Ontogeny of ovine fetal liver and kidney plasma membrane insulin receptors and fetal growth

This investigation was performed to define certain characteristics of insulin-receptor interaction during the last 2 months of gestation in fetal sheep liver and kidney. Twenty-one sheep carrying a total of 46 fetuses were sacrificed at various gestational ages from 94 days to term; fetal and maternal livers and kidneys were analyzed by a radioreceptor assay for insulin binding characteristics. Specific binding of insulin to partially purified ovine fetal liver and kidney plasma membranes increased as gestation approached term, at which time specific binding was two- to fourfold greater to fetal than to maternal tissues. Associated with increased specific binding were late gestational increases in affinity of insulin for receptors in both fetal liver and kidney and an earlier increase in insulin receptor concentration in fetal kidney. These observations in fetal sheep liver and kidney are similar to reported observations in other species. However, the increase in specific binding of insulin to male fetal liver membranes was exponential; in contrast, there was no apparent increase in specific binding to female fetal liver membranes during the gestational interval surveyed. Both the weights and the vertebral column lengths of these fetuses were shown by multivariate analysis to be significantly affected by the interaction between specific binding of insulin and fetal sex. However, in 30 additional sheep fetuses we observed no difference between male and female fetuses in the increase with time in liver glycogen content. The lack of sex difference in this postreceptor event is consonant with the demonstrated dissociation between liver insulin receptors and glycogen synthesis in the late fetal rat. Our observations suggest that late gestational differences between male and female sheep fetuses in insulin specific binding to liver and, possibly, to other tissues such as cartilage, muscle, and/or fat, that are coupled to postreceptor events may account for differences in fetal growth between the sexes.     

Lactic Acidosis in Diabetes

Lactic acidosis is occasionally responsible for metabolic acidosis in diabetics. It may occur in the presence of normal blood levels of the ketone bodies, and such cases are often described as having “non-ketotic diabetic acidosis.” Lactic acid may contribute to the metabolic acidosis in patients with true diabetic ketoacidosis, but the blood lactate concentrations in these patients are not usually very high. In some patients the ketoacidosis is replaced by a lactic acidosis during treatment. This usually occurs in association with a serious underlying disorder and is associated with a poor prognosis. A transient increase in blood lactate concentration was in fact observed in most patients after the beginning of treatment, but the significance of this finding is uncertain.     

Dextran-induced Agglutination of Streptococcus mutans, and Its Potential Role in the Formation of Microbial Dental Plaques

Glucose-grown washed cells of streptococci similar to Streptococcus mutans, which contain cell-bound dextransucrase, have been observed to agglutinate upon the addition of high molecular weight dextran. Low molecular weight dextran or unrelated polysaccharides were ineffective. Agglutination also occurred upon addition of sucrose, which can be converted into dextran, but not with other mono- and disaccharides. Other bacteria, including species capable of synthesizing dextrans, were not observed to exhibit this phenomenon. Cells of S. mutans agglutinated upon addition of dextran over a wide pH range, but maximal sensitivity to dextran occurred at pH 8.5. At this pH, such cells can be used for a simple, specific, and exquisitely sensitive qualitative assay for high molecular weight dextran, for addition of 6 ng of dextran with a molecular weight of 2 x 10(6) (i.e., approximately three molecules per cell) caused detectable agglutination. High concentrations of glucose, levan, and dextran of molecular weight of 2 x 10(4) inhibited the reaction. Fluorescein-labeled cells of S. mutans were observed to adhere to dextran-containing plaques and dextran-treated teeth, suggesting that this phenomenon may be of importance in the formation of streptococcal dental plaques. The mechanism responsible for dextraninduced agglutination appears to involve the affinity of a receptor site, possibly dextransucrase, on the surface of several cells for common dextran molecules.     

THE DEGENERATIVE CHANGES IN PANCREATIC ACINAR CELLS CAUSED BY DL-ETHIONINE

Degeneration of pancreatic acinar cells in rats injected with ethionine was studied by electron microscopy. The most conspicuous morphologic lesions occurred in the ergastoplasm. There was a widening of the endoplasmic reticulum, a decrease in number of membrane-associated ribosomes, and a development of fine and coarse vacuoles containing agranular disoriented membranes. Cytoplasmic ribosomes unassociated with membranes were less numerous. Nuclear changes consisted of a coarsening and clumping of the nuclear chromatin, chromatin margination, and increased osmiophilia and vacuolation of the nucleolus. Eight to ten days after the beginning of ethionine injections, changes in zymogen granules, mitochondria, and the Golgi apparatus appeared, but only after extensive damage to the acinar cell. The effects were consistent with ethionine's known interference with protein metabolism but also suggest disturbance in ribonucleic acid metabolism. The ergastoplasmic changes after ethionine were similar in some respects to the early lesions produced in liver parenchymal cells by fasting, to the changes occurring in animals on protein-free diets, or to some of the liver changes produced by azo dye carcinogens. The ribosomal and ergastoplasmic changes represent early morphologic expressions of the biochemical effect of ethionine.     

Factors in the Testing and Application of Algicides

A review is presented of some of the factors affecting the laboratory testing and practical applications of chemicals toxic to algae. The basic factor demonstrated is that the amount of chemical required to inhibit the growth of algae is dependent on the amount of algae present and not on the volume of water in which the algae are dispersed. It is shown how a chemical can be tested for algistatic or algicidal properties, thus enabling one to decide how best to apply a particular chemical. The selectivity of chemicals and the development of resistance in algae towards certain chemicals is demonstrated. Also, it is shown how certain algae can appear to be resistant to chemical treatments because of their growth habit or their production of extracellular products which affect the toxicity of added chemicals. With a better understanding of how various factors can influence the effectiveness of toxic chemicals, it is hoped that the selection of a chemical and method of application to a particular problem will be more successful.