Hepatic blood flow, oxygen consumption and bile production in the isolated perfused rat liver of D-galactosamine induced hepatitis were measured. Relationship between these parameters and the histological lesions of the liver was examined.
A marked decrease in hepatic blood flow, a decrease in oxygen consumption and a decrease in bile production were recorded. A decrease in hepatic blood flow was thought to have an intimate relationship with following histological changes of the liver; 1) a decrease in sinusoidal space resulted from liver cell swelling and Kupffer cell proliferation, 2) leucocytic infiltration in many sinusoids and 3) destruction of sinusoids.
The localized circulatory disturbance in the liver lobule which was induced by the morphological lesions described above is thought to play an important role in development of the focal or widespread necrosis of the liver lobule of the D-galactosamine hepatitis.

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LDH zymograms of sera from patients with hepatic disorders were studied by using a technique of agar-gel electrophoresis. Elevated activities of LDH₅ were frequently observed in various liver diseases. In acute hepatitis, LDH₅ activities still elevated even after the serum total LDH activities returned to the normal level in the recovery stage. In primary hepatoma, activities of LDH₅ showed a tendency to be higher than those of LDH₄. On the other hand, in metastatic liver cancer activities of LDH₃ as well as LDH4 were increased distinctly, and activities of LDH₄ appeared to be higher than those of LDH₅. Therefore, the differences of the zymographic patterns of LDH between primary and metastatic liver cancer seemed to be useful for differentiating the both types of liver cancer.

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Guanase in sera from the patients with hepatobiliary diseases, who admitted to Okayama University Hospital, was studied to elucidate the clinical significance of the enzyme. The activity of serum guanase was assayed by the method of Coodley using guanine as a substrate.
The normal level of the enzyme activity was found to be 4.5±2.4mU. An elevation of the activity was characteristic for hepatic diseases and the lack of a rise was observed in other non-hepatic diseases. The most remarkable increase of the activity was demonstrated in an early stage of acute icteric hepatitis. However, the elevated activity decreased much faster than the serum glutamic pyruvic transaminase during the course of the disease. In other hepatobiliary diseases, such as chronic hepatitis, liver cirrhosis, hepatic cancer and biliary obstruction, the guanase activity remained to be essentially normal, unless there was concomitant acute and extensive liver-cell damage.

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The indirect immunofluorescence technique was employed to detect HBc-Ag in liver tissue of various liver diseases. The liver tissues to be tested were incubated with the primary sera with anti-HBc, but with no anti-HBs, and then were stained with FITC-labelled goat anti-human immunoglobulins.
The specific fluorescence for HBc-Ag was observed in the nuclei or peri-nuclear area of the hepatocytes. Three patterns of the localization of HBc-Ag in hepatocyte were observed, that are; (1) intranuclear, diffuse, (2) intranuclear, speckled and (3) nucleomembranous or perinuclear cytoplasmic.
HBc-Ag in hepatic tissue was positive in 13 cases out of 22 with various liver diseases positive for HBs-Ag in serum. They were 4 out of 12 asymptomatic HBs-Ag carriers, 6 out of 7 chronic hepatitis and each one of cirrhosis, primary hepatoma and malignant reticulosis with hepatic fibrosis, respectively. No HBc-Ag was detected in the liver of 9 patients with negative HBs-Ag in serum.

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Both ot HB-Ag and HB-Ab in the sera from 159 students of the Nursing School of Kure National Hospital, were once a half year measured by the method of IAHA and PHA respectively for a year. All students are dwelt in the domitory and 2 or 4 persons ina room, whose menbers are exchanged occasionally.
High level of HB-Ag was detected in six students who were thought to be all asymptomatic carriers. HB-Ab could detected in the sera of 7 cases out of 32 students who live with these 6 asymptomatic carriers in the same room. In the addition, HB-Ab also could detect in 27 out of 121 remainders who did not live with asymptomatic carriers in the same room.
From the above results, then, the approximately same detection rate of HB-Ab are obtained to be 21.9% (7/32) and 19.0% (27/121) for each group, respectively.
Forthermore, authors could not find the case whose HB-Ab titer in the sera was elevated after living with HB-Ag carriers and also the same results about HB-Ab detection was found.
It could be concluded that the possibility of HB-Ag infection from HB-Ag carriers as only inmates are not so distinct.

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Glycyrrhizine (Gly) is widely used as the therapeutic agent for chronic hepatitis, especially in Japan. However, the effect of Gly on the damaged liver cells is still unknown. Therefore, for the purpose to elucidate its mechanism, the influence of Gly on the injured liver cells was studied biochemically and morphologically using D-galactosamine induced hepatitis in which the biochemical lesions have been figured out. That is, at least two major components, i.e. UTP-defficiency and following accumulation of UDP-hexosamine are supposed to be re- sponsible for the induction of liver injury.
Gly (20mg/150g of body weight) inhibited liver cell injury, but never repaired protein synthesis, while Uridine (1.2mg/g of body weight) repaired not only inhibited protein synthesis, but also morphological lesions.
We suggested in this article that Gly might affect injured plasma menbrane of liver cells by D-galactosamine which was reported by Reutter and Bachmann.

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