rudyvdbrink/CitationDatabase huggingface dataset:
Antimitochondrial Antibody-associated Myopathy with Slowly Progressive Cardiac Dysfunction.
Internal medicine (Tokyo, Japan), 2021

A 45-year-old woman was referred to our hospital for the evaluation of proximal muscle weakness and serum creatine kinase elevation [corrected]. She had atrial fibrillation and left ventricular asynergy. She was diagnosed with myopathy, accompanied by cardiomyopathy of unknown etiology. She was treated with prednisolone. After long-term follow-up and a detailed examination, the patient was diagnosed with antimitochondrial antibody (AMA)-associated myopathy with cardiac involvement. Although the patient received medical treatment, including beta-blockers and prednisolone, her cardiac function deteriorated progressively. Physicians should consider AMA-associated myopathy when diagnosing myopathies of unknown etiology. The presence of cardiac involvement should be proactively investigated in AMA-associated myopathy.
Antidepressant drug use in glioblastoma patients: an epidemiological view.
Neuro-oncology practice, 2020

Antidepressant drugs have shown antitumor activity in preclinical glioblastoma studies. Antidepressant drug use, as well as its association with survival, in glioblastoma patients has not been well characterized on a population level.
Selective calcification of rat brain lesions caused by systemic administration of kainic acid.
Histology and histopathology, 2003

Dystrophic calcification of previously damaged areas of nervous tissue occurs in a wide range of human diseases. The relationship between astroglial and microglial reactions and deposits of calcium salts was studied for up to five months in rats with a brain lesion produced by systemic administration of kainate. The morphology and atomic composition of the calcium salt deposits was also studied. Two types of lesions, sclerotic and liquefactive, were observed. In sclerotic lesions hyperplasia and hypertrophy of astrocytes partially substituted for the lost neurons, reaching a maximum in about twenty-five days after treatment. In liquefactive lesions, the astrocytic reaction occurred only around the liquefactive area. Microglial reaction was similar in both types of lesion and reached its highest expression in about twenty-five days. Calcium deposits were observed in the sclerotic but not in the liquefactive lesions. Clearly distinguishable granules of calcium salts were observed in sclerotic lesions under scanning electron microscopy after only five days post-injection. The size of calcified granules increased with time reaching 40 micro m or more in diameter at five months. The atomic composition of these deposits, studied by X-ray microanalysis, showed a time-dependent increase in calcium concentration. While there was no clear relationship between astroglial and microglial reactions and calcium salt deposits, the systemic injection of kainate produced progressively larger and more concentrated calcium deposits in sclerotic, but not in liquefactive lesions.
Prior Expectations of Motion Direction Modulate Early Sensory Processing.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2020

Perception is a process of inference, integrating sensory inputs with prior expectations. However, little is known regarding the temporal dynamics of this integration. It has been proposed that expectation plays a role early in the perceptual process, biasing sensory processing. Alternatively, others suggest that expectations are integrated only at later, postperceptual decision-making stages. The current study aimed to dissociate between these hypotheses. We exposed human participants (male and female) to auditory cues predicting the likely direction of upcoming moving dot patterns, while recording neural activity using magnetoencephalography (MEG). Participants' reports of the moving dot directions were biased toward the direction predicted by the cues. To investigate when expectations affected sensory representations, we used inverted encoding models to decode the direction represented in early sensory signals. Strikingly, the cues modulated the direction represented in the MEG signal as early as 150 ms after visual stimulus onset. While this may not reflect a modulation of the initial feedforward sweep, it does reveal a modulation of early sensory representations. Exploratory analyses showed that the neural modulation was related to perceptual expectation effects: participants with a stronger perceptual bias toward the predicted direction also revealed a stronger reflection of the predicted direction in the MEG signal. For participants with this perceptual bias, a correlation between decoded and perceived direction already emerged before visual stimulus onset, suggesting that the prestimulus state of the visual cortex influences sensory processing. Together, these results suggest that expectations play an integral role in the neural computations underlying perception.
Role of Rho-associated coiled-coil containing protein kinase in the spinal cord injury induced neuropathic pain.
The spine journal : official journal of the North American Spine Society, 2021

Spinal cord injury (SCI) can lead to increased phosphorylation of p38 in spinal cord microglia. This is one of the main causes for the development of persistent pain. Recently, we reported our study on the activation of p38 mitogen-activated protein kinases (MAPK) in spinal microglia, which has been considered the key molecule for the onset and maintenance of neuropathic pain after peripheral nerve injury, using a rat model. We also reported that the RhoA/Rho-associated coiled-coil containing protein kinase (ROCK) pathway mediates p38 activation in spinal microglia in peripheral nerve injury. But the precise mechanisms of neuropathic pain induced by SCI are still unclear.
Probabilistic mapping of language networks from high frequency activity induced by direct electrical stimulation.
Human brain mapping, 2020

Direct electrical stimulation (DES) at 50 Hz is used as a gold standard to map cognitive functions but little is known about its ability to map large-scale networks and specific subnetwork. In the present study, we aim to propose a new methodological approach to evaluate the specific hypothesis suggesting that language errors/dysfunction induced by DES are the result of large-scale network modification rather than of a single cortical region, which explains that similar language symptoms may be observed after stimulation of different cortical regions belonging to this network. We retrospectively examined 29 patients suffering from focal drug-resistant epilepsy who benefitted from stereo-electroencephalographic (SEEG) exploration and exhibited language symptoms during a naming task following 50 Hz DES. We assessed the large-scale language network correlated with behavioral DES-induced responses (naming errors) by quantifying DES-induced changes in high frequency activity (HFA, 70-150 Hz) outside the stimulated cortical region. We developed a probabilistic approach to report the spatial pattern of HFA modulations during DES-induced language errors. Similarly, we mapped the pattern of after-discharges (3-35 Hz) occurring after DES. HFA modulations concurrent to language symptoms revealed a brain network similar to our current knowledge of language gathered from standard brain mapping. In addition, specific subnetworks could be identified within the global language network, related to different language processes, generally described in relation to the classical language regions. Spatial patterns of after-discharges were similar to HFA induced during DES. Our results suggest that this new methodological DES-HFA mapping is a relevant approach to map functional networks during SEEG explorations, which would allow to shift from "local" to "network" perspectives.
Exploring social cognition in schizophrenia.
European archives of psychiatry and clinical neuroscience, 2017

The aim of the study was to compare social cognition between groups of patients diagnosed with schizophrenia and healthy controls and to replicate two previous studies using tests of social cognition that may be particularly sensitive to social cognitive deficits in schizophrenia. Thirty-eight first-admitted patients with schizophrenia and 38 healthy controls solved 11 "imaginary conversation (i.e., theory of mind)" items, 10 "psychological understanding" items, and 10 "practical understanding" items. Statistical tests were made of unadjusted and adjusted group differences in models adjusting for intelligence and neuropsychological test performance. Healthy controls performed better than patients on all types of social cognitive tests, particularly on "psychological understanding." However, after adjusting for intelligence and neuropsychological test performance, all group differences became nonsignificant. When intelligence and global cognitive functioning is taken into account, schizophrenia patients and healthy controls perform similarly on social cognitive tests.
Association of Sex With Frequent and Mild ABCA4 Alleles in Stargardt Disease.
JAMA ophthalmology, 2020

The mechanisms behind the phenotypic variability and reduced penetrance in autosomal recessive Stargardt disease (STGD1), often a blinding disease, are poorly understood. Identification of the unknown disease modifiers can improve patient and family counseling and provide valuable information for disease management.
Single-nucleus characterization of adult mouse spinal dynorphin-lineage cells and identification of persistent transcriptional effects of neonatal hindpaw incision.
Pain, 2021

Neonatal tissue damage can have long-lasting effects on nociceptive processing in the central nervous system, which may reflect persistent injury-evoked alterations to the normal balance between synaptic inhibition and excitation in the spinal dorsal horn. Spinal dynorphin-lineage (pDyn) neurons are part of an inhibitory circuit which limits the flow of nociceptive input to the brain and is disrupted by neonatal tissue damage. To identify the potential molecular underpinnings of this disruption, an unbiased single-nucleus RNAseq analysis of adult mouse spinal pDyn cells characterized this population in depth and then identified changes in gene expression evoked by neonatal hindpaw incision. The analysis revealed 11 transcriptionally distinct subpopulations (ie, clusters) of dynorphin-lineage cells, including both inhibitory and excitatory neurons. Investigation of injury-evoked differential gene expression identified 15 genes that were significantly upregulated or downregulated in adult pDyn neurons from neonatally incised mice compared with naive littermate controls, with both cluster-specific and pan-neuronal transcriptional changes observed. Several of the identified genes, such as Oxr1 and Fth1 (encoding ferritin), were related to the cellular stress response. However, the relatively low number of injury-evoked differentially expressed genes also suggests that posttranscriptional regulation within pDyn neurons may play a key role in the priming of developing nociceptive circuits by early-life injury. Overall, the findings reveal novel insights into the molecular heterogeneity of a key population of dorsal horn interneurons that has previously been implicated in the suppression of mechanical pain and itch.
Placebo-induced pain reduction is associated with negative coupling between brain networks at rest.
NeuroImage, 2020

Placebos can reduce pain by inducing beliefs in the effectiveness of an actually inert treatment. Such top-down effects on pain typically engage lateral and medial prefrontal regions, the insula, somatosensory cortex, as well as the thalamus and brainstem during pain anticipation or perception. Considering the level of large-scale brain networks, these regions spatially align with fronto-parietal/executive control, salience, and sensory-motor networks, but it is unclear if and how placebos alter interactions between them during rest. Here, we investigated how placebo analgesia affected intrinsic network coupling. Ninety-nine human participants were randomly assigned to a placebo or control group and underwent resting-state fMRI after pain processing. Results revealed inverse coupling between two resting-state networks in placebo but not control participants. Specifically, networks comprised the bilateral somatosensory cortex and posterior insula, as well as the brainstem, thalamus, striatal regions, dorsal and rostral anterior cingulate cortex, and the anterior insula, respectively. Across participants, more negative between-network coupling was associated with lower individual pain intensity as assessed during a preceding pain task, and there was no significant relation with expectations of medication effectiveness in the placebo group. Altogether, these findings provide initial evidence that placebo analgesia affects the intrinsic communication between large-scale brain networks, even in the absence of pain. We suggest a theoretical model where placebo analgesia might affect processing within a descending pain-modulatory network, potentially segregating it from somatosensory regions that may code for painful experiences.
Electron microscopic localization of M2-muscarinic receptors in cholinergic and noncholinergic neurons of the laterodorsal tegmental and pedunculopontine nuclei of the rat mesopontine tegmentum.
The Journal of comparative neurology, 2016

Muscarinic m2 receptors (M2Rs) are implicated in autoregulatory control of cholinergic output neurons located within the pedunculopontine (PPT) and laterodorsal tegmental (LTD) nuclei of the mesopontine tegmentum (MPT). However, these nuclei contain many noncholinergic neurons in which activation of M2R heteroceptors may contribute significantly to the decisive role of the LTD and PPT in sleep-wakefulness. We examined the electron microscopic dual immunolabeling of M2Rs and the vesicular acetylcholine transporter (VAchT) in the MPT of rat brain to identify the potential sites for M2R activation. M2R immunogold labeling was predominately seen in somatodendritic profiles throughout the PPT/LTD complex. In somata, M2R immunogold particles were often associated with Golgi lamellae and cytoplasmic endomembrannes, but were rarely in contact with the plasma membrane, as was commonly seen in dendrites. Approximately 36% of the M2R-labeled somata and 16% of the more numerous M2R-labeled dendrites coexpressed VAchT. M2R and M2R/VAchT-labeled dendritic profiles received synapses from inhibitory- and excitatory-type axon terminals, over 88% of which were unlabeled and others contained exclusively M2R or VAchT immunoreactivity. In axonal profiles M2R immunogold was localized to plasmalemmal and cytoplasmic regions and showed a similar distribution in many VAchT-negative glial profiles. These results provide ultrastructural evidence suggestive of somatic endomembrane trafficking of M2Rs, whose activation serves to regulate the postsynaptic excitatory and inhibitory responses in dendrites of cholinergic and noncholinergic neurons in the MPT. They also suggest the possibility that M2Rs in this brain region mediate the effects of acetylcholine on the release of other neurotransmitters and on glial signaling. J. Comp. Neurol. 524:3084-3103, 2016. © 2016 Wiley Periodicals, Inc.
Antidepressant and pro-motivational effects of repeated lamotrigine treatment in a rat model of depressive symptoms.
Heliyon, 2018

The antiepileptic lamotrigine is approved for maintenance treatment of bipolar disorder and augmentation therapy in treatment-resistant depression. Previous preclinical investigations showed lamotrigine antidepressant-like effects without addressing its possible activity on motivational aspects of anhedonia, a symptom clinically associated with poor treatment response and with blunted mesolimbic dopaminergic responsiveness to salient stimuli in preclinical models. Thus, in rats expressing a depressive-like phenotype we studied whether repeated lamotrigine administration restored behavioral responses to aversive and positive stimuli and the dopaminergic response to sucrose in the nucleus accumbens shell (NAcS), all disrupted by stress exposure.
Neuroprotective activity of ursodeoxycholic acid in CHMP2B
Neurobiology of disease, 2020

Frontotemporal dementia (FTD) is one of the most prevalent forms of early-onset dementia. It represents part of the FTD-Amyotrophic Lateral Sclerosis (ALS) spectrum, a continuum of genetically and pathologically overlapping disorders. FTD-causing mutations in CHMP2B, a gene encoding a core component of the heteromeric ESCRT-III Complex, lead to perturbed endosomal-lysosomal and autophagic trafficking with impaired proteostasis. While CHMP2B mutations are rare, dysfunctional endosomal-lysosomal signalling is common across the FTD-ALS spectrum. Using our established Drosophila and mammalian models of CHMP2B
Chiari I malformation with neurogenic hypertension after suboccipital decompression.
Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery, 2021

Patients with Chiari I malformations have a spectrum of symptoms related to craniocervical structural compression. Neurogenic hypertension has been reported in some patients with this disorder, with resolution of hypertension after suboccipital decompressions in some cases. The pathophysiology of neurogenic hypertension in these patients is thought to be related to ventrolateral medullary compression. The important role of the ventrolateral medulla in blood pressure control has been studied extensively. In this report, we present the case of a pediatric patient diagnosed with a Chiari I malformation who developed hypertension after a suboccipital decompression. We believe that this case demonstrates the important role of the ventrolateral medulla in neurogenic hypertension.
A qualitative exploration of SMART Recovery meetings in Australia and the role of a digital platform to support routine outcome monitoring.
Addictive behaviors, 2020

Previous research has reported on the benefits of mutual support groups. However, such groups do not routinely collect data on participant outcomes. Moreover, the effect of collecting outcomes measures on these groups is unknown. The objective of this mixed methods study was to elicit participant views on using a novel, purpose built digital platform for routine outcome monitoring (ROM) as a standard component of a mutual support group. SMART Recovery, or the Self-Management and Recovery Training program, is group-based and uses professional clinicians to facilitate discussion and foster mutual support for a range of addictive behaviours, alongside Cognitive Behavioural Therapy and Motivational Interviewing techniques. This paper reports on the qualitative component of this study and how participants perceive ROMs, and the potential shift to technological resources. Twenty semi-structured telephone interviews were conducted with participants from SMART Recovery groups across New South Wales, Australia. Participants discussed their use of mutual support within group meetings to manage their recovery, including: naming their goals in front of peers; learning from clinicians and group discussion; and developing reciprocal and caring relationships. They also described any previous experience with routine outcomes measures and how digital technologies might enhance or hinder group function. Participants valued mutual support groups and reported that digital technologies could be complementary to physical, weekly group meetings. They were also concerned that the introduction of technological resources might pose a threat to physical meetings, thereby risking their access to mutual support. Findings have implications for the implementation of ROM when delivered via digital mechanisms, and indicate threats and opportunities that warrant consideration for future initiatives.
Biased interpretation in paranoia and its modification.
Journal of behavior therapy and experimental psychiatry, 2020

Cognitive models of psychosis implicate interpretation biases as one of the mechanisms involved in the formation and maintenance of symptoms. First we measured the strength of association between interpretation biases and psychosis-relevant traits. Next we manipulated these biases and quantified the effects of doing so on psychosis-relevant outcomes.
COVID-19 pandemic lockdown and problematic eating behaviors in a student population.
Journal of behavioral addictions, 2020

Since mid-March 2020, over 3 billion people have been confined as a result of the COVID-19 pandemic. Problematic eating behaviors are likely to be impacted by the pandemic through multiple pathways. This study examined the relationships between stress related to lockdown measures and binge eating and dietary restriction in a population of French students during the first week of confinement.
Lipocalin2 promotes cell proliferation and migration in ovarian cancer through activation of the ERK/GSK3β/β-catenin signaling pathway.
Life sciences, 2020

Lipocalin2 (Lcn2) has been shown to be a vital regulator of tumorigenesis in a variety of different cancers. However, its expression patterns and possible roles in ovarian cancer remain obscure. The aim of this study was to investigate the expression of Lcn2 in ovarian cancer cells and to determine any potential association between Lcn2 and ovarian tumor development and cancer progression. Our results indicated that Lcn2 was upregulated in tumor tissue from ovarian cancer patients as well as in three ovarian cancer cell lines compared to normal tissues and cells. Overexpression of Lcn2 promoted both cell proliferation and migration in ovarian cancer cells. Conversely, knockdown of Lcn2 in cell lines suppressed both migration and proliferation. Moreover, upregulation of Lcn2 contributed to tumor growth in nude mice in vivo. Mechanistically, Lcn2 was found to lead to tumor progression in ovarian cancer cells through activation of the ERK/GSK3β/β-catenin signaling pathway. In summary, Lcn2 promotes cell proliferation and migration in ovarian cancer through activation of the ERK/GSK3β/β-catenin signaling pathway, suggesting that Lcn2 might be a novel therapeutic target for ovarian cancer.
Genes and cognition.
Wiley interdisciplinary reviews. Cognitive science, 2011

Explaining individual differences in human cognition has been a prominent goal of psychological research during the last century. Converging lines of evidence from human and animal research have shown that these differences are under the influence of genetic factors. However, identifying the specific genes involved is not an easy task. The complexities of the human genome and of the definition of the concept of cognition itself are obvious reasons why understanding the genetics of cognitive abilities is so complicated. About 20,000 genes are thought to have an impact on the development and functionality of the brain and each and every one of these may in fact have an effect on information processing, and therefore on cognition. In addition, the concept of cognition itself is very broad and has often been the subject of intense debate. It is therefore important to provide a precise definition of the cognitive phenotype before analyzing the genetic influences acting on it. Furthermore, the genetics of cognition can be investigated by multiple approaches that can be applied not only to human, but also to animal research. An overview of these methods and some of the results obtained is provided in an attempt to highlight the multidisciplinary complexity of studying the genetic bases of human cognition. Furthermore, some directions for future studies are suggested, highlighting the importance of analyzing gene-environment interactions and avoiding deterministic approaches. WIREs Cogni Sci 2011 2 345-352 DOI: 10.1002/wcs.135 For further resources related to this article, please visit the WIREs website.