Annals of Occupational and Environmental Medicine

Gyung Jae Oh

5 Articles

The Prevalence of Musculoskeletal Symptoms and the Ergonomic Risk Factors among Oriental Melon-growing Farmers: Kyu Jung Bae, Kyoung Sook Lee, Yong Ku Kong, Gyung Jae Oh, Soo Jin Lee; Korean Journal of Occupational and Environmental Medicine 2011;23(1):1-8. Published online March 31, 2011; DOI: https://doi.org/10.35371/kjoem.2011.23.1.1

OBJECTIVES
The purpose of this study was to investigate the prevalence of musculoskeletal symptoms in oriental melon-growing farmers and to evaluate the ergonomic risk factors of melon cultivation.
METHODS
The study included 217 subjects growing oriental melons mainly in 3 villages. Subjects were interviewed by means of a structured questionnaire. Instruments used the general features and symptom table of NIOSH to evaluate tasks using ergonomic tools (REBA, OWAS).
RESULTS
A total of 202 final respondents answered. The prevalence of musculoskeletal symptoms based on the NIOSH standard criteria was 162 (75.2%). The prevalence per body part for lower back, knee and shoulder were 102 (50.5%), 86 (42.6%) and 71 (35.1%), respectively. The prevalence of pain complaints of the musculoskeletal symptom was 91 (45.0%). The prevalence of complaints per body part of lower back, knee and shoulder were 54 (26.7%), 41 (20.3%) and 37 (18.3%), respectively. Logistic regression analysis showed men were at higher risk compared to women (OR=2.409, 95% CI=1.071~5.389), and ore than 30 years of work having a higher risk compared to less than 30 years of work (OR=2.445, 95% CI=1.150~5.197). High risk tasks were moving around boxes and nursery plants for planting, transplanting nursery plants, and picking melons.
CONCLUSIONS
Musculoskeletal symptoms were very highly prevalent in oriental melon-growing farmers, showing up in 75.2% of cases. They were exposed to ergonomic high risk factors such as squatting. These risk factors must be improved in some way.

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Effects of Growth and Quantity according to Form of High Bed in Cultivation of Korean Melon
Do Yeon Won, Ji Hye Choi, Chang Hyeon Baek, Na Yun Park, Min Gu Kang, Young Jin Seo
Journal of Bio-Environment Control.2023; 32(4): 513. CrossRef
Evaluation of the prevalence of musculoskeletal symptoms, presumptive diagnosis, medical care use, and sick leave among female school meal service workers
Young Hoon Moon, Young Joon Yang, Sang Yoon Do, Jae Yoon Kim, Chul Gab Lee, Hong Jae Chae, Soo Hyeon Kim, Han Soo Song
Annals of Occupational and Environmental Medicine.2019;[Epub] CrossRef
Analysis of Working Posture for Construction Workers Using OWAS Method
Ran-i Eom, Yejin Lee
Fashion & Textile Research Journal.2018; 20(6): 704. CrossRef
Workers’ experiences with compensated sick leave due to musculoskeletal disorder: a qualitative study
Min Choi, Hyoung-Ryoul Kim, Jinwoo Lee, Hye-Eun Lee, Junsu Byun, Jong Uk Won
Annals of Occupational and Environmental Medicine.2014;[Epub] CrossRef
Development of Oriental Melon Harvesting Robot in Greenhouse Cultivation
Yu Shin Ha, Tae Wook Kim
Protected horticulture and Plant Factory.2014; 23(2): 123. CrossRef
Work-related Musculoskeletal Disorders among Agricultural Workers
Soo-Jin Lee, Hwan-Jin Park
Journal of the Ergonomics Society of Korea.2011; 30(4): 525. CrossRef

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E ffect of Nitric Oxide (NO) or Hydrogen Peroxide (H2O2) in the Nickel Induced cytotoxicity in RAW 264.7 Cell: Gyung Jae Oh, Keun Sang Kwon; Korean Journal of Occupational and Environmental Medicine 2003;15(1):61-71. Published online March 31, 2003; DOI: https://doi.org/10.35371/kjoem.2003.15.1.61

Abstract PDF: OBJECTIVES
Nickel (Ni) is present in many industrial working environments and consumer products, and is one of the leading cause of allergic contact dermatitis, which is a typical delayed (type IV) hypersensitivity reaction. However, the mechanism by which nickel causes this pathology is not well known. The contact dermatitis induced by nickel is mediated, primarily, through macrophages. This property was similar to autotoxicity related nitric oxide (NO) production. NO mediated cytotoxicity was dependent on both H2O2 and peroxynitrite (OONO-). The purpose of this study was to elucidate the role of NO/H2O2 in the cytotoxicity induced by nickel. Therefore, this study was designed to examine whether nickel could modulate NO/H2O2 production and how the Ni may affect ATP production, intracellular GSH level, and cell viability.
METHODS
This study was based on the observations of cultures of RAW 264.7 cells, which originated from a tumor in a Balb/c mouse that had been induced by the Abelson murine leukemia virus. RAW 264.7 cells were treated with either Ni, N- onomethyl-L- arginine (NMLA), catalase, and DTT for 24-72 h. The cytotoxicity of the nickel was measured via the cell viability and NO2-, H2O2, GSH, and the mitochondrial function was evaluated by the adenosine triphosphate (ATP) production in the RAW 264.7 cells.
RESULTS
The NO2- synthesis of RAW 264.7 cells increased with the increase in concentrations of Ni up to 50-micrometer, after 24 and 48 h of exposure, but then decreased at concentrations greater than 50-micrometer, and with time periods exceeding 48 h. In contrast, viability of cells and intracellular GSH level decreased in the presence of Ni in a dose and time dependent manner. However, the H2O2 synthesis of RAW 264.7 cells was not changed in the all experimental conditions. The NO2- synthesis of the cells was higher than control, whereas ATP, GSH and viability were lower than control in addition of Ni and the pretreatment of catalase or DTT prior to addition of Ni.
CONCLUSIONS
These results suggest that NO plays an important role in the cytotoxicity of Ni. Cytotoxicity of Ni may exert through modulation of NO production and associate with a decrease in intracellular GSH levels.

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Cadmium-induced Apoptosis in HL-60 Cells Via Signal Transduction: Nam Song Kim, Gyung Jae Oh, Kwang Ho Cho, Mee Sun Hyun, Yoo Chang Kim, Tae Ho Sung, Jung Ho Youm, Keun Sang Kwon; Korean Journal of Occupational and Environmental Medicine 2002;14(1):1-12. Published online March 31, 2002; DOI: https://doi.org/10.35371/kjoem.2002.14.1.1

Abstract PDF

OBJECTIVES
Apoptosis is a process of active cell death, distinct from necrosis and characterized by specific morphological and biochemical features. Apoptosis induced by metals and metal-related deleterious conditions has only recently been studied. Although the toxic effects of heavy metals are well described, little is known about the mechanism of apoptosis via cadmium toxicity. Therefore, this study is designed to define the induction mechanism of apoptosis by which cadmium exerts its cytotoxic effect on human promyelocytic leukemic HL-60 cells. The cytotoxic effects of cadmium on HL-60 cells are studied in regards to apoptotic signal transduction pathways.
METHODS
The mode of cadmium-induced apoptosis was investigated in HL-60 cells. HL-60 cells were treated with various concentrations of cadmium and antioxidants after which the viability of the cells were measured by MTT assay. The morphological features of cadmium- induced apoptosis were evaluated by fluoromicroscopy and the DNA fragmentation was analyzed using 1.5% agarose gel electrophorosis. Kinase activity was assayed by autoradiography and activity of NF-kappaB and nuclear proteins were measured by EMSA.
RESULTS
Cadmium (125 microM) induces the characteristic morphological features of apoptosis, which are characterized by a shrinkage of the cytoplasm and a condensation of chromatin. In addition, cadmium induced the ladder pattern of DNA fragmentation. Antioxidants(Sodium nitroprusside, glutathione and N-acethylcysteine), which were not toxic to the cells, did not suppress apoptosis induced by cadmium. Cadmium enhances the expression of several classes of genes at elevated cytotoxic concentrations. Poly(ADP-ribose) polymerase(PARP) was predominantly in the fragmented form when doses of 125 microM were used. Since PARP is cleaved by CPP32 (caspase-3), we next determined if cadmium was capable of effecting changes in CPP32 activity. The results of these experiments showed that cadmium increased caspase-3 activity in a time dependent manner, corresponding to the time of appearance of fragmented PARP. Cadmium also increased the phosphotransferase activities of c-JUN N-terminal kinase (JNK). Furthermore, cadmium increased the activation of transcriptional factors including the activation of protein-1 (AP-1) and NF-kappaB .
CONCLUSIONS
These results suggest that cadmium induces the apoptotic death of HL-60 cells via the activation of a DEVD-specific caspase, JNK and transcriptional factors such as AP-1 and NF-kappaB .

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The association between blood cadmium level, frequency and amount of gejang (marinated crab) intake
Chang Yul Choi, Gun Il Park, Young Seok Byun, Man Joong Jeon, Kwang Hae Choi, Joon Sakong
Annals of Occupational and Environmental Medicine.2016;[Epub] CrossRef

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Role of Nitric Oxide in the Nickel and Cobalt Induced Cytotoxicity in RAW 264.7 cell: Jung Ho Youm, Gyung Jae Oh, Young Cheun Yoo; Korean Journal of Occupational and Environmental Medicine 2001;13(3):274-285. Published online September 30, 2001; DOI: https://doi.org/10.35371/kjoem.2001.13.3.274

Abstract PDF: OBJECTIVES
The nickel and cobalt present in many industrial working environments and consumer products. They are two of the leading causes of allergic contact dermatitis, which is a typical delayed(type IV) hypersensitivity reaction. However, the mechanism by which nickel and cobalt causes this pathology is not well known. The nickel and cobalt induced contact dermatitis is mediated primarily through macrophages. This mechanism is similar to the autotoxicity procedure for NO. Therefore, this study was designed to examine whether the metals could modulate NO production and how the metals may affect ATP production and cell viability. In summary, the purpose of this study was to elucidate the role of NO in the nickel and cobalt induced cytotoxicity.
METHODS
This study is based on observations of cultures of RAW 264.7 cells which are originated from a tumor of Balb/c mouse that was induced by Abelson murine leukemia virus. RAW 264.7 cells were treated with either Ni, Co, Ni plus Co, or Nmonomethyl-L- arginine(NMLA) for 24-72 h. The cytotoxicity of the nickel and cobalt was measured by cell viability and NO2-, and mitochondrial function was evaluated by adenosine triphosphate(ATP) production in RAW 264.7 cells. In addition, the morphology of cells was observed using an inverted microsope.
RESULTS
The NO2- synthesis of RAW 264.7 cells increased with increasing concentrations of Ni and Co up to 50 microM after 24 and 48 h of exposure to Ni and Co but then decreased if the concentration was greater than 50 microM and the time period was greater than 48 h. However, the viability of cells was decreased by Ni and Co exposure in a dose and time dependent manner. Therefore, 50 microM Ni or Co and 48 h of treatment were used in this study. A complete inhibition of NO2- synthesis by Ni or/and Co occurred when iNOS inhibitor, NMLA, were pretreated prior to addition of Ni or/and Co, whereas Ni or/and Co induced decrease of synthesis of ATP and viability completely recovered when NMLA were pretreated prior to addition of Ni or/and Co. Ni or/and Co(50 microM) induced the characteristic morphological features of cytotoxicity which is characterized by a shrinkage of cytoplasm and irregular shape of the cells, but the pretreatment of NMLA resulted in a recovered morphological change of the cells to their normal appearance.
CONCLUSIONS
These results suggest that NO plays an important role in the pathogenesis of the cytotoxicity of nickel and cobalt, and nickel and cobalt may exert their toxicities by means of modulation of NO production. The results from this study may facilitate further understanding the role of NO on nickel and cobalt induced immune and inflammatory processes.

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Effect of Mercury Chloride on Peritoneal Macrophage or EMT-6 cell from Balb/c mice: Dai Ha Koh, Jung Ho Youm, No Suk Ki, Gyung Jae Oh, Kuen Sang Kwon, Sung Yeup Kim, Nam Song Kim; Korean Journal of Occupational and Environmental Medicine 1996;8(2):201-209. Published online September 30, 1996; DOI: https://doi.org/10.35371/kjoem.1996.8.2.201

Abstract PDF: The effect of treatment of mercury chloride on the nitrite and nitrate synthesis was observed in peritoneal macrophages from Balb/c mice and EMT-6 cells in vitro. The cells were cultured in Dulbecco's modified Eagle's medium (DMEM) with cytokines. Amounts of nitrite and nitrate in the culture media after 24 and 36 hours of culture were about 2-fold, and 3-fold of those measured after 12 hours respectively. There were very close associations between the amounts of nitrite and nitrate measured in the culture media, according to culture time. The survival rate of peritoneal macrophages was significantly decreased by mercury chloride added into the media in dose-dependent manner, however the survivals of EMT-6 cells were not influenced by mercury chloride concentration in media. Nitrite and nitrate syntheses were dose-dependently decreased by mercury chloride added in culture media. These results reported here suggest that the disorder of cell mediated immunity by mercurials could be related to the inhibition of nitric oxide synthesis which seems to be caused by the inhibition of metabolism of cells.

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