Effects of thermal gradient on failure of a thermoplastic composite pipe (TCP) riser leg

Acknowledgements The authors wish to thank Dr Oleksandr Menshykov and Dr Maryna Menshykova of the Centre for Micro- and Nanomechanics, University of Aberdeen, for providing MATLAB script for validation purposes. Corrigendum to “Effects of thermal gradient on failure of a thermoplastic composite pipe (TCP) riser leg” [Int. J. Pres. Ves. Pip. 172 (2019) 90–99] at https://doi.org/10.1016/j.ijpvp.2020.104172Peer reviewedPostprin

Evolution of internal pores within AlSi10Mg manufactured by laser powder bed fusion under tension : As-built and heat treated conditions

Acknowledgements The authors gratefully acknowledge the financial support of the Engineering and Physical Sciences Research Council (EPSRC) under grant reference EP/R021694/1, “3D in-situ based methodology for optimizing the mechanical performance of selective laser melted aluminium alloys”.Peer reviewedPublisher PD

Pim kinases phosphorylate multiple sites on Bad and promote 14-3-3 binding and dissociation from Bcl-X(L)

BACKGROUND: Pim-1, 2 and 3 are a group of enzymes related to the calcium calmodulin family of protein kinases. Over-expression of Pim-1 and Pim-2 in mice promotes the development of lymphomas, and up-regulation of Pim expression has been observed in several human cancers. RESULTS: Here we show that the pim kinases are constitutively active when expressed in HEK-293 cells and are able to phosphorylate the Bcl-2 family member Bad on three residues, Ser112, Ser136 and Ser155 in vitro and in cells. In vitro mapping showed that Pim-2 predominantly phosphorylated Ser112, while Pim-1 phosphorylated Ser112, but also Ser136 and Ser155 at a reduced rate compared to Ser112. Pim-3 was found to be the least specific for Ser112, and the most effective at phosphorylating Ser136 and Ser155. Pim-3 was also able to phosphorylate other sites in Bad in vitro, including Ser170, another potential in vivo site. Mutation of Ser136 to alanine prevented the phosphorylation of Ser112 and Ser155 by Pim kinases in HEK-293 cells, suggesting that this site must be phosphorylated first in order to make the other sites accessible. Pim phosphorylation of Bad was also found to promote the 14-3-3 binding of Bad and block its association with Bcl-X(L). CONCLUSION: All three Pim kinase family members predominantly phosphorylate Bad on Ser112 and in addition are capable of phosphorylating Bad on multiple sites associated with the inhibition of the pro-apoptotic function of Bad in HEK-293 cells. This would be consistent with the proposed function of Pim kinases in promoting cell proliferation and preventing cell death

Classifying shape of internal pores within AlSi10Mg alloy manufactured by laser powder bed fusion using 3D X-ray micro computed tomography : influence of processing parameters and heat treatment

The authors gratefully acknowledge the support provided by the EPSRC (grant EP/R021694/1). The authors also wish to thank Rosie Bird at the University of Aberdeen for assisting with Avizo.Peer reviewedPostprin

Proteomic analysis of Rhizoctonia solani identifies infection-specific, redox associated proteins and insight into adaptation to different plant hosts

Rhizoctonia solani is an important root infecting pathogen of a range of food staples worldwide including wheat, rice, maize, soybean, potato and others. Conventional resistance breeding strategies are hindered by the absence of tractable genetic resistance in any crop host. Understanding the biology and pathogenicity mechanisms of this fungus is important for addressing these disease issues, however, little is known about how R. solani causes disease. This study capitalises on recent genomic studies by applying mass spectrometry based proteomics to identify soluble, membrane-bound and culture filtrate proteins produced under wheat infection and vegetative growth conditions. Many of the proteins found in the culture filtrate had predicted functions relating to modification of the plant cell wall, a major activity required for pathogenesis on the plant host, including a number found only under infection conditions. Other infection related proteins included a high proportion of proteins with redox associated functions and many novel proteins without functional classification. The majority of infection only proteins tested were confirmed to show transcript up-regulation during infection including a thaumatin which increased susceptibility to R. solani when expressed in Nicotiana benthamiana. In addition, analysis of expression during infection of different plant hosts highlighted how the infection strategy of this broad host range pathogen can be adapted to the particular host being encountered. Data are available via ProteomeXchange with identifier PXD002806

Mass-spectrometry data for Rhizoctonia solani proteins produced during infection of wheat and vegetative growth

© 2016. Rhizoctonia solani is an important root infecting pathogen of a range of food staples worldwide including wheat, rice, maize, soybean, potato, legumes and others. Conventional resistance breeding strategies are hindered by the absence of tractable genetic resistance in any crop host. Understanding the biology and pathogenicity mechanisms of this fungus is important for addressing these disease issues, however, little is known about how R. solani causes disease. The data described in this article is derived from applying mass spectrometry based proteomics to identify soluble, membrane-bound and culture filtrate proteins produced under wheat infection and vegetative growth conditions. Comparisons of the data for sample types in this set will be useful to identify metabolic pathway changes as the fungus switches from saprophytic to a pathogenic lifestyle or pathogenicity related proteins contributing to the ability to cause disease on wheat. The data set is deposited in the PRIDE archive under identifier PRIDE: PXD002806

Vestiges of the proto-Caribbean seaway: origin of the San Souci Volcanic Group, Trinidad

Outcrops of volcanic–hypabyssal rocks in Trinidad document the opening of the proto-Caribbean seaway during Jurassic–Cretaceous break-up of the Americas. The San Souci Group on the northern coast of Trinidad comprises the San Souci Volcanic Formation (SSVF) and passive margin sediments of the ~ 130–125 Ma Toco Formation. The Group was trapped at the leading edge of the Pacific-derived Caribbean Plate during the Cretaceous–Palaeogene, colliding with the para-autochthonous margin of Trinidad during the Oligocene–Miocene. In-situ U–Pb ion probe dating of micro-zircons from a mafic volcanic breccia reveal the SSVF crystallised at 135.0 ± 7.3 Ma. The age of the SSVF is within error of the age of the Toco Formation. Assuming a conformable contact, geodynamic models indicate a likely origin for the SSVF on the passive margin close to the northern tip of South America. Immobile element and Nd–Hf radiogenic isotope signatures of the mafic rocks indicate the SSVF was formed by ≪10% partial melting of a heterogeneous spinel peridotite source with no subduction or continental lithospheric mantle component. Felsic breccias within the SSVF are more enriched in incompatible elements, with isotope signatures that are less radiogenic than the mafic rocks of the SSVF. The felsic rocks may be derived from re-melting of mafic crust. Although geochemical comparisons are drawn here with proto-Caribbean igneous outcrops in Venezuela and elsewhere in the Caribbean more work is needed to elucidate the development of the proto-Caribbean seaway and its rifted margins. In particular, ion probe dating of micro-zircons may yield valuable insights into magmatism and metamorphism in the Caribbean, and in altered basaltic terranes more generally

Roles of the TRAF6 and Pellino E3 ligases in MyD88 and RANKL signaling

It is widely accepted that the essential role of TRAF6 in vivo is to generate the Lys63-linked ubiquitin (K63-Ub) chains needed to activate the "master" protein kinase TAK1. Here, we report that TRAF6 E3 ligase activity contributes to but is not essential for the IL-1-dependent formation of K63-Ub chains, TAK1 activation, or IL-8 production in human cells, because Pellino1 and Pellino2 generate the K63-Ub chains required for signaling in cells expressing E3 ligase-inactive TRAF6 mutants. The IL-1-induced formation of K63-Ub chains and ubiquitylation of IRAK1, IRAK4, and MyD88 was abolished in TRAF6/Pellino1/Pellino2 triple-knockout (KO) cells, but not in TRAF6 KO or Pellino1/2 double-KO cells. The reexpression of E3 ligase-inactive TRAF6 mutants partially restored IL-1 signaling in TRAF6 KO cells, but not in TRAF6/Pellino1/Pellino2 triple-KO cells. Pellino1-generated K63-Ub chains activated the TAK1 complex in vitro with similar efficiently to TRAF6-generated K63-Ub chains. The early phase of TLR signaling and the TLR-dependent secretion of IL-10 (controlled by IRAKs 1 and 2) was only reduced modestly in primary macrophages from knockin mice expressing the E3 ligase-inactive TRAF6[L74H] mutant, but the late-phase production of IL-6, IL-12, and TNFα (controlled only by the pseudokinase IRAK2) was abolished. RANKL-induced signaling in macrophages and the differentiation of bone marrow to osteoclasts was similar in TRAF6[L74H] and wild-type cells, explaining why the bone structure and teeth of the TRAF6[L74H] mice was normal, unlike TRAF6 KO mice. We identify two essential roles of TRAF6 that are independent of its E3 ligase activity