bluuebunny/crossref_metadata_2025_split huggingface dataset:
A Minimally Supervised Approach for Synonym Extraction with Word Embeddings
Authors: Leeuwenberg Artuur , Vela Mihaela , Dehdari Jon , van Genabith Josef 
Published: April 2016

Abstract
In this paper we present a novel approach to minimally supervised synonym extraction. The approach is based on the word embeddings and aims at presenting a method for synonym extraction that is extensible to various languages.
We report experiments with word vectors trained by using both the continuous bag-of-words model (CBoW) and the skip-gram model (SG) investigating the effects of different settings with respect to the contextual window size, the number of dimensions and the type of word vectors. We analyze the word categories that are (cosine) similar in the vector space, showing that cosine similarity on its own is a bad indicator to determine if two words are synonymous. In this context, we propose a new measure, relative cosine similarity, for calculating similarity relative to other cosine-similar words in the corpus. We show that calculating similarity relative to other words boosts the precision of the extraction. We also experiment with combining similarity scores from differently-trained vectors and explore the advantages of using a part-of-speech tagger as a way of introducing some light supervision, thus aiding extraction.
We perform both intrinsic and extrinsic evaluation on our final system: intrinsic evaluation is carried out manually by two human evaluators and we use the output of our system in a machine translation task for extrinsic evaluation, showing that the extracted synonyms improve the evaluation metric.
3. Developing by Drawing Creativity of Children Activities
Authors: Ceauşu Felicia 
Published: April 2016

Abstract
The potential creativity elements can be expressivity, flexibility, fluency, brain sensibility as well as the qualities of the analyzers and temperamental characteristics which have an important role in triggering, developing and manifesting creativity. Here we must also take into account the relationship of the subject with the environment and educational factors. For the child, creativity has certain time limits that are determined by a multitude of factors such as: adaptation to new changes, will, creative type cognitive type, the feeling of duty and responsibility, ideal, surrounding atmosphere. In the current paperwork, we aimed to elevate the development level of creativity by plastic arts and we remarked that, in those plastic art activities where the basic method was the play, the efficient organization of the activities of plastic arts. The child is an active subject of knowledge who absorbs with lust the information proposed by the educator, he/she must be ready to receive more and more knowledge. The main task of the adults is to create optimal conditions of discovery and achievement of his/her creative possibilities and to take into consideration the individuality of each child.
In-Situ Characterization of Isotropic and Transversely Isotropic Elastic Properties Using Ultrasonic Wave Velocities
Authors: Pant S. , Laliberte J. , Martinez M. , Rocha B. 
Published: April 2016

Abstract
In this paper, a one-sided, in situ method based on the time of flight measurement of ultrasonic waves was described. The primary application of this technique was to non-destructively measure the stiffness properties of isotropic and transversely isotropic materials. The method consists of generating and receiving quasi-longitudinal and quasi-shear waves at different through-thickness propagation angles. First, analytical equations were provided to calculate the ultrasonic wave velocities. Then, an inverse method based on non-linear least square technique was used to calculate the stiffness constants using the ultrasonic wave velocities. Sensitivity analysis was performed by randomly perturbing the velocity data, thus observing the effects of perturbations on the calculated stiffness constants. An improved algorithm was proposed and tested to reduce the effects of random errors. Based on the sensitivity analysis, minimum number of angles required to inversely calculate the stiffness constants were suggested for isotropic and transversely isotropic material. The method was experimentally verified on an isotropic 7050-T7451 aluminum with two different thicknesses and a transversely isotropic composite laminate fabricated using 24 plies of CYCOM 977-2 12 k HTA unidirectional carbon fiber reinforced polymer (CFRP) prepregs. The results demonstrated that this technique is able to accurately measure the material properties of isotropic material. As for the transversely isotropic material, this method was able to accurately measure the material properties if the experimental errors can be reduced to less than 1 %.
Quasi-Static, Cyclic Fatigue and Fracture Behavior of Alloy Steel for Structural Applications: Influence of Orientation
Authors: Gowda S. , Hotz C. , Manigandan K. , Srivatsan T. S. , Patnaik A. , Payer J. 
Published: April 2016

Abstract
In this paper, the results of a study aimed at understanding the extrinsic influence of test specimen orientation, with respect to a wrought alloy-steel plate, on the stress-controlled cyclic fatigue properties and fracture behavior of a structural steel is highlighted. The alloy steel chosen was ASTM A572 grade 50. Samples of this alloy steel, prepared from both the longitudinal and transverse orientations, were cyclically deformed over a range of maximum stress and the corresponding number of cycles to failure (NF) was recorded. The influence of test specimen orientation and intrinsic microstructural effects on cyclic fatigue life and fracture behavior are presented and discussed. Overall, the macroscopic fracture mode was essentially identical regardless of orientation of the test specimen with respect to the wrought plate. The microscopic mechanisms governing cyclic deformation, fatigue life, and final fracture behavior are presented in light of the mutually interactive influences of magnitude of applied stress, intrinsic microstructural effects, orientation of test specimen, and deformation characteristics of the key microstructural constituents.
Physiological Properties of Neurons in Bat Entorhinal Cortex Exhibit an Inverse Gradient along the Dorsal–Ventral Axis Compared to Entorhinal Neurons in Rat
Authors: Heys James G. , Shay Christopher F. , MacLeod Katrina M. , Witter Menno P. , Moss Cynthia F. , Hasselmo Michael E. 
Published: April 2016

Medial entorhinal cortex (MEC) grid cells exhibit firing fields spread across the environment on the vertices of a regular tessellating triangular grid. In rodents, the size of the firing fields and the spacing between the firing fields are topographically organized such that grid cells located more ventrally in MEC exhibit larger grid fields and larger grid-field spacing compared with grid cells located more dorsally. Previous experiments in brain slices from rodents have shown that several intrinsic cellular electrophysiological properties of stellate cells in layer II of MEC change systematically in neurons positioned along the dorsal–ventral axis of MEC, suggesting that these intrinsic cellular properties might control grid-field spacing. In the bat, grid cells in MEC display a functional topography in terms of grid-field spacing, similar to what has been reported in rodents. However, it is unclear whether neurons in bat MEC exhibit similar gradients of cellular physiological properties, which may serve as a conserved mechanism underlying grid-field spacing in mammals. To test whether entorhinal cortex (EC) neurons in rats and bats exhibit similar electrophysiological gradients, we performed whole-cell patch recordings along the dorsal–ventral axis of EC in bats. Surprisingly, our data demonstrate that the sag response properties and the resonance properties recorded in layer II neurons of entorhinal cortex in the Egyptian fruit bat demonstrate an inverse relationship along the dorsal–ventral axis compared with the rat.SIGNIFICANCE STATEMENTAs animals navigate, neurons in medial entorhinal cortex (MEC), termed grid cells, discharge at regular spatial intervals. In bats and rats, the spacing between the firing fields of grid cells changes systematically along the dorsal–ventral axis of MEC. It has been proposed that these changes could be generated by systematic differences in the intrinsic cellular physiology of neurons distributed along the dorsal–ventral axis of MEC. The results from our study show that key intrinsic physiological properties of neurons in entorhinal cortex of the bat and rat change in the opposite direction along the dorsal–ventral axis of entorhinal cortex, suggesting that these intrinsic physiological properties cannot account in the same way across species for the change in grid-field spacing shown along the dorsal–ventral axis.
Wiring Specificity and Synaptic Diversity in the Mouse Lateral Central Amygdala
Authors: Hou Wen-Hsien , Kuo Ning , Fang Ge-Wei , Huang Hsien-Sung , Wu Kun-Pin , Zimmer Andreas , Cheng Jen-Kun , Lien Cheng-Chang 
Published: April 2016

The central amygdala (CeA) nucleus, a subcortical structure composed of mostly GABA-releasing (GABAergic) neurons, controls fear expression via projections to downstream targets in the hypothalamus and brainstem. The CeA consists of the lateral (CeL) and medial (CeM) subdivisions. The CeL strongly gates information transfer to the CeM, the main output station of the amygdala, but little is known about the functional organization of local circuits in this region. Using cluster analysis, we identified two major electrophysiologically distinct CeL neuron classes in mouse amygdala slices, the early-spiking (ES) and late-spiking (LS) neurons. These two classes displayed distinct autaptic transmission. Compared with LS neurons, ES neurons had strong and depressing autapses, which enhanced spike-timing precision. With multiple patch-clamp recordings, we found that CeL neurons made chemical, but not electrical, synapses. Analysis of individual connections revealed cannabinoid type 1 receptor-mediated suppression of the ES, but not of the LS cell output synapse. More interestingly, the efficacy of the ES→LS or LS→ES synapse was ∼2-fold greater than that of the LS→LS or ES→ES synapse. When tested at 20 Hz, synapses between different neurons, but not within the same class, were markedly depressing and were more powerful to sculpt activity of postsynaptic neurons. Moreover, neurons of different classes also form synapses with higher degree of connectivity. We demonstrate that ES and LS neurons represent two functionally distinct cell classes in the CeL and interactions between presynaptic and postsynaptic neurons dictate synaptic properties between neurons.SIGNIFICANCE STATEMENTThe central lateral amygdala (CeL) is a key node in fear circuits, but the functional organization of local circuits in this region is largely unknown. The CeL consists of mostly GABAergic inhibitory neurons with different functional and molecular features. Here, we report that the presynaptic cell class determines functional properties of autapses and cannabinoid-mediated modulation of synaptic transmission between neurons, whereas presynaptic versus postsynaptic cell classes dictate the connectivity, efficacy, and dynamics of GABAergic synapses between any two neurons. The wiring specificity and synaptic diversity have a great impact on neuronal output in amygdala inhibitory networks. Such synaptic organizing principles advance our understanding of the significance of physiologically defined neuronal phenotypes in amygdala inhibitory networks.
Sphingosine-1-Phosphate (S1P) Impacts Presynaptic Functions by Regulating Synapsin I Localization in the Presynaptic Compartment
Authors: Riganti Loredana , Antonucci Flavia , Gabrielli Martina , Prada Ilaria , Giussani Paola , Viani Paola , Valtorta Flavia , Menna Elisabetta , Matteoli Michela , Verderio Claudia 
Published: April 2016

Growing evidence indicates that sphingosine-1-P (S1P) upregulates glutamate secretion in hippocampal neurons. However, the molecular mechanisms through which S1P enhances excitatory activity remain largely undefined. The aim of this study was to identify presynaptic targets of S1P action controlling exocytosis. Confocal analysis of rat hippocampal neurons showed that S1P applied at nanomolar concentration alters the distribution of Synapsin I (SynI), a presynaptic phosphoprotein that controls the availability of synaptic vesicles for exocytosis. S1P induced SynI relocation to extrasynaptic regions of mature neurons, as well as SynI dispersion from synaptic vesicle clusters present at axonal growth cones of developing neurons. S1P-induced SynI relocation occurred in a Ca2+-independent but ERK-dependent manner, likely through the activation of S1P3receptors, as it was prevented by the S1P3receptor selective antagonist CAY1044 and in neurons in which S1P3receptor was silenced. Our recent evidence indicates that microvesicles (MVs) released by microglia enhance the metabolism of endogenous sphingolipids in neurons and stimulate excitatory transmission. We therefore investigated whether MVs affect SynI distribution and whether endogenous S1P could be involved in the process. Analysis of SynI immunoreactivity showed that exposure to microglial MVs induces SynI mobilization at presynaptic sites and growth cones, whereas the use of inhibitors of sphingolipid cascade identified S1P as the sphingolipid mediating SynI redistribution. Our data represent the first demonstration that S1P induces SynI mobilization from synapses, thereby indicating the phosphoprotein as a novel target through which S1P controls exocytosis.SIGNIFICANCE STATEMENTGrowing evidence indicates that the bioactive lipid sphingosine and its metabolite sphingosine-1-P (S1P) stimulate excitatory transmission. While it has been recently clarified that sphingosine influences directly the exocytotic machinery by activating the synaptic vesicle protein VAMP2 to form SNARE fusion complexes, the molecular mechanism by which S1P promotes neurotransmission remained largely undefined. In this study, we identify Synapsin I, a presynaptic phosphoprotein involved in the control of availability of synaptic vesicles for exocytosis, as the key target of S1P action. In addition, we provide evidence that S1P can be produced at mature axon terminals as well as at immature growth cones in response to microglia-derived signals, which may be important to stabilize nascent synapses and to restore or potentiate transmission.
α-Synuclein Mutation Inhibits Endocytosis at Mammalian Central Nerve Terminals
Authors: Xu Jianhua , Wu Xin-Sheng , Sheng Jiansong , Zhang Zhen , Yue Hai-Yuan , Sun Lixin , Sgobio Carmelo , Lin Xian , Peng Shiyong , Jin Yinghui , Gan Lin , Cai Huaibin , Wu Ling-Gang 
Published: April 2016

α-Synuclein (α-syn) missense and multiplication mutations have been suggested to cause neurodegenerative diseases, including Parkinson's disease (PD) and dementia with Lewy bodies. Before causing the progressive neuronal loss, α-syn mutations impair exocytosis, which may contribute to eventual neurodegeneration. To understand how α-syn mutations impair exocytosis, we developed a mouse model that selectively expressed PD-related human α-syn A53T (h-α-synA53T) mutation at the calyx of Held terminals, where release mechanisms can be dissected with a patch-clamping technique. With capacitance measurement of endocytosis, we reported that h-α-synA53T, either expressed transgenically or dialyzed in the short term in calyces, inhibited two of the most common forms of endocytosis, the slow and rapid vesicle endocytosis at mammalian central synapses. The expression of h-α-synA53Tin calyces also inhibited vesicle replenishment to the readily releasable pool. These findings may help to understand how α-syn mutations impair neurotransmission before neurodegeneration.SIGNIFICANCE STATEMENTα-Synuclein (α-syn) missense or multiplication mutations may cause neurodegenerative diseases, such as Parkinson's disease and dementia with Lewy bodies. The initial impact of α-syn mutations before neuronal loss is impairment of exocytosis, which may contribute to eventual neurodegeneration. The mechanism underlying impairment of exocytosis is poorly understood. Here we report that an α-syn mutant, the human α-syn A53T, inhibited two of the most commonly observed forms of endocytosis, slow and rapid endocytosis, at a mammalian central synapse. We also found that α-syn A53T inhibited vesicle replenishment to the readily releasable pool. These results may contribute to accounting for the widely observed early synaptic impairment caused by α-syn mutations in the progression toward neurodegeneration.
l-Lactate-Mediated Neuroprotection against Glutamate-Induced Excitotoxicity Requires ARALAR/AGC1
Authors: Llorente-Folch Irene , Rueda Carlos B. , Pérez-Liébana Irene , Satrústegui Jorgina , Pardo Beatriz 
Published: April 2016

ARALAR/AGC1/Slc25a12, the aspartate-glutamate carrier from brain mitochondria, is the regulatory step in the malate-aspartate NADH shuttle, MAS. MAS is used to oxidize cytosolic NADH in mitochondria, a process required to maintain oxidative glucose utilization. The role of ARALAR was analyzed in two paradigms of glutamate-induced excitotoxicity in cortical neurons: glucose deprivation and acute glutamate stimulation. ARALAR deficiency did not aggravate glutamate-induced neuronal deathin vitro, although glutamate-stimulated respiration was impaired. In contrast, the presence ofl-lactate as an additional source protected against glutamate-induced neuronal death in control, but not ARALAR-deficient neurons.l-Lactate supplementation increased glutamate-stimulated respiration partially prevented the decrease in the cytosolic ATP/ADP ratio induced by glutamate and substantially diminished mitochondrial accumulation of 8-oxoguanosine, a marker of reactive oxygen species production, only in the presence, but not the absence, of ARALAR. In addition,l-lactate potentiated glutamate-induced increase in cytosolic Ca2+, in a way independent of the presence of ARALAR. Interestingly,in vivo, the loss of half-a-dose of ARALAR inaralar+/−mice enhanced kainic acid-induced seizures and neuronal damage with respect to control animals, in a model of excitotoxicity in which increasedl-lactate levels andl-lactate consumption have been previously proven. These results suggest that,in vivo, an inefficient operation of the shuttle in thearalarhemizygous mice prevents the protective role ofl-lactate on glutamate excitotoxiciy and that the entry and oxidation ofl-lactate through ARALAR-MAS pathway is required for its neuroprotective function.SIGNIFICANCE STATEMENTLactate now stands as a metabolite necessary for multiple functions in the brain and is an alternative energy source during excitotoxic brain injury. Here we find that the absence of a functional malate-aspartate NADH shuttle caused byaralar/AGC1 disruption causes a block in lactate utilization by neurons, which prevents the protective role of lactate on excitotoxicity, but not glutamate excitotoxicity itself. Thus, failure to use lactate is detrimental and is possibly responsible for the exacerbatedin vivoexcitotoxicity inaralar+/−mice.
cGMP-Dependent Protein Kinase Encoded byforagingRegulates Motor Axon Guidance inDrosophilaby Suppressing Lola Function
Authors: Peng Qionglin , Wang Yijin , Li Meixia , Yuan Deliang , Xu Mengbo , Li Changqing , Gong Zhefeng , Jiao Renjie , Liu Li 
Published: April 2016

Correct pathfinding and target recognition of a developing axon are exquisitely regulated processes that require multiple guidance factors. Among these factors, the second messengers, cAMP and cGMP, are known to be involved in establishing the guidance cues for axon growth through different intracellular signaling pathways. However, whether and how cGMP-dependent protein kinase (PKG) regulates axon guidance remains poorly understood. Here, we show that the motor axons of intersegmental nerve b (ISNb) in theDrosophilaembryo display targeting defects during axon development in the absence offoraging(for), a gene encoding PKG.In vivotag expression revealed PKG to be present in the ventral nerve code at late embryonic stages, supporting its function in embryonic axon guidance. Mechanistic studies showed that the transcription factorlongitudinal lacking(lola) genetically interacts withfor.PKG physically associates with the LolaT isoform via the C-terminal zinc-finger-containing domain. Overexpression of PKG leads to the cytoplasmic retention of LolaT in S2 cells, suggesting a role for PKG in mediating the nucleocytoplasmic trafficking of Lola. Together, these findings reveal a novel function of PKG in regulating the establishment of neuronal connectivity by sequestering Lola in the cytoplasm.SIGNIFICANCE STATEMENTAxon pathfinding and target recognition are important processes in the formation of specific neuronal connectivity, which rely upon precise coordinated deployment of multiple guidance factors. This paper reveals the role of cGMP-dependent protein kinase (PKG) in regulating the pathfinding and targeting of the developing axons inDrosophila. Moreover, our study indicates that PKG regulates the cytoplasmic-nuclear trafficking of the transcription factor LolaT, suggesting a mechanism of PKG in directing motor axon guidance. These findings highlight a new function of PKG in axon guidance by suppressing a transcription factor.
Rapid Adaptation Induces Persistent Biases in Population Codes for Visual Motion
Authors: Zavitz Elizabeth , Yu Hsin-Hao , Rowe Elise G. , Rosa Marcello G.P. , Price Nicholas S. C. 
Published: April 2016

Each visual experience changes the neural response to subsequent stimuli. If the brain is unable to incorporate these encoding changes, the decoding, or perception, of subsequent stimuli is biased. Although the phenomenon of adaptation pervades the nervous system, its effects have been studied mainly in isolation, based on neuronal encoding changes induced by an isolated, prolonged stimulus. To understand how adaptation-induced biases arise and persist under continuous, naturalistic stimulation, we simultaneously recorded the responses of up to 61 neurons in the marmoset (Callithrix jacchus) middle temporal area to a sequence of directions that changed every 500 ms. We found that direction-specific adaptation following only 0.5 s of stimulation strongly affected encoding for up to 2 s by reducing both the gain and the spike count correlations between pairs of neurons with preferred directions close to the adapting direction. In addition, smaller changes in bandwidth and preferred direction were observed in some animals. Decoding individual trials of adaptation-affected activity in simultaneously recorded neurons predicted repulsive biases that are consistent with the direction aftereffect. Surprisingly, removing spike count correlations by trial shuffling did not impact decoding performance or bias. When adaptation had the largest effect on encoding, the decoder made the most errors. This suggests that neural and perceptual repulsion is not a mechanism to enhance perceptual performance but is instead a necessary consequence of optimizing neural encoding for the identification of a wide range of stimulus properties in diverse temporal contexts.SIGNIFICANCE STATEMENTAlthough perception depends upon decoding the pattern of activity across a neuronal population, the encoding properties of individual neurons are unreliable: a single neuron's response to repetitions of the same stimulus is variable, and depends on both its spatial and temporal context. In this manuscript, we describe the complete cascade of adaptation-induced effects in sensory encoding and show how they predict population decoding errors consistent with perceptual biases. We measure the time course of adaptation-induced changes to the response properties of neurons in isolation, and to the correlation structure across pairs of simultaneously recorded neurons. These results provide novel insight into how and for how long adaptation affects the neural code, particularly during continuous, naturalistic vision.