduction in IGF2 level. This study identifies IGF2 as a relevant factor deregulated in HD, operating as a disease modifier that buffers the accumulation of abnormal protein species.
Association of hypnotizability and deep sleep: any role for interoceptive sensibility?
Experimental brain research, 2020

The aim of the study was to investigate the possible association of hypnotizability and deep sleep (N3) duration, and whether the interoceptive sensibility influences this association. This was motivated by the proneness of highly hypnotizable individuals to easily change their psychophysiological state, i.e., from wakefulness to hypnosis and sleep, and by the positive association observed between hypnotizability and interoceptive sensibility. Forty-seven healthy participants previously enrolled in a polysomnographic night sleep study completed the questionnaire for Multidimensional Assessment of Interoceptive Awareness (MAIA) and underwent hypnotic assessment through the Stanford Hypnotic Susceptibility Scale, form A (SHSS,A). Results showed that N3 duration is not linearly correlated with hypnotizability. Controlling for a few MAIA scales did not modify the relation between hypnotizability and deep sleep. A polynomial relation indicates that N3 duration and N3 percentage of the total sleep time increase with hypnotizability in the low-to-medium range of hypnotizability and decrease in the medium-to-high range. In conclusion, hypnotic assessment predicts N3 duration and their association is not modified by interoceptive awareness/sensitivity.
Alertness fluctuations when performing a task modulate cortical evoked responses to transcranial magnetic stimulation.
NeuroImage, 2020

Transcranial magnetic stimulation (TMS) has been widely used in human cognitive neuroscience to examine the causal role of distinct cortical areas in perceptual, cognitive and motor functions. However, it is widely acknowledged that the effects of focal cortical stimulation can vary substantially between participants and even from trial to trial within individuals. Recent work from resting state functional magnetic resonance imaging (fMRI) studies has suggested that spontaneous fluctuations in alertness over a testing session can modulate the neural dynamics of cortical processing, even when participants remain awake and responsive to the task at hand. Here we investigated the extent to which spontaneous fluctuations in alertness during wake-to-sleep transition can account for the variability in neurophysiological responses to TMS. We combined single-pulse TMS with neural recording via electroencephalography (EEG) to quantify changes in motor and cortical reactivity with fluctuating levels of alertness defined objectively on the basis of ongoing brain activity. We observed rapid, non-linear changes in TMS-evoked responses with decreasing levels of alertness, even while participants remained responsive in the behavioural task. Specifically, we found that the amplitude of motor evoked potentials peaked during periods of EEG flattening, whereas TMS-evoked potentials increased and remained stable during EEG flattening and the subsequent occurrence of theta ripples that indicate the onset of NREM stage 1 sleep. Our findings suggest a rapid and complex reorganization of active neural networks in response to spontaneous fluctuations of alertness over relatively short periods of behavioural testing during wake-to-sleep transition.
Effects of restricted basilar papillar lesions and hair cell regeneration on auditory forebrain frequency organization in adult European starlings.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009

The frequency organization of neurons in the forebrain Field L complex (FLC) of adult starlings was investigated to determine the effects of hair cell (HC) destruction in the basal portion of the basilar papilla (BP) and of subsequent HC regeneration. Conventional microelectrode mapping techniques were used in normal starlings and in lesioned starlings either 2 d or 6-10 weeks after aminoglycoside treatment. Histological examination of the BP and recordings of auditory brainstem evoked responses confirmed massive loss of HCs in the basal portion of the BP and hearing losses at frequencies >2 kHz in starlings tested 2 d after aminoglycoside treatment. In these birds, all neurons in the region of the FLC in which characteristic frequencies (CFs) normally increase from 2 to 6 kHz had CF in the range of 2-4 kHz. The significantly elevated thresholds of responses in this region of altered tonotopic organization indicated that they were the residue of prelesion responses and did not reflect CNS plasticity. In the long-term recovery birds, there was histological evidence of substantial HC regeneration. The tonotopic organization of the high-frequency region of the FLC did not differ from that in normal starlings, but the mean threshold at CF in this frequency range was intermediate between the values in the normal and lesioned short-recovery groups. The recovery of normal tonotopicity indicates considerable stability of the topography of neuronal connections in the avian auditory system, but the residual loss of sensitivity suggests deficiencies in high-frequency HC function.
Examining the independent and joint effects of genomic and exposomic liabilities for schizophrenia across the psychosis spectrum.
Epidemiology and psychiatric sciences, 2020

Psychosis spectrum disorder has a complex pathoetiology characterised by interacting environmental and genetic vulnerabilities. The present study aims to investigate the role of gene-environment interaction using aggregate scores of genetic (polygenic risk score for schizophrenia (PRS-SCZ)) and environment liability for schizophrenia (exposome score for schizophrenia (ES-SCZ)) across the psychosis continuum.
Are we witnessing the swan song of neoliberalism?
MEDICC review, 2020

Dr José Ramón Acosta-Sariego is full professor of basic and preclinical scienc-es at the Medical University of Havana's Victoria de Girón Institute, where he also chairs the Scientifi c Research Ethics Committee. He serves as vice-chair of the Board of Directors of UNESCO's Latin American and Caribbean Bioethics Net-work (REDBioética) and in 2020, UNES-CO's Director-General appointed him to its 36-member International Bioethics Committee. Dr Acosta-Sariego has been academic coordinator for the bioethics master's degree program at the Univer-sity of Havana since its inception in 2006, is president of the Neuroethics Chapter of the Cuban Neurosciences Society and is a member of the Cuban National Bioeth-ics Committee.
Altered third-party punishment in Huntington's disease: A study using neuroeconomic games.
Brain and behavior, 2021

Huntington's disease (HD) is a heritable degenerative brain disease caused by a mutation in the huntingtin gene with excessive repeats of the base triplet cytosine-adenine-guanine (CAG), which codes for the aminoacid glutamine. HD is associated with a broad spectrum of neurocognitive dysfunction, including deficits in social cognition. The appreciation of fairness rules and reciprocity has not been studied in HD. Based on theoretical considerations suggesting that brain regions known to be affected from HD are involved in economic decision-making, the present study sought to examine HD patients' performance in two neuroeconomic games.
Energy Metabolism and Ketogenic Diets: What about the Skeletal Health? A Narrative Review and a Prospective Vision for Planning Clinical Trials on this Issue.
International journal of molecular sciences, 2021

The existence of a common mesenchymal cell progenitor shared by bone, skeletal muscle, and adipocytes cell progenitors, makes the role of the skeleton in energy metabolism no longer surprising. Thus, bone fragility could also be seen as a consequence of a "poor" quality in nutrition. Ketogenic diet was originally proven to be effective in epilepsy, and long-term follow-up studies on epileptic children undergoing a ketogenic diet reported an increased incidence of bone fractures and decreased bone mineral density. However, the causes of such negative impacts on bone health have to be better defined. In these subjects, the concomitant use of antiepileptic drugs and the reduced mobilization may partly explain the negative effects on bone health, but little is known about the effects of diet itself, and/or generic alterations in vitamin D and/or impaired growth factor production. Despite these remarks, clinical studies were adequately designed to investigate bone health are scarce and bone health related aspects are not included among the various metabolic pathologies positively influenced by ketogenic diets. Here, we provide not only a narrative review on this issue, but also practical advice to design and implement clinical studies on ketogenic nutritional regimens and bone health outcomes. Perspectives on ketogenic regimens, microbiota, microRNAs, and bone health are also included.
A randomised controlled comparison of serratus anterior plane, pectoral nerves and intercostal nerve block for post-thoracotomy analgesia in adult cardiac surgery.
Indian journal of anaesthesia, 2020

Enhanced recovery after cardiac surgery is centred around multimodal analgesia which is becoming increasingly feasible with the advent of safer regional analgesic techniques such as fascial plane blocks. We designed this prospective, single-blind, randomised controlled study to compare the efficacy of serratus anterior plane block (SAPB), pectoral nerves (Pecs) II block, and intercostal nerve block (ICNB) for post-thoracotomy analgesia in cardiac surgery.
Hemodynamic and behavioral peculiarities in response to emotional stimuli in children with attention deficit hyperactivity disorder: An fNIRS study.
Journal of affective disorders, 2020

Children with attention deficit hyperactivity disorder (ADHD) exhibit behavioral inhibition deficits, which often lead to emotional dysregulation (ED) affecting individual ability to control emotions and behavioral responses. In ADHD, ED is associated with poor outcomes and comorbidities, with both externalizing and internalizing disorders. This work aims to evaluate sensitivity to emotional stimuli in children with ADHD using functional Near Infrared Spectroscopy (fNIRS).
Report on the 5'th scientific meeting of the "Verein zur Förderung des Wissenschaftlichen Nachwuchses in der Neurologie" (NEUROWIND e.V.) held in Motzen, Germany, Oct. 25th - Oct. 27th, 2013.
Experimental & translational stroke medicine, 2013

From october 25th - 27th 2013, the 5th NEUROWIND e.V. meeting was held in Motzen, Brandenburg, Germany. This year more than 60 doctoral students and postdocs from over 25 different groups working in German university hospitals or research institutes attended the meeting to discuss their latest findings in the fields of neuroimmunology, neurodegeneration and neurovascular research. All participants appreciated the stimulating environment in Motzen, Brandenburg, and people took the opportunity for scientific exchange, discussion about ongoing projects and already started further collaborations. Like in the previous years, the symposium was regarded as a very well organized platform to support research of young investigators in Germany.According to the major aim of NEUROWIND e.V. to support younger researchers in Germany the 3rd NEUROWIND YOUNG SCIENTIST AWARD for experimental neurology was awarded to Ruth Stassart working in the group of Klaus Armin Nave and Wolfgang Brück (MPI Göttingen and Department of Neuropathology, Göttingen Germany). The successful work was published in Nature Neuroscience entitled "A role for Swann cell-derived neuregulin-1 in remyelination". This outstanding paper deals with the function of Schwann cell neuregulin as an endogenous factor for myelin repair. The award is endowed with 20.000 Euro sponsored by Merck Serono GmbH, Darmstadt, Germany (unrestricted educational grant).This year's keynote lecture was given by Albert Ludolph, Head of the Department of Neurology at the University Clinic of Ulm. Dr. Ludolph highlighted the particular role of individual scientists for the development of research concepts in Alzheimer´s disease (AD) and frontotemporal dementia (FTD).
Spatio-temporal feature learning with reservoir computing for T-cell segmentation in live-cell [Formula: see text] fluorescence microscopy.
Scientific reports, 2021

Advances in high-resolution live-cell [Formula: see text] imaging enabled subcellular localization of early [Formula: see text] signaling events in T-cells and paved the way to investigate the interplay between receptors and potential target channels in [Formula: see text] release events. The huge amount of acquired data requires efficient, ideally automated image processing pipelines, with cell localization/segmentation as central tasks. Automated segmentation in live-cell cytosolic [Formula: see text] imaging data is, however, challenging due to temporal image intensity fluctuations, low signal-to-noise ratio, and photo-bleaching. Here, we propose a reservoir computing (RC) framework for efficient and temporally consistent segmentation. Experiments were conducted with Jurkat T-cells and anti-CD3 coated beads used for T-cell activation. We compared the RC performance with a standard U-Net and a convolutional long short-term memory (LSTM) model. The RC-based models (1) perform on par in terms of segmentation accuracy with the deep learning models for cell-only segmentation, but show improved temporal segmentation consistency compared to the U-Net; (2) outperform the U-Net for two-emission wavelengths image segmentation and differentiation of T-cells and beads; and (3) perform on par with the convolutional LSTM for single-emission wavelength T-cell/bead segmentation and differentiation. In turn, RC models contain only a fraction of the parameters of the baseline models and reduce the training time considerably.
Massively parallel techniques for cataloguing the regulome of the human brain.
Nature neuroscience, 2020

Complex brain disorders are highly heritable and arise from a complex polygenic risk architecture. Many disease-associated loci are found in non-coding regions that house regulatory elements. These elements influence the transcription of target genes-many of which demonstrate cell-type-specific expression patterns-and thereby affect phenotypically relevant molecular pathways. Thus, cell-type-specificity must be considered when prioritizing candidate risk loci, variants and target genes. This Review discusses the use of high-throughput assays in human induced pluripotent stem cell-based neurodevelopmental models to probe genetic risk in a cell-type- and patient-specific manner. The application of massively parallel reporter assays in human induced pluripotent stem cells can characterize the human regulome and test the transcriptional responses of putative regulatory elements. Parallel CRISPR-based screens can further functionally dissect this genetic regulatory architecture. The integration of these emerging technologies could decode genetic risk into medically actionable information, thereby improving genetic diagnosis and identifying novel points of therapeutic intervention.
Proboscis Extension Reflex in 
Bio-protocol, 2017

The proboscis extension reflex (PER) is a common classical conditioned reflex which is widely used in the neurology and ethology. In honeybees, PER experiments can train bees to associate an odor with a reward or punishment. Here we present a variation of the PER experiment in
Spinal and Peripheral Mechanisms Individually Lead to the Development of Remifentanil-induced Hyperalgesia.
Neuroscience, 2020

The present study was performed to determine neuronal loci and individual molecular mechanisms responsible for remifentanil-induced hyperalgesia. The effect of methylnaltrexone (MNX) on remifentanil-induced behavioral hyperalgesia was assessed to distinguish contributions of the peripheral and/or central nervous system to remifentanil-induced hyperalgesia. Phosphorylation of p38 mitogen-activated protein kinase (p38MAPK) in the dorsal root ganglion (DRG) neurons after remifentanil infusion, and the effect of a p38MAPK inhibitor on remifentanil-induced hyperalgesia were analyzed to investigate involvement of p38MAPK in the peripheral mechanisms of remifentanil-induced hyperalgesia. Spinal levels of prodynorphin mRNA after remifentanil infusion, and the effect of the BK2 bradykinin receptor antagonist on remifentanil-induced hyperalgesia were investigated to assess potential spinal mechanisms. The effects of MNX and BK2 antagonists on remifentanil-induced exacerbation of post-incisional hyperalgesia were also investigated using behavioral analysis. Remifentanil infusion induced hyperalgesia in the early (4 h to 2 days) and late (8-14 days) post-infusion periods. MNX inhibited hyperalgesia only during the early post-infusion period. p38MAPK phosphorylation was observed in the DRG neuron, and the p38MAPK inhibitor inhibited hyperalgesia during the early post-infusion period. Prodynorphin expression increased in the spinal cord, and a BK2 antagonist inhibited hyperalgesia during the late post-infusion period. Remifentanil-induced exacerbation of incisional hyperalgesia was inhibited by MNX and the BK2 antagonist. The present study demonstrated that remifentanil activates peripheral and spinal neurons to promote chronologically distinctive hyperalgesia. p38MAPK phosphorylation in the DRG neuron leads to peripherally-driven hyperalgesia during the early post-infusion period, while spinal dynorphin-bradykinin signaling promotes hyperalgesia during the late post-infusion period.
Smartphone App to Address Loneliness Among College Students: Pilot Randomized Controlled Trial.
JMIR mental health, 2020

Loneliness is a widespread and significant problem on college campuses. Prolonged loneliness in young adulthood is a risk factor for concurrent and future mental health problems and attrition, making college a critical time for support. Cognitive and behavioral interventions show promise for decreasing loneliness and can be widely disseminated through technology.
Language comprehension in the social brain: Electrophysiological brain signals of social presence effects during syntactic and semantic sentence processing.
Cortex; a journal devoted to the study of the nervous system and behavior, 2020

Although, evolutionarily, language emerged predominantly for social purposes, much has yet to be uncovered regarding how language processing is affected by social context. Social presence research studies the ways in which the presence of a conspecific affects processing, but has yet to be thoroughly applied to language processes. The principal aim of this study was to see how syntactic and semantic language processing might be subject to mere social presence effects by studying Event-Related brain Potentials (ERP). In a sentence correctness task, participants read sentences with a semantic or syntactic anomaly while being either alone or in the mere presence of a confederate. Compared to the alone condition, the presence condition was associated with an enhanced N400 component and a more centro-posterior LAN component (interpreted as an N400). The results seem to imply a boosting of heuristic language processing strategies, proper of lexico-semantic operations, which actually entails a shift in the strategy to process morphosyntactic violations, typically based on algorithmic or rule-based strategies. The effects cannot be related to increased arousal levels. The apparent enhancement of the activity in the precuneus while in presence of another person suggests that the effects conceivably relate to social cognitive and attentional factors. The present results suggest that understanding language comprehension would not be complete without considering the impact of social presence effects, inherent to the most natural and fundamental communicative scenarios.