Increased lipid content in the rat axotomized superior cervical ganglion

Transection of postganglionic nerves of the rat superior cervical ganglion results in significant increases in the concentration of lipid as well as the total content of lipid in the ganglion. The purpose of this work was to characterize the effect of axotomy on the major classes of lipid in the ganglion and to examine possible relationships among increases in lipid content and changes in steady-state concentrations of metabolites utilized in lipid biosynthesis. Major classes of lipids in axotomized and contralateral intact ganglia were compared using the Folch extraction and partitioning scheme. Analyses of lipids were carried out 7 days after axotomy because total lipid content was increased maximally at that time. The increase in lipid content in axotomized ganglia was related primarily to an increase in phospholipids. Amounts of gangliosides, cerebrosides, cholesterol, and proteolipid protein did not change significantly after axotomy. The elevation of phospholipid content was accompanied by increases in steady-state concentrations of α-glycerophosphate and decreases in Coenzyme A in the ganglion; however, concentrations of acetyl CoA and long-chain acyl CoA compounds did not change significantly in axotomized ganglia. Increases in α-glycerophosphate do not appear to arise from enhanced utilization of glucose because α-glycerophosphate dehydrogenase activity was decreased in axotomized ganglia and the incorporation of [U-¹⁴C] glucose into lipids in explants of the axotomized ganglia in vitro was not elevated. In contrast, incorporation of [U-¹⁴C] glycerol into lipids of explants from axotomized ganglia was increased in vitro. The results suggest that utilization of extracellular glycerol for phospholipid biosynthesis may be enhanced in the rat's axotomized superior cervical ganglion.     

Histogenesis of the papillary Clara cell adenoma.

The origin of the endocrine cells in the respiratory tract and the gastrointestinal tract is still a matter of debate. In the original concept of the amine precursor uptake and decarboxylation (APUD) system, all APUD cells were considered to be derived from the neural crest. More recently it has been proposed that the APUD cell types of the gastrointestinal and respiratory tracts originate from neuroendocrine-programmed ectoblast. Still other investigators have reported observations that favor a direct endodermal origin of these cell types. Based on the assumption that in teratomas different tissue types which in normal embryogenesis are derived from the neuroectoderm might be expected to occur together, we investigated a series of cystic ovarian teratomas and testicular teratocarcinomas for the presence of brain tissue and of different types of APUD cells. In the ovarian teratomas, intestinal and respiratory APUD cell types were found almost exclusively without coexistence of brain tissue, whereas melanocytes, which are of neuroectodermal origin, occurred mostly together with brain tissue. In the testicular teratocarcinomas, intestinal types of APUD cells occurred without brain tissue. Peptide hormone production was found in appropriate tissues. It can therefore be concluded that in teratomas appropriate intestinal and respiratory APUD cells differentiate in and presumably descend directly from intestinal and respiratory epithelium.     

Hemostatic mechanisms, independent of platelet aggregation, arrest gastric mucosal bleeding.

Platelet adhesion, aggregation, and subsequent plug formation play a major role in the control of cutaneous and vascular hemostasis. Little is known, however, about the hemostatic processes in gastric mucosal tissue. A method for evaluating bleeding from a standard incision in the gastric mucosa of the rat, rabbit, and dog has therefore been developed. By using pharmacological agents that interfere with platelet aggregation and blood coagulation, the mechanism of gastric hemostasis has been compared to that in the vasculature, using the rat mesenteric artery. Intravenous infusion of prostacyclin (0.5 micrograms X kg-1 X min-1), which inhibits platelet aggregation directly, or administration of the thromboxane synthase inhibitor 1-benzylimidazole (50 mg X kg-1) significantly prolonged bleeding in the mesenteric artery yet failed to alter gastric mucosal bleeding. In contrast, a low dose of heparin (100 units X kg-1), which interferes with the clotting process, had no effect on mesenteric bleeding but substantially prolonged bleeding from the gastric mucosa. These findings suggest that, unlike in the skin or vasculature, platelet aggregation plays a minimal role in the initial hemostatic events in the gastric mucosa and that the arrest of gastric hemorrhage is brought about largely by processes primarily involving the coagulation system.     

Distemper virus infection in ferrets: an animal model of measles-induced immunosuppression.

Distemper virus is very similar antigenically to measles virus, and the disease produced in ferrets by distemper is a systemic illness quite similar to measles infection in humans. Using an attenuated strain of distemper virus, we produced a mild systemic illness in ferrets and were able to study the effects of the viral infection on cell-mediated immunity (CMI). Beginning on day 5 after viral inoculation and continuing to day 30, infected ferrets showed a marked lymphopenia, with a reduction in total numbers of all lymphocyte subpopulations studied. Transformation of circulating lymphocytes to the mitogens phytohemagglutinin, concanavalin A, and pokeweed mitogen was suppressed on day 5, reached a nadir by days 8 to 11, and returned toward normal by days 23 to 30 after viral inoculation. Production of macrophage migration inhibitory factor by splenic macrophages was diminished during distemper infection. In contrast to marked suppression of these in vitro assays for CMI, delayed hypersensitivity skin test responses were only slightly diminished in animals infected with distemper virus. This model should prove useful in exploring the mechanisms of measles induced immunosuppression.