Xorphanol.

Xorphanol is a new mixed agonist-antagonist from the morphinan class of analgesics. On the basis of animal experiments, the physical dependence liability of xorphanol is predicted to be of a low order in man. Conceptually, xorphanol is of interest since in vitro experiments have revealed anti-naloxone properties and resistance to antagonism by opioid antagonists. At the practical level, xorphanol is a well tolerated, orally active analgesic that provides effective pain relief clinically.

Transplantation studies on induced and spontaneous nodules from B6C3F1 mouse liver.

The present research was designed to assess the potential for progressive growth of hyperplastic, adenomatous, and carcinomatous mouse liver lesions grafted into syngeneic hosts and to determine the effect of treatment type, donor age, and metastatic potential on this parameter. Lesions were obtained from male B6/C3F1 mice fed on an open formula (NIH-007) diet or the same diet mixed with a chlorinated hydrocarbon pesticide (3,5-dichloro-(N-1,1-dimethyl-2-propyl)benzamide) (DcB). Animals were killed at 18 or 24 months of age. Hosts for transplanting were killed at 8 months, or when grafts reached 2 cm in diameter. Lesions diagnosed as nonmalignant (hyperplastic or benign) were more likely to grow after transplantation if obtained after 24 months, rather than after 18 months (0.025 less than p less than 0.05). There was a close correlation between donor lesion morphology and ability to grow in a recipient mouse (p less than 0.0005; 36% of the hyperplastic, 32% of the adenomatous and 79%, of the malignant lesions grew). The majority of lesions retained the morphologic appearance of the donor lesions. Transplanted lesions from control mice were more likely to grow than were those from DCB-treated mice (0.01 less than p less than 0.025). This correlation was particularly strong for hyperplastic nodules. Metastatic capability in the donor animals correlated positively with both growth potential (p less than 0.01) and growth rate (p less than 0.05) in recipient mice. These findings suggest that progression toward autonomous growth may occur both within the original host and during a prolonged transplantation period, making data interpretation difficult. Lesion morphology alone may not be adequate for assessing capacity for autonomous growth. Other factors, such as evidence of metastasis or local invasion in the primary host, may be required to make more meaningful diagnosis.

Enzymatic alterations in mouse hepatic nodules induced by a chlorinated hydrocarbon pesticide.

Male C57BL/6 X C3H/anf F1 mice were either untreated or fed 3,5-dichloro(N-1, 1-dimethyl-2-propynyl)benzamide, a chlorinated hydrocarbon pesticide, for 12, 18 or 24 months. Mice in the highest dose group showed evidence of chronic liver toxicity including necrosis and an increased incidence of tumors diagnosed malignant by histological assessment. The increase in malignant tumors was not accompanied by an increased mortality. Glucose-6-phosphatase and alkaline phosphatase were good markers for mouse hepatic nodules. gamma-Glutamyl transpeptidase was not a good marker and was irregularly present in these lesions. Nodules also had a relative decrease in aryl hydrocarbon hydroxylase activity and an increase in the K form of the glycolytic enzyme, pyruvate kinase. Treatment type, as well as nodular morphology, had an effect on enzyme activity in the case of each of the markers.

Hemolytic ghost cell glaucoma. Further studies.

Three variations of ghost cell glaucoma that occur following cataract extraction are presented. The most common variant occurred when a large, anterior chamber and vitreous hemorrhage complicated the immediate postoperative course. Weeks later, as the anterior chamber hemorrhage cleared, ghost cells that had formed within the vitreous cavity passed forward into the anterior chamber and obstructed the aqueous outflow channels. Ultramicroscopy of aqueous specimens confirmed that RBC ghost were the major aqueous component and were therefore the cause of the glaucoma, distinguishing this glaucoma from glaucoma due to macrophages and RBC debris. Scanning and transmission electron microscopy of hemorrhagic vitreous showed that RBCs disintegrated into ghosts and denatured extracellular hemoglobin aggregates. The latter, common in the vitreous, were bound within vitreous strands, accounting for their absence in the anterior chambers of patients with ghost cell glaucoma. In correlation with clinical findings, perfusion studies showed that neither fresh RBCs nor ghosts could pass through an intact anterior hyaloid face.