Evidence of a subenergy gap in the overdoped regime of Y_{1-x}Ca_{x}Ba_{2}Cu_{3}O_{7-\delta} thin films from THz Spectroscopy

We measured the terahertz (THz) complex conductivity of Ca doped YBa_{2}Cu_{3}O_{7-\delta} thin films in the frequency range of 0.1 to 3 THz (3 to 100 cm^{-1}) and at a temperature range of 20 to 300 K. The films were measured using both time domain and frequency domain THz methods. We showed evidence for the existence of a sub-gap in overdoped Y_{1-x}Ca_{x}Ba_{2}Cu_{3}O_{7-\delta} samples doped with 5% and 10% Ca. Evidence for the opening of this sub-gap appears as a sharp decrease in the spectrum of the real part of conductivity at frequencies equivalent to a gap energy of 1 meV and is more prominent with increased doping. This decrease in conductivity can be explained by using d-wave pairing symmetry with an imaginary part of is or id_{xy} which suggests node removal.Comment: 7 pages, 7 figure

Structure and mechanical properties of the welded joints of large-diameter pipes

The structure and mechanical properties of the technological welded joints of large-diameter pipes of strength class K60 produced by two companies are studied. Along with standard mechanical properties (σ0.2, σu, δ, ψ), specific work of deformation a (tensile toughness) and true rupture strength Sf are estimated from an analysis of the stress-strain diagrams constructed in true coordinates. The mechanical behavior is found to be different for samples cut from different zones of a welded joint (central weld, heat-affected zone, and base metal). The mutual correlation between parameters a, S f, and impact toughness KCV is considered. © 2013 Pleiades Publishing, Ltd

Module sectional category of products

Adapting a result of Félix–Halperin–Lemaire concerning the Lusternik–Schnirelmann category of products, we prove the additivity of a rational approximation for Schwarz’s sectional category with respect to products of certain fibrations.J.C. is supported by the Polish National Science Centre Grant 2016/21/ P/ST1/03460 within the European Unions Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie Grant Agreement No. 665778 and by the Belgian Interuniversity Attraction Pole (IAP) within the framework “Dynamics, Geometry and Statistical Physics” (DYGEST P7/18). L.V. is partially supported by Portuguese Funds through FCT – Fundação para a Ciência e a Tecnologia, within the Project UID/MAT/00013/2013

Women playwrights in post-apartheid South Africa : Yael Farber, Lara Foot-Newton, and the call for Ubuntu

This chapter explores how these two contemporary South African female playwrights are using specific aesthetics to address legacies of apartheid violence in the post-apartheid context. It analyses Yael Farber's post TRC plays 'A Woman in Waiting' (1999), 'Amajuba' (2002), 'He left Quietly' (2003) and 'Molora' (2007); and Lara Foot-Newton's 'Tshepang: The Third testament' (2003), 'Karoo Moose' (2007) and 'Reach!' (2007)

Zinc deficiency activates S100A8 inflammation in the absence of COX-2 and promotes murine oral-esophageal tumor progression

Zinc (Zn)-deficiency (ZD) is implicated in the pathogenesis of human oral-esophageal cancers. Previously, we showed that in ZD mice genetic deletion of cyclooxygenase-2 (Cox-2) enhances N-nitrosomethylbenzylamine-induced forestomach carcinogenesis. By contrast, Cox-2 deletion offers protection in Zn-sufficient (ZS) mice. We hypothesize that ZD activates pathways insensitive to COX-2 inhibition, thereby promoting carcinogenesis. This hypothesis is tested in a Cox-2−/− mouse tongue cancer model that mimics pharmacologic blockade of COX-2 by firstly examining transcriptome profiles of forestomach mucosa from Cox-2−/− and wild-type mice on a ZD vs. ZS diet, and secondly investigating the roles of identified markers in mouse forestomach/tongue preneoplasia and carcinomas. In Cox-2−/− mice exposed to the tongue carcinogen 4-nitroquinoline 1-oxide, dietary ZD elicited tongue/esophagus/forestomach carcinomas that were prevented by ZS. The precancerous ZD:Cox-2−/−vs. ZS:Cox-2−/− forestomach had an inflammatory signature with upregulation of the proinflammation genes S100a8 and S100a9. Bioinformatics analysis revealed overrepresentation of inflammation processes comprising S100a8/a9 and an nuclear factor (NF)-κB network with connectivity to S100A8. Immunohistochemistry revealed co-overexpression of S100A8, its heterodimeric partner S100A9, the receptor for advanced glycation end-products (RAGE), NF-κB p65, and cyclin D1, in ZD:Cox-2−/− forestomach/tongue preneoplasia and carcinomas, evidence for the activation of a RAGE-S100A8/A9 inflammatory pathway. Accumulation of p53 in these carcinomas indicated activation of additional inflammatory pathways. Zn-replenishment in ZD:Cox-2−/−mice reversed the inflammation and inhibited carcinogenesis. Thus, ZD activates alternative inflammation-associated cancer pathways that fuel tumor progression and bypass the antitumor effect of Cox-2 ablation. These findings have important clinical implications, as combination cancer therapy that includes Zn may improve efficacy

Atomic structure of dislocation kinks in silicon

We investigate the physics of the core reconstruction and associated structural excitations (reconstruction defects and kinks) of dislocations in silicon, using a linear-scaling density-matrix technique. The two predominant dislocations (the 90-degree and 30-degree partials) are examined, focusing for the 90-degree case on the single-period core reconstruction. In both cases, we observe strongly reconstructed bonds at the dislocation cores, as suggested in previous studies. As a consequence, relatively low formation energies and high migration barriers are generally associated with reconstructed (dangling-bond-free) kinks. Complexes formed of a kink plus a reconstruction defect are found to be strongly bound in the 30-degree partial, while the opposite is true in the case of 90-degree partial, where such complexes are found to be only marginally stable at zero temperature with very low dissociation barriers. For the 30-degree partial, our calculated formation energies and migration barriers of kinks are seen to compare favorably with experiment. Our results for the kink energies on the 90-degree partial are consistent with a recently proposed alternative double-period structure for the core of this dislocation.Comment: 12 pages, two-column style with 8 postscript figures embedded. Uses REVTEX and epsf macros. Also available at http://www.physics.rutgers.edu/~dhv/preprints/index.html#rn_di

Integration of metabolomics, transcriptomics, and microRNA expression profiling reveals a miR-143-HK2-glucose network underlying zinc-deficiency-associated esophageal neoplasia

Esophageal squamous cell carcinoma (ESCC) in humans is a deadly disease associated with dietary zinc (Zn)-deficiency. In the rat esophagus, Zn-deficiency induces cell proliferation, alters mRNA and microRNA gene expression, and promotes ESCC. We investigated whether Zn-deficiency alters cell metabolism by evaluating metabolomic profiles of esophageal epithelia from Zn-deficient and replenished rats vs sufficient rats, using untargeted gas chromatography time-of-flight mass spectrometry (n = 8/group). The Zn-deficient proliferative esophagus exhibits a distinct metabolic profile with glucose down 153-fold and lactic acid up 1.7-fold (P \u3c 0.0001), indicating aerobic glycolysis (the Warburg effect ), a hallmark of cancer cells. Zn-replenishment rapidly increases glucose content, restores deregulated metabolites to control levels, and reverses the hyperplastic phenotype. Integration of metabolomics and our reported transcriptomic data for this tissue unveils a link between glucose down-regulation and overexpression of HK2, an enzyme that catalyzes the first step of glycolysis and is overexpressed in cancer cells. Searching our published microRNA profile, we find that the tumor-suppressor miR-143, a negative regulator of HK2, is down-regulated in Zn-deficient esophagus. Using in situ hybridization and immunohistochemical analysis, the inverse correlation between miR-143 down-regulation and HK2 overexpression is documented in hyperplastic Zndeficient esophagus, archived ESCC-bearing Zn-deficient esophagus, and human ESCC tissues. Thus, to sustain uncontrolled cell proliferation, Zn-deficiency reprograms glucose metabolism by modulating expression of miR-143 and its target HK2. Our work provides new insight into critical roles of Zn in ESCC development and prevention. © Fong et al