Sizing up the competition: Quantifying the influence of the mental lexicon on auditory, visual, and audiovisual spoken word recognition

A central question in research on spoken word recognition is whether spoken words are recognized relationally, in the context of other words in the mental lexicon: McClelland & Elman, 1986; Norris, 1994; Luce & Pisoni, 1998). The current research evaluated metrics for measuring the influence of the mental lexicon on spoken word recognition in auditory-only: A-only), visual-only: V-only) and audiovisual: AV) conditions, and assessed the extent to which lexical properties influence recognition similarly across modality of input. Lexical competition: the extent to which perceptually similar words influence recognition of a stimulus word) was quantified using metrics that are well-established in the literature, as well as a novel statistical method for calculating perceptual confusability, based on the Phi-square statistic. The Phi-square statistic proved an effective measure for assessing lexical competition and explained significant variance in A-only and V-only spoken word identification beyond that accounted for by traditional metrics. Because these values include the influence of all words in the lexicon: rather than only perceptually very similar words), it suggests that even perceptually distant words may receive some activation, and therefore provide competition, during spoken word recognition. Spoken word recognition in A-only, V-only, and AV was sensitive to modality-specific lexical competition and stimulus frequency. These findings extend the scope of activation-competition models of spoken word recognition and suggest that the perceptual and lexical properties underlying spoken word recognition are not unique to the A-only domain

Characterization of the DNA-damaging impact of food-borne acrylamide in vivo

Die alpha,beta-ungesättigte Carbonylverbindung Acrylamid entsteht beim Erhitzen von kohlenhydratreichen Lebensmitteln aus der Reaktion von Aminosäuren (hauptsächlich Asparagin) und reduzierenden Zuckern als Nebenprodukt der Maillard-Reaktion. In Langzeitstudien an Ratten wurde ein kanzerogenes Potential von Acrylamid nachgewiesen, was zu seiner Klassifizierung als „wahrscheinlich kanzerogen am Menschen“ (Kategorie 2a) durch die International Agency for Research on Cancer führte. Als Auslöser der Kanzerogenität von Acrylamid wird ein genotoxischer Mechanismus vermutet, der auf der Reaktion von Glycidamid mit der DNA unter Ausbildung des Hauptadduktes N7-Glycidamid-Guanin (N7-GA-Guanin) basiert. Das Ziel der vorliegenden Arbeit war die Untersuchung der genotoxischen Wirkung von Acrylamid in vivo anhand des modifizierten Comet Assays sowie der massenspektrometrischen Untersuchung von N7-GA-Guanin-Addukten. Die Problematik wurde in zwei Teilprojekten bearbeitet. Zum einen wurde die Auswirkung verschiedener Lebensmittelmatrices auf die genotoxische Wirkung von Acrylamid in der Ratte im Vergleich zur Acrylamid-Aufnahme über Trinkwasser per Schlundsonde untersucht. Dazu wurden jeweils drei Ratten über maximal neun Tage mit Acrylamid-Dosen von 50 µg/kg KG/d in Trinkwasser oder Brotkruste bzw. 100 µg/kg KG/d in Trinkwasser (Schlundsonde), geschnittenen und rekonstituierten Pommes Frites sowie Lebkuchen behandelt. Zusätzlich wurde jeweils drei Tiere einmalig eine Dosis von 450 µg bzw. 900 µg Acrylamid/kg KG in Trinkwasser mittels Schlundsonde verabreicht, was der maximalen Aufnahmemenge über neun Tage entspricht. Außerdem wurde zwei Tieren einmalig 10 mg Acrylamid/kg KG in Trinkwasser per Schlundsonde gegeben. Die Tötung der Tiere sowie Blut- und Organentnahme erfolgten 24 Stunden nach der letzten Acrylamid-Gabe. Die Untersuchung der Blut- und Leberzellen mittels modifiziertem Comet Assay ließ auf keine signifikante DNA-Schädigung der mit 50 oder 100 µg Acrylamid/kg KG behandelten Tiere schließen. Auch die einmalige Verabreichung von 450 µg bzw. 900 µg Acrylamid/kg KG im Trinkwasser führte zu keiner signifikanten Erhöhung der DNA-Schädigung. Lediglich nach der Gabe von 10 mg Acrylamid/kg KG wurden DNA-Schäden in Blut und Leber detektiert. In den Geweben der für maximal neun Tage mit 50 oder 100 µg Acrylamid/kg KG im Trinkwasser oder Lebensmittel behandelten Ratten wurden keine N7-GA-Guanin-Addukte detektiert und lagen somit unterhalb der Nachweisgrenze von 1 Addukt/10E8 Nukleotide. Nach einmaliger Verabreichung von 450 µg Acrylamid/kg KG wurden in allen Organen der behandelten Tiere N7-GA-Guanin-Addukte detektiert, die allerdings unterhalb der Bestimmungsgrenze von 3 Addukten/10E8 Nukleotide lagen. Die einmalige Gabe von 900 µg und 10 mg Acrylamid/kg KG führte zu quantifizierbaren Addukten in allen untersuchten Organen. Im zweiten Teil dieser Arbeit wurde die zeit- und dosisabhängige Bildung von N7-GA-Guanin-Addukten in der DNA aus Leber, Niere und Lunge weiblicher Sprague-Dawley Ratten untersucht. Dazu wurden die Ratten zunächst einmalig mit 1 mg oder 10 mg Acrylamid/kg KG per Schlundsonde behandelt und die Gewebeproben nach 8, 16 oder 24 Stunden entnommen und untersucht. Nach Ermittlung des Zeitpunktes der maximalen N7-GA-Guanin-Adduktbildung wurden weitere Ratten einmalig mit 0,1 mg, 0,5 mg, 3 mg oder 6 mg Acrylamid/kg KG behandelt. Neben der N7-GA-Guanin-Adduktbildung wurde die Bildung der Mercaptursäuren von Acrylamid und Glycidamid mittels HPLC-MS/MS untersucht. Die Mercaptursäuren AAMA und GAMA entstehen als Abbauprodukte der Glutathionkonjugate von Acrylamid und Glycidamid und werden über den Urin ausgeschieden. Die dosisabhängige Bildung von N7-GA-Guanin-Addukten wurde 16 Stunden nach Verabreichung von Acrylamiddosen zwischen 0,1 mg und 10 mg/kg KG untersucht. Die N7-GA-Guanin-Addukte konnten erst ab einer Dosis von 1 mg Acrylamid/kg KG in der DNA der Tiere quantifiziert werden. Die Adduktbildung in der 0,1 mg Acrylamid/kg KG-Gruppe lag unterhalb der Nachweisgrenze, während die Addukte in der 0,5 mg Acrylamid/kg KG-Gruppe zwar nachweisbar, aber nicht quantifizierbar waren. Im Bereich von 1 bis 10 mg Acrylamid/kg KG wurde ein dosisabhängiger Anstieg der N7-GA-Guanin-Addukte beobachtet. Die Ergebnisse der gemessenen Mercaptursäuren zeigen insgesamt, dass 53-55 % der Acrylamid-Dosis von 1 und 10 mg/kg KG innerhalb von 24 Stunden als Mercaptursäuren ausgeschieden werden und dadurch eine effektive Entgiftung von Acrylamid gewährleistet ist. Anhand der ausgeschiedenen GAMA-Menge lässt sich rückschließen, dass 14-18 % der verabreichten 1 und 10 mg Acrylamid/kg KG innerhalb von 24 Stunden zu Glycidamid metabolisiert werden. Die Untersuchung der Mercaptursäuren im 16-Stunden-Sammelurin nach Gabe von 0,1 bis 10 mg Acrylamid/kg KG zeigte, dass die absolute Ausscheidung von AAMA und GAMA linear mit der Dosis ansteigt.Acrylamide is an alpha,beta-unsaturated carbonyl compound that is generated during the heating of carbohydrate-rich food. In long-term animal trials acrylamide was found to be carcinogenic. Therefore, it is classified by International Agency for Research on Cancer as probably carcinogenic to humans (group 2a). The biological activity of acrylamide is considered to be mainly determined by its metabolic activation into genotoxic glycidamide (GA). Glycidamide is able to react with DNA bases to form glycidamide-DNA adducts, especially with the N7 of guanine. The aim of this work was to investigate the genotoxicity of acrylamide in vivo using the modified Comet Assay to detect DNA damage and a HPLC-MS/MS method to determine N7-GA-guanine adducts. In the first part of this work the influence of food matrices on genotoxicity of acrylamide was investigated. Therefore, three Sprague-Dawley rats per group received acrylamide doses of 50 or 100 µg/kg bw/d in drinking water per gavage or in different food matrices for up to nine days. As food matrices bread crust, gingerbread and French fries (sliced from potatoes with normal plant texture or reconstituted from potato starch representing a dough-like texture) were chosen. In an additional trial, three rats received a single dose of 450 or 900 µg acrylamide/kg bw, respectively. These doses represent the maximum exposure against acrylamide over nine days. Furthermore, two rats received a single dose of 10 mg acrylamide/kg bw in drinking water. All animals were sacrificed 24 hours after the last dosing and blood and tissues (liver, kidney, lung, testes) were removed for testing. The results of the Comet Assay showed no significantly increased DNA damage in blood and liver cells after treatment of rats with 50 or 100 µg acrylamide/kg bw for up to nine days nor after application of a single dose of 450 or 900 µg acrylamide/kg bw. DNA damage was only increased in blood and liver cells of animals dosed with 10 mg acrylamide/kg bw. N7-GA guanine adducts were not detectable in tissues of animals treated for up to nine days with 50 or 100 µg acrylamide/kg bw/d (detection limit: 1 adduct/10E8 nucleotides). After a single dose of 450 µg acrylamide/kg bw N7-GA guanine adducts were detectable, but not quantifiable in all investigated tissues (quantification limit: 3 adducts/10E8 nucleotides). The single treatment of three rats with 900 µg and 10 mg acrylamide/kg bw leads to quantifiable adducts in DNA isolated from all investigated tissues. In the second part of this work the time- and dose-dependent formation of N7-GA guanine adducts was investigated. Additionally, the mercapturic acids of acrylamide and glycidamide, AAMA and GAMA, were determined in the urine of acrylamide-treated rats by HPLC-MS/MS. AAMA and GAMA are the degradation products of acrylamide and glycidamide glutathione conjugates and can be used as biomarkers of toxification and detoxification of acrylamide and glycidamide, respectively. First of all, Sprague-Dawley rats were treated with single doses of 1 or 10 mg acrylamide/kg bw in drinking water per gavage for 8, 16 or 24 hours to determine the best time point to investigate N7-GA guanine adducts. This investigation results in a slight maximum of N7-GA guanine adduct formation after 16 hours. Thereafter, further animals were dosed with 0.1-6 mg acrylamide/kg bw to investigate a dose-dependent formation of N7-GA guanine adducts 16 hours after the application. But even after 16 hours the N7-GA guanine adducts were only quantifiable in the groups dosed with 1 mg acrylamide/kg bw or higher. Within the range of 1 and 10 mg acrylamide/kg bw the N7-GA guanine adduct formation increased in dependence of dose. In contrast, mercapturic acids of acrylamide and glycidamide were detectable in the urine of all acrylamide-treated animals. Within 24 hours, 53-55 % of acrylamide dose were excreted with urine as AAMA and GAMA

No evidence that siblings’ gender affects personality across nine countries

Does growing up with a sister rather than a brother affect personality? In this article, we provide a comprehensive analysis of the effects of siblings’ gender on adults’ personality, using data from 85,887 people from 12 large representative surveys covering nine countries (United States, United Kingdom, The Netherlands, Germany, Switzerland, Australia, Mexico, China, and Indonesia). We investigated the personality traits of risk tolerance, trust, patience, locus of control, and the Big Five. We found no meaningful causal effects of the gender of the next younger sibling and no associations with the gender of the next older sibling. Given the high statistical power and consistent results in the overall sample and relevant subsamples, our results suggest that siblings’ gender does not systematically affect personality

No Evidence That Siblings’ Gender Affects Personality Across Nine Countries

Does growing up with a sister rather than a brother affect personality? In this article, we provide a comprehensive analysis of the effects of siblings’ gender on adults’ personality, using data from 85,887 people from 12 large representative surveys covering nine countries (United States, United Kingdom, The Netherlands, Germany, Switzerland, Australia, Mexico, China, and Indonesia). We investigated the personality traits of risk tolerance, trust, patience, locus of control, and the Big Five. We found no meaningful causal effects of the gender of the next younger sibling and no associations with the gender of the next older sibling. Given the high statistical power and consistent results in the overall sample and relevant subsamples, our results suggest that siblings’ gender does not systematically affect personality

Proceedings from the 2018 Canadian Association for the Study of the Liver Single Topic Conference—Decompensated Cirrhosis : from clinic to transplant

Actes publiés dans le Canadian Liver Journal; vol. 2, no. 4, Fall 2019, p. 137-170

Differential cross section measurements for the production of a W boson in association with jets in proton–proton collisions at √s = 7 TeV

Measurements are reported of differential cross sections for the production of a W boson, which decays into a muon and a neutrino, in association with jets, as a function of several variables, including the transverse momenta (pT) and pseudorapidities of the four leading jets, the scalar sum of jet transverse momenta (HT), and the difference in azimuthal angle between the directions of each jet and the muon. The data sample of pp collisions at a centre-of-mass energy of 7 TeV was collected with the CMS detector at the LHC and corresponds to an integrated luminosity of 5.0 fb[superscript −1]. The measured cross sections are compared to predictions from Monte Carlo generators, MadGraph + pythia and sherpa, and to next-to-leading-order calculations from BlackHat + sherpa. The differential cross sections are found to be in agreement with the predictions, apart from the pT distributions of the leading jets at high pT values, the distributions of the HT at high-HT and low jet multiplicity, and the distribution of the difference in azimuthal angle between the leading jet and the muon at low values.United States. Dept. of EnergyNational Science Foundation (U.S.)Alfred P. Sloan Foundatio

Impacts of the Tropical Pacific/Indian Oceans on the Seasonal Cycle of the West African Monsoon

The current consensus is that drought has developed in the Sahel during the second half of the twentieth century as a result of remote effects of oceanic anomalies amplified by local land–atmosphere interactions. This paper focuses on the impacts of oceanic anomalies upon West African climate and specifically aims to identify those from SST anomalies in the Pacific/Indian Oceans during spring and summer seasons, when they were significant. Idealized sensitivity experiments are performed with four atmospheric general circulation models (AGCMs). The prescribed SST patterns used in the AGCMs are based on the leading mode of covariability between SST anomalies over the Pacific/Indian Oceans and summer rainfall over West Africa. The results show that such oceanic anomalies in the Pacific/Indian Ocean lead to a northward shift of an anomalous dry belt from the Gulf of Guinea to the Sahel as the season advances. In the Sahel, the magnitude of rainfall anomalies is comparable to that obtained by other authors using SST anomalies confined to the proximity of the Atlantic Ocean. The mechanism connecting the Pacific/Indian SST anomalies with West African rainfall has a strong seasonal cycle. In spring (May and June), anomalous subsidence develops over both the Maritime Continent and the equatorial Atlantic in response to the enhanced equatorial heating. Precipitation increases over continental West Africa in association with stronger zonal convergence of moisture. In addition, precipitation decreases over the Gulf of Guinea. During the monsoon peak (July and August), the SST anomalies move westward over the equatorial Pacific and the two regions where subsidence occurred earlier in the seasons merge over West Africa. The monsoon weakens and rainfall decreases over the Sahel, especially in August.Peer reviewe

Optimasi Portofolio Resiko Menggunakan Model Markowitz MVO Dikaitkan dengan Keterbatasan Manusia dalam Memprediksi Masa Depan dalam Perspektif Al-Qur`an

Risk portfolio on modern finance has become increasingly technical, requiring the use of sophisticated mathematical tools in both research and practice. Since companies cannot insure themselves completely against risk, as human incompetence in predicting the future precisely that written in Al-Quran surah Luqman verse 34, they have to manage it to yield an optimal portfolio. The objective here is to minimize the variance among all portfolios, or alternatively, to maximize expected return among all portfolios that has at least a certain expected return. Furthermore, this study focuses on optimizing risk portfolio so called Markowitz MVO (Mean-Variance Optimization). Some theoretical frameworks for analysis are arithmetic mean, geometric mean, variance, covariance, linear programming, and quadratic programming. Moreover, finding a minimum variance portfolio produces a convex quadratic programming, that is minimizing the objective function ðð¥with constraintsð ð 𥠥 ðandð´ð¥ = ð. The outcome of this research is the solution of optimal risk portofolio in some investments that could be finished smoothly using MATLAB R2007b software together with its graphic analysis

Penilaian Kinerja Keuangan Koperasi di Kabupaten Pelalawan

This paper describe development and financial performance of cooperative in District Pelalawan among 2007 - 2008. Studies on primary and secondary cooperative in 12 sub-districts. Method in this stady use performance measuring of productivity, efficiency, growth, liquidity, and solvability of cooperative. Productivity of cooperative in Pelalawan was highly but efficiency still low. Profit and income were highly, even liquidity of cooperative very high, and solvability was good