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  1. Article: CD83 expression induced by CpG-DNA stimulation in a macrophage cell line RAW 264.7 Min Chul Park1, Dongbum Kim2, Younghee Lee3 & Hyung-Joo Kwon1,2,*

    Park, M.C., Hallym University, Chuncheon, Republic of Korea / Kim, D.B., Hallym University, Chuncheon, Republic of Korea / Lee, Y.H., Chungbuk National University, Cheongju, Republic of korea / Kwon, H.J., Hallym University, Chuncheon, Republic of Korea

    Biochemistry and Molecular Biology reports

    (Sep 2013)  Volume v. 46, Issue (9), Page(s) p. 448–453

    Abstract: CpG-DNA has various immunomodulatory effects in dendritic cells, B cells, and macrophages. While induction of cytokines by CpG-DNA has been well documented in macrophages, the expression of costimulatory molecules in CpG-DNA treated macrophages has not ... ...

    Abstract CpG-DNA has various immunomodulatory effects in dendritic cells, B cells, and macrophages. While induction of cytokines by CpG-DNA has been well documented in macrophages, the expression of costimulatory molecules in CpG-DNA treated macrophages has not yet been defined. Therefore, we investigated the effects of CpG-DNA on the expression of costimulatory molecules in RAW 264.7 cells. The surface expression of CD80 was slightly increased and CD83 expression was significantly increased in response to CpG-DNA. However, the expression of CD86 and MHC class II was not changed. As expression of CD83 mRNA was also increased by CpG-DNA, CD83 expression is regulated at a transcriptional level. To understand the contribution of signaling pathways to CD83 induction, we used pathway specific inhibitors. The NF-κB inhibitor significantly reduced surface expression of CD83 as well as phagocytic activity of RAW 264.7 cells. Therefore, CD83 expression may contribute to the immunostimulatory effects of CpG-DNA in macrophage cells
    Keywords MACROPHAGE ; MACROFAGOS ; MACROPHAGES
    Language English
    Document type Article
    ISSN 1976-6696
    Database AGRIS - International Information System for the Agricultural Sciences and Technology

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  2. Article: CD83 expression induced by CpG-DNA stimulation in a macrophage cell line RAW 264.7 Min Chul Park1, Dongbum Kim2, Younghee Lee3 & Hyung-Joo Kwon1,2,*

    Park, M.C., Hallym University, Chuncheon, Republic of Korea / Kim, D.B., Hallym University, Chuncheon, Republic of Korea / Lee, Y.H., Chungbuk National University, Cheongju, Republic of korea / Kwon, H.J., Hallym University, Chuncheon, Republic of Korea

    Biochemistry and Molecular Biology reports

    (Sep 2013)  Volume v. 46, Issue (9), Page(s) p. 448–453

    Abstract: CpG-DNA has various immunomodulatory effects in dendritic cells, B cells, and macrophages. While induction of cytokines by CpG-DNA has been well documented in macrophages, the expression of costimulatory molecules in CpG-DNA treated macrophages has not ... ...

    Abstract CpG-DNA has various immunomodulatory effects in dendritic cells, B cells, and macrophages. While induction of cytokines by CpG-DNA has been well documented in macrophages, the expression of costimulatory molecules in CpG-DNA treated macrophages has not yet been defined. Therefore, we investigated the effects of CpG-DNA on the expression of costimulatory molecules in RAW 264.7 cells. The surface expression of CD80 was slightly increased and CD83 expression was significantly increased in response to CpG-DNA. However, the expression of CD86 and MHC class II was not changed. As expression of CD83 mRNA was also increased by CpG-DNA, CD83 expression is regulated at a transcriptional level. To understand the contribution of signaling pathways to CD83 induction, we used pathway specific inhibitors. The NF-κB inhibitor significantly reduced surface expression of CD83 as well as phagocytic activity of RAW 264.7 cells. Therefore, CD83 expression may contribute to the immunostimulatory effects of CpG-DNA in macrophage cells
    Keywords MACROPHAGE ; MACROFAGOS ; MACROPHAGES
    Language English
    Document type Article
    ISSN 1976-6696
    Database AGRIS - International Information System for the Agricultural Sciences and Technology

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  3. Article ; Online: Association between Moving to a High-Volume Hospital in the Capital Area and the Mortality among Patients with Cancer: A Large Population-Based Cohort Study.

    Choi, Jung-Kyu / Kim, Se-Hyung / Park, Myung-Bae

    International journal of environmental research and public health

    2021  Volume 18, Issue 7

    Abstract: This study aimed to identify the association between moving to a high-volume hospital and the mortality of patients with cancer living in the district. The study population comprised participants diagnosed with cancer within the past nine years (2004- ... ...

    Abstract This study aimed to identify the association between moving to a high-volume hospital and the mortality of patients with cancer living in the district. The study population comprised participants diagnosed with cancer within the past nine years (2004-2012). The final sample included 8197 patients with cancer, 3939 were males (48.1%), and 4258 were females (51.9%). A Cox proportional hazard model was used to estimate the hazard ratio (HR) for death. Confounding variables including sex, age, type of social security, income level, disability, and utilization volume were incorporated into the model. Among patients with cancer living in the district, 2874 (35.1%) used healthcare services in Seoul. About 10% (
    MeSH term(s) Cohort Studies ; Female ; Hospitals, High-Volume ; Humans ; Income ; Male ; Neoplasms ; Proportional Hazards Models ; Seoul
    Language English
    Publishing date 2021-04-06
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1660-4601
    ISSN (online) 1660-4601
    DOI 10.3390/ijerph18073812
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Association between Moving to a High-Volume Hospital in the Capital Area and the Mortality among Patients with Cancer

    Jung-kyu Choi / Se-Hyung Kim / Myung-Bae Park

    International Journal of Environmental Research and Public Health, Vol 18, Iss 3812, p

    A Large Population-Based Cohort Study

    2021  Volume 3812

    Abstract: This study aimed to identify the association between moving to a high-volume hospital and the mortality of patients with cancer living in the district. The study population comprised participants diagnosed with cancer within the past nine years (2004– ... ...

    Abstract This study aimed to identify the association between moving to a high-volume hospital and the mortality of patients with cancer living in the district. The study population comprised participants diagnosed with cancer within the past nine years (2004–2012). The final sample included 8197 patients with cancer, 3939 were males (48.1%), and 4258 were females (51.9%). A Cox proportional hazard model was used to estimate the hazard ratio (HR) for death. Confounding variables including sex, age, type of social security, income level, disability, and utilization volume were incorporated into the model. Among patients with cancer living in the district, 2874 (35.1%) used healthcare services in Seoul. About 10% ( n = 834) of patients died during the follow-up period. The HR for death in females (HR: 0.68, 95% CI: 0.58–0.81) was lower than that in males. Additionally, the HR for the death of patients using healthcare services in Seoul (HR: 1.30, 95% CI: 1.11–1.53) was higher than those patients who did not use healthcare services in Seoul. Among patients utilizing services in the province, wealthier patients’ survival probability was significantly higher than that of others. The cause of income differences should be identified, and accessibility to medical use of low-income families should be enhanced to prevent mortality of patients from cancer disparities.
    Keywords patient movement ; mortality ; cancer ; income ; Medicine ; R
    Subject code 610
    Language English
    Publishing date 2021-04-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Fructose impairs fat oxidation: Implications for the mechanism of western diet-induced NAFLD.

    Inci, Mustafa Kutlu / Park, Se-Hyung / Helsley, Robert N / Attia, Suzanna L / Softic, Samir

    The Journal of nutritional biochemistry

    2022  Volume 114, Page(s) 109224

    Abstract: Increased fructose intake from sugar-sweetened beverages and highly processed sweets is a well-recognized risk factor for the development of obesity and its complications. Fructose strongly supports lipogenesis on a normal chow diet by providing both, a ... ...

    Abstract Increased fructose intake from sugar-sweetened beverages and highly processed sweets is a well-recognized risk factor for the development of obesity and its complications. Fructose strongly supports lipogenesis on a normal chow diet by providing both, a substrate for lipid synthesis and activation of lipogenic transcription factors. However, the negative health consequences of dietary sugar are best observed with the concomitant intake of a HFD. Indeed, the most commonly used obesogenic research diets, such as "Western diet", contain both fructose and a high amount of fat. In spite of its common use, how the combined intake of fructose and fat synergistically supports development of metabolic complications is not fully elucidated. Here we present the preponderance of evidence that fructose consumption decreases oxidation of dietary fat in human and animal studies. We provide a detailed review of the mitochondrial β-oxidation pathway. Fructose affects hepatic activation of fatty acyl-CoAs, decreases acylcarnitine production and impairs the carnitine shuttle. Mechanistically, fructose suppresses transcriptional activity of PPARα and its target CPT1α, the rate limiting enzyme of acylcarnitine production. These effects of fructose may be, in part, mediated by protein acetylation. Acetylation of PGC1α, a co-activator of PPARα and acetylation of CPT1α, in part, account for fructose-impaired acylcarnitine production. Interestingly, metabolic effects of fructose in the liver can be largely overcome by carnitine supplementation. In summary, fructose decreases oxidation of dietary fat in the liver, in part, by impairing acylcarnitine production, offering one explanation for the synergistic effects of these nutrients on the development of metabolic complications, such as NAFLD.
    MeSH term(s) Animals ; Humans ; Non-alcoholic Fatty Liver Disease/etiology ; Non-alcoholic Fatty Liver Disease/metabolism ; Fructose/metabolism ; PPAR alpha/metabolism ; Liver/metabolism ; Carnitine/metabolism ; Diet, Western/adverse effects ; Dietary Fats/pharmacology ; Diet, High-Fat
    Chemical Substances Fructose (30237-26-4) ; acylcarnitine ; PPAR alpha ; Carnitine (S7UI8SM58A) ; Dietary Fats
    Language English
    Publishing date 2022-11-18
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1014929-6
    ISSN 1873-4847 ; 0955-2863
    ISSN (online) 1873-4847
    ISSN 0955-2863
    DOI 10.1016/j.jnutbio.2022.109224
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Adipocyte-Derived PXR Signaling Is Dispensable for Diet-Induced Obesity and Metabolic Disorders in Mice.

    Wang, Fang / Liu, Jingwei / Hernandez, Rebecca / Park, Se-Hyung / Lai, Ying-Jing / Wang, Shuxia / Blumberg, Bruce / Zhou, Changcheng

    Drug metabolism and disposition: the biological fate of chemicals

    2023  Volume 51, Issue 9, Page(s) 1207–1215

    Abstract: Pregnane X receptor (PXR) is a xenobiotic receptor that can be activated by numerous chemicals including endogenous hormones, dietary steroids, pharmaceutical agents, and environmental chemicals. PXR has been established to function as a xenobiotic ... ...

    Abstract Pregnane X receptor (PXR) is a xenobiotic receptor that can be activated by numerous chemicals including endogenous hormones, dietary steroids, pharmaceutical agents, and environmental chemicals. PXR has been established to function as a xenobiotic sensor to coordinately regulate xenobiotic metabolism by regulating the expression of many enzymes and transporters required for xenobiotic metabolism. Recent studies have implicated a potentially important role for PXR in obesity and metabolic disease beyond xenobiotic metabolism, but how PXR action in different tissues or cell types contributes to obesity and metabolic disorders remains elusive. To investigate the role of adipocyte PXR in obesity, we generated a novel adipocyte-specific PXR deficient mouse model (PXR
    MeSH term(s) Male ; Mice ; Animals ; Pregnane X Receptor/metabolism ; Receptors, Steroid/genetics ; Receptors, Steroid/metabolism ; Xenobiotics/metabolism ; Obesity/etiology ; Obesity/metabolism ; Adipocytes/metabolism ; Insulin Resistance ; Diet, High-Fat/adverse effects
    Chemical Substances Pregnane X Receptor ; Receptors, Steroid ; Xenobiotics
    Language English
    Publishing date 2023-05-25
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 186795-7
    ISSN 1521-009X ; 0090-9556
    ISSN (online) 1521-009X
    ISSN 0090-9556
    DOI 10.1124/dmd.123.001311
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Erratum to: Non-nucleoside reverse transcriptase inhibitor efavirenz activates PXR to induce hypercholesterolemia and hepatic steatosis [J Hepatol (2019); 70 (5): 930-940].

    Gwag, Taesik / Meng, Zhaojie / Sui, Yipeng / Helsley, Robert N / Park, Se-Hyung / Wang, Shuxia / Greenberg, Richard N / Zhou, Changcheng

    Journal of hepatology

    2021  Volume 74, Issue 4, Page(s) 1003–1004

    Language English
    Publishing date 2021-01-30
    Publishing country Netherlands
    Document type Published Erratum
    ZDB-ID 605953-3
    ISSN 1600-0641 ; 0168-8278
    ISSN (online) 1600-0641
    ISSN 0168-8278
    DOI 10.1016/j.jhep.2021.01.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: Reply: Response to Significance of the Regular Publication of Statistics on National Health Indicators in Academic Journals and the Prospects of Korea National Antimicrobial Use Analysis System (KONAS).

    Kim, Bongyoung / Kim, Yong Chan / Kim, Hyung-Sook / Park, Se Yoon / Choi, Jun Yong

    Infection & chemotherapy

    2024  Volume 55, Issue 4, Page(s) 512–514

    Language English
    Publishing date 2024-01-05
    Publishing country Korea (South)
    Document type Letter
    ZDB-ID 2573798-3
    ISSN 2093-2340
    ISSN 2093-2340
    DOI 10.3947/ic.2023.0107
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Perinatal Bisphenol A Exposure Increases Atherosclerosis in Adult Male PXR-Humanized Mice.

    Sui, Yipeng / Park, Se-Hyung / Wang, Fang / Zhou, Changcheng

    Endocrinology

    2018  Volume 159, Issue 4, Page(s) 1595–1608

    Abstract: Bisphenol A (BPA) is a base chemical used extensively in numerous consumer products, and human exposure to BPA is ubiquitous. Higher BPA exposure has been associated with an increased risk of atherosclerosis and cardiovascular disease (CVD) in multiple ... ...

    Abstract Bisphenol A (BPA) is a base chemical used extensively in numerous consumer products, and human exposure to BPA is ubiquitous. Higher BPA exposure has been associated with an increased risk of atherosclerosis and cardiovascular disease (CVD) in multiple human population-based studies. However, the underlying mechanisms responsible for the associations remain elusive. We previously reported that BPA activates the xenobiotic receptor pregnane X receptor (PXR), which has proatherogenic effects in animal models. Because BPA is a potent agonist for human PXR but does not affect rodent PXR activity, a suitable PXR-humanized apolipoprotein E-deficient (huPXR•ApoE-/-) mouse model was developed to study BPA's atherogenic effects. Chronic BPA exposure increased atherosclerosis in the huPXR•ApoE-/- mice. We report that BPA exposure can also activate human PXR signaling in the heart tubes of huPXR•ApoE-/- embryos, and perinatal BPA exposure exacerbated atherosclerosis in adult male huPXR•ApoE-/- offspring. However, atherosclerosis development in female offspring was not affected by perinatal BPA exposure. Perinatal BPA exposure did not affect plasma lipid levels but increased aortic and atherosclerotic lesional fatty acid transporter CD36 expression in male huPXR•ApoE-/- offspring. Mechanistically, PXR epigenetically regulated CD36 expression by increasing H3K4me3 levels and decreasing H3K27me3 levels in the CD36 promoter in response to perinatal BPA exposure. The findings from the present study contribute to our understanding of the association between BPA exposure and increased atherosclerosis or CVD risk in humans, and activation of human PXR should be considered for future BPA risk assessment.
    MeSH term(s) Animals ; Aorta/drug effects ; Aorta/metabolism ; Apolipoproteins E/genetics ; Apolipoproteins E/metabolism ; Atherosclerosis/metabolism ; Benzhydryl Compounds/administration & dosage ; CD36 Antigens/genetics ; CD36 Antigens/metabolism ; Cholesterol/blood ; Environmental Pollutants/administration & dosage ; Gene Expression Regulation/drug effects ; Male ; Mice ; Mice, Knockout ; Phenols/administration & dosage ; Pregnane X Receptor ; Receptors, Steroid/metabolism ; Signal Transduction/drug effects
    Chemical Substances Apolipoproteins E ; Benzhydryl Compounds ; CD36 Antigens ; Environmental Pollutants ; Phenols ; Pregnane X Receptor ; Receptors, Steroid ; Cholesterol (97C5T2UQ7J) ; bisphenol A (MLT3645I99)
    Language English
    Publishing date 2018-03-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 427856-2
    ISSN 1945-7170 ; 0013-7227
    ISSN (online) 1945-7170
    ISSN 0013-7227
    DOI 10.1210/en.2017-03250
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Deficiency of Adipocyte IKKβ Affects Atherosclerotic Plaque Vulnerability in Obese LDLR Deficient Mice.

    Lu, Weiwei / Park, Se-Hyung / Meng, Zhaojie / Wang, Fang / Zhou, Changcheng

    Journal of the American Heart Association

    2019  Volume 8, Issue 12, Page(s) e012009

    Abstract: Background Obesity-associated chronic inflammation has been known to contribute to atherosclerosis development, but the underlying mechanisms remain elusive. Recent studies have revealed novel functions of IKK β (inhibitor of NF -κB [nuclear factor κB] ... ...

    Abstract Background Obesity-associated chronic inflammation has been known to contribute to atherosclerosis development, but the underlying mechanisms remain elusive. Recent studies have revealed novel functions of IKK β (inhibitor of NF -κB [nuclear factor κB] kinase β), a key coordinator of inflammation through activation of NF -κB, in atherosclerosis and adipose tissue development. However, it is not clear whether IKK β signaling in adipocytes can also affect atherogenesis. This study aims to investigate the impact of adipocyte IKK β expression on atherosclerosis development in lean and obese LDLR (low-density lipoprotein receptor)-deficient ( LDLR
    MeSH term(s) Adaptor Proteins, Signal Transducing/deficiency ; Adipocytes/enzymology ; Animals ; I-kappa B Kinase/deficiency ; Male ; Mice, Obese ; Plaque, Atherosclerotic/etiology
    Chemical Substances Adaptor Proteins, Signal Transducing ; Ldlrap1 protein, mouse ; I-kappa B Kinase (EC 2.7.11.10)
    Language English
    Publishing date 2019-06-15
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2653953-6
    ISSN 2047-9980 ; 2047-9980
    ISSN (online) 2047-9980
    ISSN 2047-9980
    DOI 10.1161/JAHA.119.012009
    Database MEDical Literature Analysis and Retrieval System OnLINE

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