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한주은,강경아 대한류마티스 건강전문학회 2000 근관절건강학회지 Vol.7 No.1
The arthritis patients suffer from psychological, social and spiritual problems as well as physical problems because the arthritis is not curable and has chronic pain, joint deformity, limitation of activity and physical dysfunction for all of his life. Especially if they do not fond the meaning in their lives, they will experience spiritual distress seriously. Therefore, it is important that nurses help the patients to find the meaning in their lives and to reduce spiritual distress. The purpose of this study is to provide a basis for nursing intervention strategies to minimize the arthritis patients' spiritual distress and understand the relationship between the meaning of life and the spiritual distress in arthritis patients. The samples were composed of 157 arthritis patients. Data collection was carried out from October 1, 1998 to February 28, 1999. Data were analyzed using a SAS Program for descriptive statistic, Pearson correlation, t-test, ANOVA, linear regression. The results were as follow, 1. The scores on the meaning of life scale ranged from 51 to 130 with a mean of 93. 2. The scores on the spiritual distress scale ranged from 26 to 91 with a mean of 60. 3. There were significant correlations between the meaning of life and the spiritual distress(r=.53, p=.00). 4. The linear regression analysis showed that the meaning of life explained 13% of the spiritual distress. 5. In the degree of the meaning of life and the spiritual distress according to the general characteristics, the level of the meaning of life in arthritis patients was different by the duration of incidence(F=2.71, p=.03). In conclusion, the nursing intervention strategies to reduce the spiritual distress in arthritis patients must take into account the meaning of life.
박영만,임영,강성규,김지홍,이종욱,최용휴,김경아 大韓産業醫學會 1999 대한직업환경의학회지 Vol.11 No.2
Aplastic anemia is characterized by pancytopenia with hypocellular bone marrow. Fifty percent of the cases are idiopathic and the rest are caused by various agents including drugs, chemicals, radiation and viruses. It is difficult to link specific etiologic agents, especially chemicals to the development of aplastic anemia because multiple or unknown exposures may be involved in. Benzene, a common industrial chemical and a component of gasoline, may lead progressively to pancytopenia, aplastic anemia and leukemia when exposed. A petrochemical worker with aplastic anemia was referred to our hospital to evaluate a relationship between the job history and the disease. He worked in the petrochemical plant for 21 years and was exposed to low-level benzene. There was not anyother etiologic agent except benzene and this is the case report of aplastic anemia which possibly due to benzene exposure.
Kang, Kyoung Ah,Piao, Mei Jing,Hyun, Yu Jae,Zhen, Ao Xuan,Cho, Suk Ju,Ahn, Mee Jung,Yi, Joo Mi,Hyun, Jin Won Nature Publishing Group UK 2019 Experimental and molecular medicine Vol.51 No.4
<▼1><P>Luteolin, a dietary flavone, modulates various signaling pathways involved in carcinogenesis. In this study, we investigated the molecular mechanism that underlies the apoptotic effects of luteolin mediated by DNA demethylation of the nuclear factor erythroid 2-related factor 2 (Nrf2) promoter and the interaction of Nrf2 and p53, a tumor suppressor, in human colon cancer cells. Luteolin increased the expression of apoptosis-related proteins and antioxidant enzymes. In DNA methylation, luteolin inhibited the expression of DNA methyltransferases, a transcription repressor, and increased the expression and activity of ten-eleven translocation (TET) DNA demethylases, a transcription activator. Methyl-specific polymerase chain reaction and bisulfite genomic sequencing indicated that luteolin decreased the methylation of the Nrf2 promoter region, which corresponded to the increased mRNA expression of Nrf2. In addition, luteolin increased TET1 binding to the Nrf2 promoter, as determined using a chromatin immunoprecipitation (ChIP) assay. TET1 knockdown decreased the percentages of luteolin-treated cells in sub-G<SUB>1</SUB> phase and cells with fragmented nuclei. Furthermore, complex formation between p53 and Nrf2 was involved in the apoptotic effects of luteolin. These results provide insight into the mechanism that underlies the anticancer effects of luteolin on colon cancer, which involve the upregulation of Nrf2 and its interaction with the tumor suppressor.</P></▼1><▼2><P><B>Cancer: Cell-killing plant compound exerts antioxidant effects</B></P><P>A molecule found in fruits, vegetables and herbs helps kill colon cancer cells by activating a master regulator of detoxifying enzymes. Jin Won Hyun from Jeju National University School of Medicine in South Korea and colleagues treated human colon cancer cells with luteolin, a molecule that occurs naturally in many food plants. They showed that luteolin increased the levels of proteins involved in cell death and antioxidant responses by causing DNA-modifying enzymes to strip suppressive chemical markers off the gene encoding Nrf2, a protein that regulates antioxidant effects. Nrf2 levels subsequently increased and the protein interacted with the tumor suppressor p53 to facilitate destruction of the colon cancer cells. The findings offer a mechanistic basis for using luteolin to help prevent and treat cancer.</P></▼2>
Luteolin induces apoptotic cell death via antioxidant activity in human colon cancer cells
Kang, Kyoung Ah,Piao, Mei Jing,Ryu, Yea Seong,Hyun, Yu Jae,Park, Jeong Eon,Shilnikova, Kristina,Zhen, Ao Xuan,Kang, Hee Kyoung,Koh, Young Sang,Jeong, Yong Joo,Hyun, Jin Won Spandidos Publications 2017 International journal of oncology Vol.51 No.4
<P>The present study determined whether luteolin induces HT-29 colon cancer cell death through an antioxidant effect such as the activation of antioxidant enzymes. Luteolin decreased cell viability in human colon cancer cells (HT-29), whereas it had no effect on normal colon cells (FHC). Luteolin induced apoptosis by activating the mitochondria-mediated caspase pathway in HT-29 cells. Luteolin caused loss of the mitochondrial membrane action potential, increased mitochondrial Ca2+ level, upregulated Bax, downregulated Bcl-2, induced the release of cytochrome c from mitochondria to the cytosol, and increased the levels of the active forms of caspase-9 and caspase-3. Luteolin-induced apoptosis was accompanied by the activation of intracellular and mitochondrial reactive oxygen species scavenging through the activation of antioxidant enzymes, such as superoxide dismutase and catalase in HT-29 cells. Luteolin increased the level of reduced glutathione (GSH) and the expression of GSH synthetase, which catalyzes the second step of GSH biosynthesis. The apoptotic effect of luteolin was mediated by the activation of the mitogen-activated protein kinase signaling pathway. The present results indicate that luteolin induces apoptosis by promoting antioxidant activity and activating MAPK signaling in human colon cancer cells.</P>
Oxidative Stress, Nrf2, and Epigenetic Modification Contribute to Anticancer Drug Resistance
Kang, Kyoung Ah,Hyun, Jin Won Korean Society of ToxicologyKorea Environmental Mu 2017 Toxicological Research Vol.33 No.1
Nuclear factor E2-related factor 2 (Nrf2), a transcription factor, controls the expression of genes encoding cytoprotective proteins, including antioxidant enzymes that combat oxidative and electrophilic stress to maintain redox homeostasis. However, recent studies demonstrated that, in cancer, aberrant activation of Nrf2 by epigenetic alterations promotes high expression of cytoprotective proteins, which can decrease the efficacy of anticancer drugs used for chemotherapy. In this review, we summarize recent findings regarding the relationship between oxidative stress, Nrf2, epigenetic modification, and anticancer drug resistance, which should aid in development of new strategies to improve chemotherapeutic efficacy.
Cytoprotective Effects of KIOM-79 on Streptozotocin Induced Cell Damage by Inhibiting ERK and AP-1
Kang, Kyoung Ah,Lee, Kyoung Hwa,Kim, So Young,Kim, Hee Sun,Kim, Jin Sook,Hyun, Jin Won Pharmaceutical Society of Japan 2007 Biological & pharmaceutical bulletin Vol.30 No.5
<P>The present study investigated the potential cytoprotective properties of a combination of plant extracts (KIOM-79) obtained from <I>Magnolia officinalis</I>, <I>Pueraria lobata</I>, <I>Glycyrrhiza uralensis</I>, and <I>Euphorbia pekinensis</I>, against the oxidative stresses induced by streptozotocin (STZ) in a rat pancreatic β-cells (RINm5F). KIOM-79 was found to scavenge intracellular reactive oxygen species (ROS), thereby preventing DNA damage and lipid peroxidation. The KIOM-79 inhibited apoptosis of the β-cells exposed to STZ <I>via</I> radical scavenging activity and activation of antioxidant enzymes. KIOM-79 inhibited activation of extracellular regulated kinase (ERK) induced by STZ and inhibited DNA binding activity of an activator protein-1 (AP-1), a downstream transcription factor of ERK. Taken together, these findings suggest that KIOM-79 protects against STZ induced cell death in RINm5F cells by inhibiting ROS generation and the ERK pathway.</P>
Cytotoxic Effect of 7β-Hydroxycholesterol on Human NCI-H460 Lung Cancer Cells
Kang, Kyoung Ah,Chae, Sungwook,Lee, Kyoung Hwa,Park, Moon Taek,Lee, Su Jae,Lee, Yun Sil,Hyun, Jin Won Pharmaceutical Society of Japan 2005 Biological & pharmaceutical bulletin Vol.28 No.8
<P>The cytotoxic activity of 7β-hydroxycholesterol (7β-OHC) was evaluated on human NCI-H460 lung cancer cells. 7β-OHC decreased clonogenic survival of NCI-H460 in a dose dependent pattern. 7β-OHC induced apoptosis in NCI-H460, with the characteristic features like increase in sub-G<SUB>1</SUB> hypodiploid (apoptotic) cells, and apoptotic body formation, as evidenced by flow cytometry and fluorescence microscope, respectively. Apoptosis was also associated with loss of mitochondrial transmembrane potential, and the activation of caspases 9 and 3. 7β-OHC resulted in generation of reactive oxygen species (ROS) during apoptosis. On the whole, the results indicated that 7β-OHC inhibited the proliferation of NCI-H460 cells through apoptosis <I>via</I> caspase activation.</P>
Kang, Kyoung-Ah,Zhang, Rui,Piao, Mei-Jing,Park, Min-Jeong,Kwon, Ae-Ran,Kim, Bum-Joon,You, Ho-Jin,Chung, Myung-Hee,Hyun, Jin-Won Korean Society for Biotechnology and Bioengineerin 2007 Biotechnology and Bioprocess Engineering Vol.12 No.2
8-Hydroxydeoxyguanosine $(oh^8dG)$ treatment induced senescence-like changes in KG-1 cells, a human acute myelocytic leukemia cell line. The $oh^8dG-treated$ cells stained positive for senescence associated ${\beta}-galactosidase$ $(SA-{\beta}-galactosidase)$ and had enlarged cell shape, both of which are senescence indexes. The $oh^8dG-treated$ cells were also cell growth inhibited and arrested at $G_1$ in the cell cycle. The accumulation of cdk (cyclin dependent kinase) inhibitors, such as p16, p21, and p27, also implies that cellular senescence was induced in $oh^8dG-treated$ cells. However, these changes were not accompanied by cell differentiation or telomerase activity. Taken together, we conclude that $oh^8dG$ treatment of KG-1 cells induces cellular senescence.