Up- and down-quark masses from QCD sum rules

The QCD up- and down-quark masses are determined from an optimized QCD Finite Energy Sum Rule (FESR) involving the correlator of axial-vector current divergences. In the QCD sector this correlator is known to five loop order in perturbative QCD (PQCD), together with non-perturbative corrections from the quark and gluon condensates. This FESR is designed to reduce considerably the systematic uncertainties arising from the hadronic spectral function. The determination is done in the framework of both fixed order and contour improved perturbation theory. Results from the latter, involving far less systematic uncertainties, are: \bar{m}_u (2\, \mbox{GeV}) = (2.6 \, \pm \, 0.4) \, {\mbox{MeV}}, \bar{m}_d (2\, \mbox{GeV}) = (5.3 \, \pm \, 0.4) \, {\mbox{MeV}}, and the sum $\bar{m}_{ud} \equiv (\bar{m}_u \, + \, \bar{m}_d)/2$, is \bar{m}_{ud}({ 2 \,\mbox{GeV}}) =( 3.9 \, \pm \, 0.3 \,) {\mbox{MeV}}.Comment: A Mathematica^(C) file pertaining to numerical evaluations is attached as Ancillar

Measurement of electron screening in muonic lead

Energies of the transitions between high-lying (n≥6) states of muonic lead were accurately determined. The results are interpreted as a ∼2% test of the electron screening. The agreement between experiment and theory is good if it is assumed that the refilling of the electron K shell is fast. The present results furthermore severely restrict possible ionization of the electron L shell

Swimming exercise enhances brain plasticity in fish

It is well-established that sustained exercise training can enhance brain plasticity and boost cognitive performance in mammals, but this phenomenon has not received much attention in fish. The aim of this study was to determine whether sustained swimming exercise can enhance brain plasticity in juvenile Atlantic salmon. Brain plasticity was assessed by both mapping the whole telencephalon transcriptome and conducting telencephalic region-specific microdissections on target genes. We found that 1772 transcripts were differentially expressed between the exercise and control groups. Gene ontology (GO) analysis identified 195 and 272 GO categories with a significant overrepresentation of up- or downregulated transcripts, respectively. A multitude of these GO categories was associated with neuronal excitability, neuronal signalling, cell proliferation and neurite outgrowth (i.e. cognition-related neuronal markers). Additionally, we found an increase in proliferating cell nuclear antigen (pcna) after both three and eight weeks of exercise in the equivalent to the hippocampus in fish. Furthermore, the expression of the neural plasticity markers synaptotagmin (syt) and brain-derived neurotrophic factor (bdnf) were also increased due to exercise in the equivalent to the lateral septum in fish. In conclusion, this is the first time that swimming exercise has been directly linked to increased telencephalic neurogenesis and neural plasticity in a teleost, and our results pave the way for future studies on exercise-induced neuroplasticity in fish.</p

Parallel Gaussian Process Optimization with Upper Confidence Bound and Pure Exploration

In this paper, we consider the challenge of maximizing an unknown function f for which evaluations are noisy and are acquired with high cost. An iterative procedure uses the previous measures to actively select the next estimation of f which is predicted to be the most useful. We focus on the case where the function can be evaluated in parallel with batches of fixed size and analyze the benefit compared to the purely sequential procedure in terms of cumulative regret. We introduce the Gaussian Process Upper Confidence Bound and Pure Exploration algorithm (GP-UCB-PE) which combines the UCB strategy and Pure Exploration in the same batch of evaluations along the parallel iterations. We prove theoretical upper bounds on the regret with batches of size K for this procedure which show the improvement of the order of sqrt{K} for fixed iteration cost over purely sequential versions. Moreover, the multiplicative constants involved have the property of being dimension-free. We also confirm empirically the efficiency of GP-UCB-PE on real and synthetic problems compared to state-of-the-art competitors

Germline TP53 mutational spectrum in French Canadians with breast cancer

Abstract Background Specific germline mutations in the hereditary breast-ovarian cancer susceptibility (HBC/HBOC) genes, BRCA1, BRCA2 and PALB2, have been shown to recur in French Canadians of Quebec, Canada, and this has been attributed to common ancestors. Germline TP53 mutation carriers are known to segregate in Li-Fraumeni syndrome families, which feature young age of onset breast cancer. We have reported rare TP53 mutation carriers in French Canadian HBC families, though none recurred possibly due to the limited number of cancer families investigated. Here we describe TP53 germline mutations found in French Canadian cancer families provided from hereditary cancer clinics; investigate 37 new BRCA1 and BRCA2 mutation-negative HBC/HBOC families for the TP53 mutations; and assess the frequency of TP53 mutations in a 1235 French Canadian breast cancer cases not selected for family history of cancer. Methods TP53 mutation-positive pedigrees from French Canadian cancer families were provided from local hereditary cancer clinics. Bidirectional Sanger sequencing of all protein encoding exons of TP53 was performed using peripheral blood lymphocyte DNA from breast/ovarian cancer probands from 37 HBC/HBOC families of French Canadian descent. Targeted bidirectional Sanger sequencing assay of regions containing the identified TP53 mutations was performed on 1235 French Canadian breast cancer cases not selected for family history cancer. Results Five new TP53 mutations were identified in six pedigrees from hereditary cancer clinics. No deleterious mutations were identified in cancer probands from 37 HBC/HBOC families. A targeted mutation screen of the 1235 breast cancer cases identified a c.844C>T [p.Arg282Trp] mutation carrier. This mutation was also found among the six mutation-positive cancer families provided by the local hereditary cancer clinics. The targeted screen also uncovered a new TP53 mutation, c.685T>C [p.Cys229Arg] that was found in two breast cancer cases. All TP53 mutation carriers were among the 656 women with breast cancer diagnosed less than 50 years of age. Conclusions In all six new TP53 mutations were identified in French Canadians, where two each occurred in independently ascertained cases/families. Although all newly identified breast cancer mutation carriers reported a family history of cancer, none were consistent with features of Li-Fraumeni syndrome families