The purpose of this study is to investigate the effect of job stress and social support on the organizational effectiveness of hospital employees and to examine the role of social support in the experience of job stress among the employees. Previous studies have yielded mixed results regarding the role of social support. Some studies provide supporting evidence for the buffering effect of social support, while others do not. Still others report findings about reverse buffering effects. These inconsistent findings are, in part, accounted for by methodological problems such as poor measurement, small sample size, and the existence of high multicollinearity. To examine more rigorously the role of social support in relation to the negative effects of job stress, this study was carefully designed to overcome methodolgical shortcomings found in the past research. In addition, unlike the previous studies, which were concerned mostly with health-related variables as consequences of job stress, in this study, three work-related variables (job satisfaction, organizational commitment, and intent to stay) which had close relationships with organizational effectiveness were examined as output variables. The sample used in this study consisted of 353 employees from a university hospital in the suburbs of seoul. Data were collected with self-administered questionnaires and analyzed using canonical analysis and hierarchical regression analysis. The results of this study indicate that; (l) job stress has negative main effects on job satisfaction, organizational commitment, and intent to stay; (2) social support has positive main effects on the same three output variables, (3) social support does not moderate the harmful effects of job stress on the three outcome variables, and (4) the three-way interaction effects of (social support * job stress * gender) and of (social support * job stress * education) are not supported The implications of these findings for the management of human resources are discussed.
Humans ; Job Satisfaction ; Surveys and Questionnaires ; Sample Size ; Seoul

No abstract available.
Nevus

BACKGROUND: The aim of this study was to compare the efficacy of ketorolac, paracetamol, and paracetamol plus morphine on pain relief after thyroidectomy. METHODS: Eighty patients were randomly allocated to one of the 4 groups: normal saline (group C), ketorolac 30 mg (group K), paracetamol 1 g (group P), and paracetamol 700 mg plus morphine 3 mg (group PM). Each regimen was administered intravenously (IV) 30 min. before the end of surgery. If pain was not relieved, patients received an IV bolus of pethidine hydrochloride 25 mg. Pain intensity using a visual analogue scale (VAS) was recorded at 0.5, 1, 2, 4, and 6 hr after the end of surgery. RESULTS: VAS at 0.5 and 1 hr after the end of surgery were significantly lower in group K, group P, and group PM than in group C (P < 0.05). The number of patients receiving pethidine hydrochloride at 0.5 and 1 hr after the end of surgery was significantly lower in group K, group P, and group PM than in group C (P < 0.05). There was no significant difference among the groups in the incidences of adverse events associated with study medications and patient satisfaction (P > 0.05). CONCLUSIONS: Paracetamol 1 g IV possesses a similar analgesic efficacy to ketorolac 30 mg IV after thyroidectomy. Paracetamol may represent an alternative to ketorolac for pain prevention after mildly to moderately painful surgery in situations where the use of NSAIDs is unsuitable.
Acetaminophen ; Analgesics ; Anti-Inflammatory Agents, Non-Steroidal ; Humans ; Incidence ; Ketorolac ; Meperidine ; Morphine ; Patient Satisfaction ; Thyroidectomy

OBJECTIVE: The aim of this study is to evaluate the role of tumor suppressor genes, p53 and Rb gene, as well as apoptosis in the carcinogenesis of ovarian epithelial tumors. And the value of these factors as prognostic markers to tell the transformation of borderline tumors to overt carcinomas is also studied. METHOD: Thirty cases of ovarian epithelial benign and borderline tumors and invasive carcinoma were used and the expression of the p53 protein and Rb gene protein were evaluated by immunohistochemical method. The apoptosis was evaluated by TUNNEL method. RESULTS: Positive rate of p53 expression in benign, borderline and invasive tumors were 0, 28, and 94 %, respectively. And also, p53 was highly expressed in chemoresistant cases (2/3), in residual tumor (4/5) and in recurred cancer (2/2). Rb protein was partly lost in the borderline tumors, but the rate of Rb protein loss in both borderline tumors and invasive carcinomas were similar. Apoptosis were more active in overt carcinomas than in borderline and benign tumors. In borderline tumors, p53 protein was expressed as 28.6% positivity, and apoptosis was expressed as 28.6% negativity, which showed indirectly that there was apoptosis induction effect of p53. In ten cases of invasive carcinomas showing highly expressed p53, apoptosis revealed all positive reaction except 2 cases, and Rb protein revealed variously. This result supported the apoptosis imduction effect of p53, but it was difficult to find the association of expression degree between the two tumor supressor genes CONCLUSION: In conclusion, the values of p53 is a discriminating factor of malignancy from benign and the expression of p53 is related with clinical aggressivity such as recurrence and residual cancers. Apoptosis are more active in overt carcinoma than in benign & borderline tumor, and in borderline tumor the expression of p53 is related to apoptosis induction which results to carcinomatous change.
Apoptosis* ; Carcinogenesis ; Genes, Retinoblastoma* ; Genes, Tumor Suppressor ; Neoplasm, Residual ; Recurrence ; Retinoblastoma Protein

No abstract available.
Onychomycosis

No abstract available.
Candida ; Onychomycosis

No abstract available.
Aged* ; Dementia* ; Gyeongsangbuk-do* ; Humans ; Prevalence*

No abstract available.
Aged* ; Dementia* ; Gyeongsangbuk-do* ; Humans ; Prevalence*

No abstract available.
Mucopolysaccharidosis II*

No abstract available.
Mucopolysaccharidosis II*