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톨루엔을 포함한 유기용제의 직업적 폭로로 인한 신경내분비계 영향
이채언,이종태,정의화,손혜숙,문덕환,전진호,강정학,이창희,김휘동,김종한,정귀옥 大韓産業醫學會 1995 대한직업환경의학회지 Vol.7 No.2
Long term occupational exposure to solvent mixtures may cause adverse effects to the central nervous system with neurobehavioral symptoms. And some organic slovents have been suggested to cause impairment of tuberoinfundibular dopaminergic activity and neurochemical mechanisms controlling pituitary secretion. For the purpose of assessing neuroendocrine effects in occupational solvents exposure, hormonal study settings (shoes-manufacturing industry & fishing products industry) and compared with nonexposed controls(33 men, 85 women). Male workers exposed to solvent mixtures had significantly lower plasma level of follicle-stimulating hormone(FSH) than nonexposed male controls. While female workers exposed to solvent mixtures had significantly lower plasma levels of growth hormone(GH), and thyroid-stimulating hormone(TSH) than nonexposed female controls. The results of significant decrease in plasma concentrations of pituitary hormones(FSH, GH, and TSH) in workers exposed solvent mixtures indicate that occupational exposure to solvent mixtures may induce neuroendocrine effects through an effect on hypothalamic pituitary axis.
Chun, Sung Won,Song, Young Tack,Lee, Jai Hak,Chang, Suk Kyun,Kim, Jin,Cho, Won Il,Lee, Jong Seo,Kim, Eung Kook,Kim, Chang Soo,Kim, Seung Nam,Choo, Sang Yong CATHOLIC MEDICAL CENTER 1995 Bulletin of the Clinical Research Institute Vol.23 No.2
Carcinogenesis of colorectal carcinoma is known as a series of genetic changes such as point mutation of ras oncogene and genetic alterations of chromosomes 5q, 17p and 18q. The mutation of p53 gene on chromosome 17p is known to be required for malignant transformation of colorectal tumors and occurred near the transition from benign to malignant growth and caused the accumulation of the mutant p53 protein to high levels in cancer clells. To examine the correlation between the expression of the mutant p53 protein and disease severity of colorectal tumors, 115 paraffin-embedded tissue sections of variable patients were utilized: 15 normal colon tissues(group 1), 30 colorectal adenoma(group 2), and 70 colorectal adenoearcinoma (group 3). The expression of the mutant p53 protein was examined immunohistochemically using monoclonal antibody against the mutant p53 protein. The expression rate of the mutant p53 protein of each group was analyzed according to the clinical stage, pathologic parameters of tumor invasion (Iymph node involvement, Iymphatic invasion, perineural invasion, vein invasion), tumor location, and differentiation grade. The results were as follows: 1. There was no positive expression of the mutant p53 protein in group 1 and 2, but 41.4% of positive expression rate in group 3. 2. In group 3, the positive expression rate of the mutant p53 protein was gradually decreased from 50.0%(4.8) of Dukes'A, 48.0%(12.25) of Dukes'B, 40.9%(9/22) of Dukes'C to 26.7%(4.15) of Dukes'D. The difference between that of Dukes'A, B, C and that of Dukes'D was statistically significant(P<0.05). 3. The positive expression rates of the mutant p53 protein in group 3 without Iymph node involvement, Iymphatic invasion, perineural invasion and vein invasion were 48.5%(16.33), 47.8%(11/23), 50.O%(25.50) and 44.1%(26/59) respectively, which were significantly higher than 39.4%(13.37), 38.3%(18.47), 20.0%(4/20) and 27.3%(3.11) in group 3 with positive pathologic findings(P<0.05, p<0.01). 4. The positive expression rates of the mutant p53 protein in group 3 of rectum, sigmoid colon transverse and descending colon, and cecum and ascending colon were 48.7%(19/39), 33.3%(4/13), 22.2%(2/9) and 40.0%(4.10) respectively. Cancers of rectum, cecum and ascending colon revealed significantly higher rates of positivity than other site. 5. The positive expression rates of the mutant p53 protein in group 3 of well, moderately, and poorly differentiated adenocarcinoma and mucinous carcinoma were 45.5%(5.11), 45.3%(24.53) and 0%(O/6). Well and moderately differentiated adenocarcinoma revealed significantly higher positive expression rate than poorly differentiated adenocarcinoma and mucinous carcinoma. With the above results, the positive expression of the mutant p53 protein seems to be specific to colorectal adenocarcinoma, and the expression rate of which was reciprocally parallel to the clinical stage and severity of pathologic findings. In conclusion, the expression of the mutant p53 protein might have a prognostic value in colorectal cancer patients.