Metabolic Control of Avocado Fruit Growth (Isoprenoid Growth Regulators and the Reaction Catalyzed by 3-Hydroxy-3-Methylglutaryl Coenzyme A Reductase).

The effect of isoprenoid growth regulators on avocado (Persea americana Mill. cv Hass) fruit growth and mesocarp 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR) activity was investigated during the course of fruit ontogeny. Both normal and small-fruit phenotypes were used to probe the interaction between the end products of isoprenoid biosynthesis and the activity of HMGR in the metabolic control of avocado fruit growth. Kinetic analysis of the changes in both cell number and size revealed that growth was limited by cell number in phenotypically small fruit. In small fruit a 70% reduction in microsomal HMGR activity was associated with an increased mesocarp abscisic acid (ABA) concentration. Application of mevastatin, a competitive inhibitor of HMGR, reduced the growth of normal fruit and increased mesocarp ABA concentration. These effects were reversed by co-treatment of fruit with mevalonic acid lactone, isopentenyladenine, or N-(2-chloro-4-pyridyl)-N-phenylurea, but were not significantly affected by either gibberellic acid or stigmasterol. However, stigmasterol appeared to partially restore fruit growth when co-injected with mevastatin in either phase II or III of fruit growth. In vivo application of ABA reduced fruit growth and mesocarp HMGR activity and accelerated fruit abscission, effects that were reversed by co-treatment with isopentenyladenine. Together, these observations indicate that ABA accumulation down-regulates mesocarp HMGR activity and fruit growth, and that in situ cytokinin biosynthesis modulates these effects during phase I of fruit ontogeny, whereas both cytokinins and sterols seem to perform this function during the later phases.

Tick-bite fever in South Africa. The occurrence of severe cases on the Witwatersrand.

Tick-bite fever, the variety of tick typhus occurring in southern Africa, is caused by Rickettsia conori var. pijperi and is transmitted by hard or ixodid ticks. It is usually a mild disease, especially in children and young adults, but in middle-aged and elderly patients (and sometimes in young adults) it may assume a severe form. This is characterized by high fever, severe headache, delirium, stupor and occasionally coma, and a profuse maculopapular rash which becomes haemorrhagic and is associated with petechiae in the skin and later, but rarely, by the development of gangrene of the fingers and toes. During these severe attacks the central nervous system may be involved and marked disorders of liver and kidney function sometimes lead to kidney failure and the need for treatment and dialysis in an intensive care unit. Three illustrative cases are described in which diagnosis was delayed. One patient died; 2 patients responded to administration of tetracycline. The danger of allowing tick-infested dogs onto one's bed is stressed. Infections transmitted by dog ticks tend to be more severe than those acquired via ticks from the bushveld, possibly because they so often occur in middle-aged and elderly patients. Serological tests have recently indicated that there are antigenic differences between 'suburban' and 'bushveld' strains; these clearly require further study.

Bradykinin-stimulated prostaglandin E2 production by endothelial cells and its modulation by antiinflammatory compounds.

Prostaglandin production was studied in cultures of pig aorta endothelial cells using radioimmunoassay, radiochromatography, and smooth muscle bioassay. PGE2 was produced in higher concentrations than other prostaglandins. Bradykinin produced a rapid dose-related stimulation of PGE2 production. These results provided the basis for establishment of a simplified test system for investigating new compounds which alter prostaglandin synthesis and might therefore affect inflammatory response. It was also observed that these endothelial cells do not metabolize prostaglandins via 15-hydroxyprostaglandin dehydrogenase.

Further observations on the relationship and distribution of Schistosoma margrebowiei and S. leiperi in central southern Africa.

A further survey in East Caprivi, Chobe National Park, Okavango swamps and Kavango was undertaken in June 1976. No evidence of lechwe schistosomes was found in droppings of African buffalo (Syncerus caffer) nor baboons (Papio ursinus) living in lechwe habitats. It was thought that they were not capable of spreading or maintaining these parasites outside the confines of the known distribution of Kobus sp. The role of goats was equivocal but probably they too are poor hosts. Kavango, an endemic area of S. haematobium and S. mansoni, was thought to be free of all animal schistosomes, thus confirming the hypotheses that (1) cattle and goats are poor hosts of the lechwe schistosomes and (2) S. mattheei was blocked from entering the territory by the presence of lechwe schistosomes in the surrounding areas. Evidence of schistosomes was not found in cattle and goats at Maun for the same reasons. The prevalence of S. mansoni at Maun has increased alarmingly over the past 20 years with a simultaneous disappearance of lechwe from the area. S. margrebowiei and S. leiperi eggs were found in lechwe and tsessebe droppings some 80 km north of Maun. A high proportion of children with negative excreta from "non-endemic" areas in East Caprivi had positive CFT and/or skin tests, suggestive of exposure to lechwe schistosomes resulting in a possible immunity to S. mansoni and S. haematobium.