Isolated rat liver nuclei incubated with ¹⁴C-leucine in vitro were extracted with 50mM Tris-HCl buffer (pH 7.4) and 1 M NaCl successively. "Nuclear residual fraction" remained after extraction was solubilized with 8 M urea in 50mM NaHCO₃C-Na₂CCO₃C (pH 9.5). About 90% of protein and the incorporated radioactivity of "nuclear residual fraction" was solubilized in 8 M urea-50mM sodium carbonate buffer extract. The urea extract was further fractionated into 3 fractions by chromatography on DEAE-cellulose. The fraction II, which was eluted from the column with 0.05 M NaCl and contained 80% of radioactivity of the urea extract, was rich in glutamic and aspartic acid. The fraction II was separated into 3 protein bands, and one major and a few minor radioactive bands on acrylamide gel electrophoresis.

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Nuclear membrane fraction obtained from rat liver was able to incorporate ¹⁴C-leucine into its proteins. The incorporation of ¹⁴CC-leucine increased almost linearly during 2 hr incubation. Optimal pH of the incorporation was found to be between 6.0 and 6.5. The rate at which ¹⁴C-leucine was incorporated into protein was proportional to the added amount of membrane fraction up to 400μg.
The possibility that the contaminated mitochondrial fraction is responsible for the incorporation of ¹⁴C-leucine by nuclear membrane fraction was ruled out.

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Blood pressures pre- and post-ligation of hepatic artery at the several key points of the hepatic vascular pathway in both the normal and the choline deficient diet induced liver cirrhosis of rats were measured.
The mean portal venous and intrahepatic terminal portal vein pressure in the cirrhotic rat elevated by 102mm H₂O and 40mm H₂O from the normal level respectively, while no remarkable pressure change was there in the central vein and in the inferior vena cava. Hepatic artery ligation produced a decrease by 22mm H₂O in portal vein pressure and a decrease by 10mm H₂O in terminal portal vein pressure in the cirrhotic rat, in contrast to a decrease by 9mm H₂O in the portal vein and by 1.6mm H₂O in the terminal portal vein in the normal rat. There Was no significant pressure change in the ccntral veln and in the inferior vena cava.
The difference of blood pressure in the portal vein between the normal and the cirrhotic rat was calculated to compose of an increase in vascular resistance in the intrahepatic portal vein-56%, an increase in vascular resistance in the sinusoid-27% and pressure transmitted from the hepatic artery-13%.

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The purpose of this study is to analyse some changes which contributed to the disintegration of the biliary epithelial cell and to clarify the details of the fine structure of the affected cell. The needle biopsy of the liver was performed in normal cases (2 cases) and various hepatic diseases (50 cases) under peritoneoscopic observation, and a large number of biliary epithelial cells were observed electromicroscopically.
The degenerative findings which contributed tc the disintegration of the biliary epithelial cell consist of two changes: 1) "dark cell metamorphosis" and 2) "light cell metamorphosis". The "dark" epithelial cell retracts from its neighbours and finally falls down into the ductal lumen (1a) or falls out at the basal side of the duct because of the rupture of the basal membrane (1b). The "light" epithelial cell forms large edematous microvilli ("bleb" formation) and falls down in the ductal lumen because of the rupture of the edematous microvilli (2a). These affected epithelial cells were observed commonly in all observed cases of hepatic injury and there were no specific differences among each diseases.
When each of the epithelial cells of the bile duct become "dark" progressively, the bile duct is to be disorganized as a whole. This findings was observed in cases with extrahepatic biliary obstruction and cholangitis.
No specific change of the organelles in the cytoplasm which may have a correlation to the disintegration of the biliary epithelial cell was clarified.

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We described here histological changes of the interlobular bile ducts found in chronic hepatitis.
Fourteen liver biopsy specimens (12.2%) from 14 cases exhibited abnormal interlobular bile duct epithelium in 115 biopsy specimens from 99 patients with chronic hepatitis. Abnormal bile ducts had swollen, vacuolized or flat epithelial cells with karyopyknosis or karyorrhexis. The epithelium was often infiltrated by inflammatory cells. Eosinophilic degeneration of epithelial cells was also found. The portal tracts containing abnormal bile ducts were infiltrated with dense inflammatory cells, occasionally forming follicles.
In this study no granuloma was found and papillary appearance was not observed in bile duct epithelium. Plasma cells were found slightly in the portal tracts in only one case.
It should be mentioned that these findings differed from bile duct lesions found in early stage of primary biliary cirrhosis.

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The origin and the structure of alcoholic hyalin were studied by light and electron microscopy in thirty-three liver biopsy specimens from patients with alcoholic disease, primary biliary cirrhosis, hepatoma or diethylaminoethoxyhexestrol-induced liver injury. Hyalin was classified into two types, namely coarse type and fine type. Most hepatocytes with hyalin showed nucleus degeneration. Hyalin was scarcely stained with ribonucleic acid staining. On the other hand, numerous bosophile substances were revealed inthe hepatocytes around the cells with severe necrobiosis and fine type of hyalin. Ultrastructurally hyalin at an early stage was composed of filamentous components and, floccular, partly granular structures considered to be degenerated glycogen particles as well as ribosome-like particles scattered throughout the hyalin meshwork. Besides, altered rough surfaced endoplasmic reticulum (rER) and polysomes were increased around the early hyalin. Filamentous structures were partly merged with disorganized rER, showing a close similarity to the membrane of rER. Therefore the early hyalin could be considered to be related closely to the endoplasmic reticulum, particularly denatured structures of rER and occasionally of glycogen particles.

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Serum levels of hepatitis B antigen (HB-Ag)and α-fetoprotein (AFP) in the patients with chronic liver diseases were measured by the methods of immune adherence and radioimmunoassay, respectively.
The incidence of positive HB-Ag was higher in active form of chronic hepatitis or liver cirrhosis than in inactive form of these diseases. The difference between the incidences of HB-Ag in active form and in inactive form was more characteristic in the precirrhotic stage of chronic hepatitis or in the early stage of liver cirrhosis than in the other stages of these diseases.
The incidence of positive AFP was higher in liver cirrhosis, especially in active form, than in chronic hepatitis and that was highest in hepatocellural carcinoma (95%). It was also showed that the incidence of positive HB-Ag in hepatocellural carcinoma with liver cirrhosis (44.1%) was higher than in liver cirrhosis without carcinoma (27.7%).

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