julilili42/papers huggingface dataset:
Role of Morpho-Syntactic Features in Estonian Proficiency Classification
2013-06-01

• We developed an approach to perform proficiency classification for learners of Estonian as a second language. • Using a publicly accessible Estonian learner corpus, we show that – morpho-syntactic features in learner texts are useful predictors. – cascades of binary classifiers perform better than performing the classification in a single step. Related Work • SLA researchers studied the characteristic features of learner texts at different proficiency levels. (e.g., Tono, 2000; Vyatkina, 2012; Lu, 2012) • Automated assessment of student essays is also an active research area. (e.g., Yannakoudakis, Briscoe &amp;amp; Medlock, 2011; Burstein, 2013) • Contemporary research primarily focused on learner errors across proficiency levels. (e.g., Dickinson, Kübler &amp;amp; Meyer, 2012) • But, the role of morpho-syntactic features in proficiency classification was not explored before. Estonian Morphology • Estonian is agglutinative. Word forms can be formed by joining the morphemes together.- e.g., jalgades –&amp;gt;jalga+de+s (stem for foot +plural marker+inessive case marker) • It is fusional i.e., word forms can be formed by changing the stem.- e.g., jalg (foot, nominative), jala (genitive), jalga (partitive) • It has 14 productive cases (grammatical and semantic cases).- Cases express relations between words and are sometimes used instead of postpositions (jalal and jala peal have the same meaning: on the foot) • Cases have different alternative case endings.- e.g., Valid allative plural forms for jalg (foot) are: jalgadele, jalule, jalgele- We model some of these morphological characteristics as features for the learner proficiency classification task. The Corpus • The Estonian Interlanguage Corpus (EIC) consists of texts written by learners of Estonian as a Second Language (Eslon, 2007). • It mainly consists of short answers, essays and personal letters. • It also has error annotations but we did not use them in this paper. • Here is a numeric description of the corpus:
Synthesis of 6-Ethyl-1,2,9-trioxopyrrolo[3,2-f ]quinoline-8-carboxylic Acid
2013-06-01

Abstract Interaction of 6-amino-1-ethyl-4-oxoquinoline-3-carboxylic ester (7) with chloral hydrate and hydroxylamine hydrochloride gave the corresponding isonitroso-acetamido derivative 8 which, upon treatment with concentrated sulfuric acid, was converted regioselectively into 1,2,9-trioxopyrrolo[ 3,2- f ]quinoline-8-carboxylic acid (3). This novel tricyclic system was isolated in good yield as a stable hydrate 3H. Structural assignments of the new compounds are based on microanalytical and spectral (MS and NMR) data
SFS-TUE: Compound Paraphrasing with a Language Model and Discriminative Reranking
2013-06-01

This paper presents an approach for generating free paraphrases of compounds (task 4 at SemEval 2013) by decomposing the training data into a collection of templates and fillers and recombining/scoring these based on a generative language model and discriminative MaxEnt reranking. The system described in this paper achieved the highest score (with a very small margin) in the (default) isomorphic setting of the scorer, for which it was optimized, at a disadvantage to the non-isomorphic score.
Mechanisms of genetic epilepsies
2013-06-01

Abstract Epilepsy is one of the most common neurological disorders. As early as the time of Hippocrates (460-370 BC), it was reported on as the “holy disease”. Today it is known that an epileptic seizure is a consequence of synchronous discharges of neuronal populations in the brain, which abruptly and usually without an observable cause evoke involuntary behavioural dysfunction or impaired consciousness. Epilepsies can have various causes and lead to extensive implications for the everyday life of affected patients. Up to 50% of all epilepsies are caused by genetic defects, in particular the so-called idiopathic epilepsies, which occur without easily observable structural alterations in the brain. Genetically caused dysfunctions of neuronal ion channels play a central role in the formation of such epilepsies. The ion channels control the ion flux over the cell membrane of neurons and thus present the basis for the excitability of these neurons. Therefore, medications used in epilepsy treatment affect predominantly ion channels. However, common anticonvulsants have limited success, not only because one third of epilepsy patients exhibit pharmacoresistance, but also because of the secondary effects which can dramatically affect their quality of life. Furthermore, current therapeutic approaches are mainly symptomatic and do not act on the epileptogenic mechanisms, which are still largely unknown. In this review article we will highlight the current main topics of our research on genetically caused epilepsies, their pathomechanisms and therapeutic options.
Non-LTE Model Spectra for Gaseous Planetary Debris Disks around WDs
2013-06-01

Abstract Metal-rich dust disks around white dwarfs are thought to be the debris of tidally disrupted rocky bodies. While normally the number of features to study the planetary material directly is very limited, ancillary gas disks around some of these white dwarfs provide the opportunity to do so. We used our Tübingen Accretion Disk code AcDc , assuming non-LTE conditions, to model the gaseous spectrum component. We investigated the chemical mixture as well as the surface density and effective temperature, and utilized the Ca ii infrared triplet to determine the geometry of the disk.
On the uniform pricing puzzle in recorded music
2013-06-01

This paper proposes a possible explanation for uniform pricing in the recorded music industry, based on a pooling equilibrium across different quality types. We show that an ex ante ability to invest in the probability of success – which we identify with record companies’ artists and repertoire (A&amp;R) expenditures – makes such a pooling equilibrium more likely.
Active control of radiative and nonradiative processes in coupled quantum systems embedded in a &#x03BB;/2-microresonator
2013-06-01

In this paper, the interaction of closely-spaced coupled quantum systems in a photonic environment is studied. A simple model based on rate equations is introduced, allowing to describe the influence, e.g., of a resonator on the radiative and nonradiative processes, such as Förster resonant energy transfer, in the coupled system. The validity of the model is tested by comparing results to measured spectra of the fluorescent protein DsRed in a λ/2-microresonator. This approach will prove useful for studying the radiative and nonradiative behaviour of inseparable fluorescent compounds such as complex biological molecules.
Stress-vs-time signals allow the prediction of structurally catastrophic events during fracturing of immature cartilage and predetermine the biomechanical, biochemical, and structural impairment
2013-06-01

Objective: Trauma-associated cartilage fractures occur in children and adolescents with clinically significant incidence. Several studies investigated biomechanical injury by compressive forces but the injury-related stress has not been investigated extensively. In this study, we hypothesized that the biomechanical stress occurring during compressive injury predetermines the biomechanical, biochemical, and structural consequences. We specifically investigated whether the stress-vs-time signal correlated with the injurious damage and may allow prediction of cartilage matrix fracturing. Methods: Superficial and deeper zones disks (SZDs, DZDs; immature bovine cartilage) were biomechanically characterized, injured (50% compression, 100%/s strain-rate), and re-characterized. Correlations of the quantified functional, biochemical and histological damage with biomechanical parameters were zonally investigated. Results: Injured SZDs exhibited decreased dynamic stiffness (by 93.04. Â±. 1.72%), unresolvable equilibrium moduli, structural damage (2.0. Â±. 0.5 on a 5-point-damage-scale), and 1.78-fold increased sGAG loss. DZDs remained intact. Measured stress-vs-time-curves during injury displayed 4 distinct shapes, which correlated with histological damage (p
Mechanismen genetischer Epilepsien
2013-06-01

Abstract Mechanisms of genetic epilepsies. Epilepsy is one of the most common neurological disorders. Already at the time of Hippocrates (460 - 370 BC) it was reported on as the “holy disease” (Fröscher 2004). Today it is known that an epileptic seizure is a consequence of synchronous discharges of neuronal populations in the brain, which abruptly and usually without an observable cause evoke involuntary behavioural dysfunction or impaired consciousness. Epilepsies can have various causes and lead to extensive implications for the everyday life of affected patients. Up to 50 % of all epilepsies are caused by genetic defects, in particular the so-called idiopathic epilepsies which occur without easily observable structural alterations of the brain. Genetically caused dysfunctions of neuronal ion channels play a central role in the formation of such epilepsies. The ion channels control the ion flux over the cell membrane of neurons and thus present the basis for the excitability of these neurons. Therefore, medications used for epilepsy treatment affect predominantly ion channels. However, the common anticonvulsants have limited success, not only because one third of epilepsy patients exhibits pharmacoresistance, but also because of the secondary effects which can dramatically affect their quality of life. Furthermore, current therapeutic approaches are mainly symptomatic and do not act on the epileptogenic mechanisms which are still largely unknown. In this review article we will highlight the current main topics of our research on genetically caused epilepsies, their pathomechanisms and therapeutic options.
Metabolomics approach for predicting response to neoadjuvant chemotherapy for breast cancer
2013-06-01

Breast cancer is a clinically heterogeneous disease, which necessitates a variety of treatments and leads to different outcomes. As an example, only some women will benefit from chemotherapy. Identifying patients who will respond to chemotherapy and thereby improve their long-term survival has important implications to treatment protocols and outcomes, while identifying non responders may enable these patients to avail themselves of other investigational approaches or other potentially effective treatments. In this study, serum metabolite profiling was performed to identify potential biomarker candidates that can predict response to neoadjuvant chemotherapy for breast cancer. Metabolic profiles of serum from patients with complete (n = 8), partial (n = 14) and no response (n = 6) to chemotherapy were studied using a combination of nuclear magnetic resonance (NMR) spectroscopy, liquid chromatography-mass spectrometry (LC-MS) and statistical analysis methods. The concentrations of four metabolites, three (threonine, isoleucine, glutamine) from NMR and one (linolenic acid) from LC-MS were significantly different when comparing response to chemotherapy. A prediction model developed by combining NMR and MS derived metabolites correctly identified 80% of the patients whose tumors did not show complete response to chemotherapy. These results show promise for larger studies that could result in more personalized treatment protocols for breast cancer patients.
The habit for voting, “civic duty” and travel distance
2013-06-01

There is a rich literature addressing the paradox of not voting and election turnout from both theoretical and empirical perspectives. By taking advantage of a unique dataset from an “experimental” setting, this paper is the first to estimate the utility that drives the “civic duty” or the habit for voting. Consistent with the general turnout literature, education level, marital status, household size, and distance all affect the persistence of voter participation.
Inhibitory control and decision making under risk in bulimia nervosa and binge‐eating disorder
2013-06-03

ABSTRACT Objective To investigate neuropsychological mechanisms of impulsivity in patients with bulimia nervosa (BN) and binge‐eating disorder (BED). Method Nineteen BN patients and 31 age‐ and body‐mass‐index (BMI)‐matched healthy controls (c‐BN) as well as 54 overweight and obese BED patients and 43 age‐ and BMI‐matched healthy controls (c‐BED) were investigated using an inhibitory control task (stop signal task, SST) and a decision‐making under risk task (game of dice task, GDT). Results Compared to c‐BN, BN patients demonstrated significant greater stop signal reaction times in the SST, but no differences for the frequency of risky decisions in the GDT. BED patients did not differ from c‐BED in the SST or the GDT. Discussion BN but not BED patients differed from their respective control groups concerning the “stopping” component of impulsivity. These differences in motor inhibition may contribute to the behavioral distinctions in binge‐eating behavior between BN and BED. © 2013 Wiley Periodicals, Inc. (Int J Eat Disord 2013; 46:721–728)
Arabidopsis μ-adaptin subunit AP1M of adaptor protein complex 1 mediates late secretory and vacuolar traffic and is required for growth
2013-06-03

Adaptor protein (AP) complexes are the predominant coat proteins of membrane vesicles in post-Golgi trafficking of mammalian cells. Each AP complex contains a specific medium subunit, μ-adaptin, that selects cargo proteins bearing sequence-specific sorting motifs. Much less is known about the AP complexes and their μ subunits in plants. Because of uncertain homology, the μ-adaptins of Arabidopsis have been designated muA through muD [Happel et al. (2004) Plant J 37(5):678–693]. Furthermore, only muD has been assigned to a specific AP complex, AP-3, involved in Golgi-vacuolar trafficking [Niihama et al. (2009) Plant Cell Physiol 50(12):2057–2068, Zwiewka et al. (2011) Cell Res 21(12):1711–1722, and Wolfenstetter et al. (2012) Plant Cell 24(1):215–232]. In contrast, the μ subunit of neither the post-Golgi trafficking AP-1 complex nor the endocytic AP-2 complex has been identified. Here, we report the functional analysis of redundant AP-1 μ-adaptins AP1M1 (also known as muB1) and AP1M2 (also known as muB2). Coimmunoprecipitation revealed that both AP1M2 and its less strongly expressed isoform AP1M1 are complexed with the large subunit γ-adaptin of AP-1. In addition, AP1M2 was localized at or near the trans -Golgi network. Knockout mutations of AP1M2 impaired pollen function and arrested plant growth whereas the ap1m1 ap1m2 double mutant was nearly pollen-lethal. At the cellular level, the absence of AP1M2 entailed inhibition of multiple trafficking pathways from the trans -Golgi network to the vacuole and to the plasma membrane in interphase and to the plane of cell division in cytokinesis. Thus, AP-1 is crucial in post-Golgi trafficking in plant cells and required for cell division and plant growth.
Zinc Oxide Nanoparticles Induce Necrosis and Apoptosis in Macrophages in a p47phox- and Nrf2-Independent Manner
2013-06-03

In view of the steadily increasing use of zinc oxide nanoparticles in various industrial and consumer applications, toxicological investigations to evaluate their safety are highly justified. We have investigated mechanisms of ZnO nanoparticle-induced apoptosis and necrosis in macrophages in relation to their important role in the clearance of inhaled particulates and the regulation of immune responses during inflammation. In the murine macrophage RAW 264.7 cell line, ZnO treatment caused a rapid induction of nuclear condensation, DNA fragmentation, and the formation of hypodiploid DNA nuclei and apoptotic bodies. The involvement of the essential effector caspase-3 in ZnO-mediated apoptosis could be demonstrated by immunocytochemical detection of activated caspase-3 in RAW 264.7 cells. ZnO specifically triggered the intrinsic apoptotic pathway, because Jurkat T lymphocytes deficient in the key mediator caspase-9 were protected against ZnO-mediated toxicity whereas reconstituted cells were not. ZnO also caused DNA strand breakage and oxidative DNA damage in the RAW 264.7 cells as well as p47(phox) NADPH oxidase-dependent superoxide generation in bone marrow-derived macrophages. However, ZnO-induced cell death was not affected in bone marrow-derived macrophages of mice deficient in p47(phox) or the oxidant responsive transcription factor Nrf2. Taken together, our data demonstrate that ZnO nanoparticles trigger p47(phox) NADPH oxidase-mediated ROS formation in macrophages, but that this is dispensable for caspase-9/3-mediated apoptosis. Execution of apoptotic cell death by ZnO nanoparticles appears to be NADPH oxidase and Nrf2-independent but rather triggered by alternative routes.
transparent, a gene affecting stripe formation in Zebrafish, encodes the mitochondrial protein Mpv17 that is required for iridophore survival
2013-06-03

Summary In the skin of adult zebrafish, three pigment cell types arrange into alternating horizontal stripes, melanophores in dark stripes, xanthophores in light interstripes and iridophores in both stripes and interstripes. The analysis of mutants and regeneration studies revealed that this pattern depends on interactions between melanophores and xanthophores; however, the role of iridophores in this process is less understood. We describe the adult viable and fertile mutant transparent (tra), which shows a loss or strong reduction of iridophores throughout larval and adult stages. In addition, in adults only the number of melanophores is strongly reduced, and stripes break up into spots. Stripes in the fins are normal. By cell transplantations we show that tra acts cell-autonomously in iridophores, whereas the reduction in melanophores in the body occurs secondarily as a consequence of iridophore loss. We conclude that differentiated iridophores are required for the accumulation and maintenance of melanophores during pigment pattern formation. The tra mutant phenotype is caused by a small deletion in mpv17, an ubiquituously expressed gene whose protein product, like its mammalian and yeast homologs, localizes to mitochondria. Iridophore death might be the result of mitochondrial dysfunction, consistent with the mitochondrial DNA depletion syndrome observed in mammalian mpv17 mutants. The specificity of the tra phenotype is most likely due to redundancy after gene multiplication, making this mutant a valuable model to understand the molecular function of Mpv17 in mitochondria.
GRAVITATIONAL FRACTIONATION OF ISOTOPES AND DISSOLVED COMPONENTS AS A FIRST-ORDER PROCESS IN CRUSTAL FLUIDS
2013-06-03

Abstract The origin of ore-forming hydrothermal fluids and mechanisms of ore formation are commonly inferred from chemical and isotopic signatures. Fluid mixing and fluid-rock interaction are well-known processes that modify and produce these signatures, respectively. We propose that gravitational fractionation is an additional, hitherto not considered process that can significantly affect fluid signatures. Gravitational fractionation is the tendency for heavier components in a fluid to concentrate at the base of a reservoir. In stagnant fluids, gravitational fractionation can lead to significant changes in isotopic signatures, but also halogen ratios, within tens of millions of years. Rising fractionated fluids can give the same signatures that are classically and potentially erroneously interpreted as indicating mixing of surface-derived and deeper fluids. Recognition of gravitational fractionation as an additional first-order process affecting fluid composition necessitates a thorough reevaluation of models for crustal fluid flow, especially for the formation of unconformity-related hydrothermal ore deposits.
Mitochondrial Substrate Availability and Its Role in Lipid-Induced Insulin Resistance and Proinflammatory Signaling in Skeletal Muscle
2013-06-04

The relationship between glucose and lipid metabolism has been of significant interest in understanding the pathogenesis of obesity-induced insulin resistance. To gain insight into this metabolic paradigm, we explored the potential interplay between cellular glucose flux and lipid-induced metabolic dysfunction within skeletal muscle. Here, we show that palmitate (PA)-induced insulin resistance and proinflammation in muscle cells, which is associated with reduced mitochondrial integrity and oxidative capacity, can be attenuated under conditions of glucose withdrawal or glycolytic inhibition using 2-deoxyglucose (2DG). Importantly, these glucopenic-driven improvements coincide with the preservation of mitochondrial function and are dependent on PA oxidation, which becomes markedly enhanced in the absence of glucose. Intriguingly, despite its ability to upregulate mitochondrial PA oxidation, glucose withdrawal did not attenuate PA-induced increases in total intramyocellular diacylglycerol and ceramide. Furthermore, consistent with our findings in cultured muscle cells, we also report enhanced insulin sensitivity and reduced proinflammatory tone in soleus muscle from obese Zucker rats fed a 2DG-supplemented diet. Notably, this improved metabolic status after 2DG dietary intervention is associated with markedly reduced plasma free fatty acids. Collectively, our data highlight the key role that mitochondrial substrate availability plays in lipid-induced metabolic dysregulation both in vitro and in vivo.
Acute Normovolemic Hemodilution in the Pig Is Associated with Renal Tissue Edema, Impaired Renal Microvascular Oxygenation, and Functional Loss
2013-06-05

Abstract Background: The authors investigated the impact of acute normovolemic hemodilution (ANH) on intrarenal oxygenation and its functional short-term consequences in pigs. Methods: Renal microvascular oxygenation (μP o 2 ) was measured in cortex, outer and inner medulla via three implanted optical fibers by oxygen-dependent quenching of phosphorescence. Besides systemic hemodynamics, renal function, histopathology, and hypoxia-inducible factor-1α expression were determined. ANH was performed in n = 18 pigs with either colloids (hydroxyethyl starch 6% 130/0.4) or crystalloids (full electrolyte solution), in three steps from a hematocrit of 30% at baseline to a hematocrit of 15% (H3). Results: ANH with crystalloids decreased μP o 2 in cortex and outer medulla approximately by 65% ( P &lt; 0.05) and in inner medulla by 30% ( P &lt; 0.05) from baseline to H3. In contrast, μP o 2 remained unaltered during ANH with colloids. Furthermore, renal function decreased by approximately 45% from baseline to H3 ( P &lt; 0.05) only in the crystalloid group. Three times more volume of crystalloids was administered compared with the colloid group. Alterations in systemic and renal regional hemodynamics, oxygen delivery and oxygen consumption during ANH, gave no obvious explanation for the deterioration of μP o 2 in the crystalloid group. However, ANH with crystalloids was associated with the highest formation of renal tissue edema and the highest expression of hypoxia-inducible factor-1α, which was mainly localized in distal convoluted tubules. Conclusions: ANH to a hematocrit of 15% statistically significantly impaired μP o 2 and renal function in the crystalloid group. Less tissue edema formation and an unimpaired renal μP o 2 in the colloid group might account for a preserved renal function.
A User Centred Approach for Bringing BCI Controlled Applications to End-Users
2013-06-05

In the past 20 years research on BCI has been increasing almost exponentially. While a great deal of experimentation was dedicated to offline analysis for improving signal detection and translation, online studies with the target population are less common. Although BCIs are also developed for entertainment and thus potentially for healthy users, the main focus for BCI applications that are aiming at communication and control are people with severe motor impairment. There is a great need for translational studies that test BCI at home with the target population. Further, long-term studies with users in the field are required to improve reliability of BCI control. The user centred approach appears suitable to foster such studies.