• BMB Reports
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• 제53권4호
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• pp.181-190
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• 2020

Protein phosphatase 4 (PP4), one of serine/threonine phosphatases, is involved in many critical cellular pathways, including DNA damage response (DNA repair, cell cycle regulation, and apoptosis), tumorigenesis, cell migration, immune response, stem cell development, glucose metabolism, and diabetes. PP4 has been steadily studied over the past decade about wide spectrum of physiological activities in cells. Given the many vital functions in cells, PP4 has great potential to develop into the finding of key working mechanisms and effective treatments for related diseases such as cancer and diabetes. In this review, we provide an overview of the cellular and molecular mechanisms by which PP4 impacts and also discuss the functional significance of it in cell health.

• 한국콘크리트학회:학술대회논문집
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• 한국콘크리트학회 2003년도 가을 학술발표회 논문집
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• pp.331-334
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• 2003

Since regulation or specification for the reinforcing method are quite ambiguous, structural design for the reinforcement can be subjectively and arbitrarily conducted. Thus, reasonable limitation and guide for the quantity of the reinforcement are required for the safe use of the structure after repair. In order to guarantee the safety of the structural member several items should be considered; reinforcing limit to avoid the brittle failure, least required strength of the existing member before reinforcement in order not to fail under the new serviceability load condition when reinforcing steel plates or CFRP sheets are harmed or subjected to fire.

• 생명과학회지
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• 제28권1호
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• pp.116-129
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• 2018

생물체는 스트레스에 대처하기 위한 항상성 유지 기작을 가지고 있으나, 만성적이고 반복적인 스트레스는 카테콜아민과 같은 스트레스 호르몬의 과도한 방출로 인해 인체에 해로운 영향을 미친다. 교감신경계와 암과의 관련성을 분석하는 연구는 스트레스가 암을 악화시킬 수 있다는 오랜 가설을 바탕으로 이루어졌다. 다수의 전임상연구와 역학 연구결과는 교감신경계의 주요 신호전달경로인 ${\beta}$-adrenergic signaling을 조절하는 것이 암의 진행을 억제할 수 있음을 보여주고 있다. 교감신경계의 활성화는 암세포의 oncogene과 DNA repair 유전자 조절, 생존과 사멸 조절, EMT 및 전이 조절, 면역계와 혈관신생 조절, 세포외기질과 간엽세포 조절, 지방세포 조절 등을 통해 암세포와 종양미세환경에 광범위하게 영향을 미칠 수 있다. 오늘날 암의 성장과 관련된 분자적 기전을 차단하는 표적항암치료가 각광받고 있으나, 보상경로의 활성화와 항암제 내성 출현 및 여러 부작용으로 말미암아 임상적 실패를 거듭하면서 암의 생병리를 다방면에서 조절하는 전략이 새로운 치료법으로 대두되고 있다. 본 총설에서는 이러한 암의 전신적 조절인자로서 교감신경계가 암의 형성과 발전에 미치는 영향을 요약하고, 향후 새로운 암 치료전략으로서 ${\beta}$-adrenergic signaling을 조절하는 약물의 임상적 활용가능성에 대해 논의하고자 한다.

• Asian Pacific Journal of Cancer Prevention
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• 제16권1호
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• pp.9-21
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• 2015

Cancer, a serious public health problem in worldwide, results from an excessive and uncontrolled proliferation of the body cells without obvious physiological demands of organs. The gastrointestinal tract, including the esophagus, stomach and intestine, is a unique organ system. It has the highest cancer incidence and cancer-related mortality in the body and is influenceed by both genetic and environmental factors. Among the various chemical elements recognized in the nature, some of them including zinc, iron, cobalt, and copper have essential roles in the various biochemical and physiological processes, but only at low levels and others such as cadmium, lead, mercury, arsenic, and nickel are considered as threats for human health especially with chronic exposure at high levels. Cadmium, an environment contaminant, cannot be destroyed in nature. Through impairment of vitamin D metabolism in the kidney it causes nephrotoxicity and subsequently bone metabolism impairment and fragility. The major mechanisms involved in cadmium carcinogenesis could be related to the suppression of gene expression, inhibition of DNA damage repair, inhibition of apoptosis, and induction of oxidative stress. In addition, cadmium may act through aberrant DNA methylation. Cadmium affects multiple cellular processes, including signal transduction pathways, cell proliferation, differentiation, and apoptosis. Down-regulation of methyltransferases enzymes and reduction of DNA methylation have been stated as epigenetic effects of cadmium. Furthermore, increasing intracellular free calcium ion levels induces neuronal apoptosis in addition to other deleterious influence on the stability of the genome.

• 대한의생명과학회지
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• 제22권1호
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• pp.18-23
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• 2016

Ultraviolet (UV) irradiation induces cellular damage. A variety of cellular responses for repairing cellular damage including DNA damage occur after UV irradiation. During the repair processes, expression and activation of various molecules are regulated depending on the types of cellular damage. Parkin is an E3 ligase and act as a tumor suppressor. Recently, it has been reported that Parkin is involved in the DNA repair process. In the current study, we investigated whether UVB irradiation influences expression of Parkin. Parkin expression transiently decreased after UVB irradiation both at the mRNA and protein levels, but returned to normal levels thereafter. Taken together with cell viability data, Parkin expression is down-regulated during UVB-induced suppression of cell growth and is increased again in accordance with recovery of UVB-induced cell growth inhibition. However, Parkin overexpression or knockdown did not influence UVB-induced cell growth inhibition and recovery. We propose that Parkin could be a useful molecular marker for evaluating conditions of cells after UVB irradiation.

• Archives of Plastic Surgery
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• 제40권4호
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• pp.304-311
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• 2013

With an increasing emphasis on microsurgery skill acquisition through simulated training, the need has been identified for standardised training programmes in microsurgery. We have reviewed microsurgery training courses available across the six continents of the World. Data was collected of relevant published output from PubMed, MEDLINE (Ovid), and EMBASE (Ovid) searches, and from information available on the Internet of up to six established microsurgery course from each of the six continents of the World. Fellowships and courses that concentrate on flap harvesting rather than microsurgical techniques were excluded. We identified 27 centres offering 39 courses. Total course length ranged from 20 hours to 1,950 hours. Student-to-teacher ratios ranged from 2:1 to 8:1. Only two-thirds of courses offered in-vivo animal models. Instructions in microvascular end-to-end and end-to-side anastomoses were common, but peripheral nerve repair or free groin flap transfer were not consistently offered. Methods of assessment ranged from no formal assessment, where an instructor monitored and gave instant feedback, through immediate assessment of patency and critique on quality of repair, to delayed re-assessment of patency after a 12 to 24 hours period. Globally, training in microsurgery is heterogeneous, with variations primarily due to resource and regulation of animal experimentation. Despite some merit to diversity in curricula, there should be a global minimum standard for microsurgery training.

• Journal of Microbiology and Biotechnology
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• 제23권9호
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• pp.1293-1303
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• 2013

Antibiotic resistance of soilborne Acinetobacter species has been poorly explored. In this study, norfloxacin resistance of a soil bacterium, Acinetobacter oleivorans DR1, was investigated. The frequencies of mutant appearance of all tested non-pathogenic Acinetobacter strains were lower than those of pathogenic strains under minimum inhibitory concentration (MIC). When the quinolone-resistance-determining region of the gyrA gene was examined, only one mutant (His78Asn) out of 10 resistant variants had a mutation. Whole transcriptome analysis using a RNA-Seq demonstrated that genes involved in SOS response and DNA repair were significantly up-regulated by norfloxacin. Determining the MICs of survival cells after norfloxacin treatment confirmed some of those cells were indeed persister cells. Ten colonies, randomly selected from among those that survived in the presence of norfloxacin, did not exhibit increased MIC. Thus, both the low mutation frequency of the target gene and SOS response under norfloxacin suggested that persister formation might contribute to the resistance of DR1 against norfloxacin. The persister frequency increased without a change in MIC when stationary phase cells, low growth rates conditions, and growth-deficient dnaJ mutant were used. Taken together, our comprehensive approach, which included mutational analysis of the target gene, persister formation assays, and RNA sequencing, indicated that DR1 survival when exposed to norfloxacin is related not only to target gene mutation but also to persister formation, possibly through up-regulation of the SOS response and DNA repair genes.

• 한국항공운항학회지
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• 제25권3호
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• pp.123-134
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• 2017

In order to advance into the MRO industry, the Aviation maintenance organization with suitable for the standards for personnel, facilities and operations should be first approved by FAA and EASA. The purpose of study is designed to arrange the standards required for personnel, facility, operation rule for approval of Repair Station maintenance organizations certified by FAA PART 145 of the US Federal Aviation Regulation. Also to consider the following differences through the comparative analysis with domestic AMO certification of the information in the Management, Maintenance Process, and Quality System for approval of maintenance organization authorized, the additional EASA PART 145. As a comparative analysis on maintenance organization certification in the country between FAA and EASA, this study could show us that domestic maintenance organization, certified manual contents are used by applying just many of the FAA system. And we could know that as part of the EASA maintenance organization certification process, airmen personnel were relatively systematically segmented and controlled. For domestic maintenance organization certification, operational as policy implications we would like to present policy implications such as the implication of rating system of Aviation Mechanic License like EASA, the financial support of the training center to resolve the shortage of the FAA or EASA license holders, operational organization as "CAMO" for systematic aviation mechanic certified system should be required, continued construction of hangar or MRO for airworthiness repair under Governmental support, and varied application of DER system from FAA accordingly.

• Toxicological Research
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• 제22권2호
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• pp.95-102
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• 2006

Exposure to soluble nickel compound produces toxic effects on immune system, but the mechanism of action remains to be elucidated. Differential gene expression was studied to understand the potential molecular mechanism responsible for acute toxicity induced by nickel acetate in spleen cells. We exposed mouse spleen cells to nickel acetate with a nontoxic dose ($40{\mu}M$) and then extracted total RNA at 6 h and 12 h after exposure. The RNA was hybridized onto 10K mouse oligonucleotide microarrays, and data were analyzed using GeneSpring 7.1. Nickel had a modest effects on expression of many genes, in the range of 1.3-3 fold. The expression profile showed time-dependent changes in expression levels of differentially expressed genes, including some important genes related to cell cycle, apoptosis and DNA repair. In hierarchical cluster analysis of duplicate experiments, 111 genes were screened out. Out of these, 44 genes showing time- dependent up-regulation (>1.5 fold) and 38 genes showing down-regulation (>1.5 fold) at all time points were chosen for further analysis. The change in the expression of three genes (GPX1, GADD45B and FAIM) after nickel treatment was validated using RT-PCR. As a rule, a number of genes appear to be coordinately regulated between cell survival and cell death from nickel toxicity. In conclusion, changes in the gene profile in the spleen after nickel treatment are complex and genes with diverse functions are modulated. These findings will be contributed to the understanding of the complicated biological effects of nickel.

• 동의생리병리학회지
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• 제25권1호
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• pp.71-77
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• 2011

Gastric ulcer has multifactorial etiology, and the development of ulcer is known to be caused by gastric acidity, pepsin secretion, gastric motility and gastric mucosal blood flow. The ulcer results from the tissue necrosis and apoptotic cell death triggered by mucosal ischemia, free radical formation and cessation of nutrient delivery. The gastric mucosa is usually exposed to a wide range of aggressive insults, and has developed efficient mechanisms to repair tissue injury. The apoptotic process of gastric mucosa is triggered by the induction of such proapoptotic gene expression, such as BAX. The Bcl-2 family of proteins plays a pivotal role in the regulation of apoptosis. The maintenance of gastric mucosa integrity depends upon the ratio between cell proliferation and cell death. Stress-inducing factors may affect Bcl-2/BAX ratio and thus the rate of apoptosis through modulation of the expression of both proteins depends upon the experimental model. In addition to the regulation of apoptosis, new vessels have to be generated in order to ensure an adequate supply of oxygen and nutrients to the healing gastric mucosa. This events are regulated by several factors. Among them, such polypeptide growth factors, such as vascular endothelial growth factor (VEGF) regulates essential cell functions involved in tissue healing including cell proliferation and differentiation. The purpose of this study was carried to investigate whether Rhei Rhizoma administration might protect apoptotic cell death and promote angiogenesis in gastric mucosa. Sprague-Dawley rats were randomly divided into 4 groups; normal, saline, cimetidine and Rhei Rhizoma-treated group. The saline, cimetidine and Rhei Rhizoma extracts were orally administrated to each group and gastric ulcer was induced by HCl-EtOH solution. After 1 hour, the stomachs were collected for histological observation and immunohistochemistry. In results, Rhei Rhizoma proves to promote to heal wound in gastric ulcer in conclusion and the significant changes of BAX, Bcl-2 and VEGF quantity in gastric mucosa were observed. These results suggest that Rhei Rhizoma extract may promote incision wound healing and has protective effects on gastric ulcer in rats.