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Pb(Mg1/3Nb2/3)O3 (PMN) ceramics have been hot-pressed and post-hot-pressing annealed at 1000 °C in a conventional tube furnace under 1 atm of oxygen and argon, respectively; their microstructures investigated via transmission electron microscopy (TEM) and crystalline phases analyzed via X-ray diffractometry (XRD). Three types of the superlattice reflections from the fundamental spots of the perovskite structure were detected in both the as-hot-pressed and annealed samples by selected-area electron diffraction (SADP). The {1/2 1/2 1/2}-type of the superlattice F-spots is observed in as-hot-pressed samples. The nanoscale ordered domains of approximately 5 nm size giving rise to F-spots are observed by dark field imaging. α-Spots of the {1/2 1/2 0}-type have appeared in post-hot-pressing-annealed samples after heat-treatment at 1000 °C in an oxygen as well as argon atmosphere. Superlattice reflections of the {1/2 1/2 1}-type, termed α′-spots, are also observed from hot-pressed samples annealed at the same temperature for 500 h in an oxygen atmosphere. The occurrence of α-spots associated with lead vacancies (VPb″) is discussed by considering that Pb(Mg1/3Nb2/3)O3 grains is consisted of the acceptor-type nanoscale ordered domains in a donor-type disordered matrix. [Copyright &y& Elsevier]

The microstructure of TiO2-excess BaTiO3 ceramics sintered by using a CO2-laser and conventional furnace has been analysed via scanning and transmission electron microscopy. Second phases located at the triple-grain junctions and along the grain boundaries of laser-sintered samples contain monoclinic-Ba6Ti17O40. They exhibit a characteristic lamellar structure arising from the solidification of the BaTiO3–Ba6Ti17O40 eutectic generated at ≈1332 °C upon fast cooling. This microstructure can be taken as the diagnostic feature to distinguish between Ba6Ti17O40 formed by solid-state reaction and that by eutectic solidification. A self-consistent crystallographic orientation relationship of (001)t//(101)m, (11¯1)t/(001)m, (11¯0)t//(1¯03)m, (11¯1¯)t//(1¯01)m and [010]m//[1¯1¯0]t between tetragonal-BaTiO3 and monoclinic-Ba6Ti17O40 has been found. The monoclinic Ba6Ti17O40 is stable below the eutectic temperature of 1332 °C after post-sintering annealing at 1000 °C for 100 h. [ABSTRACT FROM AUTHOR]

Coronavirus disease 2019 (COVID-19) is an infectious disease caused by SARS-CoV-2, a newly discovered coronavirus that exhibits many similarities with the severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS) coronaviruses (SARS-CoV and MERS-CoV, respectively). The definite pathogenesis and immunological influences of SARS-CoV-2 have not been fully elucidated. Therefore, we constructed a brief summary comparison of SARS-CoV-2, SARS-CoV, and MERS-CoV infections regarding their immunological changes. In addition, we further investigated the immunological differences between severe and nonsevere COVID-19 cases, and we searched for possible immunological predictors of the patient outcome by reviewing case series studies to date. Possible immunological predictors of a poor outcome are leukocytosis, neutrophilia, lymphopenia (both CD4 and CD8 T cells), an increased neutrophil-to-lymphocyte ratio (NLR), and increased levels of pro-inflammatory cytokines (IL-6 and TNF-α), Th1 cytokines (IL-2 and IFN-γ), regulatory T cell cytokines (IL-10) and Th17 cytokines (IL-17). A more precise immunological map needs to be established, which may assist in diagnosing this disease and facilitate immunological precision medicine treatment., (Copyright © 2021. Published by Elsevier B.V.)

Glycine N-methyltransferase (GNMT) is known for its function as a tumor suppressor gene. Since 100% of female Gnmt(-/-) mice developed hepatocellular carcinoma, we hypothesized that Gnmt(-/-) mice may have defective immune surveillance. In this study, we examined the immune modulation of GNMT in T-cell responses using experimental autoimmune encephalomyelitis (EAE). The results showed that EAE severity was reduced significantly in Gnmt(-/-) mice. Pathological examination of the spinal cords revealed that Gnmt(-/-) mice had significantly lower levels of mononuclear cell infiltration and demyelination than the wild-type mice. In addition, quantitative real-time PCR showed that expression levels of proinflammatory cytokines, including interferon (IFN)-γ and interleukin (IL)-17A, were much lower in the spinal cord of Gnmt(-/-) than in that of wild-type mice. Accordingly, myelin oligodendrocyte glycoprotein (MOG)-specific T-cell proliferation and induction of T-helper (Th)1 and Th17 cells were markedly suppressed in MOG(35-55)-induced Gnmt(-/-) mice. Moreover, the number of regulatory T (Treg) cells was increased significantly in these mice. When the T-cell receptor was stimulated, the proliferative capacity and the activation status of mTOR-associated downstream signaling were decreased significantly in Gnmt(-/-) CD4(+) T cells via an IL-2- and CD25-independent manner. Moreover, GNMT deficiency enhanced the differentiation of Treg cells without affecting the differentiation of Th1 and Th17 cells. Furthermore, the severity of EAE in mice adoptive transferred with GNMT-deficient CD4(+) T cells was much milder than in those with wild-type CD4(+) T cells. In summary, our findings suggest that GNMT is involved in the pathogenesis of EAE and plays a crucial role in the regulation of CD4(+) T-cell functions.