rudyvdbrink/CitationDatabase huggingface dataset:
Characterizing cerebral hemodynamics across the adult lifespan with arterial spin labeling MRI data from the Human Connectome Project-Aging.
NeuroImage, 2021

Arterial spin labeling (ASL) magnetic resonance imaging (MRI) has become a popular approach for studying cerebral hemodynamics in a range of disorders and has recently been included as part of the Human Connectome Project-Aging (HCP-A). Due to the high spatial resolution and multiple post-labeling delays, ASL data from HCP-A holds promise for localization of hemodynamic signals not only in gray matter but also in white matter. However, gleaning information about white matter hemodynamics with ASL is challenging due in part to longer blood arrival times in white matter compared to gray matter. In this work, we present an analytical approach for deriving measures of cerebral blood flow (CBF) and arterial transit times (ATT) from the ASL data from HCP-A and report on gray and white matter hemodynamics in a large cohort (n = 234) of typically aging adults (age 36-90 years). Pseudo-continuous ASL data were acquired with labeling duration = 1500 ms and five post-labeling delays = 200 ms, 700 ms, 1200, 1700 ms, and 2200 ms. ATT values were first calculated on a voxel-wise basis through normalized cross-correlation analysis of the acquired signal time course in that voxel and an expected time course based on an acquisition-specific Bloch simulation. CBF values were calculated using a two-compartment model and with age-appropriate blood water longitudinal relaxation times. Using this approach, we found that white matter CBF reduces (ρ = 0.39) and white matter ATT elongates (ρ = 0.42) with increasing age (p < 0.001). In addition, CBF is lower and ATTs are longer in white matter compared to gray matter across the adult lifespan (Wilcoxon signed-rank tests; p < 0.001). We also found sex differences with females exhibiting shorter white matter ATTs than males, independently of age (Wilcoxon rank-sum test; p < 0.001). Finally, we have shown that CBF and ATT values are spatially heterogeneous, with significant differences in cortical versus subcortical gray matter and juxtacortical versus periventricular white matter. These results serve as a characterization of normative physiology across the human lifespan against which hemodynamic impairment due to cerebrovascular or neurodegenerative diseases could be compared in future studies.
Detrimental effects of the 'bath salt' methylenedioxypyrovalerone on social play behavior in male rats.
Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2020

Methylenedioxypyrovalerone (MDPV) is the most popular synthetic cathinone found in products marketed as 'bath salts', widely abused among teenagers and young adults. Synthetic cathinones have pharmacological effects resembling those of psychostimulants, which are known to disrupt a variety of social behaviors. However, despite the popular use of MDPV by young people in social contexts, information about its effects on social behavior is scarce. To investigate the impact of MDPV on social behavior at young age, and the underlying neurobehavioral mechanisms, we focused on social play behavior. Social play behavior is the most characteristic social behavior displayed by young mammals and it is crucial for neurobehavioral development. Treatment with MDPV reduced social play behavior in both juvenile and young adult male rats, and its play-suppressant effect was subject to tolerance but not sensitization. As the behavioral effects of MDPV have been ascribed to dopaminergic and noradrenergic neurotransmission, and given the role of these neurotransmitters in social play, we investigated the involvement of dopamine and noradrenaline in the play-suppressant effects of MDPV. The effects of MDPV on social play were blocked by either the α2 adrenoceptor antagonist RX821002 or the dopamine receptor antagonist flupenthixol, given alone or together at sub-effective doses. In sum, MDPV selectively suppresses the most vigorous social behavior of developing rats through both noradrenergic and dopaminergic mechanisms. This study provides important preclinical evidence of the deleterious effects of MDPV on social behavior, and as such increases our understanding of the neurobehavioral effects of this popular cathinone.
Motor Function in the Late Phase After Stroke: Stroke Survivors' Perspective.
Annals of rehabilitation medicine, 2020

To examine the association between observer-assessed functional status and perceived recovery in the late phase after stroke. The study also aimed to determine whether observer-assessed functional improvements as a result of horse-riding therapy (H-RT) are related to enhanced perception of stroke recovery.
Behavioral and oculomotor evidence for visual simulation of object movement.
Journal of vision, 2019

We regularly interact with moving objects in our environment. Yet, little is known about how we extrapolate the future movements of visually perceived objects. One possibility is that movements are experienced by a mental visual simulation, allowing one to internally picture an object's upcoming motion trajectory, even as the object itself remains stationary. Here we examined this possibility by asking human participants to make judgments about the future position of a falling ball on an obstacle-filled display. We found that properties of the ball's trajectory were highly predictive of subjects' reaction times and accuracy on the task. We also found that the eye movements subjects made while attempting to ascertain where the ball might fall had significant spatiotemporal overlap with those made while actually perceiving the ball fall. These findings suggest that subjects simulated the ball's trajectory to inform their responses. Finally, we trained a convolutional neural network to see whether this problem could be solved by simple image analysis as opposed to the more intricate simulation strategy we propose. We found that while the network was able to solve our task, the model's output did not effectively or consistently predict human behavior. This implies that subjects employed a different strategy for solving our task, and bolsters the conclusion that they were engaging in visual simulation. The current study thus provides support for visual simulation of motion as a means of understanding complex visual scenes and paves the way for future investigations of this phenomenon at a neural level.
Pain phenotypes classified by machine learning using electroencephalography features.
NeuroImage, 2020

Pain is a multidimensional experience mediated by distributed neural networks in the brain. To study this phenomenon, EEGs were collected from 20 subjects with chronic lumbar radiculopathy, 20 age and gender matched healthy subjects, and 17 subjects with chronic lumbar pain scheduled to receive an implanted spinal cord stimulator. Analysis of power spectral density, coherence, and phase-amplitude coupling using conventional statistics showed that there were no significant differences between the radiculopathy and control groups after correcting for multiple comparisons. However, analysis of transient spectral events showed that there were differences between these two groups in terms of the number, power, and frequency-span of events in a low gamma band. Finally, we trained a binary support vector machine to classify radiculopathy versus healthy subjects, as well as a 3-way classifier for subjects in the 3 groups. Both classifiers performed significantly better than chance, indicating that EEG features contain relevant information pertaining to sensory states, and may be used to help distinguish between pain states when other clinical signs are inconclusive.
A population-based study of head injury, cognitive function and pathological markers.
Annals of clinical and translational neurology, 2021

To assess associations between head injury (HI) with loss of consciousness (LOC), ageing and markers of later-life cerebral pathology; and to explore whether those effects may help explain subtle cognitive deficits in dementia-free individuals.
History of the Nordic psychiatric cooperation.
Nordic journal of psychiatry, 2012

The Nordic countries include Denmark, Finland, Iceland, Norway and Sweden as well the Faroe Islands, Greenland, Svalbard and Åland. The countries share much common history as well as common traits in their respective societies. As early as 1906, a Scandinavian Psychiatric Association was suggested. The first Nordic Psychiatric Congress was held in Copenhagen 1913. After the First World War, at the 6th Nordic Psychiatric Congress in Stockholm 1935, a Nordic Psychiatric Association was founded and it was decided that a Nordic Journal of Psychiatry should be founded. After the Second World War, at the 8th Nordic Psychiatric Congress in Copenhagen 1946, the Nordic Psychiatric Association was terminated. At this time, the most important task of the Association, to found a Nordic Journal of Psychiatry, had been achieved. After 1946, there has been a close cooperation between the Nordic countries but no common Nordic Psychiatric Association. Today, the Nordic Psychiatric Cooperation is active and ongoing. The 30th Nordic Psychiatric Congress is scheduled to be held in Tromsö, in 2012. The Nordic Journal of Psychiatry is publishing its 64 th volume. The Journal is indexed in the important international databases and the impact factor is increasing. The Joint Committee of the Nordic psychiatric associations has established itself as the owner of the Journal and the organizer of the congresses. There are also a series of Nordic cooperations in a series of different fields, such as the Scandinavian Societies of Biological Psychiatry, the Scandinavian College of Neuropsychopharmacology (SCNP), the bi-annual Nordic Psychoanalytical Congresses, the Scandinavian Psychoanalytic Review, the Nordic Association of Psychiatric Epidemiology, NAPE, and so on.
Targeted immunotherapy trials for idiopathic inflammatory myopathies.
Journal of neurology, 2013

The idiopathic inflammatory myopathies (IIM) are a group of muscle diseases with complex immunopathogenesis that varies between disease subgroups, and possibly between patients within the same subgroup. There exists no universal consensus on optimum management, so that no "standard" therapy has been developed. Treatment-refractive IIM remains a clinical challenge. Progress in the development and application of molecular biology techniques and biological therapeutics are evolving into a new scientific frontier in the management of autoimmune diseases. This review offers an update on those components of the humoral and cellular immunity deemed potential targets for biological therapeutics (monoclonal antibodies and fusion proteins) that have been approved by the US FDA for treatment of immunological disorders. A futuristic approach is envisioned in which each individual will receive targeted therapy tailored to patient-specific immune mechanisms. Risk-benefit and cost analyses should determine whether such targeted therapy is appropriate and feasible for refractive and/or newly diagnosed disease.
The Critical Role of Peripheral Targets in Triggering Rapid Neural Effects of Intravenous Cocaine.
Neuroscience, 2020

Direct interaction of cocaine with centrally located monoamine transporters is the primary mechanism underlying its reinforcing properties. It is also often assumed that this drug action is responsible for all the physiological and behavioral effects of this drug. The goal of this review is to challenge this basic mechanism and demonstrate the importance of peripheral actions of cocaine in inducing its initial, rapid neural effects. The use of high-resolution electrophysiological, neurochemical and physiological techniques revealed that the effects of intravenous cocaine at behaviorally relevant doses are exceptionally rapid and transient correlating with strong, quick, and transient increases in blood cocaine levels. Some of these effects are mimicked by cocaine-methiodide, a cocaine analog that cannot cross the blood-brain barrier and they are resistant to dopamine (DA) receptor blockade. Therefore, it appears that rapid neural effects of cocaine result from its direct interaction with receptive sites on afferents of sensory nerves densely innervating blood vessels. This interaction creates a rapid neural signal to the CNS that results in generalized neural activation and subsequent changes in different physiological parameters. This drug's action appears to be independent from cocaine's action on central neurons, which requires a definite time to occur and induce neural and physiological effects with longer latencies and durations. The co-existence in the same drug on two timely distinct actions with their subsequent interaction in the CNS could explain consistent changes in physiological and behavioral effects of cocaine following their repeated use, playing a role in the development of drug-seeking and drug-taking behavior.
Anosognosia for theory of mind deficits: A single case study and a review of the literature.
Neuropsychologia, 2020

Being aware of one's own ability to interact socially is crucial to everyday life. After a brain injury, patients may lose their capacity to understand others' intentions and beliefs, that is, the Theory of Mind (ToM). To date, the debate on the association between ToM and other cognitive deficits (in particular executive functions and behavioural disorders) remains open and data regarding awareness of ToM deficits are meagre. By means of an ad-hoc neuropsychological battery of tests, we report on a patient who suffers from ToM deficits and is not aware of these disorders, although aware of his other symptoms. The study is accompanied by a review of the literature (PRISMA guidelines) demonstrating that ToM deficits are independent of executive functions. Furthermore, an advanced lesion analysis including tractography was executed. The results indicate that: i) ToM deficits can be specific and independent of other cognitive symptoms; ii) unawareness may be specific for ToM impairment and not involve other disorders and iii) the medial structures of the limbic, monitoring and attentional systems may be involved in anosognosia for ToM impairment.
Group II metabotropic glutamate receptor activation in the basolateral amygdala mediates individual differences in stress-induced changes in rapid eye movement sleep.
Progress in neuro-psychopharmacology & biological psychiatry, 2021

Group II metabotropic glutamate receptors (mGluR2/3s) have been implicated in stress and trauma related disorders including post-traumatic stress disorder (PTSD). PTSD is characterized by flashbacks, anxiety, and sleep disturbances. While many people are exposed to trauma in their lifetime, only a small percentage go on to develop PTSD, indicating individual differences in stress and emotional processing. Wistar strain rats display directionally different rapid-eye movement sleep (REM) responses to footshock stress, with resilient rats having no change or an increase in REM and vulnerable rats having a significant reduction in REM compared to baseline. The basolateral nucleus of the amygdala (BLA) is key in regulating individual differences in stress-induced alterations in sleep. Group II metabotropic glutamate receptors (mGluR2/3s) negatively modulate glutamate and are implicated in fear, fear memory, and sleep. The current study evaluated the effect of mGluR2/3 agonist LY379268 (LY37) in BLA on stress and fear memory induced changes in sleep, EEG spectra, behavioral fear expression and physiological stress. These data indicate that vulnerable rats treated with LY37 have an attenuation of the REM reductions generally seen in vulnerable rats. Furthermore, LY37 altered EEG spectra in the delta (0.5-4.5 Hz) and theta (5-9.5 Hz) frequency. LY37 did not impact behavioral fear expression or physiological stress. Therefore, mGluR2/3s within BLA are implicated in regulating individual differences in sleep responses to fear- and stress-related memories.
Ghrelin Signaling Affects Feeding Behavior, Metabolism, and Memory through the Vagus Nerve.
Current biology : CB, 2020

Vagal afferent neuron (VAN) signaling sends information from the gut to the brain and is fundamental in the control of feeding behavior and metabolism [1]. Recent findings reveal that VAN signaling also plays a critical role in cognitive processes, including affective motivational behaviors and hippocampus (HPC)-dependent memory [2-5]. VANs, located in nodose ganglia, express receptors for various gut-derived peptide signals; however, the function of these receptors with regard to feeding behavior, metabolism, and memory control is poorly understood. We hypothesized that VAN-mediated processes are influenced by ghrelin, a stomach-derived orexigenic hormone, via communication to its receptor (GHSR) expressed on gut-innervating VANs. To examine this hypothesis, rats received nodose ganglia injections of an adeno-associated virus (AAV) expressing short hairpin RNAs targeting GHSR (or a control AAV) for RNAi-mediated VAN-specific GHSR knockdown. Results reveal that VAN GHSR knockdown induced various feeding and metabolic disturbances, including increased meal frequency, impaired glucose tolerance, delayed gastric emptying, and increased body weight compared to controls. Additionally, VAN-specific GHSR knockdown impaired HPC-dependent contextual episodic memory and reduced HPC brain-derived neurotrophic factor expression, but did not affect anxiety-like behavior or general activity levels. A functional role for endogenous VAN GHSR signaling was further confirmed by results revealing that VAN signaling is required for the hyperphagic effects of ghrelin administered at dark onset, and that gut-restricted ghrelin-induced increases in VAN firing rate require intact VAN GHSR expression. Collective results reveal that VAN GHSR signaling is required for both normal feeding and metabolic function as well as HPC-dependent memory.
Sympathetic nervous system dominance during stress recovery mediates associations between stress sensitivity and social anxiety symptoms in female adolescents.
Development and psychopathology, 2020

Social anxiety disorder (SAD) is commonly diagnosed during adolescence and is associated with psychological stress reactivity and heightened physiological arousal. No study, however, has systematically examined which aspects of autonomic nervous system function mediate likely links between stress sensitivity and social anxiety symptoms in adolescents. Here, we assessed 163 adolescents (90 females; 12.29 ± 1.39 years) with respect to life stress and social anxiety symptoms, and measured respiratory sinus arrhythmia (RSA) and skin conductance levels (SCL) during a psychosocial stress paradigm. We operationalized stress sensitivity as the residual variance in subjective stress severity after accounting for objective severity and changes in autonomic regulation using standardized change scores in RSA and SCL. In females only, stress sensitivity and social anxiety symptoms were significantly correlated with each other (p < .001) and with autonomic regulation during both reactivity and recovery (all ps < 0.04). Further, sympathetic nervous system dominance during recovery specifically mediated associations between stress sensitivity and social anxiety symptoms (B = 1.06, 95% CI: 0.02-2.64). In contrast, in males, stress sensitivity, autonomic regulation during reactivity or recovery, and social anxiety symptoms were not significantly associated (all ps > 0.1). We interpret these results in the context of psychobiological models of SAD and discuss implications for interventions targeting autonomic processes.
The Impact of Physical Enrichment in the Structure of the Medial Prefrontal Cortex and Nucleus Accumbens of the Adult Male Rat Brain.
Neuroscience, 2021

Rodents' behavioural analysis can be influenced by several factors, including housing. The PhenoWorld (PhW) is an enriched housing and testing paradigm, which proved to be relevant for screening depressive-like behaviours in rats, being remarkably sensitive for hedonic behaviour. Herein, we assessed neuronal plasticity as a consequence of living in the PhW, by comparing the structure of the medial prefrontal cortex (mPFC) and the nucleus accumbens (NAc), two brain areas involved in the circuitry regulating motivation and reward. Our findings indicate that male rats living in the PhW display increased mPFC layer II volumes, as well as increased immature spine densities and total numbers in the mPFC pyramidal neurons. The NAc volumes and NAc medium spiny neurons branching tend also to be higher in animals experiencing the physical enrichment provided in the PhW, but significant differences were not found between animals living in PhW compared to animals living in standard cages (STD6). These results demonstrate that living in a more naturalistic complex environment, closer to real life experience, impacts on the structure of brain regions implicated in complex multidimensional disorders.
Down syndrome cell adhesion molecule like-1 (DSCAML1) links the GABA system and seizure susceptibility.
Acta neuropathologica communications, 2020

The Ihara epileptic rat (IER) is a mutant model with limbic-like seizures whose pathology and causative gene remain elusive. In this report, via linkage analysis, we identified Down syndrome cell adhesion molecule-like 1(Dscaml1) as the responsible gene for IER. A single base mutation in Dscaml1 causes abnormal splicing, leading to lack of DSCAML1. IERs have enhanced seizure susceptibility and accelerated kindling establishment. Furthermore, GABAergic neurons are severely reduced in the entorhinal cortex (ECx) of these animals. Voltage-sensitive dye imaging that directly presents the excitation status of brain slices revealed abnormally persistent excitability in IER ECx. This suggests that reduced GABAergic neurons may cause weak sustained entorhinal cortex activations, leading to natural kindling via the perforant path that could cause dentate gyrus hypertrophy and epileptogenesis. Furthermore, we identified a single nucleotide substitution in a human epilepsy that would result in one amino acid change in DSCAML1 (A2105T mutation). The mutant DSCAML1
Strategies for Cancer Immunotherapy Using Induced Pluripotency Stem Cells-Based Vaccines.
Cancers, 2020

Despite improvements in cancer therapy, metastatic solid tumors remain largely incurable. Immunotherapy has emerged as a pioneering and promising approach for cancer therapy and management, and in particular intended for advanced tumors unresponsive to current therapeutics. In cancer immunotherapy, components of the immune system are exploited to eliminate cancer cells and treat patients. The recent clinical successes of immune checkpoint blockade and chimeric antigen receptor T cell therapies represent a turning point in cancer treatment. Despite their potential success, current approaches depend on efficient tumor antigen presentation which are often inaccessible, and most tumors turn refractory to current immunotherapy. Patient-derived induced pluripotent stem cells (iPSCs) have been shown to share several characteristics with cancer (stem) cells (CSCs), eliciting a specific anti-tumoral response when injected in rodent cancer models. Indeed, artificial cellular reprogramming has been widely compared to the biogenesis of CSCs. Here, we will discuss the state-of-the-art on the potential implication of cellular reprogramming and iPSCs for the design of patient-specific immunotherapeutic strategies, debating the similarities between iPSCs and cancer cells and introducing potential strategies that could enhance the efficiency and therapeutic potential of iPSCs-based cancer vaccines.