Incidental Ovarian Lesions

Incidental ovarian lesions are diagnostic challenges owing to their wide disease spectrum, ranging from normal findings to malignant ovarian tumors. There are several physiologic ovarian lesions that may not require any follow-up or treatment. While some lesions demonstrate their benign nature on imaging, some significant radiologic features may suggest malignant potential. Therefore, precise interpretation of imaging findings and proper recommendations for clinicians by radiologists are essential for managing incidental ovarian lesions to avoid unnecessary examinations or invasive treatments. The aim of this review is to describe the radiologic findings of commonly encountered incidental ovarian lesions on ultrasonography or computed tomography and to explain the management plan according to the stratified risk for malignancy in each ovarian lesion.

Effects of norepinephrine and neuropeptide Y on the contractility of small mesenteric artery from 2K1C and DOCA-salt hypertensive rats

The present study was conducted to investigate the possible role of the sympathetic nervous system in two-kidney, one clip (2K1C) and deoxycorticosterone acetate (DOCA)-salt hypertension. 2K1C and DOCA-salt hypertension were made in Sprague-Dawley rats. Four weeks after induction of hypertension, systolic blood pressure measured in conscious state was significantly higher in 2K1C (216+/-18 mmHg) and DOCA-salt (205+/-29 mmHg) groups than that in control (128+/-4 mmHg). The third branches (<300 micrometer in outer diameter) of the mesenteric artery were isolated and cut into ring segments of 2apprx3 mm in length. Each ring segment was mounted in tissue bath and connected to a force displacement transducer for measurement of isometric tension. The arterial rings were contracted by application of norepinephrine (NE) in a dose-dependent manner. The amplitude of the NE-induced contraction of the vessels was significantly larger in hypertension than in control. The NE-induced contraction was significantly enhanced by neuropeptide Y (NPY) in hypertension. Reciprocally, NPY-elicited vasocontraction was increased by NE in hypertension. These results suggest that the sympathetic nervous system contributes to the development of 2K1C and DOCA-salt hypertension.