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Behavior of R/C cylindrical shell under lateral load
Hara, Takashi,Shigematsu, Tsunemi,Tamura, Takahiro Techno-Press 2003 Structural Engineering and Mechanics, An Int'l Jou Vol.16 No.3
In this paper, the structural behavior of R/C cylindrical panel is analyzed by experimental results. To avoid the geometric imperfection, R/C shell specimens are made by use of a stiff steel mold. From experimental results, the load carrying behavior of R/C cylindrical panel is presented under an external lateral pressure. Even if R/C shell does not posses geometric imperfections, the inaccuracy of the reinforcement position strongly affects to the ultimate strength and the failure patterns of such shells. To explain these effects, FEM nonlinear analyses are done under the same conditions as those of experiments. The behavior of R/C cylindrical shells are well simulated under the consideration of both the geometric imperfection and several inaccuracies.
HUGE DIRECT NUMERICAL SIMULATION OF TURBULENT COMBUSTION
Mamoru Tanahashi,Takehiko Seo,Makoto Sato,Akihiko Tsunemi,Toshio Miyauchi 한국전산유체공학회 2008 한국전산유체공학회지 Vol.13 No.4
Current state and perspective of DNS of turbulence and turbulent combustion are discussed with feature trend of the fastest supercomputer in the world. Based on the perspective of DNS of turbulent combustion, possibility of perfect simulations of IC engine is shown. In 2020, the perfect simulation will be realized with 30 billion grid points by 1 EXAFlops supercomputer, which requires 4 months CPU time. The CPU time will be reduced to about 4 days if several developments were achieved in the current fundamental researches. To shorten CPU time required for DNS of turbulent combustion, two numerical methods are introduced to full-explicit full-compressible DNS code. One is compact finite difference filter to reduce spatial resolution requirements and numerical oscillations in small scales, and another is well-known point-implicit scheme to avoid quite small time integration of the order of nanosecond for fully explicit DNS. A vailability and accuracy of these numerical methods have been confirmed carefully for auto-ignition, planar laminar flame and turbulent premixed flames. To realize DNS of IC engine with realistic kinetic mechanism, several DNS of elemental combustion process in IC engines has been conducted.
HUGE DIRECT NUMERICAL SIMULATION OF TURBULENT COMBUSTION - TOWARD PERFECT SIMULATION OF IC ENGINE -
Tanahashi, Mamoru,Seo, Takehiko,Sato, Makoto,Tsunemi, Akihiko,Miyauchi, Toshio Korea Society of Computational Fluids Engineering 2008 한국전산유체공학회지 Vol.13 No.4
Current state and perspective of DNS of turbulence and turbulent combustion are discussed with feature trend of the fastest supercomputer in the world. Based on the perspective of DNS of turbulent combustion, possibility of perfect simulations of IC engine is shown. In 2020, the perfect simulation will be realized with 30 billion grid points by 1EXAFlops supercomputer, which requires 4 months CPU time. The CPU time will be reduced to about 4 days if several developments were achieved in the current fundamental researches. To shorten CPU time required for DNS of turbulent combustion, two numerical methods are introduced to full-explicit full-compressible DNS code. One is compact finite difference filter to reduce spatial resolution requirements and numerical oscillations in small scales, and another is well-known point-implicit scheme to avoid quite small time integration of the order of nanosecond for fully explicit DNS. Availability and accuracy of these numerical methods have been confirmed carefully for auto-ignition, planar laminar flame and turbulent premixed flames. To realize DNS of IC engine with realistic kinetic mechanism, several DNS of elemental combustion process in IC engines has been conducted.
Mechanism of Macrophage-Derived Chemokine/CCL22 Production by HaCaT Keratinocytes
( Chizuko Yano ),( Hidehisa Saeki ),( Mayumi Komine ),( Shinji Kagami ),( Yuichiro Tsunemi ),( Mamitaro Ohtsuki ),( Hidemi Nakagawa ) 대한피부과학회 2015 Annals of Dermatology Vol.27 No.3
Background: CC chemokine ligand 17 (CCL17) and CCL22 are the functional ligands for CCR4. We previously reported that inhibitors of nuclear factor-kappa B and p38 mitogen- activated protein kinase (p38 MAPK), but not of extracellular signal-related kinase (ERK), inhibited tumor necrosis factor (TNF)-α- and interferon (IFN)-γ-induced production of CCL17 by the human keratinocyte cell line, HaCaT. Further, an inhibitor of epidermal growth factor receptor (EGFR) enhanced the CCL17 production by these keratinocytes. Objective: To identify the mechanism underlying CCL22 production by HaCaT cells. Methods: We investigated the signal transduction pathways by which TNF-α and IFN-γ stimulate HaCaT cells to produce CCL22 by adding various inhibitors. Results: TNF-α- and IFN-γ- induced CCL22 production was inhibited by PD98059, PD153035, Bay 11-7085, SB202190, c-Jun N-terminal kinase (JNK) inhibitor II, and Janus kinase (JAK) inhibitor 1. Conclusion: Our results indicate that CCL22 production in HaCaT cells is dependent on ERK, EGFR, p38 MAPK, JNK, and JAK and is mediated by different signal pathways from those regulating CCL17 production. Altogether, our previous and present results suggest that EGFR activation represses CCL17 but enhances CCL22 production by these cells. (Ann Dermatol 27(2) 152∼156, 2015)
( Satoshi Takeuchi ),( Hidehisa Saeki ),( Shoji Tokunaga ),( Makoto Sugaya ),( Hanako Ohmatsu ),( Yuichiro Tsunemi ),( Hideshi Torii ),( Koichiro Nakamura ),( Tamihiro Kawakami ),( Yoshinao Soma ),( E 대한피부과학회 2012 Annals of Dermatology Vol.24 No.2
Background: Pruritis caused by atopic dermatitis (AD) is not always well controlled by topical corticosteroid therapy, but use of tacrolimus often helps to soothe such intractable pruritis in clinical settings. Objective: To determine the anti-pruritic efficacy of topical tacrolimus in treating AD in induction and maintenance therapy. Methods: Prior to the study, patients were randomly allocated into two groups, induction therapy followed by tacrolimus monotherapy maintenance, and induction therapy followed by emollient- only maintenance. In the induction therapy, the patients were allowed to use topical tacrolimus and emollients in addition to a low dose (<10 g/week) of topical steroids. Patients showing relief from pruritis were allowed to proceed to maintenance therapy. Recurrence of pruritis in maintenance therapy was examined as a major endpoint. Results: Two-thirds of patients (44/68; 64.7%) showed relief from pruritis after induction therapy. Pruritis recurred in 23.8% (5/21) of the tacrolimus monotherapy group and in 100% (21/21) of the emollient group during maintenance period, a difference that was statistically significant. Conclusion: Use of topical tacrolimus is effective in controlling pruritis of AD compared to emollient. (Ann Dermatol 24(2) 144∼150, 2012)
Mechanism of Macrophage-Derived Chemokine/CCL22 Production by HaCaT Keratinocytes
( Chizuko Yano ),( Hidehisa Saeki ),( Mayumi Komine ),( Shinji Kagami ),( Yuichiro Tsunemi ),( Mamitaro Ohtsuki ),( Hidemi Nakagawa ) 대한피부과학회 2015 Annals of Dermatology Vol.27 No.2
Background: CC chemokine ligand 17 (CCL17) and CCL22 are the functional ligands for CCR4. We previously reported that inhibitors of nuclear factor-kappa B and p38 mitogen- activated protein kinase (p38 MAPK), but not of extracellular signal-related kinase (ERK), inhibited tumor necrosis factor (TNF)-α- and interferon (IFN)-γ-induced production of CCL17 by the human keratinocyte cell line, HaCaT. Further, an inhibitor of epidermal growth factor receptor (EGFR) enhanced the CCL17 production by these keratinocytes. Objective: To identify the mechanism underlying CCL22 production by HaCaT cells. Methods: We investigated the signal transduction pathways by which TNF-α and IFN-γ stimulate HaCaT cells to produce CCL22 by adding various inhibitors. Results: TNF-α- and IFN-γ- induced CCL22 production was inhibited by PD98059, PD153035, Bay 11-7085, SB202190, c-Jun N-terminal kinase (JNK) inhibitor II, and Janus kinase (JAK) inhibitor 1. Conclusion: Our results indicate that CCL22 production in HaCaT cells is dependent on ERK, EGFR, p38 MAPK, JNK, and JAK and is mediated by different signal pathways from those regulating CCL17 production. Altogether, our previous and present results suggest that EGFR activation represses CCL17 but enhances CCL22 production by these cells.(Ann Dermatol 27(2) 152∼156, 2015)