Changes in Calcium Reserves in Breeding Lesser Snow Geese (Chen caerulescens caerulescens)

Calcium and fat reserves of the femur medullary bone were examined in sexually mature lesser snow geese (Chen caerulescens caerulescens) collected during the 1974–1975 season. In females, femur calcium and fat levels increased by 80 and 30%, respectively, during the spring migration, much of the increase taking place while the birds staged in southwestern Manitoba and North Dakota prior to their departure for the breeding area. In males. femur calcium levels showed no seasonal change but femur fat increased in a manner similar to that found in the females, although the increase was not as great (17%). In the females, femur fat content fell by 40% during egg-laying whereas in males a decrease in femur lipid was not evident until incubation was well underway. Femur calcium levels in females declined during egg production and early incubation, showing a 56% decrease over spring migratory levels, indicating that dietary calcium intake was limited during the nesting period. However, the low femur calcium levels in birds collected during the spring were not significantly different from those of wintering birds, suggesting that no calcium deficiencies were apparent. Plasma calcium levels in males remained relatively constant throughout the year, although there was some elevation in May. Plasma calcium levels in the females increased almost threefold during egg laying and returned to pre-laying levels during incubation. Medullary bone was evident only in reproducing females and appeared during spring migration, concomitant with increased femur weight, fat and calcium content. Medullary bone degradation commenced during the first week of incubation and no medullary bone was in evidence by molt. Calcium reserves of medullary bone accounted for only 17.2% of the calcium required for eggshell production, suggesting that. at least during the laying period, the female must depend on some exogenous source, perhaps from grit or brackish water.     

Structure-function analysis of epidermal growth factor: site directed mutagenesis and nuclear magnetic resonance

The role of leucine-47 in determining the structure and activity of human epidermal growth factor was examined using site-directed mutagenesis. Wild type protein and four variants in which Leu47 was replaced by valine, glutamate, aspartate and alanine were produced from yeast. 1H NMR experiments demonstrated that substitution of Leu47 had little effect on the protein structure. The observed reduction in receptor binding affinity caused by the substitutions could thus be attributed to perturbation of a residue directly involved in receptor interactions.     

c-Myc Regulates Proliferation and Fgf10 Expression in Airway Smooth Muscle after Airway Epithelial Injury in Mouse

During lung development, Fibroblast growth factor 10 (Fgf10), which is expressed in the distal mesenchyme and regulated by Wnt signaling, acts on the distal epithelial progenitors to maintain them and prevent them from differentiating into proximal (airway) epithelial cells. Fgf10-expressing cells in the distal mesenchyme are progenitors for parabronchial smooth muscle cells (PSMCs). After naphthalene, ozone or bleomycin-induced airway epithelial injury, surviving epithelial cells secrete Wnt7b which then activates the PSMC niche to induce Fgf10 expression. This Fgf10 secreted by the niche then acts on a subset of Clara stem cells to break quiescence, induce proliferation and initiate epithelial repair. Here we show that conditional deletion of the Wnt target gene c-Myc from the lung mesenchyme during development does not affect proper epithelial or mesenchymal differentiation. However, in the adult lung we show that after naphthalene-mediated airway epithelial injury c-Myc is important for the activation of the PSMC niche and as such induces proliferation and Fgf10 expression in PSMCs. Our data indicate that conditional deletion of c-Myc from PSMCs inhibits airway epithelial repair, whereas c-Myc ablation from Clara cells has no effect on airway epithelial regeneration. These findings may have important implications for understanding the misregulation of lung repair in asthma and COPD.