Some circadian rhythms can become disorganized due to rotating shift work. This lack of organization, termed desynchronization, can produce a group of symptoms such as insomnia, GI disturbance and fatigue among many rotating shift workers. The magnitude of these symptoms are influenced by personal and environmental factors and the patterns of shift work. This study was carried out to investigate the subjective symptoms related to rotational schedules of shift work after personal and environmental factors adjusted. 182 male workers in rapidly rotating shift system and 86 male workers in weekly rotating shift system were conducted the questionnaire on personal factors and subjective sleep, GI and fatigue symptoms. Major findings obtained from this study are as follows: 1. The symptoms of 'feeling tired at work' and 'being irritable' were more frequent in weekly rotating shift workers(P<0.05), and the mean of symptom score was significantly higher in weekly rotating shift workers(P<0.01). 2. According to 6 hours of sleeping which is a definite elevation point of fatigue, there was not a significant difference between two groups in sleeping hours. Among workers in rapidly rotating shift system, the mean of symptom score was significantly higher in workers of less than 6 hours of sleeping(P<0.05), but it was not different among weekly rotating shift workers. 3. The symptoms of GI disturbance were more frequent in weekly rotating shift workers but statistically mot significant. 4. The positive rate of mental and physical fatigue symptoms were significantly higher in weekly rotating shift workers(P<0.01) and mental and physical fatigue symptoms were more frequent in them(P<0.01). 5. After the effect of the factors that were significantly different between two groups by X2-test were controlled, the mean score of sleep disturbance was significantly higher in weekly rotating shift workers(P<0.01) and mental physical fatigue symptoms were more frequent in them(P<0.01). Based on these study results, subjective symptoms were more common in the weekly rotating shift workers. In future, medical examination and laboratory test will be also administered to evaluate a more accurate health outcomes and the review of current shift schedules will be required.
Appointments and Schedules ; Circadian Rhythm ; Fatigue ; Humans ; Male ; Surveys and Questionnaires ; Sleep Initiation and Maintenance Disorders

No abstract available.
Antibody Formation* ; Immunoglobulin A* ; T-Lymphocytes*

BACKGROUND: It is well known that IgA isotype switching is induced by TGF-beta1. LPS-activated mouse normal B cells well differentiate into IgA secreting plasma cells under the influence of TGF-beta1. Nevertheless, there are lots of difficulties in studying normal B cells in detail because it is not simple to obtain highly purified B cells, showing low reproducibility and transfection efficacy, moreover impossible to keep continuous culture. To overcome these obstacles, it is desperately needed to develop B cell line which acts like normal B cells. In the present study, we investigated whether CH12F3-2A lymphoma cells are appropriate for studying IgA isotype switching event. METHODS: CH12F3-2A B cell line was treated with LPS and TGF-beta1, then levels of germ-line (GL) transcripts were measured by RT-PCR, and GLalpha promoter activity was measured by luciferase assay. In addition, membrane IgA (mIgA) expression and IgA secretion were determined by FACS and ELISA, respectively. RESULTS: TGF-beta1, regardless of the presence of LPS, increased level of GLalpha transcripts but not GLgamma2b transcripts. However, IgA secretion was increased dramatically by co-stimulation of LPS and TGF-beta1. Both mIgA and IgA secretion in the presence of TGF-beta1 were further increased by over-expression of Smad3/4. Finally, GLalpha promoter activity was increased by TGF-beta1. CONCLUSION: CH12F3-2A cell line acts quite similarly to the normal B cells which have been previously reported regarding IgA expression. Thus, CH12F3-2A lymphoma cell line appears to be adequate for the investigation of the mechanism(s) of IgA isotype switching at the cellular and molecular levels.
Animals ; B-Lymphocytes ; Cell Line ; Enzyme-Linked Immunosorbent Assay ; Immunoglobulin A* ; Immunoglobulin Class Switching* ; Luciferases ; Lymphoma* ; Membranes ; Mice* ; Plasma Cells ; Transfection ; Transforming Growth Factor beta1

This study was conducted to evaluate the effect of VDT work on eyes and vision among workers in a TV manufacturing plant. The study subjects consisted of 264 screen workers and 74 non-screen workers who were less than 40 years old male and had no history of opthalmic diseases such as corneal opacities, trauma, keratitis, etc and whose visual acuity on pre-employment health examination by Han's test chart was 1.0 or above. The screen workers were divided into two groups by actual time for screen work in a day; Group 1, 60 workers, lesser than 4 hours a day and group 11, 204 workers, more than 4 hours a day. From July to October 1992 a questionnaire was administered to all the study subjects for the general charateristics and subjective eye symptoms after which the opthalmologic tests such as visual acuity, spherical equivalent, lacrimal function, ocular pressure, slit lamp test, fundoscopy were conducted by one opthalmologist. The proportion of workers whose present visual acuity was decreased more than 0. 15 in comparison with that on the pre-employment health examination by Han's test chart was 20.6% in Group Ii, 15.0% in Group I and 14.9% in non-screen workers. However, the differences in proportion were not statistically significant. The proportion of workers with decreased visual acuity was not associated with the age, working duration, use of magnifying glass and type of shift work (independent variables) in all of the three groups. However, screen workers working under poor illumination had a higher proportion of persons with decreased visual acuity than those working under adequate illumination (P<0.05). The proportion of workers whose near vision was decreased was 27.5% in Group II, 18.3% in Group I, and 28.4% in non-screen workers and these differences in proportion were not statistically significant. Changes of near vision were not associated with 4 independent variables in all of the three groups. Six out of sever-subjective eye symptoms except tearing were more common in Group I than in non-screen workers and more common in Group II than in Group I (P<0.01). Mean of the total scores for seven subjective symptoms of each worker (2 points for always, 1 point for sometimes, 0 point for never) was not significantly different between workers with decreased visual acuity and workers with no vision change. However, mean of the total scores for Group II was higher than those for the Group I and non-screen workers (P < 0. 01). Total eye symptom scores were significantly correlated with the grade of screen work, use of magnifying glass, and type of shift work. There was no independent variable which was correlated with the difference in visual acuity between the pre-employment health examination and the present state, the difference between far and near visions, lacrimal function, ocular pressure, and spherical equivalent. Multiple linear regression analysis for the subjective eye symptom scores revealed a positive linear relationship with actual time for screen work and shift work(P<0.01). In this study it was not observed that the VDT work decreased visual acuity but it induces subjective eye symptoms such as eye fatigue, blurred vision, ocular discomfort, etc. Maintenance of adequate illumination in the, work place and control of excessive VDT work are recommended to prevent such eye symptoms.
Adult ; Asthenopia ; Corneal Opacity ; Glass ; Humans ; Keratitis ; Lighting ; Linear Models ; Male ; Plants* ; Surveys and Questionnaires ; Tears ; Vision, Ocular ; Visual Acuity ; Workplace

In a TV component manufacturing factory, 102 male workers aged 20~39 years old were participated in testing for physical fitness. At the same time, worker's periodic health examination was done. Test battery for physical fitness include grip strength, trunk flexing, standing long jump, side step, single leg balance with eye close, push ups and Harvard step test. As a result of testing for physical fitness, synthetically, there is no difference between manufacturing workers and officers. By bioelectrical impedance test, it means a declining tendency to all 7 factors in the obese workers, and so, it is important for obese workers not only to promote physical fitness but also to promote health. Excluding grip strength and single leg balance with eye close, 5 fitness factors are negatively associated with degree of diastolic Blood pressure, but it is statistically not significant. And levels of SGOT & SGPT have no association with physical fitness factors.
Alanine Transaminase ; Aspartate Aminotransferases ; Blood Pressure ; Electric Impedance ; Exercise Test ; Hand Strength ; Health Promotion ; Humans ; Leg ; Male* ; Physical Fitness* ; Pilot Projects*

Background: Kelch-like ECH-associated protein 1 (KEAP1)–nuclear factor erythroid- 2-related factor 2 (NRF2) pathway is a major regulator protecting cells from oxidative and metabolic stress. Studies have revealed that this pathway is involved in mediating resistance to cytotoxic chemotherapy and immunotherapy; however, its implications in oncogene-addicted tumors are largely unknown. This study aimed to elucidate whether this pathway could be a potential therapeutic target for epidermal growth factor receptor (EGFR)-mutant non-small cell lung cancer. Methods: We measured the baseline expression of NRF2 using EGFR-mutant parental cells and acquired gefitinib resistant cells. We investigated whether NRF2 inhibition affected cell death in vitro and tumor growth in vivo using a xenograft mouse model, and compared the transcriptional changes before and after NRF2 inhibition. Results: Baseline NRF2 expression was enhanced in PC9 and PC9 with gefitinib resistance (PC9/GR) cells than in other cell lines, with a more prominent expression in PC9/ GR. The NRF2 inhibitor induced NRF2 downregulation and cell death in a dose-dependent manner. Cotreatment with an NRF2 inhibitor enhanced osimertinib-induced cell death in vitro, and potentiated tumor growth inhibition in a PC9/GR xenograft model. Finally, RNA sequencing revealed that NRF2 inhibition resulted in the altered expression of multiple genes involved in various signaling pathways. Conclusion We identified that NRF2 inhibition enhanced cell death and inhibited tumor growth in tyrosine kinase inhibitor (TKI)-resistant lung cancer with EGFR-mutation. Thus, NRF2 modulation may be a novel therapeutic strategy to overcome the resistance to EGFR-TKIs.

Background: Kelch-like ECH-associated protein 1 (KEAP1)–nuclear factor erythroid- 2-related factor 2 (NRF2) pathway is a major regulator protecting cells from oxidative and metabolic stress. Studies have revealed that this pathway is involved in mediating resistance to cytotoxic chemotherapy and immunotherapy; however, its implications in oncogene-addicted tumors are largely unknown. This study aimed to elucidate whether this pathway could be a potential therapeutic target for epidermal growth factor receptor (EGFR)-mutant non-small cell lung cancer. Methods: We measured the baseline expression of NRF2 using EGFR-mutant parental cells and acquired gefitinib resistant cells. We investigated whether NRF2 inhibition affected cell death in vitro and tumor growth in vivo using a xenograft mouse model, and compared the transcriptional changes before and after NRF2 inhibition. Results: Baseline NRF2 expression was enhanced in PC9 and PC9 with gefitinib resistance (PC9/GR) cells than in other cell lines, with a more prominent expression in PC9/ GR. The NRF2 inhibitor induced NRF2 downregulation and cell death in a dose-dependent manner. Cotreatment with an NRF2 inhibitor enhanced osimertinib-induced cell death in vitro, and potentiated tumor growth inhibition in a PC9/GR xenograft model. Finally, RNA sequencing revealed that NRF2 inhibition resulted in the altered expression of multiple genes involved in various signaling pathways. Conclusion We identified that NRF2 inhibition enhanced cell death and inhibited tumor growth in tyrosine kinase inhibitor (TKI)-resistant lung cancer with EGFR-mutation. Thus, NRF2 modulation may be a novel therapeutic strategy to overcome the resistance to EGFR-TKIs.

Background: Kelch-like ECH-associated protein 1 (KEAP1)–nuclear factor erythroid- 2-related factor 2 (NRF2) pathway is a major regulator protecting cells from oxidative and metabolic stress. Studies have revealed that this pathway is involved in mediating resistance to cytotoxic chemotherapy and immunotherapy; however, its implications in oncogene-addicted tumors are largely unknown. This study aimed to elucidate whether this pathway could be a potential therapeutic target for epidermal growth factor receptor (EGFR)-mutant non-small cell lung cancer. Methods: We measured the baseline expression of NRF2 using EGFR-mutant parental cells and acquired gefitinib resistant cells. We investigated whether NRF2 inhibition affected cell death in vitro and tumor growth in vivo using a xenograft mouse model, and compared the transcriptional changes before and after NRF2 inhibition. Results: Baseline NRF2 expression was enhanced in PC9 and PC9 with gefitinib resistance (PC9/GR) cells than in other cell lines, with a more prominent expression in PC9/ GR. The NRF2 inhibitor induced NRF2 downregulation and cell death in a dose-dependent manner. Cotreatment with an NRF2 inhibitor enhanced osimertinib-induced cell death in vitro, and potentiated tumor growth inhibition in a PC9/GR xenograft model. Finally, RNA sequencing revealed that NRF2 inhibition resulted in the altered expression of multiple genes involved in various signaling pathways. Conclusion We identified that NRF2 inhibition enhanced cell death and inhibited tumor growth in tyrosine kinase inhibitor (TKI)-resistant lung cancer with EGFR-mutation. Thus, NRF2 modulation may be a novel therapeutic strategy to overcome the resistance to EGFR-TKIs.

Background: Kelch-like ECH-associated protein 1 (KEAP1)–nuclear factor erythroid- 2-related factor 2 (NRF2) pathway is a major regulator protecting cells from oxidative and metabolic stress. Studies have revealed that this pathway is involved in mediating resistance to cytotoxic chemotherapy and immunotherapy; however, its implications in oncogene-addicted tumors are largely unknown. This study aimed to elucidate whether this pathway could be a potential therapeutic target for epidermal growth factor receptor (EGFR)-mutant non-small cell lung cancer. Methods: We measured the baseline expression of NRF2 using EGFR-mutant parental cells and acquired gefitinib resistant cells. We investigated whether NRF2 inhibition affected cell death in vitro and tumor growth in vivo using a xenograft mouse model, and compared the transcriptional changes before and after NRF2 inhibition. Results: Baseline NRF2 expression was enhanced in PC9 and PC9 with gefitinib resistance (PC9/GR) cells than in other cell lines, with a more prominent expression in PC9/ GR. The NRF2 inhibitor induced NRF2 downregulation and cell death in a dose-dependent manner. Cotreatment with an NRF2 inhibitor enhanced osimertinib-induced cell death in vitro, and potentiated tumor growth inhibition in a PC9/GR xenograft model. Finally, RNA sequencing revealed that NRF2 inhibition resulted in the altered expression of multiple genes involved in various signaling pathways. Conclusion We identified that NRF2 inhibition enhanced cell death and inhibited tumor growth in tyrosine kinase inhibitor (TKI)-resistant lung cancer with EGFR-mutation. Thus, NRF2 modulation may be a novel therapeutic strategy to overcome the resistance to EGFR-TKIs.

Background: Kelch-like ECH-associated protein 1 (KEAP1)–nuclear factor erythroid- 2-related factor 2 (NRF2) pathway is a major regulator protecting cells from oxidative and metabolic stress. Studies have revealed that this pathway is involved in mediating resistance to cytotoxic chemotherapy and immunotherapy; however, its implications in oncogene-addicted tumors are largely unknown. This study aimed to elucidate whether this pathway could be a potential therapeutic target for epidermal growth factor receptor (EGFR)-mutant non-small cell lung cancer. Methods: We measured the baseline expression of NRF2 using EGFR-mutant parental cells and acquired gefitinib resistant cells. We investigated whether NRF2 inhibition affected cell death in vitro and tumor growth in vivo using a xenograft mouse model, and compared the transcriptional changes before and after NRF2 inhibition. Results: Baseline NRF2 expression was enhanced in PC9 and PC9 with gefitinib resistance (PC9/GR) cells than in other cell lines, with a more prominent expression in PC9/ GR. The NRF2 inhibitor induced NRF2 downregulation and cell death in a dose-dependent manner. Cotreatment with an NRF2 inhibitor enhanced osimertinib-induced cell death in vitro, and potentiated tumor growth inhibition in a PC9/GR xenograft model. Finally, RNA sequencing revealed that NRF2 inhibition resulted in the altered expression of multiple genes involved in various signaling pathways. Conclusion We identified that NRF2 inhibition enhanced cell death and inhibited tumor growth in tyrosine kinase inhibitor (TKI)-resistant lung cancer with EGFR-mutation. Thus, NRF2 modulation may be a novel therapeutic strategy to overcome the resistance to EGFR-TKIs.