Effect of glucocorticoids on alpha-fetoprotein synthesis and liver structure in mice acutely poisoned with carbon tetrachloride]

Experiments on male C57BL mice demonstrated that the CCl4 inhalation for 15 minutes in a concentration of 0.05 ml to 4 l of air caused deep dystrophic lesions of the liver with the signs of necrobiosis. The signs of regeneration and cellular infiltration appeared almost in 24 hours accompanied by the secretion of alpha-fetoprotein into the blood. The foci of necrobiosis disappeared completely in 4 days, being replaced by the lymphoid cells with large hepatocytes in the circumference. In the animals given hydrocortisone (20 mg/kg) or dexamethasone (2 mg/kg) for therapeutic or prophylactic purpose the regenerative processes were decreased, and the number of animals producing alpha-fetoproteins fell from 92 to 60--65%.     

Glial cells in the pineal gland of mice and rats

Summary Antigenic markers characteristic of astrocytes and their differentiative states (i.e., glial fibrillary acidic protein (GFAP), vimentin, and M1 and C1 antigens) were investigated in the pineal gland of mouse and rat using double immunolabeling techniques. In both species the socalled interstitial cells as characterized by TEM were shown to be astrocytes, since they expressed vimentin, but neither fibronectin (a marker for fibroblasts and endothelial cells) nor the neuron-specific L1 antigen or tetanus toxin receptors. Subpopulations of vimentin-positive pineal astrocytes were also GFAP- and C1- antigen-positive. M1- antigenpositive cells were not detected.It is concluded that a considerable proportion of interstitial cells in the pineal gland of rat and mouse are immature astrocytes which, in contrast to other parts of the central nervous system, persist into adulthood.Supported in part by Deutsche Forschungsgemeinschaft (Scha 185/9-4)S.-K. Huang was a recipient of a Humboldt Foundation fellowship.     

Hepatotrophic growth factor in blood of mice treated with carbon tetrachloride

The presence of a human hepatocyte growth factor (hHGF)-like DNA-synthesis promoter in platelet-poor serum of mice with liver injury was examined. Activity of the serum for stimulating DNA synthesis in cultured rat hepatocytes was low in untreated or vehicle-treated mice, but markedly increased 24 h after carbon tetrachloride administration and then dropped to normal levels prior to the peak of liver DNA synthesis. The effect of the serum was additive with the maximal effects of mouse and human epidermal growth factors, but not with that of hHGF. The growth-stimulating factor in the mouse serum, like hHGF, had affinity for heparin and was heat-labile. These results indicate that the level of a serum hHGF-like hepatocyte growth factor increased in mice treated with carbon tetrachloride prior to liver regeneration.     

Loss of blood and carbon tetrachloride poisoning]

In rats the induced enhancement of glutamic-pyruvic transaminase and leucine aminopeptidase activity in plasma to 5.2 mMol CC14/kg (per 05) is potentiated after repeated drawing of blood. The DL50 of CC14 following oral application in rats after loss of blood is reduced significant comparatively to controls and to animals with increased content of haemoglobin in blood.     

Mammary gland involution is delayed by activated Akt in transgenic mice

Activation of the antiapoptotic protein kinase Akt is induced by a number of growth factors that regulate mammary gland development. Akt is expressed during mammary gland development, and expression decreases at the onset of involution. To address Akt actions in mammary gland development, transgenic mice were generated expressing constitutively active Akt in the mammary gland under the control of the mouse mammary tumor virus (MMTV) promoter. Analysis of mammary glands from these mice reveals a delay in both involution and the onset of apoptosis. Expression of tissue inhibitor of metalloproteinase-1 (TIMP-1), an inhibitor of matrix metalloproteinases (MMPs), is prolonged and increased in the transgenic mice, suggesting that disruption of the MMP:TIMP ratio may contribute to the delayed mammary gland involution observed in the transgenic mice.