Histochemical studies of adenosine triphosphatase activity of liver cells exposed to ribonuclease

It has been revealed that ribonuclease (RNase) can penetrate into living cells and inhibits amino acid incorporation into proteins resulting in the suppression of protein synthesis and growth of living cells. BHIDE, BRACHET&#185;, KAUFMAN and DAs have proven that the RNase penetrates into onion root-tip cells and induces a number of mitotic abnormalities. KIMOTO and others&#178; also have revealed that RNase injection into mice results in the reduction of cytoplasmic basophilia with the morphologic change of endoplasmic reticulum and the disturbances in DNA synthesis as demonstrated histochemically on pancreatic exocrine cells and liver cells. But there is little information so far on the mechanisms of penetration of RNase into living cells. PILLERI&#179; and SCHUMAKER4 in Brachet's laboratory have demonstrated the uptake of RNase by pinocytosis in amoebae and cancer cells. This may suggest the penetration of RNase through the membrane of the endoplasmic reticulum in the cells whose RNase contents are low5, however it is reasonablly supposed that some phosphatase may be concerned with the permeability of RNase.</p

Acid ribonuclease activity of hepatoma cells

Activities of intracellular RNase of the liver cytoplasm, normal liver cells exposed to 3'-Me-DAB and heaptoma cells, have been studied in correlation with the contents of RNA and DNA and morphologic changes of the cells with or without treating RNase. The data showed that in hepatoma cells the intracellular acid RNase activity decreases with the decrease of RNA and unchanged DNA contents and alkaline RNase activity. Morphologic observation proved that hepatoma cells show a small low massed vesicular or vacuolar endoplasmic reticulum having ribosomes. For the exposure to RNase the hepatoma cells proved to be much less resistant comparing to normal liver cells. The former lost the granules and was destroyed in its endoplasmic reticulum, whereas the latter retained ribosomes and ER. From these experiments it has been speculated that acid RNase in the cell may be involved in RNA synthesis and alkaline RNase in RNA decompostition, though the effect of the difference in concentration in the case given RNase experimentally can not be neglected.</p

Glucose-6-phosphatase activity in regenerating cholangiole cells and hepatoma cells

Histogenesis of hepatic cancer has been analysed by observing glycogen by PAS staining and the histochemically demonstrable G-6-Pase activity on the liver of rats fed with 3'-Me-DAB or 3'-Ni-DAB. By observations on normal hepatic tissue it has been revealed that these two reactions are specific to the cytoplasm of liver parenchymal cells. Observations on the liver from the early stage of dye feeding, up to 100 days, show a marked proliferation of cholangioles in 3'-Me-DAB feeding on polished rice but only a poor reaction of cholangioles in 3'-Me-DAB feeding with synthetic diet. After 15-16 weeks of 3'-Me-DAB feeding cancer develops, a great erpart of which is consisted of cholangiocellular carcinoma and a portion, hepatocellular carcinoma. Histochemical observations on G-6-Pase and glycogen reveal that regenerating cholangiole and adenomatous tissues seem to have poles, on one side, the cells differentiate to liver parenchymal cells and on the other side, they differentiate to bile duct cells. Cancers develop mainly from these regenerating adenomatous tissues and they develop to cholangiocellular cancer or to hepatocellular cancer. The histogenesis of the latter can be traced histochemically. In the cases fed with 3'-Ni-DAB, the activity of cholangiole cells and the development of adenomatous tissue are rather poor with the delayed cancer formation. However, in these cases the majority of cancers are of hepatocellular carcinoma and the developmental mode of hepatocellular cancer can easily be traced by the G-6-Pase activity.</p

Turbid intrusion below the thermal staircase in the seasonal thermocline of Lake Biwa

Thermal 'staircase', a layer of constant temperature between the sheets of the steep gradients, was formed in the seasonal thermocline, which was 2.5 m above the bottom at a point of 18 m deep on the boundary slope in Lake Biwa. Following a sediment resuspension event when a moderate onshore wind blew, bed materials should be suspended up to the thermocline, then settled down forming a staircase above the turbid intrusion. Comparing the observed downward hear flux with the settling flux of sediment, it was found that double-diffusive convection would play an important role on the formation of the whole structure consisting of the staircase and turbid intrusion along with chemical anomalies and dense population of phytoplankters, which were fed by nutrients supplied from the bottom sediment under a typical condition of drought. Laboratory experiments were conducted to demonstrate the thermal and sediment processes in the stratified lake. Resuspension process due to surface and internal waves was examined using a tank with a sloping bottom, while the settling process was investigated by using a deep, diffusive tank. Formative process and scales of the staircase and intrusion were discussed relating with the intensity of resuspension and the buoyancy fluxes

22q11欠失症候群モデルマウスの神経発達障害には、マイクロRNAが介在するCxcr4/Cxcl12シグナリングの欠損が寄与する

22q11 deletion syndrome (22q11DS) frequently accompanies psychiatric conditions, some of which are classified as schizophrenia and bipolar disorder in the current diagnostic categorization. However, it remains elusive how the chromosomal microdeletion leads to the mental manifestation at the mechanistic level. Here we show that a 22q11DS mouse model with a deletion of 18 orthologous genes of human 22q11 (Df1/+ mice) has deficits in migration of cortical interneurons and hippocampal dentate precursor cells. Furthermore, Df1/+ mice show functional defects in Chemokine receptor 4/Chemokine ligand 12 (Cxcr4/Cxcl12; Sdf1) signaling, which reportedly underlie interneuron migration. Notably, the defects in interneuron progenitors are rescued by ectopic expression of Dgcr8, one of the genes in 22q11 microdeletion. Furthermore, heterozygous knockout mice for Dgcr8 show similar neurodevelopmental abnormalities as Df1/+ mice. Thus, Dgcr8-mediated regulation of microRNA is likely to underlie Cxcr4/Cxcl12 signaling and associated neurodevelopmental defects. Finally, we observe that expression of CXCL12 is decreased in olfactory neurons from sporadic cases with schizophrenia compared with normal controls. Given the increased risk of 22q11DS in schizophrenia that frequently shows interneuron abnormalities, the overall study suggests that CXCR4/CXCL12 signaling may represent a common downstream mediator in the pathophysiology of schizophrenia and related mental conditions.博士（医学）・乙1331号・平成26年3月17