• Journal of The Korean Society of Inherited Metabolic disease
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• 제5권1호
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• pp.76-87
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• 2005

Various disorders cause hyperammonemia during childhood. Amongthem are those caused by inherited defects in urea synthesis and related metabolic pathways. These disorders can be grouped into two types: disorders of the enzymes that comprise the urea cycle, and disorders of the transporters or metabolites of theamino acids related to the urea cycle. Principal clinical features of these disorders are caused by elevated levels of blood ammonium. Additional disease-specific symptoms are related to the particular metabolic defect. These specific clinical manifestations are often due to an excess or lack of specific amino acids. Treatment of urea cycle disorders and related metabolic diseases consists of nutritional restriction of proteins, administration of specific amino acids, and use of alternative pathways for discarding excess nitrogen. Although combinations of these treatments are extensively employed, the prognosis of severe cases remains unsatisfactory. Liver transplantation is one alternative for which a better prognosis is reported.

• Proceedings of the Korean Society of Embryo Transfer Conference
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• 한국수정란이식학회 2006년도 The 6th Intermational Symposium on Developmental Biotechnology
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• pp.59-59
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• 2006

• BMB Reports
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• 제49권10호
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• pp.527-528
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• 2016

In embryonic stem cells (ESCs), cell cycle regulation is deeply connected to pluripotency. Especially, core transcription factors (CTFs) which are essential to maintaining the pluripotency transcription programs should be reset during M/G1 transition. However, it remains unknown about how CTFs are governed during cell cycle progression. Here, we describe that the regulation of Oct4 by Aurora kinase b (Aurkb)/protein phosphatase 1 (PP1) axis during the cell cycle is important for resetting Oct4 to pluripotency and cell cycle related target genes in determining the identity of ESCs. Aurkb starts to phosphorylate Oct4(S229) at the onset of G2/M phase, inducing the dissociation of Oct4 from chromatin, whereas PP1 binds Oct4 and dephosphorylates Oct4(S229) during M/G1 transition, which resets Oct4-driven transcription for pluripotency and the cell cycle. Furthermore, Aurkb phosphormimetic and PP1 binding-deficient mutations in Oct4 disrupt the pluripotent cell cycle, lead to the loss of pluripotency in ESCs, and decrease the efficiency of somatic cell reprogramming. Based on our findings, we suggest that the cell cycle is directly linked to pluripotency programs in ESCs.

• BMB Reports
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• 제46권6호
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• pp.289-294
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• 2013

To maintain cellular homeostasis against the demands of the extracellular environment, a precise regulation of kinases and phosphatases is essential. In cell cycle regulation mechanisms, activation of the cyclin-dependent kinase (CDK1) and cyclin B complex (CDK1:cyclin B) causes a remarkable change in protein phosphorylation. Activation of CDK1:cyclin B is regulated by two auto-amplification loops-CDK1:cyclin B activates Cdc25, its own activating phosphatase, and inhibits Wee1, its own inhibiting kinase. Recent biological evidence has revealed that the inhibition of its counteracting phosphatase activity also occurs, and it is parallel to CDK1:cyclin B activation during mitosis. Phosphatase regulation of mitotic kinases and their substrates is essential to ensure that the progression of the cell cycle is ordered. Outlining how the mutual control of kinases and phosphatases governs the localization and timing of cell division will give us a new understanding about cell cycle regulation.

• Journal of Korean Neurosurgical Society
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• 제66권6호
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• pp.642-651
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• 2023

Objective : Endothelial colony-forming cells (ECFCs) have been reported to play an important role in the pathogenesis of moyamoya disease (MMD). We have previously observed stagnant growth in MMD ECFCs with functional impairment of tubule formation. We aimed to verify the key regulators and related signaling pathways involved in the functional defects of MMD ECFCs. Methods : ECFCs were cultured from peripheral blood mononuclear cells of healthy volunteers (normal) and MMD patients. Low-density lipoproteins uptake, flow cytometry, high content screening, senescence-associated β-galactosidase, immunofluorescence, cell cycle, tubule formation, microarray, real-time quantitative polymerase chain reaction, small interfering RNA transfection, and western blot analyses were performed. Results : The acquisition of cells that can be cultured for a long time with the characteristics of late ECFCs was significantly lower in the MMD patients than the normal. Importantly, the MMD ECFCs showed decreased cellular proliferation with G1 cell cycle arrest and cellular senescence compared to the normal ECFCs. A pathway enrichment analysis demonstrated that the cell cycle pathway was the major enriched pathway, which is consistent with the results of the functional analysis of ECFCs. Among the genes associated with the cell cycle, cyclin-dependent kinase inhibitor 2A (CDKN2A) showed the highest expression in MMD ECFCs. Knockdown of CDKN2A in MMD ECFCs enhanced proliferation by reducing G1 cell cycle arrest and inhibiting senescence through the regulation of CDK4 and phospho retinoblastoma protein. Conclusion : Our study suggests that CDKN2A plays an important role in the growth retardation of MMD ECFCs by inducing cell cycle arrest and senescence.

• 대한상한금궤의학회지
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• 제8권1호
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• pp.67-85
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• 2016

Objectives: In this paper, two cases which showed the meaningful results on the patients' chief complaints were analyzed. The patients were treated with the Mahwang-Haengin-Gamcho-seokgo-tang herbal medication based on Shanghanlun disease pattern identification diagnostic system. Methods: The patients were diagnosed based on Shanghanlun, disease pattern identification diagnostic system. In case 1, the change of menstruation cycle was noted and pre-menstrual discomforts were measured with Menstrual Distress Questionnaire(MDQ). In case 2, Quality of life questionnaire for adult Korean asthmatics (QLQAKA) was used to estimate the quality of the patient's life. Results: All the symptoms were improved after the Mahwang-Haengin-Gamcho-seokgotang treatment. In case 1, the menstruation cycle decreased to 30 days average. MDQ score decreased 143 to 103. In case 2, the change of the QLQAKA score as 1.647 average point is considered as a meaningful improvement. Conclusion: With great difference to a 'Symptom-Medicine' diagnostic system, the disease pattern identification diagnostic system seeks the pathologic pattern through the patient's whole life. More studies and multiple cases based on the diagnostic system are needed to prove this possibility later.

• Journal of the Korean Society of Food Culture
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• 제11권4호
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• pp.527-538
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• 1996

The contents of articles on nutrition in life cycle, health and disease in the Korean daily newspapers were analyzed for the evaluation of the trends in nutrition information in mass media. Among 922 articles pressed from January 1960 to June 1996, articles on nutrition in life cycle were most frequently appeared, which is followed by articles on nutrition in disease, health foods and other related food and nutrition informations. There was a deep contrast in that the proportion of articles on nutrition in life clyle decreased from 58% in the 60's to 33% in the 90's, and those of nutrition in disease, and health foods increased from 23% and 5% in 60's to 34% and 18% in 90's, respectively.

• Korean System Dynamics Review
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• 제6권1호
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• pp.17-32
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• 2005

An agricultural commodity production cycle model consisting of corn, beef, and dairy sectors was constructed for the purpose of exploring the propagating effects of large-scale disruptive events. In an initial proof-of-concept exercise, we considered an agricultural disruption scenario in which foot-and-mouth disease (FMD) is introduced into the U.S., causing a large-scale outbreak of the disease in both beef and dairy cattle. The magnitude of disruption to the beef and dairy sectors are presented under the existing W response policy and then improvements under two alternative policies are shown.

• Journal of Life Science
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• 제20권8호
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• pp.1281-1286
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• 2010

Gaucher disease (GD) is caused by glucocerebrosidase functional deficiency and the most prevalent lysosomal storage disorder (LSD), with an incidence of about 1 in 20,000 new births. Resveratrol, one kind of phytoalexin, is a produced naturally by several plants and has anti-tumor, anti-aging, anti-inflammatory and neuro-protective effects. In this paper we provide the cellular protective effect of resveratrol in both type I and type II Gaucher disease cells. Resveratrol treatment did not show any significant change in the p21 and p53 mRNA expression level, however expression level of the p21 protein, a cell cycle arrest factor, shows significant increment in both types of Gaucher disease cells. These cell cycle arrest patterns were confirmed by both MTT assay measurement and microscopy detection. In comparison, expression level of poly ADP ribose polymerase (PARP), an apoptosis indicator protein, was significantly decreased in both type I and II Gaucher disease cells after treatment with resveratrol. This result indicates that resveratrol relievescellular apoptotic stress fromtype I and II Gaucher disease cells. Therefore, we demonstrate that resveratrol inhibits cell proliferation via p21 activity and activates cellular repair systems for Gaucher disease cells. Our results provide at least one of the molecular mechanisms of Gaucher disease and may allow the verification of potential drug targets for therapeutic trials.

• Journal of The Korean Society of Inherited Metabolic disease
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• 제5권1호
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• pp.88-93
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• 2005