TESTOSTERONE-INDUCED CELL PROLIFERATION IN THE ACCESSORY SEX GLANDS OF MICE AT VARIOUS TIMES AFTER CASTRATION

The proliferative response to testosterone in the accessory sex glands (seminal vesicle and coagulating gland) of castrated male Balb/c mice has been examined by pulse and continuous thymidine-labelling experiments, and by the fraction of labelled mitoses technique. Progressive reductions in cellularity followed castration, and by varying the time elapsing between castration and the initiation of testosterone treatment, it was clear that the size of the response depended upon the number of cells in the tissue, relative to the normal complement. Interpretation of FLM data was difficult in periods where proliferative rates changed rapidly. We have attempted to explain the cell kinetic events by postulating a G₀ compartment, from which cells are stimulated to enter the proliferative cycle before subsequently returning to an out of cycle state. It was thought unlikely that substantial changes in cell cycle time occurred. In both the accessory sex glands, the overall form of the continuous thymidine labelling curves showed that most proliferative cells entered DNA synthesis in a shorter time after stimulation at 14 days after castration than they did at 3 days after castration. The data were not consistent with cells moving deeper into G₀ with time after castration. In the seminal vesicle almost all epithelial cells were potentially proliferative by 3 days after castration. In the coagulating gland only 30% were potentially proliferative at 3 days, increasing to 85% at 14 days after castration. However, such proportional increases represented much smaller changes in terms of absolute numbers of cells, because of a concomitant decline in cellularity from 3 to 14 days after castration.     

The action of the adenosylhomocysteine hydrolase inhibitor, 3-deazaadenosine,on phagocytic function of mouse macrophages and human monocytes

An inhibitor of adenosylhomocysteine hydrolase, 3-deazaadenosine, caused profound inhibition of phagocytosis of opsonized erythrocytes by mouse resident peritoneal macrophages $\text{in}\text{vitro}$. The inhibition was evident at concentrations as low as 2×10^?7M, and increased with increasing concentration and time of exposure to the analogue. It was not associated with detachment of the macrophage monolayers or with loss of cell viability. Although the inhibition was not reversible, progression of the functional impairment was interrupted by washing out the analogue. In striking contrast, phagocytic function of human blood monocytes was unaffected by 3-deazaadenosine.     

Preliminary observations on the birth and development ofPropithecus verreauxi to the age of six months

In this paper, preliminary observations are presented on the ontogency of one of the Malagasy prosimians,Propithecus verreauxi. Observations were carried out in the course of an eighteen-month study of the social organization and ecology of four, free-ranging groups. Parturition is described, together with data on the development of locomotor and feeding behavior, and on the changing nature of the infant's relationship with its mother and with other members of the group. The final section compares the results of this study with those of previous studies ofP. verreauxi and other lemur species. Tentative conclusions are drawn concerning aspects of social ontogeny inP. verreauxi and areas for future research are suggested which would clarify some of the remaining problems.     

Inhibition of prostaglandin biosynthesis by sulphasalazine and its metabolites

Sulphasalazine (SZ) inhibits prostaglandin (PG) biosynthesis $\text{in vitro}$ with a potency comparable to that of aceylsalicylate. The metabolites of SZ, sulphapyridine and 5-aminosalicylic acid, were of considerably lower potency as inhibitors of PG biosynthesis in the synthetase preparations used. The inhibition of prostaglandin production by SZ could at least partly account for the clinical utility of sulphasalazine in ulcerative colitis. Sulphapyridine may help to maintain inhibitory concentrations of SZ by restraining bacterial breakdown of the active drug.     

Effects of Cortisol and Dexamethasone on Insulin Signalling Pathways in Skeletal Muscle of the Ovine Fetus during Late Gestation

Before birth, glucocorticoids retard growth, although the extent to which this is mediated by changes in insulin signalling pathways in the skeletal muscle of the fetus is unknown. The current study determined the effects of endogenous and synthetic glucocorticoid exposure on insulin signalling proteins in skeletal muscle of fetal sheep during late gestation. Experimental manipulation of fetal plasma glucocorticoid concentration was achieved by fetal cortisol infusion and maternal dexamethasone treatment. Cortisol infusion significantly increased muscle protein levels of Akt2 and phosphorylated Akt at Ser473, and decreased protein levels of phosphorylated forms of mTOR at Ser2448 and S6K at Thr389. Muscle GLUT4 protein expression was significantly higher in fetuses whose mothers were treated with dexamethasone compared to those treated with saline. There were no significant effects of glucocorticoid exposure on muscle protein abundance of IR-β, IGF-1R, PKCζ, Akt1, calpastatin or muscle glycogen content. The present study demonstrated that components of the insulin signalling pathway in skeletal muscle of the ovine fetus are influenced differentially by naturally occurring and synthetic glucocorticoids. These findings may provide a mechanism by which elevated concentrations of endogenous glucocorticoids retard fetal growth.