• Journal of the Korean Society for Nondestructive Testing
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• v.27 no.6
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• pp.541-549
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• 2007

This work describes an investigation into the feasibility of using an acoustic emission (AE) technique to evaluate the integrity of a composite actuator with a PZT ceramic under electromechanical cyclic loading. AE characteristics have been analyzed in terms of the behavior of the AE count rate and signal waveform in association with the performance degradation of the composite actuator during the cyclic tests. The results showed that the fatigue cracking of the composite actuator with a PZT ceramic occurred only in the PZT ceramic layer, and that the performance degradation caused by the fatigue damage varied immensely depending on the existence of a protecting composite bottom layer. We confirmed the correlations between the fatigue damage mechanisms and AE signal types for the actuators that exhibited multiple modes of fatigue damage; transgranular micro damage, intergranular fatigue cracking, and breakdown by a short circuiting were related to a burst type signal showing a shortly rising and slowly decaying waveform with a comparably low voltage, a continuous type signal showing a gradual rising and slowly decaying waveform with a very high voltage and a burst and continuous type signal with a high voltage, respectively. Results from the present work showed that the evolution of fatigue damage in the composite actuator with a PZT ceramic can be nondestructively identified via in situ AE monitoring and microscopic observations.

• The Plant Pathology Journal
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• v.39 no.5
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• pp.449-465
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• 2023

Plants are challenged by various pathogens throughout their lives, such as bacteria, viruses, fungi, and insects; consequently, they have evolved several defense mechanisms. In addition, plants have developed localized and systematic immune responses due to biotic and abiotic stress exposure. Animals are known to activate DNA damage responses (DDRs) and DNA damage sensor immune signals in response to stress, and the process is well studied in animal systems. However, the links between stress perception and immune response through DDRs remain largely unknown in plants. To determine whether DDRs induce plant resistance to pathogens, Arabidopsis plants were treated with bleomycin, a DNA damage-inducing agent, and the replication levels of viral pathogens and growth of bacterial pathogens were determined. We observed that DDR-mediated resistance was specifically activated against viral pathogens, including turnip crinkle virus (TCV). DDR increased the expression level of pathogenesis-related (PR) genes and the total salicylic acid (SA) content and promoted mitogen-activated protein kinase signaling cascades, including the WRKY signaling pathway in Arabidopsis. Transcriptome analysis further revealed that defense-and SA-related genes were upregulated by DDR. The atm-2atr-2 double mutants were susceptible to TCV, indicating that the main DDR signaling pathway sensors play an important role in plant immune responses. In conclusion, DDRs activated basal immune responses to viral pathogens.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.11
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• pp.4405-4409
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• 2014

Reactive oxygen species (ROS), highly reactive molecules, are produced by living organisms as a result of normal cellular metabolism and environmental factors, and can damage nucleic acids and proteins, thereby altering their functions. The human body has several mechanisms to counteract oxidative stress by producing antioxidants. A shift in the balance between oxidants and antioxidants in favor of oxidants is termed as "oxidative stress". Paradoxically, there is a large body of research demonstrating the general effect of oxidative stress on signaling pathways, less is known about the initial and direct regulation of signaling molecules by ROS, or what we term the "oxidative interface." This review focuses on the molecular mechanisms through which ROS directly interact with critical signaling molecules to initiate signaling in a broad variety of cellular processes, such as proliferation and survival (MAP kinases and PI3 kinase), ROS homeostasis, and antioxidant gene regulation (Ref-1 and Nrf-2). This review also deals with classification as well as mechanisms of formation of free radicals, examining their beneficial and deleterious effects on cellular activities and focusing on the potential role of antioxidants in preventing and repairing damage caused by oxidative stress. A discussion of the role of phytochemical antioxidants in oxidative stress, disease and the epigenome is included.

• IMMUNE NETWORK
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• v.2 no.4
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• pp.208-216
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• 2002

Background: Reactive oxygen and nitrogen are produced by rheumatoid arthritis (RA) synovial tissue and can induce mutations in key genes. Normally, this process is prevented by a DNA mismatch repair (MMR) system that maintains sequence fidelity. Key members of the MMR system include MutS${\alpha}$ (comprised of hMSH2 and hMSH6), which can sense and repair single base mismatches and 8-oxoguanine, and MutS${\beta}$ (comprised of hMSH2 and hMSH3), which repairs longer insertion/deletion loops. Methods: To provide further evidence of DNA damage, we analyzed synovial tissues for microsatellite instability (MSI). MSI was examined by PCR on genomic DNA of paired synovial tissue and peripheral blood cells (PBC) of RA patients using specific primer sequences for 5 key microsatellites. Results: Surprisingly, abundant MSI was observed in RA synovium compared with osteoarthritis (OA) tissue. Western blot analysis of the same tissues for the expression of MMR proteins demonstrated decreased hMSH6 and increased hMSH3 in RA synovium. To evaluate potential mechanisms of MMR regulation in arthritis, fibroblast-like synoviocytes (FLS) were isolated from synovial tissues and incubated with the nitric oxide donor S-nitroso-N-acetylpenicillamine (SNAP). Western blot analysis demonstrated constitutive expression of hMSH2, 3 and 6 in RA and OA FLS. When FLS were cultured with SNAP, the RA synovial pattern of MMR expression was reproduced (high hMSH3, low hMSH6). Conclusion: Therefore, oxidative stress can relax the DNA MMR system in RA by suppressing hMSH6. Decreased hMSH6 can subsequently interfere with repair of single base mutations, which is the type observed in RA. We propose that oxidative stress not only creates DNA adducts that are potentially mutagenic, but also suppresses the mechanisms that limit the DNA damage.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.17
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• pp.7043-7048
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• 2014

Inhibition of heat shock protein 90 (Hsp90) leads to inappropriate processing of proteins involved in DNA damage repair pathways after DNA damage and may enhance tumor cell radio- and chemotherapy sensitivity. To investigate the potentiation of antitumor efficacy of lidamycin (LDM), an enediyne agent by the Hsp90 inhibitorgeldanamycin (GDM), and possible mechanisms, we have determined effects on ovarian cancer SKOV-3, hepatoma Bel-7402 and HepG2 cells by MTT assay, apoptosis assay, and cell cycle analysis. DNA damage was investigated with H2AX C-terminal phosphorylation (${\gamma}H2AX$) assays. We found that GDM synergistically sensitized SKOV-3 and Bel-7402 cells to the enediyne LDM, and this was accompanied by increased apoptosis. GDM pretreatment resulted in a greater LDM-induced DNA damage and reduced DNA repair as compared with LDM alone. However, in HepG2 cells GDM did not show significant sensitizing effects both in MTT assay and in DNA damage repair. Abrogation of LDM-induced $G_2/M$ arrest by GDM was found in SKOV-3 but not in HepG2 cells. Furthermore, the expression of ATM, related to DNA damage repair responses, was also decreased by GDM in SKOV-3 and Bel-7402 cells but not in HepG2 cells. These results demonstrate that Hsp90 inhibitors may potentiate the antitumor efficacy of LDM, possibly by reducing the repair of LDM-induced DNA damage.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.2
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• pp.209-219
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• 1997

Previous studies have demonstrated that oxidative stress involving generation of reactive oxygen species (ROS) is responsible for the cytotoxic action of $TNF{\alpha}$. Protective effect of small heat shock proteins (small HSP) against diverse oxidative stress conditions has been suggeted. Although overexpression of small hsp was shown to provide an enhanced survival of $TNF{\alpha}$-sensitive cells when challenged with $TNF{\alpha}$, neither the nature of $TNF{\alpha}$-induced cytotoxicity nor the protective mechanism of small HSP has not been completely understood. In this study, we have attempted to determine whether $TNF{\alpha}$ induces oxidative DNA damage in $TNF{\alpha}$-sensitive L929 cells. We chose to measure the level of 8-hydroxy-2'-deoxyguanosine (8 ohdG), which has been increasingly recognized as one of the most sensitive markers of oxidative DNA damage. Our results clearly demonstrated that the level of 8 ohdG increased in L929 cells in a $TNF{\alpha}$ dose-dependent manner. Subsequently, we asked whether small HSP has a protective effect on $TNF{\alpha}$-induced oxidative DNA damage. To accomplish this goal, we have stably transfected L929 cells with mouse small hsp cDNA (hsp25) since these cells are devoid of endogenous small hsps. We found that $TNF{\alpha}$-induced 8 ohdG was decreased in cells overexpressing exogenous small hsp. We also found that the cell killing activity of $TNF{\alpha}$ was decreased in these cells as measured by clonogenic survival. Taken together, results from the current study show that cytotoxic mechanism of $TNF{\alpha}$ involves oxidative damage of DNA and that overexpression of the small hsp reduces this oxidative damage. We suggest that the reduction of oxidative DNA damage is one of the most important protective mechanisms of small HSP against $TNF{\alpha}$.

• Environmental Analysis Health and Toxicology
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• v.21 no.2 s.53
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• pp.127-138
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• 2006

In urban areas, diesel exhaust particles (DEP) are probably a major component of particulate matters, especially in Korea where drive many diesel vehicles. The aim of this study was to investigate genotoxic effects of DEP using single ceil gel electrophoresis. In order to evaluate the mechanisms of DEP genotoxicity, the rat microsome mediated and DNA repair enzyme treated comet assays together with conventional comet assay were performed. Total diesel particles (DEPT) was collected without site fractionation from diesel engine bus and dichloromethane extract was obtained. The organic extract of DEPT revealed DNA damage itself in NIH/3T3 cells. The level of DNA breaks plus oxidative DNA lesions and microsome mediated DNA damage was assessed by modified single cell gel eletrophoresis. DEPT was able to induce oxidative DNA damage as well as microsome mediated DNA damage. Vitamin C as an model antioxidant reduced DNA damage in endonuclase III treated comet assay. One of flavonoid, galangin as a CYP1A1 inhibitor. reduced DNA damage in the presence of S-9 mixture. $DEP_T$ is the sources of oxidative stress, but antioxidants can significantly reduce oxidative DNA dmage. And $DEP_T$ may contain indirect mutagens which can be inhibited by CYP1A1 inhibitors. The ethanol extracts of the mixed vegetables (BV) or the mixed fruits (BF) were evaluated for their in vitro antigenotoxic effects. BV and BF showed potent Inhibitory effects against DEPT induced DNA damage with oxidative DNA lesions and in the prescence of S-9 mixture. These results indicate that BV and BF could prevent cellular DNA damage by inhibiting oxidative stress and suppressing cytochrome P4501A1 in cell culture.

• BMB Reports
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• v.51 no.8
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• pp.400-405
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• 2018

Chronic stress induces neuronal cell death, which can cause nervous system disorders including Parkinson's disease and Alzheimer's disease. In this study, we evaluated the neuroprotective effects of Clematis terniflora extract (CTE) against corticosterone-induced apoptosis in rat pheochromocytoma (PC12) cells, and also investigated the underlying molecular mechanisms. At concentrations of 300 and $500{\mu}g/ml$, CTE significantly decreased apoptotic cell death and mitochondrial damage induced by $200{\mu}M$ corticosterone. CTE decreased the expression levels of endoplasmic reticulum (ER) stress proteins GRP78, GADD153, and mitochondrial damage-related protein BAD, suggesting that it downregulates ER stress evoked by corticosterone. Furthermore, our results suggested that these protective effects were mediated by the upregulation of p-AKT and p-ERK1/2, which are involved in cell survival signaling. Collectively, our results indicate that CTE can lessen neural damage caused by chronic stress.

• Geomechanics and Engineering
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• v.11 no.3
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• pp.421-438
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• 2016

Explosions inside transportation tunnels might result in failure of tunnel structures. This study investigated the failure mechanisms of circular cast-iron tunnels in saturated soil subjected to medium internal blast loading. This issue is crucial to tunnel safety as many transportation tunnels run through saturated soils. At the same time blast loading on saturated soils may induce residual excess pore pressure, which may result in soil liquefaction. A series of numerical simulations were carried out using Finite Element program LS-DYNA. The effect of soil liquefaction was simulated by the Federal Highway soil model. It was found that the failure modes of tunnel lining were differed with different levels of blast loading. The damage and failure of the tunnel lining was progressive in nature and they occurred mainly during lining vibration when the main event of blast loading was over. Soil liquefaction may lead to more severe failure of tunnel lining. Soil deformation and soil liquefaction were determined by the coupling effects of lining damage, lining vibration, and blast loading. The damage of tunnel lining was a result of internal blast loading as well as dynamic interaction between tunnel lining and saturated soil, and stress concentration induced by a ventilation shaft connected to the tunnel might result in more severe lining damage.

• Structural Engineering and Mechanics
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• v.75 no.4
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• pp.445-454
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• 2020

Structural damage identification (SDI) is a crucial step in structural health monitoring. However, some of the existing SDI methods cannot provide enough identification accuracy and efficiency in practice. A novel whale optimization algorithm (WOA) based method is proposed for SDI by weighting modal data and flexibility assurance criterion in this study. At first, the SDI problem is mathematically converted into a constrained optimization problem. Unlike traditional objective function defined using frequencies and mode shapes, a new objective function on the SDI problem is formulated by weighting both modal data and flexibility assurance criterion. Then, the WOA method, due to its good performance of fast convergence and global searching ability, is adopted to provide an accurate solution to the SDI problem, different predator mechanisms are formulated and their probability thresholds are selected. Finally, the performance of the proposed method is assessed by numerical simulations on a simply-supported beam and a 31-bar truss structures. For the given multiple structural damage conditions under environmental noises, the WOA-based SDI method can effectively locate structural damages and accurately estimate severities of damages. Compared with other optimization methods, such as particle swarm optimization and dragonfly algorithm, the proposed WOA-based method outperforms in accuracy and efficiency, which can provide a more effective and potential tool for the SDI problem.