The Korean Social Workers' Burn-out Factors and Personal Traits in the Hospice and Palliative Care / 한국호스피스완화의료학회지

PURPOSE: This study investigated the Korean social workers' burn-out factors and personal traits in hospice and palliative care field, and also examined the effect and correlation between their professionality, social support and supervision. METHODS: Data (N=46) from 46 social workers working at hospice and palliative care field were collected, and the data were analyzed for the inferential statistics using t-test, ANOVA, correlation and multiple regression with the SPSS 12.0 program. RESULTS: General factors of the burn-out were age and work experience. The effect of the organization environment is greatly dependant on social support and supervision, and the burn-out were protected when workers got an emotional support from their family. For the workers with supervision, the less negative feeling, the better for the burn-out protection. Furthermore, the low burn-out was thought about when professional organization, self regulation, job vocation and autonomy were utilized. Regression analysis needed that the burn-out were protected well when individual autonomy among expertise was guaranteed. As for social support, vertical support was able to protect physical burn-out. CONCLUSION: The training program for social workers in hospices and palliative care field is essential to reduce and prevent the burn-out. Hospice should be more activated and a training program with up-to-date knowledge and information should be adopted.

Repression of TNF-alpha-induced IL-8 expression by the glucocorticoid receptor-beta involves inhibition of histone H4 acetylation

Increased expression of a number of proinflammatory genes, including IL-8, is associated with inflammatory conditions such as asthma. Glucocorticoid receptor (GR)beta, one of the GR isoforms, has been suggested to be upregulated in asthma associated with glucocorticoid insensitivity and to work as a dominant negative inhibitor of wild type GRalpha. However, recent data suggest that GRbeta is not a dominant negative inhibitor of GRalpha in the transrepressive process and has its own functional role. We investigated the functional role of GRbeta expression in the suppressive effect of glucocorticoids on tumor necrosis factor (TNF)-alpha-induced IL-8 release in an airway epithelial cell line. GRbeta expression was induced by treatment of epithelial cells with either dexamethasone or TNF-alpha. GRbeta was able to inhibit glucocorticoid-induced transcriptional activation mediated by binding to glucocorticoid response elements (GREs). The suppressive effect of dexamethasone on TNF-alpha-induced IL-8 transcription was not affected by GRbeta overexpression, rather GRbeta had its own weak suppressive activity on TNF-alpha-induced IL-8 expression. Overall histone deacetylase activity and histone acetyltransferase activity were not changed by GRbeta overexpression, but TNF-alpha-induced histone H4 acetylation at the IL-8 promoter was decreased with GRbeta overexpression. This study suggests that GRbeta overexpression does not affect glucocorticoid-induced suppression of IL-8 expression in airway epithelial cells and GRbeta induces its own histone deacetylase activity around IL-8 promoter site.

Repression of TNF-alpha-induced IL-8 expression by the glucocorticoid receptor-beta involves inhibition of histone H4 acetylation

Increased expression of a number of proinflammatory genes, including IL-8, is associated with inflammatory conditions such as asthma. Glucocorticoid receptor (GR)beta, one of the GR isoforms, has been suggested to be upregulated in asthma associated with glucocorticoid insensitivity and to work as a dominant negative inhibitor of wild type GRalpha. However, recent data suggest that GRbeta is not a dominant negative inhibitor of GRalpha in the transrepressive process and has its own functional role. We investigated the functional role of GRbeta expression in the suppressive effect of glucocorticoids on tumor necrosis factor (TNF)-alpha-induced IL-8 release in an airway epithelial cell line. GRbeta expression was induced by treatment of epithelial cells with either dexamethasone or TNF-alpha. GRbeta was able to inhibit glucocorticoid-induced transcriptional activation mediated by binding to glucocorticoid response elements (GREs). The suppressive effect of dexamethasone on TNF-alpha-induced IL-8 transcription was not affected by GRbeta overexpression, rather GRbeta had its own weak suppressive activity on TNF-alpha-induced IL-8 expression. Overall histone deacetylase activity and histone acetyltransferase activity were not changed by GRbeta overexpression, but TNF-alpha-induced histone H4 acetylation at the IL-8 promoter was decreased with GRbeta overexpression. This study suggests that GRbeta overexpression does not affect glucocorticoid-induced suppression of IL-8 expression in airway epithelial cells and GRbeta induces its own histone deacetylase activity around IL-8 promoter site.

The prevalence of adverse drug reactions to a short course anti-tuberculosis regimen / 대한내과학회지

BACKGROUND: Anti-tuberculosis drugs used in combination cause adverse drug reactions, but the prevalence of the reactions and risk factors have not been determined. This study aims to identify the prevalence and risk factors of adverse drug reactions (ADR) to the use of first line anti-tuberculosis drugs. METHODS: A total of 435 newly diagnosed patients with tuberculosis (44.1 years+/-19.0 years) were eligible for this study. All patients received daily oral isoniazid (300 or 400 mg), rifampicin (450 or 600 mg) and ethambutol (800 mg) for 6 months, and pyrazinamide (20 mg/kg) for 2 months. Blood tests were performed regularly (before treatment, 2 weeks after treatment, and bimonthly there after). Patients were interviewed 2 months and 6 months after treatment. A serious ADR was defined as any ADR that resulted in the discontinuation of one or more of the drugs. RESULTS: An ADR was noted in 52.6% of all patients. Gastrointestinal (19.3%), cutaneous (17.7%), hepatic (13.8%), renal (12.6%), and neurological (10.3%) ADRs were frequent and hematological (4.4%), musculoskeletal (3.0%) ADRs were less frequent. A skin ADR was associated with an elevated baseline of liver enzymes (odds ratio, 3.48; 95% CI, 1.2 to 9.9), whereas a hepatic ADR was associated with a history of chronic liver disease (odds ratio, 4.82; 95% CI, 1.7 to 13.2). The prevalence of any serious ADR was 9.7%. Occurrence of any serious ADR was associated with a history of chronic liver disease (odds ratio, 4.29; 95% CI, 1.4 to 13.6). CONCLUSIONS: Anti-tuberculosis drugs given in combination frequently caused a ADR and the findings suggest that a patient receiving anti-tuberculosis treatment should be closely monitored.

Expression of mRNA of GATA-3 and T-bet in the peripheral blood mononuclear cells of atopic asthmatics / 대한내과학회지

BACKGROUND: It is well known that the expression of Th2 cytokines are up-regulated in the atopic asthma. The study was to investigate the expression of transcription factors, such as GATA-3, c-maf, T-bet which are known to be involved in the T cell differentiation in the peripheral blood mononuclear cells (PBMCs) of atopic asthmatics. METHODS: PBMCs were obtained from non-atopic controls and atopic asthmatics and cultured for 48 hours, and then 12-o-tetracanoylphorbol-13-acetate (PMA) and calcium ionophore (ionomycin) were added. mRNA of GATA-3, c-maf, T-bet, IL-4, IL-5, IL-13 and IFN-gamma were measured by RT-PCR RESULTS: mRNAs of Th2 cytokines, such as IL-4, IL-5 and IL-13 were expressed higher in the atopic asthmatics, and that of Th1 cytokine, IFN-gamma was expressed higher in the non-atopic controls. GATA-3 and c-maf were expressed higher and T-bet was expressed lower in the atopic asthmatics. Expressions of GATA-3, c-maf and T-bet were not changed with the stimulation of PMA/Ionomycin. CONCLUSION: This study suggest that GATA-3, c-maf and T-bet participate in the Th2 type inflammation in atopic asthmatics, like GATA-3 and c-maf as stimulatory factors, and T-bet as inhibitory factor.

Effect of GRbeta expression on steroid-induced transcriptional activity in airway epithelial cells / 천식및알레르기

BACKGROUND: It has been known that GRbeta(90 kDa), an alternative splicing variant, can not bind ligand and may act as a domiant negative inhibitor of GRalpha. But there is little report on the effect of GRbeta on steroid-induced transrepression, and GRbeta as a dominant negative inhibitor is still uncertain. OBJECTIVE: The aim of this study is to investigate the functional role of GRbeta expression in steroid-induced transcriptional activity. METHODS: Steroid-induced transactivation was measured by using pGRE luciferase reporter gene in A549 cell line and steroid-induced transrepression was measured by using stable A549 IgGkappa-NFkappaB luciferase cell line, which contained the minimal IL-8 promoter region. Effect of GRbeta expression on steroid-induced transactivation or transrepression were investigated by comparing the results with or without pCMV GRbeta transfection by lipopectamine plus method. TNF-alpha was used as an activator of IL-8 and RU486 was used as a steroid antagonist. RESULTS: GRbeta expression inhibited steroid-induced transactivation, but did not inhibit steroid-induced transrepression. GRbeta expression caused transrepression of IL-8 under the pretreatment of RU486. CONCLUSION: The study suggests that GRbeta may not act as a dominant negative inhibitor of GRalpha, in the steroid-induced transrepression. Furthermore GRbeta looks having a suppressive activity on IL-8 transactivation.