rudyvdbrink/CitationDatabase huggingface dataset:
Eating less from bigger packs: Preventing the pack size effect with diet primes.
Appetite, 2016

An increase in the package size of food has been shown to lead to an increase in energy intake from this food, the so-called pack size effect. Previous research has shown that providing diet-concerned individuals with a reminder, or prime, of their dieting goal can help them control their consumption. Here, we investigated if providing such a prime is also effective for reducing the magnitude of the pack size effect. We conducted two experiments in which the cover of a dieting magazine (Experiment 1) and diet-related commercials (Experiment 2) served as diet goal primes. Both experiments had a 2 (pack size: small vs. large) × 2 (prime: diet vs. control) × 2 (dietary restraint: high vs. low) between participants design. We measured expected consumption of four snack foods in Experiment 1 (N = 477), and actual consumption of M&M's in Experiment 2 (N = 224). Results showed that the diet prime reduced the pack size effect for both restrained and unrestrained eaters in Experiment 1 and for restrained eaters only in Experiment 2. Although effect sizes were small, these findings suggest that a diet prime motivates restrained eaters to limit their consumption, and as a result the pack size has less influence on the amount consumed. We discuss limitations of this research as well as potential avenues for further research and theoretical and practical implications.
TRH injected into the nucleus accumbens shell releases dopamine and reduces feeding motivation in rats.
Behavioural brain research, 2016

The thyrotropin-releasing hormone (TRH), an anorexigenic factor that reduces food intake in food-restricted animals, may be involved in motivation for food. Injected centrally, TRH impairs acquisition of food-rewarded behavior. Through the TRH-R1 receptors, TRH injected in the nucleus accumbens increases dopamine content-perhaps the mechanism by which the peptide modulates food motivation. This, however, is still to be demonstrated. We sought to evaluate dopamine release by microdialysis after a TRH injection into the nucleus accumbens shell in free-moving fasted rats. In addition, we assessed dopamine content and turnover by HPLC and the relationship with the motivation for food by analyzing the performance of rats during a progressive-ratio (PR) operant-conditioning test. Finally, we determined serum leptin and triiodothyronine (T3) levels in order to evaluate the animals' metabolic response to food restriction and the impact of intra-accumbal TRH administration on circulating hormones. Intra-accumbal injections of TRH reduced food intake in food-restricted rats-compared to counterparts treated with saline-, without further decreasing T3 or leptin levels, which dropped due to their dietary regime. TRH-injected rats had lower breaking points on the PR schedule, which indicated lower motivation to eat. Accordingly, compared to saline-treated animals, dopamine release and turnover increased in the nucleus accumbens of TRH-injected rats, a finding that suggests a relationship between motivation for food and TRH-induced release of dopamine.
Multitarget-Directed Ligands Combining Cholinesterase and Monoamine Oxidase Inhibition with Histamine H
Angewandte Chemie (International ed. in English), 2017

The therapy of complex neurodegenerative diseases requires the development of multitarget-directed drugs (MTDs). Novel indole derivatives with inhibitory activity towards acetyl/butyrylcholinesterases and monoamine oxidases A/B as well as the histamine H
Estrous cycle variations in GABA(A) receptor phosphorylation enable rapid modulation by anabolic androgenic steroids in the medial preoptic area.
Neuroscience, 2012

Anabolic androgenic steroids (AAS), synthetic testosterone derivatives that are used for ergogenic purposes, alter neurotransmission and behaviors mediated by GABA(A) receptors. Some of these effects may reflect direct and rapid action of these synthetic steroids at the receptor. The ability of other natural allosteric steroid modulators to alter GABA(A) receptor-mediated currents is dependent upon the phosphorylation state of the receptor complex. Here we show that phosphorylation of the GABA(A) receptor complex immunoprecipitated by β(2)/β(3) subunit-specific antibodies from the medial preoptic area (mPOA) of the mouse varies across the estrous cycle; with levels being significantly lower in estrus. Acute exposure to the AAS, 17α-methyltestosterone (17α-MeT), had no effect on the amplitude or kinetics of inhibitory postsynaptic currents in the mPOA of estrous mice when phosphorylation was low, but increased the amplitude of these currents from mice in diestrus, when it was high. Inclusion of the protein kinase C (PKC) inhibitor, calphostin, in the recording pipette eliminated the ability of 17α-MeT to enhance currents from diestrous animals, suggesting that PKC-receptor phosphorylation is critical for the allosteric modulation elicited by AAS during this phase. In addition, a single injection of 17α-MeT was found to impair an mPOA-mediated behavior (nest building) in diestrus, but not in estrus. PKC is known to target specific serine residues in the β(3) subunit of the GABA(A) receptor. Although phosphorylation of these β(3) serine residues showed a similar profile across the cycle, as did phosphoserine in mPOA lysates immunoprecipitated with β2/β3 antibody (lower in estrus than in diestrus or proestrus), the differences were not significant. These data suggest that the phosphorylation state of the receptor complex regulates both the ability of AAS to modulate receptor function in the mPOA and the expression of a simple mPOA-dependent behavior through a PKC-dependent mechanism that involves the β(3) subunit and other sites within the GABA(A) receptor complex.
NMMGenerator: an automatic neural mass model generator from population graphs.
Journal of neural engineering, 2021

Neural mass models are among the most popular mathematical models of brain activity, since they enable the rapid simulation of large-scale networks involving different neural types at a spatial scale compatible with electrophysiological experiments (e.g. local field potentials). However, establishing neural mass model (NMM) equations associated with specific neuronal network architectures can be tedious and is an error-prone process, restricting their use to scientists who are familiar with mathematics. In order to overcome this challenge, we have developed a user-friendly software that enables a user to construct rapidly, under the form of a graph, a neuronal network with its populations and connectivity patterns. The resulting graph is then automatically translated into the corresponding set of differential equations, which can be solved and displayed within the same software environment. The software is proposed as open access, and should assist in offering the possibility for a wider audience of scientists to develop NMM corresponding to their specific neuroscience research questions.
Mitochondrial dysfunction is a trigger of Alzheimer's disease pathophysiology.
Biochimica et biophysica acta, 2010

Mitochondria are uniquely poised to play a pivotal role in neuronal cell survival or death because they are regulators of both energy metabolism and cell death pathways. Extensive literature exists supporting a role for mitochondrial dysfunction and oxidative damage in the pathogenesis of Alzheimer's disease. This review discusses evidence indicating that mitochondrial dysfunction has an early and preponderant role in Alzheimer's disease. Furthermore, the link between mitochondrial dysfunction and autophagy in Alzheimer's disease is also discussed. As a result of insufficient digestion of oxidatively damaged macromolecules and organelles by autophagy, neurons progressively accumulate lipofuscin that could exacerbate neuronal dysfunction. Since autophagy is the major pathway involved in the degradation of protein aggregates and defective organelles, an intense interest in developing autophagy-related therapies is growing among the scientific community. The final part of this review is devoted to discuss autophagy as a potential target of therapeutic interventions in Alzheimer's disease pathophysiology.
Biomarkers and phenotypic expression in Alzheimer's disease: exploring the contribution of frailty in the Alzheimer's Disease Neuroimaging Initiative.
GeroScience, 2021

The present study aimed at investigating if the main biomarkers of Alzheimer's disease (AD) neuropathology and their association with cognitive disturbances and dementia are modified by the individual's frailty status. We performed a cross-sectional analysis of data from participants with normal cognition, mild cognitive impairment (MCI), and AD dementia enrolled in the Alzheimer's Disease Neuroimaging Initiative 2 (ADNI2) study. Frailty was operationalized by computing a 40-item Frailty Index (FI). The following AD biomarkers were considered and analyzed according to the participants' frailty status: CSF Aβ
Normal Reference Interval of WBC Count After On - Pump Coronary Artery Bypass Graft; When Values Could Be Misleading.
Anesthesiology and pain medicine, 2018

Applying the cardiopulmonary pump produces inflammatory responses and induces leukocytosis. White Blood Cell (WBC) count has a diagnostic value for detecting different infections. In this study, we want to redefine the normal value reference intervals of WBC count in Coronary Artery Bypass Graft (CABG) patients, to prevent misdiagnose leukocytosis as a sign of infection.
Pharmacological rescue of adult hippocampal neurogenesis in a mouse model of X-linked intellectual disability.
Neurobiology of disease, 2017

Oligophrenin-1 (OPHN1) is a Rho GTPase activating protein whose mutations cause X-linked intellectual disability (XLID). How loss of function of Ophn1 affects neuronal development is only partly understood. Here we have exploited adult hippocampal neurogenesis to dissect the steps of neuronal differentiation that are affected by Ophn1 deletion. We found that mice lacking Ophn1 display a reduction in the number of newborn neurons in the dentate gyrus. A significant fraction of the Ophn1-deficient newly generated neurons failed to extend an axon towards CA3, and showed an altered density of dendritic protrusions. Since Ophn1-deficient mice display overactivation of Rho-associated protein kinase (ROCK) and protein kinase A (PKA) signaling, we administered a clinically approved ROCK/PKA inhibitor (fasudil) to correct the neurogenesis defects. While administration of fasudil was not effective in rescuing axon formation, the same treatment completely restored spine density to control levels, and enhanced the long-term survival of adult-born neurons in mice lacking Ophn1. These results identify specific neurodevelopmental steps that are impacted by Ophn1 deletion, and indicate that they may be at least partially corrected by pharmacological treatment.
Dynamic extrinsic pacing of the HOX clock in human axial progenitors controls motor neuron subtype specification.
Development (Cambridge, England), 2021

Rostro-caudal patterning of vertebrates depends on the temporally progressive activation of HOX genes within axial stem cells that fuel axial embryo elongation. Whether the pace of sequential activation of HOX genes, the 'HOX clock', is controlled by intrinsic chromatin-based timing mechanisms or by temporal changes in extrinsic cues remains unclear. Here, we studied HOX clock pacing in human pluripotent stem cell-derived axial progenitors differentiating into diverse spinal cord motor neuron subtypes. We show that the progressive activation of caudal HOX genes is controlled by a dynamic increase in FGF signaling. Blocking the FGF pathway stalled induction of HOX genes, while a precocious increase of FGF, alone or with GDF11 ligand, accelerated the HOX clock. Cells differentiated under accelerated HOX induction generated appropriate posterior motor neuron subtypes found along the human embryonic spinal cord. The pacing of the HOX clock is thus dynamically regulated by exposure to secreted cues. Its manipulation by extrinsic factors provides synchronized access to multiple human neuronal subtypes of distinct rostro-caudal identities for basic and translational applications.This article has an associated 'The people behind the papers' interview.
Network plasticity in cortical assemblies.
The European journal of neuroscience, 2008

To investigate distributed synaptic plasticity at the cell assembly level, we used dissociated cortical networks from embryonic rats grown on grids of 60 extracellular substrate-embedded electrodes (micro-electrode arrays). We developed a set of experimental plasticity protocols based on the pairing of tetanic bursts (20 Hz) with low-frequency stimuli (< or = 1 Hz), delivered through two separate channels of the array (i.e. associative tetanic stimulation). We tested our protocols on a large data set of 26 stable cultures, selected on the basis of both their initial level of spontaneous firing and the capability of low-frequency test stimuli to evoke spikes. Our main results are summarized as follows: (i) low-frequency stimuli produce neither short- nor long-term changes in the evoked response of the network; (ii) associative tetanic stimulation is able to induce plasticity in terms of a significant increase or decrease of the evoked activity in the whole network; (iii) the amount of change (i.e. increase or decrease of the evoked firing) strongly depends on the specific features of the applied protocols; and (iv) the potentiation induced by a specific associative protocol can last several hours. The results obtained demonstrate that large in vitro cortical assemblies display long-term network potentiation, a mechanism considered to be involved in the memory formation at cellular level. This pilot study could represent a relevant step towards understanding plastic properties at the neuronal population level.
In vivo assessment of the human cerebral microcirculation and its glycocalyx: A technical report.
Journal of neuroscience methods, 2018

The cerebral microcirculation and its glycocalyx, a matrix coating the luminal endothelium, are key regulators of capillary permeability and cerebral blood flow. Microvascular abnormalities are described in several neurological disorders. However, assessment of the cerebral microcirculation and glycocalyx has mainly been performed ex vivo.
Face selectivity properties of monkey temporal cortical neurons predicted by computer vision.
Neuron, 2012

In this issue of Neuron, Ohayon et al. (2012) utilize fMRI-guided single-cell recordings to demonstrate the importance of contrast polarity features for face-selective responses in macaque temporal cortex, as predicted by a computer vision face detection algorithm.
Involuntary sustained firing of plantar flexor motor neurones: effect of electrical stimulation parameters during tendon vibration.
European journal of applied physiology, 2021

Simultaneous application of tendon vibration and neuromuscular electrical stimulation (NMES) induces an involuntary sustained torque. We examined the effect of different NMES parameters (intensity, pattern of stimulation and pulse width) on the magnitude of the evoked involuntary torque.
Minireview: Hormones and human sexual orientation.
Endocrinology, 2011

Many people believe that sexual orientation (homosexuality vs. heterosexuality) is determined by education and social constraints. There are, however, a large number of studies indicating that prenatal factors have an important influence on this critical feature of human sexuality. Sexual orientation is a sexually differentiated trait (over 90% of men are attracted to women and vice versa). In animals and men, many sexually differentiated characteristics are organized during early life by sex steroids, and one can wonder whether the same mechanism also affects human sexual orientation. Two types of evidence support this notion. First, multiple sexually differentiated behavioral, physiological, or even morphological traits are significantly different in homosexual and heterosexual populations. Because some of these traits are known to be organized by prenatal steroids, including testosterone, these differences suggest that homosexual subjects were, on average, exposed to atypical endocrine conditions during development. Second, clinical conditions associated with significant endocrine changes during embryonic life often result in an increased incidence of homosexuality. It seems therefore that the prenatal endocrine environment has a significant influence on human sexual orientation but a large fraction of the variance in this behavioral characteristic remains unexplained to date. Genetic differences affecting behavior either in a direct manner or by changing embryonic hormone secretion or action may also be involved. How these biological prenatal factors interact with postnatal social factors to determine life-long sexual orientation remains to be determined.
Reversal of Alcohol-Induced Dysregulation in Dopamine Network Dynamics May Rescue Maladaptive Decision-making.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2016

Alcohol is the most commonly abused substance among adolescents, promoting the development of substance use disorders and compromised decision-making in adulthood. We have previously demonstrated, with a preclinical model in rodents, that adolescent alcohol use results in adult risk-taking behavior that positively correlates with phasic dopamine transmission in response to risky options, but the underlying mechanisms remain unknown. Here, we show that adolescent alcohol use may produce maladaptive decision-making through a disruption in dopamine network dynamics via increased GABAergic transmission within the ventral tegmental area (VTA). Indeed, we find that increased phasic dopamine signaling after adolescent alcohol use is attributable to a midbrain circuit, including the input from the pedunculopontine tegmentum to the VTA. Moreover, we demonstrate that VTA dopamine neurons from adult rats exhibit enhanced IPSCs after adolescent alcohol exposure corresponding to decreased basal dopamine levels in adulthood that negatively correlate with risk-taking. Building on these findings, we develop a model where increased inhibitory tone on dopamine neurons leads to a persistent decrease in tonic dopamine levels and results in a potentiation of stimulus-evoked phasic dopamine release that may drive risky choice behavior. Based on this model, we take a pharmacological approach to the reversal of risk-taking behavior through normalization of this pattern in dopamine transmission. These results isolate the underlying circuitry involved in alcohol-induced maladaptive decision-making and identify a novel therapeutic target.
Independent Component Decomposition of Human Somatosensory Evoked Potentials Recorded by Micro-Electrocorticography.
International journal of neural systems, 2017

High-density surface microelectrodes for electrocorticography (ECoG) have become more common in recent years for recording electrical signals from the cortex. With an acceptable invasiveness/signal fidelity trade-off and high spatial resolution, micro-ECoG is a promising tool to resolve fine task-related spatial-temporal dynamics. However, volume conduction - not a negligible phenomenon - is likely to frustrate efforts to obtain reliable and resolved signals from a sub-millimeter electrode array. To address this issue, we performed an independent component analysis (ICA) on micro-ECoG recordings of somatosensory-evoked potentials (SEPs) elicited by median nerve stimulation in three human patients undergoing brain surgery for tumor resection. Using well-described cortical responses in SEPs, we were able to validate our results showing that the array could segregate different functional units possessing unique, highly localized spatial distributions. The representation of signals through the root-mean-square (rms) maps and the signal-to-noise ratio (SNR) analysis emphasizes the advantages of adopting a source analysis approach on micro-ECoG recordings in order to obtain a clear picture of cortical activity. The implications are twofold: while on one side ICA may be used as a spatial-temporal filter extracting micro-signal components relevant to tasks for brain-computer interface (BCI) applications, it could also be adopted to accurately identify the sites of nonfunctional regions for clinical purposes.
Screening for fetal growth restriction using ultrasound and the sFLT1/PlGF ratio in nulliparous women: a prospective cohort study.
The Lancet. Child & adolescent health, 2018

Fetal growth restriction is a major determinant of perinatal morbidity and mortality. This condition has no gold standard definition, but a widely used proxy is delivery of a small for gestational age infant (<10th percentile) combined with an adverse pregnancy outcome. Effective screening for fetal growth restriction is an area of unmet clinical need. We aimed to determine the diagnostic effectiveness of a combination of ultrasonic fetal biometry and measurement of the ratio of soluble fms-like tyrosine kinase receptor 1 (sFLT1) to placental growth factor (PlGF) in predicting adverse pregnancy outcomes associated with delivery of a small for gestational age infant.
SIRT1 promotes the central adaptive response to diet restriction through activation of the dorsomedial and lateral nuclei of the hypothalamus.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010

Diet restriction retards aging and extends lifespan by triggering adaptive mechanisms that alter behavioral, physiological, and biochemical responses in mammals. Little is known about the molecular pathways evoking the corresponding central response. One factor that mediates the effects of diet restriction is the mammalian nicotinamide adenine dinucleotide (NAD)-dependent deacetylase SIRT1. Here we demonstrate that diet restriction significantly increases SIRT1 protein levels and induces neural activation in the dorsomedial and lateral hypothalamic nuclei. Increasing SIRT1 in the brain of transgenic (BRASTO) mice enhances neural activity specifically in these hypothalamic nuclei, maintains a higher range of body temperature, and promotes physical activity in response to different diet-restricting paradigms. These responses are all abrogated in Sirt1-deficient mice. SIRT1 upregulates expression of the orexin type 2 receptor specifically in these hypothalamic nuclei in response to diet-restricting conditions, augmenting response to ghrelin, a gut hormone whose levels increase in these conditions. Our results suggest that in the hypothalamus, SIRT1 functions as a key mediator of the central response to low nutritional availability, providing insight into the role of the hypothalamus in the regulation of metabolism and aging in mammals.
Variation in noninvasive ventilation use in amyotrophic lateral sclerosis.
Neurology, 2019

We sought to examine prevalence and predictors of noninvasive ventilation (NIV) in a composite cohort of patients with amyotrophic lateral sclerosis (ALS) followed in a clinical trials setting (Pooled Resource Open-Access ALS Clinical Trials database).