• International Journal of High-Rise Buildings
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• v.10 no.4
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• pp.323-334
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• 2021

Concrete structures may rarely collapse in fire incidents but fire induced damage to structural members is inevitable as a result of material degradation and thermal expansion. This requires certain repairing measures to be applied to restore the performance of post-fire members. A brief review on investigation of post-fire damage of concrete material and concrete structural members is presented in this paper, followed by a review of post-fire repair research regarding various types of repairing techniques (FRP, steel plate, and concrete section enlargement) and different type of structural members including columns, beams, and slabs. Particularly, the fire scenarios adopted in these studies leading to damage are categorized as three levels according to the duration of gas-phase temperature above 600℃ (t₆₀₀). The repair effectiveness in terms of recovered performance of concrete structural members compared to the initial undamaged performance has been summarized and compared regarding the repairing techniques and fire intensity levels. The complied results have shown that recovering the ultimate strength is achievable but the stiffness recovery is difficult. Moreover, the current fire loading scenarios adopted in the post-fire repair research are mostly idealized as constant heating rates or standard fire curves, which may have produced unrealistic fire damage patterns and the associated repairing techniques may be not practical. For future studies, the realistic fire impact and the system-level structural damage investigation are necessary.

• International Journal of Concrete Structures and Materials
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• v.6 no.3
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• pp.199-207
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• 2012

Concrete is an economical construction material and for that reason it is widely used in buildings and infrastructures. The use of deicing salts, expansion joint failure, and freeze-thaw cycles have led to concrete bridge girders experiencing corrosion of steel reinforcement and becoming unsafe for driving. The goal of this research is to assess the effectiveness of current and possible repair techniques for the end region of damaged prestressed concrete girders. To do this, three American Association of State Highway and Transportation prestressed concrete girders were tested to failure, repaired, and retested. Three different repair materials were tested including carbon fiber, glass fiber, and surface mounted rods. Each different repair material was also tested with and without injected epoxy. Comparisons were then made to determine if injecting epoxy had a positive effect on stiffness and strength recovery as well as which repair type regained the largest percentage of original strength.

• 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.

• 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.41 no.2
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• pp.127-133
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• 2018

Chromatin remodeling factors are involved in many cellular processes such as transcription, replication, and DNA damage response by regulating chromatin structure. As one of chromatin remodeling factors, remodeling and spacing factor 1 (RSF1) is recruited at double strand break (DSB) sites and regulates ataxia telangiectasia mutated (ATM) -dependent checkpoint pathway upon DNA damage for the efficient repair. RSF1 is overexpressed in a variety of cancers, but regulation of RSF1 levels remains largely unknown. Here, we showed that protein levels of RSF1 chromatin remodeler are temporally upregulated in response to different DNA damage agents without changing the RSF1 mRNA level. In the absence of SNF2h, a binding partner of RSF1, the RSF1 protein level was significantly diminished. Intriguingly, the level of RSF1-3SA mutant lacking ATM-mediated phosphorylation sites significantly increased, and upregulation of RSF1 levels under DNA damage was not observed in cells overexpressing ATM kinase. Furthermore, failure in the regulation of RSF1 level caused a significant reduction in DNA repair, whereas reconstitution of RSF1, but not of RSF1-3SA mutants, restored DSB repair. Our findings reveal that temporal regulation of RSF1 levels at its post-translational modification by SNF2h and ATM is essential for efficient DNA repair.

• Steel and Composite Structures
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• v.26 no.2
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• pp.151-161
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• 2018

The application of carbon fiber reinforced polymer (CFRP) composites for rehabilitation of steel structures has become vital in recent years. This paper presents an experimental program and a finite element (FE) modelling approach to study the effectiveness of CFRP patch for repair of notch damaged circular hollow sectional (CHS) steel beams. The proposed modeling approach is unique because it takes into account the orthotropic behavior and stacking sequence of composite materials. Parametric study was conducted to investigate the effect of initial damage (i.e., notch depth) on flexural performance of the notched beams and effectiveness of the repair system using the validated FE models. Results demonstrated the ability of CFRP patch to repair notched CHS steel beams, restoring them to their original flexural stiffness and strength. The effect of composite patch repair technique on post-elastic stiffness was more pronounced compared to the elastic stiffness. Composite patch repair becomes more effective when the level of initial damage of beam increases.

• International Journal of Concrete Structures and Materials
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• v.9 no.3
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• pp.345-367
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• 2015

Past earthquakes have signaled the increased collapse vulnerability of mainshock-damaged bridge piers and urgent need of repair interventions prior to subsequent cascading hazard events, such as aftershocks, triggered by the mainshock (MS). The overarching goal of this study is to quantify the collapse vulnerability of mainshock-damaged substandard RC bridge piers rehabilitated with different repair jackets (FRP, conventional thick steel and hybrid jacket) under aftershock (AS) attacks of various intensities. The efficacy of repair jackets on post-MS resilience of repaired bridges is quantified for a prototype two-span single-column bridge bent with lap-splice deficiency at column-footing interface. Extensive number of incremental dynamic time history analyses on numerical finite element bridge models with deteriorating properties under back-to-back MS-AS sequences were utilized to evaluate the efficacy of different repair jackets on the post-repair behavior of RC bridges subjected to AS attacks. Results indicate the dramatic impact of repair jacket application on post-MS resilience of damaged bridge piers-up to 45.5 % increase of structural collapse capacity-subjected to aftershocks of multiple intensities. Besides, the efficacy of repair jackets is found to be proportionate to the intensity of AS attacks. Moreover, the steel jacket exhibited to be the most vulnerable repair intervention compared to CFRP, irrespective of the seismic sequence (severe MS-severe or moderate AS) or earthquake type (near-fault or far-fault).

• Environmental Mutagens and Carcinogens
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• v.9 no.1
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• pp.13-22
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• 1989

The effect of novobiocin (NOV), and inhibitor of topoisomerase II, on ethyl methanesulfonate (EMS)-or bleomycin (BLM)-induced DNA repair synthesis was examined during the cell cycle of Chinese hamster ovary (CHO)-K1 cells. Three assays were employed in this study: cell survival, alkaline elution and unscheduled DNA synthesis. EMS was effective at killing CHO cells in G1 phase, wheras BLM preferentially killed cells in G2 and S phases. EMS induced the much more amount of DNA damage in G1 phase, while BLM induced in G2 phase than the other phases. The both of pre- and post-treatment with BOV inhibitied EMS- or BLM-induced DNA repair synthesis in G1 and G2 phases, and pretreatment with NOV inhibited more effectively than the post-treated group. These results suggested that CHO cells exhibited a differential sensitivity to cell lethality and DNA damage in relation to cell cycle according to used chemical agents, and that DNA topoisomerase II participated in an initial stage of DNA repair.

• BMB Reports
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• v.48 no.6
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• pp.354-359
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• 2015

Vascular smooth muscle cells (VSMCs) undergo death during atherosclerosis, a widespread cardiovascular disease. Recent studies suggest that oxidative damage occurs in VSMCs and induces atherosclerosis. Here, we analyzed oxidative damage repair in VSMCs and found that VSMCs are hypersensitive to oxidative damage. Further analysis showed that oxidative damage repair in VSMCs is suppressed by a low level of poly (ADP-ribosyl)ation (PARylation), a key post-translational modification in oxidative damage repair. The low level of PARylation is not caused by the lack of PARP-1, the major poly(ADP-ribose) polymerase activated by oxidative damage. Instead, the expression of poly(ADP-ribose) glycohydrolase, PARG, the enzyme hydrolyzing poly(ADP-ribose), is significantly higher in VSMCs than that in the control cells. Using PARG inhibitor to suppress PARG activity facilitates oxidative damage-induced PARylation as well as DNA damage repair. Thus, our study demonstrates a novel molecular mechanism for oxidative damage-induced VSMCs death. This study also identifies the use of PARG inhibitors as a potential treatment for atherosclerosis. [BMB Reports 2015; 48(6): 354-359]

• Journal of Ginseng Research
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• v.28 no.1
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• pp.18-26
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• 2004

The effect of Panax ginseng administration in muscle inflammatory process induced after eccentric exercise, that causes myofibrillar disruption, was studied. Changes in lipid peroxidation, inflammation, glycogen levels in muscle and release of myocellular proteins to blood were measured. The analyses were performed immediately after eccentric exercise and over week since this period are necessary for the muscle damage-repair cycle. The ginseng extract (100 mg kg$^{-1}$ ) was orally administered to rats for three months, before the eccentric exercise performance. The results showed the protective role of ginseng against skeletal muscle damage. This effect could be associated with their membrane stabilising capacity since creatine kinase (CK) activity was significantly decreased 96 h post-exercise from 523$\pm$70 to 381$\pm$53 and 120 h post-exercise from 443$\pm$85 to 327$\pm$75 in treated animals. $\beta$-glucuronidase activity, as indicator of inflammation, showed a significant reduction of about 15-25% in soleus, vastus and triceps in these post-exercise times. The lipid peroxidation, measured by malondyaldehyde levels, was significantly decreased in the 24 h post-exercise period in soleus and vastus intermedius muscles and on the recovery period. Finally ginseng administration reduced significantly the decrease of the glycogen levels immediately after exercise and when the regenerative process took place (72-168 h post exercise). Collectively, the results have showed that ginseng did not inhibit the vital inflammatory response process associated with the muscle damage-repair cycle but presumably ameliorate the injury.