• Journal of the Korean Society for Precision Engineering
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• v.19 no.8
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• pp.71-76
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• 2002

In this study low cycle fatigue (LCF) behavior of 12Cr steel at high temperature are described. Secondly, comparisons between predicted lives and experimental lives are made for the several sample life prediction models. Two minute hold period in either tension or compression reduce the number of cycles to failure by about a factor of two. Twenty minute hold periods in compression lead to shorter lives than 2 minute hold periods in compression. Experiments showed that life predictions from classical phenomenological models have limitations. More LCF experiments should be pursued to gain understanding of the physical damage mechanisms and to allow the development of physically-based models which can enhance the accuracy of the predictions of components. From a design point-of-view, life prediction has been judged acceptable for these particular loading conditions but extrapolations to thermo-mechanical fatigue loading, for example, require more sophisticated models including physical damage mechanisms.

• Transactions of the Korean Society of Mechanical Engineers A
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• v.24 no.5 s.176
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• pp.1084-1092
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• 2000

Responses of ultrasonic back scattered energy and AE (Acoustic Emission) characteristics related to the progressive damage of $[0/90-{2}]_s$ and $[0/90-{4}]_s$ crossply laminates were studied. It was found that the ultrasonic backscattered energy was sensitive to the matrix cracking but not sensitive to other failure mechanisms. However, AE was proved to be sensitive to matrix cracking as well as other failure mechanisms.AE signals were analyzed by investigating the amplitude and number of counts per event for corresponding applied strain. Loading and unloading tests were conducted separately. AE results showed Kaiser effect in the crossply composite laminates and ultrasonic results supported the AE results.

• Biomedical Science Letters
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• v.11 no.2
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• pp.103-108
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• 2005

2-Deoxyribonolactone (dL) arises as a major DNA damage induced by a variety of agents, involving free radical attack and oxidation of C1'-deoxyribose in DNA. We investigated whether dL lesions can be repaired in mammalian cells and the mechanisms underlying the role of DNA polymerase $\beta$ in processing of dL lesions. Pol $\beta$ appeared to be trapped by dL residues, resulting in stable DNA-protein cross-links. However, repair DNA synthesis at site-specific dL sites occurred effectively in cell-free extracts, but predominantly accompanied by long-patch base excision repair (BER) pathway. Reconstitution of long-patch BER demonstrated that FEN1 was capable of removing the displaced flap DNA containing a 5'-dL residue. Cellular repair of dL lesions was largely dependent on the DNA polymerase activity of Pol $\beta$. Our observations reveal repair mechanisms of dL and define how mammalian cells prevent cytotoxic effects of oxidative DNA lesions that may threaten the genetic integrity of DNA.

• Structural Engineering and Mechanics
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• v.5 no.6
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• pp.679-689
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• 1997

The damage of concrete subjected to multiaxial complex loading involves strong anisotropy due to its highly heterogeneous nature and the geometrically anisotropic characteristic of the microcracks. A comprehensive description of concrete damage is proposed by introducing a fourth-order anisotropic damage tenser. The evolution of damage is assumed to be related to the principal components of the current states of stress and damage. The unilateral effect of damage due to the closure and opening of microcracks is taken into account by introducing projection tensors that are also determined by the current state of stress. The proposed damage model considers the different kinds of damage mechanisms that result in different failure modes and different patterns of microdefects that cause different unilateral effects. This damage model is embedded in a thermomechanically consistent constitutive equation in which hardening and the triaxial compression caused shear-enhanced compaction can also be taken into account. The validity of the proposed model is verified by comparing theoretical and experimental results of plain and steel fiber reinforced concrete subjected to complex triaxial stress histories.

• Physical Therapy Korea
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• v.5 no.2
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• pp.106-117
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• 1998

The pain is common among individuals with physical disabilities. It can interfere with therapy since patients with pain can become uncooperative and reluctant to move. This paper reviews the natural physiological mechanisms that can reduce pain perception, and considers physiological mechanisms which contribute to clinical pain by describing how the pain system changes its sensitivity depending upon the body's needs. The peripheral and central mechanisms contributing to sensitised nociceptive system are described with reference to the symptoms of clinical pain such as hyperalgesia, allodynia sopntaneous 'on-going'-projected and referred pain. It is suggested that in some chronic pain the nociceptive system maintains a state of sensitivity despite the absence of on-going tissue damage and under such circumstances the nociceptive system itself may have become dysfunctional. Such situations are often initiated by damage to nervous tissue which results in changes in the activity and organization of neuronal circuits within the central nervous system. The ability of the nociceptive system to operate in a suppressed state is also discussed with reference to pain modulation. The physical therapist can help facilitate the activation of these mechanisms through a combination of noninvasive modalities, functional activities, and the therapeutic use of self.

• Proceedings of the Korean Society of Toxicology Conference
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• 2006.11a
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• pp.55-64
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• 2006

The fetal central nervous system (CNS) is sensitive to diverse environmental factors, such as alcohol, heavy metals, irradiation, mycotoxins, neurotransmitters, and DNA damage, because a large number of processes occur during an extended period of development. Fetal neural damage is an important issue affecting the completion of normal CNS development. As many concepts about the brain development have been recently revealed, it is necessary to compare the mechanism of developmental abnormalities induced by extrinsic factors with the normal brain development. To clarify the mechanism of fetal CNS damage, we used one experimental model in which 5-azacytidine (5AZC), a DNA damaging and demethylating agent, was injected to the dams of rodents to damage the fetal brain. 5AzC induced cell death (apoptosis)and cell cycle arrest in the fetal brain, and it lead to microencephaly in the neonatal brain. We investigated the mechanism of apoptosis and cell cycle arrest in the neural progenitor cells in detail, and demonstrated that various cell cycle regulators were changed in response to DNA damage. p53, the guardian of genome, played a main role in these processes. Further, using DNA microarray analysis, tile signal cascades of cell cycle regulation were clearly shown. Our results indicate that neural progenitor cells have the potential to repair the DNA damages via cell cyclearrest and to exclude highly affected cells through the apoptotic process. If the stimulus and subsequent DNA damage are high, brain development proceeds abnormally and results in malformation in the neonatal brain. Although the mechanisms of fetal brain injury and features of brain malformation afterbirth have been well studied, the process between those stages is largely unknown. We hypothesized that the fetal CNS has the ability to repair itself post-injuring, and investigated the repair process after 5AZC-induced damage. Wefound that the damages were repaired by 60 h after the treatment and developmental processes continued. During the repair process, amoeboid microglial cells infiltrated in the brain tissue, some of which ingested apoptotic cells. The expressions of genes categorized to glial cells, inflammation, extracellular matrix, glycolysis, and neurogenesis were upregulated in the DNA microarray analysis. We show here that the developing brain has a capacity to repair the damage induced by the extrinsic stresses, including changing the expression of numerous genes and the induction of microglia to aid the repair process.

• Molecules and Cells
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• v.19 no.2
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• pp.167-179
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• 2005

The cells of metazoans respond to DNA damage by either arresting their cell cycle in order to repair the DNA, or by undergoing apoptosis. This response is highly conserved across species, and many of the genes involved in this DNA damage response have been shown to be inactivated in human cancers. This suggests the importance of DNA damage response with regard to the prevention of cancer. The DNA damage checkpoint responses vary greatly depending on the developmental context, cell type, gene expression profile, and the degree and nature of the DNA lesions. More valuable information can be obtained from studies utilizing whole organisms in which the molecular basis of development has been well established, such as Drosophila. Since the discovery of the Drosophila p53 orthologue, various aspects of DNA damage responses have been studied in Drosophila. In this review, I will summarize the current knowledge on the DNA damage checkpoint response in Drosophila. With the ease of genetic, cellular, and cytological approaches, Drosophila will become an increasingly valuable model organism for the study of mechanisms inherent to cancer formation associated with defects in the DNA damage pathway.

• Proceedings of the Korean Vacuum Society Conference
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• 2013.08a
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• pp.155.1-155.1
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• 2013

The goals of this study are to elucidate the plasma effects on DNA molecules to apply some plasma based applications and also to find out the mechanisms of plasma-induced DNA damage in biomolecule. Nonthermal atmospheric pressure plasma has much potential for medical, agricultural and food applications for the future. The atmospheric pressure plasma jet (APPJ) contains radicals, charged particles, low energy electrons, excited molecules and UV light. It has been started doing experiments using APPJ at the early 21th. And some recent results showed that APPJ has a possibility to apply to new fields like mentioned above. But it is kind of at the very early stages of plasma based application. It is definitely necessary much of theoretical and experimental studies to further understanding to use nonthermal atmospheric pressure plasma in biomedical, agriculture and food parts. Here we introduce a new experimental system to study plasma effects on biomolecules. And we will show some recent results of LEE-induced DNA damage using electron irradiation apparatus under ultra-high vacuum.

• Journal of Life Science
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• v.23 no.8
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• pp.963-969
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• 2013

Although it is popularly believed that vitamin C protects cells from various genotoxicants, the degrees and mechanisms of itsprotective actions are not fully understood. In this study, vitamin C's protective effects against various genotoxicants were quantified, together with subsequent analyses on the mechanisms of these protective effects. Comet assay was employed to measure the degree of DNA damage in Chinese hamster ovary cells (CHO-K1) exposed to five genotoxicants, $H_2O_2$, $HgCl_2$, N-methyl-N-nitro-N-nitrosoguanidine (MNNG), 4-nitroquinoline-1-oxide (4NQO), and UV-irradiation. In cases cells were treated with $H_2O_2$, $HgCl_2$, and 4NQO together with vitamin C, the damage to DNA decreased to the level of the control group. In cases of UV-irradiation, the protective effect of vitamin C appeared, but did not reach the control levels. Interestingly, vitamin C did not have protective effects against the genotoxicity of MNNG. The degrees of DNA damage of cells treated with vitamin C prior to exposure togenotoxicants were 28~49% lower than those of cells treated with vitamin C after being exposed to genotoxicants. In conclusion, vitamin C had strong antioxidanteffects against genotoxicants by being a primary antioxidant blocking genotoxicity reaching the cells, rather than being a secondary antioxidant acting on post-exposure DNA repair processes. However, vitamin C's protective effects appearto be limited, as there are genotoxicants, such as MNNG, whosegenotoxicityis not affected by vitamin C. Therefore, the results of this study warrant furtherstudies on toxic mechanisms of genotoxicants and their interactions with protective mechanisms of vitamin C.

• Radiation Oncology Journal
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• v.32 no.3
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• pp.103-115
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• 2014

To summarize current knowledge regarding mechanisms of radiation-induced normal tissue injury and medical countermeasures available to reduce its severity. Advances in radiation delivery using megavoltage and intensity-modulated radiation therapy have permitted delivery of higher doses of radiation to well-defined tumor target tissues. Injury to critical normal tissues and organs, however, poses substantial risks in the curative treatment of cancers, especially when radiation is administered in combination with chemotherapy. The principal pathogenesis is initiated by depletion of tissue stem cells and progenitor cells and damage to vascular endothelial microvessels. Emerging concepts of radiation-induced normal tissue toxicity suggest that the recovery and repopulation of stromal stem cells remain chronically impaired by long-lived free radicals, reactive oxygen species, and pro-inflammatory cytokines/chemokines resulting in progressive damage after radiation exposure. Better understanding the mechanisms mediating interactions among excessive generation of reactive oxygen species, production of pro-inflammatory cytokines and activated macrophages, and role of bone marrow-derived progenitor and stem cells may provide novel insight on the pathogenesis of radiation-induced injury of tissues. Further understanding the molecular signaling pathways of cytokines and chemokines would reveal novel targets for protecting or mitigating radiation injury of tissues and organs.