Superconformal Ward Identities for Green Functions with Multiple Supercurrent Insertions

Superconformal Ward identities for N=1 supersymmetric quantum field theories in four dimensions are convenienty obtained in the superfield formalism by combining diffeomorphisms and Weyl transformations on curved superspace. Using this approach we study the superconformal transformation properties of Green functions with one or more insertions of the supercurrent to all orders in perturbation theory. For the case of two insertions we pay particular attention to fixing the additional counterterms present, as well as to the purely geometrical anomalies which contribute to the transformation behaviour. Moreover we show in a scheme-independent way how the quasi-local terms in the Ward identities are related to similar terms which contribute to the supercurrent two and three point functions. Furthermore we relate our superfield approach to similar studies which use the component formalism by discussing the implications of our approach for the components of the supercurrent and of the supergravity prepotentials.Comment: 35 pages, AMSLaTeX Problems with older LaTeX versions fixed, no change of conten

Conformal Transformation Properties of the Supercurrent in Four Dimensional Supersymmetric Theories

We investigate the superconformal transformation properties of Green functions with one or more insertions of the supercurrent in N=1 supersymmetric quantum field theories. These Green functions are conveniently obtained by coupling the supercurrent and its trace to a classical supergravity background. We derive flat space superconformal Ward identities from diffeomorphisms and Weyl transformations on curved superspace. For the classification of potential quantum superconformal anomalies in the massless Wess-Zumino model on curved superspace a perturbative approach is pursued, using the BPHZ scheme for renormalisation. By deriving a local Callan-Symanzik equation the usual dilatational anomalies are identified and it is shown that no further superconformal anomalies involving the dynamical fields are present.Comment: 35 pages, AMS-LaTex, four ps figures. Two remarks added, misprints corrected. To be published in Nuclear Physics

Introduction: meeting the challenges of Workplace English Communication in the 21st century

Open access article. Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) applies[Abstract not available]Ye

PP2A methylesterase PME-1 suppresses anoikis and is associated with therapy relapse of PTEN-deficient prostate cancers

While organ-confined prostate cancer (PCa) is mostly therapeutically manageable, metastatic progression of PCa remains an unmet clinical challenge. Resistance to anoikis, a form of cell death initiated by cell detachment from the surrounding extracellular matrix, is one of the cellular processes critical for PCa progression towards aggressive disease. Therefore, further understanding of anoikis regulation in PCa might provide therapeutic opportunities. Here, we discover that PCa tumors with concomitant inhibition of two tumor suppressor phosphatases, PP2A and PTEN, are particularly aggressive, having less than 50% 5-year secondary-therapy-free patient survival. Functionally, overexpression of PME-1, a methylesterase for the catalytic PP2A-C subunit, inhibits anoikis in PTEN-deficient PCa cells. In vivo, PME-1 inhibition increased apoptosis in in ovo PCa tumor xenografts, and attenuated PCa cell survival in zebrafish circulation. Molecularly, PME-1-deficient PC3 cells display increased trimethylation at lysines 9 and 27 of histone H3 (H3K9me3 and H3K27me3), a phenotype known to correlate with increased apoptosis sensitivity. In summary, our results demonstrate that PME-1 supports anoikis resistance in PTEN-deficient PCa cells. Clinically, these results identify PME-1 as a candidate biomarker for a subset of particularly aggressive PTEN-deficient PCa

Modelling human choices: MADeM and decision‑making

Research supported by FAPESP 2015/50122-0 and DFG-GRTK 1740/2. RP and AR are also part of the Research, Innovation and Dissemination Center for Neuromathematics FAPESP grant (2013/07699-0). RP is supported by a FAPESP scholarship (2013/25667-8). ACR is partially supported by a CNPq fellowship (grant 306251/2014-0)

25th annual computational neuroscience meeting: CNS-2016

The same neuron may play different functional roles in the neural circuits to which it belongs. For example, neurons in the Tritonia pedal ganglia may participate in variable phases of the swim motor rhythms [1]. While such neuronal functional variability is likely to play a major role the delivery of the functionality of neural systems, it is difficult to study it in most nervous systems. We work on the pyloric rhythm network of the crustacean stomatogastric ganglion (STG) [2]. Typically network models of the STG treat neurons of the same functional type as a single model neuron (e.g. PD neurons), assuming the same conductance parameters for these neurons and implying their synchronous firing [3, 4]. However, simultaneous recording of PD neurons shows differences between the timings of spikes of these neurons. This may indicate functional variability of these neurons. Here we modelled separately the two PD neurons of the STG in a multi-neuron model of the pyloric network. Our neuron models comply with known correlations between conductance parameters of ionic currents. Our results reproduce the experimental finding of increasing spike time distance between spikes originating from the two model PD neurons during their synchronised burst phase. The PD neuron with the larger calcium conductance generates its spikes before the other PD neuron. Larger potassium conductance values in the follower neuron imply longer delays between spikes, see Fig. 17.Neuromodulators change the conductance parameters of neurons and maintain the ratios of these parameters [5]. Our results show that such changes may shift the individual contribution of two PD neurons to the PD-phase of the pyloric rhythm altering their functionality within this rhythm. Our work paves the way towards an accessible experimental and computational framework for the analysis of the mechanisms and impact of functional variability of neurons within the neural circuits to which they belong

Social entrepreneurship: Prospects for the study of market based activity and social change

Social entrepreneurship constitutes a distinct organizing model that uses market activity to overcome social problems. This chapter introduces key elements of this model, including a focus on understanding the causal architecture and institutional embeddedness of social problems, the pursuit of multiple interrelated goals to effect social change, creative governance arrangements, and the contingencies of social entrepreneurship across contexts. We discuss these elements in light of the motives and challenges of social initiatives in the corporate sectors (corporate social responsibility; CSR), in particular how social problems are subjugated to a financial logic, in order to generate a constructive debate on learning potential for the corporate sector from social entrepreneurship. We conclude with an outlook on research gaps and opportunities as the study of social entrepreneurship moves beyond a phase of exploration

Gastrointestinal bleeding and endoscopic findings in critically and non‐critically ill patients with corona virus disease 2019 (COVID‐19): results from Lean European Open Survey on SARS‐CoV‐2 (LEOSS) and COKA registries

BACKGROUND: Corona virus disease 2019 (COVID‐19) patients are at increased risk for thromboembolic events. It is unclear whether the risk for gastrointestinal (GI) bleeding is also increased. METHODS: We considered 4128 COVID‐19 patients enrolled in the Lean European Open Survey on SARS‐CoV‐2 (LEOSS) registry. The association between occurrence of GI bleeding and comorbidities as well as medication were examined. In addition, 1216 patients from COKA registry were analyzed focusing on endoscopy diagnostic findings. RESULTS: A cumulative number of 97 patients (1.8%) with GI bleeding were identified in the LEOSS registry and COKA registry. Of 4128 patients from the LEOSS registry, 66 patients (1.6%) had a GI bleeding. The rate of GI bleeding in patients with intensive care unit (ICU) admission was 4.5%. The use of therapeutic dose of anticoagulants showed a significant association with the increased incidence of bleeding in the critical phase of disease. The Charlson comorbidity index and the COVID‐19 severity index were significantly higher in the group of patients with GI bleeding than in the group of patients without GI bleeding (5.83 (SD = 2.93) vs. 3.66 (SD = 3.06), p < 0.01 and 3.26 (SD = 1.69) vs. 2.33 (SD = 1.53), p < 0.01, respectively). In the COKA registry 31 patients (2.5%) developed a GI bleeding. Of these, the source of bleeding was identified in upper GI tract in 21 patients (67.7%) with ulcer as the most frequent bleeding source (25.8%, n = 8) followed by gastroesophageal reflux (16.1%, n = 5). In three patients (9.7%) GI bleeding source was located in lower GI tract caused mainly by diverticular bleeding (6.5%, n = 2). In seven patients (22.6%) the bleeding localization remained unknown. CONCLUSION: Consistent with previous research, comorbidities and disease severity correlate with the incidence of GI bleeding. Also, therapeutic anticoagulation seems to be associated with a higher risk of GI bleeding. Overall, the risk of GI bleeding seems not to be increased in COVID‐19 patients

Involvement of K+ channels in the relaxant effects of YC-1 in vascular smooth muscle

Seitz S, Wegener J, Rupp J, et al. Involvement of K+ channels in the relaxant effects of YC-1 in vascular smooth muscle. European Journal of Pharmacology. 1999;382(1):11-18.This study addresses the question whether K+ channels are involved in the vasorelaxant effects of 3-(5′-hydroxymethyl-2′-furyl)-1-benzyl-indazole (YC-1 ). In rat aorta, guinea pig aorta, and guinea pig a. carotis, YC-1 inhibited contractions induced by phenylephrine (3 μM) more potently than those induced by K+(48 mM). In rat aorta, tetraethylammonium (10 mM), charybdotoxin (0.2 μM), and iberiotoxin (0.1 μM), but not glibenclamide (10 μM), attenuated the relaxant effects of YC-1. In guinea pig a. carotis, YC-1 (30 μM) induced a hyperpolarisation which was antagonised by 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ; 50 μM). In rat aorta, YC-1 (30 μM) increased the rate constant of 86Rb-efflux. The effect of YC-1 was potentiated by zaprinast (10 μM), but inhibited by ODQ (50 μM) or charybdotoxin (0.2 μM). In smooth muscle cells from rat aorta, YC-1 (10 μM) increased BKCa channel activity. It is suggested that YC-1-induced vasorelaxation is partially mediated by the activation of K+ channels