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is much more acceptable. This catalyst cost represents only the cost due to inability to recover the zinc and does not represent the costs involved in various recovery schemes.Following the hydrogenation step the zinc is distributed about equally between the liquid and solid products. In the liquid, the zinc is primarily, but not exclusively, in the water phase. The zinc content of the organic phase is greatly reduced by water washing. The zinc associated with the char is much more difficult to recover. Some of the char associated zinc is water soluble and even more is soluble in hydrochloric acid. Still more is rendered soluble by the use of cold concentrated nitric acid or hot 6 N nitric acid.Table V lists the overall recovery of the zinc catalyst by the application of two water rinse steps on the liquid portion and three different char treatment procedures for zinc removal. The first char treatment procedure, -combined with the water rinse treatment of the liquid, results in a 98.2% recovery of the zinc. The second char procedure represents a 99.0% recovery of the zinc, and the third a 98.3% recovery of the zinc. More stringent acid treatment procedures would result in more complete catalyst recovery, but at the expense of greater char oxidation. Because of the small scale of the operation, it has not been possible to make a realistic evaluation of the cost factors in catalyst recovery as yet.Literature Cited

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This animal study was performed to ascertain whether the regeneration of membrane-protected bone defects can be accelerated by the controlled application of basic fibroblast growth factor (FGF-2) using a new drug delivery system. Standardized alveolar bone defects were made surgically in 9 beagle dogs, and FGF-2 was administered using specially made collagen minipellets. A minipellet containing either 0.15 microgram FGF-2 (FGF) or 0 microgram FGF-2 (placebo) was placed in the defect or no minipellet was used (control), and bone regeneration was evaluated radiologically, histologically, and histometrically 8 weeks after the operation. Radiographs showed a surprisingly large radiopaque region in FGF sites compared with placebo or control sites. Histologically, mature bone filled the majority of the inner space of the membrane-protected defect in FGF sites. New bone formation was also seen in the control and the placebo sites, however, it filled less than half the area of the defect. Histometrically, the area of regenerated bone in FGF sites was significantly higher than in the other sites (P < 0.01). These results demonstrate that the controlled application of FGF-2 accelerates bone regeneration in membrane-protected bone defects in the canine model.

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