The microstructure of the Ni-base superalloy IN617 that had undergone prolonged aging (approximately 65,000 hours) at a series of temperatures from 482°C to 871°C has been characterized by microhardness measurements, optical microscopy, scanning electron microscopy (SEM), and transmission electron microscopy (TEM). Cr 23 C 6 , Mo-rich eta-M 6 C, and Ti(C,N) constitute the major primary coarse precipitates both within the grains and along the grain boundaries. The secondary carbides were mostly fine Cr 23 C 6 , which had a cube-on-cube orientation relationship (OR) with the fcc matrix, and at long times were present in cuboidal and plate-shape forms within the grains and as films along the grain boundaries. Fine, eta-M 6 C carbides were also observed at low to intermediate temperatures with an OR given by [011] carbide//[011] matrix, " 1 " 11 À Á carbide// " 1 " 11 À Á matrix. The coarse eta-M 6 C carbides increased in extent at 871°C, whereas the counterpart fine carbides were absent. The c¢ phase was found to be present at all aging temperatures up to 871°C, with a volume fraction ranging from very low to approximately 5 pct at 593°C, where the peak in microhardness occurs. The observations have also suggested that the presence of a very small amount of c¢ at temperatures as high as 871°C at long times may be associated with a reaction between the fine eta-carbides and the c matrix. Ultrafine precipitates of the intermetallic phase Ni 2 (Cr,Mo) with the Pt 2 Mo-type structure was observed in addition to c¢ in samples aged for 28,300 hours at the lowest aging temperature of 482°C. These precipitates were absent in samples aged at higher temperatures. The various observations made have suggested that the long-term thermal stability of the IN617 alloy is reasonably good over a wide temperature range of 538°C to 704°C, whereas at higher temperatures (871°C), the substantial decrease in the volume fraction of c¢ and coarsening and clustering of the carbides lead to a large drop in the microhardness. A modified time-temperature-transformation (TTT) diagram was constructed based on the results of this study and comparison with previous reports.

No abstract

Advances in scientific technology in the early twentieth century have facilitated the development of synthetic plastics that are lightweight, rigid, and can be easily molded into a desirable shape without changing their material properties. Thus, plastics become ubiquitous and indispensable materials that are used in various manufacturing sectors, including clothing, automotive, medical, and electronic industries. However, strong physical durability and chemical stability of synthetic plastics, most of which are produced from fossil fuels, hinder their complete degradation when they are improperly discarded after use. In addition, accumulated plastic wastes without degradation have caused severe environmental problems, such as microplastics pollution and plastic islands. Thus, the usage and production of plastics is not free from environmental pollution or resource depletion. In order to lessen the impact of climate change and reduce plastic pollution, it is necessary to understand and address the current plastic life cycles. In this review, "sustainable biopolymers" are suggested as a promising solution to the current plastic crisis. The desired properties of sustainable biopolymers and bio-based and bio/chemical hybrid technologies for the development of sustainable biopolymers are mainly discussed.

Cell migration and angiogenesis are key steps in tumor metastasis. However, the mechanism of migration regulated by vascular endothelial growth factor (VEGF), a potent regulator of angiogenesis, is not completely understood. This study examined the relationship between VEGF and migration, along with the mechanism involved in the VEGF-regulated migration of human gastric cancer cells. The level of cell migration was increased by recombinant human (rh)VEGF-165 in the VEGF receptor-2-expressing SNU-601 cells. Interleukin (IL)-18 is associated with the malignant progression of tumors. Accordingly, this study examined the effect of IL-18 on the migration of cancer cells in order to identify the factors involved in VEGF-enhanced migration. Inhibiting IL-18 markedly reduced the level of VEGF-enhanced migration, and IL-18 increased cell migration directly through filamentous-actin polymerization and tensin downregulation. It was confirmed that rhVEGF-165 increased IL-18 production significantly. An antioxidant and an extracellular signal-regulated kinase (ERK)1/2-specific inhibitor blocked rhVEGF-165-enhanced IL-18 production. Accordingly, rhVEGF-165 increased the generation of region of interest (ROI) and activated the ERK1/2 pathway. These results suggest that rhVEGF-165 enhances IL-18 production via the generation of ROI and ERK1/2 phosphorylation, which results in the increased migration of gastric cancer cells.

The culture supernatants of LK1 cells, murine erythroleukemia cells, showed B cell-stimulating activity. Purification and NH2-terminal sequence analysis revealed that one of the candidates was murine IgE-dependent histamine-releasing factor (IgE-HRF), which is known to induce histamine from basophils. Recombinant IgE-HRF (rHRF) obtained from Escherichia coli- or 293-transformed embryonal kidney cells was tested for B cell-stimulating activity. Both rHRFs stimulated B cell proliferation in a dose-dependent manner. However, boiling or anti-HRF Ab abolished the B cell stimulatory effects of rHRF. Recombinant HRF showed strong synergistic effects with IL-2, IL-4, and IL-5 for B cell activation, with maximal activity in the presence of anti-CD40 Ab. Recombinant HRF increased MHC class II expression of B cells. It also increased Ig production from B cells. Treatment with polymyxin B, a neutralizing peptide antibiotic of LPS, did not reduce the activity of rHRF. In addition, FACS analysis using PE-conjugated rHRF showed that HRF bound to B cells. Recombinant HRF up-regulated the expression of IL-1 and IL-6 in B cells. In vivo administration of rHRF or the cDNA for rHRF increased total and Ag-specific Ig synthesis. Taken together, these results indicate that HRF stimulates B cell activation and function.