rudyvdbrink/CitationDatabase huggingface dataset:
Does Head Orientation Influence 3D Facial Imaging? A Study on Accuracy and Precision of Stereophotogrammetric Acquisition.
International journal of environmental research and public health, 2021

This study investigates the reliability and precision of anthropometric measurements collected from 3D images and acquired under different conditions of head rotation. Various sources of error were examined, and the equivalence between craniofacial data generated from alternative head positions was assessed. 3D captures of a mannequin head were obtained with a stereophotogrammetric system (Face Shape 3D MaxiLine). Image acquisition was performed with no rotations and with various pitch, roll, and yaw angulations. On 3D images, 14 linear distances were measured. Various indices were used to quantify error magnitude, among them the acquisition error, the mean and the maximum intra- and inter-operator measurement error, repeatability and reproducibility error, the standard deviation, and the standard error of errors. Two one-sided tests (TOST) were performed to assess the equivalence between measurements recorded in different head angulations. The maximum intra-operator error was very low (0.336 mm), closely followed by the acquisition error (0.496 mm). The maximum inter-operator error was 0.532 mm, and the highest degree of error was found in reproducibility (0.890 mm). Anthropometric measurements from alternative acquisition conditions resulted in significantly equivalent TOST, with the exception of Zygion (l)-Tragion (l) and Cheek (l)-Tragion (l) distances measured with pitch angulation compared to no rotation position. Face Shape 3D Maxiline has sufficient accuracy for orthodontic and surgical use. Precision was not altered by head orientation, making the acquisition simpler and not constrained to a critical precision as in 2D photographs.
Activation of transient receptor potential vanilloid 2-expressing primary afferents stimulates synaptic transmission in the deep dorsal horn of the rat spinal cord and elicits mechanical hyperalgesia.
The European journal of neuroscience, 2014

Probenecid, an agonist of transient receptor vanilloid (TRPV) type 2, was used to evaluate the effects of TRPV2 activation on excitatory and inhibitory synaptic transmission in the dorsal horn (DH) of the rat spinal cord and on nociceptive reflexes induced by thermal heat and mechanical stimuli. The effects of probenecid were compared with those of capsaicin, a TRPV1 agonist. Calcium imaging experiments on rat dorsal root ganglion (DRG) and DH cultures indicated that functional TRPV2 and TRPV1 were expressed by essentially non-overlapping subpopulations of DRG neurons, but were absent from DH neurons and DH and DRG glial cells. Pretreatment of DRG cultures with small interfering RNAs against TRPV2 suppressed the responses to probenecid. Patch-clamp recordings from spinal cord slices showed that probenecid and capsaicin increased the frequencies of spontaneous excitatory postsynaptic currents (sEPSCs) and spontaneous inhibitory postsynaptic currents in a subset of laminae III-V neurons. In contrast to capsaicin, probenecid failed to stimulate synaptic transmission in lamina II. Intrathecal or intraplantar injections of probenecid induced mechanical hyperalgesia/allodynia without affecting nociceptive heat responses. Capsaicin induced both mechanical hyperalgesia/allodynia and heat hyperalgesia. Activation of TRPV1 or TRPV2 in distinct sets of primary afferents increased the sEPSC frequencies in a largely common population of DH neurons in laminae III-V, and might underlie the development of mechanical hypersensitivity following probenecid or capsaicin treatment. However, only TRPV1-expressing afferents facilitated excitatory and/or inhibitory transmission in a subpopulation of lamina II neurons, and this phenomenon might be correlated with the induction of thermal heat hyperalgesia.
Phosphorylation of Rpt6 regulates synaptic strength in hippocampal neurons.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012

It has become increasingly evident that protein degradation via the ubiquitin proteasome system plays a fundamental role in the development, maintenance and remodeling of synaptic connections in the CNS. We and others have recently described the activity-dependent regulation of proteasome activity and recruitment of proteasomes into spine compartments involving the phosphorylation of the 19S ATPase subunit, Rpt6, by the plasticity kinase Ca(2+)/calmodulin-dependent protein kinase II α (CaMKIIα) (Bingol and Schuman, 2006; Djakovic et al., 2009; Bingol et al, 2010). Here, we investigated the role of Rpt6 phosphorylation on proteasome function and synaptic strength. Utilizing a phospho-specific antibody we verified that Rpt6 is phosphorylated at Serine 120 (S120) by CaMKIIα. In addition, we found that Rpt6 is phosphorylated by CaMKIIα in an activity-dependent manner. Furthermore, we showed that a serine 120 to aspartic acid phospho-mimetic mutant of Rpt6 (S120D) increases its resistance to detergent extraction in rat hippocampal dendrites, indicating phosphorylated Rpt6 may promote the tethering of proteasomes to scaffolds and cytoskeletal components. Expression of Rpt6 S120D decreased miniature EPSC (mEPSC) amplitude, while expression of a phospho-dead mutant (S120A) increased mEPSC amplitude. Surprisingly, homeostatic scaling of mEPSC amplitude produced by chronic application of bicuculline or tetrodotoxin is both mimicked and occluded by altered Rpt6 phosphorylation. Together, these data suggest that CaMKII-dependent phosphorylation of Rpt6 at S120 may be an important regulatory mechanism for proteasome-dependent control of synaptic remodeling in slow homeostatic plasticity.
Abnormal 5-HT modulation of stress behaviors in the Kv4.2 knockout mouse.
Neuroscience, 2010

The Kv4.2 gene codes for an essential subunit of voltage-gated A-type potassium channels that are involved in dendritic signal integration and synaptic plasticity. Detailed cellular characterization in CA1 pyramidal neurons of the hippocampus has shown that knocking out the Kv4.2 gene increases neuronal excitability and promotes long-term potentiation. However, the overall behavioral consequences of these modifications have not been fully explored. Given the growing connection between neuronal plasticity and affect processing in the hippocampus and other Kv4.2 expressing regions, we proposed to investigate whether the absence of this gene would alter the stress response of mice to the forced swimming and tail suspension tests (TSTs) for depression-like behavior. Kv4.2 knockout (KO) mice, generated in the 129SvEv background, demonstrated elevated immobility and a loss of swimming, as well as antidepressant resistance to the selective 5-HT reuptake inhibitor fluoxetine (FLX). Characterization of a relatively new head movement behavior category, responsive to serotonergic treatment in wildtype (WT) mice, supported conclusions of abnormal 5-HT modulation. Electrophysiology recordings in the prefrontal cortex showed a blunting of postsynaptic response to direct 5-HT application following a single period of swim stress only in the animals without the Kv4.2 subunit. Based on our findings, we hypothesize that Kv4.2 KO mice may have an exaggerated 5-HT response to stress leading to a premature desensitization of postsynaptic receptors and a loss of continued behavior modulation. These results may shed some light on the involvement of A-type potassium channels in the effective action of selective serotonin reuptake inhibitor (SSRI) antidepressants.
Genome-wide meta-analysis identifies new loci and functional pathways influencing Alzheimer's disease risk.
Nature genetics, 2019

Alzheimer's disease (AD) is highly heritable and recent studies have identified over 20 disease-associated genomic loci. Yet these only explain a small proportion of the genetic variance, indicating that undiscovered loci remain. Here, we performed a large genome-wide association study of clinically diagnosed AD and AD-by-proxy (71,880 cases, 383,378 controls). AD-by-proxy, based on parental diagnoses, showed strong genetic correlation with AD (r
A cognitive neuroscience approach to individual differences in sensitivity to reward.
Neurotoxicity research, 2008

The Reinforcement Sensitivity Theory proposes that a neurobiological system, the Behavioral Activation System, defines individual differences on the subject's sensitivity and reactivity to appetitive stimuli associated with mesocorticolimbic structures, while this system does not mediate aversive stimulus processing. However, Jeffrey A. Gray's model also predicts the system's antagonism between this appetitive system and another aversive stimulus sensitive system, the Behavioral Inhibitory System/Fight-Flight-Freeze System, mostly associated with limbic structures. Therefore, direct modulation of brain activation during appetitive stimulus processing should be expected from the Behavioral Activation System, while inverse modulation during aversive stimulus processing may be expected to reflect the system's antagonism. Using the Sensitivity to Reward scale of the SPSR questionnaire to assess individual differences in the activity of the reward system, we present different behavioral and neuroimaging data to illustrate our view. The first experiment was based on a simple letter-judgment task while viewing erotic and aversive pictures selected from the International Affective Picture System. A second experiment employed a task performed by participants to detect infrequent aversive (i.e., stop) signals when responding to reward. The results from these studies were consistent with the idea that Behavioral Activation System-related personality traits mediate the brain activation associated with appetitive stimulus processing in reward-related areas, while it also showed its antagonism to aversive systems through a negative mediation on the limbic cortex activation. To conclude, sensitivity to reward may be understood as a form of impulsivity related to both better appetitive learning and poorer aversive learning.
A RAC/CDC-42-independent GIT/PIX/PAK signaling pathway mediates cell migration in C. elegans.
PLoS genetics, 2008

P21 activated kinase (PAK), PAK interacting exchange factor (PIX), and G protein coupled receptor kinase interactor (GIT) compose a highly conserved signaling module controlling cell migrations, immune system signaling, and the formation of the mammalian nervous system. Traditionally, this signaling module is thought to facilitate the function of RAC and CDC-42 GTPases by allowing for the recruitment of a GTPase effector (PAK), a GTPase activator (PIX), and a scaffolding protein (GIT) as a regulated signaling unit to specific subcellular locations. Instead, we report here that this signaling module functions independently of RAC/CDC-42 GTPases in vivo to control the cell shape and migration of the distal tip cells (DTCs) during morphogenesis of the Caenorhabditis elegans gonad. In addition, this RAC/CDC-42-independent PAK pathway functions in parallel to a classical GTPase/PAK pathway to control the guidance aspect of DTC migration. Among the C. elegans PAKs, only PAK-1 functions in the GIT/PIX/PAK pathway independently of RAC/CDC42 GTPases, while both PAK-1 and MAX-2 are redundantly utilized in the GTPase/PAK pathway. Both RAC/CDC42-dependent and -independent PAK pathways function with the integrin receptors, suggesting that signaling through integrins can control the morphology, movement, and guidance of DTC through discrete pathways. Collectively, our results define a new signaling capacity for the GIT/PIX/PAK module that is likely to be conserved in vertebrates and demonstrate that PAK family members, which are redundantly utilized as GTPase effectors, can act non-redundantly in pathways independent of these GTPases.
Syndemic effects of HIV risk behaviours: results from the NHANES study.
Epidemiology and infection, 2019

The aim of the present study is to use the syndemic framework to investigate the risk of contracting HIV in the US population. Cross-sectional analyses are from The National Health and Nutrition Examination Survey. We extracted and aggregated data on HIV antibody test, socio-demographic characteristics, alcohol use, drug use, depression, sexual behaviours and sexually transmitted diseases from cycle 2009-2010 to 2015-2016. We carried out weighted regression among young adults (20-39 years) and adults (40-59 years) separately. In total, 5230 men and 5794 women aged 20-59 years were included in the present analyses. In total, 0.8% men and 0.2% women were tested HIV-positive. Each increasing HIV risk behaviour was associated with elevated odds of being tested HIV-positive (1.15, 95% CI 1.15-1.15) among young adults and adults (1.61, 95% CI 1.61-1.61). Multi-faceted, community-based interventions are urgently required to reduce the incidence of HIV in the USA.
Inferring decoding strategies for multiple correlated neural populations.
PLoS computational biology, 2018

Studies of neuron-behaviour correlation and causal manipulation have long been used separately to understand the neural basis of perception. Yet these approaches sometimes lead to drastically conflicting conclusions about the functional role of brain areas. Theories that focus only on choice-related neuronal activity cannot reconcile those findings without additional experiments involving large-scale recordings to measure interneuronal correlations. By expanding current theories of neural coding and incorporating results from inactivation experiments, we demonstrate here that it is possible to infer decoding weights of different brain areas at a coarse scale without precise knowledge of the correlation structure. We apply this technique to neural data collected from two different cortical areas in macaque monkeys trained to perform a heading discrimination task. We identify two opposing decoding schemes, each consistent with data depending on the nature of correlated noise. Our theory makes specific testable predictions to distinguish these scenarios experimentally without requiring measurement of the underlying noise correlations.
Synaptic targeting and functional modulation of GluK1 kainate receptors by the auxiliary neuropilin and tolloid-like (NETO) proteins.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011

Auxiliary proteins modify the biophysical function and pharmacological properties of ionotropic glutamate receptors and likely are important components of receptor signaling complexes in vivo. The neuropilin and tolloid-like proteins (NETO) 1 and NETO2, two closely related CUB domain-containing integral membrane proteins, were identified recently as auxiliary proteins that slowed GluK2a kainate receptor current kinetics without impacting receptor membrane localization. Here we demonstrate that NETO2 profoundly slows the desensitization rate of GluK1 kainate receptors, promotes plasma membrane localization of transfected receptors in heterologous cells and rat hippocampal neurons, and targets GluK1-containing receptors to synapses. Conversely, the closely related protein NETO1 increases the rate of GluK1 receptor desensitization. Incorporation of NETO proteins into kainate receptor-signaling complexes therefore extends the temporal range of receptor gating by over an order of magnitude. The presence of these auxiliary proteins could underlie some of the unusual aspects of kainate receptor function in the mammalian CNS.
Electrophysiological indexes of ToM and non-ToM humor in healthy adults.
Experimental brain research, 2020

The cognitive processes involved in humor comprehension were analyzed by directly comparing the time course of brain activity associated with the perception of slapstick humor and that associated with the comprehension of humor requiring theory of mind (ToM). Four different comic strips (strips containing humorous scenes that required ToM, non-ToM humorous strips, non-humorous semantically coherent strips and non-humorous semantically incoherent strips) were presented to participants, while their EEG response was recorded. Results showed that both of the humorous comic strips and the semantically incongruent strip elicited an N400 effect, suggesting similar cognitive mechanisms underlying the processing of incongruent and humorous comic strips. The results also showed that the humorous ToM strips elicited a frontal late positive (LP) response, possibly reflecting the active deployment of ToM abilities such as perspective-taking and empathy that allow for the resolution and interpretation of apparently incongruent situations. In addition, the LP response was positively correlated with ratings of perceived amusement as well as individual empathy scores, suggesting that the increased LP response to ToM humorous strips reflects the combined activation of neural mechanisms involved in the experience of amusement and ToM abilities. Overall, humor comprehension appears to demand distinct cognitive steps such as the detection of incongruent semantic components, the construction of semantic coherence, and the appreciation of humoristic elements such as maladaptive emotional reactions. Our results show that the deployment of these distinct cognitive steps is at least partially dependent on individual empathic abilities.
Targeting mitochondria for neuroprotection in Parkinson's disease.
Antioxidants & redox signaling, 2012

Several genetic causes of familial Parkinson's disease (PD) have now been identified and include mutations of genes encoding mitochondrial proteins. Mitochondrial complex I toxins can induce dopaminergic cell death and produce a parkinsonian state. Importantly, defects of mitochondrial function have been identified in postmortem substantia nigra from pathologically proven cases of PD.
Resting-state brain oscillations predict trait-like cognitive styles.
Neuropsychologia, 2018

Anecdotal reports suggest the existence of individual differences in peoples' cognitive styles for solving problems, in particular, the tendency to rely on insight (the "aha" phenomenon) versus deliberate analytical thought. We hypothesized that such stable individual differences exist and are associated with trait-like individual differences in resting-state brain activity. We tested this idea by recording participants' resting-state electroencephalograms (RS-EEGs) on 4 occasions over approximately 7 weeks and then tasking them with solving anagrams and compound remote associates problems that are solvable by either strategy. We found that peoples' tendency to solve problems consistently by insight or by analysis spans both tasks and time. Moreover, we discovered trait-like individual differences in the balance between frontal and posterior resting-state brain activity and in temporal-lobe hemispheric asymmetries that predict, at least weeks in advance, the tendency to solve by insight versus analysis. The discovery of an insight-analytic dimension of cognitive style and its neural basis in resting state brain activity suggests new avenues for the development of neuroscience-based methods for intellectual, educational, and vocational assessment.
Quantum dot-loaded monofunctionalized DNA icosahedra for single-particle tracking of endocytic pathways.
Nature nanotechnology, 2016

Functionalization of quantum dots (QDs) with a single biomolecular tag using traditional approaches in bulk solution has met with limited success. DNA polyhedra consist of an internal void bounded by a well-defined three-dimensional structured surface. The void can house cargo and the surface can be functionalized with stoichiometric and spatial precision. Here, we show that monofunctionalized QDs can be realized by encapsulating QDs inside DNA icosahedra and functionalizing the DNA shell with an endocytic ligand. We deployed the DNA-encapsulated QDs for real-time imaging of three different endocytic ligands-folic acid, galectin-3 (Gal3) and the Shiga toxin B-subunit (STxB). Single-particle tracking of Gal3- or STxB-functionalized QD-loaded DNA icosahedra allows us to monitor compartmental dynamics along endocytic pathways. These DNA-encapsulated QDs, which bear a unique stoichiometry of endocytic ligands, represent a new class of molecular probes for quantitative imaging of endocytic receptor dynamics.
Axon Dynamics during Neocortical Laminar Innervation.
Cell reports, 2015

The cerebral cortex is a densely interconnected structure with neural circuits that form between cortical laminae and also between distinct cortical areas. However, the precise cell biological and developmental mechanisms that underlie the formation of these neural circuits remain unknown. Here, we visualize laminar innervation of the developing mouse cerebral cortex by layer II/III pyramidal neurons in real time, describing cytoskeletal dynamics during this process. We find that layer II/III pyramidal neurons achieve local laminar-specific innervation through the stabilization of collateral axon branches in target laminae. We also find that loss of neural activity does not abolish local laminar-specific innervation and that cells within the local environment are the likely source of cues that direct layer-specific cortical innervation.
Dual Dopaminergic Regulation of Corticostriatal Plasticity by Cholinergic Interneurons and Indirect Pathway Medium Spiny Neurons.
Cell reports, 2018

Endocannabinoid (eCB)-mediated long-term depression (LTD) requires dopamine (DA) D2 receptors (D2Rs) for eCB mobilization. The cellular locus of the D2Rs involved in LTD induction remains highly debated. We directly examined the role in LTD induction of D2Rs expressed by striatal cholinergic interneurons (Chls) and indirect pathway medium spiny neurons (iMSNs) using neuron-specific targeted deletion of D2Rs. Deletion of Chl-D2Rs (Chl-Drd2KO) impaired LTD induction in both subtypes of MSNs. LTD induction was restored in the Chl-Drd2KO mice by an M1-selective muscarinic acetylcholine receptor antagonist. In contrast, after the deletion of iMSN-D2Rs (iMSN-Drd2KO), LTD induction was intact in MSNs. Separate interrogation of direct pathway and iMSNs revealed a deficit in LTD induction only at synapses onto iMSNs that lack D2Rs. LTD induction in iMSNs was restored by D2R agonist application. Our findings suggest that Chl D2Rs strongly modulate LTD induction in MSNs, with iMSN-D2Rs having a weaker, iMSN-specific, modulatory effect.
Triiodothyronine accelerates and enhances the antipsychotic effect of risperidone in acute schizophrenia.
Journal of psychiatric research, 2016

In acute psychotic schizophrenia patients we investigated if the combination of triiodothyronine (T3) plus risperidone was more effective when compared to risperidone monotherapy. Thirty-two in-patients meeting the DSM-IV-TR diagnostic criteria for schizophrenia and without thyroid disease received risperidone (flexibly adjusted dose for tolerability) and were randomized to additionally receive either T3 (25 μg daily; risperidone plus T3 group) or placebo (risperidone plus placebo group). Treatment lasted until meeting the response to treatment criteria defined as score of ≤ 3 on the Clinical Global Impression Severity and Improvement scales. Acute psychotic episode symptom severity was evaluated using the Brief Psychiatric Rating Scale (BPRS) at treatment initiation and at the final study assessment. Fourteen patients were randomized to receive risperidone plus T3 and eighteen to receive risperidone plus placebo. The time until treatment response was shorter in the risperidone plus T3 group relative to the risperidone plus placebo group (25.5 ± 4.4 days vs 32.2 ± 8.2 days, respectively; p = 0.001). Moreover, there was a greater reduction of BPRS-total score (p = 0.01) in the risperidone plus T3 group relative to the risperidone plus placebo group. Treatment with T3 was associated with shorter time to treatment response (β = -0.440, p = 0.022) and with greater improvement in BPRS score (β = 0.240, p = 0.053), independent of patients' gender, age, baseline BPRS score and mean risperidone dose. The study confirms that addition of T3 to risperidone was associated with accelerated and enhanced treatment response in acutely psychotic schizophrenic patients.