rudyvdbrink/CitationDatabase huggingface dataset:
Aberrations of anterior insular cortex functional connectivity in nontreatment-seeking alcoholics.
Psychiatry research. Neuroimaging, 2019

An emergent literature suggests that resting state functional magnetic resonance imaging (rsfMRI) functional connectivity (FC) patterns are aberrant in alcohol use disorder (AUD) populations. The salience network (SAL) is an established set of brain regions prominent in salience attribution and valuation, and includes the anterior insular cortex (AIC). The SAL is thought to play a role in AUD through directing increased attention to interoceptive cues of intoxication. There is very little information on the salience network (SAL) in AUD, and, in particular, there are no data on SAL FC in currently drinking, nontreatment seeking individuals with AUD (NTS). rsfMRI data from 16 NTS and 21 social drinkers (SD) were compared using FC correlation maps from ten seed regions of interest in the bilateral AIC. As anticipated, SD subjects demonstrated greater insular FC with frontal and parietal regions. We also found that, compared to SD, NTS had higher insular FC with hippocampal and medial orbitofrontal regions. The apparent overactivity in brain networks involved in salience, learning, and behavioral control in NTS suggests possible mechanisms in the development and maintenance of AUD.
Delayed injury of hippocampal interneurons after neonatal hypoxia-ischemia and therapeutic hypothermia in a murine model.
Hippocampus, 2018

Delayed hippocampal injury and memory impairments follow neonatal hypoxia-ischemia (HI) despite the use of therapeutic hypothermia (TH). Death of hippocampal pyramidal cells occurs acutely after HI, but characterization of delayed cell death and injury of interneurons (INs) is unknown. We hypothesize that injury of INs after HI is: (i) asynchronous to that of pyramidal cells, (ii) independent of injury severity, and (iii) unresponsive to TH. HI was induced in C57BL6 mice at p10 with unilateral right carotid ligation and 45 min of hypoxia (FiO
Spatial and temporal expression of folate-related transporters and metabolic enzymes during mouse placental development.
Placenta, 2012

It is well understood that maternal folate deficiency can cause abnormal fetal development. However, the extent to which placental development and function are also dependent upon folate uptake and metabolism remains unclear. To understand which trophoblast cell types may be affected by folate deficiency or abnormal folate metabolism, we completed a comprehensive spatial and temporal protein expression analysis of folate receptor (Folr), folate transporters (proton-coupled folate receptor [Slc46a1 or PCFT] and reduced folate carrier-1 [Rfc1]) and folate metabolic enzymes (5,10-methylenetetrahydrofolate reductase [Mthfr] and methionine synthase [Mtr]) in histological sections of mouse placentas from early development (E8.5) until term (E18.5). We observed that the highest level of protein expression was during early development (E8.5-E10.5), prior to the formation of the three main layers of the mature placenta suggesting that folate uptake and metabolism may be required for placental development, itself. As expected, the labyrinth trophoblast cells, which are responsible for nutrient transport, expressed these proteins throughout pregnancy, including robust expression in the sinusoidal trophoblast giant cells that line the maternal blood spaces. Other trophoblast giant cell (TGC) subtypes (parietal-TGCs and canal-TGCs), whose function does not include nutrient transport, expressed folate transporters and enzymes from E8.5 onwards. Remarkably, these proteins were also detected in glycogen trophoblast cells from E12.5-E18.5 suggesting a new role in folate uptake and metabolism for these cells. Together, these data provide evidence that folate may be necessary for normal placental development and function, and perturbations in its availability or metabolism may lead to secondary effects on fetal development.
Diagnostic Utility of Repetitive Nerve Stimulation in a Large Cohort of Patients With Myasthenia Gravis.
Journal of clinical neurophysiology : official publication of the American Electroencephalographic Society, 2017

Optimizing the diagnostic utility of repetitive nerve stimulation in myasthenia gravis (MG) may include tailoring the examination to clinical phenotype. Therefore, we analyzed all available repetitive nerve stimulation parameters in a large cohort of patients with confirmed MG diagnosis.
Ligand regulation of the quaternary organization of cell surface M3 muscarinic acetylcholine receptors analyzed by fluorescence resonance energy transfer (FRET) imaging and homogeneous time-resolved FRET.
The Journal of biological chemistry, 2010

Flp-In(TM) T-REx(TM) 293 cells expressing a wild type human M(3) muscarinic acetylcholine receptor construct constitutively and able to express a receptor activated solely by synthetic ligand (RASSL) form of this receptor on demand maintained response to the muscarinic agonist carbachol but developed response to clozapine N-oxide only upon induction of the RASSL. The two constructs co-localized at the plasma membrane and generated strong ratiometric fluorescence resonance energy transfer (FRET) signals consistent with direct physical interactions. Increasing levels of induction of the FRET donor RASSL did not alter wild type receptor FRET-acceptor levels substantially. However, ratiometric FRET was modulated in a bell-shaped fashion with maximal levels of the donor resulting in decreased FRET. Carbachol, but not the antagonist atropine, significantly reduced the FRET signal. Cell surface homogeneous time-resolved FRET, based on SNAP-tag technology and employing wild type and RASSL forms of the human M(3) receptor expressed stably in Flp-In(TM) TREx(TM) 293 cells, also identified cell surface dimeric/oligomeric complexes. Now, however, signals were enhanced by appropriate selective agonists. At the wild type receptor, large increases in FRET signal to carbachol and acetylcholine were concentration-dependent with EC(50) values consistent with the relative affinities of the two ligands. These studies confirm the capacity of the human M(3) muscarinic acetylcholine receptor to exist as dimeric/oligomeric complexes at the surface of cells and demonstrate that the organization of such complexes can be modified by ligand binding. However, conclusions as to the effect of ligands on such complexes may depend on the approach used.
Dying in hospital: Qualitative study among caregivers of terminally ill patients who are transferred to the emergency department.
Presse medicale (Paris, France : 1983), 2018

Most people in France die in the hospital, even though a majority would like to die at home. These end-of-life hospital admissions sometimes occur in the emergency setting, in the hours preceding death.
Quality of sleep predicts increased frontoparietal network connectivity in patients with mild cognitive impairment.
Neurobiology of aging, 2020

High quality of sleep may mitigate the impact of pathophysiological mechanisms in mild cognitive impairment (MCI) through functional connectivity reorganization of neural networks underlying higher cognitive functions. Thirty-eight patients with MCI stratified into high and low quality of sleep in accordance with a self-reported questionnaire for sleep habits, and 38 controls underwent resting-state functional magnetic resonance imaging. Independent component analysis was used to reconstruct the default mode network and frontoparietal network (FPN). High quality of sleep was associated with increased FPN connectivity among patients with MCI. Moreover, a positive coupling of connectivity between networks was found in MCI reporting high quality of sleep, congruently with the pattern observed in controls, whereas this coupling was disrupted in MCI with low quality of sleep. An association between FPN connectivity and language scores was observed in MCI. These findings suggest a relationship between sleep quality and FPN connectivity in MCI that may underlie compensatory mechanisms to overcome advancing neurodegeneration.
A novel Tungsten-based fiducial marker for multi-modal brain imaging.
Journal of neuroscience methods, 2019

Multi-modal brain image registration is a prerequisite for accurate mapping of brain structure and function in neuroscience. Image registration is commonly performed using automated software; however, its accuracy decreases when images differ in modality, contrast, uniformity, and resolution. This limitation could be overcome by using an external reference point; however, high-contrast agents in multi-modal imaging have not been previously reported.
Patterned assembly and neurogenesis in the chick dorsal root ganglion.
The Journal of comparative neurology, 2010

The birth of small-diameter TrkA+ neurons that mediate pain and thermoreception begins approximately 24 hours after the cessation of neural crest cell migration from progenitors residing in the nascent dorsal root ganglion. Although multiple geographically distinct progenitor pools have been proposed, this study is the first to comprehensively characterize the derivation of small-diameter neurons. In the developing chick embryo we identify novel patterns in neural crest cell migration and colonization that sculpt the incipient ganglion into a postmitotic neuronal core encapsulated by a layer of proliferative progenitor cells. Furthermore, we show that this outer progenitor layer is composed of three spatially, temporally, and molecularly distinct progenitor zones, two of which give rise to distinct populations of TrkA+ neurons.
Precision Technique for Splenectomy Limits Mouse Stress Responses for Accurate and Realistic Measurements for Investigating Inflammation and Immunity.
Bio-protocol, 2019

Splenectomy in an animal model requires a standardized technique utilizing best practice to avoid variability which can result in adverse impact to the animal resulting in flawed physiologic responses simply due to technique rather than to the studied variables. In the case of the spleen, often investigators are analyzing the animal immune or inflammatory responses. Surgical splenectomy involves many variables from the training and expertise of the surgeon, which directly correlates to surgical technique to the length of operation and ease of the procedure. This operation, in turn, impacts blood loss and insensible fluid losses, sterile technique, unintended trauma to the spleen and surrounding organs, the length of the incision and the duration of the operation with more prolonged exposure to anesthetic agents. All these variables ultimately play a significant role in the experiment since they directly affect the response of the model in terms of inflammation, immune activation, or even suppression. Undesired variables such as these go unnoticed and lead to inaccurate and misleading data.
Morphine produces circuit-specific neuroplasticity in the bed nucleus of the stria terminalis.
Neuroscience, 2008

The bed nucleus of the stria terminalis (BST) is a brain structure located at the interface of the cortex and the cerebrospinal trunk. The BST is a cluster of nuclei organized in a complex intrinsic network that receives inputs from cortical and subcortical sources, and that sends a widespread top-down projection. There is growing evidence that the BST is a key component in the neurobiological basis of substance abuse. In the present study, the regulation of excitatory inputs onto identified neurons in the BST was examined in rats treated chronically with morphine. Neurons projecting to the ventral tegmental area (VTA) were identified by retrograde transport of fluorescent microspheres and recorded in the whole-cell voltage clamp configuration in brain slices. Selective excitatory inputs to these neurons were electrically evoked with electrodes placed in the medial and lateral aspects of the dorsal BST. The chronic morphine treatment selectively increased AMPA-dependent excitatory postsynaptic currents in a subset of inputs activated by dorso-lateral stimulation in the BST. Inputs activated by medial stimulation were not affected by morphine. Likewise, the inputs to neurons that did not project to the VTA were not changed by morphine. Altogether, these results extend the understanding of neuronal circuits intrinsically sensitive to drugs of abuse within the BST.
Sandwich masking eliminates both visual awareness of faces and face-specific brain activity through a feedforward mechanism.
Journal of vision, 2011

It is generally agreed that considerable amounts of low-level sensory processing of visual stimuli can occur without conscious awareness. On the other hand, the degree of higher level visual processing that occurs in the absence of awareness is as yet unclear. Here, event-related potential (ERP) measures of brain activity were recorded during a sandwich-masking paradigm, a commonly used approach for attenuating conscious awareness of visual stimulus content. In particular, the present study used a combination of ERP activation contrasts to track both early sensory-processing ERP components and face-specific N170 ERP activations, in trials with versus without awareness. The electrophysiological measures revealed that the sandwich masking abolished the early face-specific N170 neural response (peaking at ~170 ms post-stimulus), an effect that paralleled the abolition of awareness of face versus non-face image content. Furthermore, however, the masking appeared to render a strong attenuation of earlier feedforward visual sensory-processing signals. This early attenuation presumably resulted in insufficient information being fed into the higher level visual system pathways specific to object category processing, thus leading to unawareness of the visual object content. These results support a coupling of visual awareness and neural indices of face processing, while also demonstrating an early low-level mechanism of interference in sandwich masking.
IKKβ deficiency in myeloid cells ameliorates Alzheimer's disease-related symptoms and pathology.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014

Alzheimer's disease (AD) is characterized by extracellular amyloid-β (Aβ) deposits and microglia-dominated inflammatory activation. Innate immune signaling controls microglial inflammatory activities and Aβ clearance. However, studies examining innate immunity in Aβ pathology and neuronal degeneration have produced conflicting results. In this study, we investigated the pathogenic role of innate immunity in AD by ablating a key signaling molecule, IKKβ, specifically in the myeloid cells of TgCRND8 APP-transgenic mice. Deficiency of IKKβ in myeloid cells, especially microglia, simultaneously reduced inflammatory activation and Aβ load in the brain and these effects were associated with reduction of cognitive deficits and preservation of synaptic structure proteins. IKKβ deficiency enhanced microglial recruitment to Aβ deposits and facilitated Aβ internalization, perhaps by inhibiting TGF-β-SMAD2/3 signaling, but did not affect Aβ production and efflux. Therefore, inhibition of IKKβ signaling in myeloid cells improves cognitive functions in AD mice by reducing inflammatory activation and enhancing Aβ clearance. These results contribute to a better understanding of AD pathogenesis and could offer a new therapeutic option for delaying AD progression.
Population profiles of child-reported psychotic-like experiences and their differential association with other psychopathologies.
The British journal of clinical psychology, 2020

Childhood psychotic-like experiences (PLEs) increase risk for concurrent and future psychiatric disorders but are common in the population. Strategies are needed to identify vulnerable individuals who may benefit from monitoring or targeted intervention. This study aimed to delineate profiles of childhood PLEs that might be differentially associated with other psychopathologies, and multiple psychopathology.
Pharmacological Rescue of Long-Term Potentiation in Alzheimer Diseased Synapses.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2017

Long-term potentiation (LTP) is an activity-dependent and persistent increase in synaptic transmission. Currently available techniques to measure LTP are time-intensive and require highly specialized expertise and equipment, and thus are not well suited for screening of multiple candidate treatments, even in animal models. To expand and facilitate the analysis of LTP, here we use a flow cytometry-based method to track chemically induced LTP by detecting surface AMPA receptors in isolated synaptosomes: fluorescence analysis of single-synapse long-term potentiation (FASS-LTP). First, we demonstrate that FASS-LTP is simple, sensitive, and models electrically induced LTP recorded in intact circuitries. Second, we conducted FASS-LTP analysis in two well-characterized Alzheimer's disease (AD) mouse models (3xTg and Tg2576) and, importantly, in cryopreserved human AD brain samples. By profiling hundreds of synaptosomes, our data provide the first direct evidence to support the idea that synapses from AD brain are intrinsically defective in LTP. Third, we used FASS-LTP for drug evaluation in human synaptosomes. Testing a panel of modulators of cAMP and cGMP signaling pathways, FASS-LTP identified vardenafil and Bay-73-6691 (phosphodiesterase-5 and -9 inhibitors, respectively) as potent enhancers of LTP in synaptosomes from AD cases. These results indicate that our approach could provide the basis for protocols to study LTP in both healthy and diseased human brains, a previously unattainable goal.
Optimizing Sleep in the Military: Challenges and Opportunities.
Chest, 2019

Historically, scientific knowledge gaps-including a lack of information regarding the minimum amount of sleep needed to sustain nominally adequate, militarily relevant performance, and nescience of the potential impact of chronic sleep restriction on health and psychological well-being-have hindered decision-making vis-à-vis sleep/alertness management in operational environments. However, against a backdrop of increasing awareness of the importance of sleep for sustaining both performance and health, military researchers are currently doing the following: (1) developing a comprehensive, individualized sleep/alertness management system to optimize the general effectiveness of military personnel (ie, without regard to the potential relationship between sleep and specific aspects of military performance, thus sidestepping what has historically been an impediment to development of such a system); and (2) investigating the prevalence, potentially unique etiology (eg, resulting from the interaction of long-term exposure to combat-related stressors and sleep restriction), and treatment of sleep disorders and comorbidities in the military population.
On-board recordings reveal no jamming avoidance in wild bats.
Proceedings. Biological sciences, 2015

Animals often deal with situations in which vast sensory input is received simultaneously. They therefore must possess sophisticated mechanisms to select important input and ignore the rest. In bat echolocation, this problem is at its extreme. Echolocating bats emit sound signals and analyse the returning echoes to sense their environment. Bats from the same species use signals with similar frequencies. Nearby bats therefore face the difficulty of distinguishing their own echoes from the signals of other bats, a problem often referred to as jamming. Because bats commonly fly in large groups, jamming might simultaneously occur from numerous directions and at many frequencies. Jamming is a special case of the general phenomenon of sensory segregation. Another well-known example is the human problem of following conversation within a crowd. In both situations, a flood of auditory incoming signals must be parsed into important versus irrelevant information. Here, we present a novel method, fitting wild bats with a miniature microphone, which allows studying jamming from the bat's 'point of view'. Previous studies suggested that bats deal with jamming by shifting their echolocation frequency. On-board recordings suggest otherwise. Bats shifted their frequencies, but they did so because they were responding to the conspecifics as though they were nearby objects rather than avoiding being jammed by them. We show how bats could use alternative measures to deal with jamming instead of shifting their frequency. Despite its intuitive appeal, a spectral jamming avoidance response might not be the prime mechanism to avoid sensory interference from conspecifics.
Bridging the gap between functional and anatomical features of cortico-cerebellar circuits using meta-analytic connectivity modeling.
Human brain mapping, 2014

Theories positing that the cerebellum contributes to cognitive as well as motor control are driven by two sources of information: (1) studies highlighting connections between the cerebellum and both prefrontal and motor territories, (2) functional neuroimaging studies demonstrating cerebellar activations evoked during the performance of both cognitive and motor tasks. However, almost no studies to date have combined these two sources of information and investigated cortico-cerebellar connectivity during task performance. Through the use of a novel neuroimaging tool (Meta-Analytic Connectivity Modelling) we demonstrate for the first time that cortico-cerebellar connectivity patterns seen in anatomical studies and resting fMRI are also present during task performance. Consistent with human and nonhuman primate anatomical studies cerebellar lobules Crus I and II were significantly coactivated with prefrontal and parietal cortices during task performance, whilst lobules HV, HVI, HVIIb, and HVIII were significantly coactivated with the pre- and postcentral gyrus. An analysis of the behavioral domains showed that these circuits were driven by distinct tasks. Prefrontal-parietal-cerebellar circuits were more active during cognitive and emotion tasks whilst motor-cerebellar circuits were more active during action execution tasks. These results highlight the separation of prefrontal and motor cortico-cerebellar loops during task performance, and further demonstrate that activity within these circuits relates to distinct functions.
Sleep Parameters and Overnight Urinary Melatonin Production in Children With Persistent Post-concussion Symptoms.
Pediatric neurology, 2020

Sleep disturbance is common after a mild traumatic brain injury (mTBI) in children, yet its biology is poorly understood. We aimed to explore sleep-related problems (SRPs), sleep-activity patterns, and endogenous melatonin production in children with different recovery trajectories following mTBI. We hypothesized that children with delayed recovery would have more SRPs and abnormal sleep-activity patterns, which would correlate with lower overnight melatonin production.