Behavioral dominance between female color morphs of a Lake Victoria cichlid fish

Species that exhibit genetic color polymorphism are suitable for studying the evolutionary forces that maintain heritable phenotypic variation in nature. Male color morphs often differ in behavioral dominance, affecting the evolution of color polymorphisms. However, behavioral dominance among female color morphs has received far less attention. We studied a polymorphic population of the cichlid fish Neochromis omnicaeruleus from Lake Victoria, in which 3 distinct female color morphs coexist, black-and-white blotched (WB), orange blotched (OB), and plain (P) color morphs. First, we investigated dominance relationships among female morphs using triadic and dyadic encounters in the laboratory. In triadic encounters, both WB and OB females dominated plain, whereas WB females dominated OB females. Dominance of WB over OB was confirmed using dyadic encounters. In a second experiment, blotched (WB or OB) and plain full-sib sisters were bred by crossing a blotched and a plain parent. In dyadic encounters, WB female morphs dominated their plain sisters, suggesting that dominance of WB females is a pleiotropic effect of color or that genes coding for color and those influencing behavioral dominance are genetically linked, explaining the association between color and behavioral dominance despite gene flow. We conclude that behavioral dominance asymmetries exist among female color morphs of the fish N. omnicaeruleus, and discuss possible mechanisms that may account for the tight association between color and behavioral dominance.

Estimating Annual CO2 Flux for Lutjewad Station Using Three Different Gap-Filling Techniques

Long-term measurements of CO2 flux can be obtained using the eddy covariance technique, but these datasets are affected by gaps which hinder the estimation of robust long-term means and annual ecosystem exchanges. We compare results obtained using three gap-fill techniques: multiple regression (MR), multiple imputation (MI), and artificial neural networks (ANNs), applied to a one-year dataset of hourly CO2 flux measurements collected in Lutjewad, over a flat agriculture area near the Wadden Sea dike in the north of the Netherlands. The dataset was separated in two subsets: a learning and a validation set. The performances of gap-filling techniques were analysed by calculating statistical criteria: coefficient of determination (R2), root mean square error (RMSE), mean absolute error (MAE), maximum absolute error (MaxAE), and mean square bias (MSB). The gap-fill accuracy is seasonally dependent, with better results in cold seasons. The highest accuracy is obtained using ANN technique which is also less sensitive to environmental/seasonal conditions. We argue that filling gaps directly on measured CO2 fluxes is more advantageous than the common method of filling gaps on calculated net ecosystem change, because ANN is an empirical method and smaller scatter is expected when gap filling is applied directly to measurements.

Net CO 2 surface emissions at Bern, Switzerland inferred from ambient observations of CO 2 , δ(O 2 /N 2 ), and 222 Rn using a customized radon tracer inversion

The 222Radon tracer method is a powerful tool to estimate local and regional surface emissions of, e.g., greenhouse gases. In this paper we demonstrate that in practice, the method as it is commonly used, produces inaccurate results in case of nonhomogeneously spread emission sources, and we propose a different approach to account for this. We have applied the new methodology to ambient observations of CO2 and 222Radon to estimate CO2 surface emissions for the city of Bern, Switzerland. Furthermore, by utilizing combined measurements of CO2 and δ(O2/N2) we obtain valuable information about the spatial and temporal variability of the main emission sources. Mean net CO2 emissions based on 2 years of observations are estimated at (11.2 ± 2.9) kt km−2 a−1. Oxidative ratios indicate a significant influence from the regional biosphere in summer/spring and fossil fuel combustion processes in winter/autumn. Our data indicate that the emissions from fossil fuels are, to a large degree, related to the combustion of natural gas which is used for heating purposes.

Three decades of global methane sources and sinks

Methane is an important greenhouse gas, responsible for about 20 of the warming induced by long-lived greenhouse gases since pre-industrial times. By reacting with hydroxyl radicals, methane reduces the oxidizing capacity of the atmosphere and generates ozone in the troposphere. Although most sources and sinks of methane have been identified, their relative contributions to atmospheric methane levels are highly uncertain. As such, the factors responsible for the observed stabilization of atmospheric methane levels in the early 2000s, and the renewed rise after 2006, remain unclear. Here, we construct decadal budgets for methane sources and sinks between 1980 and 2010, using a combination of atmospheric measurements and results from chemical transport models, ecosystem models, climate chemistry models and inventories of anthropogenic emissions. The resultant budgets suggest that data-driven approaches and ecosystem models overestimate total natural emissions. We build three contrasting emission scenarios � which differ in fossil fuel and microbial emissions � to explain the decadal variability in atmospheric methane levels detected, here and in previous studies, since 1985. Although uncertainties in emission trends do not allow definitive conclusions to be drawn, we show that the observed stabilization of methane levels between 1999 and 2006 can potentially be explained by decreasing-to-stable fossil fuel emissions, combined with stable-to-increasing microbial emissions. We show that a rise in natural wetland emissions and fossil fuel emissions probably accounts for the renewed increase in global methane levels after 2006, although the relative contribution of these two sources remains uncertain.

Atmospheric CO₂, δ(O₂/N₂) and δ13CO2 measurements at Jungfraujoch, Switzerland: results from a flask sampling intercomparison program

We present results from an intercomparison program of CO2, δ(O2/N2) and δ13CO2 measurements from atmospheric flask samples. Flask samples are collected on a bi-weekly basis at the High Altitude Research Station Jungfraujoch in Switzerland for three European laboratories: the University of Bern, Switzerland, the University of Groningen, the Netherlands and the Max Planck Institute for Biogeochemistry in Jena, Germany. Almost 4 years of measurements of CO2, δ(O2/N2) and δ13CO2 are compared in this paper to assess the measurement compatibility of the three laboratories. While the average difference for the CO2 measurements between the laboratories in Bern and Jena meets the required compatibility goal as defined by the World Meteorological Organization, the standard deviation of the average differences between all laboratories is not within the required goal. However, the obtained annual trend and seasonalities are the same within their estimated uncertainties. For δ(O2/N2) significant differences are observed between the three laboratories. The comparison for δ13CO2 yields the least compatible results and the required goals are not met between the three laboratories. Our study shows the importance of regular intercomparison exercises to identify potential biases between laboratories and the need to improve the quality of atmospheric measurements.

Dramaturgie der Seuche. Zur Verarbeitung von Aids in Literatur, Theater und Film

Gegenstand / Untersuchungskorpus Die massenmediale Aufbereitung von Aids ist bereits seit den Anfängen der geisteswissenschaftlichen Beschäftigung mit diesem Thema ein zentraler Gegenstand kritischer Betrachtung. Demgegenüber stellt sich die systematische Erforschung des Beitrages von eher fiktionalen Gattungen zur gesellschaftlichen Verarbeitung von Aids ein Forschungsdesiderat dar. Die Dissertation „Dramaturgie der Seuche“ schliesst mit der Fokussierung auf Literatur, Theater und Film diese Lücke. Die dezidiert interdisziplinäre Auswahl des Untersuchungskorpus’ liefert eine Zusammenschau der Funktionen, die diese Gattungen im Laufe der Zeit innerhalb des Aids-Diskurses übernommen haben. Die Arbeit zeigt die komplexen Wechselverhältnisse zwischen den Massenmedien, den fiktionalen Gattungen sowie der medizinischen Kommunikation auf. Fragedesign auf der Höhe der aktuellen Forschung Gegenwärtig ist erneut ein Interesse kultur- und sozialwissenschaftlicher Disziplinen am Thema Aids zu beobachten. Eine junge Forschergeneration nimmt sich des Themas an und beleuchtet die Auseinandersetzung mit Aids an Hand neuer Fragestellungen und mit neuen Methoden. Im Mittelpunkt dieser wissenschaftlichen Auseinandersetzung stehen die reflektierte Historisierung und Kontextualisierung des Aids-Diskurses seit den 1980er-Jahren. Die Dissertation „Dramaturgie der Seuche“ positioniert sich mit ihrer Frage nach der Struktur und der Entwicklung der gesellschaftlichen Auseinandersetzung mit Aids seit den Anfängen bis zur Gegenwart innerhalb dieses aktuellen Forschungsfeldes. Die Herangehensweise unterscheidet sich damit deutlich von den Forschungen der 1990er-Jahre, die eher von Betroffenheit und/oder unmittelbarer Kritik am Aids-Diskurs in den Massenmedien geprägt war. Zugleich verschafft die kritische Re-Lektüre der zentralen Publikationen zum Thema Aids, etwa von Susan Sontag oder Sander L. Gilman, diesen eine kritische Aktualisierung. Innovatives Methodendesign Um dem interdiszplinären Korpus und der kulturwissenschaftlich inspirierten Fragestellung gerecht zu werden, entwirft die Dissertation ein innovatives Methodendesign, das diskursanalytische und systemtheoretische Ansätze mit theater-, literatur- und filmwissenschaftlichen Analyseinstrumenten synthetisiert. Dieses leistet in der Anwendung sowohl eine präzise und adäquate Tiefenanalyse der untersuchten Texte, Bilder und Filme als auch eine Auswertung dieser Ergebnisse auf einer abstrakteren Ebene, die die komplexe Struktur der Entwicklung des Aids-Diskurses seit den 1980er-Jahren bis heute überzeugend und anschaulich darlegt. Das entworfene Methodendesign lässt sich auf andere Gegenstände anwenden und verspricht ebenso präzise wie innovative Ergebnisse. Ergebnisse: Nutzen für die Öffentlichkeit Die analytische Auseinandersetzung mit der letzten grossen Seuche innerhalb der westlichen Welt birgt nicht nur in der Rückschau auf die letzten Dekaden einen Mehrwert für die Öffentlichkeit. Die regelmässige Wiederkehr von epidemischen Szenarien – BSE, SARS, Vogel- und Schweinegrippe und jüngst EHEC – zeigt, dass ein kritischer Blick auf die sich wiederholenden dramaturgischen Muster des Redens über ansteckende Krankheiten nottut. Die Dissertation „Dramaturgie der Seuche“ trägt dazu bei, die Muster des Seuchendiskurses zu erkennen und reflektiert und kritisch mit der Berichterstattung in den Medien wie auch mit den kursierenden Urban Legends umzugehen. Der Aufbau der Argumentation und der sprachliche Stil verbinden wissenschaftliche Genauigkeit mit Allgemeinverständlichkeit. Dadurch wird die Arbeit breit rezipierbar.

Self-control in social decision making: A neurobiological perspective

Self-control is defined as the process in which thoughts, emotions, or prepotent responses are inhibited to efficiently enact a more focal goal. Self-control not only allows for more adaptive individual decision making but also promotes adaptive social decision making. In this chapter, we examine a burgeoning area of interdisciplinary research: the neuroscience of self-control in social decision making. We examine research on self-control in complex social contexts examined from a social neuroscience perspective. We review correlational evidence from neuroimaging studies and causal evidence from neuromodulation studies (i.e., brain stimulation). We specifically highlight research that shows that self-control involves the lateral prefrontal cortex (PFC) across a number of social domains and behaviors. Research has also begun to directly integrate nonsocial with social forms of self-control, showing that the basic neurobiological processes involved in stopping a motor response appear to be involved in social contexts that require self-control. Further, neural traits, such as baseline activation in the lateral PFC, can explain sources of individual differences in self-control capacity. We explore whether techniques that change brain functioning could target neural mechanisms related to self-control capacity to potentially enhance self-control in social behavior. Finally, we discuss several research questions ripe for examination. We broadly suggest that future research can now turn to exploring how neural traits and situational affordances interact to impact self-control in social decision making in order to continue to elucidate the processes that allow people to maintain and realize stable goals in a dynamic and often uncertain social environment.

Genetic Engineering of Induced Pluripotent Stem Cells and Reprogramming to Motor Neurons to Elucidate Selective Motor Neuron Death in Amyotrophic Lateral Sclerosis

Amyotrophic lateral sclerosis (ALS) is a progressive motor neuron disease, fatal within 1 to 5 years after onset of symptoms. About 3 out of 100’000 persons are diagnosed with ALS and there is still no cure available [1, 2]. 95% of all cases occur sporadically and the aetiology remains largely unknown [3]. However, up to now 16 genes were identified to play a role in the development of familial ALS. One of these genes is FUS that encodes for the protein fused in sarcoma (FUS). Mutations in this gene are responsible for some cases of sporadic as well as of inherited ALS [4]. FUS belongs to the family of heterogeneous nuclear ribonucleoproteins and is predicted to be involved in several cellular functions like transcription regulation, RNA splicing, mRNA transport in neurons and microRNA processing [5] Aberrant accumulation of mutated FUS has been found in the cytoplasm of motor neurons from ALS patients [6]. The mislocalization of FUS is based on a mutation in the nuclear localization signal of FUS [7]. However, it is still unclear if the cytoplasmic localization of FUS leads to a toxic gain of cytoplasmic function and/or a loss of nuclear function that might be crucial in the course of ALS. The goal of this project is to characterize the impact of ALS-associated FUS mutations on in vitro differentiated motor neurons. To this end, we edit the genome of induced pluripotent stem cells (iPSC) using transcription activator-like effector nucleases (TALENs) [8,9] to create three isogenic cell lines, each carrying an ALS-associated FUS mutation (G156E, R244C and P525L). These iPSC’s will then be differentiated to motor neurons according to a recently established protocol [10] and serve to study alterations in the transcriptome, proteome and metabolome upon the expression of ALS-associated FUS. With this approach, we hope to unravel the molecular mechanism leading to FUS-associated ALS and to provide new insight into the emerging connection between misregulation of RNA metabolism and neurodegeneration, a connection that is currently implied in a variety of additional neurological diseases, including spinocerebellar ataxia 2 (SCA-2), spinal muscular atrophy (SMA), fragile X syndrome, and myotonic dystrophy. [1] Cleveland, D.W. et al. (2001) Nat Rev Neurosci 2(11): 806-819 [2] Sathasivam, S. (2010) Singapore Med J 51(5): 367-372 [3] Schymick, J.C. et al. (2007) Hum Mol Genet Vol 16: 233-242 [4] Pratt, A.J. et al. (2012). Degener Neurol Neuromuscul Dis 2012(2): 1-14 [5] Lagier-Tourenne, C. Hum Mol Genet, 2010. 19(R1): p. R46-64 [6] Mochizuki, Y. et al. (2012) J Neurol Sci 323(1-2): 85-92 [7] Dormann, D. et al. (2010) EMBO J 29(16): 2841-2857 [8] Hockemeyer, D. et al. (2011) Nat Biotech 29(8): 731-734 [9] Joung, J.K. and J.D. Sander (2013) Nat Rev Mol Cell Biol 14(1): 49-55 [10]Amoroso, M.W. et al. (2013) J Neurosci 33(2): 574-586.

Multidisciplinary consensus on assessment of unruptured intracranial aneurysms: proposal of an international research group.

BACKGROUND AND PURPOSE To address the increasing need to counsel patients about treatment indications for unruptured intracranial aneurysms (UIA), we endeavored to develop a consensus on assessment of UIAs among a group of specialists from diverse fields involved in research and treatment of UIAs. METHODS After composition of the research group, a Delphi consensus was initiated to identify and rate all features, which may be relevant to assess UIAs and their treatment by using ranking scales and analysis of inter-rater agreement (IRA) for each factor. IRA was categorized as very high, high, moderate, or low. RESULTS Ultimately, 39 specialists from 4 specialties agreed (high or very high IRAs) on the following key factors for or against UIA treatment decisions: (1) patient age, life expectancy, and comorbid diseases; (2) previous subarachnoid hemorrhage from a different aneurysm, family history for UIA or subarachnoid hemorrhage, nicotine use; (3) UIA size, location, and lobulation; (4) UIA growth or de novo formation on serial imaging; (5) clinical symptoms (cranial nerve deficit, mass effect, and thromboembolic events from UIAs); and (6) risk factors for UIA treatment (patient age and life expectancy, UIA size, and estimated risk of treatment). However, IRAs for features rated with low relevance were also generally low, which underlined the existing controversy about the natural history of UIAs. CONCLUSIONS Our results highlight that neurovascular specialists currently consider many features as important when evaluating UIAs but also highlight that the appreciation of natural history of UIAs remains uncertain, even within a group of highly informed individuals.

Cross-sectional study of 168 patients with hepatorenal tyrosinaemia and implications for clinical practice

BackgroundHepatorenal tyrosinaemia (Tyr 1) is a rare inborn error of tyrosine metabolism. Without treatment, patients are at high risk of developing acute liver failure, renal dysfunction and in the long run hepatocellular carcinoma. The aim of our study was to collect cross-sectional data.MethodsVia questionnaires we collected retrospective data of 168 patients with Tyr 1 from 21 centres (Europe, Turkey and Israel) about diagnosis, treatment, monitoring and outcome. In a subsequent consensus workshop, we discussed data and clinical implications.ResultsEarly treatment by NTBC accompanied by diet is essential to prevent serious complications such as liver failure, hepatocellular carcinoma and renal disease. As patients may remain initially asymptomatic or develop uncharacteristic clinical symptoms in the first months of life newborn mass screening using succinylacetone (SA) as a screening parameter in dried blood is mandatory for early diagnosis. NTBC-treatment has to be combined with natural protein restriction supplemented with essential amino acids. NTBC dosage should be reduced to the minimal dose allowing metabolic control, once daily dosing may be an option in older children and adults in order to increase compliance. Metabolic control is judged by SA (below detection limit) in dried blood or urine, plasma tyrosine (<400 ¿M) and NTBC-levels in the therapeutic range (20¿40 ¿M). Side effects of NTBC are mild and often transient.Indications for liver transplantation are hepatocellular carcinoma or failure to respond to NTBC. Follow-up procedures should include liver and kidney function tests, tumor markers and imaging, ophthalmological examination, blood count, psychomotor and intelligence testing as well as therapeutic monitoring (SA, tyrosine, NTBC in blood).ConclusionBased on the data from 21 centres treating 168 patients we were able to characterize current practice and clinical experience in Tyr 1. This information could form the basis for clinical practice recommendations, however further prospective data are required to underpin some of the recommendations.

16p11.2 600 kb Duplications confer risk for typical and atypical Rolandic epilepsy

Rolandic epilepsy (RE) is the most common idiopathic focal childhood epilepsy. Its molecular basis is largely unknown and a complex genetic etiology is assumed in the majority of affected individuals. The present study tested whether six large recurrent copy number variants at 1q21, 15q11.2, 15q13.3, 16p11.2, 16p13.11 and 22q11.2 previously associated with neurodevelopmental disorders also increase risk of RE. Our association analyses revealed a significant excess of the 600 kb genomic duplication at the 16p11.2 locus (chr16: 29.5-30.1 Mb) in 393 unrelated patients with typical (n = 339) and atypical (ARE; n = 54) RE compared with the prevalence in 65,046 European population controls (5/393 cases versus 32/65,046 controls; Fisher's exact test P = 2.83 × 10(-6), odds ratio = 26.2, 95% confidence interval: 7.9-68.2). In contrast, the 16p11.2 duplication was not detected in 1738 European epilepsy patients with either temporal lobe epilepsy (n = 330) and genetic generalized epilepsies (n = 1408), suggesting a selective enrichment of the 16p11.2 duplication in idiopathic focal childhood epilepsies (Fisher's exact test P = 2.1 × 10(-4)). In a subsequent screen among children carrying the 16p11.2 600 kb rearrangement we identified three patients with RE-spectrum epilepsies in 117 duplication carriers (2.6%) but none in 202 carriers of the reciprocal deletion. Our results suggest that the 16p11.2 duplication represents a significant genetic risk factor for typical and atypical RE.