On the Atomic Photoeffect in Non-relativistic QED

In this paper we present a mathematical analysis of the photoelectric effect for one-electron atoms in the framework of non-relativistic QED. We treat photo-ionization as a scattering process where in the remote past an atom in its ground state is targeted by one or several photons, while in the distant future the atom is ionized and the electron escapes to spacial infinity. Our main result shows that the ionization probability, to leading order in the fine-structure constant, $\alpha$, is correctly given by formal time-dependent perturbation theory, and, moreover, that the dipole approximation produces an error of only sub-leading order in $\alpha$. In this sense, the dipole approximation is rigorously justified.Comment: 25 page

An experimentally-validated computational framework for CMAS degradation of environmental barrier coatings

The work addresses reactions between silicate deposits, generically known as CMAS, and yttrium disilicate (YDS), a candidate environmental barrier coating (EBC) for SiC/SiC composites. The primary goal is to elucidate effects of deposit composition, exposure temperature and time on the extent of YDS recession as well as the associated compositional and morphological evolution of reacting phases. Phase equilibrium calculations are used to assess deposits of twelve different compositions at 1300°C and 1400°C; experimental observations of YDS recession are reported for three of these compositions at both temperatures. The results show that recession depths reach terminal values for exposure times ≥ 100h. Terminal recession depths are sensitive to deposit composition but only weakly affected by temperature. Deposits with high initial Ca:Si ratio react most severely with YDS, forming a thick layer containing an apatite reaction product interpenetrated by residual melt. The severity of the reaction decreases with decreasing Ca:Si ratio, and is least severe for deposits with insufficient Ca:Si ratio to produce apatite. Please click Additional Files below to see the full abstract

CMAS challenges to CMC-T/EBC systems

Gas turbine technology is undergoing a major transition with the recent implementation of SiC based ceramic composites (CMCs) in aircraft engines. While the potential improvement in temperature capability (≥1500°C) is unprecedented, there are a number of issues that limit the full exploitation of such potential. In addition to the longstanding concern for low temperature oxidative embrittlement and the limited temperature capability of current bond coats and matrices, the susceptibility of the protective SiO2 to volatilization in the combustion environment requires the use of environmental barrier coatings (EBCs) to achieve durability targets. Most EBC concepts, however, are based on silicates and are thus susceptible to degradation by molten silicate deposits generically known as CMAS originating from mineral debris ingested into engines with the intake air. This presentation will discuss the thermodynamic and mechanistic foundation of the degradation of EBCs by CMAS, recent progress in establishing the relevant phase equilibria for these systems, and the role of the CMAS composition on the extent of degradation, as well as perspective on mitigation. (Research supported by ONR, AFOSR and the P&W Center of Excellence in Composites at UCSB.

CMS physics technical design report : Addendum on high density QCD with heavy ions

Peer reviewe

Identification of TMEM126A as OXA1L-interacting protein reveals cotranslational quality control in mitochondria

Cellular proteostasis requires transport of polypeptides across membranes. Although defective transport processes trigger cytosolic rescue and quality control mechanisms that clear translocases and membranes from unproductive cargo, proteins that are synthesized within mitochondria are not accessible to these mechanisms. Mitochondrial-encoded proteins are inserted cotranslationally into the inner membrane by the conserved insertase OXA1L. Here, we identify TMEM126A as a OXA1L-interacting protein. TMEM126A associates with mitochondrial ribosomes and translation products. Loss of TMEM126A leads to the destabilization of mitochondrial translation products, triggering an inner membrane quality control process, in which newly synthesized proteins are degraded by the mitochondrial iAAA protease. Our data reveal that TMEM126A cooperates with OXA1L in protein insertion into the membrane. Upon loss of TMEM126A, the cargo-blocked OXA1L insertase complexes undergo proteolytic clearance by the iAAA protease machinery together with its cargo

Genetic Variation in Selenoprotein Genes, Lifestyle, and Risk of Colon and Rectal Cancer

BACKGROUND: Associations between selenium and cancer have directed attention to role of selenoproteins in the carcinogenic process. METHODS: We used data from two population-based case-control studies of colon (n = 1555 cases, 1956 controls) and rectal (n = 754 cases, 959 controls) cancer. We evaluated the association between genetic variation in TXNRD1, TXNRD2, TXNRD3, C11orf31 (SelH), SelW, SelN1, SelS, SepX, and SeP15 with colorectal cancer risk. RESULTS: After adjustment for multiple comparisons, several associations were observed. Two SNPs in TXNRD3 were associated with rectal cancer (rs11718498 dominant OR 1.42 95% CI 1.16,1.74 pACT 0.0036 and rs9637365 recessive 0.70 95% CI 0.55,0.90 pACT 0.0208). Four SNPs in SepN1 were associated with rectal cancer (rs11247735 recessive OR 1.30 95% CI 1.04,1.63 pACT 0.0410; rs2072749 GGvsAA OR 0.53 95% CI 0.36,0.80 pACT 0.0159; rs4659382 recessive OR 0.58 95% CI 0.39,0.86 pACT 0.0247; rs718391 dominant OR 0.76 95% CI 0.62,0.94 pACT 0.0300). Interaction between these genes and exposures that could influence these genes showed numerous significant associations after adjustment for multiple comparisons. Two SNPs in TXNRD1 and four SNPs in TXNRD2 interacted with aspirin/NSAID to influence colon cancer; one SNP in TXNRD1, two SNPs in TXNRD2, and one SNP in TXNRD3 interacted with aspirin/NSAIDs to influence rectal cancer. Five SNPs in TXNRD2 and one in SelS, SeP15, and SelW1 interacted with estrogen to modify colon cancer risk; one SNP in SelW1 interacted with estrogen to alter rectal cancer risk. Several SNPs in this candidate pathway influenced survival after diagnosis with colon cancer (SeP15 and SepX1 increased HRR) and rectal cancer (SepX1 increased HRR). CONCLUSIONS: Findings support an association between selenoprotein genes and colon and rectal cancer development and survival after diagnosis. Given the interactions observed, it is likely that the impact of cancer susceptibility from genotype is modified by lifestyle