rudyvdbrink/CitationDatabase huggingface dataset:
Visual field improvement in neglect after virtual reality intervention: a single-case study.
Neurocase, 2021

A patient suffering from visuo-spatial neglect was investigated as a special interest case during a study on the effectiveness of "restorative approaches" after visual field loss. This patient trained with our newly developed Virtual Reality (VR) system "Salzburg Visual Field Trainer" for 254 days. Perimetric results show a visual field expansion of 48.8% (left eye) and 36.8% (right eye) translating to an improvement of approximately 5.5° to 10.5° of visual angle. Further, subjective self-report shows improvements of up to 317% in visual field functionality. Our results indicate that patients suffering from visuo-spatial neglect could benefit from a VR-based restorative intervention.
The Transition from Evaluation to Selection Involves Neural Subspace Reorganization in Core Reward Regions.
Neuron, 2020

Economic choice proceeds from evaluation, in which we contemplate options, to selection, in which we weigh options and choose one. These stages must be differentiated so that decision makers do not proceed to selection before evaluation is complete. We examined responses of neurons in two core reward regions, orbitofrontal (OFC) and ventromedial prefrontal cortex (vmPFC), during two-option choice with asynchronous offer presentation. Our data suggest that neurons selective during the first (presumed evaluation) and second (presumed comparison and selection) offer epochs come from a single pool. Stage transition is accompanied by a shift toward orthogonality in the low-dimensional population response manifold. Nonetheless, the relative position of each option in driving responses in the population subspace is preserved. The orthogonalization we observe supports the hypothesis that the transition from evaluation to selection leads to reorganization of response subspace and suggests a mechanism by which value-related signals are prevented from prematurely driving choice.
Resveratrol promotes the arcuate nucleus architecture remodeling to produce more anorexigenic neurons in high-fat-diet-fed mice.
Nutrition (Burbank, Los Angeles County, Calif.), 2018

Adult hypothalamic neurogenesis has been considered a central regulator of energy balance. Resveratrol (RSV), a natural polyphenol, influences the body fat mass and reduces the amount of adipose tissue. The present study was designed to evaluate the effect of RSV on dynamic of hypothalamic neurons in a diet-induced obesity model of mice.
Rgma-Induced Neo1 Proteolysis Promotes Neural Tube Morphogenesis.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019

Neuroepithelial cell (NEC) elongation is one of several key cell behaviors that mediate the tissue-level morphogenetic movements that shape the neural tube (NT), the precursor of the brain and spinal cord. However, the upstream signals that promote NEC elongation have been difficult to tease apart from those regulating apico-basal polarity and hingepoint formation, due to their confounding interdependence. The Repulsive Guidance Molecule a (Rgma)/Neogenin 1 (Neo1) signaling pathway plays a conserved role in NT formation (neurulation) and is reported to regulate both NEC elongation and apico-basal polarity, through signal transduction events that have not been identified. We examine here the role of Rgma/Neo1 signaling in zebrafish (sex unknown), an organism that does not use hingepoints to shape its hindbrain, thereby enabling a direct assessment of the role of this pathway in NEC elongation. We confirm that Rgma/Neo1 signaling is required for microtubule-mediated NEC elongation, and demonstrate via cell transplantation that Neo1 functions cell autonomously to promote elongation. However, in contrast to previous findings, our data do not support a role for this pathway in establishing apical junctional complexes. Last, we provide evidence that Rgma promotes Neo1 glycosylation and intramembrane proteolysis, resulting in the production of a transient, nuclear intracellular fragment (NeoICD). Partial rescue of Neo1a and Rgma knockdown embryos by overexpressing
Audio-visual synchrony and spatial attention enhance processing of dynamic visual stimulation independently and in parallel: A frequency-tagging study.
NeuroImage, 2017

The neural processing of a visual stimulus can be facilitated by attending to its position or by a co-occurring auditory tone. Using frequency-tagging, we investigated whether facilitation by spatial attention and audio-visual synchrony rely on similar neural processes. Participants attended to one of two flickering Gabor patches (14.17 and 17 Hz) located in opposite lower visual fields. Gabor patches further "pulsed" (i.e. showed smooth spatial frequency variations) at distinct rates (3.14 and 3.63 Hz). Frequency-modulating an auditory stimulus at the pulse-rate of one of the visual stimuli established audio-visual synchrony. Flicker and pulsed stimulation elicited stimulus-locked rhythmic electrophysiological brain responses that allowed tracking the neural processing of simultaneously presented Gabor patches. These steady-state responses (SSRs) were quantified in the spectral domain to examine visual stimulus processing under conditions of synchronous vs. asynchronous tone presentation and when respective stimulus positions were attended vs. unattended. Strikingly, unique patterns of effects on pulse- and flicker driven SSRs indicated that spatial attention and audiovisual synchrony facilitated early visual processing in parallel and via different cortical processes. We found attention effects to resemble the classical top-down gain effect facilitating both, flicker and pulse-driven SSRs. Audio-visual synchrony, in turn, only amplified synchrony-producing stimulus aspects (i.e. pulse-driven SSRs) possibly highlighting the role of temporally co-occurring sights and sounds in bottom-up multisensory integration.
In Vitro Optogenetic Characterization of Neuropeptide Release from Prefrontal Cortical Somatostatin Neurons.
Neuroscience, 2019

Somatostatin is a neuropeptide thought to play a role in a variety of neuropsychiatric disorders, and is important for healthy aging and behavioral resiliency. Physiological conditions underlying somatostatin peptidergic release are not well-defined. Using a combination of optogenetic and biochemical approaches in transgenic mice, we demonstrate an assay for the induction and inhibition of somatostatin release in mouse acute brain slices.
The ovarian hormone estradiol plays a crucial role in the control of food intake in females.
Physiology & behavior, 2011

Despite a strong male bias in both basic and clinical research, it is becoming increasingly accepted that the ovarian hormone estradiol plays an important role in the control of food intake in females. Estradiol's feeding inhibitory effect occurs in a variety of species, including women, but the underlying mechanism has been studied most extensively in rats and mice. Accordingly, much of the data reviewed here is derived from the rodent literature. Adult female rats display a robust decrease in food intake during estrus and ovariectomy promotes hyperphagia and weight gain, both of which can be prevented by a physiological regimen of estradiol treatment. Behavioral analyses have demonstrated that the feeding inhibitory effect of estradiol is mediated entirely by a decrease in meal size. In rats, estradiol appears to exert this action indirectly via interactions with peptide and neurotransmitter systems implicated in the direct control of meal size. Here, I summarize research examining the neurobiological mechanism underlying estradiol's anorexigenic effect. Central estrogen receptors (ERs) have been implicated and activation of one ER subtype in particular, ERα, appears both sufficient and necessary for the estrogenic control of food intake. Future studies are necessary to identify the critical brain areas and intracellular signaling pathways responsible for estradiol's anorexigenic effect. A clearer understanding of the estrogenic control of food intake is prerequisite to elucidating the biological factors that contribute to obesity and eating disorders, both of which are more prevalent in women, compared to men.
The structure of semantic representation shapes controlled semantic retrieval.
Memory (Hove, England), 2021

An essential aim in the research on semantic cognition is to understand the interplay between the structure of semantic representation and controlled processes that operate on it to generate flexible behaviours. To evaluate the link between semantic network connectivity and semantic control functions (semantic inhibition and switching), we employed a network theory approach and revealed that controlled semantic processing was reliably associated with connectivity of conceptual representation. In particular, our results show that efficient information flow afforded by high connectivity of semantic network is coupled with superior switching but poor inhibition ability. These findings suggest that the network architectures that facilitate efficient semantic activation spreading aid flexible transitions between semantic clusters but impede inhibition employed to suppress inappropriate or interfering semantic representations. Overall, our study provides a novel insight into the mechanisms underlying controlled semantic processing that is recruited to disentangle from habitual structure of semantic representation.
EEG/fMRI contributions to our understanding of genetic generalized epilepsies.
Epilepsy & behavior : E&B, 2014

The first reports of combined EEG and fMRI used for evaluation of epileptic spikes date back to the mid-90s. At that time, the technique was called EEG-triggered fMRI--the "triggered" corresponded to an epilepsy specialist reviewing live EEG while the patient was located in the scanner; after the spike was identified, a scan was initiated to collect the data. Since then major progress has been made in combined EEG/fMRI data collection and analyses. These advances allow studying the electrophysiology of genetic generalized epilepsies (GGEs) in vivo in greater detail than ever. In addition to continuous data collection, we now have better methods for removing physiologic and fMRI-related artifacts, more advanced understanding of the hemodynamic response functions, and better computational methods to address the questions regarding the origins of the epileptiform discharge generators in patients with GGEs. These advances have allowed us to examine numerous cohorts of children and adults with GGEs while not only looking for spike and wave generators but also examining specific types of GGEs (e.g., juvenile myoclonic epilepsy or childhood absence epilepsy), drug-naïve patients, effects of medication resistance, or effects of epileptiform abnormalities and/or seizures on brain connectivity. While the discussion is ongoing, the prevailing thought is that the GGEs as a group are a network disorder with participation from multiple nodes including the thalami and cortex with the clinical presentation depending on which node of the participating network is affected by the disease process. This review discusses the contributions of EEG/fMRI to our understanding of GGEs.
How reliable is ictal duration to differentiate psychogenic nonepileptic seizures from epileptic seizures?
Epilepsy & behavior : E&B, 2017

We sought to investigate (1) differences in ictal duration between psychogenic nonepileptic seizures (PNES) and epileptic seizures (ES), (2) the odds of being PNES when seizures last ≥5min, and (3) the value of ictal duration as a diagnostic test to differentiate PNES from ES. We retrospectively reviewed video-EEG recordings and tabulated ictal durations of all PNES and ES. We estimated the mean ictal durations of PNES and ES using linear mixed models. The odds of being PNES when seizures last ≥5min were estimated using logistic regression. We used receiver operating characteristics (ROC) curves to study the overall diagnostic accuracy of ictal duration in differentiating PNES from ES. We studied 441 ES and 341 PNES recorded from 138 patients. The mean ictal duration of PNES (148.7s, 95% CI: 115.2-191.8) was significantly longer (p<0.001) than that of ES (47.7s, 95% CI: 37.6-60.6). The odds of being PNES was about 24 times higher (Odds ratio: 23.8, 95% CI: 7.9-71.3) when the ictal duration was ≥5min. The ROC curve yielded an area under the curve of 0.80 (95% CI 0.73-0.88). Youden's index identified 123.5s as the optimal threshold to diagnose PNES with 65% sensitivity and 93% specificity. Our results indicate that ictal duration is a useful test to raise suspicion of PNES. When a seizure lasts ≥5min, it is 24 times more likely to be PNES with the potential risk of misdiagnosis as status epilepticus.
External Validation of Scoring Models to Predict Shunt Insertion after Aneurysmal Subarachnoid Hemorrhage.
World neurosurgery, 2021

The current study is an external validation of 4 scoring models proposed in the literature for predicting ventriculoperitoneal shunt insertion after aneurysmal subarachnoid hemorrhage (aSAH) using retrospective patient data from Sheffield Teaching Hospital (STH).
Phosphorylation of the cryptochrome 1 C-terminal tail regulates circadian period length.
The Journal of biological chemistry, 2013

The Cryptochrome (CRY) proteins are critical components of the mammalian circadian clock and act to rhythmically repress the activity of the transcriptional activators CLOCK and BMAL1 at the heart of the clock mechanism. The CRY proteins are part of a large repressive complex, the components of which are not completely known. Using mass spectroscopy, we identified the catalytic subunit of DNA-dependent protein kinase as a CRY-interacting protein and found that loss or inhibition of this kinase results in circadian rhythms with abnormally long periods. We then identified serine 588 in the C-terminal tail of mouse CRY1 as a potential DNA-PK phosphorylation site but surprisingly found that the phosphomimetic mutation S588D also results in long period rhythms, similar to the loss of DNA-PK. Consistent with this, we found that phosphorylation of this site is increased in cells lacking DNA-PK, suggesting that DNA-PK negatively regulates the phosphorylation of this site most likely through indirect means. Furthermore, we found that phosphorylation of this site increases the stability of the CRY1 protein and prevents FBXL3-mediated degradation. The phosphorylation of this site is robustly rhythmic in mouse liver nuclei, peaking in the middle of the circadian day at a time when CRY1 levels are declining. Therefore, these data suggest a new role for the C-terminal tail of CRY1 in which phosphorylation rhythmically regulates CRY1 stability and contributes to the proper circadian period length.
Prediction of motor outcome based on diffusion tensor tractography findings in thalamic hemorrhage.
The International journal of neuroscience, 2013

Little is known about the usefulness of diffusion tensor tractography (DTT) findings of the corticospinal tract (CST) in terms of predicting motor outcome after thalamic hemorrhage. We investigated the predictive value of DTT for motor outcome in patients with thalamic hemorrhage.
Pharmacological convergence reveals a lipid pathway that regulates C. elegans lifespan.
Nature chemical biology, 2019

Phenotypic screening has identified small-molecule modulators of aging, but the mechanism of compound action often remains opaque due to the complexities of mapping protein targets in whole organisms. Here, we combine a library of covalent inhibitors with activity-based protein profiling to coordinately discover bioactive compounds and protein targets that extend lifespan in Caenorhabditis elegans. We identify JZL184-an inhibitor of the mammalian endocannabinoid (eCB) hydrolase monoacylglycerol lipase (MAGL or MGLL)-as a potent inducer of longevity, a result that was initially perplexing as C. elegans does not possess an MAGL ortholog. We instead identify FAAH-4 as a principal target of JZL184 and show that this enzyme, despite lacking homology with MAGL, performs the equivalent metabolic function of degrading eCB-related monoacylglycerides in C. elegans. Small-molecule phenotypic screening thus illuminates pure pharmacological connections marking convergent metabolic functions in distantly related organisms, implicating the FAAH-4/monoacylglyceride pathway as a regulator of lifespan in C. elegans.
Clozapine-induced gastroesophageal rumination in 22q11.2 Deletion Syndrome. A case report on gastroesophageal side effects management without renouncing clozapine's effectiveness.
Clinical case reports, 2021

Despite entailing more severe and uncommon side effects in 22q11.2DS compared to idiopathic schizophrenia, we strongly believe that clozapine should continue to be considered the gold standard for all treatment-resistant schizophrenia, even in 22qDS.
Transgenic mouse models for studying adult neurogenesis.
Frontiers in biology, 2016

The mammalian hippocampus shows a remarkable capacity for continued neurogenesis throughout life. Newborn neurons, generated by the radial neural stem cells (NSCs), are important for learning and memory as well as mood control. During aging, the number and responses of NSCs to neurogenic stimuli diminish, leading to decreased neurogenesis and age-associated cognitive decline and psychiatric disorders. Thus, adult hippocampal neurogenesis has garnered significant interest because targeting it could be a novel potential therapeutic strategy for these disorders. However, if we are to use neurogenesis to halt or reverse hippocampal-related pathology, we need to understand better the core molecular machinery that governs NSC and their progeny. In this review, we summarize a wide variety of mouse models used in adult neurogenesis field, present their advantages and disadvantages based on specificity and efficiency of labeling of different cell types, and review their contribution to our understanding of the biology and the heterogeneity of different cell types found in adult neurogenic niches.
Morphology of subcortical brain nuclei is associated with autonomic function in healthy humans.
Human brain mapping, 2018

The autonomic nervous system (ANS) is a brain body interface which serves to maintain homeostasis by influencing a plethora of physiological processes, including metabolism, cardiorespiratory regulation and nociception. Accumulating evidence suggests that ANS function is disturbed in numerous prevalent clinical disorders, including irritable bowel syndrome and fibromyalgia. While the brain is a central hub for regulating autonomic function, the association between resting autonomic activity and subcortical morphology has not been comprehensively studied and thus was our aim. In 27 healthy subjects [14 male and 13 female; mean age 30 years (range 22-53 years)], we quantified resting ANS function using validated indices of cardiac sympathetic index (CSI) and parasympathetic cardiac vagal tone (CVT). High resolution structural magnetic resonance imaging scans were acquired, and differences in subcortical nuclei shape, that is, 'deformation', contingent on resting ANS activity were investigated. CSI positively correlated with outward deformation of the brainstem, right nucleus accumbens, right amygdala and bilateral pallidum (all thresholded to corrected P < 0.05). In contrast, parasympathetic CVT negatively correlated with inward deformation of the right amygdala and pallidum (all thresholded to corrected P < 0.05). Left and right putamen volume positively correlated with CVT (r = 0.62, P = 0.0047 and r = 0.59, P = 0.008, respectively), as did the brainstem (r = 0.46, P = 0.049). These data provide novel evidence that resting autonomic state is associated with differences in the shape and volume of subcortical nuclei. Thus, subcortical morphological brain differences in various disorders may partly be attributable to perturbation in autonomic function. Further work is warranted to investigate these findings in clinical populations. Hum Brain Mapp 39:381-392, 2018. © 2017 Wiley Periodicals, Inc.
M2 microglia promotes neurogenesis and oligodendrogenesis from neural stem/progenitor cells via the PPARγ signaling pathway.
Oncotarget, 2017

Neural stem/progenitor cells (NSPCs) are an important source of cells for cell replacement therapy after nerve injury. How to induce NSPCs differentiation towards neurons and oligodendrocytes is a challenging issue in neuroscience research. In the present study, we polarized microglia into M1 and M2 phenotype, used their supernatants to induce NSPCs differentiation, and investigated the effects of different microglia phenotypes on NSPCs differentiation and their mechanisms. We discovered that, after exposure to M1 phenotype supernatant, NSPCs differentiated into fewer Tuj-1+ and Olig2+ cells, but more GFAP+ cells. Meanwhile, a significantly increased number of Tuj-1+ and Olig2+ cells and smaller number of GFAP+ cells were generated by M2 microglia supernatant-induced NSPCs differentiation. We also observed that 15d-PGJ2, an endogenous ligand of PPARγ, was elevated in M2 phenotype supernatant and could activate PPARγ expression in NSPCs, whereas use of the PPARγ inhibitor GW9662, could reduce the percentage of differentiated neurons and oligodendrocytes. Our study results confirm that M2 microglia supernatant can activate the PPARγ signaling pathway and promote neurogenesis and oligodendrogenesis from NSPCs differentiation. The present study provides a further theoretical basis for induction of NSPCs oriented differentiation.
Nerve growth factor and associated nerve sprouting contribute to local mechanical hyperalgesia in a rat model of bone injury.
European journal of pain (London, England), 2012

To clarify the mechanism of tenderness after bone injury, we investigated changes in the withdrawal threshold to mechanical stimuli, nerve distribution and nerve growth factor (NGF)-expression in a rat model of bone injury without immobilization for bone injury healing. Rats were divided into three groups as follows: (1) rats incised in the skin and periosteum, followed by drilling a hole in the tibia [bone lesion group (BLG)]; (2) those incised in the skin and periosteum without bone drilling [periosteum lesion group (PLG)]; and (3) those incised in the skin [skin lesion group (SLG)]. Mechanical hyperalgesia continued for 28 days at a lesion in the BLG, 21 days in PLG and 5 days in SLG after treatments, respectively. Endochondral ossification was observed on days 5-28 in BLG and on days 5-21 in PLG. Nerve growth appeared in deep connective tissue (DCT) at day 28 in BLG. Nerve fibres increased in both cutaneous tissue and DCT at day 7 in PLG, but they were not found at day 28. Mechanical hyperalgesia accompanied with endochondral ossification and nerve fibres increasing at the lesion in both BLG and PLG. NGF was expressed in bone-regenerating cells during the bone injury healing. Anti-NGF and trk inhibitor K252a inhibited hyperalgesia in the different time course. This study shows that localized tenderness coincides with the bone healing and involves NGF expression and nerve sprouting after bone injury. The findings present underlying mechanisms and provide pathophysiological relevance of local tenderness to determination of bone fracture and its healing.