Plastic deformation of polycrystals of Co

The plastic behaviour of Co3(Al, W) polycrystals with the L12 structure has been investigated in compression from 77 to 1273 K. The yield stress exhibits a rapid decrease at low temperatures (up to room temperature) followed by a plateau (up to 950 K), then it increases anomalously with temperature in a narrow temperature range between 950 and 1100 K, followed again by a rapid decrease at high temperatures. Slip is observed to occur exclusively on {111} planes at all temperatures investigated. The rapid decrease in yield stress observed at low temperatures is ascribed to a thermal component of solid-solution hardening that occurs during the motion of APB-coupled dislocations whose core adopts a planar, glissile structure. The anomalous increase in yield stress is consistent with the thermally activated cross-slip of APB-coupled dislocations from (111) to (010), as for many other L12 compounds. Similarities and differences in the deformation behaviour and operating mechanisms among Co3(Al, W) and other L12 compounds, such as Ni3Al and Co3Ti, are discussed

マッキ ジンフゼン トウニョウビョウ カンジャ ニオケル ケットウ カンリ シヒョウ : HbA1c ノ モンダイテン

We have investigated the validity of HbA1c values measured as the index of glycemic controls in diabetics with end-stage renal disease（ESRD）. HbA1c levels for diabetics with ESRD undergoing haemodialysis were lower than indicated by their blood glucose control. However, the changes in glycated albumin in relation to the blood glucose control in the dialysis patients matched those in diabetics without renal dysfunction. Diabetics with stage４or５chronic kidney disease（CKD）not on haemodialysis had significantly lower values of HbA1c and shorter RBC lifespan compared with patients without renal dysfunction. When assessing blood glucose control based solely on HbA1c, erroneous result may be obtained in diabetics with ESRD

Mechanical strain attenuates cytokine-induced ADAMTS9 expression via transient receptor potential vanilloid type 1

The synovial fluids of patients with osteoarthritis (OA) contain elevated levels of inflammatory cytokines, which induce the expression of a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) and of the matrix metalloproteinase (MMP) in chondrocytes. Mechanical strain has varying effects on organisms depending on the strength, cycle, and duration of the stressor; however, it is unclear under inflammatory stimulation how mechanical strain act on. Here, we show that mechanical strain attenuates inflammatory cytokine-induced expression of matrix-degrading enzymes. Cyclic tensile strain (CTS), as a mechanical stressor, attenuated interleukin (IL)-1β and tumor necrosis factor (TNF)-α-induced mRNA expression of ADAMTS4, ADAMTS9, and MMP-13 in normal chondrocytes (NHAC-kn) and in a chondrocytic cell line (OUMS-27). This effect was abolished by treating cells with mechano-gated channel inhibitors, such as gadolinium, transient receptor potential (TRP) family inhibitor, ruthenium red, and with pharmacological and small interfering RNA-mediated TRPV1 inhibition. Furthermore, nuclear factor κB (NF-κB) translocation from the cytoplasm to the nucleus resulting from cytokine stimulation was also abolished by CTS. These findings suggest that mechanosensors such as the TRPV protein are potential therapeutic targets in treating OA

Host-produced ADAMTS4 Inhibits Early-Stage Tumor Growth

Several research groups demonstrated that ‘a disintegrin-like and metalloproteinase with thrombospondin type 1 motifs (ADAMTS)’-family proteases play roles in cancer progression. However, the origins and contributions of these proteases are not known. Here, we demonstrate an association between host-produced ADAMTS4 and early-stage tumor growth. Murine Lewis lung carcinoma (LLC) tumors showed marked expressions of Adamts4 and Adamts5. We examined the contributions and distributions of host-derived Adamts4 and Adamts5 on tumor growth, using Adamts4LacZ/LacZ and Adamts5LacZ/LacZ knockout mice. Interestingly, the Adamts4LacZ/LacZ mice showed enhanced tumor growth compared to wild-type mice at 5-, 10- and 12-days post-inoculation, whereas the Adamts5LacZ/LacZ mice did not show significant differences in tumor growth. We next examined LacZ distribution in LLC tumor-bearing Adamts4LacZ/LacZ mice by β-galactosidase (β-gal) staining. We found that the β-gal-positive signals were strictly localized at the interior areas of the tumor at 10 days post-inoculation. Multiple staining demonstrated that most of the β-gal-positive cells were localized at the tumor vasculature in Adamts4LacZ/LacZ mice. Interestingly, β-gal-positive signals were not co-localized with biglycan after 10 days post-inoculation, excluding the biglycan cleavage by host-derived ADAMTS4. Taken together, these findings illustrate that host-derived ADAMTS4 was expressed at the tumor vessels and was associated with early-stage tumor growth