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No abstract

A human congenital pseudarthrosis of the tibia, unresponsive to conventional treatment, was stimulated to healing by direct electric current. The method was modeled after prior experimental work in vivo in rabbits. X-ray photographs, histological techniques, and electron microscopy confirmed the presence of newly formed bone in the defect region.

Dietary zinc deficiency has been shown to decrease the in vivo incor.poration of thymidine into the nuclear DNA of liver parenchymal cells in the rat. A single injection of 100 pg of zinc was sufficient to rapidly reverse the effect of zinc deficiency on the synthesis of DNA.Zinc is essential for nucleic acid and protein synthesis of several species of microorganisms and plants (Underwood, '62). Studies by Fujioka and Lieberman (' 64) of the effect of ethylene diamine tetra acetic acid (EDTA) perfusion on deoxyribonucleic acid (DNA) synthesis in the partially hepatectomized rat suggested that zinc is also necessary for DNA synthesis in mammals. Preliminary observations in zincdeficient and pair-fed control rats and more recent studies by Buchanan and Hsu ('68) in zinc-deficient and ad libitum control rats indicate that this may indeed be true.The present studies were done to test Lieberman's hypothesis in zinc deficient rats of different ages and to determine whether the effect was due primarily to lack of zinc or simply due to inanition. MATERIALS AND METHODSTwenty-seven weanling Spr ague-Dawley rats were fed a biotin-enriched purified diet containing sprayed egg white as the protein source, having a zinc content of < 1 ppm.They were given glass-distilled water from plastic containers and housed in plastic or stainless steel cages in an air-conditioned, relatively dust-free environment.Twelve animals were divided into pairs by weight and sex (Groups I-VI). One of each pair was injected with either 500 clg of zinc intraperitoneally (IP) at weekly intervals or 100 pg every other day. The zinc injected animals were fed an amount of diet equal to what their pair mates had consumed on the previous day (pair-fed).Fifteen of the rats were divided into groups of three by weight and sex (Groups VII-XI). All were fed the diet alone until J. CELL PHYSIOL., 73: 81-84.signs of zinc deficiency became apparent (Macapinlac, '64). Groups VII and VIII were treated as follows: one member was injected with 100 pg of zinc every other day and fed the diet ad libitum, a second member of the group was injected with 100 clg of zinc every other day and pair-fed with the third member (the zinc deficient animal) who received the diet alone. The treatments were continued for ten days by which time signs of zinc deficiency had disappeared in the zinc-supplemented control animals. Groups IX, X, and XI were treated as follows: all were fed the diet alone until severely ill with zinc deficiency. The two control members of each group were then injected with 100 clg of zinc IP. The zinc deficient and one of the control animals were then fasted for 24 hours. The second control animal was fed the diet ad libitum for 24 hours.After completion of the various treatments described, the animals were injected IP with 0.25-1.0 ~c of high specific activity H3-thymidine3 per gram of body weight; members of each group were given the same dose of tracer. Twenty-four hours later the rats were killed by decapitation and a portion of their livers fixed...

No abstract