Diet and retarded growth.

The diets of 36 children below the third centile for height but with no organic disease were compared with the diets of a control group. In most cases retarded growth was associated with a long-continued deficiency in calorie intake. When the diets were reassessed about a year later the shortfall in calorie intake was significantly reduced. This improvement, which tended to be followed by an increase in the rate of growth in height, might have been due to alteration in the child''s circumstances or improvement in the family attitudes and feeding habits or both. Advice given at the clinic is thought to have played a part in bringing these changes about.     

Neuronal cytoskeleton and growth.

The involvement of the cytoskeleton in the expression of neuronal morphology is most obvious in its support of neurite extension and the motile activity of growth cones. Techniques permitting direct observation of the dynamics of proteins in living cells, along with attempts to assay protein function in vivo, are testing existing models for cytoskeletal function in neurons, as well as generating more detailed models at the molecular level.     

Peptide growth factor interactions in embryonic and fetal growth.

Peptide growth factors are expressed by multiple tissues in the animal and human embryo and fetus. They undergo specific interactions which control the rate of cellular proliferation, tissue differentiation and the induction of specific morphogenic events such as mesoderm formation in the embryo. Biologic control may not only be exerted at the level of growth factor synthesis and receptor expression but by the sequestration and storage of growth factors by extracellular matrix molecules. In the case of insulin-like growth factors (IGFs), storage maybe mediated by attachment to specific IGF-binding proteins which may additionally modulate biological potency. Basic fibroblast growth factor (basic FGF) and transforming growth factor-beta (TGF beta) directly bind to glycosaminoglycan molecules. Release of growth factors from these stores may be by local proteolytic action. A sequential expression of basic FGF, IGF-II and TGF beta occurs in the ovine fetal epiphyseal growth plate as chondrocytes progress from a proliferative to a postmitotic, hypertrophic state. Cellular phenotype may be largely explained by the relative amounts of these autocrine growth factors within the growth plate.     

Skeletal-muscle growth and protein turnover.

Because of turnover, protein synthesis and breakdown can each be involved in the regulation of the growth of tissue protein. To investigate the regulation of skeletal-muscle-protein growth we measured rates of protein synthesis and breakdown in growing rats during development on a good diet, during development on a marginally low-protein diet and during rehabilitation on a good diet after a period of severe protein deficiency. Rates of protein synthesis were measured in vivo with a constant intravenous infusion of [14C]tyrosine. The growth rate of muscle protein was measured and the rate of breakdown calculated as breakdown rate=synthesis rate-growth rate. These measurements showed that during development on a good diet there was a fall with age in the rate of protein synthesis resulting from a fall in capacity (RNA concentration) and activity (synthesis rate per unit of RNA). There was a fall with age in the breakdown rate so that the rate was highest in the weaning rats, with a half-life of 3 days. There was a direct correlation between the fractional growth and breakdown rates. During rehabilitation on the good diet, rapid growth was also accompanied by high rates of protein breakdown. During growth on the inadequate diet protein synthesis rates were lesss than in controls, but growth occurred because of decreased rates of protein breakdown. This compression was not complete, however, since ultimate muscle size was only one-half that of controls. It is suggested that increased rates of protein breakdown are a necessary accompaniment to muscle growth and may result from the way in which myofibrils proliferate.     

From growth arrest to growth suppression.

Since the introduction of the cell cycle concept two approaches to study growth regulation of cells have been proposed. One claims that cells are naturally quiescent, requiring a stimulatory encouter with growth factors for induction of cell division. The other considers cellular multiplication as the natural steady-state; cessation of multiplication is thus a restriction imposed on the system. In the latter case emphasis is mainly on the signals involved in arrest of multiplication. This Prospect focuses on specific events occurring in mammalian cells at growth arrest, senescence, and terminal differentiation, specifically emphasizing the growth inhibitory factors, tumor suppressor genes, and other signals for growth suppression.     

Oocyte growth.

The main elements of reproduction are exposed with emphasis on its preparation during the larval stage. The system oocyte-nurse cells-follicular cells is described and the principal features of egg morphogenesis are indicated. Two types of problems are concentrated on : 1) sequential determination of growth and evolution of the follicle in the ovarian tube, 2) morphological and biochemical aspects of chorion formation. Variation in the functioning of the oocyte's morphogenetic system is explored with discussion of the role of larval alimentation, temperature, hormonal environment and genetic factors.