• 한국생물공학회:학술대회논문집
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• 2005.04a
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• pp.587-588
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• 2005

• 한국생물공학회:학술대회논문집
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• 2005.10a
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• pp.795-796
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• 2005

• Biomolecules & Therapeutics
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• v.15 no.3
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• pp.192-198
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• 2007

Emodin (1,3,8-trihydroxy-6-methylanthraquinone) is a major constituent of rhubarb. Although it has been claimed to have a wild spectrum of therapeutic value, its side effects, especially in human kidney cells have not been well characterized. In this study, we have carried out in vitro genetic toxicity test of emodin and microarray analysis of differentially expressed genes in response to emodin. The result of Ames test showed mutations with emodin treatment in base substitution strain TA1535 both with and without exogenous metabolic activation. Likewise, emodin showed mutations in frame shift TA98 both with and without exogenous metabolic activation. The result of COMET assay in L5178Y cells with emodin treatment showed DNA damage both with and without exogenous metabolic activation. Emodin did not increase micronuclei in CHO cells both with and without exogenous metabolic activation. 150 Genes were selected as differentially expressed genes in response to emodin by microarray analysis and these genes would be candidate biomarkers of genetic toxic action of emodin.

• Biomolecules & Therapeutics
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• v.15 no.3
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• pp.199-204
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• 2007

Carbamates have excellent insecticidal activities against a broad spectrum of insects. They possess knocking-down, fast-killing, and systemic effects, however, they are toxic to mammals. In this study, we have carried out in vitro genetic toxicity test of methylcarbamate and microarray analysis of differentially expressed genes in response to methylcarbamate. Methylcarbamate did not show mutations in base substitution strain TA1535 both with and without exogenous metabolic activation. Methylcarbamate did not show mutations in frame shift TA98 both with and without exogenous metabolic activation. Methylcarbamate showed DNA damage based on single cell gel/comet assay in L5178Y cells both with and without exogenous metabolic activation. Methylcarbamate did not increase micronuclei in CHO cells both with and without exogenous metabolic activation. Microarray analysis of gene expression profiles in L5178Y cells in response to methylcarbamate selected differentially expressed 132 genes that could be candidate biomarkers of genetic toxic action of methylcarbamate.

• Journal of Microbiology and Biotechnology
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• v.27 no.9
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• pp.1681-1691
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• 2017

This study investigated the effect of proline addition on the salt tolerance of Tetragenococcus halophilus. Salt stress led to the accumulation of intracellular proline in T. halophilus. When 0.5 g/l proline was added to hyperhaline medium, the biomass increased 34.6% (12% NaCl) and 27.7% (18% NaCl) compared with the control (without proline addition), respectively. A metabolomic approach was employed to reveal the cellular metabolic responses and protective mechanisms of proline upon salt stress. The results showed that both the cellular membrane fatty acid composition and metabolite profiling responded by increasing unsaturated and cyclopropane fatty acid proportions, as well as accumulating some specific intracellular metabolites (environmental stress protector). Higher contents of intermediates involved in glycolysis, the tricarboxylic acid cycle, and the pentose phosphate pathway were observed in the cells supplemented with proline. In addition, addition of proline resulted in increased concentrations of many organic osmolytes, including glutamate, alanine, citrulline, N-acetyl-tryptophan, and mannitol, which may be beneficial for osmotic homeostasis. Taken together, results in this study suggested that proline plays a protective role in improving the salt tolerance of T. halophilus by regulating the related metabolic pathways.

• Biomolecules & Therapeutics
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• v.14 no.4
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• pp.246-252
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• 2006

1,2-Dibromoethane(DBE) has been widely used as a soil fumigant, an additive to leaded gasoline and an industrial solvent. In this study, we have carried out in vitro genetic toxicity test of 1,2-dibromoethane and microarray analysis of differentially expressed genes in response to 1,2-dibromoethane. 1,2-Dibromoethane showed mutations in base substitution strain TA1535 both with and without exogenous metabolic activation. 1,2-Dibromoethane showed mutations in frame shift TA98 both with and without exogenous metabolic activation. 1,2-Dibromoethane showed DNA damage based on single cell gel/comet assay in L5178Y cells both with and without exogenous metabolic activation. 1,2-Dibromoethane increased micronuclei in CRO cells both with and without exogenous metabolic activation. Microarray analysis of gene expression profiles in L5178Y cells in response to 1,2-dibromoethane selected differentially expressed 241 genes that would be candidate biomarkers of genetic toxic action of 1,2-dibromoethane.

• The Korean Journal of Physiology and Pharmacology
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• v.28 no.2
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• pp.107-112
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• 2024

27-Hydroxycholesterol (27OHChol), a prominent cholesterol metabolite present in the bloodstream and peripheral tissues, is a kind of immune oxysterol that elicits immune response. Recent research indicates the involvement of 27OHChol in metabolic inflammation (meta-inflammation) characterized by chronic responses associated with metabolic irregularities. 27OHChol activates monocytic cells such that they secrete pro-inflammatory cytokines and chemokines, and increase the expression of cell surface molecules such as pattern-recognition receptors that play key roles in immune cell-cell communication and sensing metabolism-associated danger signals. Levels of 27OHChol increase when cholesterol metabolism is disrupted, and the resulting inflammatory responses can contribute to the development and complications of metabolic syndrome, including obesity, insulin resistance, and cardiovascular diseases. Since 27OHChol can induce chronic immune response by activating monocyte-macrophage lineage cells that play a crucial role in meta-inflammation, it is essential to understand the 27OHChol-induced inflammatory responses to unravel the roles and mechanisms of action of this cholesterol metabolite in chronic metabolic disorders.

• BMB Reports
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• v.52 no.6
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• pp.360-372
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• 2019

Macrophages play an essential role not only in mediating the first line of defense but also in maintaining tissue homeostasis. In response to extrinsic factors derived from a given tissue, macrophages activate different functional programs to produce polarized macrophage populations responsible for inducing inflammation against microbes, removing cellular debris, and tissue repair. However, accumulating evidence has revealed that macrophage polarization is pivotal in the pathophysiology of metabolic syndromes and cancer, as well as in infectious and autoimmune diseases. Recent advances in transcriptomic and metabolomic studies have highlighted the link between metabolic rewiring of macrophages and their functional plasticity. These findings imply that metabolic adaption to their surrounding microenvironment instructs activation of macrophages with functionally distinct phenotypes, which in turn probably leads to the pathogenesis of a wide spectrum of diseases. In this review, we have introduced emerging concepts in immunometabolism with focus on the impact on functional activation of macrophages. Furthermore, we have discussed the implication of macrophage plasticity on the pathogenesis of metabolic syndromes and cancer, and how the disease microenvironment manipulates macrophage metabolism with regard to the pathophysiology.

• Radiation Oncology Journal
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• v.27 no.3
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• pp.111-119
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• 2009

Purpose: This study aimed at assessing the value of fluorine-18 fluorodeoxyglucose positron emission tomography ($^{18}F$-FDG PET) for predicting the response of locally advanced rectal cancer to neoadjuvant CRT. Materials and Methods: Between August 2006 and January 2008, we prospectively enrolled 20 patients with locally advanced rectal cancer and who were treated with neoadjuvant CRT at the Korea Institute of Radiological and Medical Sciences. The treatment consisted of radiation therapy and chemotherapy, and this was followed by curative resection 6 weeks later. All the patients underwent $^{18}F$-FDG PET/CT both before CRT and 6 weeks after completing CRT. The measurements of the FDG uptake ($SUV_{max}$), the absolute difference (${\Delta}SUV_{max}$) and the percent $SUV_{max}$ difference (response index, $RI_{SUV}$) between the pre- and post-CRT $^{18}F$-FDG PET/CT scans were assessed. The measurements of the metabolic volume, the absolute difference (${\Delta}$metabolic volume) and the percent metabolic volume difference (response index, $RI_{metabolic\;volume}$) were also assessed. Results: Of the 20 patients who underwent surgery, 11 patients (55%) were classified as responders according to Dworak's classification. The post-CRT $SUV_{max}$ was significantly lower than the pre-CRT $SUV_{max}$. However, there were no significant differences in the $SUV_{max}$ and the metabolic volume reduction between the responders and non-responders. We used a minimum $SUV_{max}$ reduction of 67% as the cut-off value for defining a response, with a sensitivity of 45.5%, a specificity of 88.9%, a positive predictive value of 77% and a negative predictive value of 53.8%. Conclusion: Although there were no statistically significant results in this study, other studies have revealed that $^{18}F$-FDG PET/CT has the potential to assess the tumor response to neoadjuvant CRT in patients with locally advanced rectal cancer.

• Molecules and Cells
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• v.46 no.12
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• pp.727-735
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• 2023

Stem cells require high amounts of energy to replicate their genome and organelles and differentiate into numerous cell types. Therefore, metabolic stress has a major impact on stem cell fate determination, including self-renewal, quiescence, and differentiation. Lysosomes are catabolic organelles that influence stem cell function and fate by regulating the degradation of intracellular components and maintaining cellular homeostasis in response to metabolic stress. Lysosomal functions altered by metabolic stress are tightly regulated by the transcription factor EB (TFEB) and TFE3, critical regulators of lysosomal gene expression. Therefore, understanding the regulatory mechanism of TFEB-mediated lysosomal function may provide some insight into stem cell fate determination under metabolic stress. In this review, we summarize the molecular mechanism of TFEB/TFE3 in modulating stem cell lysosomal function and then elucidate the role of TFEB/TFE3-mediated transcriptional activity in the determination of stem cell fate under metabolic stress.