The administration of trivalent chromium (Cr (III)) caused a significant enhancement of RNA synthesis in rat liver after partial hepatectomy. Cr was accumulated in the liver cell nuclei and concentrated in the nucleoli. Of RNAs synthesized in the nuclei, nucleolar RNA synthesis was most enhanced by the administration of Cr (III). Furthermore, DNA synthesis in the Cr (III)-administered rat liver after partial hepatectomy was initiated a little earlier and was less synchronized than in control rats.

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Resting cells (G₀ cells) of the uterine surface epithelium in castrated mice began to synthesize DNA with high synchrony from 10hr after the injection of 50ng of estradiol-17β with or without 5.5μg of clomiphene citrate. Highly synthesis in G₀ cells elicited with estradiol was delayed approximately 5hr when the simultaneous administration of 0.5mg of progesterone was given. In Go cells of castrated mice which received 5.5μg of clomiphene or 55μg of clomiphene plus 50 ng of estradiol, DNA synthesis with partial synchrony began 15hr after the injection. The effects of estradiol were completely suppressed by the administration of 55μg of clomiphene. It is suggested that the inhibitory action of clomiphene may be due to the competitive blocking of estrogen binding, while progesterone suppresses the estrogen-induced DNA synthesis of the surface epithelium and transfers them to the G₀ cell-compartment.

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When an excised section of larval integument is implanted into a larva, the growth rate of the epidermal cells of the implanted tissue increases to form a cyst in vivo. In order to clarify the processes associated with in vivo cyst formation in the sweet potato hornworm, Agrius convolvuli, we investigated the progression thereof using light- and electron microscopy. Immunohistochemical techniques using eCBP (epidermal carotenoid binding protein) as a specific marker for detecting larval epidermal cells, and BrdU-incorporation for examining DNA synthesis in the epidermal cells were also undertaken. The results indicated that in vivo cyst formation proceeded through the following five phases: (1) hemocytes aggregate around the periphery of the transplanted integument, (2) forming a thick mass of aggregated cells. This is followed by (3) DNA synthesis, not only in the cells near the periphery, but also in the entire epidermal cell layer. Then, (4) the epidermal cells at the leading edge penetrate the cell mass until continuity of the integument is complete, (5) finally they secrete new cuticle inside the cyst. Given the simplicity, high reproducibility and ease with which these experimental procedures can be conducted, the system of in vivo cyst formation in insect is a useful model for studying the more detailed mechanisms associated with wound recovery, such as epidermal elongation at the site of integument damage.

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Nivalenol, a toxic product isolated from the rice grains infected with Fusarium nivale, was shown to inhibit the multiplication of HeLa cells completely at a concentration of 0.5μg/ml or higher. At the concentration of 5μg/ml, protein and DNA syntheses were almost entirely suppressed, whereas little or no inhibition took place in RNA synthesis. The inhibitory effects on both DNA and protein syntheses were similar with respect to the rapidity and severity.
Cell cycle analysis revealed that, in addition to direct effect on S phase, the toxin affected the entry of G1 cells into S phase and that of G2 cells into mitosis. These results are discussed with special reference to the similarity of the action to that of well-known inhibitors for protein synthesis.

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