DNA from B6C3F1 mouse and Fischer 344 rat liver tumors induced by N-nitrosodiethylamine (DEN) were examined for the ability to induce morphological transformation of NIH3T3 cells. DNAs from 14 of 33 of the mouse liver tumors induced by a single injection of DEN at 12 or 15 days of age were positive in this assay while DNA from only one of 28 DEN-induced rat liver tumors was active. Southern blot analysis of the NIH3T3 transformants derived from the mouse liver tumors revealed amplified and/or rearranged restriction fragments homologous to the H-ras proto-oncogene. DNA from two independent foci induced by the rat tumor DNA did not hybridize to probes for members of the ras gene family or c-raf. Activating mutations in the H-ras genes from the DEN-induced mouse liver tumors were characterized by selective oligonucleotide hybridization and the detection of a new XbaI restriction site by Southern blot analysis. In activated H-ras genes from the DEN-induced mouse liver tumor DNA, seven of 14 had a CG----AT transversion at the first base of the 61st codon, three of 14 had an AT----GC transition and four of 14 had the AT----TA transversion at the second base of codon 61. This spectrum of mutations is very similar to that recently observed in activated H-ras genes found in spontaneously occurring B6C3F1 mouse liver tumors. Taken together, the data suggest that the DEN-induced rat and mouse liver carcinogenesis may involve genetic targets other than or in addition to the H-ras gene.
The author demonstrates - contrary to all existing opinions - that without doubt insulin demand increases very early and relative continually; it stagnates only in the last weeks of pregnancy. Therefore gravid women have a resource of insulin - sufficient to guarantee (for sake of fetus) a constant level of blood-glucose. The author argues, that it may be taken for granted, that above all other hormones human placental lactogen (HPL) is responsible for regulation of carbohydrate metabolism during pregnancy. One of the most important consequences of these results is the necessity, to control the renal insulin demand of pregnant women at brief intervals (not longer than 14 days). That is the most certain way to protect fetus from injury (fetopathia!), caused by anomal high concentration of maternal blood-glucose. Moreover: alteration of insulin demand signal the condition of placenta, thus enabling the physician to act in due time.
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