Alveolar hydatid disease of the liver: Brief review and spectrum of adjacent organ invasion

The purpose of this study is to show the spectrum of adjacent organ invasion and to make a brief review of hepatic alveolar hydatid disease (AHD), using CT and MR imaging. We retrospectively reviewed CT and MR images of three patients with various adjacent organ invasions surgically and histologically proven to be AHD. Local invasion to right kidney and adrenal, right hemidiaphragm and lung were detected in one patient, right adrenal in another patient and gall bladder, duodenum, gastric wall and pancreas invasion in the other. AHD may rarely extend to the gall bladder, stomach, duodenum, pancreas, right adrenal and kidney, diaphragm, pleura and lung. The extension of the disease outside the liver is usually encountered in patients with large, peripherally located masses in the advanced stage of the disease.     

Deprivation of form vision suppresses diurnal cycling of retinal levels of leu-enkephalin

Deprivation of form vision by the fitting of translucent occluders suppressed the diurnal cycling of enkephalinergic amacrine cells (the ENSLI amacrine cells), in the chicken. Daily periods of normal vision or enforcing temporal contrast using strobe lighting appeared to restore normal functioning of the ENSLI cells. These results suggest that the ENSLI cells are involved in retinal circuits that assess the quality of the visual image and control eye growth.     

The 21-aminosteroid antioxidant, U74389F, prevents estradiol-induced depletion of hypothalamic β-endorphin in adult female rats

A single intramuscular injection of 2 mg estradiol valerate (EV) results in neuronal degeneration and β-endorphin depletion in the hypothalamic arcuate nucleus of adult female rats. We have hypothesized that peroxidase-positive astrocytes in this brain region oxidize estrogens and catecholestrogens to semiquinone radicals which mediate oxidative neuronal injury. In the present study, dietary administration of the potent antioxidant 21-aminosteroid, U-74389F, completely blocked EV-induced β-endorphin depletion in the hypothalami of adult female rats. Neither EV nor 21-aminosteroid treatment had any effect on hypothalamic concentrations of neuropeptide Y and Met-enkephalin, confirming that the estradiol lesion is fairly selective for the β-endorphin cell population. The present findings support the hypothesis that the toxic effect of estradiol on hypothalamic β-endorphin neurons is mediated by free radicals.