rudyvdbrink/CitationDatabase huggingface dataset:
Age differences in the fronto-striato-parietal network underlying serial ordering.
Neurobiology of aging, 2020

Maintaining the ability to arrange thoughts and actions in an appropriate serial order is crucial for complex behavior. We aimed to investigate age differences in the fronto-striato-parietal network underlying serial ordering using functional magnetic resonance imaging. We exposed 25 young and 27 older healthy adults to a digit ordering task, where they had to reorder and recall sequential digits or simply to recall them. We detected a network comprising of the lateral and medial prefrontal, posterior parietal, and striatal regions. In young adults, the prefrontal and parietal regions were more activated and more strongly connected with the supplementary motor area for "reorder & recall" than "pure recall" trials (psychophysiological interaction, PPI). In older adults, the prefrontal and parietal activations were elevated, but the PPI was attenuated. Individual adults who had a stronger PPI performed more accurately in "reorder & recall" trials. The decreased PPI appeared to be compensated by increased physiological correlations between the prefrontal/parietal cortex and the striatum, and by that between the striatum and the supplementary motor area.
A prognostic role for Low tri-iodothyronine syndrome in acute stroke patients: A systematic review and meta-analysis.
Clinical neurology and neurosurgery, 2018

Low triiodothyronine (T3) syndrome could be a powerful prognostic factor for acute stroke; yet, a prognostic role for low T3 has not been given enough importance in stroke management. This meta-analysis aimed to evaluate whether low T3 among acute stroke patients could be used as a prognostic biomarker for stroke severity, functional outcome, and mortality.
Management of opioid-induced constipation for people in palliative care.
International journal of palliative nursing, 2015

Constipation is common in the palliative population. Opioid medications, which are frequently prescribed to this cohort, represent a significant risk factor for this condition. Opioid-induced constipation may be of such severity that opioid doses are reduced or missed, and analgesia and quality of life are therefore reduced. However, underlying chronic constipation, local and systemic disease effects, and other medications may also precipitate constipation in this population. The assessment and treatment of constipation in a palliative individual should be undertaken in a fashion similar to that used in non-palliative patients. Initial management should include minimising exposure to predisposing factors and general measures such as encouraging hydration, fibre intake and mobility. Pharmacological treatment should commence with a stool softener and a stimulant laxative. Recently published literature demonstrates that newer laxatives, including lubiprostone (a chloride channel activator) and prucalopride (a 5-HT4 receptor agonist) can effectively treat opioid-induced constipation. For patients not responding to laxatives, opioid antagonists (non-specific or peripherally acting μ-opioid receptor antagonists) can be co-prescribed with laxatives. These agents have also proven efficacy in treating opioid-induced constipation. This review discusses the recent literature regarding the management of opioid-induced constipation and provides a rational approach to assessing and managing constipation in the palliative population.
Dynamic aspects of musical imagery.
Annals of the New York Academy of Sciences, 2012

Auditory imagery can represent many aspects of music, such as the starting pitches of a tune or the instrument that typically plays it. In this paper, I concentrate on more dynamic, or time-sensitive aspects of musical imagery, as demonstrated in two recently published studies. The first was a behavioral study that examined the ability to make emotional judgments about both heard and imagined music in real time. The second was a neuroimaging study on the neural correlates of anticipating an upcoming tune, after hearing a cue tune. That study found activation of several sequence-learning brain areas, some of which varied with the vividness of the anticipated musical memory. Both studies speak to the ways in which musical imagery allows us to judge temporally changing aspects of the represented musical experience. These judgments can be quite precise, despite the complexity of generating the rich internal representations of imagery.
Exercise-induced Hypoalgesia Is Impaired in Chronic Whiplash-associated Disorders (WAD) With Both Aerobic and Isometric Exercise.
The Clinical journal of pain, 2020

Exercise-induced hypoalgesia (EIH) can be impaired in patients with chronic pain and may be dependent on exercise type. Factors predictive of EIH are not known. This study aimed to: (1) compare EIH in participants with chronic whiplash-associated disorders (WAD) to asymptomatic controls, (2) determine if EIH differs between aerobic and isometric exercise, (3) determine predictors of EIH.
Associations between maternal psychological distress and salivary cortisol during pregnancy: A mixed-models approach.
Psychoneuroendocrinology, 2018

Maternal psychological distress during pregnancy is related to adverse child behavioral and emotional outcomes later in life, such as ADHD and anxiety/depression. The underlying mechanisms for this, however, are still largely unknown. The hypothalamic-pituitary-adrenal (HPA)-axis, with its most important effector hormone cortisol, has been proposed as a mechanism, but results have been inconsistent. The current study investigated the association between maternal psychological distress (i.e. anxiety and depressive symptoms) and maternal cortisol levels during pregnancy using a mixed models approach.
Gut microbes and the brain: paradigm shift in neuroscience.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014

The discovery of the size and complexity of the human microbiome has resulted in an ongoing reevaluation of many concepts of health and disease, including diseases affecting the CNS. A growing body of preclinical literature has demonstrated bidirectional signaling between the brain and the gut microbiome, involving multiple neurocrine and endocrine signaling mechanisms. While psychological and physical stressors can affect the composition and metabolic activity of the gut microbiota, experimental changes to the gut microbiome can affect emotional behavior and related brain systems. These findings have resulted in speculation that alterations in the gut microbiome may play a pathophysiological role in human brain diseases, including autism spectrum disorder, anxiety, depression, and chronic pain. Ongoing large-scale population-based studies of the gut microbiome and brain imaging studies looking at the effect of gut microbiome modulation on brain responses to emotion-related stimuli are seeking to validate these speculations. This article is a summary of emerging topics covered in a symposium and is not meant to be a comprehensive review of the subject.
Nephropathic cystinosis: an international consensus document.
Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 2014

Cystinosis is caused by mutations in the CTNS gene (17p13.2), which encodes for a lysosomal cystine/proton symporter termed cystinosin. It is the most common cause of inherited renal Fanconi syndrome in young children. Because of its rarity, the diagnosis and specific treatment of cystinosis are frequently delayed, which has a significant impact on the overall prognosis. In this document, we have summarized expert opinions on several aspects of the disease to improve knowledge and provide guidance for diagnosis and treatment.
IGF-1 promotes beta-amyloid production by a secretase-independent mechanism.
Biochemical and biophysical research communications, 2009

Beta-amyloid peptide (Abeta) is generated via the sequential proteolysis of beta-amyloid precursor protein (APP) by beta- and gamma-secretases, and plays a crucial role in the pathogenesis of Alzheimer's disease (AD). Here, we sought to clarify the role of insulin-like growth factor-1 (IGF-1), implicated in the AD pathomechanism, in the generation of Abeta. Treatment of neuroblastoma SH-SY5Y cells expressing AD-associated Swedish mutant APP with IGF-1 did not alter cellular levels of APP, but significantly increased those of beta-C-terminal fragment (beta-CTF) and secreted Abeta. IGF-1 also enhanced APP phosphorylation at Thr668. Treatment of beta-CTF-expressing cells with IGF-1 increased the levels of beta-CTF and secreted Abeta. The IGF-1-induced augmentation of beta-CTF was observed in the presence of gamma-secretase inhibitors, but not in cells expressing beta-CTF with a Thr668 to alanine substitution. These results suggest that IGF-1 promotes Abeta production through a secretase-independent mechanism involving APP phosphorylation.
Analysis of brain atrophy and local gene expression in genetic frontotemporal dementia.
Brain communications, 2020

Frontotemporal dementia is a heterogeneous neurodegenerative disorder characterized by neuronal loss in the frontal and temporal lobes. Despite progress in understanding which genes are associated with the aetiology of frontotemporal dementia, the biological basis of how mutations in these genes lead to cell loss in specific cortical regions remains unclear. In this work we combined gene expression data for 16,772 genes from the Allen Institute for Brain Science atlas with brain maps of gray matter atrophy in symptomatic
Toward Omics-Based, Systems Biomedicine, and Path and Drug Discovery Methodologies for Depression-Inflammation Research.
Molecular neurobiology, 2016

Meta-analyses confirm that depression is accompanied by signs of inflammation including increased levels of acute phase proteins, e.g., C-reactive protein, and pro-inflammatory cytokines, e.g., interleukin-6. Supporting the translational significance of this, a meta-analysis showed that anti-inflammatory drugs may have antidepressant effects. Here, we argue that inflammation and depression research needs to get onto a new track. Firstly, the choice of inflammatory biomarkers in depression research was often too selective and did not consider the broader pathways. Secondly, although mild inflammatory responses are present in depression, other immune-related pathways cannot be disregarded as new drug targets, e.g., activation of cell-mediated immunity, oxidative and nitrosative stress (O&NS) pathways, autoimmune responses, bacterial translocation, and activation of the toll-like receptor and neuroprogressive pathways. Thirdly, anti-inflammatory treatments are sometimes used without full understanding of their effects on the broader pathways underpinning depression. Since many of the activated immune-inflammatory pathways in depression actually confer protection against an overzealous inflammatory response, targeting these pathways may result in unpredictable and unwanted results. Furthermore, this paper discusses the required improvements in research strategy, i.e., path and drug discovery processes, omics-based techniques, and systems biomedicine methodologies. Firstly, novel methods should be employed to examine the intracellular networks that control and modulate the immune, O&NS and neuroprogressive pathways using omics-based assays, including genomics, transcriptomics, proteomics, metabolomics, epigenomics, immunoproteomics and metagenomics. Secondly, systems biomedicine analyses are essential to unravel the complex interactions between these cellular networks, pathways, and the multifactorial trigger factors and to delineate new drug targets in the cellular networks or pathways. Drug discovery processes should delineate new drugs targeting the intracellular networks and immune-related pathways.
Fasting-induced changes in hepatic thyroid hormone metabolism in male rats are independent of autonomic nervous input to the liver.
Endocrinology, 2014

During fasting, profound changes in the regulation of the hypothalamus-pituitary-thyroid axis occur in order to save energy and limit catabolism. In this setting, serum T3 and T4 are decreased without an appropriate TSH and TRH response reflecting central down-regulation of the hypothalamus-pituitary-thyroid axis. Hepatic thyroid hormone (TH) metabolism is also affected by fasting, because type 3 deiodinase (D3) is increased, which is mediated by serum leptin concentrations. A recent study showed that fasting-induced changes in liver TH sulfotransferases (Sults) and uridine 5'-diphospho-glucuronosyltransferase (Ugts) depend on a functional melanocortin system in the hypothalamus. However, the pathways connecting the hypothalamus and the liver that induce these changes are currently unknown. In the present study, we investigated in rats whether the fasting-induced changes in hepatic TH metabolism are regulated by the autonomic nervous system. We selectively cut either the sympathetic or the parasympathetic input to the liver. Serum and liver TH concentrations, deiodinase expression, and activity and Sult and Ugt expression were measured in rats that had been fasted for 36 hours or were fed ad libitum. Fasting decreased serum T3 and T4 concentrations, whereas intrahepatic TH concentrations remained unchanged. D3 expression and activity increased, as was the expression of constitutive androstane receptor, Sult1b1, and Ugt1a1, whereas liver D1 was unaffected. Neither sympathetic nor parasympathetic denervation affected the fasting-induced alterations. We conclude that fasting-induced changes in liver TH metabolism are not regulated via the hepatic autonomic input in a major way and more likely reflect a direct effect of humoral factors on the hepatocyte.
Blood plasma inflammation markers during epileptogenesis in post-status epilepticus rat model for temporal lobe epilepsy.
Epilepsia, 2013

Brain inflammation occurs during epileptogenesis and may contribute to the development and progression of temporal lobe epilepsy. Recently, several studies have indicated that seizures may also increase specific blood plasma cytokine levels in animal models as well as in human patients with epilepsy, suggesting that peripheral inflammation may serve as a biomarker for epilepsy. Moreover, studies in epilepsy animal models have shown that peripheral inflammation may play either a pathogenic or neuroprotective role.
Alterations in the Gut-Microbial-Inflammasome-Brain Axis in a Mouse Model of Alzheimer's Disease.
Cells, 2021

Alzheimer's disease (AD), a progressive neurodegenerative disorder characterized by memory loss and cognitive decline, is a major cause of death and disability among the older population. Despite decades of scientific research, the underlying etiological triggers are unknown. Recent studies suggested that gut microbiota can influence AD progression; however, potential mechanisms linking the gut microbiota with AD pathogenesis remain obscure. In the present study, we provided a potential mechanistic link between dysbiotic gut microbiota and neuroinflammation associated with AD progression. Using a mouse model of AD, we discovered that unfavorable gut microbiota are correlated with abnormally elevated expression of gut NLRP3 and lead to peripheral inflammasome activation, which in turn exacerbates AD-associated neuroinflammation. To this end, we observe significantly altered gut microbiota compositions in young and old 5xFAD mice compared to age-matched non-transgenic mice. Moreover, 5xFAD mice demonstrated compromised gut barrier function as evident from the loss of tight junction and adherens junction proteins compared to non-transgenic mice. Concurrently, we observed increased expression of NLRP3 inflammasome and IL-1β production in the 5xFAD gut. Consistent with our hypothesis, increased gut-microbial-inflammasome activation is positively correlated with enhanced astrogliosis and microglial activation, along with higher expression of NLRP3 inflammasome and IL-1β production in the brains of 5xFAD mice. These data indicate that the elevated expression of gut-microbial-inflammasome components may be an important trigger for subsequent downstream activation of inflammatory and potentially cytotoxic mediators, and gastrointestinal NLRP3 may promote NLRP3 inflammasome-mediated neuroinflammation. Thus, modulation of the gut microbiota may be a potential strategy for the treatment of AD-related neurological disorders in genetically susceptible hosts.
Closure of Patent Foramen Ovale Versus Medical Therapy in Patients With Cryptogenic Stroke or Transient Ischemic Attack: Updated Systematic Review and Meta-Analysis.
Stroke, 2018

Previous systematic reviews and meta-analyses compared the efficacy and safety of patent foramen ovale (PFO) closure versus medical treatment in patients with cryptogenic stroke or transient ischemic attack (TIA). Recently, new evidence from randomized trials became available.
Cueing color imagery: A critical analysis of imagery-perception congruency effects.
Journal of experimental psychology. Learning, memory, and cognition, 2019

The relation between mental imagery and visual perception is a long debated topic in experimental psychology. In a recent study, Wantz, Borst, Mast, and Lobmaier (2015) demonstrated that color imagery could benefit color perception in a task that involved generating imagery in response to a cue prior to a forced-choice color discrimination task. Here, we scrutinized whether the method of Wantz et al. warrants strong inferences about the role of color imagery in color perception. In Experiments 1-3, we demonstrate that the imagery effect reported by Wantz et al. does replicate nicely using their method but does not occur when cue-target contingencies and a redundancy between the imagery and response dimensions are removed from their method. In Experiments 4-6, we explored cued imagery effects further using a method in which the cued imagery dimension was orthogonal to the response dimension. The results of these experiments demonstrate that a compelling endogenously cued imagery effect does not occur for lone targets but does occur for singleton color targets embedded amid homogenous color distractors. (PsycINFO Database Record (c) 2019 APA, all rights reserved).
Searching for the elements of thought: reply to Franklin, Mrazek, Broadway, and Schooler (2013).
Psychological bulletin, 2013

Understanding thoughts with no perceptual basis is a complex problem, and the commentary by Franklin, Mrazek, Broadway, and Schooler (2013) highlighted some of the difficulties that can occur when theorizing about this topic. They argued that the suppression of external input during internal thought arises from the selection of internal information. However, once a process of competition has been resolved in favor of self-generated content, it is still necessary to explain the stability of that content over time. It is proposed that perceptual decoupling and the associated attenuation of external input make environmental information less likely to gain access to limited resources explaining how internal thoughts persist over time. Franklin and colleagues also claimed that perceptual decoupling is unnecessary for an internal train of thought because statements of necessity cannot be drawn from correlational evidence. However, experimentally induced internal trains of thought also compete with concurrent external information, and this mutual inhibition is easily explained by assuming perceptual decoupling is necessary for the integrity of a detailed internal train of thought. I argue that the fundamental advantage of the process-occurrence framework is to highlight that self-generated thought is an emergent property from a general-purpose cognitive architecture and that models such as these will deepen our understanding more effectively than those focused on describing specific mental states.
Netrin-1 overexpression promotes white matter repairing and remodeling after focal cerebral ischemia in mice.
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2013

Damage of oligodendrocytes after ischemia has negative impact on white matter integrity and neuronal function. In this work, we explore whether Netrin-1 (NT-1) overexpression facilitates white matter repairing and remodeling. Adult CD-1 mice received stereotactic injection of adeno-associated virus carrying NT-1 gene (AAV-NT-1). One week after gene transfer, mice underwent 60 minutes of middle cerebral artery occlusion. The effect of NT-1 on neural function was evaluated by neurobehavioral tests. Proliferated oligodendrocyte progenitor cells (OPCs), newly matured oligodendrocytes, and remyelination were semi-quantified by immunohistochemistry. The role of NT-1 in oligodendrogenesis was further explored by examining specific NT-1 receptors and their function. Netrin-1 overexpression was detected in neurons and astrocytes 2 weeks after AAV-NT-1 gene transfer and significantly improved the neurobehavioral outcomes compared with the control (P<0.05). In comparison with the control, proliferated OPCs, newly matured oligodendrocytes, and remyelination were greatly increased in the ipsilateral hemisphere of AAV-NT-1-transduced mice. Furthermore, both NT-1 receptors deleted in colorectal carcinoma and UNC5H2 were expressed on OPCs whereas only UNC5H2 was expressed in myelinated axons. Our study indicated that NT-1 promoted OPC proliferation, differentiation, and increased remyelination, suggesting that NT-1 is a promising factor for white matter repairing and remodeling after ischemia.
Superoxide anions modulate the effects of angiotensin-(1-7) in the rostral ventrolateral medulla on cardiac sympathetic afferent reflex and sympathetic activity in rats.
Neuroscience, 2012

Both angiotensin (Ang)-(1-7) and Ang II in the rostral ventrolateral medulla (RVLM) increase renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP) and enhance the cardiac sympathetic afferent reflex (CSAR). NAD(P)H oxidase-derived superoxide anions in the RVLM mediate the effects of Ang II on CSAR and sympathetic activity. However, whether the superoxide anions mediate the effects of Ang-(1-7) in RVLM is still unclear. This study was designed to determine whether superoxide anions mediate the effects of Ang-(1-7) in the RVLM, including increasing the RSNA and MAP and enhancing the CSAR, and to determine whether NAD(P)H oxidase is the major origin of the superoxide anions in rats. RSNA and MAP were recorded in sinoaortic-denervated and cervical-vagotomized rats with urethane and α-chloralose anesthesia. The CSAR was evaluated by the RSNA and MAP responses to the epicardial application of capsaicin. Bilateral RVLM microinjection of the superoxide anion scavengers tempol or tiron, or the NAD(P)H oxidase inhibitor apocynin inhibited the effects of Ang-(1-7) in RVLM, while the superoxide dismutase (SOD) inhibitor diethyldithiocarbamic acid (DETC) potentiated the effects of Ang-(1-7). Ang-(1-7) increased but Mas receptor antagonist D-Alanine-Ang-(1-7) (A-779) decreased the NAD(P)H oxidase activity and superoxide anion level in the RVLM. The Ang-(1-7)-induced increases in NAD(P)H oxidase activity and superoxide anion level were abolished by pre-treating the RVLM with apocynin or A-779 but not the AT(1) receptor antagonist losartan. The epicardial application of capsaicin increased NAD(P)H oxidase activity and superoxide anion level; the effect was inhibited by A-779 and enhanced by Ang-(1-7). These results indicate that superoxide anions are involved in modulating the effects of Ang-(1-7) and Mas receptor in the RVLM: increasing the RSNA and MAP and enhancing the CSAR. The enzyme of NAD(P)H oxidase is a major source of the superoxide anions that modulate the effects of Ang-(1-7) in the RVLM.