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203 results on '"Yoo, Jung-Yoon"'

6. Relationship Between Asymptomatic Hyperuricemia and the Hypertriglyceridemic-Waist Phenotype in Korean Adults: A Cross-Sectional Study

Author

Oh,Ji-Eun, Yu,Sung Ryul, Yoo,Jung-Yoon, Shin,Kyung-A, Oh,Ji-Eun, Yu,Sung Ryul, Yoo,Jung-Yoon, and Shin,Kyung-A

Abstract

Ji-Eun Oh,1 Sung Ryul Yu,2 Jung-Yoon Yoo,3,* Kyung-A Shin4,* 1Department of Biomedical Laboratory Science, Far East University, Eumseong, Republic of Korea; 2Department of Clinical Laboratory Science, Semyung University, Jecheon, Republic of Korea; 3Department of Biomedical Laboratory Science, Yonsei University MIRAE Campus, Wonju-si, Republic of Korea; 4Department of Clinical Laboratory Science, Shinsung University, Dangjin, Republic of Korea*These authors contributed equally to this workCorrespondence: Kyung-A Shin, Department of Clinical Laboratory Science, Shinsung University, Daehak-ro 1, Jeongmi-myeon, Dangjin, Chungnam, 31801, Republic of Korea, Tel +82-41-350-1408, Fax +82-41-350-1045, Email mobitz2@hanmail.net Jung-Yoon Yoo, Department of Biomedical Laboratory Science, Yonsei University MIRAE Campus, 1 Yonseidae-gil, Wonju-si, Gangwon-do, 26493, Republic of Korea, Tel +82-33-760-2861, Fax +82-33-760-2561, Email jy_yoo@yonsei.ac.krPurpose: Visceral fat accumulation can negatively affect uric acid metabolism in healthy adults. The hypertriglyceridemic-waist (HTGW) phenotype is a predictor of diabetes and cardiometabolic risk. This study aimed to investigate the association between the HTGW phenotype and asymptomatic hyperuricemia in Korean adults.Patients and Methods: The study included 23,240 adults, aged 20– 80 years who underwent comprehensive health examinations at a general hospital in Gyeonggi Province, Korea, from January 2020 to December 2022. The HTGW phenotype was defined as the simultaneous presence of elevated serum triglyceride (TG) levels and increased waist circumference (WC). The diagnostic capability of the HTGW phenotype for hyperuricemia and its association with the condition were assessed using the receiver operating characteristic (ROC) curve and logistic regression analysis.Results: The prevalence of hyperuricemia in the HTGW phenotype was 3.44 times higher than that in the normal TG normal waist (NTNW) phenotyp

Published
2024

10. Promotion of Colitis in B Cell-Deficient C57BL/6 Mice Infected with Enterotoxigenic Bacteroides fragilis.

Author

Jo, Minjeong, Hwang, Soonjae, Lee, Chang-Gun, Hong, Ju-Eun, Kang, Da-Hye, Yoo, Sang-Hyeon, Kim, Woo-Seung, Yoo, Jung-Yoon, and Rhee, Ki-Jong

Subjects
INFLAMMATORY bowel diseases, BACTEROIDES fragilis, LABORATORY mice, COLITIS, ENTERITIS, LARGE intestine, WEIGHT loss
Abstract

Enterotoxigenic Bacteroides fragilis (ETBF) causes colitis and is implicated in inflammatory bowel diseases and colorectal cancer. The ETBF-secreted B. fragilis toxin (BFT) causes cleavage of the adherence junction, the E-cadherin, resulting in the large intestine showing IL-17A inflammation in wild-type (WT) mice. However, intestinal pathology by ETBF infection is not fully understood in B-cell-deficient mice. In this study, ETBF-mediated inflammation was characterized in B-cell-deficient mice (muMT). WT or muMT C57BL/6J mice were orally inoculated with ETBF and examined for intestinal inflammation. The indirect indicators for colitis (loss of body weight and cecum weight, as well as mortality) were increased in muMT mice compared to WT mice. Histopathology and inflammatory genes (Nos2, Il-1β, Tnf-α, and Cxcl1) were elevated and persisted in the large intestine of muMT mice compared with WT mice during chronic ETBF infection. However, intestinal IL-17A expression was comparable between WT and muMT mice during infection. Consistently, flow cytometry analysis applied to the mesenteric lymph nodes showed a similar Th17 immune response in both WT and muMT mice. Despite elevated ETBF colonization, the ETBF-infected muMT mice showed no histopathology or inflammation in the small intestine. In conclusion, B cells play a protective role in ETBF-induced colitis, and IL-17A inflammation is not attributed to prompted colitis in B-cell-deficient mice. Our data support the fact that B cells are required to ameliorate ETBF infection-induced colitis in the host. [ABSTRACT FROM AUTHOR]

Published
2024
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13. Supplementary Figures from EPB41L5 Mediates TGFβ-Induced Metastasis of Gastric Cancer

Author

Jeong, Mi-Hyeon, primary, Park, Soo-Yeon, primary, Lee, Seung-Hyun, primary, Seo, JaeSung, primary, Yoo, Jung-Yoon, primary, Park, Seung-Ho, primary, Kim, Mi Jeong, primary, Lee, SooYeon, primary, Jang, Subhin, primary, Choi, Hyo-Kyoung, primary, Lee, Jae Eun, primary, Shin, Su-Jin, primary, Choi, Kyung-Chul, primary, Cheong, Jae-Ho, primary, and Yoon, Ho-Geun, primary

Published
2023
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22. Human induced pluripotent stem cell line YCMi007-A generated from a dilated cardiomyopathy patient with a heterozygous dominant c.613C > T (p. Arg205Trp) variant of the TNNT2 gene

Author

Jeon, Sae-Bom, primary, Kim, Hyoeun, additional, Chun, Kyeong-Hyeon, additional, Oh, Jaewon, additional, Kwon, Chulan, additional, Choi, Hyo-Kyoung, additional, Kim, Sangwoo, additional, Kim, Hyoung-Pyo, additional, Kim, In-Cheol, additional, Yoo, Jung-Yoon, additional, Park, Sahng Wook, additional, Kang, Seok-Min, additional, and Lee, Seung-Hyun, additional

Published
2023
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28. Feature Based Extended Target Tracking Using Automotive 2D LIDAR

Author

Hyung-Chan Cho, Seul-Ki Han, Yoo-Jung Yoon, Dahye Ham, and Won-Sang Ra

Subjects
Lidar, business.industry, Computer science, Feature based, Automotive industry, Computer vision, Artificial intelligence, Electrical and Electronic Engineering, business, Tracking (particle physics)
Published
2021

31. Genetic and epigenetic changes in the eutopic endometrium of women with endometriosis: association with decreased endometrial αvβ3 integrin expression

Author

Joshi, Niraj R, primary, Kohan-Ghadr, Hamid-Reza, additional, Roqueiro, Damian S, additional, Yoo, Jung Yoon, additional, Fru, Karenne, additional, Hestermann, Eli, additional, Yuan, Lingwen, additional, Ho, Shuk-Mei, additional, Jeong, Jae-Wook, additional, Young, Steven L, additional, Lessey, Bruce A, additional, and Fazleabas, Asgerally T, additional

Published
2021
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32. Mitochondrial tumor suppressor 1 is a target of AT-rich interactive domain 1A and progesterone receptor in the murine uterus

Author

Chang, Hye Jin, Teasley, Hanna E., Yoo, Jung-Yoon, Kim, Tae Hoon, and Jeong, Jae-Wook

Subjects
0301 basic medicine, AT-rich Interactive Domain 1A (ARID1A), ARID1A, medicine.drug_class, Progesterone Receptor, lcsh:Animal biochemistry, Uterus, Biology, Article, law.invention, Andrology, 03 medical and health sciences, law, Progesterone receptor, medicine, lcsh:QP501-801, Mitochondrial Tumor Suppressor 1 (MTUS1), lcsh:SF1-1100, Estrogen, Reverse transcription polymerase chain reaction, 030104 developmental biology, medicine.anatomical_structure, Animal Reproduction and Physiology, Suppressor, Immunohistochemistry, Animal Science and Zoology, lcsh:Animal culture, Food Science, Hormone
Abstract

Objective Progesterone receptor (PGR) and AT-rich interactive domain 1A (ARID1A) have important roles in the establishment and maintenance of pregnancy in the uterus. In present studies, we examined the expression of mitochondrial tumor suppressor 1 (MTUS1) in the murine uterus during early pregnancy as well as in response to ovarian steroid hormone treatment. Methods We performed quantitative reverse transcription polymerase chain reaction and immunohistochemistry analysis to investigate the regulation of MTUS1 by ARID1A and determined expression patterns of MTUS1 in the uterus during early pregnancy. Results The expression of MTUS1 was detected on day 0.5 of gestation (GD 0.5) and then gradually increased until GD 3.5 in the luminal and glandular epithelium. However, the expression of MTUS1 was significantly reduced in the uterine epithelial cells of Pgrcre/+Arid1af/f and Pgr knockout (PRKO) mice at GD 3.5. Furthermore, MTUS1 expression was remarkably induced after P4 treatment in the luminal and glandular epithelium of the wild-type mice. However, the induction of MTUS1 expression was not detected in uteri of Pgrcre/+Arid1af/f or PRKO mice treated with P4. Conclusion These results suggest that MTUS1 is a novel target gene by ARID1A and PGR in the uterine epithelial cells.

Published
2018

39. EPB41L5 Mediates TGFβ-Induced Metastasis of Gastric Cancer

Author

Jeong, Mi-Hyeon, primary, Park, Soo-Yeon, additional, Lee, Seung-Hyun, additional, Seo, JaeSung, additional, Yoo, Jung-Yoon, additional, Park, Seung-Ho, additional, Kim, Mi Jeong, additional, Lee, SooYeon, additional, Jang, Subhin, additional, Choi, Hyo-Kyoung, additional, Lee, Jae Eun, additional, Shin, Su-Jin, additional, Choi, Kyung-Chul, additional, Cheong, Jae-Ho, additional, and Yoon, Ho-Geun, additional

Published
2019
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45. Protein Inhibitor of Activated STAT3 (PIAS3) Is Down-Regulated in Eutopic Endometrium of Women with Endometriosis1

Author

Yoo, Jung-Yoon, Jeong, Jae-Wook, Fazleabas, Asgerally T., Tayade, Chandrakant, Young, Steven L., and Lessey, Bruce A.

Subjects
STAT3 Transcription Factor, Endometrium, Interferon-gamma, Disease Progression, Endometriosis, Animals, Down-Regulation, Humans, Female, Articles, Phosphorylation, Protein Inhibitors of Activated STAT, Papio
Abstract

Endometriosis is a major cause of chronic pelvic pain and infertility. Activation of STAT3 appears central to the inflammatory phenotype of eutopic endometrium in women with endometriosis. However, the molecular mechanism by which this occurs remains unknown. Our objective is to determine how STAT3 activity is regulated in endometriosis. Protein inhibitor of activated STAT3 (PIAS3) is a negative regulator of STAT3 activity. We examined the levels of PIAS3 in endometrium from women with and without endometriosis using Western blot analysis and immunohistochemistry. Levels of PIAS3 are significantly lower, in contrast with phosphorylation of STAT3, in women with endometriosis compared to women without endometriosis. Furthermore, induction of endometriosis in the baboon showed a significant reduction of PIAS3 expression during the progression of the disease. Interferon-γ (INFγ) reduces PIAS3 protein levels and increases phospho-STAT3 levels through CXCL10 in endometrial cells, Ishikawa, and 12Z cells. These results suggest that attenuation of PIAS3 causes aberrant activation of STAT3 in endometriosis, leading to inflammatory changes that may impair fertility or cause pain.

Published
2016

49. Serine/threonine kinase 31 promotes PDCD5‐mediated apoptosis in p53‐dependent human colon cancer cells.

Author

Kwak, Sungmin, Lee, Seung‐Hyun, Han, Eun‐Jung, Park, Soo‐Yeon, Jeong, Mi‐Hyeon, Seo, Jaesung, Park, Seung‐Ho, Sung, Gi‐Jun, Yoo, Jung‐Yoon, Yoon, Ho‐Geun, and Choi, Kyung‐Chul

Subjects
SERINE/THREONINE kinases, APOPTOSIS, COLON cancer, ETOPOSIDE, CANCER cells
Abstract

Although programed cell death 5 (PDCD5) is an important protein in p53‐mediated proapoptotic signaling, very little is known about PDCD5‐related cell death. In this study, we report that serine/threonine kinase 31 (STK31) interacts with PDCD5, which maintains the stability of PDCD5. STK31 overexpression significantly activated PDCD5 stabilization and p53‐mediated apoptosis in response to etoposide (ET). However, STK31 knockdown did not enhance apoptosis by ET treatment. Moreover, when STK31 was depleted, PDCD5 inhibited the activation of the p53 signaling pathway with ET, indicating that the PDCD5–STK31 network has an essential role in p53 activation. Importantly, STK31 activated the p53 signaling pathway by genotoxic stress through positive regulation of PDCD5‐mediated apoptosis. We thus demonstrated that overexpression of STK31 greatly inhibited tumorigenic growth and increased the chemosensitivity of HCT116 human colorectal carcinoma cells. Taken together, these findings demonstrate that the STK31–PDCD5 complex network regulates apoptosis of cancer cells, and STK31 is a positive apoptosis regulator that inhibits tumorigenesis of colon cancer cells by inducing PDCD5‐mediated apoptosis in response to genotoxic stress. STK31 stabilizes PDCD5 proteins by genotoxic stress. STK31 promotes p53‐mediated apoptosis via PDCD5. Knockdown of STK31 reduces the levels of PDCD5 and p53. STK31 reduces the tumorigenicity of colon cancer cells. [ABSTRACT FROM AUTHOR]

Published
2019
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