Report on thermal aging effects on tensile properties of ferritic-martensitic steels.

This report provides an update on the evaluation of thermal-aging induced degradation of tensile properties of advanced ferritic-martensitic steels. The report is the first deliverable (level 3) in FY11 (M3A11AN04030103), under the Work Package A-11AN040301, 'Advanced Alloy Testing' performed by Argonne National Laboratory, as part of Advanced Structural Materials Program for the Advanced Reactor Concepts. This work package supports the advanced structural materials development by providing tensile data on aged alloys and a mechanistic model, validated by experiments, with a predictive capability on long-term performance. The scope of work is to evaluate the effect of thermal aging on the tensile properties of advanced alloys such as ferritic-martensitic steels, mod.9Cr-1Mo, NF616, and advanced austenitic stainless steel, HT-UPS. The aging experiments have been conducted over a temperature of 550-750 C for various time periods to simulate the microstructural changes in the alloys as a function of time at temperature. In addition, a mechanistic model based on thermodynamics and kinetics has been used to address the changes in microstructure of the alloys as a function of time and temperature, which is developed in the companion work package at ANL. The focus of this project is advanced alloy testing and understanding the effects of long-term thermal aging on the tensile properties. Advanced materials examined in this project include ferritic-martensitic steels mod.9Cr-1Mo and NF616, and austenitic steel, HT-UPS. The report summarizes the tensile testing results of thermally-aged mod.9Cr-1Mo, NF616 H1 and NF616 H2 ferritic-martensitic steels. NF616 H1 and NF616 H2 experienced different thermal-mechanical treatments before thermal aging experiments. NF616 H1 was normalized and tempered, and NF616 H2 was normalized and tempered and cold-rolled. By examining these two heats, we evaluated the effects of thermal-mechanical treatments on material microstructures and associated mechanical properties during long-term aging at elevated temperatures. Thermal aging experiments at different temperatures and periods of time have been completed: 550 C for up to 5000 h, 600 C for up to 7500 h, and 650 C for more than 10,000 h. Tensile properties were measured on thermally aged specimens and aging effect on tensile behavior was assessed. Effects of thermal aging on deformation and failure mechanisms were investigated by using in-situ straining technique with simultaneous synchrotron XRD measurements

The p75 Neurotrophin Receptor Mediates Neuronal Apoptosis and Is Essential for Naturally Occurring Sympathetic Neuron Death

Abstract. To determine whether the p75 neurotrophin receptor (p75NTR) plays a role in naturally occurring neuronal death, we examined neonatal sympathetic neurons that express both the TrkA tyrosine kinase receptor and p75NTR. When sympathetic neuron survival is maintained with low quantities of NGF or KCl, the neurotrophin brain-derived neurotrophic factor (BDNF), which does not activate Trk receptors on sympathetic neurons, causes neuronal apoptosis and increased phosphorylation of c-jun. Function-blocking antibody studies indicate that this apoptosis is due to BDNF-mediated activation of p75NTR. To determine the physiological relevance of these culture findings, we examined sympathetic neurons in BDNF−/− and p75NTR−/− mice. In BDNF−/− mice, sympathetic neuron number is increased relative to BDNF+/+ littermates, and in p75NTR−/− mice, the normal period of sympathetic neuron death does not occur, with neuronal attrition occurring later in life. This deficit in apoptosis is intrinsic to sympathetic neurons, since cultured p75NTR−/− neurons die more slowly than do their wild-type counterparts. Together, these data indicate that p75NTR can signal to mediate apoptosis, and that this mechanism is essential for naturally occurring sympathetic neuron death

Genetics and Pathogenesis of Diffuse Large B-Cell Lymphoma.

BACKGROUND: Diffuse large B-cell lymphomas (DLBCLs) are phenotypically and genetically heterogeneous. Gene-expression profiling has identified subgroups of DLBCL (activated B-cell-like [ABC], germinal-center B-cell-like [GCB], and unclassified) according to cell of origin that are associated with a differential response to chemotherapy and targeted agents. We sought to extend these findings by identifying genetic subtypes of DLBCL based on shared genomic abnormalities and to uncover therapeutic vulnerabilities based on tumor genetics. METHODS: We studied 574 DLBCL biopsy samples using exome and transcriptome sequencing, array-based DNA copy-number analysis, and targeted amplicon resequencing of 372 genes to identify genes with recurrent aberrations. We developed and implemented an algorithm to discover genetic subtypes based on the co-occurrence of genetic alterations. RESULTS: We identified four prominent genetic subtypes in DLBCL, termed MCD (based on the co-occurrence of MYD88L265P and CD79B mutations), BN2 (based on BCL6 fusions and NOTCH2 mutations), N1 (based on NOTCH1 mutations), and EZB (based on EZH2 mutations and BCL2 translocations). Genetic aberrations in multiple genes distinguished each genetic subtype from other DLBCLs. These subtypes differed phenotypically, as judged by differences in gene-expression signatures and responses to immunochemotherapy, with favorable survival in the BN2 and EZB subtypes and inferior outcomes in the MCD and N1 subtypes. Analysis of genetic pathways suggested that MCD and BN2 DLBCLs rely on "chronic active" B-cell receptor signaling that is amenable to therapeutic inhibition. CONCLUSIONS: We uncovered genetic subtypes of DLBCL with distinct genotypic, epigenetic, and clinical characteristics, providing a potential nosology for precision-medicine strategies in DLBCL. (Funded by the Intramural Research Program of the National Institutes of Health and others.).This research was supported by the Intramural Research Program of the NIH, Center for Cancer Research, National Cancer Institute and by a National Cancer Institute Strategic Partnering to Evaluate Cancer Signatures (SPECS II) grant (5U01CA157581-05). R.S. was supported by the Dr Mildred Scheel Stiftung für Krebsforschung (Deutsche Krebshilfe). D.J.H. was a Kay Kendall Leukaemia Fund Intermediate research fellow. M.K. was supported by the National Institutes of Health Oxford-Cambridge Scholars Program and the Washington University in St. Louis Medical Scientist Training Progra

Metal dusting behavior of coatings.

Surface modification by preoxidation and/or by coatings and alternative materials are being examined at ANL to alleviate the metal dusting problem. Oxide coatings have the advantage that they can minimize carbon-producing reactions (by reducing the availability of catalytic surface) and can also act as a barrier to minimize carbon ingress and pitting of the substrate alloy. We have selected in-situ development of oxide scales, pack diffusion of Al or Cr/Si, and thermal spray of FeAl as avenues for further study. Preliminary tests showed virtually no carbon in pre-oxidized layers of Al-, Cr-, and Si-enriched layers that were subjected to metal dusting environments

Report on thermal aging effects on tensile properties of ferritic-martensitic steels.

This report provides an update on the evaluation of thermal-aging induced degradation of tensile properties of advanced ferritic-martensitic steels. The report is the first deliverable (level 3) in FY11 (M3A11AN04030103), under the Work Package A-11AN040301, 'Advanced Alloy Testing' performed by Argonne National Laboratory, as part of Advanced Structural Materials Program for the Advanced Reactor Concepts. This work package supports the advanced structural materials development by providing tensile data on aged alloys and a mechanistic model, validated by experiments, with a predictive capability on long-term performance. The scope of work is to evaluate the effect of thermal aging on the tensile properties of advanced alloys such as ferritic-martensitic steels, mod.9Cr-1Mo, NF616, and advanced austenitic stainless steel, HT-UPS. The aging experiments have been conducted over a temperature of 550-750 C for various time periods to simulate the microstructural changes in the alloys as a function of time at temperature. In addition, a mechanistic model based on thermodynamics and kinetics has been used to address the changes in microstructure of the alloys as a function of time and temperature, which is developed in the companion work package at ANL. The focus of this project is advanced alloy testing and understanding the effects of long-term thermal aging on the tensile properties. Advanced materials examined in this project include ferritic-martensitic steels mod.9Cr-1Mo and NF616, and austenitic steel, HT-UPS. The report summarizes the tensile testing results of thermally-aged mod.9Cr-1Mo, NF616 H1 and NF616 H2 ferritic-martensitic steels. NF616 H1 and NF616 H2 experienced different thermal-mechanical treatments before thermal aging experiments. NF616 H1 was normalized and tempered, and NF616 H2 was normalized and tempered and cold-rolled. By examining these two heats, we evaluated the effects of thermal-mechanical treatments on material microstructures and associated mechanical properties during long-term aging at elevated temperatures. Thermal aging experiments at different temperatures and periods of time have been completed: 550 C for up to 5000 h, 600 C for up to 7500 h, and 650 C for more than 10,000 h. Tensile properties were measured on thermally aged specimens and aging effect on tensile behavior was assessed. Effects of thermal aging on deformation and failure mechanisms were investigated by using in-situ straining technique with simultaneous synchrotron XRD measurements