Chiral corrections to the SU(2)×SU(2)SU(2)\times SU(2) Gell-Mann-Oakes-Renner relation

The next to leading order chiral corrections to the $SU(2)\times SU(2)$ Gell-Mann-Oakes-Renner (GMOR) relation are obtained using the pseudoscalar correlator to five-loop order in perturbative QCD, together with new finite energy sum rules (FESR) incorporating polynomial, Legendre type, integration kernels. The purpose of these kernels is to suppress hadronic contributions in the region where they are least known. This reduces considerably the systematic uncertainties arising from the lack of direct experimental information on the hadronic resonance spectral function. Three different methods are used to compute the FESR contour integral in the complex energy (squared) s-plane, i.e. Fixed Order Perturbation Theory, Contour Improved Perturbation Theory, and a fixed renormalization scale scheme. We obtain for the corrections to the GMOR relation, $\delta_\pi$, the value $\delta_\pi = (6.2, \pm 1.6)$. This result is substantially more accurate than previous determinations based on QCD sum rules; it is also more reliable as it is basically free of systematic uncertainties. It implies a light quark condensate $\simeq \equiv |_{2\,\mathrm{GeV}} = (- 267 \pm 5 MeV)^3$. As a byproduct, the chiral perturbation theory (unphysical) low energy constant $H^r_2$ is predicted to be $H^r_2 (\nu_\chi = M_\rho) = - (5.1 \pm 1.8)\times 10^{-3}$, or $H^r_2 (\nu_\chi = M_\eta) = - (5.7 \pm 2.0)\times 10^{-3}$.Comment: A comment about the value of the strong coupling has been added at the end of Section 4. No change in results or conslusion

B meson decay constants f(Bc), f(Bs) and f(B) from QCD sum rules

Finite energy QCD sum rules with Legendre polynomial integration kernels are used to determine the heavy meson decay constant f(Bc), and revisit f(B) and f(Bs). Results exhibit excellent stability in a wide range of values of the integration radius in the complex squared energy plane, and of the order of the Legendre polynomial. Results are f(Bc) = 528 +/- 19 MeV, f(B) = 186 +/- 14 MeV, and f(Bs) = 222 +/- 12 MeV

Weinberg like sum rules revisited

The generalized Weinberg sum rules containing the difference of isovector vector and axial-vector spectral functions saturated by both finite and infinite number of narrow resonances are considered. We summarize the status of these sum rules and analyze their overall agreement with phenomenological Lagrangians, low-energy relations, parity doubling, hadron string models, and experimental data.Comment: 31 pages, noticed misprints are corrected, references are added, and other minor corrections are mad

Corrosion resistance of anodic layers grown on 304L stainless steel at different anodizing times and stirring speeds

Different chemical and physical treatments have been used to improve the properties and functionalities of steels. Anodizing is one of the most promising treatments, due to its versatility and easy industrial implementation. It allows the growth of nanoestructured oxide films with interesting properties able to be employed in different industrial sectors. The present work studies the influence of the anodizing time (15, 30, 45 and 60 min), as well as the stirring speed (0, 200, 400, and 600 rpm), on the morphology and the corrosion resistance of the anodic layers grown in 304L stainless steel. The anodic layers were characterized morphologically, compositionally, and electrochemically, in order to determine the influence of the anodization parameters on their corrosion behavior in a 0.6 mol L-1 NaCl solution. The results show that at 45 and 60 min anodizing times, the formation of two microstructures is favored, associated with the collapse of the nanoporous structures at the metal-oxide interphace. However, both the stirring speed and the anodizing time have a negligeable effect on the corrosion behavior of the anodized 304L SS samples, since their electrochemical values are similar to those of the non-anodized ones

LEMUR: Large European Module for solar Ultraviolet Research. European contribution to JAXA's Solar-C mission

Understanding the solar outer atmosphere requires concerted, simultaneous solar observations from the visible to the vacuum ultraviolet (VUV) and soft X-rays, at high spatial resolution (between 0.1" and 0.3"), at high temporal resolution (on the order of 10 s, i.e., the time scale of chromospheric dynamics), with a wide temperature coverage (0.01 MK to 20 MK, from the chromosphere to the flaring corona), and the capability of measuring magnetic fields through spectropolarimetry at visible and near-infrared wavelengths. Simultaneous spectroscopic measurements sampling the entire temperature range are particularly important. These requirements are fulfilled by the Japanese Solar-C mission (Plan B), composed of a spacecraft in a geosynchronous orbit with a payload providing a significant improvement of imaging and spectropolarimetric capabilities in the UV, visible, and near-infrared with respect to what is available today and foreseen in the near future. The Large European Module for solar Ultraviolet Research (LEMUR), described in this paper, is a large VUV telescope feeding a scientific payload of high-resolution imaging spectrographs and cameras. LEMUR consists of two major components: a VUV solar telescope with a 30 cm diameter mirror and a focal length of 3.6 m, and a focal-plane package composed of VUV spectrometers covering six carefully chosen wavelength ranges between 17 and 127 nm. The LEMUR slit covers 280" on the Sun with 0.14" per pixel sampling. In addition, LEMUR is capable of measuring mass flows velocities (line shifts) down to 2 km/s or better. LEMUR has been proposed to ESA as the European contribution to the Solar C mission.Comment: 35 pages, 14 figures. To appear on Experimental Astronom

Distinct Actin and Lipid Binding Sites in Ysc84 Are Required during Early Stages of Yeast Endocytosis

During endocytosis in S. cerevisiae, actin polymerization is proposed to provide the driving force for invagination against the effects of turgor pressure. In previous studies, Ysc84 was demonstrated to bind actin through a conserved N-terminal domain. However, full length Ysc84 could only bind actin when its C-terminal SH3 domain also bound to the yeast WASP homologue Las17. Live cell-imaging has revealed that Ysc84 localizes to endocytic sites after Las17/WASP but before other known actin binding proteins, suggesting it is likely to function at an early stage of membrane invagination. While there are homologues of Ysc84 in other organisms, including its human homologue SH3yl-1, little is known of its mode of interaction with actin or how this interaction affects actin filament dynamics. Here we identify key residues involved both in Ysc84 actin and lipid binding, and demonstrate that its actin binding activity is negatively regulated by PI(4,5)P2. Ysc84 mutants defective in their lipid or actin-binding interaction were characterized in vivo. The abilities of Ysc84 to bind Las17 through its C-terminal SH3 domain, or to actin and lipid through the N-terminal domain were all shown to be essential in order to rescue temperature sensitive growth in a strain requiring YSC84 expression. Live cell imaging in strains with fluorescently tagged endocytic reporter proteins revealed distinct phenotypes for the mutants indicating the importance of these interactions for regulating key stages of endocytosis

CRISPR-Cas9 screens in human cells and primary neurons identify modifiers of C9ORF72 dipeptide-repeat-protein toxicity.

Hexanucleotide-repeat expansions in the C9ORF72 gene are the most common cause of amyotrophic lateral sclerosis and frontotemporal dementia (c9ALS/FTD). The nucleotide-repeat expansions are translated into dipeptide-repeat (DPR) proteins, which are aggregation prone and may contribute to neurodegeneration. We used the CRISPR-Cas9 system to perform genome-wide gene-knockout screens for suppressors and enhancers of C9ORF72 DPR toxicity in human cells. We validated hits by performing secondary CRISPR-Cas9 screens in primary mouse neurons. We uncovered potent modifiers of DPR toxicity whose gene products function in nucleocytoplasmic transport, the endoplasmic reticulum (ER), proteasome, RNA-processing pathways, and chromatin modification. One modifier, TMX2, modulated the ER-stress signature elicited by C9ORF72 DPRs in neurons and improved survival of human induced motor neurons from patients with C9ORF72 ALS. Together, our results demonstrate the promise of CRISPR-Cas9 screens in defining mechanisms of neurodegenerative diseases

Timeliness of national notifiable diseases surveillance system in Korea: a cross-sectional study

<p>Abstract</p> <p>Background</p> <p>With the increase of international travels, infectious disease control is gaining a greater importance across regional borders. Adequate surveillance system function is crucial to prevent a global spread of infectious disease at the earliest stage. There have been limited reports on the characteristics of infectious disease surveillance in Asia. The authors studied the timeliness of the Korean National Notifiable Disease Surveillance System with regard to major notifiable diseases from 2001 to 2006.</p> <p>Methods</p> <p>Six notifiable infectious diseases reported relatively frequently were included in this study. Five diseases were selected by the criteria of reported cases > 100 per year: typhoid fever, shigellosis, mumps, scrub typhus, and hemorrhagic fever with renal syndrome. In addition, dengue fever was also included to represent an emerging disease, despite its low number of cases. The diseases were compared for the proportion notified within the recommended time limits, median time lags, and for the cumulative distribution of time lags at each surveillance step between symptom onset and date of notification to the Korea Centers for Disease Control and Prevention (KCDC).</p> <p>Results</p> <p>The proportion of cases reported in time was lower for disease groups with a recommended time limit of 1 day compared with 7 days (60%–70% vs. > 80%). The median time from disease onset to notification to KCDC ranged between 6 and 20 days. The median time from onset to registration at the local level ranged between 2 and 15 days. Distribution of time lags showed that main delays arose in the time from onset to diagnosis. There were variations in timeliness by disease categories and surveillance steps.</p> <p>Conclusion</p> <p>Time from disease onset to diagnosis generally contributed most to the delay in reporting. It is needed to promote public education and to improve clinical guidelines. Rapid reporting by doctors should be encouraged, and unification of recommended reporting time limit can be helpful. Our study also demonstrates the utility of the overall assessment of time-lag distributions for disease-specific strategies to improve surveillance.</p