Exploring failure modes of alumina scales on FeCrAl and FeNiCrAl alloys in a nitriding environment

Two high-temperature FeCrAl and FeNiCrAl alloys were exposed in a strongly nitriding environment at 900 \ub0C and the morphology of nitridation was studied. Quasi-in-situ experiments revealed that nitridation started at specific surface sites directly related to the alloy microstructure where the alumina scale was permeable to nitrogen. FeCrAl alloy grains with (112) orientation formed outward-growing alumina scales and were susceptible to nitridation. Outward-growing scales and substrate nitridation was also observed at chromium carbide precipitates in the FeNiCrAl alloy. Both alloys suffered nitridation at reactive element-rich (Y and Zr) inclusions larger than a certain critical size. The latter type of attack is caused by cracks and pores in the scale. The findings open new avenues of research for developing the next generation of high temperature alloys with superior properties

Prognostic Impact of Array-based Genomic Profiles in Esophageal Squamous Cell Cancer

Background: Esophageal squamous cell carcinoma (ESCC) is a genetically complex tumor type and a major cause of cancer related mortality. Although distinct genetic alterations have been linked to ESCC development and prognosis, the genetic alterations have not gained clinical applicability. We applied array-based comparative genomic hybridization (aCGH) to obtain a whole genome copy number profile relevant for identifying deranged pathways and clinically applicable markers. Methods: A 32 k aCGH platform was used for high resolution mapping of copy number changes in 30 stage I-IV ESCC. Potential interdependent alterations and deranged pathways were identified and copy number changes were correlated to stage, differentiation and survival. Results: Copy number alterations affected median 19% of the genome and included recurrent gains of chromosome regions 5p, 7p, 7q, 8q, 10q, 11q, 12p, 14q, 16p, 17p, 19p, 19q, and 20q and losses of 3p, 5q, 8p, 9p and 11q. High-level amplifications were observed in 30 regions and recurrently involved 7p11 (EGFR), 11q13 (MYEOV, CCND1, FGF4, FGF3, PPFIA, FAD, TMEM16A, CTTS and SHANK2) and 11q22 (PDFG). Gain of 7p22.3 predicted nodal metastases and gains of 1p36.32 and 19p13.3 independently predicted poor survival in multivariate analysis. Conclusion: aCGH profiling verified genetic complexity in ESCC and herein identified imbalances of multiple central tumorigenic pathways. Distinct gains correlate with clinicopathological variables and independently predict survival, suggesting clinical applicability of genomic profiling in ESCC

Identification of multiple risk loci and regulatory mechanisms influencing susceptibility to multiple myeloma

Genome-wide association studies (GWAS) have transformed our understanding of susceptibility to multiple myeloma (MM), but much of the heritability remains unexplained. We report a new GWAS, a meta-analysis with previous GWAS and a replication series, totalling 9974 MM cases and 247,556 controls of European ancestry. Collectively, these data provide evidence for six new MM risk loci, bringing the total number to 23. Integration of information from gene expression, epigenetic profiling and in situ Hi-C data for the 23 risk loci implicate disruption of developmental transcriptional regulators as a basis of MM susceptibility, compatible with altered B-cell differentiation as a key mechanism. Dysregulation of autophagy/apoptosis and cell cycle signalling feature as recurrently perturbed pathways. Our findings provide further insight into the biological basis of MM

Author Correction: Identification of multiple risk loci and regulatory mechanisms influencing susceptibility to multiple myeloma

Correction to: Nature Communications; https://doi.org/10.1038/s41467-018-04989-w, published online 13 September 2018

Identification of multiple risk loci and regulatory mechanisms influencing susceptibility to multiple myeloma

Genome-wide association studies (GWAS) have transformed our understanding of susceptibility to multiple myeloma (MM), but much of the heritability remains unexplained. We report a new GWAS, a meta-analysis with previous GWAS and a replication series, totalling 9974 MM cases and 247,556 controls of European ancestry. Collectively, these data provide evidence for six new MM risk loci, bringing the total number to 23. Integration of information from gene expression, epigenetic profiling and in situ Hi-C data for the 23 risk loci implicate disruption of developmental transcriptional regulators as a basis of MM susceptibility, compatible with altered B-cell differentiation as a key mechanism. Dysregulation of autophagy/apoptosis and cell cycle signalling feature as recurrently perturbed pathways. Our findings provide further insight

Amundsen versus Scott : are growth paths related to firm performance?

In the race to the South Pole, Roald Amundsen's expedition covered an equal distance each day, irrespective of weather conditions, while Scott's pace was erratic. Amundsen won the race and returned without loss of life, while Scott and his men died. We investigate how firms' sales growth deviate from the long-run average growth path. Our baseline results suggest that growth path volatility is associated with higher growth of sales and profits, but is also associated with higher exit rates. This is driven by firms with negative growth rates. For positive-growth firms, volatility is negatively associated with both sales growth and survival

Could collaborative research between two major libraries help consolidate digital preservation and break the “project cycle”?

The successful preservation of digital assets requires maintenance, continuity of service, and proactive stewardship.1 An ongoing challenge for Bodleian Libraries (of Oxford University) and Cambridge University Library (CUL) has been taking outputs from time-bound digital preservation projects and turning them into ongoing uninterrupted services. This is not a challenge which is specific to Bodleian Libraries and CUL, but it has been recognized as a difficult transition for many organizations to make. The Digital Preservation at Oxford and Cambridge (DPOC) project (2016–2018) is a collaboration between Bodleian Libraries and CUL which is supported and funded by The Polonsky Foundation. Bodleian Libraries and CUL have historically strong ties, and have previously collaborated on digital preservation projects. Both organizations also have experience creating digital preservation resources, for which stewardship at the end of projects has been transferred over to staff within the libraries for maintenance. However, siloed preservation activities have so far not translated into institution-wide, ongoing programmatic digital preservation activities