pinecone/core-2020-05-10-deduplication huggingface dataset:
Emotion recognition specialization and context-dependent risk of anxiety and depression in adolescents

BACKGROUND: Some adolescents function poorly in apparently benign environments, while others thrive despite hassles and difficulties. The aim of this study was to examine if adolescents with specialized skills in the recognition of either positive or negative emotions have a context-dependent risk of developing an anxiety or depressive disorder during adolescence, depending on exposure to positive or harsh parenting.  \ud
METHODS: Data came from a large prospective Dutch population study (N = 1539). At age 11, perceived parental rejection and emotional warmth were measured by questionnaire, and emotion recognition skills by means of a reaction-time task. Lifetime diagnoses of anxiety and depressive disorders were assessed at about age 19, using a standardized diagnostic interview.  \ud
RESULTS: Adolescents who were specialized in the recognition of positive emotions had a relatively high probability to develop an anxiety disorder when exposed to parental rejection (Bspecialization*rejection = 0.23, P < 0.01) and a relatively low probability in response to parental emotional warmth (Bspecialization*warmth = -0.24, P = 0.01), while the opposite pattern was found for specialists in negative emotions. The effect of parental emotional warmth on depression onset was likewise modified by emotion recognition specialization (B = -0.13, P = 0.03), but the effect of parental rejection was not (B = 0.02, P = 0.72). In general, the relative advantage of specialists in negative emotions was restricted to fairly uncommon negative conditions.  \ud
CONCLUSIONS: Our results suggest that there is no unequivocal relation between parenting behaviors and the probability to develop an anxiety or depressive disorder in adolescence, and that emotion recognition specialization may be a promising way to distinguish between various types of context-dependent reaction patterns
Neural basis of nonanalytical reasoning expertise during clinical evaluation

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                  153485.pdf (publisher's version ) (Open Access)INTRODUCTION: Understanding clinical reasoning is essential for patient care and medical education. Dual-processing theory suggests that nonanalytic reasoning is an essential aspect of expertise; however, assessing nonanalytic reasoning is challenging because it is believed to occur on the subconscious level. This assumption makes concurrent verbal protocols less reliable assessment tools. METHODS: Functional magnetic resonance imaging was used to explore the neural basis of nonanalytic reasoning in internal medicine interns (novices) and board-certified staff internists (experts) while completing United States Medical Licensing Examination and American Board of Internal Medicine multiple-choice questions. RESULTS: The results demonstrated that novices and experts share a common neural network in addition to nonoverlapping neural resources. However, experts manifested greater neural processing efficiency in regions such as the prefrontal cortex during nonanalytical reasoning. CONCLUSIONS: These findings reveal a multinetwork system that supports the dual-process mode of expert clinical reasoning during medical evaluation
Association of cerebral white matter lesions with cognitive function and mood in Japanese elderly people: a population-based study.

[Background] To determine the relationships between regional white matter lesions (WMLs), lifestyle factors, and cognitive, motor function and mood. [Methods] A comprehensive evaluation, including brain MRI, blood tests, the Unified Parkinson's Disease Rating Scale, the Mini Mental State Examination, and the Geriatric Depression Scale, was performed for people aged 65 years or older living in Ama-cho on October 1, 2009. Participants were classified by severity of periventricular hyperintensities (PVH) and deep white matter hyperintensities (DWMH) using the Fazekas score. [Results] Of 900 eligible participants, 688 (76.4%) were enrolled, including 303 men. Significant predictors of severe PVH were older age, lower low-density lipoprotein cholesterol (LDL-C) levels, elevated blood pressure (BP), cerebral infarction, and no current alcohol use. Significant predictors of severe DWMH were older age, lower 1, 5-anhydroglucitol (1, 5-AG) levels, elevated BP, cerebral infarction, and no current alcohol use. Higher cognitive function was associated with younger age, female sex, mild DWMH, more years of education, and higher high-density lipoprotein cholesterol levels. Depressive symptoms were associated with lower 1, 5-AG levels, lower LDL-C levels, moderate to severe PVH, and no current alcohol use. [Conclusions] White matter lesions in elderly people were related to hypertension and impaired glucose tolerance. The severity of WMLs was associated with cognitive function and mood
PMCA4 (ATP2B4) mutation in familial spastic paraplegia causes delay in intracellular calcium extrusion

Background: Familial spastic paraplegia (FSP) is a heterogeneous group of disorders characterized primarily by progressive lower limb spasticity and weakness. More than 50 disease loci have been described with different modes of inheritance. Recently, we described a novel missense mutation (c.803G>A, p.R268Q) in the plasma membrane calcium ATPase (PMCA4, or ATP2B4) gene in a Chinese family with autosomal dominant FSP. Further to this finding, here we describe the functional effect of this mutation. Methods: As PMCA4 removes cytosolic calcium, we measured transient changes and the time-dependent decay of cytosolic calcium level as visualized by using fura-2 fluorescent dye with confocal microscopy in human SH-SY5Y neuroblastoma cells overexpressing either wild-type or R268Q mutant PMCA4. Results: Overexpressing both wild-type and R268Q PMCA4 significantly reduced maximum calcium surge after KCl-induced depolarization as compared with vector control cells. However, cells overexpressing mutant PMCA4 protein demonstrated significantly higher level of calcium surge when compared with wild-type. Furthermore, the steady-state cytosolic calcium concentration in these mutant cells remained markedly higher than the wild-type after SERCA inhibition by thapsigargin. Conclusion: Our result showed that p.R268Q mutation in PMCA4 resulted in functional changes in calcium homeostasis in human neuronal cells. This suggests that calcium dysregulation may be associated with the pathogenesis of FSP. © 2015 The Authors. Brain and Behavior published by Wiley Periodicals, Inc.published_or_final_versio
DTI and VBM reveal white matter changes without associated gray matter changes in patients with idiopathic restless legs syndrome

BACKGROUND AND PURPOSE\ud
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We evaluated cerebral white and gray matter changes in patients with iRLS in order to shed light on the pathophysiology of this disease.\ud
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METHODS\ud
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Twelve patients with iRLS were compared to 12 age- and sex-matched controls using whole-head diffusion tensor imaging (DTI) and voxel-based morphometry (VBM) techniques. Evaluation of the DTI scans included the voxelwise analysis of the fractional anisotropy (FA), radial diffusivity (RD), and axial diffusivity (AD).\ud
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RESULTS\ud
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Diffusion tensor imaging revealed areas of altered FA in subcortical white matter bilaterally, mainly in temporal regions as well as in the right internal capsule, the pons, and the right cerebellum. These changes overlapped with changes in RD. Voxel-based morphometry did not reveal any gray matter alterations.\ud
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CONCLUSIONS\ud
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We showed altered diffusion properties in several white matter regions in patients with iRLS. White matter changes could mainly be attributed to changes in RD, a parameter thought to reflect altered myelination. Areas with altered white matter microstructure included areas in the internal capsule which include the corticospinal tract to the lower limbs, thereby supporting studies that suggest changes in sensorimotor pathways associated with RLS
The neural correlates of subjectively perceived and passively matched loudness perception in auditory phantom perception

International audienceIntroduction: A fundamental question in phantom perception is determining whether the brain creates a network that represents the sound intensity of the auditory phantom as measured by tinnitus matching (in dB), or whether the phantom perception is actually only a representation of the subjectively perceived loudness. Methods: In tinnitus patients, tinnitus loudness was tested in two ways, by a numeric rating scale for subjectively perceived loudness and a more objective tinnitus-matching test, albeit it is still a subjective measure. Results: Passively matched tinnitus does not correlate with subjective numeric rating scale, and has no electrophysiological correlates. Subjective loudness, in a whole-brain analysis, is correlated with activity in the left anterior insula (alpha), the rostral/dorsal anterior cingulate cortex (beta), and the left parahip-pocampus (gamma). A ROI analysis finds correlations with the auditory cortex (high beta and gamma) as well. The theta band links gamma band activity in the auditory cortex and parahippocampus via theta–gamma nesting. Conclusions: Apparently the brain generates a network that represents subjectively perceived tinnitus loudness only, which is context dependent. The subjective loudness network consists of the anterior cingulate/insula, the parahippocam-pus, and the auditory cortex. The gamma band activity in the parahippocampus and the auditory cortex is functionally linked via theta–gamma nested lagged phase synchronization
The impact of transcranial direct current stimulation on inhibitory control in young adults

Background: 

There is increasing evidence that the dorso-lateral prefrontal cortex (DLPFC), a brain region related to reward and motivational processes, is involved in effective response inhibition and that decreased activity in this region coincides with reduced inhibitory capacity. Using transcranial direct current stimulation (tDCS) to manipulate cortical activation, this study examined whether cross-hemispheric tDCS over the DLPFC affected performance on an inhibitory control task.

Methods: 

Neurologically intact participants performed a modified Stroop color-word matching task before and after completing one of two tDCS conditions; (1) anodal stimulation over the left DLPFC or (2) sham tDCS.

Results: 

There was a statistically significant effect of tDCS condition on Stroop reaction time (RT) pre-post tDCS change scores. Participants who received anodal stimulation over the left DLPFC demonstrated statistically significant faster RT change scores on the Stroop items compared to participants in the sham condition. Although errors on Stroop incongruent items decreased before and after receiving the tDCS treatment, there were no significant differences in errors on Stroop items between the anodal stimulation over left DLPFC and sham tDCS conditions. Anodal tDCS, which is known to elevate neural excitation, may have enhanced activation levels in the left DLPFC and minimized impairment of inhibitory control, resulting in better task performance.

Conclusions: 

Current findings provide preliminary evidence that increased excitation of the left DLPFC improves inhibitory control and are a step toward understanding the potential of tDCS for moderating deficits in inhibitory control.Full Tex
A P300-based cognitive assessment battery

© 2015 The Authors. Brain and Behavior published by Wiley Periodicals, Inc.Background: It is well established that some patients who are diagnosed as being in a vegetative state or a minimally conscious state show reliable signs of volition that may only be detected by measuring neural responses. A pertinent question is whether these patients are capable of higher cognitive processes. Methods: Here, we develop a series of EEG paradigms that probe several core aspects of cognition at the bedside without the need for motor responses and explore the sensitivity of this approach in a group of healthy controls. Results: Using analysis of ERPs alone, this method can determine with high reliability whether individual participants are able to attend a stimulus stream, maintain items in working memory, or solve complex grammatical reasoning problems. Conclusion: We suggest that this approach could form the basis of a brain-based battery for assessing higher cognition in patients with severe motor impairments or disorders of consciousness
Intraventricular cerebrospinal fluid temperature analysis using MR diffusion-weighted imaging thermometry in Parkinson's disease patients, multiple system atrophy patients, and healthy subjects

[Purpose]We examined the temperature of the intraventricular cerebrospinal fluid (Tv) in patients with Parkinson's disease (PD) and those with multiple system atrophy (MSA) in comparison with healthy subjects, and we examined normal changes in this temperature with aging. [Methods]Tv was estimated by magnetic resonance (MR) diffusion-weighted imaging (DWI) thermometry in 36 PD patients (19 males, 17 females), 34 MSA patients (17 males, 17 females), 64 age-matched controls (27 men, 37 women), and 114 all-age adult controls (47 men, 67 women; 28–89 years old). The volume of lateral ventricles was also estimated using FreeSurfer in all subjects. Tv and ventricular volume data were compared among the PD and MSA patients and age-matched controls. We also evaluated the relationship between Tv and age in the 114 all-age controls, controlling for ventricular volume. Men and women were analyzed separately. [Results]The male PD and MSA patients had significantly higher Tv values compared to the male controls, with no significant difference in ventricular volume among them. There was no significant difference in Tv between the female patients and controls. In the all-age male controls, there was a significant negative correlation between Tv and age controlling for ventricular volume, and this was not observed in the women. [Conclusion]DWI thermometry is a useful and easy method for demonstrating an altered intracranial environment in male patients and healthy controls, but not in females. DWI thermometry can thus be used to help to explore the pathophysiology of Parkinsonian syndromes and to differentiate individuals affected by neurodegenerative disease with autonomic dysfunction from those without it
Blood pressure differences between patients with lacunar and nonlacunar infarcts

Background Elevated blood pressure is frequently seen in acute stroke, and patients with lacunar and nonlacunar infarcts may have different underlying mechanisms for increase in blood pressure. The impact of hypertension as a risk factor may also vary. The aims of the present study were to investigate blood pressure in patients presenting with lacunar syndromes but with different anatomical subtypes of stroke, to explore the impact of subtype on blood pressure, and to identify stroke-related factors associated with hypertension.
Methods Consecutive patients presenting with an acute lacunar syndrome were enrolled. Patients were classified into a lacunar or nonlacunar group based on radiological verified infarcts. Blood pressure was measured. Between-group differences were analyzed by χ2-test, t-test, and Mann–Whitney U test, as appropriate. We performed linear regression to analyze the association between blood pressure and lacunar infarct, and multiple linear regression to adjust for other covariates.
Results One hundred thirteen patients were included. Seventy five percent had lacunar and 25% nonlacunar infarcts. There was no significant difference in clinical severity between the two groups. In the linear regression model, we found a significant association between blood pressure and lacunar infarct. No other factor was significantly associated with blood pressure in the two groups.
Conclusions Lacunar infarcts may be independently associated with higher blood pressure compared to nonlacunar infarcts with the same clinical severity. Blood pressure differences between different subtypes of stroke may not be related to clinical severity but to the underlying cause of stroke
Blunted responses to reward in remitted post-traumatic stress disorder

Background: Recent evidence suggests blunted responses to rewarding stimuli in patients with post-traumatic stress disorder (PTSD). However, it is not clear whether these alterations in reward processing normalize in remitted PTSD patients.\ud
Methods: We tested behavioral and physiological responses to monetary reward in a spatial memory task in 13 accident survivors with remitted PTSD, 14 accident survivors who never had PTSD, and 16 nontrauma-exposed subjects. All accident survivors were recruited from two samples of severely physically injured patients, who had participated in previous prospective studies on the incidence of PTSD after accidental injury approximately 10 years ago. Reaction time, accuracy, skin conductance responses, and self-reported mood were assessed during the task.\ud
Results: Accident survivors who never had PTSD and nontrauma exposed controls reported significantly higher positive mood in the reinforced versus nonreinforced condition (P < 0.045 and P < 0.001, respectively), while there was no effect of reinforcement in remitted PTSD subjects.\ud
Conclusions: Our findings suggest an alteration of the reward system in remitted PTSD. Further research is needed to investigate whether altered reward processing is a residual characteristic in PTSD after remission of symptoms or, alternatively, a preexisting risk factor for the development of PTSD after a traumatic event
Open‐field arena boundary is a primary object of exploration for  Drosophila

Drosophila  adults, when placed into a novel open‐field arena, initially exhibit an elevated level of activity followed by a reduced stable level of spontaneous activity and spend a majority of time near the arena edge, executing motions along the walls. In order to determine the environmental features that are responsible for the initial high activity and wall‐following behavior exhibited during exploration, we examined wild‐type and visually impaired mutants in arenas with different vertical surfaces. These experiments support the conclusion that the wall‐following behavior of  Drosophila  is best characterized by a preference for the arena boundary, and not thigmotaxis or centrophobicity. In circular arenas,  Drosophila  mostly move in trajectories with low turn angles. Since the boundary preference could derive from highly linear trajectories, we further developed a simulation program to model the effects of turn angle on the boundary preference. In an hourglass‐shaped arena with convex‐angled walls that forced a straight versus wall‐following choice, the simulation with constrained turn angles predicted general movement across a central gap, whereas  Drosophila  tend to follow the wall. Hence, low turn angled movement does not drive the boundary preference. Lastly, visually impaired  Drosophila  demonstrate a defect in attenuation of the elevated initial activity. Interestingly, the visually impaired  w 1118   activity decay defect can be rescued by increasing the contrast of the arena's edge, suggesting that the activity decay relies on visual detection of the boundary. The arena boundary is, therefore, a primary object of exploration for  Drosophila .    In an open field arena, Drosophila spend the majority of time at the arena boundary even when additional vertical surfaces are present in the interior. The visually impaired white files have defects in the attenuation of exploratory activity. by increasing the contrast of the boundary, we can rescue this defect in white mutants, demonstrating that the boundary is a primary object of exploration in an open field arena
Selective inhibition of dopamine-beta-hydroxylase enhances dopamine release from noradrenergic terminals in the medial prefrontal cortex

Introduction: Disulfiram has been claimed to be useful in cocaine addiction therapy, its efficacy being attributed to dopamine-beta-hydroxylase (DBH) inhibition. Our previous results indicate that disulfiram and the selective DBH inhibitor nepicastat increase extracellular dopamine (DA) in the rat medial prefrontal cortex (mPFC), and markedly potentiated cocaine-induced increase. Concomitantly, in rats with cocaine self-administration history, cocaine-seeking behavior induced by drug priming was prevented, probably through overstimulation of D1 receptors due to the DA increase. The present research was aimed at studying the neurochemical mechanisms originating the enhanced DA release. Methods: Noradrenergic system ablation was attained by intracerebroventricular (i.c.v.) administration of the neurotoxin anti-DBH-saporin (aDBH-sap). DA, noradrenaline (NA), and DOPAC were assessed by HPLC after ex vivo tissue extraction or in vivo microdialysis. Control and denervated rats were subjected to microdialysis in the mPFC and caudate nucleus to evaluate the effect of nepicastat-cocaine combination on extracellular DA levels and their regulation by α2-adrenoceptors. Results: Fifteen days after neurotoxin or its vehicle administration, tissue and extracellular NA were reduced to less than 2% the control value, while extracellular DA was increased by approximately 100%. In control rats, nepicastat given alone and in combination with cocaine increased extracellular DA by about 250% and 1100%, respectively. In denervated rats, nepicastat slightly affected extracellular DA, while in combination with cocaine increased extracellular DA by 250%. No differences were found in the caudate nucleus. Clonidine almost totally reversed the extracellular DA elevation produced by nepicastat-cocaine combination, while it was ineffective in denervated rats. Conclusions: This research shows that the increase of extracellular DA produced by nepicastat alone or in combination with cocaine was prevented by noradrenergic denervation. The results indicate that nepicastat enhances DA release from noradrenergic terminals supposedly by removing NA from α2-autoreceptors. In addition to the inhibition of DA uptake, the latter mechanism may explain the synergistic effect of cocaine on nepicastat-induced DA release
Molecular neuropathology of the synapse in sheep with CLN5 Batten disease

© 2015 Published by Wiley Periodicals, Inc. Aims: Synapses represent a major pathological target across a broad range of neurodegenerative conditions. Recent studies addressing molecular mechanisms regulating synaptic vulnerability and degeneration have relied heavily on invertebrate and mouse models. Whether similar molecular neuropathological changes underpin synaptic breakdown in large animal models and in human patients with neurodegenerative disease remains unclear. We therefore investigated whether molecular regulators of synaptic pathophysiology, previously identified in Drosophila and mouse models, are similarly present and modified in the brain of sheep with CLN5 Batten disease. Methods: Gross neuropathological analysis of CLN5 Batten disease sheep and controls was used alongside postmortem MRI imaging to identify affected brain regions. Synaptosome preparations were then generated and quantitative fluorescent Western blotting used to determine and compare levels of synaptic proteins. Results: The cortex was particularly affected by regional neurodegeneration and synaptic loss in CLN5 sheep, whilst the cerebellum was relatively spared. Quantitative assessment of the protein content of synaptosome preparations revealed significant changes in levels of seven out of eight synaptic neurodegeneration proteins investigated in the motor cortex, but not cerebellum, of CLN5 sheep (α-synuclein, CSP-α, neurofascin, ROCK2, calretinin, SIRT2, and UBR4). Conclusions: Synaptic pathology is a robust correlate of region-specific neurodegeneration in the brain of CLN5 sheep, driven by molecular pathways similar to those reported in Drosophila and rodent models. Thus, large animal models, such as sheep, represent ideal translational systems to develop and test therapeutics aimed at delaying or halting synaptic pathology for a range of human neurodegenerative conditions