• 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.

• The Korean Journal of Physiology and Pharmacology
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• v.27 no.5
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• pp.427-436
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• 2023

Mitotic arrest deficient 2 like 2 (Mad2L2, also known as Mad2B), the human homologue of the yeast Rev7 protein, is a regulatory subunit of DNA polymerase ζ that shares high sequence homology with Mad2, the mitotic checkpoint protein. Previously, we demonstrated the involvement of Mad2B in the cisplatin-induced DNA damage response. In this study, we extend our findings to show that Mad2B is recruited to sites of DNA damage in human cancer cells in response to cisplatin treatment. We found that in undamaged cells, Mad2B exists in a complex with Polζ-Rev1 and the APC/C subunit Cdc27. Following cisplatin-induced DNA damage, we observed an increase in the recruitment of Mad2B and Cdc20 (the activators of the APC/C), to the complex. The involvement of Mad2B-Cdc20-APC/C during DNA damage has not been reported before and suggests that the APC/C is activated following cisplatin-induced DNA damage. Using an in vitro ubiquitination assay, our data confirmed Mad2B-dependent activation of APC/C in cisplatin-treated cells. Mad2B may act as an accelerator for APC/C activation during DNA damage response. Our data strongly suggest a role for Mad2B-APC/C-Cdc20 in the ubiquitination of proteins involved in the DNA damage response.

• BMB Reports
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• v.34 no.6
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• pp.489-495
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• 2001

DNA damage by UV and environmental agents are the major cause of genomic instability that needs to be repaired, otherwise it give rise to cancer. Accordingly, mammalian cells operate several DNA repair pathways that are not only responsible for identifying various types of DNA damage but also involved in removing DNA damage. In mammals, nucleotide excision repair (NER) machinery is responsible for most, if not all, of the bulky adducts caused by UV and chemical agents. Although most of the proteins involved in NER pathway have been identified, only recently have we begun to gain some insight into the mechanism by which proteins recognize damaged DNA. Binding of Xeroderma pigmentosum group C protein (XPC)-hHR23B complex to damaged DNA is the initial damage recognition step in NER, which leads to the recruitment of XPA and RPA to form a damage recognition complex. Formation of damage recognition complex not only stabilizes low affinity binding of XPA to the damaged DNA, but also induces structural distortion, both of which are likely necessary for the recruitment of TFIIH and two structure-specific endonucleases for dual incision.

• Nuclear Engineering and Technology
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• v.56 no.1
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• pp.114-122
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• 2024

Irradiation-induced defects and the precipitates in the wrapper material of the Indian Fast Breeder Test Reactor (FBTR), SS 316 are analyzed using the synchrotron source-based Angle Dispersive X-Ray Diffraction (ADXRD) technique with X-rays of energy 17.185 keV (wavelength ~0.72146 Å). The differences and similarities in the high displacement damage samples as a function of dpa (displacement per atom) and dpa rate in the range of 2.9 × 10^-7- 9 × 10^-7 dpa/s are studied. Ferrite and M₂₃C₆ are commonly observed in the present set of high displacement damage 40-74 dpa SS 316 samples irradiated at temperatures in the range of 400-483 ℃. Also, the dislocation density has increased as a function of the irradiation dose. The X-ray diffraction peak profile parameters quantified such as peak shift and asymmetry show that the irradiation-induced defects are sensitive to the dpa rate-irradiation temperature combinations. The increase in yield strength as a function of displacement damage is also correlated to the dislocation density.

• Journal of the Korean Society for Aeronautical & Space Sciences
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• v.46 no.2
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• pp.141-149
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• 2018

This paper presents a neural network controller design for complex damage to a blended wing Unmanned Aerial Vehicle(UAV): partial loss of main wing and vertical tail. Longitudinal/lateral axis instability and the change of flight dynamics is investigated via numerical simulation. Based on this, neural network based adaptive controller combined with two types of feedback linearization are designed in order to compensate for the complex damage. Performance of two kinds of dynamic inversion controllers is analyzed against complex damage. According to the structure of the dynamic inversion controller, the performance difference is confirmed in normal situation and under damaged situation. Numerical simulation verifies that the instability from the complex damage of the UAV can be stabilized via the proposed adaptive controller.

• The Korean Society of Law and Medicine
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• v.11 no.1
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• pp.91-116
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• 2010

As Complex Regional Pain Syndrome (CRPS) is a new and rare illness, medical cause for it has not yet been clearly found out. Nevertheless, the patients continue to file lawsuits for damage compensation against wrongdoers or their insurers, claiming that the cause of the illness is certain actions of the wrongdoers. Moreover, the claim amount reaches to hundreds of millions of won through billions of won unlike other illnesses. Therefore, CRPS has become an important legal issue in the damage compensation lawsuit. Even though the wound is slight, the development and result may be serious in the case of CRPS. As a result, a sharp conflict arises even regarding medical diagnosis of CRPS in the lawsuit. And, even if the medical diagnosis of CRPS is admitted, severe debates occurs with regard to many issues, which include the causation between accident and CRPS in connection with establishment of damage compensation liability and scope of liability like anamnesis, determination standard of aftereffect disability, and scope of admitted aftereffect medical expense in connection with scope of damage compensation. In this study, I will review fundamental medical research on CRPS up to now and discuss principal legal issues in the damage compensation lawsuit focusing on lower court rulings.

• Journal of Environmental Impact Assessment
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• v.20 no.2
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• pp.141-150
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• 2011

The construction of photovoltaic complex in mountainous area is quickly increasing recently so that the environment assessment in constructing photovoltain complex in mountainous area was performed by comparison of $CO_{2{\cdot}}$ reduction and forest damage. The case studies for environmental value assessment, which construct photovoltaic complex in mountainous area, show that the losses of around 5.1billion won arise during 15 years. The government's official target for spreading photovoltaic energy until year 2030 can be satisfied when considering other alternative sites, improvement of technology and the alternative sites of an idle space of a building or a disused site, etc, except an undeveloped mountainous area. The construction of photovoltaic complex in mountainous area can cause the great damage to the environment, especially undeveloped mountainous area such as Baekdudaegan, and this defeat its own purpose of using photovoltaic energy. Therefore, the spread of photovoltaic complex through the additional damage of forest should be sublated.

• Korean Journal of Environmental Biology
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• v.21 no.4
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• pp.410-414
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• 2003

The effect of treatment with pine needle oil complex (complex of pine needle oil and Korean medicinal herbs) upon rat hepatocytes exposed to alcohol was investigated. We compared body weight gain and ratios of liver and kidney to body weight and the serum biochemistry of rats administered both alcohol and Pine needle oil complex to control rats treated with alcohol alone. Pine needle oil complex treatment resulted in a significant reduction in the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and triglycerides (TG) compared to the control rats. These data suggest that Pine needle oil complex represents an excellent candidate for protection of rat hepatocytes from alcohol-mediated damage.

• THE INTERNATIONAL COMMERCE & LAW REVIEW
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• v.15
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• pp.119-136
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• 2001

The purpose of this paper is to consider how to decide the cause of loss or damage to the transport goods when maritime accident occurs. In marine insurance, the underwriter is liable for any loss or damage proximately caused by a risk insured(MIA Art.55). So it is very important to determine the proximate cause of loss or damage to ascertain whether it is to be recoverable under the policy. But there is no definite conception or rule what is the proximate cause. It was left to the tribunal as a question of fact. In this paper, I will suggest the general rules to determine the proximate cause of loss or damage of the transport goods in marine insurance. First, in MIA 1906, there is the rule of proximate causation and it has been established the effective causation by cases since 1918. Second, in Institute Cargo Clauses(B) & (C), there are rules of considerably relaxed standards to determine the causation of loss of or damage using the "attributable to" and "caused by" basis. Third, it is noted, under the complex causation situation, there are difference basises to decide the liability of underwriters between the case of successive occurrence of single risk and the case of concurrent occurrence of several risks. Forth, in practice, it couldn't be ascertained the underwrier's liability by a definite rule and it should be fully considered the circumstances and conditions of the loss.

• Molecules and Cells
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• v.26 no.1
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• pp.5-11
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• 2008

Stalled DNA replication forks activate specific DNA repair mechanism called post-replication repair (PRR) pathways that simply bypass DNA damage. The bypassing of DNA damage by PRR prevents prolonged stalling of DNA replication that could result in double strand breaks (DSBs). Proliferating cell nuclear antigen (PCNA) functions to initiate and choose different bypassing pathways of PRR. In yeast, DNA replication forks stalled by DNA damage induces monoubiquitination of PCNA at K164, which is catalyzed by Rad6/Rad18 complex. PCNA monoubiquitination triggers the replacement of replicative polymerase with special translesion synthesis (TLS) polymerases that are able to replicate past DNA lesions. The PCNA interaction motif and/or the ubiquitin binding motif in most TLS polymerases seem to be important for the regulation of TLS. The TLS pathway is usually error-prone because TLS polymerases have low fidelity and no proofreading activity. PCNA can also be further polyubiquitinated by Ubc13/ Mms2/Rad5 complex, which adds an ubiquitin chain onto monoubiquitinated K164 of PCNA. PCNA polyubiquitination directs a different PRR pathway known as error-free damage avoidance, which uses the newly synthesized sister chromatid as a template to bypass DNA damage presumably through template switching mechanism. Mammalian homologues of all of the yeast PRR proteins have been identified, thus PRR is well conserved throughout evolution. Mutations of some PRR genes are associated with a higher risk for cancers in mice and human patients, strongly supporting the importance of PRR as a tumor suppressor pathway.