Accuracy of frozen section diagnosis for ovarian tumors according to histologic type and malignant potential / 부인종양

OBJECTIVE: The purpose of this was to evaluate accuracy of frozen section diagnosis for ovarian tumors according to histologic type and malignant potential. METHODS: We compared the frozen section and final diagnosis of patients with ovarian tumors from April 2001 to April 2006. Of these 1138 cases, 628 cases (55.2%) were epithelial ovarian tumors. Benign, borderline, and malignant epithelial tumors were 380 (60.5%), 87 (13.9%), and 161 (25.6%) cases. The accuracy of frozen section diagnosis was analyzed according to histologic type and malignancy potential. RESULTS: The overall accuracy of frozen section diagnosis was 93.9%. The accuracy for benign, borderline, and malignant tumors were 93%, 92%, and 98%, respectively. The accuracy of frozen section diagnosis was significantly low in mucinous tumors and borderline malignant tumors. However the borderline malignancy was the only independent factor associated with the inaccuracy of frozen section diagnosis (OR: 12.2, 95% CI: 6.5-23.1). The sensitivity for immature teratoma was as low as 63.6%. CONCLUSION: Our data shows that the accuracy is low in mucinous tumors, borderline tumors, and immature teratomas and the borderline malignancy is independent factor associated with inaccuracy of frozen section diagnosis.

The roles of arachidonic acid and calcium in the angiotensin II-induced inhibition of Na+ uptake in renal proximal tubule cells

Angiotensin II (ANG II) has a biphasic effect on Na+ transport in proximal tubule: low doses of ANG II increase the Na+ transport, whereas high doses of ANG II inhibit it. However, the mechanisms of high dose ANG II-induced inhibition on Na+ uptake are poorly understood. Thus the aim of the present study was to investigate signal transduction pathways involved in the ANG II-induced inhibition of Na+ uptake in the primary cultured rabbit renal proximal tubule cells (PTCs) in hormonally defined serum-free medium. ANG II (10-9 M)-induced inhibition of Na+ uptake was blocked by losartan (10-8 M, AT1 antagonist), but not by PD123319 (10-8 M, AT2 antagonist) (P < 0.05). ANG II-induced inhibition of Na+ uptake was also completely abolished by neomycin (10-4 M, PLC inhibitor), W-7 (10-4 M, calmodulin antagonist), and AACOCF3 (10-6 M, PLA2 inhibitor) (P < 0.05). ANG II significantly increased (3H)arachidonic acid (AA) release compared to control. The ANG II-induced (3H)AA release was blocked by losartan, AACOCF3, neomycin, and W-7, but not by PD123319. ANG II-induced (3H)AA release in the presence of extracellular Ca2+ was greater than in Ca2+-free medium, and it was partially blocked by TMB-8 (10-4 M, intracelluar Ca2+ mobilization blocker). However, in the absence of extracellular Ca2+, it was completely blocked by TMB-8. In addition, econazole (10-6 M, cytochrome P-450 monooxygenase inhibitor) and indomethacin (10-6 M, cyclooxygenase inhibitor) blocked ANG II-induced inhibition of Na+ uptake, but NGDA (10-6 M, lipoxygenase inhibitor) did not affect it. In conclusion, PLA2-mediated AA release is involved in ANG II-induced inhibition of Na+ uptake and is modulated by (Ca2+)i in the PTCs.