Mellin moments of spin dependent and independent PDFs of the pion and rho meson

We compute the second moments of pion and rho parton distribution functions in lattice QCD with Nf=2+1 flavors of improved Wilson fermions. We determine both singlet and nonsinglet flavor combinations and, for the first time, take disconnected contributions fully into account. In the case of the rho, we also calculate the additional contribution arising from the b1 structure function. The numerical analysis includes 26 ensembles, mainly generated by the CLS effort, with pion masses ranging from 420 down to 214 MeV and with 5 different lattice spacings in the range of 0.1 to 0.05 fm. This enables us to take the continuum limit, as well as to resolve the quark mass dependencies reliably. Additionally we discuss the contaminations of rho correlation functions by two-pion states

Scale setting and the light baryon spectrum in Nf=2+1N_f=2+1 QCD with Wilson fermions

We determine the light baryon spectrum on ensembles generated by the Coordinated Lattice Simulations (CLS) effort, employing $N_f=2+1$ flavours of non-perturbatively improved Wilson fermions. The hadron masses are interpolated and extrapolated within the quark mass plane, utilizing three distinct trajectories, two of which intersect close to the physical quark mass point and the third one approaching the SU(3) chiral limit. The results are extrapolated to the continuum limit, utilizing six different lattice spacings ranging from $a\approx 0.10\,$fm down to below $0.04\,$fm. The light pion mass varies from $M_{\pi}\approx 429\,$MeV down to $127\,$MeV. In general, the spatial extent is kept larger than four times the inverse pion mass and larger than $2.3\,$fm, with additional small and large volume ensembles to investigate finite size effects. We determine the Wilson flow scales $\sqrt{t_{0,{\rm ph}}}=0.1449^{(7)}_{(9)}\,$fm and $t_0^*\approx t_{0,{\rm ph}}$ from the octet cascade ($\Xi$ baryon). Determining the light baryon spectrum in the continuum limit, we find the nucleon mass $m_N=941.7^{(6.5)}_{(7.6)}\,$MeV and the other stable baryon masses to agree with their experimental values within sub-percent level uncertainties. Moreover, we determine SU(3) and SU(2) chiral perturbation theory low energy constants, including the octet and the $\Omega$ baryon sigma~terms $\sigma_{\pi N}=43.9(4.7)\,$MeV, $\sigma_{\pi\Lambda}=28.2^{(4.3)}_{(5.4)}\,$MeV, $\sigma_{\pi\Sigma}=25.9^{(3.8)}_{(6.1)}\,$MeV, $\sigma_{\pi\Xi}=11.2^{(4.5)}_{(6.4)}\,$MeV and $\sigma_{\pi\Omega}=6.9^{(5.3)}_{(4.3)}\,$MeV, as well as various parameters, renormalization factors and improvement coefficients that are relevant for simulations with our lattice action.Comment: 128 pages, many figure

Charmonium resonances on the lattice

The nature of resonances and excited states near decay thresholds is encoded in scattering amplitudes, which can be extracted from single-particle and multiparticle correlators in finite volumes. Lattice calculations have only recently reached the precision required for a reliable study of such correlators. The distillation method represents a significant improvement insofar as it simplifies quark contractions and allows one to easily extend the operator basis used to construct interpolators. We present preliminary results on charmonium bound states and resonances on the Nf = 2+1 CLS ensembles. The long term goal of our investigation is to understand the properties of the X resonances that do not fit into conventional models of quark-antiquark mesons. We tune various parameters of the distillation method and the charm quark mass. As a first result, we present the masses of the ground and excited states in the 0++ and 1−− channel

Divalproex sodium modulates nuclear localization of ataxin-3 and prevents cellular toxicity caused by expanded ataxin-3

In the era of computational biology, functional annotation remains a major challenge. Recent annotation methods are based on the guilt by association assumption and rely on data integration to identify functional partners. However, most of these methods suffer from data heterogeneity and a lack of biological context specificity which would probably explain the high rate of false positives among predictions. This thesis develops an approach of molecular data integration controlling their heterogeneity in order to annotate Arabidopsis thaliana genes involved in stress response. The major contributions of this thesis are: (1) functional annotation of groups of co-expressed genes by omics data integration (2) the construction of a coregulatory gene network through a cross-analysis of the coexpressed groups strengthening the functional links between genes (3) the development of a supervised learning method for the inference of gene function centered on the GO Slim terms with a control of the FDR. By identifying a decision rule by term, this method was used to predict the function of 47 orphan or partially annotated genes.À l'ère de la biologie computationnelle, l'annotation fonctionnelle reste un défi central. Les méthodes d’annotation récentes reposent sur l’hypothèse d’association par culpabilité et s’appuient sur l’intégration de données pour la recherche de partenaires fonctionnels. Cependant, la majorité de ces méthodes souffrent de l’hétérogénéité des données et du manque de spécificité du contexte biologique ce qui expliquerait un taux élevé de faux positifs parmi les prédictions. Ce travail de thèse développe une approche intégrative de données moléculaires contrôlant leur hétérogénéité pour annoter des gènes d’Arabidopsis thaliana impliqués dans la réponse aux stress. Les contributions majeures de cette thèse sont: (1) l'annotation fonctionnelle de groupes de gènes coexprimés par l'intégration de données omiques (2) la construction d'un réseau de corégulation par une analyse transversale des groupes coexprimés qui renforce les liens fonctionnels entre les gènes. (3) le développement d’une méthode d’apprentissage supervisé pour l’inférence de fonction centrée sur les termes de la GO Slim en contrôlant le FDR. En identifiant une règle de décision par terme, cette méthode a permis de prédire la fonction de 47 gènes partiellement annotés ou orphelins

Divalproex sodium modulates nuclear localization of ataxin-3 and prevents cellular toxicity caused by expanded ataxin-3

Background & aims: Spinocerebellar ataxia type 3 (SCA3), also known as Machado-Joseph disease (MJD), is an autosomal dominantly inherited neurodegenerative disorder and the most common form of SCA worldwide. It is caused by the expansion of a polyglutamine (polyQ) tract in the ataxin-3 protein. Nuclear localization of the affected protein is a key event in the pathology of SCA3 via affecting nuclear organization, transcriptional dysfunction, and seeding aggregations, finally causing neurodegeneration and cell death. So far, there is no effective therapy to prevent or slow the progression of SCA3.Methods: In this study, we explored the effect of divalproex sodium as an HDACi in SCA3 cell models and explored how divalproex sodium interferes with pathogenetic processes causing SCA3.Results: We found that divalproex sodium rescues the hypoacetylation levels of histone H3 and attenuates cellular cytotoxicity induced by expanded ataxin-3 partly via preventing nuclear transport of ataxin-3 (particularly heat shock-dependent).Conclusion: Our study provides novel insights into the mechanisms of action of divalproex sodium as a possible treatment for SCA3, beyond the known regulation of transcription