• Korean Security Journal
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• no.57
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• pp.57-84
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• 2018

This study assumes that the perception of the ex-prisoner's against stigma will affect trust in interpersonal relationship. Prior studies have suggested that there is a stigma at the base of the awareness where people avoid and discriminate against ex-prisoner's. This in turn affects ex-prisoner's' recividicism, but there is no study about ex-prisoner's perception of stigma in Korea. Although stigma can be explained in numerous ways, this study is based on the opinion of Phillips(2016), which divides the subscale of stigma as perceived public stigma, perceived personnel stigma, and self stigma. He insisted that ex-prisoner's believe perceived public stigma higher than self-stigma. these results are consistent with this study. However, it is important to note that although ex-prisoner's are more aware of public stigma than self-stigma, they are actually more influenced by self stigma in pereonal relationships. This means that ex-prisoner's are more susceptible to internal psychological awareness than external social recognition. Therefore, the development and intervention of the program to overcome the internal self-stigma of the released prisoner is required. In this study, first, stigma, especially self-stigma turned out to have influence on the interpersonal trust. Therefore, as self-stigma level increased, the interpersonal trust decreased in most cases. Second, it was shown that stigma has the greatest influence on children out of family members, co-workers out of social relationship, self trust out of general relationship in. This confirms that stigma is a factor that greatly influences relationship between important people for ex-prisoner's. Third, since self-sigma negatively reestablish self-identity, make individuals recognize themselves as deviators and show bad lifestyle, which lead them to become habitual offender, ex-prisoner's need to make efforts to overcome self-stigma, and development and intervention of program that can make ex-prisoner's have positive self identity is requested. Fourth, although participants in the study were only male, it seems that there is difference in recognition of stigma by gender, and influence of stigma not only on interpersonal relationships, but also on social reintegration and recidivism imply that these might be good future research topics.

• Tuberculosis and Respiratory Diseases
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• v.50 no.1
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• pp.52-66
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• 2001

Background : NF-${\kappa}B$ is the most important transcriptional factor in IL-8 gene expression. Triptolide is a new compound that recently has been shown to inhibit NF-${\kappa}B$ activation. The purpose of this study is to investigate how triptolide inhibits NF-${\kappa}B$-dependent IL-8 gene transcription in lung epithelial cells and to pilot the potential for the clinical application of triptolide in inflammatory lung diseases. Methods : A549 cells were used and triptolide was provided from Pharmagenesis Company (Palo Alto, CA). In order to examine NF-${\kappa}B$-dependent IL-8 transcriptional activity, we established stable A549 IL-8-NF-${\kappa}B$-luc. cells and performed luciferase assays. IL-8 gene expression was measured by RT-PCR and ELISA. A Western blot was done for the study of $I{\kappa}B{\alpha}$ degradation and an electromobility shift assay was done to analyze NF-${\kappa}B$ DNA binding. p65 specific transactivation was analyzed by a cotransfection study using a Gal4-p65 fusion protein expression system. To investigate the involvement of transcriptional coactivators, we perfomed a transfection study with CBP and SRC-1 expression vectors. Results : We observed that triptolide significantly suppresses NF-${\kappa}B$-dependent IL-8 transcriptional activity induced by IL-$1{\beta}$ and PMA. RT-PCR showed that triptolide represses both IL-$1{\beta}$ and PMA-induced IL-8 mRNA expression and ELISA confirmed this triptolide-mediated IL-8 suppression at the protein level. However, triptolide did not affect $I{\kappa}B{\alpha}$ degradation and NF-$_{\kappa}B$ DNA binding. In a p65-specific transactivation study, triptolide significantly suppressed Gal4-p65T Al and Gal4-p65T A2 activity suggesting that triptolide inhibits NF-${\kappa}B$ activation by inhibiting p65 transactivation. However, this triptolide-mediated inhibition of p65 transactivation was not rescued by the overexpression of CBP or SRC-1, thereby excluding the role of transcriptional coactivators. Conclusions : Triptolide is a new compound that inhibits NF-${\kappa}B$-dependent IL-8 transcriptional activation by inhibiting p65 transactivation, but not by an $I{\kappa}B{\alpha}$-dependent mechanism. This suggests that triptolide may have a therapeutic potential for inflammatory lung diseases.