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The influence of the initial resistivity on the life stability of thin In 2 O 3 -SnO 2 films deposited onto cold substrates was investigated. We tried to improve the life stability with protective layers. A method of producing thin films with low initial resistivities is presented and the influence of the substrate on the initial resistivity is described.

Pyruvate kinase isoenzymes type M1 and M2 from dog muscle, lung and tumor have been isolated. The K0.5 for phosphoenol pyruvate have been determined to be 0.04 mM for dog muscle type M1, 0.24 mM for lung type M2 and 0.28 mM for tumor type M2 isoenzymes. The activator constant ka of L-serine is 240 nM from lung and 70 nM from tumor isoenzyme. Consistent with the assumption of a special form of pyruvate kinase M2 in dog tumor cells different isoelectric points and amino acid compositions have been found for the isoenzymes of lung and tumor.

Primary hepatocellular carcinoma was induced by treatment with the initiator N’nitrosomorpholine followed by the promoting agents phenobarbital or Clofibrate. In those tumors, the activities of pyruvate kinase, fructose 1,6-bisphosphatase and lactate dehydrogenase were reduced. A reduction in the activities of pyruvate kinase and fructose 1,6-bisphosphatase along with an increase in malic enzyme activity were observed in the host livers of tumor-bearing rats and in livers of rats pretreated with the promoter alone, suggesting that these changes may be a general effect of the xenobiotic which serves as the tumor promoter in chemical-induced hepatocarcinogenesis. Such changes were independent of the promoter used, whereas alterations in the enzymes gamma-glutamyltransferase and glucose 6-phosphate dehydrogenase were dependent on the promoter type. Enolase activity was not affected by any treatment. In a second experiment, relevant carbohydrate metabolites, amino acid levels and selected carbohydrate metabolizing enzyme activities were determined in hepatic tumors from rats which had received phenobarbital as the promoting drug. Serine dehydratase and glucose 6-phosphatase were strongly depressed when compared to host livers and livers from rats treated only with N’nitrosomorpholine. On the other hand, glucokinase activity was reduced in tumors as well as in host livers of tumor-bearing rats, while phosphofructokinase and 6-phosphogluconate dehydrogenase activities were unaltered in all livers. The decrease in pyruvate kinase, fructose 1,6-bisphosphatase, serine dehydratase and the subsequent decrease in pyruvate and alanine in hepatocellular carcinoma were positively correlated with an increase in fructose 1,6-bisphosphate and glycine.