rudyvdbrink/CitationDatabase huggingface dataset:
Prevalence of Vitamin D Deficiency in Patients Undergoing Elective Spine Surgery: A Cross-Sectional Analysis.
World neurosurgery, 2015

Decreased bone density secondary to osteoporosis and osteomalacia represents a significant risk factor for bony fracture and spinal instrumentation failure. We evaluated the incidence of vitamin D deficiency in patients undergoing elective spinal instrumentation to investigate which patient-level risk factors are associated with deficient vitamin D levels.
Latrophilin-2 and latrophilin-3 are redundantly essential for parallel-fiber synapse function in cerebellum.
eLife, 2020

Latrophilin-2 (Lphn2) and latrophilin-3 (Lphn3) are adhesion GPCRs that serve as postsynaptic recognition molecules in CA1 pyramidal neurons of the hippocampus, where they are localized to distinct dendritic domains and are essential for different sets of excitatory synapses. Here, we studied Lphn2 and Lphn3 in the cerebellum. We show that latrophilins are abundantly and differentially expressed in the cerebellar cortex. Using conditional KO mice, we demonstrate that the Lphn2/3 double-deletion but not the deletion of Lphn2 or Lphn3 alone suppresses parallel-fiber synapses and reduces parallel-fiber synaptic transmission by ~50% without altering release probability. Climbing-fiber synapses, conversely, were unaffected. Even though ~50% of total cerebellar Lphn3 protein is expressed in Bergmann glia, Lphn3 deletion from Bergmann glia did not detectably impair excitatory or inhibitory synaptic transmission. Our studies demonstrate that Lphn2 and Lphn3 are selectively but redundantly required in Purkinje cells for parallel-fiber synapses.
Individual differences in speech-in-noise perception parallel neural speech processing and attention in preschoolers.
Hearing research, 2017

From bustling classrooms to unruly lunchrooms, school settings are noisy. To learn effectively in the unwelcome company of numerous distractions, children must clearly perceive speech in noise. In older children and adults, speech-in-noise perception is supported by sensory and cognitive processes, but the correlates underlying this critical listening skill in young children (3-5 year olds) remain undetermined. Employing a longitudinal design (two evaluations separated by ∼12 months), we followed a cohort of 59 preschoolers, ages 3.0-4.9, assessing word-in-noise perception, cognitive abilities (intelligence, short-term memory, attention), and neural responses to speech. Results reveal changes in word-in-noise perception parallel changes in processing of the fundamental frequency (F0), an acoustic cue known for playing a role central to speaker identification and auditory scene analysis. Four unique developmental trajectories (speech-in-noise perception groups) confirm this relationship, in that improvements and declines in word-in-noise perception couple with enhancements and diminishments of F0 encoding, respectively. Improvements in word-in-noise perception also pair with gains in attention. Word-in-noise perception does not relate to strength of neural harmonic representation or short-term memory. These findings reinforce previously-reported roles of F0 and attention in hearing speech in noise in older children and adults, and extend this relationship to preschool children.
Regulation of postsynaptic structure and function by an A-kinase anchoring protein-membrane-associated guanylate kinase scaffolding complex.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009

A-kinase anchoring protein (AKAP) 79/150 is a scaffold protein found in dendritic spines that recruits the cAMP-dependent protein kinase (PKA) and protein phosphatase 2B-calcineurin (CaN) to membrane-associated guanylate kinase (MAGUK)-linked AMPA receptors (AMPARs) to control receptor phosphorylation and synaptic plasticity. However, AKAP79/150 may also coordinate regulation of AMPAR activity with spine structure directly through MAGUK binding and membrane-cytoskeletal interactions of its N-terminal targeting domain. In cultured hippocampal neurons, we observed that rat AKAP150 expression was low early in development but then increased coincident with spine formation and maturation. Overexpression of human AKAP79 in immature or mature neurons increased the number of dendritic filopodia and spines and enlarged spine area. However, RNA interference knockdown of AKAP150 decreased dendritic spine area only in mature neurons. Importantly, AKAP79 overexpression in immature neurons increased AMPAR postsynaptic localization and activity. Neither the AKAP79 PKA nor CaN anchoring domain was required for increasing dendritic protrusion numbers, spine area, or AMPAR synaptic localization; however, an internal region identified as the MAGUK binding domain was found to be essential as shown by expression of a MAGUK binding mutant that formed mainly filopodia and decreased AMPAR synaptic localization and activity. Expression of the AKAP79 N-terminal targeting domain alone also increased filopodia numbers but not spine area. Overall, these results demonstrate a novel structural role for AKAP79/150 in which the N-terminal targeting domain induces dendritic filopodia and binding to MAGUKs promotes spine enlargement and AMPAR recruitment.
Microstructure assessment of grey matter nuclei in adult tourette patients by diffusion tensor imaging.
Neuroscience letters, 2011

Tourette syndrome (TS) is a neuropsychiatric disorder with the cardinal symptoms of motor and vocal tics. The onset occurs during childhood; many patients experience a subsequent reduction of tic frequency and severity suggesting that the pathways involved play a significant developmental role. Research has mainly focused on the cortico-striato-thalamo-cortical circuit, but clinical symptoms and recent neuroimaging studies suggest the involvement of limbic structures as well. We acquired diffusion-weighted data at 1.5 T in fifteen adult patients fulfilling the DSM-IV-TR criteria for TS and in a healthy control group. Based on the Harvard-Oxford subcortical structural atlas we investigated the microstructure of grey matter nuclei such as the nucleus accumbens, the amygdala, the putamen, the pallidum and the thalamus. The basal ganglia and the thalamus show in the direct comparison between patients and control subjects no significant differences in the diffusion indices. However, within the Tourette group the correlation coefficients between diffusion parameters and measures of tic severity indicate that the individual microstructure of the basal ganglia has an influence on the individual clinical phenotype. The microstructure assessment of the amygdala and nucleus accumbens in TS revealed a significant difference for the left nucleus accumbens and the right amygdala. Our findings suggest two pathophysiologic patterns in TS. One pattern could indicate altered connectivity based on the correlation between the increased mean and axial diffusivity in the basal ganglia and tic severity. The other pattern is characterized by the increase in radial diffusivity in the amygdala and the correlation between radial diffusivity in the nucleus accumbens and tic measures indicating potentially altered myelination.
Long-Term Risk of Hip Fracture After Ischemic Stroke.
The Neurohospitalist, 2020

Data are lacking on the long-term risk of hip fracture among patients with ischemic stroke. A better understanding of the contemporary incidence of hip fracture after ischemic stroke could benefit patient care by promoting strategies to prevent this disabling complication in stroke survivors.
The blockade of the serotoninergic receptors 5-HT5A, 5-HT6 and 5-HT7 in the basolateral amygdala, but not in the hippocampus facilitate the extinction of fear memory.
Behavioural brain research, 2019

Extinction is the learned inhibition of retrieval. It is the mainstay of exposure therapy, which is widely used to treat drug addiction, phobias and fear-related pathologies such as post-traumatic stress disorder. The serotonin (5-HT) system is positioned to modulate the extinction circuitry via ascending 5-HT projections that innervate certain brain structures including the hippocampus and the basolateral amygdala (BLA). The most recently described serotoninergic receptors 5-HT5A, 5-HT6, 5-HT7 affect different memory processes and so are putative therapeutic targets for disorders related to cognition; however, their role in the extinction of contextual fear conditioning (CFC) has not been studied yet. Here we investigate the role of these receptors in the CA1 region of the hippocampus and the BLA in the extinction of CFC. For this, male rats were implanted with cannulae in the CA1 or in the BLA region through which they received immediately or 3 h after extinction training of CFC infusions of SB699551 (10 μg/side), 5-HT5A antagonist; WAY-208466 (0.04 μg/side), 5-HT6 agonist; SB-271046A (10 μg/side), 5-HT6 antagonist; AS-19 (5 μg/side), 5-HT7 agonist; SB-269970 (5 μg/side), 5-HT7 antagonist. After 24 h, animals were submitted to a 3 min extinction test. Results show that the infusion immediately after extinction training of 5-HT5A, 5-HT6 and 5-HT7 antagonists, and 3 h after extinction training of 5-HT5A and 5-HT7 antagonists in the BLA region, but not in CA1, facilitates the extinction of CFC memory.
The Subjective Value of Cognitive Effort is Encoded by a Domain-General Valuation Network.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019

Cognitive control is necessary for goal-directed behavior, yet people treat cognitive control demand as a cost, which discounts the value of rewards in a similar manner as other costs, such as delay or risk. It is unclear, however, whether the subjective value (SV) of cognitive effort is encoded in the same putatively domain-general brain valuation network implicated in other cost domains, or instead engages a distinct frontoparietal network, as implied by recent studies. Here, we provide rigorous evidence that the valuation network, with core foci in the ventromedial prefrontal cortex and ventral striatum, also encodes SV during cognitive effort-based decision-making in healthy, male and female adult humans. We doubly dissociate this network from frontoparietal regions that are instead recruited as a function of decision difficulty. We show that the domain-general valuation network jointly and independently encodes both reward benefits and cognitive effort costs. We also demonstrate that cognitive effort SV signals predict choice and are influenced by state and trait motivation, including sensitivity to reward and anticipated task performance. These findings unify cognitive effort with other cost domains, and suggest candidate neural mechanisms underlying state and trait variation in willingness to expend cognitive effort.
Intra-arterial stroke therapy: recanalization strategies, patient selection and imaging.
Neuroimaging clinics of North America, 2011

With more than 700,000 strokes per year resulting in greater than 160,000 deaths per year, stroke remains the leading cause of disability and third leading cause of death in the United States. Despite an overall decline in stroke mortality over the past 40 years, the total number of stroke deaths continues to increase, suggesting an increase in stroke incidence. The last 20 years of neuroscience advances have moved stroke from a condition that is monitored clinically and imaged serially as it evolves to an entity that can be treated acutely, with remarkable alterations in its natural history.
Prediction of Choice from Competing Mechanosensory and Choice-Memory Cues during Active Tactile Decision Making.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019

Perceptual decision making is an active process where animals move their sense organs to extract task-relevant information. To investigate how the brain translates sensory input into decisions during active sensation, we developed a mouse active touch task where the mechanosensory input can be precisely measured and that challenges animals to use multiple mechanosensory cues. Male mice were trained to localize a pole using a single whisker and to report their decision by selecting one of three choices. Using high-speed imaging and machine vision, we estimated whisker-object mechanical forces at millisecond resolution. Mice solved the task by a sensory-motor strategy where both the strength and direction of whisker bending were informative cues to pole location. We found competing influences of immediate sensory input and choice memory on mouse choice. On correct trials, choice could be predicted from the direction and strength of whisker bending, but not from previous choice. In contrast, on error trials, choice could be predicted from previous choice but not from whisker bending. This study shows that animal choices during active tactile decision making can be predicted from mechanosensory and choice-memory signals, and provides a new task well suited for the future study of the neural basis of active perceptual decisions.
Amyloid pathology is associated with progressive monoaminergic neurodegeneration in a transgenic mouse model of Alzheimer's disease.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008

beta-Amyloid (Abeta) pathology is an essential pathogenic component in Alzheimer's disease (AD). However, the significance of Abeta pathology, including Abeta deposits/oligomers and glial reactions, to neurodegeneration is unclear. In particular, despite the Abeta neurotoxicity indicated by in vitro studies, mouse models with significant Abeta deposition lack robust and progressive loss of forebrain neurons. Such results have fueled the view that Abeta pathology is insufficient for neurodegeneration in vivo. In this study, because monoaminergic (MAergic) neurons show degenerative changes at early stages of AD, we examined whether the APPswe/PS1DeltaE9 mouse model recapitulates progressive MAergic neurodegeneration occurring in AD cases. We show that the progression forebrain Abeta deposition in the APPswe/PS1DeltaE9 model is associated with progressive losses of the forebrain MAergic afferents. Significantly, axonal degeneration is associated with significant atrophy of cell bodies and eventually leads to robust loss (approximately 50%) of subcortical MAergic neurons. Degeneration of these neurons occurs without obvious local Abeta or tau pathology at the subcortical sites and precedes the onset of anxiety-associated behavior in the mice. Our results show that a transgenic mouse model of Abeta pathology develops progressive MAergic neurodegeneration occurring in AD cases.
Steroid-Based Amphiphiles for Membrane Protein Study: The Importance of Alkyl Spacers for Protein Stability.
Chembiochem : a European journal of chemical biology, 2018

Membrane proteins allow effective communication between cells and organelles and their external environments. Maintaining membrane protein stability in a non-native environment is the major bottleneck to their structural study. Detergents are widely used to extract membrane proteins from the membrane and to keep the extracted protein in a stable state for downstream characterisation. In this study, three sets of steroid-based amphiphiles-glyco-diosgenin analogues (GDNs) and steroid-based pentasaccharides either lacking a linker (SPSs) or containing a linker (SPS-Ls)-have been developed as new chemical tools for membrane protein research. These detergents were tested with three membrane proteins in order to characterise their ability to extract membrane proteins from the membrane and to stabilise membrane proteins long-term. Some of the detergents, particularly the SPS-Ls, displayed favourable behaviour with the tested membrane proteins. This result indicates the potential utility of these detergents as chemical tools for membrane protein structural study and a critical role of the simple alkyl spacer in determining detergent efficacy.
The spatiotemporal organization of episodic memory and its disruption in a neurodevelopmental disorder.
Scientific reports, 2019

Recent theories of episodic memory (EM) posit that the hippocampus provides a spatiotemporal framework necessary for representing events. If such theories hold true, then does the development of EM in children depend on the ability to first bind spatial and temporal information? And does this ability rely, at least in part, on normal hippocampal function? We investigated the development of EM in children 2-8 years of age (Study 1) and its impairment in Williams Syndrome, a genetic neurodevelopmental disorder characterized by visuospatial deficits and irregular hippocampal function, (Study 2) by implementing a nonverbal object-placement task that dissociates the what, where, and when components of EM. Consistent with the spatiotemporal-framework view of hippocampal EM, our results indicate that the binding of where and when in memory emerges earliest in development, around the age of 3, and is specifically impaired in WS. Space-time binding both preceded and was critical to full EM (what + where + when), and the successful association of objects to spatial locations seemed to mediate this developmental process.
Parvalbumin and calbindin expression in parallel thalamocortical pathways in a gleaning bat, Antrozous pallidus.
The Journal of comparative neurology, 2014

The pallid bat (Antrozous pallidus) listens to prey-generated noise to localize and hunt terrestrial prey while reserving echolocation to avoid obstacles. The thalamocortical connections in the pallid bat are organized as parallel pathways that may serve echolocation and prey localization behaviors. Thalamic inputs to the cortical echolocation call- and noise-selective regions originate primarily in the suprageniculate nucleus (SG) and ventral division of medial geniculate body (MGBv), respectively. Here we examined the distribution of parvalbumin (PV) and calbindin (CB) expression in cortical regions and thalamic nuclei of these pathways. Electrophysiology was used to identify cortical regions selective for echolocation calls and noise. Immunohistochemistry was used to stain for PV and CB in the auditory cortex and MGB. A higher percentage (relative to Nissl-stained cells) of PV(+) cells compared with CB(+) cells was found in both echolocation call- and noise-selective regions. This was due to differences in cortical layers V-VI, but not layers I-IV. In the MGB, CB(+) cells were present across all divisions of the MGB, with a higher percentage in the MGBv than the SG. Perhaps the most surprising result was the virtual absence of PV staining in the MGBv. PV staining was present only in the SG. Even in the SG, the staining was mostly diffuse in the neuropil. These data support the notion that calcium binding proteins are differentially distributed in different processing streams. Our comparative data, however, do not support a general mammalian pattern of PV/CB staining that distinguishes lemniscal and nonlemniscal pathways.
Socioeconomic status and inflammation: a meta-analysis.
Molecular psychiatry, 2020

Socioeconomic status (SES), often conceptualized as income, education, or occupation, is associated with risk for disease morbidity and psychopathology. Recent research has focused on the potential biological mechanisms linking lower SES and poor outcomes; much of this work has examined the relationship between SES and markers of systemic inflammation. The strength of the estimated association between SES and inflammatory markers varies widely across individual studies. Thus, we used meta-analytic techniques to quantify the magnitude of this relationship. To accomplish this, PubMed and PsycINFO were searched for papers that reported on SES and two commonly measured systemic inflammatory markers, C-reactive protein (CRP) and interleukin-6 (IL-6). Peer-reviewed, empirical papers conducted in non-patient populations were included. Data from 43 papers (N = 111,156) reporting a total of 63 relevant effect sizes were included in analyses. SES, broadly defined, was significantly associated with both levels of CRP (Z = 0.12; 95% CI, 0.09-0.16) and IL-6 (Z = 0.15; 95% CI, 0.12-0.18); individuals with lower SES showed higher levels of systemic inflammation. Subanalyses demonstrated that studies operationalizing SES as either levels of income or educational attainment also found significant associations with both CRP and IL-6. Moderator analyses revealed that effect sizes varied based on sample characteristics and analysis approaches. Lower SES is associated with significantly elevated levels of inflammatory markers of disease risk. Thus, pro-inflammatory pathways are likely an important mechanism translating socioeconomic inequalities into mental and physical health disparities.
A White Paper on the medical and social needs of people with epilepsy and intellectual disability: the Task Force on Intellectual Disabilities and Epilepsy of the International League Against Epilepsy.
Epilepsia, 2014

This White Paper builds on the publication of the International League Against Epilepsy (ILAE) and International Bureau for Epilepsy (IBE) report "Listening for a change-medical and social needs of people with intellectual disability who have epilepsy" (Listening for a change the medical and social needs of people with epilepsy and intellectual disability, ILAE, 2013). The Paper presents an overview of the recommendations of the report, which aim to improve the health and social care of this important population of people with epilepsy worldwide. Actions in four domains are indicated: (1) the development of standards and initiatives that would enhance diagnosis, pathways to investigation, and treatment; (2) the development of guidelines for treatment, specifically best practice in the management of antiepileptic drugs including rescue medication; (3) the development of standards for primary care, multidisciplinary teamwork, and clinical consultations, with emphasis on the need to enhance communication and improve access to information; and (4) the enhancement of links among different stakeholders including medical services, educational establishments, employment services, organizations providing opportunities for social engagement, and family members. The breadth of needs of this population is a challenge to the epilepsy world, spanning all the professional groupings, care providers, and the research modalities in epilepsy.
α2-Adrenergic Receptor in Liver Fibrosis: Implications for the Adrenoblocker Mesedin.
Cells, 2020

The noradrenergic system is proposed to play a prominent role in the pathogenesis of liver fibrosis. While α1- and β-adrenergic receptors (ARs) are suggested to be involved in a multitude of profibrogenic actions, little is known about α2-AR-mediated effects and their expression pattern during liver fibrosis and cirrhosis. We explored the expression of α2-AR in two models of experimental liver fibrosis. We further evaluated the capacity of the α2-AR blocker mesedin to deactivate hepatic stellate cells (HSCs) and to increase the permeability of human liver sinusoidal endothelial cells (hLSECs). The mRNA of α2a-, α2b-, and α2c-AR subtypes was uniformly upregulated in carbon tetrachloride-treated mice vs the controls, while in bile duct-ligated mice, only α2b-AR increased in response to liver injury. In murine HSCs, mesedin led to a decrease in α-smooth muscle actin, transforming growth factor-β and α2a-AR expression, which was indicated by RT-qPCR, immunocytochemistry, and Western blot analyses. In a hLSEC line, an increased expression of endothelial nitric oxide synthase was detected along with downregulated transforming growth factor-β. In conclusion, we suggest that the α2-AR blockade alleviates the activation of HSCs and may increase the permeability of liver sinusoids during liver injury.