rudyvdbrink/CitationDatabase huggingface dataset:
Latent variable GIMME using model implied instrumental variables (MIIVs).
Psychological methods, 2020

Researchers across many domains of psychology increasingly wish to arrive at personalized and generalizable dynamic models of individuals' processes. This is seen in psychophysiological, behavioral, and emotional research paradigms, across a range of data types. Errors of measurement are inherent in most data. For this reason, researchers typically gather multiple indicators of the same latent construct and use methods, such as factor analysis, to arrive at scores from these indices. In addition to accurately measuring individuals, researchers also need to find the model that best describes the relations among the latent constructs. Most currently available data-driven searches do not include latent variables. We present an approach that builds from the strong foundations of group iterative multiple model estimation (GIMME), the idiographic filter, and model implied instrumental variables with two-stage least squares estimation (MIIV-2SLS) to provide researchers with the option to include latent variables in their data-driven model searches. The resulting approach is called latent variable GIMME (LV-GIMME). GIMME is utilized for the data-driven search for relations that exist among latent variables. Unlike other approaches such as the idiographic filter, LV-GIMME does not require that the latent variable model to be constant across individuals. This requirement is loosened by utilizing MIIV-2SLS for estimation. Simulated data studies demonstrate that the method can reliably detect relations among latent constructs, and that latent constructs provide more power to detect effects than using observed variables directly. We use empirical data examples drawn from functional MRI and daily self-report data. (PsycINFO Database Record (c) 2020 APA, all rights reserved).
Merging machines with microsurgery: clinical experience with neuroArm.
Journal of neurosurgery, 2013

It has been over a decade since the introduction of the da Vinci Surgical System into surgery. Since then, technology has been advancing at an exponential rate, and newer surgical robots are becoming increasingly sophisticated, which could greatly impact the performance of surgery. NeuroArm is one such robotic system.
Starvation promotes concerted modulation of appetitive olfactory behavior via parallel neuromodulatory circuits.
eLife, 2015

The internal state of an organism influences its perception of attractive or aversive stimuli and thus promotes adaptive behaviors that increase its likelihood of survival. The mechanisms underlying these perceptual shifts are critical to our understanding of how neural circuits support animal cognition and behavior. Starved flies exhibit enhanced sensitivity to attractive odors and reduced sensitivity to aversive odors. Here, we show that a functional remodeling of the olfactory map is mediated by two parallel neuromodulatory systems that act in opposing directions on olfactory attraction and aversion at the level of the first synapse. Short neuropeptide F sensitizes an antennal lobe glomerulus wired for attraction, while tachykinin (DTK) suppresses activity of a glomerulus wired for aversion. Thus we show parallel neuromodulatory systems functionally reconfigure early olfactory processing to optimize detection of nutrients at the risk of ignoring potentially toxic food resources.
The role of the immune system in central nervous system plasticity after acute injury.
Neuroscience, 2014

Acute brain injuries cause rapid cell death that activates bidirectional crosstalk between the injured brain and the immune system. In the acute phase, the damaged CNS activates resident and circulating immune cells via the local and systemic release of soluble mediators. This early immune activation is necessary to confine the injured tissue and foster the clearance of cellular debris, thus bringing the inflammatory reaction to a close. In the chronic phase, a sustained immune activation has been described in many CNS disorders, and the degree of this prolonged response has variable effects on spontaneous brain regenerative processes. The challenge for treating acute CNS damage is to understand how to optimally engage and modify these immune responses, thus providing new strategies that will compensate for tissue lost to injury. Herein we have reviewed the available information regarding the role and function of the innate and adaptive immune responses in influencing CNS plasticity during the acute and chronic phases of after injury. We have examined how CNS damage evolves along the activation of main cellular and molecular pathways that are associated with intrinsic repair, neuronal functional plasticity and facilitation of tissue reorganization.
Effects of a Single Head Exposure to GSM-1800 MHz Signals on the Transcriptome Profile in the Rat Cerebral Cortex: Enhanced Gene Responses Under Proinflammatory Conditions.
Neurotoxicity research, 2020

Mobile communications are propagated by electromagnetic fields (EMFs), and since the 1990s, they operate with pulse-modulated signals such as the GSM-1800 MHz. The biological effects of GSM-EMF in humans affected by neuropathological processes remain seldom investigated. In this study, a 2-h head-only exposure to GSM-1800 MHz was applied to (i) rats undergoing an acute neuroinflammation triggered by a lipopolysaccharide (LPS) treatment, (ii) age-matched healthy rats, or (iii) transgenic hSOD1
Independence of landmark and self-motion-guided navigation: a different role for grid cells.
Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2014

Recent interest in the neural bases of spatial navigation stems from the discovery of neuronal populations with strong, specific spatial signals. The regular firing field arrays of medial entorhinal grid cells suggest that they may provide place cells with distance information extracted from the animal's self-motion, a notion we critically review by citing new contrary evidence. Next, we question the idea that grid cells provide a rigid distance metric. We also discuss evidence that normal navigation is possible using only landmarks, without self-motion signals. We then propose a model that supposes that information flow in the navigational system changes between light and dark conditions. We assume that the true map-like representation is hippocampal and argue that grid cells have a crucial navigational role only in the dark. In this view, their activity in the light is predominantly shaped by landmarks rather than self-motion information, and so follows place cell activity; in the dark, their activity is determined by self-motion cues and controls place cell activity. A corollary is that place cell activity in the light depends on non-grid cells in ventral medial entorhinal cortex. We conclude that analysing navigational system changes between landmark and no-landmark conditions will reveal key functional properties.
Ischemic tolerance in an in vivo model of glutamate preconditioning.
Journal of neuroscience research, 2015

Ischemia initiates a complicated biochemical cascade of events that triggers neuronal death. This study focuses on glutamate-mediated neuronal tolerance to ischemia-reperfusion. We employed an animal model of lifelong excess release of glutamate, the glutamate dehydrogenase 1 transgenic (Tg) mouse, as a model of in vivo glutamate preconditioning. Nine- and twenty-two-month-old Tg and wild-type (wt) mice were subjected to 90 min of middle cerebral artery occlusion, followed by 24 hr of reperfusion. The Tg mice suffered significantly reduced infarction and edema volume compared with their wt counterparts. We further analyzed proteasomal activity, level of ubiquitin immunostaining, and microtubule-associated protein-2A (MAP2A) expression to understand the mechanism of neuroprotection observed in the Tg mice. We found that, in the absence of ischemia, the Tg mice exhibited higher activity of the 20S and 26S proteasomes, whereas there was no significant difference in the level of hippocampal ubiquitin immunostaining between wt and Tg mice. A surprising, significant increase was observed in MAP2A expression in neurons of the Tg hippocampus following ischemia-reperfusion compared with that in wt hippocampus. The results suggest that increased proteasome activity and MAP2A synthesis and transport might account for the effectiveness of glutamate preconditioning against ischemia-reperfusion.
A novel, nongenomic mechanism underlies retinoic acid-induced growth cone turning.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009

The vitamin A metabolite, retinoic acid (RA), is well known for its roles in neural development and regeneration. We have previously shown that RA can induce positive growth cone turning in regenerating neurons in vitro. In this study, we address the subcellular mechanisms underlying this chemo-attractive response, using identified central neurons from the adult mollusc, Lymnaea stagnalis. We show that the RA-induced positive growth cone turning was maintained in the presence of the transcriptional inhibitor, actinomycin D. We also physically transected the neurites from the cell body and showed that isolated growth cones retain the capacity to turn toward a gradient of RA. Moreover, this attractive turning is dependent on de novo local protein synthesis and Ca(2+) influx. Most of RA's actions during neurite outgrowth and regeneration require gene transcription, although these data show for the first time in any species, that the chemotropic action of RA in guiding neurite outgrowth, involves a novel, nongenomic mechanism.
The postnatal development of D-serine in the retinas of two mouse strains, including a mutant mouse with a deficiency in D-amino acid oxidase and a serine racemase knockout mouse.
ACS chemical neuroscience, 2014

D-Serine, an N-methyl D-aspartate receptor coagonist, and its regulatory enzymes, D-amino acid oxidase (DAO; degradation) and serine racemase (SR; synthesis), have been implicated in crucial roles of the developing central nervous system, yet the functional position that they play in regulating the availability of d-serine throughout development of the mammalian retina is not well-known. Using capillary electrophoresis and a sensitive method of enantiomeric amino acid separation, we were able to determine total levels of d-serine at specific ages during postnatal development of the mouse retina in two different strains of mice, one of which contained a loss-of-function point mutation for DAO while the other was a SR knockout line. Each mouse line was tested against conspecific wild type (WT) mice for each genetic strain. The universal trend in all WT and transgenic mice was a large amount of total retinal d-serine at postnatal age 2 (P2), followed by a dramatic decrease as the mice matured into adulthood (P70-80). SR knockout mice retinas had 41% less D-serine than WT retinas at P2, and 10 times less as an adult. DAO mutant mice retinas had significantly elevated levels of d-serine when compared to WT retinas at P2 (217%), P4 (223%), P8 (194%), and adulthood (227%).
BoNT-A for Post-Stroke Spasticity: Guidance on Unmet Clinical Needs from a Delphi Panel Approach.
Toxins, 2021

There is extensive literature supporting the efficacy of botulinum toxin (BoNT-A) for the treatment of post-stroke spasticity, however, there remain gaps in the routine management of patients with post-stroke spasticity. A panel of 21 Italian experts was selected to participate in this web-based survey Delphi process to provide guidance that can support clinicians in the decision-making process. There was a broad consensus among physicians that BoNT-A intervention should be administered as soon as the spasticity interferes with the patients' clinical condition. Patients monitoring is needed over time, a follow-up of 4-6 weeks is considered necessary. Furthermore, physicians agreed that treatment should be offered irrespective of the duration of the spasticity. The Delphi consensus also stressed the importance of patient-centered goals in order to satisfy the clinical needs of the patient regardless of time of onset or duration of spasticity. The findings arising from this Delphi process provide insights into the unmet needs in managing post-stroke spasticity from the clinician's perspective and provides guidance for physicians for the utilization of BoNT-A for the treatment of post-stroke spasticity in daily practice.
Narcolepsy with resolution of cataplexy and persisting orexin deficiency.
Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine, 2020

Narcolepsy type 1 is a debilitating chronic neurological disorder, whose main symptoms of excessive daytime sleepiness and cataplexy may partially improve with time, but typically do not fully resolve. The irreversible loss of orexin neurons is considered to be the pivotal mechanistic link underlying the development of cataplectic attacks in narcolepsy type 1. Here we describe a case of untreated narcolepsy type 1with low cerebrospinal orexin levels (< 50 pg/mL), where cataplexy fully resolved in the first 5-6 years after disease onset, whereas excessive daytime sleepiness persisted.
Novel GNB1 mutations disrupt assembly and function of G protein heterotrimers and cause global developmental delay in humans.
Human molecular genetics, 2017

Global developmental delay (GDD), often accompanied by intellectual disability, seizures and other features is a severe, clinically and genetically highly heterogeneous childhood-onset disorder. In cases where genetic causes have been identified, de novo mutations in neuronally expressed genes are a common scenario. These mutations can be best identified by exome sequencing of parent-offspring trios. De novo mutations in the guanine nucleotide-binding protein, beta 1 (GNB1) gene, encoding the Gβ1 subunit of heterotrimeric G proteins, have recently been identified as a novel genetic cause of GDD. Using exome sequencing, we identified 14 different novel variants (2 splice site, 2 frameshift and 10 missense changes) in GNB1 in 16 pediatric patients. One mutation (R96L) was recurrently found in three ethnically diverse families with an autosomal dominant mode of inheritance. Ten variants occurred de novo in the patients. Missense changes were functionally tested for their pathogenicity by assaying the impact on complex formation with Gγ and resultant mutant Gβγ with Gα. Signaling properties of G protein complexes carrying mutant Gβ1 subunits were further analyzed by their ability to couple to dopamine D1R receptors by real-time bioluminescence resonance energy transfer (BRET) assays. These studies revealed altered functionality of the missense mutations R52G, G64V, A92T, P94S, P96L, A106T and D118G but not for L30F, H91R and K337Q. In conclusion, we demonstrate a pathogenic role of de novo and autosomal dominant mutations in GNB1 as a cause of GDD and provide insights how perturbation in heterotrimeric G protein function contributes to the disease.
Developing the FARSEEING Taxonomy of Technologies: Classification and description of technology use (including ICT) in falls prevention studies.
Journal of biomedical informatics, 2016

Recent Cochrane reviews on falls and fall prevention have shown that it is possible to prevent falls in older adults living in the community and in care facilities. Technologies aimed at fall detection, assessment, prediction and prevention are emerging, yet there has been no consistency in describing or reporting on interventions using technologies. With the growth of eHealth and data driven interventions, a common language and classification is required.
Rapid State-Dependent Alteration in K
Cell reports, 2017

In many neurons, subthreshold depolarization in the soma can transiently increase action-potential (AP)-evoked neurotransmission via analog-to-digital facilitation. The mechanisms underlying this form of short-term synaptic plasticity are unclear, in part, due to the relative inaccessibility of the axon to direct physiological interrogation. Using voltage imaging and patch-clamp recording from presynaptic boutons of cerebellar stellate interneurons, we observed that depolarizing somatic potentials readily spread into the axon, resulting in AP broadening, increased spike-evoked Ca
Social Support Protects Against Symptoms of Anxiety and Depression: Key Variations in Latinx and Non-Latinx White College Students.
Journal of Latina/o psychology, 2021

Social support protects against perceived stress and its harmful effects on psychological well-being. College students in general are at high risk for mental health disorders, and Latinx college students face unique stressors placing them at greater risk of psychological distress. Social support may be a key construct in improving outcomes for college students; however, few studies have empirically tested whether the protective effect of social support is equivalent across racial/ethnic groups. Using a series of regression models, we investigated whether social support moderates the relationship between perceived stress and endorsement of depression and anxiety symptoms in Latinx (
Sex hormone therapy and functional brain plasticity in postmenopausal women.
Neuroscience, 2011

Several studies have shown that fluctuating levels of sex hormones (estrogen and progesterone) can affect fundamental principles of brain organization, including functional cerebral asymmetries (FCAs) and interhemispheric interactions. The majority of findings come from studies investigating younger women tested during distinct hormonal phases of the menstrual cycle, an approach that does not necessarily allow for conclusions about the causal relationship between hormonal changes and functional brain organization. An alternative approach is to manipulate the hormonal status of participants directly. This research focuses on the effects of hormone therapy (HT) on FCAs and interhemispheric interactions in postmenopausal women. Functional brain organization was tested in postmenopausal women using either estrogen therapy or combined estrogen plus gestagen therapy. The results are then compared to age- and IQ-matched postmenopausal women not taking HT. The results indicate HT-related modulations in both FCAs and interhemispheric interaction. In contrast to normally cycling women, however, it seems that HT, and especially estrogen therapy, after menopause affects intrahemispheric processing rather than interhemispheric crosstalk. The findings indicate a faster and more pronounced age-related decline in intrahemispheric relative to interhemispheric processing which seems to be accompanied by a higher sensitivity to HT. Aging processes together with differences in the hormonal status (exogenous changes as a result of HT vs. endogenous changes during the menstrual cycle) may also explain divergent (cognitive) behavioral outcomes in postmenopausal women and younger women. Taken together, the findings suggest that the female brain retains its plasticity even after reproductive age and remains susceptible to the effects of sex hormones throughout the lifetime. This article is part of a Special Issue entitled: Neuroactive Steroids: Focus on Human Brain.
High-quality chromosome-level genomes of two tilapia species reveal their evolution of repeat sequences and sex chromosomes.
Molecular ecology resources, 2021

Tilapias are one of the most farmed fishes that are coined as "aquatic chicken" by the food industry. Nile tilapia and blue tilapia exhibit very recent transition of sex chromosome systems since their divergence approximately five million years ago, making them a great model for elucidating the molecular and evolutionary mechanisms of sex chromosome turnovers. Studies of their sex-determining pathways are also critical for developing genetic sex control in aquaculture. We report here the newly produced genomes of Nile tilapia and blue tilapia that integrate long-read sequencing and chromatin conformation data. The two nearly complete genomes have anchored over 97% of the sequences into linkage groups (LGs), and assembled majorities of complex repetitive regions including telomeres, centromeres and rDNA clusters. In particular, we inferred two episodes of repeat expansion at LG3 respectively in the ancestor of cichlids and that of tilapias. The consequential large heterochromatic region concentrated at one end of LG3 comprises tandem arrays of mRNA and small RNA genes, among which we have identified a candidate female determining gene Paics in blue tilapia. Paics shows female-specific patterns of single-nucleotide variants, copy numbers and expression patterns in gonads during early gonadogenesis. Our work provides a very important genomic resource for functional studies of cichlids, and suggested that unequal distribution of repeat content that impacts the local recombination rate might make some chromosomes more likely to become sex chromosomes.
Traumatic nociceptive pain activates the hypothalamus and the periaqueductal gray: a positron emission tomography study.
Pain, 1996

The study was conducted to investigate which areas of the brain respond to a painful encounter of minor dermal injury (a model of clinical pain) elicited by intracutaneous injection of a minute amount of ethanol. Four healthy volunteers (27-46 years) were subjected to positron emission tomographic (PET) investigation of regional cerebral blood flow (rCBF), using [15O]butanol as tracer. The ethanol (20 microliters, 70%) and saline (20 microliters, 0.9%) were injected intracutaneously 3 times in a single-blinded, semi-randomised manner for the pain experiment. All the injections were performed, adjacent to each other, at the lateral aspect of the right upper arm. Subjective sensory intensity of pain, unpleasantness and anxiety were rated with separate 100-mm visual analogue scales together with the Spielberger's State Anxiety Inventory (Spielberger et al. 1970) and heart rate. Paired-subtraction (pixel-by-pixel) between ethanol and saline was performed. Traumatic pain significantly caused higher ratings of intensity and affect scales, i.e., pain intensity, unpleasantness and increased sympathetic activity (evidenced by tachycardia). In contrast the anxiety rating remained unchanged. Acute traumatic nociceptive pain prominently activated the hypothalamus and periaqueductal gray (PAG). In addition, activations of the prefrontal cortex (PFC), insular, anterior cingulate cortex (ACC), posterior parietal cortex (PPC), primary motor/somatosensory areas (MI/SI: face, upper arm), supplementary motor area (SMA), and cerebellum were also demonstrated. The central processing of the pain-relevant/anticipatory arousal also engaged the PAG. This study demonstrates the involvement of the human cerebral cortex in perception, arousal, cognitive evaluative processes, and, hence, affective reactions (somatic/ autonomic outflow) associated with pain. The pain stimulus of traumatic character may, by its very nature, evoke the central processing to involve both the hypothalamus and the PAG.