OBJECTIVES: This study was performed to investigate the service needs of the beneficiaries who had enrolled in home-based management programs for cancer patients. METHODS: From March to May 2009, 676 cancer patients who were registered in home-based cancer patient management programs were selected as subjects for this study. The data were collected using a questionnaire along with a face-to-face interview performed by officers in charge of the home-based care programs of 47 regional health centers. Fifteen patients were excluded due to incomplete data, leaving 661 subjects who were ultimately enrolled in the study. RESULTS: The mean age of subjects was 64.0 +/- 12.5 years, and males comprised 45.1% (298/661) of the sample. The results of factor analysis for service needs showed that there were five main categories and Cronbach's alpha ranged from 0.593 to 0.890 for each factor. The service needs categories in order of importance were social support, information and education, psychological problems, physical symptoms and household chores. The service needs scores were significantly different when subjects were stratified by age, habitation, religion and disease classification. When we divided the subjects into complete remission, under treatment and terminally ill groups, the needs scores of the terminally ill patient group were significantly higher than those of the other groups (p<0.001). CONCLUSIONS: Service provision based on patient and beneficiary needs could be an effective intervention to reduce the economic burden of cancer management and to improve the quality of life of cancer patients receiving home-based care. Therefore, it is recommended that individual cancer patient care programs be developed and administered according to patient age, habitation and disease severity.
Family Characteristics ; Fees and Charges ; Home Care Services ; Humans ; Male ; Needs Assessment ; Patient Care ; Quality of Life ; Terminally Ill ; Surveys and Questionnaires

OBJECTIVES: This cross-sectional study investigated the relationship between job stress and psychosocial stress among nurses at a university hospital in Incheon, Korea. METHODS: A questionnaire survey was administered to 476 nurses, of which 320 (67.2%) questionnaires were returned and 299 (62.8%) were regarded as containing reliable data for analyses. A structured self-reported questionnaire was used to assess each respondent's sociodemographics, sleep quality, physical burden, job stress and psychosocial stress. Seven domains of occupational stress (e.g., Job demand, Insufficient job control, Interpersonal conflict, Job insecurity, Lack of reward, Organizational system and Occupational climates) according to the Korean Occupational Stress Scale (KOSS) were used and psychosocial stress was measured using Dr. Chang's PWI-SF (Psychosocial Well-being Index-Short Form). We estimated the relation of job stress to psychosocial stress using univariate and logistic regression analyses. RESULTS: The logistic regression analyses indicated that the groups with high stress in 'Insufficient job control' (OR=2.67, 95% C.I.=1.37-5.23), 'Interpersonal conflict' (OR=2.32, 95% C.I.=1.19-4.51), 'Job insecurity' (OR=2.51, 95% C.I.=1.17-5.36), 'Organizational system' (OR=2.80, 95% C.I.=1.39-5.63), and 'Lack of reward' (OR=2.98, 95% C.I.=1.55-5.74) were more likely to experience high psychosocial stress. CONCLUSIONS: Our results tend to suggest that job stress is associated with psychosocial stress. The importance of job stress should be acknowledged and stress management programs need to be instigated to minimize the psychosocial stress caused by job stress.
Cross-Sectional Studies ; Incheon ; Korea ; Logistic Models ; Questionnaires ; Reward

OBJECTIVE: This study was performed to evaluate the protective effects of selenium against the methyl mercury chloride (MeHgCl) induced cell apoptosis. METHODS: The effect of selenium on the MeHgCl induced cell apoptosis was observed in mouse macrophage-derived RAW 264.7 cells, in vitro. The cells were cultured in Dulbecco's modified Eagle's medium (DMEM). RESULTS: MeHgCl exerted a dose dependent cytotoxicity, as demonstrated by the MTT assay, an assay dependent, in part, on mitochondrial function. Concurrent exposure to selenium provided complete protective effects against the cytotoxicity induced by MeHgCl. Pretreatment with selenium increased the protective effects of subsquent administrations of selenium in conjunction with MeHgCl, but pretreatment of selenium alone did not provide protection against MeHgCl when given alone. Selenium administered after exposure to MeHgCl did not repair the existing MeHgCl induced cytotoxicity.Furthermore, the apoptosis induced by MeHgCl was revealed by the DNA fragmentation, using the terminal deoxynucleotidyl transferase Biotin-dUTP nick end labeling (TUNEL) assay, alterations to the nuclear morphology, by nuclei staining, and the plasma membrane lipid organization, as shown by cell flow cytometry. The apoptosis induced by MeHgCl was prevented by the concurrent exposure to selenium, or pretreatment with selenium, prior to the administration of selenium in conjunction with MeHgCl. However, no inhibittion of the MeHgCl induced apoptosis was observed with selenium pretreatment prior to exposure to MeHgCl alone, or with the administration of selenium after exposure to MeHgCl. CONCLUSIONS: These results suggest that the coexistence of selenium and MeHgCl are essential for the protective effects of selenium against the MeHgCl-induced apoptosis, and the cytotoxicity, in RAW 264.7 cells, and may involve selenium-MeHgCl binding.
Animals ; Apoptosis* ; Cell Membrane ; DNA Fragmentation ; DNA Nucleotidylexotransferase ; Flow Cytometry ; Mice ; Selenium*

PURPOSE: The purpose of this study was to evaluate diagnostic criteria using plain lateral radiography, the incidence of traumatic disc herniation and the degree of neurologic deficit in extension injury of the lower cervical spine. MATERIALS AND METHODS: We analyzed 28 patients with extension injury of the lower cervical spine, by measuring the retropharyngeal, retrotracheal space and the intervertebral space at the injured level in plain lateral radiography. We selected 40 patients as a control group for the prevertebral soft tissue space measurement. RESULTS: Widening was found in the retropharyngeal space (6.8 +/-2.9 mm) and in the retrotracheal space (15.2 +/-3.8 mm) compared with the control group (4.2 +/-0.7 mm, 12.6 +/-1.9 mm, p<0.05). No significant increase in the injured intervertebral space was observed with respect to the normal upper and lower disc space. Neurologic deficit occurred in 25 cases (89%); with root injury in 11 cases and cord injury in 14 cases. There were 19 posterior disc herniations (68%), which were associated with neurologic deficits in all cases. CONCLUSION: Extension injuries should be suspected in the presence of soft tissue injury of the anterior column without fracture or dislocation by the radiologic study of the lower cervical spine. Magnetic resonance imaging study is believed to be an essential diagnostic modality for the accurate evaluation and proper management of the lower cervical spine injuries.
Diagnosis* ; Dislocations ; Humans ; Incidence ; Magnetic Resonance Imaging ; Neurologic Manifestations ; Radiography ; Soft Tissue Injuries ; Spine*

OBJECTIVES: This study was performed to evaluate the critical role of glutathione(GSH) in methyl mercury chloride(MeHgCl)induced cell apoptosis. METHODS: The effect of GSH in MeHgCl induced cell apoptosis was observed in mouse macrophage-derived RAW 264.7 cells in vitro. The cells were cultured in Dulbecco's modified Eagle's medium(DMEM). RESULTS: MeHgCl exerted a dose dependent cytotoxicity,as demonstrated by the MTT assay, which is an assay dependent partially on the mitochondrial function. Moreover, in the presence of NAC, a GSH precursor, the MeHgCl induced cytotoxicity was significantly decreased whereas BSO, a specific GSH synthesis inhibitor,increased the MeHgCl induced cytotoxicity.The MeHgCl induced DNA fragmentation and chromatin condensation was consistent with the morphological alterations. The MeHgCl treated cells exhibited increasing annexin V-FITC binding to the phos-phatidylserine(PS)translocated from the inner to the outer leaflet of the plasma membrane and those cells with NAC pretreatment significantly exhibited decreasing annexin V-FITC binding compared to the cells treated with MeHgCl only. However BSO pretreatment markedly exhibited the increasing annexin V-FITC binding. The MeHgCl treated cells generated ROS, which was evidenced by the oxidation of dihydroethidine and the generation of the fluorescent product, ethidium. In addition, BSO pretreatment further enhanced the extent of ROS generation caused by MeHgCl whereas NAC pretreatment decreased the amount of ROS generation. MeHgCl led to a dose dependent decrease in the GSH content. Although MeHgCl exposure significantly reduced the GSH level, those cells that had a NAC pretreatment contained a higher level of GSH compared to the cells treated with MeHgCl only. In contrast, BSO pretreatment futher enhanced the extent of GSH depletion caused by MeHgCl. CONCLUSIONS: These results indicate that MeHgCl reduced the GSH content and impaired the defense against oxidative damage caused by ROS formation in RAW 264.7 cells. It is possible that these factors leads to the activation of the apoptosis signaling pathway. Ultimately these results suggest that GSH plays a crucial role in protecting the activity against MeHgCl induced apoptosis.
Animals ; Antioxidants ; Apoptosis* ; Cell Membrane ; Chromatin ; DNA Fragmentation ; Ethidium ; Glutathione* ; Mice

BACKGROUND: This study is designed to indicate the role of 3D-surface rendering of the MRI in defining and resect-ing the epileptogenic zone. METHODS: 25 healthy volunteers and 55 patients were studied. Conventional MRI and 3D-surface rendering were performed. Sulcal and gyral patterns were assesed by a neuroradiologist and a neurologist with-out the clinical informations. Chronic video-EEG monitoring with surface and subdural grid electrodes, and PET were done. Resection was performed based on data of the EEG recordings and 3D-surface rendering. RESULTS: Conventional MRI identified structural abnormality ("MRI-identifiable lesion") in 20 patients. 20 of 35 patients without structural abnormality in conventional MRI revealed abnormal sulcal and gyral patterns in 3D-surface rendering of MRI ("3D-identifiable lesion"). Subdural grid EEGs recorded focal or diffuse ictal EEG onset from the region of "3D-identifiable lesion". Histopathologic findings revealed cortical dysplasia in 48 and neocortical gliosis in seven. Overall surgical out-come, at the average follow up period of 32.5 months, showed class I in 63.6%, class II in 25.5%, and class III in 10.9%. Among 20 patients with "MRI-identifiable lesion", 80% were in class I and 20% were in class II. Among 35 patients without "MRI-identifiable lesion", 54.3% were in class I, 28.6% were class II, and 17.1% were in class III. 80% of 20 patients with "3D-identifiable lesion" showed class I and 20% of 15 patients without "3D-identifiable lesion" showed class I. CONCLUSIONS: Identification of "MRI-identifiable lesion" or "3D-identifiable lesion" was of value in defining the epileptogenic zone. Resection of "MRI-identifiable lesion" or "3D-identifiable lesion", which were epilep-togenic in EEGs, promised a good surgical outcome.
Electrodes ; Electroencephalography ; Epilepsy* ; Equidae ; Follow-Up Studies ; Gliosis ; Healthy Volunteers ; Humans ; Magnetic Resonance Imaging* ; Malformations of Cortical Development

OBJECTIVES: Apotosis induced by metals and metal-related deleterious conditions has only recently been studied. Although the toxic effects of heavy metal are well described, little is known about the mechanism of apoptosis by heavy metal toxicity. This study is designed to define the induction of apoptosis by which heavy metals exert the cytotoxic effect on human promyelocytic leukemic HL-60 cells. Methods After the incubation with CdC12, Na2SeO3 and HgC12, viability of the cells were measured by MTT assay. DNA fragmentation was analyzed by electrophoresis. For measurement of caspase 1 and 3-like proteases activity, the whole lysates were subjected to the proteolytic cleavage and then measured by using fluorospectrometry. c-JUN N-terminal kinase (JNK) activity was detected by an in vitro kinase assay. Transcriptional activities of activating protein-1 (AP-1) and nuclear factor-kB (NF-kB) were measured by elec trophoresis mobility shift assay (EMSA). RESULTS: Cadmium (l2OuiN/I) and selenium (30,iM) induce the apoptosis of HL-60 cells which is characterized by the ladder pattern of DNA fragmentation. Cadmium and selenium induce the activation of caspase-3 in a time dependent manner. They also increase the phosphotransferase activities of c-JUN N-terminal kinase (JNK) in cadmium and selenium treated HL-60 cells. Furthermore, cadmium and selenium increase the activation of transcriptional factors including AP-i and NF-kB. CONCLUSIONS: These results suggest that cadmium and selenium induce the apoptotic death of HL-60 cells via activation of DEVD-specific caspase, JNK and transcriptional factors such as AP-1 and NF-kB.
Apoptosis* ; Cadmium ; Caspase 1 ; Caspase 3 ; DNA Fragmentation ; Electrophoresis ; Electrophoretic Mobility Shift Assay ; HL-60 Cells* ; Humans ; JNK Mitogen-Activated Protein Kinases ; Metals ; Metals, Heavy* ; NF-kappa B ; Peptide Hydrolases ; Phosphotransferases ; Selenium ; Transcription Factor AP-1

OBJECTIVES: To evaluate the protective effects of glutathione (GSH) on the cytotoxicity of mercurial compounds(CH3HgCl, HgCl2) or cadmium chloride(CdCl2) in EMT-6 cells. METHODS: The compounds investigated were CH3HgCl, HgCl2, CdCl2, GSH, buthionine sulfoximine(BSO), L-2-oxothiazolidine-4-carboxylic acid(OTC). Cytotoxicity analysis consist of nitric oxide(NO) production, ATP production and cell viability. RESULTS: Mercurial compounds and cadmium chloride significantly decreased cell viability and the synthesis of NO and cellular ATP in EMT-6 cells. GSH was not toxic at concentrations of 0 - 1.6 mM. In the presence of GSH, mercurial compounds and cadmium did not decrease the production of ATP and nitrite in EMT-6 cells. The protective effects of GSH against the cytotoxicity of mercurial compounds and cadmium depended on the concentration of added GSH to the culture medium for EMT-6 cells. We evaluated the effects of intracellular GSH level on mercury- or cadmium-induced cytotoxicity by the pretreatment experiments. Pretreatment of GSH was not changed NO2- and ATP production, and pretreatment of BSO was decreased in dose- and time-dependent manner. Pretreatment of OTC was increased NO2- and ATP production in dose- and time-dependent manner. Because intracellular GSH level was increased by OTC pretreatment, the protective effect on mercury- and cadmium-induced cytotoxicity was increased. CONCLUSIONS: These results indicated that sulfhydryl compounds had the protective effects against mercury-induced cytotoxicity by the intracellular GSH levels.
Adenosine Triphosphate ; Cadmium Chloride ; Cadmium* ; Cell Survival ; Glutathione* ; Mercuric Chloride ; Nitric Oxide ; Sulfhydryl Compounds

The purpose of the present study was to elucidate the cytotoxical influence of mercurial compounds and the protective effect of selenium against mercurial compounds. The effects of mercury compounds and selenium on the syntheses of nitrite(NO2-) and ATP were observed in the cell cultures of EMT-6 cells and peritoneal macrophages from Balb/c mouse. The viabilities of EMT-6 cells and peritoneal macrophages at the end of culture were significantly decreased in dose-dependent manner by methylmercury chloride (CH3HgCl) added into the media. NO2- and ATP syntheses of the cells were dose-dependently inhibited by CH3HgCl. Simultaneous addition of the equimolar dose of selenium completely prevented mercury-induced inhibitions of NO2- and ATP syntheses, which were observed in both of EMT-6 cells and peritoneal macrophages. But these effects of selenium were not appeared in the new medium containing mercurials only which were removed the selenium after the pretreatment of selenium for 6 hours. These results suggest that protective effect of selenium against mercurial compounds was archived by the formation of a complex consisting of Se-Hg or Se-Hg-protein. Though its mechanism was not clear, the protective role of selemium against the mercury toxicity would be exhibited in the immunological system.
Adenosine Triphosphate ; Animals ; Cell Culture Techniques ; Macrophages, Peritoneal ; Mercury Compounds ; Mice ; Nitric Oxide ; Selenium*

No abstract available.
Selenium*