• 대한임상검사과학회지
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• 제43권4호
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• pp.138-144
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• 2011

Exaggerated blood pressure response during exercise has been found to increase the risk of future hypertension, left ventricular hypertrophy, cerebrovascular stroke, and CVD (cardiovascular disease) death. The aim of this study was to evaluate exercise capacity, cardiovascular factors in exaggerated blood pressure response during treadmill exercise testing. For research subjects, 72 subjects (normal blood response: 49 subjects, exaggerated blood response: 23 subjects) who received treadmill exercise test at J General Hospital were selected in this study. Exaggerated SBP (systolic blood pressure) response was defined as an SBP of 210 mmHg or greater during a maximal treadmill exercise test. The group with an exaggerated SBP response showed significantly higher values for RPP (rate pressure product) compared with the group with a normal SBP response. Subjects with METs (metabolic equivalents) had lower exaggerated SBP response than normal SBP response group. Subjects with recovery SBP had delayed exaggerated SBP response than normal SBP response group. Exaggerated SBP response to exercise is negative correlation with METs.

• 한국독성학회:학술대회논문집
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• 한국독성학회 2002년도 Current Trends in Toxicological Sciences
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• pp.73-73
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• 2002

Thioacetamide has been known to cause immune suppression. The object of the present study is to investigate the role of metabolic activation by flavin- containing monooxygenases (FMO) in thioacetamide-induced immune response. To determine whether the metabolites of thioacetamide produced by FMO causes the immunosuppression, methimazole (MMI), an FMO inhibitor, was used to block the FMO pathway.(omitted)

• Biotechnology and Bioprocess Engineering:BBE
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• 제10권5호
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• pp.385-399
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• 2005

The phenotypic response of a cell results from a well orchestrated web of complex interactions which propagate from the genetic architecture through the metabolic flux network. To rationally design cell factories which carry out specific functional objectives by controlling this hierarchical system is a challenge. Transcriptome analysis, the most mature high-throughput measurement technology, has been readily applied In strain improvement programs in an attempt to Identify genes involved in expressing a given phenotype. Unfortunately, while differentially expressed genes may provide targets for metabolic engineering, phenotypic responses are often not directly linked to transcriptional patterns, This limits the application of genome-wide transcriptional analysis for the design of cell factories. However, improved tools for integrating transcriptional data with other high-throughput measurements and known biological interactions are emerging. These tools hold significant promise for providing the framework to comprehensively dissect the regulatory mechanisms that identify the cellular control mechanisms and lead to more effective strategies to rewire the cellular control elements for metabolic engineering.

• Biomolecules & Therapeutics
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• 제26권1호
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• pp.10-18
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• 2018

Tumors are dynamic metabolic systems which highly augmented metabolic fluxes and nutrient needs to support cellular proliferation and physiological function. For many years, a central hallmark of tumor metabolism has emphasized a uniformly elevated aerobic glycolysis as a critical feature of tumorigenecity. This led to extensive efforts of targeting glycolysis in human cancers. However, clinical attempts to target glycolysis and glucose metabolism have proven to be challenging. Recent advancements revealing a high degree of metabolic heterogeneity and plasticity embedded among various human cancers may paint a new picture of metabolic targeting for cancer therapies with a renewed interest in glucose metabolism. In this review, we will discuss diverse oncogenic and molecular alterations that drive distinct and heterogeneous glucose metabolism in cancers. We will also discuss a new perspective on how aberrantly altered glycolysis in response to oncogenic signaling is further influenced and remodeled by dynamic metabolic interaction with surrounding tumor-associated stromal cells.

• Molecules and Cells
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• 제42권4호
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• pp.292-300
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• 2019

Immunometabolism, defined as the interaction of metabolic pathways with the immune system, influences the pathogenesis of metabolic diseases. Metformin and carbon monoxide (CO) are two pharmacological agents known to ameliorate metabolic disorders. There are notable similarities and differences in the reported effects of metformin and CO on immunometabolism. Metformin, an anti-diabetes drug, has positive effects on metabolism and can exert anti-inflammatory and anti-cancer effects via adenosine monophosphate-activated protein kinase (AMPK)-dependent and AMPK-independent mechanisms. CO, an endogenous product of heme oxygenase-1 (HO-1), can exert anti-inflammatory and antioxidant effects at low concentration. CO can confer cytoprotection in metabolic disorders and cancer via selective activation of the protein kinase R-like endoplasmic reticulum (ER) kinase (PERK) pathway. Both metformin and CO can induce mitochondrial stress to produce a mild elevation of mitochondrial ROS (mtROS) by distinct mechanisms. Metformin inhibits complex I of the mitochondrial electron transport chain (ETC), while CO inhibits ETC complex IV. Both metformin and CO can differentially induce several protein factors, including fibroblast growth factor 21 (FGF21) and sestrin2 (SESN2), which maintain metabolic homeostasis; nuclear factor erythroid 2-related factor 2 (Nrf2), a master regulator of the antioxidant response; and REDD1, which exhibits an anticancer effect. However, metformin and CO regulate these effects via different pathways. Metformin stimulates p53- and AMPK-dependent pathways whereas CO can selectively trigger the PERK-dependent signaling pathway. Although further studies are needed to identify the mechanistic differences between metformin and CO, pharmacological application of these agents may represent useful strategies to ameliorate metabolic diseases associated with altered immunometabolism.

• KSBB Journal
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• 제17권3호
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• pp.213-227
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• 2002

To date, the majority of biosensor technologies use binding components such as enzymes antibodies, nucleic acids and protein ligands. In contrast, the goal underlying the use of cells and tissues of animals and plants for a sensor system is to obtain systems capable of extracting information based on the biological activity, mechanisms of action and consequences of exposure to a chemical or biological agent of interest. These systems enable the interrogation of more complex biological response and offer the potential to gather higher information content from measuring physiologic and metabolic response. In these articles, same of the recent trends and applications of microbial biosensors in environmental monitoring and for use in food and fermentations have been reviewed. This endeavor presents many technological challenges to fabricate new microbial biosensors for other scientific field.

• Korean Journal of Radiology
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• 제25권6호
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• pp.591-594
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• 2024

• Korean Journal of Radiology
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• 제23권3호
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• pp.383-384
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• 2022

• Molecular & Cellular Toxicology
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• 제5권1호
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• pp.83-87
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• 2009

In this study, we assessed the stability and toxicological safety of Angelica gigas Nakai (A. gigas Nakai) extract, which is comprised of decursin and decursinol angelate (D/DA). D/DA was tested for mutagenicity using Ames Salmonella tester strains (TA102, TA1535, and TA1537) with or without metabolic activation (S9 mix). No increase in the number of revertants was observed in response to any of the doses tested (1.25, 12.5, 125, and $1,250{\mu}/mLg$). In addition, a chromosome aberration test was conducted in the Chinese hamster lung (CHL) cell line. To accomplish this, cells were treated with D/DA (3.28, 13.12, 52.46, and $209.84{\mu}g/mL$) or with Mitomycin C ($0.1{\mu}/mLg$) as a positive control in the case of no metabolic activation or benzo(a)pyrene ($20{\mu}g/mL$) in the case of metabolic activation. No significant increase in chromosome aberrations was observed in response to treatment with any of these concentrations, regardless of activation of the metabolic system. According to these results, we concluded that D/DA did not induce bacterial reverse mutation or clastogenicity in vitro in the range of concentrations evaluated in these experiments.

• 한국식품영양학회지
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• 제26권4호
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• pp.975-984
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• 2013

This study is performed to estimate the prevalence of metabolic syndrome among male workers and to identify the relationships with many related factors including anthropometry, hematological index, serum lipid level, dietary-related behaviors and health-related behaviors. According to the age groups, the 20s are significantly higher in normal and risk groups than in the metabolic syndrome (MS) group, the 30s are significantly higher in MS group than the other groups. The levels of AST and ${\gamma}$-GTP both show significant differences in the order of MS group ($30.3{\pm}8.8U/l$, $91.1{\pm}40.2U/l$) > risk group ($25.7{\pm}8.1U/l$, $41.8{\pm}20.2U/l$) > normal group ($22.8{\pm}6.0U/l$, $26.6{\pm}10.7U/l$). For the frequency of breakfast consumption, the response of 'Every day' is significantly higher in MS group than normal and risk groups, but the response of 'Not at all' is significantly higher in normal group than MS and risk groups. The drinking amount is positively correlated with ${\gamma}$-GTP in normal group, and it is negatively correlated with the hematocrit level, but it is positively correlated with the systolic blood pressure in MS group. AST is positively correlated with glucose concentrations of the MS group. The ALT is positively correlated with waist circumferences and systolic blood pressure in the risk group. The results of this study show that breakfast frequency, education level, drinking amount, drinking frequency, exercise frequency, AST, ALT and ${\gamma}$-GTP levels are all important risk factors of MS. Therefore, it is very important to maintain a healthy life style for the prevention of MS incidence.