Search

A case is reported of a 47-year-old man with symptoms of liver cirrhosis, a chronic degenerative liver disease. The patient had a history of a kidney disorder and a submassive liver necrosis (cell death) of unknown cause, from which he had recovered. Between the ages of 45 and 47, the patient had episodes of hepatic encephalopathy (nervous system impairment caused by liver failure) often associated with peritonitis (bacterial infection of the abdominal wall). He also had poor function of the portal vein, which carries blood from the abdominal organs to the liver. The patient was given a liver transplant, and analysis of the diseased liver showed nodular regenerative hyperplasia (NRH) rather than cirrhosis. Branches of the portal vein showed evidence of old clots. NRH is distinguished by multiple nodules, containing both hyperplastic (overgrown) and atrophic (wasting) liver cells, which spread throughout the liver. Central liver veins, important for liver function, may be absent or closed, but the fibrosis or inflammation typical of cirrhosis is not present. The patient's symptoms, including encephalopathy, were not typical of NRH. It is possible that the old liver disease resulted in portal vein clotting, which probably contributed to the medical picture. The study points out that medical diagnosis without cellular studies of the diseased liver can be misleading. (Consumer Summary produced by Reliance Medical Information, Inc.)

Regulated cell migration plays a critical role in normal development, whereas misregulated cell migration can cause developmental defects, tumor invasion, and metastasis. To better understand the molecular mechanisms of cell migration, we are studying the migration of a small group of follicle cells in the Drosophila ovary, the border cells. We have identified a new locus required for border cell migration, which we call stuck in place (stuk). stuk was originally identified in a screen for mutations that disrupt border cell migration in mosaic mutant clones (Liu and Montell, 1999). We examined the distribution of two markers for the border cells, Armadillo/[Beta]-catenin and E-cadherin, in stuk mutant egg chambers and found that both proteins are aberrantly distributed in border cells that fail to migrate. We have evidence that stuk is not required cell autonomously in the border cells, but instead is required in other follicle cells to promote border cell migration. This result is surprising, since all other genes required for border cell migration act solely in the border cells. Therefore, stuk is the first gene known to control border cell migration but not to be required in the border cells themselves. We will report our current efforts to map and clone the stuk gene.