Skeletal growth in a medieval population from Sudanese Nubia

Long bone growth is analyzed for 180 children from a Medieval population at Kulubnarti in Sudanese Nubia (550–1450 A.D.). A regional interpopulation comparison is made with growth data from Wadi Halfa in Lower Nubia, and an intrapopulation analysis is undertaken to assess diachronic changes in growth at Kulubnarti. Changes in growth patterns are interpreted in the context of mortality and morbidity profiles and relationships between the three variables are discussed. It is suggested that changes in the sociopolitical environment may have been responsible in part for altering levels of biological stress and impacting growth.     

Identification of tyrosine-phosphorylated colony-stimulating factor 1 (CSF-1) receptor and a 56-kilodalton protein phosphorylated in intact human cells in response to CSF-1

Colony-stimulating factor 1 (CSF-1) selectively supports the survival, proliferation, and maturation of hemopoietic cells of the monocyte/macrophage lineage. Although the cellular receptor for CSF-1, (the c-fms protein) is a protein-tyrosine kinase activated by the binding of CFS-1, the role of phosphorylation of cellular proteins in CSF-1 signal transduction is poorly understood. Therefore, we examined the CSF-1-stimulated phosphorylation of cellular proteins in human BeWo choriocarcinoma cell line (known to express the c-fms protein). BeWo cells were metabolically labeled with 32Pi, stimulated with recombinant human CSF-1, and extracted with detergent. Phosphotyrosyl proteins were isolated from detergent extracts by affinity chromatography on a highly specific antibody to phosphotyrosine. Rapid phosphorylation of 170-kd protein, followed closely by the phosphorylation of a 56-kd protein, was observed in response to CSF-1. The 170-kd phosphotyrosyl protein bound to wheat germ agglutinin and was secondarily immunoprecipitated with a specific anti-fms serum, consistent with its identity as the CSF-1 receptor. Although purified human macrophages that proliferate in culture in response to CSF-1 are not generally accessible, CSF-1 did stimulate the phosphorylation of a 56-kd protein in intact mononuclear leukocytes from human peripheral blood. Thus, the BeWo cell line may represent a good model for the study of CSF-1-stimulated cellular protein phosphorylation.     

Effect of retinoic acid on the proliferation and tumorigenicity of mouse mastocytoma cells

Retinoic acid (RA) inhibited the in vitro growth of the mouse mast cell tumor line P₈₁₅ in a dose- and time-dependent manner. The inhibition was accompanied by an increase in the amount of neutral intracellular mucopolysaccharides. Study of cell cycle kinetics showed that exposure to retinoic acid led to a slowing-down of the cell-cycle progression possibly related to a more differentiated cell population disclosed by microscopy with a lower proliferative capacity. In vivo, delays in both tumor appearance and mouse mortality were observed after injecting RA into mice bearing mastocytomas. These results suggest that RA could be of interest in the treatment of human malignant systemic mastocytosis with proliferation of immature mast cells.     

Seasonal changes in growth and standard metabolic rate of juvenile perch, Perca fluviatilis L.

The maximum growth rate of juvenile perch, PercaJuviatilis L., at different constant temperatures and in naturally changing day-lengths was studied in the laboratory. Standard metabolic rate was studied in starvation experiments at constant temperatures under short- and long-day conditions. Growth occurred in temperatures above 8 to 10°C. In winter, from mid-October until mid-April, maximal growth was considerably reduced and was relatively slow but constant. The standard metabolic rate was reduced c . 50% under short-day conditions. The seasonal change in metabolic rates, presumably controlled by an endogenous rhythm, was considered to be an adaptation to low food availability during the short winter days.     

Otolith microstructure indicating growth and mortality among plaice, Pleuronectes platessa L., post-larval sub-cohorts

Growth and mortality of post-metamorphosed plaice were studied by means of daily increments in the sagittal otoliths. The Gompertz model was the best fit to length-at-age data and there were no significant differences between length-at-age and back-calculated lengths. The microstructure pattern of the otoliths at metamorphosis was also used to estimate hatching and settlement distributions. Differential growth and mortality occurred among sub-cohorts; growth rates and mortality were higher in fish that settled earlier. In 1986, the best survival was for a sub-cohort settling in late May to early June. In contrast, in the warmer season of 1987, survival was highest for the second and third sub-cohorts settling in late April and mid May.     

Plant hormone response mutants

A variety of plant hormone response mutants has now been described, and is surveyed in this article. In addition to hormone-insensitive mutant phenotypes with defects in hormone-related features, there exist mutants apparently constitutive for the gibberellin responses, and also a mutant hyper-responsive to gibberellin. Although there is still little biochemical evidence on the nature of these mutants, the emerging picture of their genetic dominance relationships has given rise to tentative suggestions of the involvement of represser functions in hormonal control systems.     

Phosphorus concentration in barley (Hordeum vulgare L.) seed: Influence on seedling growth and dry matter production

The effect of phosphorus (P) concentration in barley seed on seedling growth has not been much investigated. Consequently, two experiments were conducted in the greenhouse to determine the effect of P concentration in barley seed (Hordeum vulgare L., cv. Empress) on the seedlings grown in sand-filled boxes receiving a culture solution without P. Seeds were selected with three P concentrations: high-P (113.0 mmol P kg⁻¹), medium-P (80.7 mmol P kg⁻¹) and low-P (54.9 mmol P kg⁻¹). At 21 days after sowing, the shoot and root yield or shoot height was the least with seedlings from low-P seed. In the other experiment, high-P and low-P seeds were wetted with distilled water or with a solution of 25.8 cmol L⁻¹ of NaH₂PO₄ for 24 h, and then grown for 31 days. Solution P had been imbibed by seeds whether low or high in native P, but only the imbibed P held by low native P seed benefited seedling dry matter accumulation and shoot elongation. The lack of benefit from seed-imbibed P on seedlings grown from high-P barley seed was associated with low recovery of the imbibed P in those seedlings.     

Density-induced down regulation of epidermal growth factor receptors

Summary Previous studies have shown that cell density can regulate the binding of several growth factors. To determine whether cell density exerts a uniform effect on the expression of epidermal growth factor (EGF) receptors, seven cell lines were examined in detail. For each cell line, EGF binding was found to decrease as cell density increases. Scatchard analysis of the binding data reveals that decreases in EGF binding are due to reductions in the number of cell surface EGF receptors. The only apparent exception is the effect of cell density on the binding of EGF to A-431 cells. For these cells, increases in cell density lead to two effects: decreases in the number of high affinity EGF receptors and increases in the total number of EGF receptors. In addition to the effects of cell density on EGF receptors, it was determined that increases in cell density can coordinately down-regulate receptors for as many as four different growth factors. Overall, the findings described in this report for EGF and those previously described for transforming growth factor type-β (TGF-β) and fibroblast growth factor (FGF) demonstrate the existence of a common mechanism for down-regulating growth factor receptors. This work was supported by grants from the Nebraska Department of Health (89-51), the National Cancer Institute (Laboratory Research Center Support Grant, CA36727), and the American Cancer Society (Core Grant ACS SIG-16). EDITOR'S STATEMENT The paper by Rizzino et al. demonstrates that receptor number decreases as a function of cell density. This may represent a mechanism by which cell proliferation is reduced as cell density increases.