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A study of response control on the passive coupling element between two parallel structures
Zhu, Hongping,Iemura, Hirokazu Techno-Press 2000 Structural Engineering and Mechanics, An Int'l Jou Vol.9 No.4
A new structure-vibration-control approach is proposed which uses a passive coupling element between two parallel structures to reduce the seismic response of a system due to earthquake excitation. Dynamic characteristics of the two coupled single-degree-freedom systems subject to stationary white-noise excitation are examined by means of statistical energy analysis (SEA) techniques. Optimal parameters of the passive coupling element such as damping and stiffness under different circumstances are determined with an emphasis on the influence of the structural parameters of the system on the optimal parameters and control effectiveness. Numerical results including the root mean square values of the response due to the filtered white-noise excitation and the time-histories of response to El Centro 1940 NS excitation are presented.
Yasushi Nakai,Yusuke Iemura,Toshiteru Miyasaka,Shunta Hori,Makito Miyake,Nagaaki Marugami,Kiyohide Fujimoto,Nobumichi Tanaka 대한핵의학회 2022 핵의학 분자영상 Vol.56 No.5
Purpose This study evaluated the clinical utility of the highest bone scan index (BSI), among other BSIs, for each bone metastatic site in patients with bone metastatic castration–resistant prostate cancer (bmCRPC). Methods Thirty patients, diagnosed with bmCRPC by bone scintigraphy, were included. Total BSI, the number of hot spots, and regional BSI on each hot spot from bone scintigraphy at diagnosis with bmCRPC were evaluated by VSBONE BSI®. Highest regional BSI was defined as the highest value among regional BSIs on each hot spot in each patient. Related factors to overall survival and skeletal-related events (SREs) were evaluated using the Cox proportional-hazards model. Results The median follow-up time from diagnosis with bmCRPC was 29.0 months. During this time, 24 patients died, of which 22 patients died from prostate cancer. On univariate analysis, alkaline phosphatase (ALP) [Hazard ratio (HR): 5.96, 95% confidence interval (CI): 2.05–17.3] and highest regional BSI (HR: 2.01, 95% CI: 1.17–7.05) had significant correlation with overall survival. On multivariate analysis, ALP (HR: 4.79, 95% CI: 1.61–14.2) had significant correlation with overall survival. SREs were found in eight patients. Only the highest regional BSI (HR: 9.99, 95% CI: 2.46–40.6) significantly correlated with SREs on univariate analysis. Conclusion Highest regional BSI may provide important information regarding prognosis and SREs in patients with bmCRPC.
Oh, K H,Yang, S W,Park, J M,Seol, J H,Iemura, S,Natsume, T,Murata, S,Tanaka, K,Jeon, Y J,Chung, C H Macmillan Publishers Limited 2011 CELL DEATH AND DIFFERENTIATION Vol.18 No.8
Apoptosis inducing factor (AIF) is a mitochondrial oxidoreductase that scavenges reactive oxygen species under normal conditions. Under certain stresses, such as exposure to N-methyl-N′-nitro-N′-nitrosoguanidine (MNNG), AIF is truncated and released from the mitochondria and translocated into the nucleus, where the truncated AIF (tAIF) induces caspase-independent cell death. However, it is unknown how cells decide to kill themselves or operate ways to survive when they encounter stresses that induce the release of tAIF. Here, we demonstrated that USP2 and CHIP contribute to the control of tAIF stability. USP2 deubiquitinated and stabilized tAIF, thus promoting AIF-mediated cell death. In contrast, CHIP ubiquitinated and destabilized tAIF, thus preventing the cell death. Consistently, CHIP-deficient cells showed an increased sensitivity to MNNG. On the other hand, knockdown of USP2 attenuated MNNG-induced cell death. Moreover, exposure to MNNG caused a dramatic decrease in CHIP level, but not that of USP2, concurrent with cell shrinkage and chromatin condensation. These findings indicate that CHIP and USP2 show antagonistic functions in the control of AIF-mediated cell death, and implicate the role of the enzymes as a switch for cells to live or die under stresses that cause tAIF release.