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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,Lee, Kyoung Hwa,Chae, Sungwook,Zhang, Rui,Jung, Myung Sun,Ham, Young Min,Baik, Jong Seok,Lee, Nam Ho,Hyun, Jin Won Wiley Subscription Services, Inc., A Wiley Company 2006 Journal of cellular biochemistry Vol.97 No.3
<P>We investigated the cytoprotective effect of phloroglucinol, which was isolated from Ecklonia cava (brown alga), against oxidative stress induced cell damage in Chinese hamster lung fibroblast (V79-4) cells. Phloroglucinol was found to scavenge 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical, hydrogen peroxide (H<SUB>2</SUB>O<SUB>2</SUB>), hydroxy radical, intracellular reactive oxygen species (ROS), and thus prevented lipid peroxidation. As a result, phloroglucinol reduced H<SUB>2</SUB>O<SUB>2</SUB> induced apoptotic cells formation in V79-4 cells. In addition, phloroglucinol inhibited cell damage induced by serum starvation and radiation through scavenging ROS. Phloroglucinol increased the catalase activity and its protein expression. In addition, catalase inhibitor abolished the protective effect of phloroglucinol from H<SUB>2</SUB>O<SUB>2</SUB> induced cell damage. Furthermore, phloroglucinol increased phosphorylation of extracellular signal regulated kinase (ERK). Taken together, the results suggest that phloroglucinol protects V79-4 cells against oxidative damage by enhancing the cellular catalase activity and modulating ERK signal pathway. © 2005 Wiley-Liss, Inc.</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.
Kang, Kyoung Ah,Wang, Zhi Hong,Zhang, Rui,Piao, Mei Jing,Kim, Ki Cheon,Kang, Sam Sik,Kim, Young Woo,Lee, Jongsung,Park, Deokhoon,Hyun, Jin Won Molecular Diversity Preservation International (MD 2010 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.11 No.11
<P>Recently, we demonstrated that myricetin exhibits cytoprotective effects against H<SUB>2</SUB>O<SUB>2</SUB>-induced cell damage via its antioxidant properties. In the present study, myricetin was found to inhibit H<SUB>2</SUB>O<SUB>2</SUB>-induced apoptosis in Chinese hamster lung fibroblast (V79-4) cells, as shown by decreased apoptotic bodies, nuclear fragmentation, sub-G<SUB>1</SUB> cell population, and disruption of mitochondrial membrane potential (Δψ<I><SUB>m</SUB></I>), which are increased in H<SUB>2</SUB>O<SUB>2</SUB>-treated cells. Western blot data showed that in H<SUB>2</SUB>O<SUB>2</SUB>-treated cells, myricetin increased the level of Bcl-2, which is an anti-apoptotic factor, and decreased the levels of Bax, active caspase-9 and -3, which are pro-apoptotic factors. And myricetin inhibited release of cytochrome c from mitochondria to cytosol in H<SUB>2</SUB>O<SUB>2</SUB>-treated cells. Myricetin-induced survival correlated with Akt activity, and the rescue of cells by myricetin treatment against H<SUB>2</SUB>O<SUB>2</SUB>-induced apoptosis was inhibited by the specific PI3K (phosphoinositol-3-kinase) inhibitor. Myricetin-mediated survival also inhibited the activation of p38 mitogen activated protein kinase (MAPK) and c-Jun <I>N</I>-terminal kinase (JNK), which are members of MAPK. Our studies suggest that myricetin prevents oxidative stress-induced apoptosis via regulation of PI3K/Akt and MAPK signaling pathways.</P>
KANG, Kyoung Ah,ZHANG, Rui,LEE, Kyoung Hwa,CHAE, Sungwook,KIM, Bum Joon,KWAK, Young Sook,PARK, Jae Woo,LEE, Nam Ho,HYUN, Jin Won JAPAN RADIATION RESEACH SOCIETY 2006 JOURNAL OF RADIATION RESEARCH Vol.47 No.1
<P>We studied the cytoprotective effect of triphlorethol-A against γ-ray radiation- induced oxidative stress. In this study, hydrogen peroxide, which is a reactive oxygen species (ROS), was detected using 2',7'-dichlorodihydrofluorescein diacetate (DCF-DA) assay. Triphlorethol-A reduced intracellular hydrogen peroxide generated by γ-ray radiation. This compound provided protection against radiation-induced membrane lipid peroxidation and cellular DNA damage which are the main targets of radiation-induced damage. Triphlorethol-A protected the cell viability damaged by the radiation through inhibition of apoptosis. Triphlorethol-A reduced the expression of bax and activated caspase 3 induced by radiation, but recovered the expression of bcl-2 decreased by radiation. Taken together, the results suggest that triphlorethol-A protects cells against oxidative damage induced by radiation through reducing ROS.</P>
Involvement of heme oxygenase-1 in Korean colon cancer.
Kang, Kyoung Ah,Maeng, Young Hee,Zhang, Rui,Yang, Young Ro,Piao, Mei Jing,Kim, Ki Cheon,Kim, Gi Young,Kim, Young Ree,Koh, Young Sang,Kang, Hee Kyoung,Hyun, Chang Lim,Chang, Weon Young,Hyun, Jin Won Saikon Pub. Co 2012 TUMOR BIOLOGY Vol.33 No.4
<P>Heme oxygenase-1 (HO-1) catabolizes heme into carbon monoxide, biliverdin, and free iron which mediate its protective effect against oxidative stress. The aim of the present study was to determine the expression level and activity of HO-1 in Korean colon cancer tissues and cell lines. HO-1 protein expression was higher (>1.5-fold) in tumor tissues than in adjacent normal tissues in 14 of 20 colon cancer patients, and HO-1 protein expression was closely correlated with HO-1 enzyme activity in cancer tissues. Immunohistochemical data confirmed that HO-1 protein was expressed at a higher level in colon cancer tissues than in normal mucosa. Furthermore, HO-1 mRNA and protein expression and enzyme activity were higher in the colon cancer cell lines Caco-2, SNU-407, SNU-1033, HT-29, and SW-403 than in the normal fetal human colon cell line FHC. Treatment with the HO-1 inhibitor zinc protoporphyrin decreased the viability of colon cancer cell lines. These data indicate that HO-1 may serve as a clinically useful biomarker of colon cancer and as a target for anticolon cancer drugs.</P>
Kang Kyoung-Ah,Lee Kyoung-Hwa,Chae Sung-Wook,Kim Jeong-Ki,Seo Jung-Yeon,Ham Yong-Ho,Lee Kee-Ho,Kim Bum-Joon,Kim Hee-Sun,Kim Dong-Hyun,Hyun Jin Won The Korean Society for Biotechnology and Bioengine 2006 Biotechnology and Bioprocess Engineering Vol.11 No.1
Telomerase activation is detected in most cancerous cells; hence, telomerase is a highly selective target for cancer therapy, which plays an important role in the apoptotic process. We have previously reported that the ginseng saponin metabolite, Compound K (20-O-D-glucopyranosyl-20(S)-protopanaxadiol, IH901), inhibits cell proliferation by inducing apoptosis and cell cycle arrest at the $G_1$ phase. The present study investigated the regulation of telomerase activity in Compound K treated U937 cells. Compound K treatment caused a reduction in telomerase activity and down-regulated the human telomerase reverse transcriptase (hTERT) gene, resulting in the decreased expressions of its protein, and of the c-Myc and Spl proteins (transcription factors of hTERT). These results indicate that the anticancer activity of Compound K could be mediated by inhibition of the telomerase activity.
Kang, Kyoung Ah,Zhang, Rui,Piao, Mei Jing,Lee, Kyoung Hwa,Kim, Bum Joon,Kim, So Young,Kim, Hee Sun,Kim, Dong Hyun,You, Ho Jin,Hyun, Jin Won Informa Healthcare 2007 Free radical research Vol.41 No.6
<P> The present study investigated the cytoprotective properties of glycitein, a metabolite formed by the transformation of glycitin by intestinal microflora, against oxidative stress. Glycitein was found to scavenge intracellular reactive oxygen species (ROS), and 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical, and thereby preventing lipid peroxidation and DNA damage. Glycitein inhibited apoptosis of Chinese hamster lung fibroblast (V79-4) cells exposed to hydrogen peroxide (H2O2) via radical scavenging activity. Glycitein abrogated the activation of c-Jun N-terminal kinase (JNK) induced by H2O2 treatment and inhibited DNA binding activity of activator protein-1 (AP-1), a downstream transcription factor of JNK. Taken together, these findings suggest that glycitein protected H2O2 induced cell death in V79-4 cells by inhibiting ROS generation and JNK activation.</P>