Computed tomography and magnetic resonance imaging findings in cases of dermoid cyst coexisting with surface epithelial tumors in the same ovary.

OBJECTIVE: The purpose of this work was to describe the computed tomography (CT) and magnetic resonance imaging (MRI) findings in cases of dermoid cysts coexisting with surface epithelial tumors in the same ovary. METHODS: The pathologic reports of 141 dermoid cysts, 97 mucinous and 35 serous tumors were reviewed. The CT and/or MR images in the cases with a dermoid cyst and a surface epithelial tumor coexisting in the same ovary were analyzed. RESULTS: Eleven cases of mucinous tumors (6 benign, 3 low-grade, and 2 malignant) coexisted with dermoid cysts. Mucinous tumors were found in coexistence with 11.3% of dermoid cysts, and dermoid cysts were found in coexistence with 7.8% of mucinous tumors. In 10 cases, 3 radiologic patterns were observed: small fatty foci in the septa of the cystic tumor, an adjacent fat-containing component and a septated cystic component, and a dermoid cyst with no detectable mucinous tumor component. No histopathologically specific differences were observed between these groups. Small amounts of mucinous components were difficult to detect, but small fatty foci were easily detected. In 1 case, mucinous carcinoma formed a mass lesion in the wall of the dermoid cyst. CONCLUSIONS: The coexistence of these two neoplasms was not rare. If a dermoid cyst accompanies a multiseptated cyst and if the multiseptal cyst contains fatty foci, these two components may be associated. Recognizing the potential for the coexistence of these two neoplasms in the same ovary is essential for making a correct diagnosis.

Mesaconitine-induced relaxation in rat aorta: role of Na+/Ca2+ exchangers in endothelial cells.

Previously, we reported that mesaconitine, an aconite alkaloid, increased intracellular Ca(2+) concentration ([Ca(2+)](i)) level in endothelium and caused relaxation in rat aorta via nitric oxide production. In the present study, we investigated the mechanisms of increase in the [Ca(2+)](i) level induced by mesaconitine in rat aorta and in human umbilical vein endothelial cells (HUVECs). Treatment with the low Na(+) buffer delayed the 30 microM mesaconitine-, but not 10 microM acetylcholine-, induced relaxation in rat aorta. Treatments with an inhibitor of Na(+)/Ca(2+) exchangers (20 microM 3',4'-dichlorobenzamil) and a reversed mode (Ca(2+) influx) inhibitor of the exchangers (30 microM 2-[2-[4-(4-nitrobenzyloxy)phenyl]ethyl]isothiourea methanesulfonate, KBR7943) showed similar effects. In HUVECs, 30 microM mesaconitine increased the [Ca(2+)](i) level in the presence of extracellular CaCl(2) and NaCl, and the response was inhibited by KBR7943. Mesaconitine increased intracellular Na(+) concentration level in HUVECs. The [Ca(2+)](i) response by mesaconitine was inhibited by 100 microM D-tubocurarine (an inhibitor of nicotinic acetylcholine receptors), but was not inhibited in the glucose-free buffer and by inhibitors of Na(+)/H(+) exchangers. These findings suggest that mesaconitine stimulated Ca(2+) influx via the Na(+)/Ca(2+) exchangers in endothelial cells and caused relaxation in the aorta. The possibility of D-tubocurarine-sensitive Na(+) channels as target(s) of mesaconitine is discussed.