Fatigue Behavior of a SiC/SiC Composite at 1000⁰C in Air and in Steam

Tension-tension fatigue behavior of a prototype Silicon Carbide/Silicon Carbide (SiC/SiC) ceramic matrix composite (CMC) material was investigated at 1000°C in laboratory air and in steam environments. The material consists of a SiC matrix reinforced with CG NICALON™ fibers woven in an eight harness satin weave (8HSW) and coated with a BN/SiC dual-layer interphase. The composite was manufactured by a Polymer Infiltration and Pyrolysis (PIP) process. A seal coat of SiC and elemental boron was applied to the test specimens after machining. The tensile stress-strain behavior was investigated and the tensile properties were measured at 1000°C. Tension-tension fatigue behavior was studied for fatigue stresses ranging from 60 to 100 MPa. The fatigue limit (based on a run-out condition of 2 x 105 cycles) was 80 MPa, which is 59% of the Ultimate Tensile Strength (UTS). The material retained 82% of its tensile strength. The presence of steam significantly degraded the fatigue performance at 1000°C. In steam the fatigue limit dropped below 60 MPa (44% UTS). Microstructural analysis revealed severe oxidation occurring in the specimens tested in steam, which resulted in accelerated damage development and failure. Through quantitative and qualitative analysis, the damage and premature failure of the composite in the steam environment is believed to be due to oxidation embrittlement. This material also showed considerably worse performance than similar SiC/SiC composites with a great deal of variability between specimens cut from different panels. The possibility exists that inadequate process control may be behind the degraded performance of the material and the panel-to-panel variability in performance

αA-crystallin confers cellular thermoresistance

AbstractThe bovine eye lens protein αA-crystallin has been overexpressed both by stable transfection of HeLa cells and by transient transfection of NIH 3T3 cells. In both experimental systems αA-crystallin overexpression results in an increased cellular thermoresistance as judged by different clonal survival assays. In contrast, similar overexpression of another stable lens protein, βB2-crystallin, does not confer thermoresistance. These results indicate that the structural relationship of αA-crystallin to the small heat shock proteins HSP25/27 and to αB-crystallin is sufficient for the shared thermoprotective function of all of these molecules and strongly suggests that the chaperone-like properties that they have in common are responsible for the conferred cellular thermoresistance

On the Form Factor for the Unitary Group

We study the combinatorics of the contributions to the form factor of the group U(N) in the large $N$ limit. This relates to questions about semiclassical contributions to the form factor of quantum systems described by the unitary ensemble.Comment: 35 page

The Non-Trapping Degree of Scattering

We consider classical potential scattering. If no orbit is trapped at energy E, the Hamiltonian dynamics defines an integer-valued topological degree. This can be calculated explicitly and be used for symbolic dynamics of multi-obstacle scattering. If the potential is bounded, then in the non-trapping case the boundary of Hill's Region is empty or homeomorphic to a sphere. We consider classical potential scattering. If at energy E no orbit is trapped, the Hamiltonian dynamics defines an integer-valued topological degree deg(E) < 2. This is calculated explicitly for all potentials, and exactly the integers < 2 are shown to occur for suitable potentials. The non-trapping condition is restrictive in the sense that for a bounded potential it is shown to imply that the boundary of Hill's Region in configuration space is either empty or homeomorphic to a sphere. However, in many situations one can decompose a potential into a sum of non-trapping potentials with non-trivial degree and embed symbolic dynamics of multi-obstacle scattering. This comprises a large number of earlier results, obtained by different authors on multi-obstacle scattering.Comment: 25 pages, 1 figure Revised and enlarged version, containing more detailed proofs and remark

Microsomal prostaglandin E2 synthase-1 is induced by conditional expression of RET/PTC in thyroid PCCL3 cells through the activation of the MEK-ERK pathway

RET/PTC rearrangements are believed to be tumor-initiating events in papillary thyroid carcinomas. We identified microsomal prostaglandin E2 synthase-1 (mPGES-1) as a RET/PTC-inducible gene through subtraction hybridization cloning and expression profiling with custom microarrays. The inducible prostaglandin E2 (PGE2) biosynthetic enzymes cyclooxygenase-2 (COX-2) and mPGES-1 are up-regulated in many cancers. COX-2 is overexpressed in thyroid malignancies compared with benign nodules and normal thyroid tissues. Eicosanoids may promote tumorigenesis through effects on tumor cell growth, immune surveillance, and angiogenesis. Conditional RET/PTC1 or RET/PTC3 expression in PCCL3 thyroid cells markedly induced mPGES-1 and COX-2. PGE2 was the principal prostanoid and up-regulated (by approximately 60-fold), whereas hydroxyeicosatetraenoic acid metabolites were decreased, consistent with shunting of prostanoid biosynthesis toward PGE2 by coactivation of the two enzymes. RET/PTC activated mPGES-1 gene transcription. Based on experiments with kinase inhibitors, with PCCL3 cell lines with doxycycline-inducible expression of RET/PTC mutants with substitutions of critical tyrosine residues in the kinase domain, and lines with inducible expression of activated mutants of H-RAS and MEK1, RET/PTC was found to regulate mPGES-1 through Shc-RAS-MEK-ERK. These data show a direct relationship between activation of a tyrosine kinase receptor oncogene and regulation of PGE2 biosynthesis. As enzymes involved in prostanoid biosynthesis can be targeted with pharmacological inhibitors, these findings may have therapeutic implications