Study of decagonal approximant and γ-brass-type compounds in Al-Cr-Fe thin films

This paper reports the preparation conditions and structure characteristics of Al-Cr-Fe very thin films (10-30 nm) obtained by the flash evaporation technique. The films are either amorphous or crystallized, depending on the thickness of the sample and temperature of the substrate. Annealing of amorphous films leads to crystallization of intermetallic phases that are all linked with quasicrystals. In particular, we have identified by transmission electron microscopy the following structures: body-centered-cubic (bcc) γ-brass phase, monoclinic λ-Al13(Cr,Fe)4 phase, and orthorhombic O1-phase, all of them already observed in this system, together with four new structures, i.e., a face-centered-cubic (fcc) γ-brass phase (superstructure of the bcc phase), monoclinic λ′-phase (related to the λ-phase) and two orthorhombic phases (1/1/; 1/1) and (1/0; 2/1) approximants of the decagonal phase). In this study, we point out the occurrence of twin defects of the λ-Al13(Cr,Fe)4 phase. Films prepared directly in the crystalline state comprise the O1 approximant. Electron energy loss spectroscopy measurements show that all films are not oxidized except for the presence of a native oxide layer that forms in ambient atmosphere with a thickness that cannot exceed 0.3 nm. Optical properties were investigated and show that films need to be large enough (>30 nm) to reproduce the properties of bulk alloys. Finally, contact angle wetting measurements reveal that the presence of such films on a substrate, even at very low thickness, considerably decreases the wetting behavior by wate

Orthonormal sequences in L2(Rd)L^2(R^d) and time frequency localization

We study uncertainty principles for orthonormal bases and sequences in $L^2(\R^d)$. As in the classical Heisenberg inequality we focus on the product of the dispersions of a function and its Fourier transform. In particular we prove that there is no orthonormal basis for $L^2(\R)$ for which the time and frequency means as well as the product of dispersions are uniformly bounded. The problem is related to recent results of J. Benedetto, A. Powell, and Ph. Jaming. Our main tool is a time frequency localization inequality for orthonormal sequences in $L^2(\R^d)$. It has various other applications.Comment: 18 page

Quantum catastrophes: a case study

The bound-state spectrum of a Hamiltonian H is assumed real in a non-empty domain D of physical values of parameters. This means that for these parameters, H may be called crypto-Hermitian, i.e., made Hermitian via an {\it ad hoc} choice of the inner product in the physical Hilbert space of quantum bound states (i.e., via an {\it ad hoc} construction of the so called metric). The name of quantum catastrophe is then assigned to the N-tuple-exceptional-point crossing, i.e., to the scenario in which we leave domain D along such a path that at the boundary of D, an N-plet of bound state energies degenerates and, subsequently, complexifies. At any fixed $N \geq 2$, this process is simulated via an N by N benchmark effective matrix Hamiltonian H. Finally, it is being assigned such a closed-form metric which is made unique via an N-extrapolation-friendliness requirement.Comment: 23 p

The TGF-β/Smad Repressor TG-Interacting Factor 1 (TGIF1) Plays a Role in Radiation-Induced Intestinal Injury Independently of a Smad Signaling Pathway

Despite advances in radiation delivery protocols, exposure of normal tissues during the course of radiation therapy remains a limiting factor of cancer treatment. If the canonical TGF-β/Smad pathway has been extensively studied and implicated in the development of radiation damage in various organs, the precise modalities of its activation following radiation exposure remain elusive. In the present study, we hypothesized that TGF-β1 signaling and target genes expression may depend on radiation-induced modifications in Smad transcriptional co-repressors/inhibitors expressions (TGIF1, SnoN, Ski and Smad7). In endothelial cells (HUVECs) and in a model of experimental radiation enteropathy in mice, radiation exposure increases expression of TGF-β/Smad pathway and of its target gene PAI-1, together with the overexpression of Smad co-repressor TGIF1. In mice, TGIF1 deficiency is not associated with changes in the expression of radiation-induced TGF-β pathway-related transcripts following localized small intestinal irradiation. In HUVECs, TGIF1 overexpression or silencing has no influence either on the radiation-induced Smad activation or the Smad3-dependent PAI-1 overexpression. However, TGIF1 genetic deficiency sensitizes mice to radiation-induced intestinal damage after total body or localized small intestinal radiation exposure, demonstrating that TGIF1 plays a role in radiation-induced intestinal injury. In conclusion, the TGF-β/Smad co-repressor TGIF1 plays a role in radiation-induced normal tissue damage by a Smad-independent mechanism

The sequence of rice chromosomes 11 and 12, rich in disease resistance genes and recent gene duplications

Background: Rice is an important staple food and, with the smallest cereal genome, serves as a reference species for studies on the evolution of cereals and other grasses. Therefore, decoding its entire genome will be a prerequisite for applied and basic research on this species and all other cereals. Results: We have determined and analyzed the complete sequences of two of its chromosomes, 11 and 12, which total 55.9 Mb (14.3% of the entire genome length), based on a set of overlapping clones. A total of 5,993 non-transposable element related genes are present on these chromosomes. Among them are 289 disease resistance-like and 28 defense-response genes, a higher proportion of these categories than on any other rice chromosome. A three-Mb segment on both chromosomes resulted from a duplication 7.7 million years ago (mya), the most recent large-scale duplication in the rice genome. Paralogous gene copies within this segmental duplication can be aligned with genomic assemblies from sorghum and maize. Although these gene copies are preserved on both chromosomes, their expression patterns have diverged. When the gene order of rice chromosomes 11 and 12 was compared to wheat gene loci, significant synteny between these orthologous regions was detected, illustrating the presence of conserved genes alternating with recently evolved genes. Conclusion: Because the resistance and defense response genes, enriched on these chromosomes relative to the whole genome, also occur in clusters, they provide a preferred target for breeding durable disease resistance in rice and the isolation of their allelic variants. The recent duplication of a large chromosomal segment coupled with the high density of disease resistance gene clusters makes this the most recently evolved part of the rice genome. Based on syntenic alignments of these chromosomes, rice chromosome 11 and 12 do not appear to have resulted from a single whole-genome duplication event as previously suggested

Pathway-Based Analysis of a Melanoma Genome-Wide Association Study: Analysis of Genes Related to Tumour-Immunosuppression

Systemic immunosuppression is a risk factor for melanoma, and sunburn-induced immunosuppression is thought to be causal. Genes in immunosuppression pathways are therefore candidate melanoma-susceptibility genes. If variants within these genes individually have a small effect on disease risk, the association may be undetected in genome-wide association (GWA) studies due to low power to reach a high significance level. Pathway-based approaches have been suggested as a method of incorporating a priori knowledge into the analysis of GWA studies. In this study, the association of 1113 single nucleotide polymorphisms (SNPs) in 43 genes (39 genomic regions) related to immunosuppression have been analysed using a gene-set approach in 1539 melanoma cases and 3917 controls from the GenoMEL consortium GWA study. The association between melanoma susceptibility and the whole set of tumour-immunosuppression genes, and also predefined functional subgroups of genes, was considered. The analysis was based on a measure formed by summing the evidence from the most significant SNP in each gene, and significance was evaluated empirically by case-control label permutation. An association was found between melanoma and the complete set of genes (pemp = 0.002), as well as the subgroups related to the generation of tolerogenic dendritic cells (pemp = 0.006) and secretion of suppressive factors (pemp = 0.0004), thus providing preliminary evidence of involvement of tumour-immunosuppression gene polymorphisms in melanoma susceptibility. The analysis was repeated on a second phase of the GenoMEL study, which showed no evidence of an association. As one of the first attempts to replicate a pathway-level association, our results suggest that low power and heterogeneity may present challenges

Genome-Wide Association Study in BRCA1 Mutation Carriers Identifies Novel Loci Associated with Breast and Ovarian Cancer Risk

BRCA1-associated breast and ovarian cancer risks can be modified by common genetic variants. To identify further cancer risk-modifying loci, we performed a multi-stage GWAS of 11,705 BRCA1 carriers (of whom 5,920 were diagnosed with breast and 1,839 were diagnosed with ovarian cancer), with a further replication in an additional sample of 2,646 BRCA1 carriers. We identified a novel breast cancer risk modifier locus at 1q32 for BRCA1 carriers (rs2290854, P = 2.7×10-8, HR = 1.14, 95% CI: 1.09-1.20). In addition, we identified two novel ovarian cancer risk modifier loci: 17q21.31 (rs17631303, P = 1.4×10-8, HR = 1.27, 95% CI: 1.17-1.38) and 4q32.3 (rs4691139, P = 3.4×10-8, HR = 1.20, 95% CI: 1.17-1.38). The 4q32.3 locus was not associated with ovarian cancer risk in the general population or BRCA2 carriers, suggesting a BRCA1-specific associat