• 한국조사연구학회지:조사연구
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• 제11권3호
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• pp.19-32
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• 2010

본 연구에서는 일반인들의 도박 중독 유병률 조사에 활용할 수 있는 단축형 조사도구를 개발하고, 도박 중독자 선별을 위한 기준점(cutoff score)을 탐색했다. 먼저 501명의 도박 이용자들을 대상으로 K-PGSI(Korean Problem Gambling Severity Index)의 단축형 척도를 개발했다. 문항을 선별하기 위해 원척도의 요인부하량과 문항-총점 간 상관, 응답자들의 반응 빈도나 전문가의 경험적 판단 등을 단계적으로 참고하여 요인타당도와 신뢰도가 양호한 네 문항의 단축형 척도를 개발했다. 다음으로 일반인 1,584명을 대상으로 단축형 척도를 교차타당화 하고, 도박 중독자 선별을 위한 기준점을 개발했다. 단축형 척도의 기준점으로 도박 중독 집단을 선별할 때 나타난 민감도(sensitivity)와 특이도(specificity)는 각각 1.00과 0.99로 모두 우수했다. 끝으로 도박 중독 유병률 조사에 본 척도를 어떻게 활용할 수 있을지 논의하였다.

• Journal of Microbiology and Biotechnology
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• 제16권1호
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• pp.84-91
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• 2006

A Saccharomyces cerevisiae pgs1 nulI mutant, which is deficient with phosphatidyl glycerol (PG) and cardiolipin (CL) biosynthesis, grows well on most fermentable carbon sources, but fails to grow on non-fermentable carbon sources such as glycerol, ethanol, and lactate. This mutant also cannot grow on galactose medium as the sole carbon source. We found that the incorporation of $[^{14}C]-galactose$, which is the first step of the galactose metabolic pathway (Leloir pathway), into the pgs 1 null mutant cell was extremely repressed. Exogenously expressed PGS1 (YCpPGS1) under indigenous promoter could completely restore the pgs1 growth defect on non-fermentable carbon sources, and dramatically recovered $[^{14}C]-galactose$ incorporation into the pgs1 mutant cell. However, PGS1 expression under the GALl promoter $(YEpP_{GAL1}-PGS1myc)$ could not complement pgs1 mutation, and the GAL2-lacZ fusion gene $(YEpP_{GAL2}-lacZ)$ also did not exhibit its $\beta-galactosidase$ activity in the pgs1 mutant. In wild-type yeast, antimycin $A(1\;{\mu}g/ml)$, which inhibits mitochondrial complex III, severely repressed not only the expression of the GAL2-lacZ fusion gene, but also uptake of $[^{14}C]-galactose$. However, exogenously expressed PGS1 partially relieved these inhibitory effects of antimycin A in both the pgs1 mutant and wild-type yeast, although it could not basically restore the growth defect on galactose by antimycin A. These results suggest that the PGSI gene product has an important role in utilization of galactose by Gal genes, and that intact mitochondrial function with PGS1 should be required for galactose incorporation into the Leloir pathway. The PGS1 gene might provide a clue to resolve the historic issue about the incapability of galactose with deteriorated mitochondrial function.