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Role of Clusterin and Tumor Necrosis Factor Receptors on the Apoptosis of Prostate Cancer Cells
주관중 대한남성과학회 2011 The World Journal of Men's Health Vol.29 No.1
Purpose: In prostate cancer, the anti-apoptotic mechanism of sulfated glycoprotein-2 (clusterin) against tumor necrosis factor-alpha (TNF-α) receptors and the action of type 2 TNF-α receptor (TNFR2) were investigated. Materials and Methods: TNF-α, agonistic-TNF type 1 receptor (TNFR1) antibody, agonistic-TNF-R2 antibody and their combination were treated in PC3 cell line with or without anti-clusterin. Cytotoxicity was assessed by trypan blue dye exclusion assay. By using flowcytometric analysis, the exact amount of apoptosis and their changes were assessed. Results: Apoptosis was significantly increased in both agonistic-TNFR1 antibody and TNF-α treated cases after blocking the activity of clusterin. The more the anti-clusterin antibody added, the more the apoptosis occurred. The increase of total apoptosis was greater in TNF-α treated cells than in agonistic-TNFR1 antibody treated ones. However, there was no increase of apoptosis in agonistic-TNFR2 antibody and TNF-α with agonistic-TNFR2 antibody treated cases, respectively. Conclusions: Clusterin prevents TNF-α induced apoptosis by affecting TNFR1. The difference in degree of apoptosis between agonistic-TNFR1 antibody treated cells and TNF-α treated ones suggests the possibility of the action of TNFR2. It may be associated with affinity of TNF-α to the tumor cell surface.
재생검을 통해 전립선암으로 진단받은 환자의 임상적 예측요인
주관중,권칠훈 대한남성과학회 2011 The World Journal of Men's Health Vol.29 No.1
Purpose: We investigated the predictive factors in patient with prostate cancer diagnosed by repeat prostate biopsy, where initial prostate biopsy results were negative for malignancy. Materials and Methods: Between March 2000 and June 2007, 1280 men with suspected prostatic cancer underwent transrectal ultrasound guided needle biopsy of the prostate, with 148 (11.6%) diagnosed as having prostate cancer. Of 1132 men whose biopsy results were negative for malignancy, 655 whose prostate specific antigen (PSA) was elevated persistently underwent second biopsy, and 462 underwent third biopsy as the same course. Twelve core biopsies were performed in the majority of patients. To determine predictive factors, we evaluated prostate volume, serum PSA, percent free PSA, PSA density (PSAD), transition zone PSAD, PSA velocity (PSAV) and pathological report of previous biopsy between the men with cancer detection and the men with negative biopsy in second and third biopsy. Results: Overall cancer detection rate was 16.3% (208/1280). From the first, second and third biopsies, the cancer detection rate were 11.6, 5.5 and 5.2%, respectively. There were significant differences in percent free PSA, transition zone PSAD, PSAV between cancer and negative biopsy groups after serial repeat biopsies (p<0.05). Multivariate logistic regression analysis revealed that the transition zone PSAD, PSAV, and presence of either atypical small acinar proliferation (ASAP) or high grade prostatic intraepithelial neoplasia (HGPIN) in initial biopsy specimen were significant predictors for prostate cancer diagnosed by repeat biopsy. Conclusions: Of the men with negative results on the first biopsy, 60 (5.4%) were diagnosed prostate cancer after serial biopsies. The transition zone PSAD, PSAV, and presence of either ASAP or HGPIN in initial biopsy specimen are predictable factors for prostate cancer detection on repeat biopsy.
트레드밀 운동이 당뇨유발 쥐의 대뇌피질에서 세포외 신호 조절 단백질 분해 효소의 발현에 미치는 영향
주관중,백성수 한국코칭능력개발원 2006 코칭능력개발지 Vol.8 No.4
본 연구는 트레드밀 운동이 당뇨유발 쥐의 일차․이차 운동피질 및 체지각 대뇌피질에서 세포외 신호 조절 단백질 분해 효소의 발현에 미치는 영양을 규명하기 위하여 7주령의 Sprague-Dawley계 수컷 흰쥐 총 48마리를 대조군 (n = 12), 당뇨유발 군 (n = 12), 당뇨 및 저강도 트레드밀 운동군 (n = 12), 당뇨 및 중강도 트레드밀 운동군 (n = 12)으로 분류하여 일일 1회, 10일 동안 운동을 실시하였다. 운동피질 및 체지각 대뇌피질에서 세포외 신호 조절 단백질 분해 효소의 발현을 관찰하기 위하여 세포외 신호 조절 단백질 분해 효소 면역조직화학법을 실시하였다. 세포외 신호 조절 단백질 분해 효소의 발현을 조사한 결과 대조군과 비교하여 당뇨유발 군에서 세포외 신호 조절 단백질 분해 효소의 발현이 운동피질 및 체지각 대뇌피질에서 유의하게 감소하였다. 트레드밀 운동은 운동피질 및 체지각 대뇌피질의 세포외 신호 조절 단백질 분해 효소의 발현을 증가시켰고, 이러한 증가 작용은 강도 의존적으로 나타났다. 본 연구결과, 트레드밀 운동이 당뇨유발 쥐의 인산화된 세포외 신호 조절 단백질 분해 효소의 발현 수준을 증가시키는 역할을 한다고 사료되며, 운동의 이러한 작용은 당뇨에 의하여 저하된 뇌의 신호 전달 기능을 정상으로 되돌려 주는 기능을 할 것으로 사료된다.