rudyvdbrink/CitationDatabase huggingface dataset:
Paediatric arachnoid cysts: Surgical outcomes from a Singapore children's hospital.
Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia, 2021

Arachnoid cysts (AC) are reported to have a prevalence of up to 2.6% in children. Most AC remain indolent, but others may expand or rupture to cause life-threatening symptoms of raised intracranial pressure. Currently, there are 2 controversial topics with regards to the management of ACs: the indications for surgery and the choice of surgical procedure. We therein report our institution's neurosurgical experience for symptomatic AC over a 22-year period and corroborate our results with published literature. This is a single institution, retrospective study conducted at KK Women's and Children's Hospital from 01 January 1998 to 31 December 2019. A total of 38 patients with ACs that required surgery were recruited. The 3 most common anatomical locations were in the middle cranial fossa (40.5%), posterior fossa (24.3%) and interhemispheric (13.5%). Typical clinical presentations included symptoms of raised intracranial pressure (34.2%), obstructive hydrocephalus (28.9%) and AC rupture (21.1%). Surgical approaches included 17 craniotomy-based procedures, 7 endoscopic fenestrations, 11 cystoperitoneal shunts, 2 burrhole drainage operations and 1 excision of spinal AC. Thirteen patients (34.2%) underwent either another operation due to the lack of resolution of their AC-related symptoms or secondary to complications directly related to their initial surgery. Average length of followup from time of first operation was 84.1 months. Overall, our results demonstrate similarities in epidemiology, clinical presentation and surgical experience, in comparison to larger cohort studies. We advocate collaborative efforts to better understanding of the pathophysiology of paediatric ACs, particularly for deciding between the various surgical treatment modalities.
MicroRNA miR124 is required for the expression of homeostatic synaptic plasticity.
Nature communications, 2015

Homeostatic synaptic plasticity is a compensatory response to alterations in neuronal activity. Chronic deprivation of neuronal activity results in an increase in synaptic AMPA receptors (AMPARs) and postsynaptic currents. The biogenesis of GluA2-lacking, calcium-permeable AMPARs (CP-AMPARs) plays a crucial role in the homeostatic response; however, the mechanisms leading to CP-AMPAR formation remain unclear. Here we show that the microRNA, miR124, is required for the generation of CP-AMPARs and homeostatic plasticity. miR124 suppresses GluA2 expression via targeting its 3'-UTR, leading to the formation of CP-AMPARs. Blockade of miR124 function abolishes the homeostatic response, whereas miR124 overexpression leads to earlier induction of homeostatic plasticity. miR124 transcription is controlled by an inhibitory transcription factor EVI1, acting by association with the deacetylase HDAC1. Our data support a cellular cascade in which inactivity relieves EVI1/HDAC-mediated inhibition of miR124 gene transcription, resulting in enhanced miR124 expression, formation of CP-AMPARs and subsequent induction of homeostatic synaptic plasticity.
Falls Risk in Relation to Activity Exposure in High-Risk Older Adults.
The journals of gerontology. Series A, Biological sciences and medical sciences, 2020

Physical activity is linked to many positive health outcomes, stimulating the development of exercise programs. However, many falls occur while walking and so promoting activity might paradoxically increase fall rates, causing injuries, and worse quality of life. The relationship between activity exposure and fall rates remains unclear. We investigated the relationship between walking activity (exposure to risk) and fall rates before and after an exercise program (V-TIME).
Therapeutic potential of resveratrol in Alzheimer's disease.
BMC neuroscience, 2008

Several epidemiological studies indicate that moderate consumption of red wine is associated with a lower incidence of dementia and Alzheimer's disease. Red wine is enriched in antioxidant polyphenols with potential neuroprotective activities. Despite scepticism concerning the bioavailability of these polyphenols, in vivo data have clearly demonstrated the neuroprotective properties of the naturally occurring polyphenol resveratrol in rodent models for stress and diseases. Furthermore, recent work in cell cultures and animal models has shed light on the molecular mechanisms potentially involved in the beneficial effects of resveratrol intake against the neurodegenerative process in Alzheimer's disease.
Identity-by-descent mapping in a Scandinavian multiple sclerosis cohort.
European journal of human genetics : EJHG, 2015

In an attempt to map chromosomal regions carrying rare gene variants contributing to the risk of multiple sclerosis (MS), we identified segments shared identical-by-descent (IBD) using the software BEAGLE 4.0's refined IBD analysis. IBD mapping aims at identifying segments inherited from a common ancestor and shared more frequently in case-case pairs. A total of 2106 MS patients of Nordic origin and 624 matched controls were genotyped on Illumina Human Quad 660 chip and an additional 1352 ethnically matched controls typed on Illumina HumanHap 550 and Illumina 1M were added. The quality control left a total of 441 731 markers for the analysis. After identification of segments shared by descent and significance testing, a filter function for markers with low IBD sharing was applied. Four regions on chromosomes 5, 9, 14 and 19 were found to be significantly associated with the risk for MS. However, all markers but for one were located telomerically, including the very distal markers. For methodological reasons, such segments have a low sharing of IBD signals and are prone to be false positives. One marker on chromosome 19 reached genome-wide significance and was not one of the distal markers. This marker was located within the GNA11 gene, which contains no previous association with MS. We conclude that IBD mapping is not sufficiently powered to identify MS risk loci even in ethnically relatively homogenous populations, or that alternatively rare variants are not adequately present.
Sensitization of TRPV1 by protein kinase C in rats with mono-iodoacetate-induced joint pain.
Osteoarthritis and cartilage, 2016

To assess the functional changes of Transient receptor potential vanilloid 1 (TRPV1) receptor and to clarify its mechanism in a rat mono-iodoacetate (MIA)-induced joint pain model (MIA rats), which has joint degeneration with cartilage loss similar to osteoarthritis.
Complement factor H in AMD: Bridging genetic associations and pathobiology.
Progress in retinal and eye research, 2018

Age-Related Macular Degeneration (AMD) is a complex multifactorial disease characterized in its early stages by lipoprotein accumulations in Bruch's Membrane (BrM), seen on fundoscopic exam as drusen, and in its late forms by neovascularization ("wet") or geographic atrophy of the Retinal Pigmented Epithelial (RPE) cell layer ("dry"). Genetic studies have strongly supported a relationship between the alternative complement cascade, in particular the common H402 variant in Complement Factor H (CFH) and development of AMD. However, the functional significance of the CFH Y402H polymorphism remains elusive. In this article, we critically review the literature surrounding the functional significance of this polymorphism. Furthermore, based on our group's studies we propose a model in which CFH H402 affects CFH binding to heparan sulfate proteoglycans leading to accelerated lipoprotein accumulation in BrM and drusen progression. We also review the literature on the role of other complement components in AMD pathobiologies, including C3a, C5a and the membrane attack complex (MAC), and on transgenic mouse models developed to interrogate in vivo the effects of the CFH Y402H polymorphism.
Low Circulating Levels of GR, FKBP5, and SGK1 in Medicated Patients With Depression Are Not Altered by Electroconvulsive Therapy.
The journal of ECT, 2020

Hypothalamic-pituitary-adrenal axis dysregulation is frequently observed in patients with depression, with increased levels of the glucocorticoid (GC) cortisol commonly reported. Hypothalamic-pituitary-adrenal axis dysregulation may be a consequence of impaired feedback inhibition due to GC receptor (GR) impairments or dysfunction, termed "glucocorticoid resistance." Here, our objective was to assess mRNA levels of GC-related markers (GR, FKBP5, serum glucocorticoid kinase 1 [SGK1]) in patients with depression versus controls and in patient samples after electroconvulsive therapy (ECT). We also examined the relationship between these GC-related markers and 24-item Hamilton Depression Rating Scale (HAM-D24) scores to assess the utility of using them as biological markers for depression or the therapeutic response to ECT.
Emergent oscillations in evolutionary simulations: oscillating networks increase switching efficacy.
Journal of cognitive neuroscience, 2010

LeDoux [LeDoux, J. E. The emotional brain. New York: Simon & Schuster, 1996] motivated the direct route in his dual-pathway model by arguing that the ability to switch rapidly between different modes of behavior is highly adaptive. This motivation was supported by evolutionary simulations [den Dulk, P., Heerebout, B. T., & Phaf, R. H. A computational study into the evolution of dual-route dynamics for affective processing. Journal of Cognitive Neuroscience, 15, 194-208, 2003], in which foraging agents, controlled by simple inheritable neural networks, navigated an artificial world while avoiding predation. After many generations, a dual-processing architecture evolved that enabled a rapid switch to avoidance behavior when a predator appeared. We added recurrent connections to a new "context" layer in the indirect pathway to provide the agents with a working memory of previous input (i.e., a "context"). Unexpectedly, agents with oscillating networks emerged that had a much higher fitness than agents without oscillations. Oscillations seemed to have similar effects on switching speed as the dual-processing architecture, but they enhanced switching efficacy to a much larger degree. There has been much neurobiological speculation on the function, if any, of neural oscillations. These findings suggest that the facilitation of switching behavior is a likely candidate. Moreover, the strongly improved adaptation in the simulations contradicts the position that neural oscillations are merely a by-product of cell firing and have no functional value [Pareti, G., & De Palma, A. Does the brain oscillate? The dispute on neuronal synchronization. Neurological Sciences, 25, 41-47, 2004].
Anti-hyperalgesia effect of nanchelating based nano particle, RAc1, can be mediated via liver hepcidin expression modulation during persistent inflammation.
International immunopharmacology, 2019

Rheumatoid arthritis (RA) is a chronic systemic inflammatory disorder accompanied with hyperalgesia, edema and pain. At least 30% of the patients failed to respond to the available treatments and medications, which yet have a lot of serious adverse effects on patients. So, using novel technologies to produce more efficient medications is needed. According to the role of iron manipulation in inflammatory process, we have synthetized RAc1 nano particle, which contains zinc and has iron chelating property. In the present study, we evaluated RAc1 nano particle effects on hyperalgesia and liver hepcidin and serum IL-1β and TNF-α expression levels during acute and chronic phases of adjuvant-induced inflammation in male rats and compared its effects with Deferoxamine.
Exploiting the therapeutic potential of ready-to-use drugs: Repurposing antibiotics against amyloid aggregation in neurodegenerative diseases.
Progress in neurobiology, 2018

Neurodegenerative diseases are chronic and progressive disorders that affect specific regions of the brain, causing gradual disability and suffering that results in a complete inability of patients to perform daily functions. Amyloid aggregation of specific proteins is the most common biological event that is responsible for neuronal death and neurodegeneration in various neurodegenerative diseases. Therapeutic agents capable of interfering with the abnormal aggregation are required, but traditional drug discovery has fallen short. The exploration of new uses for approved drugs provides a useful alternative to fill the gap between the increasing incidence of neurodegenerative diseases and the long-term assessment of classical drug discovery technologies. Drug re-profiling is currently the quickest possible transition from bench to bedside. In this way, experimental evidence shows that some antibiotic compounds exert neuroprotective action through anti-aggregating activity on disease-associated proteins. The finding that many antibiotics can cross the blood-brain barrier and have been used for several decades without serious toxic effects makes them excellent candidates for therapeutic switching towards neurological disorders. The present review is, to our knowledge, the first extensive evaluation and analysis of the anti-amyloidogenic effect of different antibiotics on well-known disease-associated proteins. In addition, we propose a common structural signature derived from the antiaggregant antibiotic molecules that could be relevant to rational drug discovery.
Network dysfunction after traumatic brain injury.
Nature reviews. Neurology, 2014

Diffuse axonal injury after traumatic brain injury (TBI) produces neurological impairment by disconnecting brain networks. This structural damage can be mapped using diffusion MRI, and its functional effects can be investigated in large-scale intrinsic connectivity networks (ICNs). Here, we review evidence that TBI substantially disrupts ICN function, and that this disruption predicts cognitive impairment. We focus on two ICNs--the salience network and the default mode network. The activity of these ICNs is normally tightly coupled, which is important for attentional control. Damage to the structural connectivity of these networks produces predictable abnormalities of network function and cognitive control. For example, the brain normally shows a 'small-world architecture' that is optimized for information processing, but TBI shifts network function away from this organization. The effects of TBI on network function are likely to be complex, and we discuss how advanced approaches to modelling brain dynamics can provide insights into the network dysfunction. We highlight how structural network damage caused by axonal injury might interact with neuroinflammation and neurodegeneration in the pathogenesis of Alzheimer disease and chronic traumatic encephalopathy, which are late complications of TBI. Finally, we discuss how network-level diagnostics could inform diagnosis, prognosis and treatment development following TBI.
Targeting Ras-Driven Cancer Cell Survival and Invasion through Selective Inhibition of DOCK1.
Cell reports, 2017

Oncogenic Ras plays a key role in cancer initiation but also contributes to malignant phenotypes by stimulating nutrient uptake and promoting invasive migration. Because these latter cellular responses require Rac-mediated remodeling of the actin cytoskeleton, we hypothesized that molecules involved in Rac activation may be valuable targets for cancer therapy. We report that genetic inactivation of the Rac-specific guanine nucleotide exchange factor DOCK1 ablates both macropinocytosis-dependent nutrient uptake and cellular invasion in Ras-transformed cells. By screening chemical libraries, we have identified 1-(2-(3'-(trifluoromethyl)-[1,1'-biphenyl]-4-yl)-2-oxoethyl)-5-pyrrolidinylsulfonyl-2(1H)-pyridone (TBOPP) as a selective inhibitor of DOCK1. TBOPP dampened DOCK1-mediated invasion, macropinocytosis, and survival under the condition of glutamine deprivation without impairing the biological functions of the closely related DOCK2 and DOCK5 proteins. Furthermore, TBOPP treatment suppressed cancer metastasis and growth in vivo in mice. Our results demonstrate that selective pharmacological inhibition of DOCK1 could be a therapeutic approach to target cancer cell survival and invasion.
A comparison of experience-dependent locomotory behaviors and biogenic amine neurons in nematode relatives of Caenorhabditis elegans.
BMC neuroscience, 2010

Survival of an animal depends on its ability to match its responses to environmental conditions. To generate an optimal behavioral output, the nervous system must process sensory information and generate a directed motor output in response to stimuli. The nervous system should also store information about experiences to use in the future. The diverse group of free-living nematodes provides an excellent system to study macro- and microevolution of molecular, morphological and behavioral character states associated with such nervous system function. We asked whether an adaptive behavior would vary among bacterivorous nematodes and whether differences in the neurotransmitter systems known to regulate the behavior in one species would reflect differences seen in the adaptive behavior among those species. Caenorhabditis elegans worms slow in the presence of food; this 'basal' slowing is triggered by dopaminergic mechanosensory neurons that detect bacteria. Starved worms slow more dramatically; this 'enhanced' slowing is regulated by serotonin.
Sex differences in the effect of chronic mild stress on mouse prefrontal cortical BDNF levels: A role of major ovarian hormones.
Neuroscience, 2017

Depression induced by stress is affected by sex, age and hormonal status of the animal and also by duration and type of the stressors. Moreover, higher prevalence of depression and comorbidities in women than men implies the need to include the sex variable in studies on animal models of depression. The present study was therefore initiated to evaluate the effect of sex and ovarian hormones on depression-like phenotypes in mice exposed to a 21-day Chronic Variable Mild Stress (CVMS) paradigm. Adult male, intact female and, ovariectomized (OVX) female mice exposed to CVMS displayed despair behavior, a depression-like phenotype, in all the groups. However, intact females alone, but not males and OVX females, showed anhedonia, another depression-like phenotype. At the molecular level, the expression of Brain-Derived Neurotrophic Factor (BDNF), a neuropeptide associated with depression, and few other stress-specific genes CRH, NR3C1, CART, and NPY were measured in the Prefrontal Cortex (PFC) region of the reward circuitry. There was a significant decrease in the BDNF protein expression along with an increase in the mRNA expression of CRH, NR3C1, CART, and NPY in intact females, but not in the other two groups of mice. OVX females resembled males in behavioral and molecular responses to CVMS. 17β-Estradiol (E2) administration, not Progesterone (P4), to OVX female stress mice, mitigated despair and enhanced hedonic capacity with an increased expression of BDNF in PFC. This study strengthens the evidence for the beneficial effects of E2 administration in stress condition.
Analysing concurrent transcranial magnetic stimulation and electroencephalographic data: A review and introduction to the open-source TESA software.
NeuroImage, 2017

The concurrent use of transcranial magnetic stimulation with electroencephalography (TMS-EEG) is growing in popularity as a method for assessing various cortical properties such as excitability, oscillations and connectivity. However, this combination of methods is technically challenging, resulting in artifacts both during recording and following typical EEG analysis methods, which can distort the underlying neural signal. In this article, we review the causes of artifacts in EEG recordings resulting from TMS, as well as artifacts introduced during analysis (e.g. as the result of filtering over high-frequency, large amplitude artifacts). We then discuss methods for removing artifacts, and ways of designing pipelines to minimise analysis-related artifacts. Finally, we introduce the TMS-EEG signal analyser (TESA), an open-source extension for EEGLAB, which includes functions that are specific for TMS-EEG analysis, such as removing and interpolating the TMS pulse artifact, removing and minimising TMS-evoked muscle activity, and analysing TMS-evoked potentials. The aims of TESA are to provide users with easy access to current TMS-EEG analysis methods and to encourage direct comparisons of these methods and pipelines. It is hoped that providing open-source functions will aid in both improving and standardising analysis across the field of TMS-EEG research.
Individual differences in the locus coeruleus-norepinephrine system: Relevance to stress-induced cardiovascular vulnerability.
Physiology & behavior, 2017

Repeated exposure to psychosocial stress is a robust sympathomimetic stressor and as such has adverse effects on cardiovascular health. While the neurocircuitry involved remains unclear, the physiological and anatomical characteristics of the locus coeruleus (LC)-norepinephrine (NE) system suggest that it is poised to contribute to stress-induced cardiovascular vulnerability. A major theme throughout is to review studies that shed light on the role that the LC may play in individual differences in vulnerability to social stress-induced cardiovascular dysfunction. Recent findings are discussed that support a unique plasticity in afferent regulation of the LC, resulting in either excitatory or inhibitory input to the LC during establishment of different stress coping strategies. This contrasting regulation of the LC by either afferent regulation, or distinct differences in stress-induced neuroinflammation would translate to differences in cardiovascular regulation and may serve as the basis for individual differences in the cardiopathological consequences of social stress. The goal of this review is to highlight recent developments in the interplay between the LC-NE and cardiovascular systems during repeated stress in an effort to advance therapeutic treatments for the development of stress-induced cardiovascular vulnerability.
Inhibitory Effects of Mas-Related Gene C Receptor on Chronic Morphine-Induced Spinal Glial Activation in Rats.
The Journal of pharmacology and experimental therapeutics, 2019

Glial activation plays a pivotal role in morphine tolerance. This study investigated effects of Mas-related gene (Mrg) C receptor on morphine-induced activation of microglia and astrocytes in the spinal cord and its underlying mechanisms. Intrathecal administration of morphine (20