Biomedical subjects

E M Essigmann

Publications and source records attributed to E M Essigmann.

3 recordsLinked to original sources

PubMed1985

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.

Animals↗

PubMed1981

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.

Alkaline Phosphatase↗

PubMed1979

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.

Aqueous Humor↗