The met-enkephalin analog FK 33-824 and naloxone do not directly influence cortisol secretion by cultured human adrenocortical cells

Systemic administration of the enkephalin analog FK 33.824 was previously shown to inhibit ACTH secretion in man. In this study, the direct action of this analog on cortisol release was studied. The enkephalin analog (1 uM and 10 uM) did not influence basal or ACTH-stimulated cortisol production by cultured isolated adrenocortical cells prepared from the hyperplastic adrenal glands from three patients with Cushing's disease. Naloxone (10 uM) had also no direct effect on cortisol release. It is concluded that the met-enkephalin analog used in this study and naloxone do affect the hypothalamo-pituitary-adrenal axis via a central effect.     

Potentiation of antibody responses by specific IgM: specificity and thymus dependency

Modulation of antibody responses induced by IgM directed against the immunogen was investigated. When IgM directed against ox erythrocytes (ORBC) was given together with trinitrophenyl (TNP)-ORBC, the subsequent antibody response to the carrier, ORBC, as well as the response to the hapten, TNP, was potentiated. In contrast, IgG with carrier specificity inhibited both responses. The hapten-specific potentiation was found in both direct and indirect plaques, and was antigen-dose dependent, i.e., no potentiation was found with the lowest antigen doses. The response to 2,4-dinitrophenyl (DNP)-labeled proteins was potentiated by a monoclonal IgM with specificity for the hapten. The effects were observed both in primary and secondary responses. One strict requirement for IgM potentiation to occur was observed. The determinant against which potentiation was achieved had to be physically linked to the determinant against which the IgM was directed, be it hapten or carrier determinants. Thus, irrelevant IgM-antigen complexes were incapable of potentiating the responses. Similar specificity requirements were found for IgG induced suppression of antibody responses. Experiments with nude mice and their euthymic littermates showed that IgM potentiation of antibody production is T-cell dependent. Furthermore, passive transfer of carrier-primed spleen cells together with antigen challenge suggests that IgM potentiation of secondary antibody responses is dependent on specific carrier-primed immune T cells.     

Influenza and Infant Mortality

Early neonatal mortality in England and Wales in the second quarter of 1970 after a major influenza epidemic was slightly but significantly higher than in the corresponding quarter of the previous year. An increase was also noted in the first quarter of 1970. Analysis of infant mortality and an index of influenza prevalence over the past quarter-century indicates that similar increases occurred in relation to four of the other five major influenza epidemics during the period, the exception being the “Asian ''flu” epidemic of the autumn of 1957. It is suggested that the increased mortality in 1970 was the consequence of an increase in the prematurity rate, but we have no evidence to indicate whether the effect is specifically due to the virus or is nonspecific in nature.     

Ultrastructure and distribution of microbodies in leaves of grasses with and without CO2-photorespiration

Summary A comparative study was made of the ultrastructure, distribution and abundance of leaf microbodies in four species of temperate grasses with high and four tropical grasses with low CO₂-photorespiration. The temperate grasses were all festucoid; the tropical grasses included two panicoid species and two chloridoid. Comparisons of relative abundance were made by computing the average numbers of microbody profiles per cell section.Although microbodies were present in the green parenchymatous leaf cells in all grasses examined, their average number per cell was in general severalfold greater in the grasses with high CO₂-photorespiration than in those with low. Furthermore, whereas in the grasses with high CO₂-photorespiration the microbodies were distributed through the mesophyll, in those with low CO₂-photorespiration they were concentrated in the vascular-bundle-sheath cells and were smaller and relatively scarce in the mesophyll cells. The leaf microbodies of the eight grass species resembled one another in general morphology, but differed to some extent in regard to size and type of inclusion. Microbodies of all four festucoid species contained numerous fibrils with a discernible substructure. Those of the two panicoid species contained clusters of round bodies with transparent cores. The equivalence of the microbodies to peroxisomes as biochemically defined was shown cytochemically by employing 3,3-diaminobenzidine for the localization of catalase, a marker enzyme for the peroxisome. This reaction was blocked by the catalase inhibitor, aminotriazole.The observations on the relative abundance and distribution of peroxisomes in leaves of grasses with high CO₂-photorespiration versus those with low are consistent with the published biochemical data on the levels and distribution of peroxisomal enzymes in representatives of plants with high and low CO₂-photorespiration, and may help explain the differences in apparent photorespiratory levels between these two groups of plants.     

THE BINDING OF BOTULINUM TOXIN TO MEMBRANE LIPIDS: SPHINGOLIPIDS, STEROIDS AND FATTY ACIDS

A number of lipids known to be constituents of nerve-ending membranes were tested for their ability to inactivate botulinum toxin. Inactivation of the toxin by a lipid was taken as presumptive evidence that the lipid might be the in vivo receptor for the toxin. Several sphingolipids (sphingosine, galactosylceramide, glucosylceramide, lactosylceramide, cytolipin K and cytolipin R), steroids (cholesterol and deoxycholic acid) and fatty acids (palmitic acid, stearic acid, prostaglandin E₁) did not affect the potency of botulinum toxin, and thus were discounted as potential toxin receptors. However, the gangliosides did inactivate botulinum toxin rapidly (in less than 5 min), within a temperature range of 2°-40°C, and at ionic strengths of 0.05-0.40. Inactivation diminished as pH fell below 6. The activity of gangliosides in suppressing the potency of botulinum toxin was a function of the number of sialic acid residues in the lipid. Thus, the data suggest that a molecule containing sialic acid may be the receptor for the toxin.