OMAE2011-49594 DEVELOPMENT OF 6% NICKEL STEEL FOR LNG STORAGE TANKS

ABSTRACT 9% Ni steel has been used for LNG storage tanks for more than four decades although 5.5% Ni steel (N-TUF CR196) was developed in the 1970's using a special heat treatment method named L-treatment. The reason why the actual application of 5.5% Ni steel has not been attained to LNG storage tanks is mainly because the requirement of fracture properties is not confirmed for the tanks. Under the circumstances of expanding demand for natural gas and double-integrity in LNG storage tanks, we restarted developing low Ni steel for LNG storage tanks by using both conventional and advanced techniques. For the application of low Ni steel to the present LNG storage tanks, both fracture initiation and propagation properties of base metal plates and welded joints should be concerned. The fracture initiation and propagation properties of base metal were compensated with the intercritical reheating process (L-treatment), and the propagation property was additionally enhanced by combining TMCP with L-treatment. In addition, the chemical composition adjustment and the homogenization treatment of solute elements were conducted for improving the fracture initiation and propagation properties of welded joints. 6% Ni steel plates were manufactured by the process of continuous casting, reheating, hot rolling, direct quenching (TMCP), L-treatment, and tempering, and their chemical composition was 0.05C-0.06Si-1.0Mn-6.3Ni-Cr-Mo. As the results of fracture property evaluation including large-scale fracture tests such as the duplex ESSO test and the wide plate tensile test, it was demonstrated that 6% Ni steel has good characteristics regarding brittle fracture initiation and propagation in base metal plates and welded joints

Canonical versus non-canonical transsynaptic signaling of neuroligin 3 tunes development of sociality in mice

社会性の発達を調節する新たな機構を発見. 京都大学プレスリリース. 2021-03-26.Neuroligin 3 (NLGN3) and neurexins (NRXNs) constitute a canonical transsynaptic cell-adhesion pair, which has been implicated in autism. In autism spectrum disorder (ASD) development of sociality can be impaired. However, the molecular mechanism underlying NLGN3-mediated social development is unclear. Here, we identify non-canonical interactions between NLGN3 and protein tyrosine phosphatase δ (PTPδ) splice variants, competing with NRXN binding. NLGN3-PTPδ complex structure revealed a splicing-dependent interaction mode and competition mechanism between PTPδ and NRXNs. Mice carrying a NLGN3 mutation that selectively impairs NLGN3-NRXN interaction show increased sociability, whereas mice where the NLGN3-PTPδ interaction is impaired exhibit impaired social behavior and enhanced motor learning, with imbalance in excitatory/inhibitory synaptic protein expressions, as reported in the Nlgn3 R451C autism model. At neuronal level, the autism-related Nlgn3 R451C mutation causes selective impairment in the non-canonical pathway. Our findings suggest that canonical and non-canonical NLGN3 pathways compete and regulate the development of sociality

Structural and thermodynamic analyses reveal critical features of glycopeptide recognition by the human PILRα immune cell receptor

金沢大学医薬保健研究域薬学系Before entering host cells, herpes simplex virus-1 uses its envelope glycoprotein B to bind paired immunoglobulin-like type 2 receptor α (PILRα) on immune cells. PILRα belongs to the Siglec (sialic acid (SA)-binding immunoglobulin-like lectin)- like family, members of which bind SA. PILRα is the only Siglec member to recognize not only the sialylated O-linked sugar T antigen (sTn) but also its attached peptide region. We previously determined the crystal structure of PILRα complexed with the sTn-linked glycopeptide of glycoprotein B, revealing the simultaneous recognition of sTn and peptide by the receptor. However, the contribution of each glycopeptide component to PILRα binding was largely unclear. Here, we chemically synthesized glycopeptide derivatives and determined the thermodynamic parameters of their interaction with PILRα. We show that glycopeptides with different sugar units linking SA and peptides (i.e. "GlcNAc-Type" and "deoxy- GlcNAc-Type" glycopeptides) have lower affinity and more enthalpy-driven binding than the wild type (i.e. GalNAc-Type glycopeptide). The crystal structures of PILRα complexed with these glycopeptides highlighted the importance of stereochemical positioning of the O4 atom of the sugar moiety. These results provide insights both for understanding the unique O-glycosylated peptide recognition by the PILRα and for the rational design of herpes simplex virus-1 entry inhibitors. © 2017 by The American Society for Biochemistry and Molecular Biology, Inc

Distinct role of T helper Type 17 immune response for Graves\u27 hyperthyroidism in mice with different genetic backgrounds.

T helper type 17 (Th17) cells, a newly identified effector T-cell subset, have recently been shown to play a role in numerous autoimmune diseases, including iodine-induced autoimmune thyroiditis in non-obese diabetic (NOD)-H2(h4) mice, which had previously been thought Th1-dominant. We here studied the role of Th17 in Graves\u27 hyperthyroidism, another thyroid-specific autoimmune disease, in a mouse model. Two genetically distinct BALB/c and NOD-H2(h4) strains with intact or disrupted IL-17 genes (IL-17(+/+) or IL-17(-/-)) were immunized with adenovirus (Ad) expressing the thyrotropin receptor (TSHR) A-subunit (Ad-TSHR289). Both IL-17(+/+) and IL-17(-/-) mice developed anti-TSHR antibodies and hyperthyroidism at equally high frequencies on the BALB/c genetic background. In contrast, some IL-17(+/+), but none of IL-17(-/-), mice became hyperthyroid on the NOD-H2(h4) genetic background, indicating the crucial role of IL-17 for development of Graves\u27 hyperthyroidism in non-susceptible NOD-H2(h4), but not in susceptible BALB/c mice. In the T-cell recall assay, splenocytes and lymphocytes from the draining lymph nodes from either mouse strains, irrespective of IL-17 gene status, produced IFN-γ and IL-10 but not other cytokines including IL-17 in response to TSHR antigen. Thus, the functional significance of Th17 may not necessarily be predictable from cytokine expression patterns in splenocytes or inflammatory lesions. In conclusion, this is, to our knowledge, the first report showing that the role of Th17 cells for the pathogenesis of a certain autoimmune disease depends on the mouse genetic backgrounds

Summary of Panel Discussion on PIXE Analysis and Accurcy

The panel discussion on PIXE analysis and accuracy took place on the afternoon of 10 October 2002. This panel discussion was organized by the organizers of the 19th symposium of PIXE in Japan in response to an informal meeting related to "PIXE as a Trace Elemental Analysis Method: Its Potential, its Limits and a Comparison with other Methods, QA/QC" at the 18th symposium of PIXE in Japan held in Chiba 2001. During the panel discussion, K. Saitoh (Environmental Research & Information Center of Akita Prefecture) served as the coordinator, and F. Nishiyama (Graduate School of Engineering, Hiroshima University) and M. Yukawa (National Institute of Radiological Sciences) acted as advisers. The following presentations were given by three panelists. The presentations of the three panelists were published in the proceeding of the 19th symposium on PIXE in Japan as part of the proceeding of panel discussions on PIXE analysis and accuracy