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A dense structure of silicon nitride ceramic was fabricated by direct ink writing using aqueous suspensions. The rheology of the suspensions was carefully tailored by the particle chemical state and the ion concentrations, without the use of any organics. The surface chemical states of the Si 3 N 4 powder were modified by calcination at 600 °C at various times. The minimum absolute value of zeta potential, calculated by the DLVO theory, was 19 mV at which the interaction was attractive interaction. Suspensions with solid volume fraction of 25–40 vol% exhibited pseudoplastic behavior with yield stresses ≥55 Pa and equilibrium storage moduli ≥ 104 Pa. These enabled suspensions to flow through the nozzle and retain the shape of the printed parts. The flexural strength of Si 3 N 4 ceramics produced using a 40 vol% suspension was 348 MPa. This strategy provides a simple process for fabricating high-performance ceramics based on the DIW. [ABSTRACT FROM AUTHOR]

Background & Aims Chronic gastrointestinal inflammation increases the risk of cancer by mechanisms that are not well understood. Indoleamine-2,3-dioxygenase 1 (IDO1) is a heme-binding enzyme that regulates the immune response via catabolization and regulation of tryptophan availability for immune cell uptake. IDO1 expression is increased during the transition from chronic inflammation to gastric metaplasia. We investigated whether IDO1 contributes to the inflammatory response that mediates loss of parietal cells leading to metaplasia. Methods Chronic gastric inflammation was induced in Ido1 −/− and CB57BL/6 (control) mice by gavage with Helicobacter felis or overexpression of interferon gamma in gastric parietal cells. We also performed studies in Jh −/− mice, which are devoid of B cells. Gastric tissues were collected and analyzed by flow cytometry, immunostaining, and real-time quantitative polymerase chain reaction. Plasma samples were analyzed by enzyme-linked immunosorbent assay. Gastric tissues were obtained from 20 patients with gastric metaplasia and 20 patients without gastric metaplasia (controls) and analyzed by real-time quantitative polymerase chain reaction; gastric tissue arrays were analyzed by immunohistochemistry. We collected genetic information on gastric cancers from The Cancer Genome Atlas database. Results H felis gavage induced significantly lower levels of pseudopyloric metaplasia in Ido1 −/− mice, which had lower frequencies of gastric B cells, than in control mice. Blood plasma from H felis −infected control mice had increased levels of autoantibodies against parietal cells, compared to uninfected control mice, but this increase was lower in Ido1 −/− mice. Chronically inflamed stomachs of Ido1 −/− mice had significantly lower frequencies of natural killer cells in contact with parietal cells, compared with stomachs of control mice. Jh −/− mice had lower levels of pseudopyloric metaplasia than control mice in response to H felis infection. Human gastric pre-neoplasia and carcinoma specimens had increased levels of IDO1 messenger RNA compared with control gastric tissues, and IDO1 protein colocalized with B cells. Co-clustering of IDO1 messenger RNA with B-cell markers was corroborated by The Cancer Genome Atlas database. Conclusions IDO1 mediates gastric metaplasia by regulating the B-cell compartment. This process appears to be associated with type II hypersensitivity/autoimmunity. The role of autoimmunity in the progression of pseudopyloric metaplasia warrants further investigation. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the role of depolarizing activation of Na+-Ca2+ exchanger (NCX) by oligodendrocyte progenitor cells (OPC) in the effect of sevoflurane on myelination. On postnatal days 7, 8, and 9, mice were exposed to 3 % sevoflurane for 2 h per day. The proliferation, differentiation, and myelin sheath of OPC were observed with immunofluorescence, quantitative real-time polymerase chain reaction (QRT-PCR), and transmission electron microscopy (TEM) at various time points. The open field, Y maze, and new object recognition tests were used to measure spatial learning and memory. siRNA was used for the knockdown NCX1 in human OPC (HOPC) before sevoflurane exposure; the Transwell migration assay was used to measure cell migration ability and Fluo 4-AM was used to measure intracellular Ca2+ concentration. Pretreatment with an NCX inhibitor attenuated the proliferation and differentiation of OPC induced by sevoflurane and induced a remarkable increase in platelet-derived growth factor receptor-alpha (PDGFRα), 2, 3-cyclic nucleotide 3-phosphodiesterase (CNPase), oligodendrocyte transcription factor 2 (Olig2), and homeodomain protein NK2 homeobox 2 (NKX2.2) levels. Pretreatment with an NCX inhibitor alleviated the sevoflurane-induced myelination disorder and cognitive impairment. The decreased cell migration and increased intracellular Ca2+ concentration observed in the siRNA-negative control group was reversed in the sevoflurane plus siRNA-NCX1 group. This study suggests that repeated sevoflurane exposure in newborn mice leads to depolarization of OPC, which leads to Ca2+ influx through NCX and affects OPC proliferation, migration, differentiation, and myelination, ultimately leading to cognitive impairment. [Display omitted] • Sevoflurane causes dysmyelination in neonatal mice. • Sevoflurane causes cognitive disorder in neonatal mice. • Abnormal myelination is one of the influencing factors of cognitive disorder. • NCX inhibitor ameliorates cognitive disorder induced by sevoflurane. • NCX may play an important role in sevoflurane induced cognitive disorder. [ABSTRACT FROM AUTHOR]