Relationship between pattern of tumor enhancement and clinicopathologic characteristics in intrahepatic cholangiocarcinoma.

AIM: Common enhancement pattern of intrahepatic cholangiocarcinoma (ICC) on computed tomography (CT) is that of hypovascular enhancement; however, in some cases, tumor shows identical enhancement in the arterial phase to that in hepatocellular carcinoma. To identify the specific characteristics of different enhancement patterns, we examined the relationship between CT enhancement pattern and clinicopathological features or postoperative prognosis. METHOD: Subjects were 43 consecutive ICC patients who had undergone hepatectomy. Enhancement patterns were divided into two types: hypovascular or delayed enhancement (Type A), and early enhancement in the arterial phase (Type B). RESULTS: Type A enhancement was observed in 23 patients and Type B in 20. Accompanying chronic viral hepatitis was significantly more frequent in Type B than Type A. Well-differentiated adenocarcinoma was significantly more frequent in Type B than Type A. Multiple tumors were significantly more frequent in Type A than Type B. Japanese TNM stage I and II was more frequent in patients with Type B than those with Type A. Disease-free or overall survival was significantly better in patients with Type B than those with Type A. CONCLUSION: Early enhancement in the arterial phase might be a useful indicator of lower malignant potential and better survival in ICC patients.

Oxidized proteins in astrocytes generated in a hyperbaric atmosphere induce neuronal apoptosis.

In the present study, we investigated the influence of the oxidative damage to astrocytes on neuronal cell survival using cultures of rat cerebral astrocytes and neurons. The exposure of astrocytes to hyperbaric oxygen induced a time-dependent apoptotic cell death, as observed by DNA ladder assessment. When astrocytes damaged by oxidative stress were cocultured with normal neurons from the cerebrum of a newborn rat, neuronal cell death was markedly induced, although normal astrocytes not subjected to hyperoxia cocultured with normal neurons showed no neuronal cell apoptosis. It was found that either the supernatant from the homogenate of astrocytes cultured in hyperbaric oxygen atmosphere or a protein mixture extracted from the supernatant induced neuronal cell death. The level of protein carbonyls, an index of protein oxidation analysis, in cultured astrocytes increased significantly with oxidative stress, and vitamin E inhibited the increase in the level of such oxidized proteins in astrocytes. Furthermore, a two-dimensional (2D) electrophoresis of a protein mixture extracted from the supernatant showed several changes in proteins. These results imply that reactive oxygen species (ROS) induced by oxidative stress attack astrocytes to induce oxidatively denatured proteins in the cells that act as a neurotoxic factor, and that vitamin E protects neurons by inhibiting astrocyte apoptosis caused by oxidative stress.