Chronic pelvic pain is a common, disabling problem among women. Although chronic pelvic pain can be produced by many conditions, some gynecologic causes are frequently overlooked and underdiagnosed, resulting in inappropriate referral and inadequate treatment. The gynecologic conditions most often unrecognized are endometriosis, adenomyosis, pelvic congestion, and less common congenital and acquired abnormalities. Transvaginal ultrasonography (US) is helpful for assessing endometriotic cysts but has a limited role in the diagnosis of adhesions or peritoneal implants. The classic magnetic resonance (MR) imaging features diagnostic of endometrioma are a cystic mass with high signal intensity on T1-weighted images and loss of signal intensity on T2-weighted images. When transvaginal US findings are suggestive of adenomyosis, MR imaging is used as the definitive imaging modality for diagnosis. High-resolution transvaginal US and MR imaging can help establish the diagnosis of adenomyosis with a high degree of accuracy, since the imaging appearance closely correlates with the histopathologic characteristics. Pelvic varices can be identified by using transvaginal US with color Doppler and Doppler spectral analysis. Three-dimensional T1 gradient-echo sequences performed after the intravenous administration of gadolinium are the most effective MR imaging sequence for demonstrating pelvic varices. Blood flow in pelvic varices appears with high signal intensity. Recent advances in radiologic imaging and therapeutic procedures make it possible to diagnose accurately the conditions producing chronic pelvic pain in most women and to guide effective treatment.

ABSTRACT

Bcl-2 protects cells against Ras-mediated apoptosis; this protection coincides with its binding to Ras. However, the protection mechanism has remained enigmatic. Here, we demonstrate that, upon apoptotic stimulation, newly synthesized Bcl-2 redistributes to mitochondria, interacts there with activated Ras, and blocks Ras-mediated apoptotic signaling. We also show, by employing bcl-2 mutants, that the BH4 domain of Bcl-2 binds to Ras and regulates its anti-apoptotic activity. Experiments with a C-terminal-truncated Ras or a farnesyltransferase inhibitor demonstrate that the CAAX motif of Ras is essential for apoptotic signaling and Bcl-2 association. The results indicate a potential mechanism by which Bcl-2 protects cells against Rasmediated apoptotic signaling.