Thirty four autopsy cases of so-called fulminant hepatitis were collected, and pathological changes of various organs were observed, grossly and histologically, mainly from the comparative view point with the hepatic changes. According to the degree of hepatic cell necrosis, a classification into four stages was used; (I) Liver with mild necrosis, (II) severe necrosis, (III) complete destruction, and (IV) beginning of regeneration of the parenchymal cells.
This classification was believed to be usable both for clinical and pathological purposes. The weight of the liver increases a little in I, continues to decreasc in II and III, and shows slight recovery in IV. That of the kidney was always above the normal lebel.
Various striking changes of other organs than the liver were found as follows, although their incidence and grade were varying from case to case; 1) Alimentary tract: Hemorrhage and inflammatory change, 2) Pancreas: Simple, acute pancreatitis with occasional cases of severe necrosis, 3) Kidney: Severe cloudy swelling due to tubular fatty degeneration and/or biliary nephrosis, 4) Lung: Hemorrhage and hemorrhagic pneumonia, 5) Myocardium: Interstitial edema and degeneration of various kinds of the myocardium, occasionally with inflammatory processes, 6) Spleen and lymph node: Necrotic or exudative change due to acute circulatory disturbance, and some inflammatory changes, 7) Collection of ascites, 8) Brain: Edematous swelling.
A tendency that these changes became severer in degree and higher in incidence according to the progression of hepatic necrosis was observed. They were believed to be caused by various factors such as acute circulatory disturbance, hemorrhagic diathesis, increase of portal pressure, outflow of the hepatic necrotic substance into the blood, and generalized intoxication partly due to infection and partly due to hepatic insufficiency, etc. all of which should result from the main disease, acute or subacute liver necrosis. In other words, so-called fulminant hepatitis is a systemic or generalized disease, which is believed to be caused not only by hepatic disturbance itself, but also by severe, various changes associating and occurring in other organs. Treatment as well as research of this disease should be carried out along this line, in future.

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Liver biopsy specimens taken from patients with Gilbert's disease, Dubin-Johnson syndrome and Rotor's hyperbilirubinemia were examined under electron microscopy and their fine structural changes were analysed by morphometric method.
In Gilbert's disease, hepatocytic microvilli facing Disse's space were significantly decreased in number and fiber formation was observed in Disse's space. Vesicular smooth surfaced endoplasmic reticulum was considerably increased whereas rough one was decreased.
In Dubin-Johnson syndrome, the bile canaliculus was dilated with stunt of its microvilli and ring-formed electron dense particles were seen in about a half of studied bile canaliculi. Characteristic granules, observed in the cytoplasm of hepatocytes were morphologically different from lipofuscin granules.
In Rotor's hyperbilirubinemia, hepatocytic microvilli were decreased in number and fiber formation was observed in Disse's space. Giant mitochondria with inclusion body in the matrix were frequently seen in comparison with other two diseases.
From above described findings, the mechanism of jaundice in those diseases was discussed.

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This study was to investigate the relationship between oxidation-reduction system and hemolysis, especially in point of malonyl-dialdehyde (MDA) of RBC in CCl₄ administrated liver disorders. Our results in acute phase for 4 weeks after injection of CCl₄ obtained the increased resistance of RBC with Parpart's method due to protective factor in internal homeostasis, the lability of RBC membrane with H₂O₂ hemolysis test, increased concentration of MDA and low activity of catalase. Good effects which had decreased concentration of MDA, stability of RBC membrane and high activity of catalase after treating with α-tocopherol acetate (VE) were shown in our data.
In acute phase of CCl₄ liver disorders, our data concluded that hemolysis tendency was caused by oxidative effect, no concerning with hexose monophosphate shunt and had better effect on hemolysis by treating with VE but chronic phase no constant data to hemolysis were obtained.

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In order to determine the localization of an increasing vascular resistance in cirrhosis of the liver, blood pressures in several key points of the hepatic vascular pathway were measured in the normal and choline deficient diet induced liver cirrhosis of the rat. Blood pressures of the intrahepatic terminal portal and central vein were measured by means of the micropuncture technique. The mean blood pressure of the normal rat was; 110mm H₂O in the portal vein (liver hilum), 68mm H₂O in the terminal portal vein, 28mm H₂O in the central vein and 20mm H₂O in the inferior vena cava at the hepatic vein orifice. The mean portal vein and the terminal portal vein blood pressure of the choline deficient diet induced cirrhosis rat elevated significantly up to 173mm H₂O and to 100mm H₂O respectively, but no significant change was detected in the central vein and in the inferior vena cava. These data suggest that an increase in vascular resistance in the cirrhotic liver is present in both the intrahepatic portal vein and the sinusoid, and not in the hepatic venous tree.

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Comparative studies on the method of lipoprotein X (LP-X) detection were performed for the purpose of its clinical application. The method based on the peculiar property of LP-X which migrated toward the cathode by electrophoresis on agar-gel. LP-X was visualized after the electrophoresis by each one of the following methods; (1) Precipitation with specific antiserum which was prepared in our laboratory, (2) Precipitation with dextran sulfate-Ca⁺⁺, (3) Staining with sudan black B. The sensitivity of the LP-X detection depended on the selection of agar and the preparation of agar-gel but not on the methods of visualization.
LP-X was detected in various kinds of disease with intrahepatic or extrahepatic cholestasis. In 85 LP-X positive patients, 5 cases (6%) was found with normal level of serum bilirubin, alkaline phosphatase. total cholesterol and GOT.

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Agarose beads were conjugated with human or bovine albumin by CNBr. One gm wet weight of Bio-Gel A5m, 100-200 mesh conjugated 30-50mg of albumin. About a half of bilirubin of jaundiced blood samples was removed by passing through the agarose-albumin column, when the amount of albumin in the beads and that in the samples were same. Batch studies showed that the amount of BSP or ¹³¹I-BSP removed by the beads was parallel to the concentration of the dye in the medium, and it decreased with the increase of the amount of free albumin in the medium. There was same tendency between human and bovine albumins. When the perfusate was circulated through the column, the percentage of BSP removed was equal to that of conjugated albumin in the system. After washing with 50% ethanol, the beads could remove more BSP from the perfusate.

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