Cirrhotic livers of different types obtained from 4 autopsy cases were submitted to three-dimensional graphic reconstruction of the nodules and blood vessels from serial histologic sections. It was disclosed that all the nodules were connected with the adjacent ones so as to form a nodular network in the space, in spite of apparent separation of nodules on the histologic picture. There were abundant holes in the network system as the result of anastomosis of the nodular chains. On the other hand, the network was in 'conjugation' with the blood vessels of the liver. Parenchymal network of the same type was found also in the livers with subacute hepatitis and chronic hepatitis. Thus the network system was regarded as the structural framework which was common between the liver cirrhosis and its precursory lesions.

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The alterations of ALP of the serum have been studied among a control, patients with diabetes mellitus, patients with liver cirrhosis, and patients with liver cirrhosis accompanied with diabetes mellitus. The average activity of serum ALP of each group was 2.0 Bodansky units(U) in the control, 2.6 U in patients with liver cirrhosis and 5.5 U in patients with liver cirrhosis accompanied with diabetes mellitus. The values of any two groups of these were statistically significant. Electrophoretic separation of the ALP isoenzymes of these groups indicated that these differences were due to the change in intestinal component of total ALP in the serum. These data indicated that intestinal ALP activity in the serum was influenced by the metabolic disorder of glucose whether or not liver cirrhosis existed. And it also indicated that increase in intestinal ALP was exaggerated in the serum of the patients with liver cirrhosis accompanied with diabetes mellitus as compared with the patients with liver cirrhosis without diabetes mellitus.

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GOT isozymes of pig liver have been purified each other, analysed by immunodiffusion and immunoelectrophoresis in agar gel, and further their hapatic cellular sites have been investigated by indirect fluorescent antibody method; supernatant GOT (s-GOT) and mitochondrial GOT (m-GOT) are quit different enzyme proteins immunologically, and the former consists of four subconponents migrating to the anode, while the later includes two subcomponents moving to the cathode and one to the anode. The specific fluorescence of s-GOT is seen in very small granules within hepatic cells, of which some positively stained cells are occuring singly or in groups throughout the lobules. Most of positively stained cells are found in the peripheral zone of the lobules. m-GOT positive cells are rather diffusely distributed throughout the lobules, and its distribution pattern is different from that of s-GOT. Cells other than hepatocytes, Kupper cells and endothelial cells in the sinusoid are not stained for s-GOT or m-GOT.

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In order to clarify the ammonia metabolism in the rat liver in both biliary obstruction and carbon-tetrachloride (CCl₄) injection, urea synthesis and ammonia removal in liver slices and arginine synthetase activity in liver homogenate were examined. Following results were obtained :
1) In biliary obstruction groups, urea synthesis and ammonia removal in liver slices were decreased with the duration of biliary obstruction. The increasing rate in urea synthesis and ammonia removal by addition of ATP and ornithine in the medium was also declined, especially in the 6-week group. Arginine synthetase activity was decreased progressively corresponding to the duration with its lowest in 6-week group.
2) In CCl₄ group, no remarkable decrease in arginine synthetase activity was illustrated compared with 6-week group, however, the grade of urea synthesis and ammonia removal in liver slices were distinctly decreased, which were accelerated prominently in the presence of ATP and ornithine.

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Clinical course and prognosis were studied in 102 patients with hepatic coma in the 18-years period from 1958 to 1975. Patients consisted of 9 fulminant hepatitis, 7 subacute hepatitis, 53 liver cirrhosis without hepatoma (40 acute type, 10 chronic type and 3 another type according to Sherlock's classification of hepatic coma) and 33 liver cirrhosis with hepatoma.
1. 4 of 9 fulminant hepatitis patients were aroused within 1 week and recovered completely.
2. All of 7 subacute hepatitis patients died within 2 weeks after the onset of hepatic coma.
3. In the period from 1958 to 1969, 20% of liver cirrhosis patients with acute type of hepatic coma recovered from the coma, and in the period from 1970 to 1975, 45% recovered.
4. 7 of 10 patients of liver cirrhosis with chronic type of hepatic coma died 4 months to 9 years from the onset of hepatic coma. 50% survival time was 2.5 years. Remained 3 patients were now beeing alive.
5. In the 12-years period from 1958 to 1969, 9 hepatoma patients with hepatic coma were hospitalized in our clinic, and in the 6-years period from 1970 to 1975, 24 were hospitalized.
6. In the period from 1958 to 1975, 31 of 71 BUN-examined patients had hepatorenal syndrome. 23 of 31 were in the period from 1970 to 1975.

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Using the technique of percutaneous transhepatic portal vein catheterization, separate measurement of intra- and extrahepatic shunts was possible. It involves injection of ^99mTc-macroaggregated albumin (MAA) at the beginning of splenic vein and of ¹³¹I-MAA in the portal trunk, followed by scanning of liver and lungs, and measurement of count of each nuclide over the set areas of these organs. Measurement of intrahepatic shunt index was carried out in 18 cases with liver disease. Intra- and extra-hepatic shunt indeces were measured in 9 out of 18 cases. Intrahepatic shunt indeces were 1.6 to 78.4% in liver cirrhosis (14cases), 4.6% in idiopathic portal hypertension (1 case), 1.0% in intrahepatic cholestasis (1case) and 4.2 to 5.4% in hepatic steatosis (2cases). Extrahepatic shunt indeces were O to 49.9% in liver cirrhosis and 1.5% in hepatic steatosis. The intrahepatic shunt indeces seemed to correlate very closely with ICG retention, and with the presence of jaundice, indicating the value of shunt measurement in assessing liver function and prognosis.
Extrahepatic shunt indeces seem to correlate with the size of collaterals opacified by portography and tend to be high in the presence of esophageal varices.

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A 63-year-old male patient of miliary tuberculosis with jaundice was reported. He was admitted to our hospital, complaining of jaundice and lumbago. Chest X-ray examination revealed chronic tuberculosis and miliary shadows throughout the lung field and liver function tests showed indications of obstructive jaundice. He developed hepatic encephalopathy and hematemesis, and died 3 days after the admission. At autopsy, the major findings were chronic tuberculosis in the lung and disseminated miliary tuberculosis in all major organs. In the liver, many miliary tubercles were distributed diffusely, especially in the portal tracts and marked fatty degenaration of the liver cell was also noted. The intestine was free from tuberculous lesions.

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