1.The Relationship between Job Stress and Musculoskeletal Symptoms in Migrant Workers.
Min Heui JO ; Kyoo Sang KIM ; Sun Wung LEE ; Tae Gyun KIM ; Hyang Woo RYU ; Mi Young LEE ; Yong Lim WON
Korean Journal of Occupational and Environmental Medicine 2009;21(4):378-387
OBJECTIVE: To investigate the musculoskeletal symptoms of migrant workers. We focused on the relationship between job stress and musculoskeletal symptoms. METHOD: A questionnaire was administered to 502 migrant workers who visited NGO migrant worker centers located in Gyung-gi province. A structured, self-reported questionnaire was administered to participants in order to capture the following information: sociodemographics, health factors including past medical history, work related characteristics, job stress, and musculoskeletal symptoms. The job stress questionnaires were used according to KOSS-26 and musculoskeletal symptoms were measured using KOSHA Code H-30-2003. We used multiple logistic regression analysis to assess the relationship between risk factors which included job stress, and musculoskeletal symptoms. RESULTS: The prevalence rate of musculoskeletal symptoms in survey subjects was 35.1%. Other than job stress factors, past medical history was the only factor that had a statistical relationship to musculoskeletal symptoms (P<0.01). In the domains of job stress, physical environment (OR 1.62, 95% CI: 1.03~2.54), job demand (OR 2.43, 95% CI: 1.46~4.03), job insecurity (OR 1.59, 95% CI: 1.03~2.47), occupational climate (OR 2.30, 95% CI: 1.27~4.19) were most likely experience musculoskeletal symptoms. CONCLUSION: The job stress factor appeared to correlate more with musculoskeletal symptoms than with sociodemographics or other factors. Hence, in order to prevent migrant worker's musculoskeletal symptoms, we believe that intervention in job stress (physical environment, job demand, job insecurity, occupational climate) is necessary.
Climate
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Humans
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Logistic Models
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Prevalence
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Questionnaires
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Risk Factors
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Transients and Migrants
2.The Characteristics of Blood Pressure Control in Chronic Renal Failure Patients Treated with Peritoneal Dialysis.
Hang Jae JUNG ; Sung Hwa BAE ; Jun Bum PARK ; Kyoo Hyang JO ; Young Jin KIM ; Jun Young DO ; Kyung Woo YOON
Yeungnam University Journal of Medicine 1999;16(2):333-341
BACKGROUND AND METHODS: In order to evaluate characteristics and modulatory factors of blood pressure in peritoneal dialysis(PD), studies were conducted on the 69 patients who had underwent peritoneal equilibration test(PET). RESULTS: The results were as follows: 1) All patients received an antihypertensive drug before PD, but, 15 of 69 patients successfully quit taking the antihypertensive drug after peritoneal dialysis. 2) During peritoneal dialysis, mean arterial pressure(MAP) was significantlydecreased for the first 3 months, and this lasted for 1 year, and antihypertensive drug requirements were significantly decreased continuously up to 9 months(p<0.005). 3) After changing the modality from hemodialysis to peritoneal dialysis. MAP(mmHg, from 107.1+/-4.5 to 98.6+/-8.8, p<0.05), antihypertensive drug requirements(from 5.6+/-2.6, to 2.0+/-2.5, p<0.01) and erythropoietin dosages(Uint/week, from 4600+/-2660 to 2000+/-1630, p<0.05) were decreased. 4) Multiple logistic regression analysis showed that MAP(p<0.01) and daily ultrafiltration volume(p<0.05) can contribute to the determination of antihypertensive drug requirements. However the relationship between antihypertensive drug requirements and PET results or dialysis adequacy indices(weekly Kt/V. weekly creatinine clearance) was not revealed. CONCLUSION: In conclusion, the prescription of antihypertensive drugs should be considered according to daily ultrafiltration volume, especially during first year after initiating PD, and follow-ups for over a year may be needed.
Antihypertensive Agents
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Blood Pressure*
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Creatinine
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Dialysis
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Erythropoietin
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Follow-Up Studies
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Humans
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Kidney Failure, Chronic*
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Logistic Models
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Peritoneal Dialysis*
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Prescriptions
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Renal Dialysis
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Ultrafiltration
3.The Clinical and Histopathologic Features according to Loss of LKB1 Protein Expression on Primary Lung Cancer.
Ki Eun HWANG ; Hyang Jeong JO ; Kang Kyoo LEE ; Hyeok SHIM ; Jung Sub SONG ; Jeong Hyun SHIN ; Seong Nam SHIN ; Seong Hoon PARK ; Kyeong Man HONG ; Jung Hyun PARK ; Jong Hoon JEONG ; Hui Jung KIM ; Hak Ryul KIM ; Sei Hoon YANG ; Eun Taik JEONG
Tuberculosis and Respiratory Diseases 2008;64(5):362-368
BACKGROUND: LKB1(STK11) is a serine/threonine kinase that functions as a tumor growth suppressor. The functions of LKB1 in lung cancer are not completely understood. This study evaluated the relationship between LKB1 protein expression and the clinicopathological features in lung cancer tissues. METHODS: The expression of LKB1 was studied in paraffin-embedded tumor blocks, which were obtained from 77 patients who had undergone surgery at Wonkwang University Hospital. The expression of the LKB1 protein was considered positive if the staining intensity in the tumor tissue adjacent to the normal airway epithelium was >30%. RESULTS: The LKB1 expression was positive in 31 (40%) of samples. Loss of LKB1 expression was significantly associated with being male, smoking history, and squamous cell carcinoma. In the peripheral sites, the loss of LKB1 expression was strongly associated with a smoking history. A loss of LKB1 expression was more frequently associated with progression according to TNM staging, particularly more than T2, N progression. CONCLUSION: There was a significant relationship between the loss of the LKB1 protein and gender, smoking history, and histological type in primary lung cancer. Although LKB1 expression was not found to be a significant prognostic factor, further studies with a larger cohort of patient's lung cancer tissue samples will be needed to confirm this.
Carcinoma, Squamous Cell
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Cohort Studies
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Epithelium
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Humans
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Lung
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Lung Neoplasms
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Male
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Neoplasm Staging
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Phosphotransferases
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Smoke
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Smoking
4.The Role and Significance of Biomarker for Plasma G-CSF in Patients with Primary Lung Cancer.
Jung Sub SONG ; So Young KIM ; Hyang Jeong JO ; Kang Kyoo LEE ; Jeong Hyun SHIN ; Seong Nam SHIN ; Dong KIM ; Seong Hoon PARK ; Young Jin LEE ; Chang Bo KO ; Mi Kung LEE ; Soon Ho CHOI ; Jong Hoon JEONG ; Jung Hyun PARK ; Hui Jung KIM ; Hak Ryul KIM ; Eun Taik JEONG ; Sei Hoon YANG
Tuberculosis and Respiratory Diseases 2009;66(6):444-450
BACKGROUND: Biomarkers for cancer have several potential clinical uses, including the following: early cancer detection, monitoring for recurrence prognostication, and risk stratification. However, no biomarker has been shown to have adequate sensitivity and specificity. Many investigators have tried to validate biomarkers for the early detection and recurrence of lung cancer. To evaluate plasma G-CSF as such a biomarker, protein levels were measured and were found to correlate with the clinicopathological features of primary lung tumors. METHODS: Between December 2006 and May 2008, 100 patients with histologically-validated primary lung cancer were enrolled into this study. To serve as controls, 127 healthy volunteers were enrolled into this study. Plasma G-CSF levels were measured in lung cancer patients using the sandwich ELISA system (R & D inc.) prior to treatment. RESULTS: The mean plasma G-CSF levels were 12.2+/-0.3 pg/mL and 46.0+/-3.8 pg/mL (mean+/-SE) in the normal and in the cancer groups, respectively. In addition, plasma G-CSF levels were higher in patients with early lung cancer than in healthy volunteers (p<.001). Plasma G-CSF levels were higher in patients who were under 65 years old or smokers. Within the cancer group, plasma G-CSF levels were higher in patients with non small cell lung cancer than in patients with small cell lung cancer (p<.05). Overall, plasma G-CSF levels were shown to increase dependent upon the type of lung cancer diagnsosed. In the order from highest to lowest, the levels of plasma G-CSF tended to decrease in the following order: large cell carcinoma, squamous cell carcinoma, adenocarcinoma, and bronchioloalveolar carcinoma. Plasma G-CSF levels tended to be higher in patients with advanced TNM stage than in localized TNM stage (I, II
5.The Effect of Autophagy to Cell Death in Nutrient-Deprived H460 Cells.
Hye Yeon JANG ; Hyang Jeong JO ; Ki Eun HWHANG ; So Young KIM ; Kang Kyoo LEE ; Sun Rock MOON ; Jeong Hyun SHIN ; Kyung Hwa CHO ; Mi Kung LEE ; Sam Youn LEE ; Soon Ah PARK ; Jong Kun PARK ; Hui Jung KIM ; Sei Hoon YANG
Tuberculosis and Respiratory Diseases 2010;69(2):81-94
BACKGROUND: Autophagy is an important adaptive mechanism in normal development and in response to changing environmental stimuli in cancer. Previous papers have reported that different types of cancer underwent autophagy to obtain amino acids as energy source of dying cells in nutrient-deprived conditions. However, whether or not autophagy in the process of lung cancer causes death or survival is controversial. Therefore in this study, we investigated whether nutrient deprivation induces autophagy in human H460 lung cancer cells. METHODS: H460, lung cancer cells were incubated in RPMI 1640 medium, and the starved media, which are BME and RPMI media without serum, including 2-deoxyl-D-glucose according to time dependence. To evaluate the viability and find out the mechanism of cell death under nutrient-deprived conditions, the MTT assay and flow cytometry were done and analyzed the apoptotic and autophagic related proteins. It is also measured the development of acidic vascular organelles by acridine orange. RESULTS: The nutrient-deprived cancer cell is relatively sensitive to cell death rather than normal nutrition. Massive cytoplasmic vacuolization was seen under nutrient-deprived conditions. Autophagic vacuoles were visible at approximately 12 h and as time ran out, vacuoles became larger and denser with the increasing number of vacuoles. In addition, the proportion of acridine orange stain-positive cells increased according to time dependence. Localization of GFP-LC3 in cytoplasm and expression of LC-3II and Beclin 1 were increased according to time dependence on nutrient-deprived cells. CONCLUSION: Nutrient deprivation induces cell death through autophagy in H460 lung cancer cells.
Acridine Orange
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Amino Acids
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Autophagy
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Cell Death
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Cytoplasm
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Flow Cytometry
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Humans
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Lung Neoplasms
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Malnutrition
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Organelles
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Proteins
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Vacuoles