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The cuticle consits of collagenous fibres and of two types of mucopolysaccharides. The whole cuticle contain PAS-positive polysaccharides, but the acid ones are localized only in the surface zone, both in the epicuticle and in the supracuticular mucoid coat. On the surface-damaged region of the cuticle bacterial infection was observed, those intact mucoid coat may be essential in protection against bacterial infection. Microvilli of the supporting cells play significant role in repairing of cuticular injuries. Acid mucopolysaccharides of the cuticle and epidermis may function as traps for heavy metals, proved by their significant heavy metal content. The cytosol of the epidermal cells possess considerable DAB-reactivity. The enzyme, responsible for the DAB-reaction, may be transported by the microvilli towards the cuticular surface and can play central role in the detoxication of organic foreign compounds.

Postnatal blood glucose and individual plasma free amino acid levels were measured in 14 newborn infants of diabetic mothers. All infants had a significantly lower blood glucose concentration than normal controls but no significant correlation was observed between the blood glucose values and any of the amino acids determined. As regards the quantitative and qualitative changes of the plasma aminogram, the total concentration of amino acids and the level of a few individual amino acids (glycine, alanine, taurine, and valine) were significantly elevated in full-term babies. However, no significant difference was found in the total plasma concentration of amino acids between premature infants of diabetic mothers and premature control infants, but the plasma alanine level was higher in the former. It is of interest that total plasma amino acid, alanine, and glycine levels were elevated in the asphyxiated babies. This suggests that the postnatal hyperaminoacidemia observed in infants of diabetic mothers was due to birth asphyxia rather than to impaired gluconeogenesis. The possible role of a defective gluconeogenesis in the etiology of postnatal hypoglycemia in infants of diabetic mothers is not supported by these data.