Delay Estimation in CDMA Communications Using A FastICA Algorithm

Abstract

Zinc concentration was lower in liver of suckling 1-d-old lethal milk (lm/lm) mutant mice than in wild-type pups, in accordance with the hypothesis of milk-induced zinc deficiency previously proposed to underlie this mutation. Despite the initial deficiency, by 3 d of age suckling lm/lm pups exhibited higher levels of hepatic zinc than did lm/lm-nursed wild-type pups. Intestinal zinc and copper concentrations were normal in 1-d-old lm/lm pups, but by 3 d of age were also higher in lm/lm pups than in wild-type pups foster-nursed on lm/lm dams. Contrary to a previous report, we found that zinc concentration in milk of lm/lm dams was not significantly different from those of controls, between 4-20 d postpartum. Mutant milk showed normal zinc distribution as determined by gel-filtration chromatography or by DEAE-cellulose chromatography of zinc-binding ligands derived from EDTA-dissociated micelles, normal copper levels, normal amounts of citrate, a zinc (II) and copper (II)-binding ligand and normal amounts of glutamate, a proposed copper (II)-binding ligand. Total mammary glands and mammary gland cytosols from lm/lm mice exhibited normal zinc concentrations. Copper levels, however, were higher in lm/lm mammary gland cytosols than in controls. These results suggest that an increased uptake and/or retention of zinc and copper in the tissues studied may underlie the signs of zinc deficiency seen in lethal milk mutant mice.

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