rudyvdbrink/CitationDatabase huggingface dataset:
Learning to minimize efforts versus maximizing rewards: computational principles and neural correlates.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014

The mechanisms of reward maximization have been extensively studied at both the computational and neural levels. By contrast, little is known about how the brain learns to choose the options that minimize action cost. In principle, the brain could have evolved a general mechanism that applies the same learning rule to the different dimensions of choice options. To test this hypothesis, we scanned healthy human volunteers while they performed a probabilistic instrumental learning task that varied in both the physical effort and the monetary outcome associated with choice options. Behavioral data showed that the same computational rule, using prediction errors to update expectations, could account for both reward maximization and effort minimization. However, these learning-related variables were encoded in partially dissociable brain areas. In line with previous findings, the ventromedial prefrontal cortex was found to positively represent expected and actual rewards, regardless of effort. A separate network, encompassing the anterior insula, the dorsal anterior cingulate, and the posterior parietal cortex, correlated positively with expected and actual efforts. These findings suggest that the same computational rule is applied by distinct brain systems, depending on the choice dimension-cost or benefit-that has to be learned.
Corticospinal excitability in idiopathic normal pressure hydrocephalus: a transcranial magnetic stimulation study.
Fluids and barriers of the CNS, 2020

Idiopathic normal pressure hydrocephalus (iNPH) is a neurodegenerative disease with an unknown etiology. Disturbed corticospinal inhibition of the motor cortex has been reported in iNPH and can be evaluated in a noninvasive and painless manner using navigated transcranial magnetic stimulation (nTMS). This is the first study to characterize the immediate impact of cerebrospinal fluid (CSF) drainage on corticospinal excitability.
Childhood body mass index in adolescent-onset anorexia nervosa.
The International journal of eating disorders, 2016

Although weight history is relevant in predicting eating disorder symptom severity, little is known about its role in the etiology of anorexia nervosa (AN). This study aimed to determine whether BMI or BMI trajectory differed between individuals who later developed adolescent-onset AN and a comparison group of HCs between school grades 1 through 6.
Comparisons between Garcia, Modo, and Longa rodent stroke scales: Optimizing resource allocation in rat models of focal middle cerebral artery occlusion.
Journal of the neurological sciences, 2016

The use of rodent stroke models allow for the understanding of stroke pathophysiology. There is currently no gold standard neurological assessment to measure deficits and recovery from stroke in rodent models. Agreement on a universal preclinical stroke scale allows for comparison of the outcomes among conducted studies. The present study aimed to compare three routinely used neurological assessments in rodent studies (i.e., Garcia, Modo, and Longa) to determine which is most effective for accurately and consistently quantifying neurological deficits in the context of focal middle cerebral artery occlusion (MCAo) in rats. Focal MCAo was induced in 22 male Wistar rats using a novel transfemoral approach. Rodents were assessed for neurological deficit pre-injury as well as 3 and 24h post-injury. Data was analyzed to determine Pearson correlation coefficients in addition to McNemar's χ(2) values between each pair of neurological assessments. All three stroke scales, Garcia, Modo, and Longa, showed statistically significant changes between the baseline and the 3-hour neurological assessments. A trend towards neurological recovery was observed in all three stroke scales between the 3 and 24-hour endpoints. The three scales were highly correlated with each other, with Garcia and Modo having the strongest correlation. Of the three pairwise analyses, the comparison between the Garcia and Longa tests demonstrated the highest McNemar's χ(2) value, indicating least marginal homogeneity between these two tests. The combination of high correlation between Garcia and Modo tests along with greatest marginal heterogeneity observed between the Garcia and Longa test lead us to recommend the use of Garcia and Longa neurological scales when researchers are hoping to capture the broadest range of neurological factors using only two stroke scales.
Pathogenic role of delta 2 tubulin in bortezomib-induced peripheral neuropathy.
Proceedings of the National Academy of Sciences of the United States of America, 2021

The pathogenesis of chemotherapy-induced peripheral neuropathy (CIPN) is poorly understood. Here, we report that the CIPN-causing drug bortezomib (Bort) promotes delta 2 tubulin (D2) accumulation while affecting microtubule stability and dynamics in sensory neurons in vitro and in vivo and that the accumulation of D2 is predominant in unmyelinated fibers and a hallmark of bortezomib-induced peripheral neuropathy (BIPN) in humans. Furthermore, while D2 overexpression was sufficient to cause axonopathy and inhibit mitochondria motility, reduction of D2 levels alleviated both axonal degeneration and the loss of mitochondria motility induced by Bort. Together, our data demonstrate that Bort, a compound structurally unrelated to tubulin poisons, affects the tubulin cytoskeleton in sensory neurons in vitro, in vivo, and in human tissue, indicating that the pathogenic mechanisms of seemingly unrelated CIPN drugs may converge on tubulin damage. The results reveal a previously unrecognized pathogenic role for D2 in BIPN that may occur through altered regulation of mitochondria motility.
Adherence to European Society for Cataract and Refractive Surgery recommendations among Italian cataract surgeons: a survey.
European journal of ophthalmology, 2016

To survey the surgical routines with regards to prophylactic strategies in a sample of Italian hospitals and compare these with European Society for Cataract and Refractive Surgery (ESCRS) guidelines.
Psychometric properties of the Gotland Scale for Depression in Italian psychiatric inpatients and its utility in the prediction of suicide risk.
Journal of affective disorders, 2011

Rutz has postulated a "male depressive syndrome" measured by the Gotland Scale of Male Depression (GSMD). The aim of the study was to assess the psychometric properties of the GSMD in a sample of male and female psychiatric inpatients.
Review of source-monitoring processes in obsessive-compulsive disorder.
World journal of psychiatry, 2020

Obsessive-compulsive disorder (OCD) is a severe mental illness characterized by persistent, intrusive and distressing obsessions and/or compulsions. Such symptoms have been conceptualized as resulting from a failure in source-monitoring processes, suggesting that patients with OCD fail to distinguish actions they perform from those they just imagine doing. In this study, we aimed to provide an updated and exhaustive review of the literature examining the relationship between source-monitoring and OCD. A systematic search in the literature through January 2019 allowed us to identify 13 relevant publications investigating source-monitoring abilities in patients with OCD or participants with subclinical compulsive symptoms. Most of the retrieved studies did not report any source-monitoring deficits in clinical and subclinical subjects compared with healthy volunteers. However, most of the studies reported that patients with OCD and subclinical subjects displayed reduced confidence in source-monitoring judgments or global cognitive confidence compared to controls. The present review highlighted some methodological and statistical limitations. Consequently, further studies are needed to explore source monitoring with regard to the subcategories of OCD symptoms (
A causal role for the anterior mid-cingulate cortex in negative affect and cognitive control.
Brain : a journal of neurology, 2016

Converging evidence has linked the anterior mid-cingulate cortex to negative affect, pain and cognitive control. It has previously been proposed that this region uses information about punishment to control aversively motivated actions. Studies on the effects of lesions allow causal inferences about brain function; however, naturally occurring lesions in the anterior mid-cingulate cortex are rare. In two studies we therefore recruited 94 volunteers, comprising 15 patients with treatment-resistant depression who had received bilateral anterior cingulotomy, which consists of lesions made within the anterior mid-cingulate cortex, 20 patients with treatment-resistant depression who had not received surgery and 59 healthy control subjects. Using the Ekman 60 faces paradigm and two Stroop paradigms, we tested the hypothesis that patients who received anterior cingulotomy were impaired in recognizing negative facial affect expressions but not positive or neutral facial expressions, and impaired in Stroop cognitive control, with larger lesions being associated with more impairment. Consistent with this hypothesis, we found that larger volume lesions predicted more impairment in recognizing fear, disgust and anger, and no impairment in recognizing facial expressions of surprise or happiness. However, we found no impairment in recognizing expressions of sadness. Also consistent with the hypothesis, we found that larger volume lesions predicted impaired Stroop cognitive control. Notably, this relationship was only present when anterior mid-cingulate cortex lesion volume was defined as the overlap between cingulotomy lesion volume and Shackman's meta-analysis-derived binary masks for negative affect and cognitive control. Given substantial evidence from healthy subjects that the anterior mid-cingulate cortex is part of a network associated with the experience of negative affect and pain, engaging cognitive control processes for optimizing behaviour in the presence of such stimuli, our findings support the assertion that this region has a causal role in these processes. While the clinical justification for cingulotomy is empirical and not theoretical, it is plausible that lesions within a brain region associated with the subjective experience of negative affect and pain may be therapeutic for patients with otherwise intractable mood, anxiety and pain syndromes.
High H1-affinity antidepressants and risk of metabolic syndrome in bipolar disorder.
Psychopharmacology, 2016

Metabolic syndrome (MetS) is common in patients with bipolar disorder, with a relative risk of 1.6-2 compared to the general population. The increased risk is believed to be due to unhealthy lifestyles and use of medications. Although antipsychotics and mood stabilizers have been associated with weight gain and MetS, the impact of antidepressants has not been comprehensively evaluated.
Antagonism between fine and coarse motion sensors depends on stimulus size and contrast.
Journal of vision, 2010

The perceived direction of motion of a brief visual stimulus that contains fine features reverses if static coarser features are added to it. Here we show that the reversal in perceived direction disappears if the stimulus is reduced in size from 2.8 deg to 0.35 deg radius. We show that for a stimulus with 1.4 deg radius, the reversals occur when the ratio between the contrast of the fine features and of the coarser features is higher than 0.8 and lower than 4. For stimulus with 0.35 deg radius, the reversals never appear for any contrast ratio. We also show that if the stimulus is presented within an annular window with small radius, errors disappear but they return if the radius is increased to 2 deg. The errors in motion discrimination described here can be explained by a model of motion sensing in which the signals from fine-scale and coarse-scale sensors are subtracted from one another (I. Serrano-Pedraza, P. Goddard, & A. M. Derrington, 2007). The model produces errors in direction when the signals in the fine and coarse sensors are approximately balanced. The errors disappear when stimulus size is reduced because the reduction in size differentially reduces the response of the low spatial frequency motion sensors.
Semaphorin 5B is a repellent cue for sensory afferents projecting into the developing spinal cord.
Development (Cambridge, England), 2014

During vertebrate development, centrally projecting sensory axons of the dorsal root ganglia neurons first reach the embryonic spinal cord at the dorsolateral margin. Instead of immediately projecting into the grey matter, they bifurcate and extend rostrally and caudally to establish the longitudinal dorsal funiculus during a stereotyped waiting period of approximately 48&emsp14;h. Collateral fibres then extend concurrently across multiple spinal segments and project to their appropriate targets within the grey matter. This rostrocaudal extension of sensory afferents is crucial for the intersegmental processing of information throughout the spinal cord. However, the precise cues that prevent premature entry during the waiting period remain to be identified. Here, we show that semaphorin 5B (Sema5B), a member of the semaphorin family of guidance molecules, is expressed in the chick spinal cord during this waiting period and dorsal funiculus formation. Sema5B expression is dynamic, with a reduction of expression apparent in the spinal cord concomitant with collateral extension. We show that Sema5B inhibits the growth of NGF-dependent sensory axons and that this effect is mediated in part through the cell adhesion molecule TAG-1. Knockdown of Sema5B in the spinal cord using RNA interference leads to the premature extension of cutaneous nociceptive axons into the dorsal horn grey matter. These premature projections predominantly occur at the site of dorsal root entry. Our results suggest that Sema5B contributes to a repulsive barrier for centrally projecting primary sensory axons, forcing them to turn and establish the dorsal funiculus.
Melatonin reduces endoplasmic reticulum stress and autophagy in liver of leptin-deficient mice.
Journal of pineal research, 2016

The sedentary lifestyle of modern society along with the high intake of energetic food has made obesity a current worldwide health problem. Despite great efforts to study the obesity and its related diseases, the mechanisms underlying the development of these diseases are not well understood. Therefore, identifying novel strategies to slow the progression of these diseases is urgently needed. Experimental observations indicate that melatonin has an important role in energy metabolism and cell signalling; thus, the use of this molecule may counteract the pathologies of obesity. In this study, wild-type and obese (ob/ob) mice received daily intraperitoneal injections of melatonin at a dose of 500 μg/kg body weight for 4 weeks, and the livers of these mice were used to evaluate the oxidative stress status, proteolytic (autophagy and proteasome) activity, unfolded protein response, inflammation and insulin signalling. Our results show, for the first time, that melatonin could significantly reduce endoplasmic reticulum stress in leptin-deficient obese animals and ameliorate several symptoms that characterize this disease. Our study supports the potential of melatonin as a therapeutic treatment for the most common type of obesity and its liver-associated disorders.
Effects of early-life abuse differ across development: infant social behavior deficits are followed by adolescent depressive-like behaviors mediated by the amygdala.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012

Abuse during early life, especially from the caregiver, increases vulnerability to develop later-life psychopathologies such as depression. Although signs of depression are typically not expressed until later life, signs of dysfunctional social behavior have been found earlier. How infant abuse alters the trajectory of brain development to produce pathways to pathology is not completely understood. Here we address this question using two different but complementary rat models of early-life abuse from postnatal day 8 (P8) to P12: a naturalistic paradigm, where the mother is provided with insufficient bedding for nest building; and a more controlled paradigm, where infants undergo olfactory classical conditioning. Amygdala neural assessment (c-Fos), as well as social behavior and forced swim tests were performed at preweaning (P20) and adolescence (P45). Our results show that both models of early-life abuse induce deficits in social behavior, even during the preweaning period; however, depressive-like behaviors were observed only during adolescence. Adolescent depressive-like behavior corresponds with an increase in amygdala neural activity in response to forced swim test. A causal relationship between the amygdala and depressive-like behavior was suggested through amygdala temporary deactivation (muscimol infusions), which rescued the depressive-like behavior in the forced swim test. Our results indicate that social behavior deficits in infancy could serve as an early marker for later psychopathology. Moreover, the implication of the amygdala in the ontogeny of depressive-like behaviors in infant abused animals is an important step toward understanding the underlying mechanisms of later-life mental disease associated with early-life abuse.
Cerebral mechanisms of hypnotic hypoesthesia. An ERP investigation on the expectancy stage of perception.
Psychophysiology, 2020

The present study aims at identifying reliable markers of neural preparatory processes during hypnosis. To this goal, we recorded the electroencephalographic activity of 23 volunteers regardless of their hypnotizability score. Somatosensory evoked potentials (SEPs) were elicited while participants received non-painful electrical stimuli on the left median nerve in the conditions of relaxation and hypnosis with suggestions of reduced sensation. SEPs analysis was focused on the pre-stimulus activity and revealed two main components: the prefrontal negativity (pN) and the somatosensory negativity (sN) over the frontal and parietal areas of the scalp, respectively. Results showed reduced amplitudes for both components under hypnosis, mostly for the pN, suggesting a change of top-down control of parietal and prefrontal areas. Furthermore, the sLORETA source imaging showed a deactivation of the lateral and anterior portions of the prefrontal cortex (PFC) during the hypnotic state. The present study highlights the downregulation of the PFC as a core aspect of the adopted hypnotic task and confirms the ability of hypnosis to modulate the activity of frontal executive functions. Further, since the majority of participants fell into the medium range of hypnotizability, the present findings could reflect the hypnosis effects in most of the population.
Epithelial-mesenchymal transition in morphogenesis, cancer progression and angiogenesis.
Experimental cell research, 2017

All organs consist of an epithelium and an associated mesenchyme, so these epithelial-mesenchymal intercations are among the most important phenomena in nature. The aim of this article is the summarize the common mechanisms involved in the establishment of epithelial mesenchymal transition in three biological processes, namely organogenesis, tumor progression and metastasis, and angiogenesis, apparently independent each from other. A common feature of these processes is the fact that specialized epithelial cells lose their features, including cell adhesion and polarity, reorganize their cytoskeleton, and acquire a mesenchymal morphology and the ability to migrate.
Neurosarcoidosis.
Current treatment options in neurology, 2013

Neurosarcoidosis can involve either the central nervous system (CNS), the peripheral nervous system (PNS), or both. The clinical manifestations are varied and include cranial neuropathy, aseptic meningitis, hydrocephalus, headache, seizure, neuropsychiatric symptoms, neuroendocrine dysfunction, myelopathy, and peripheral neuropathy. Neurologic problems that develop in sarcoidosis patients should not be assumed to represent neurosarcoidosis, as they are often attributable to another cause. The diagnostic work up of neurosarcoidosis should include an evaluation for potential extra-neural involvement and histologic confirmation of sarcoidosis. If there is no appropriate extra-neurologic organ for biopsy, a biopsy from involved neural tissue needs to be considered. Biopsy of the dura and leptomeninges is less invasive than biopsy of the brain or spinal cord parenchyma. Gadolinium-enhanced magnetic resonance imaging (MRI) of the brain and spinal cord is the most sensitive test for neurosarcoidosis, while the diagnostic specificity of cerebrospinal fluid (CSF) analysis is limited. Corticosteroids are the mainstay of treatment for neurosarcoidosis. In general, oral corticosteroids are used for mild to moderate cases, while high-dose intravenous methylprednisolone is used in severe cases or refractory cases that fail to respond to oral corticosteroids. Immunomodulating and cytotoxic agents are often required for steroid-refractory neurosarcoidosis or for patients who develop significant corticosteroid adverse effects. Methotrexate is used as a first-line corticosteroid sparing agent. Tumor necrosis factor-alpha inhibitors, including infliximab, are effective for refractory neurosarcoidosis. Cyclophosphamide is also used for refractory neurosarcoidosis patients, but, because of the drug's significant toxicity, it is usually reserved for severe cases that have failed oral therapies when tumor necrosis factor alpha antagonists cannot be obtained. In addition to anti-granulomatous therapy, treatment is frequently required for neurosarcoidosis-associated conditions, such as epilepsy and neuroendocrine dysfunction. Surgical intervention is indicated for life threatening complications such as hydrocephalus, steroid-refractory spinal cord compression, or mass lesions causing increased intracranial pressure.
Self-identification with another person's face: the time relevant role of multimodal brain areas in the enfacement illusion.
Journal of neurophysiology, 2015

The illusory subjective experience of looking at one's own face while in fact looking at another person's face can surprisingly be induced by simple synchronized visuotactile stimulation of the two faces. A recent study (Apps MA, Tajadura-Jiménez A, Sereno M, Blanke O, Tsakiris M. Cereb Cortex. First published August 20, 2013; doi:10.1093/cercor/bht199) investigated for the first time the role of visual unimodal and temporoparietal multimodal brain areas in the enfacement illusion and suggested a model in which multisensory mechanisms are crucial to construct and update self-face representation.
Extensive phosphorylation of AMPA receptors in neurons.
Proceedings of the National Academy of Sciences of the United States of America, 2016

Regulation of AMPA receptor (AMPAR) function is a fundamental mechanism controlling synaptic strength during long-term potentiation/depression and homeostatic scaling. AMPAR function and membrane trafficking is controlled by protein-protein interactions, as well as by posttranslational modifications. Phosphorylation of the GluA1 AMPAR subunit at S845 and S831 play especially important roles during synaptic plasticity. Recent controversy has emerged regarding the extent to which GluA1 phosphorylation may contribute to synaptic plasticity. Here we used a variety of methods to measure the population of phosphorylated GluA1-containing AMPARs in cultured primary neurons and mouse forebrain. Phosphorylated GluA1 represents large fractions from 12% to 50% of the total population under basal and stimulated conditions in vitro and in vivo. Furthermore, a large fraction of synapses are positive for phospho-GluA1-containing AMPARs. Our results support the large body of research indicating a prominent role of GluA1 phosphorylation in synaptic plasticity.