The investigation was undertaken to know ultrastructural changes of experimentally induced fatty livers. When subcellular organelles involving in lipid metabolism are loaded with excess of lipid, they float to a lighter fraction than an original fraction. Therefore, the lighter fraction might reflect pathogenesis of fatty livers.
The heavy subfraction of the floating lipids studied consisted of intermediate particles between storage lipids and organelles such as microsomes, Golgi and lysosomes. Membraneenclosed particles, originated in the above mentioned organelles, were large in size(Ca 0.4μ), whilc membrane free particles, probably presursors of storage lipids and secretory VLDLs, were small in size(less than 0.1μ). Fatty changes due to impaircd protein synthesis by carbon tetrachloride was characterixed by VLDL-free Golgi vacuoles. Ethanol-induced fatty changes followed a remarkable increase of Golgi derived dense bodies filled with VLDLs.

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Liver biopsy specimens of experimental acute hepatitis B in chimpanzees were studied by electron microscopy.
The hepatocytes obtained before the elevation of serum transaminase showed sporadically and unicellulally swelling of the mitochondria and vesiculation and moderate dilation of the endoplasmic reticulum.
The hepatocytes obtained after the elevation of serum transaminase, especially at the early stage, showed many lymphocytic infiltration in the sinusoid, sporadically hypertrophy of the smooth surfaced endoplasmic reticulum, and increase of microbodies.
when the serum transaminase reached the maximum level there recognized diffuse dilation of the endoplasmic reticulum with degranulation.
HB core particles, approximately 25-27 nm in diameter, were occasionally found in nuclei of hepatocytes before the elevation of serum transaminase.

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As most of the parameter proteins useful for the diagnosis of DIC are elaborated by hepatocytes, reductions of those proteins are not necessarily reliable indices of DIC when liver damage is present. On the contrary, the plasma level of cold-insoluble globulin (CIG), which is a recently characterized high molecular weight α₁-glycoprotein, has been shown to be of extrahepatic origen. And this protein was found to be significantly reduced in the DIC syndrome. Consequently, it is expected that the measurement of plasma CIG levels will be useful to differentiate DIC from liver diseases.
Plasma concentrations of CIG were measured immunochemically in sera of patients with acute hepatitis, fatty liver, chronic hepatitis and liver cirrhosis, and compared with those of normal controls or of the DIC syndrome. The plasma level of this protein was found to be significantly increased in acute hepatitis, fatty liver, chronic hepatitis and liver cirrhosis at the early and compensated stages. Only in the decompensated stage of liver cirrhosis, it was found to be significantly decreased, but not as drastic as in DIC. In our series, the lowest value for CIG in patients with a decompensated liver disease was 10mg/dl, compared to 13 of 55 Patients with DIC who lower value than this. We, threrefore, propose that DIC may be present whenever the CIG level in plasma is found to be below 10 mg/dl.
The determination of CIG in plasma seems to provide a way to differentiate DIC from liver diseases.

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Peripheral blood killer cell (K-cell) population of patients with various liver diseases, especialiy with chronic active hepatitis (CAH) was investigated by means of a plaque-assay method. Consequently, K-cell population of 14 control subjects was 5.1±2.0% (mean±SD), and that of 28 patients with chronic hepatitis was 4.5±3.2%. These 28 patients were divided into 2 groups, in one of which s-GPT level was more than five times higher than normal and in another within five times of normal value exactly when K-cell population was examined. K-cell population of 14 patients in the former group was 2.9±1.7% and significantly reduced (p<0.01). Almost all patients of this group were thought as CAH due to their clinical course and liver histology. Therefore it was thought that K-cell population could be one of immunological markers showing disease activity of chronic hepatitis. But the investigation of K-cell population might necessitate long pursuit because improvement of clinical picture was not the same time as change of K-cell population.
K-cell population was decreased also in patients withliver cirrhosis without esophageal varix or ascites and hepatoma without liver cirrhosis. In patients with acute hepatitis Kcell population was decreased in the initial stage, but increased as clinical improvement.

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The in vitro cytotoxicity of the peripheral blood lymphocytes against Chang liver cells was significantly increased in patients with chronic active hepatitis (CAH) compared with healthy controls. This cytotoxicity was blocked by the addition of liver specific lipoprotein (LSP) prepared from the human liver to the medium during the cytotoxicity assay. These results suggest that LSP includes the antigen with which the patients' lymphocytes react and that the cytotoxicity resulted from this reaction is involved in the pathogenesis of CAH.
The patients with CAH treated with prednisolone (PSL) did not exhibit the lymphocyte cytotoxicity against Chang liver cells. The PSI. also suppressed the cytotoxicity against Chang liver cells in vitro.

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In order to simplify the technique of superselective hepatic arteriography, a new catheter named "twist catheter" was designed. This catheter is made of KIFA catheter (red), and has a twisted end about 10cm. long.
Using this catheter, superselective hepatic arteriography was tried in 98 out of 147 cases. Superselective common hepatic and proper hepatic arteriographies were successful without replacement of catheter in respectively 89 cases (90.8%) and 48 cases (49%) only by twisting the catheter. Replaced right hepatic (12 cases) and left gastric arteriographies (5 cases) were also successful in all cases.
Not only simplified twist cathcter the procedure of superselective hepatic arteriography, but also shortened the X-ray exposure time expended for angiography.
Up to now, any complications due to introduction of twist catheter were not experienced.

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Forty-nine patients with primary carcinoma of the liver were surgically treated at our hospital through 1961. Four cases with minute hepatocellular carcinoma which were subjected to liver resection were investigated.
1. Twenty cases of this series underwent liver resection and their resectability was 41.7%. Of these 20 cases, 16 were concomitant with fibrosis or cirrhosis for back ground. Patients with such a cancer show poor prognosis and autopsy were performed on 10 cases. Histological findings showed marked proliferation of connective tissues and invasion of its fiber into the pseudolobules in the residual liver than the resected liver.
2. Of 4 cases with minute hepatocellular carcinoma, 2 were positive serum AFP and HBs-Ag level and 3 were found tumor stain in hepatic arteriogram and low density area in hepatoscintigram.
3. On gross specimen with minute cancer, all of them were of the single nodular type with capsule formation which were histologically found invasion of carcinoma. Tumors larger than 3.0cm in size revealed tumor necrosis, tumor thrombus in the portal vein and rupture of the hepatic capusules. Above findings indicated that those cases should be subjected to radical operation such as segmental resection or hepatic lobectomy.

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Plasma cyclic AMP concentration after glucagon injection intravenously was determined in 8 normal subjects, 15 patients with liver cirrhosis, 10 patients with chronic hepatitis, and 8 patients with acute hepatitis.
Plasma fasting cyclic AMP indicated comparatively high in patients with chronic hepatitis and hepatoma, compared with normal subjects.
Plasma cyclic AMP levels at 10 minute after glucagon injection were maximum, and peak values of cyclic AMP in acute hepatitis or chronic hepatitis were significantly higher than those in normal subjects, but those in decompensated cirrhosis were lower than those in normal subjects.
Peak value/basal value of plasma cyclic AMP(P/B ratio)is reliable diagnostic index of liver function. Because P/B ratio was correlative with rapid turnover protein (α₂-H s glycoprotein, group specific component), while negatively correlative with ICG-R 15.
Tentatively, measurement of plasma cyclic AMP responced to injected glucagon seems to be significant to understand the reserved liver function in the miscelleneous chronic liver diseases.

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Recently we have encountered a case of type B fulminant hepatitis which is thought to have been caused by blood transfusion after gastrectomy for advanced gastric cancer.
The results of examination of the donor blood (samples for cross-matching) showed that all of the 9 bottles of preserved blood were HBs antigen negative (R-PHA and RIA), but one of them had an anti-HBc level of 1:1024 (IAHA), and this was considered to have caused type B post-transfusion hepatitis.
The patient was a 47-year-old man. 1800 ml of preserved blood was transfused befbre and during the operation for gastric cancer. Three months after the operation, jaundice appeared, accompanied by a temparature up to 38.5 C. Also, slight psychoneurological abnormalities were present, and those continued for about 10 days. But only jaundice gradually disappeared. Although both the HBs antigen and the HBs antibody were negative before blood transfusion, when the hepatitis occurred the presence of HBs antigen and HBs antibody in the serum, a temporary disappearance of HBs antigen, and a overproduction of HBs antibody prior to the increase of anti-HBc were observed.
The histological findings of the liver biopsy performed 9 weeks after the onset of the fulminant hepatitis indicate the convalescent stage of acute viral hepatitis with confluent necrosis without orcein positive hepatocytes.

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A 21-year-old female survived fulminant hepatitis B by extensive treatments including chacoal hemoperfusion. However, she suffered a reelevation of SGPT with jaundice during the recovery stage (44 days from the onset of the grade 4 coma) from the fulminant episode. Both serum immune complex and serum HBs antigen-antibody immune complex were detected during the grade 4 coma of fulminant hepatitis, but the only former was positive in the second episode. Liver biopsy specimens obtained on the 8th day from the onset of the grade 4 coma revealed a conspicuous and diffuse hydropic swelling of hepatocytes which was not associated with necrosis of parenchymal cells. On the contrary, submmasive loss of parenchymal cells with marked inflammatory response was observed in the liver biopsy specimens in the acute stage of the second episode. There was no change of the antibody titers of HA virus, EB virus, Herpes Simplex virus and Cytomegarovirus before and after the second episode. Since this patient received transfusion (6 units) during the fulminant episode, the second elevation of SGPT was considered to be non A- non B hepatitis of which the incubation period was almost 40 days.

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A case of subacute hepatitis with abnormal intrahepatic bile ducts was reported.
In a 49 year old woman physical examination on admission showed remarkable jaundice and ascites. Liver function tests were as follows: total bilirubin, 26.9mg/dl; S-GOT, 139; S-GPT, 71; alkaline phosphatase, 29.5 K.A. units; γ-GTP, 354mU/ml; prothrombin time, 45%. Total proteins were 6g/dl, which included an albumin of 45.9%and γ-globulin of 27.2%. HBs antigen and α-fetoprotein were negative. Antimitochondrial antibody and other autoantibody were negative. IgM level was 392mg/dl.
Surgical liver biopsy specimens showed subacute hepatitis. Changes of interlobular bile ducts with damaged walls were found. But papillary appearance of the epithelium was not observed, plasma cells were rarely infiltrated, fbllicle fbrmation was not found and granuloma was never Seen.
In these point. the present findings differed from the bile duct lesions in CNSDC found in the early stage of PBC.

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A 26-year-old male with fulminant hepatitis had been treated twice in a day for 3 weeks with an intravenous drip infusion of regular insulin (10U) and glucagon (1mg) in 250ml of 5% glucose solution. Any other treatments had been accompanied during this period. Fortunately he had shown a good clinical course with marked improvements of liver functions, liver scintigrams and macroscopic and microscopic findings of the liver. Supplemental administration of pancreatic hormones to patients with fulminant hepatitis has beensuggested to have clinical significances.

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We recently came across two families of constitutional ICG excretory defect. Case 1 of 1st family Was detected by chance, otherwise case 2 of 2nd family Was detected when he Was hospitalized because of acute hepatitis. Laboratory findings in case 1 and in case 2 during recovery phase of acute hepatitis showed no abnormalities exccpt high plasma ICG retention and normal BSP. Histology of liver biopsy specimen of case l Was non specific reactive hepatitis and of case 2 was subsided stage of acute hepatitis. We found other 3 persons of same constitutional ICG excretory defect in these two families. In 1st family we found 3 persons with HBs-Ag positive and 3 persons with anti HBs positive.
In either 2 cases we obtained step fbrmation at about 20 minutes on the plasma ICG disappearance curve.
Labelling with ICG of serum protein from 5 persons in these two families using column chromatography containing Sphadex G-200 showed same eluting diagram as in control group. During acute phase in case 2 we observed disappearance of 2nd ICG peak.
We examined serum lipoprotein and binding percentage of ICG to each lipoprotein fraction using preparative ultracentrifugation in case 1, case 2, control group, liver cirrhosis and acute hepatitis. They showed respective binding percentage of ICG to each lipoprotein fraction owing to the lipid concentration, but we were failed to obtain diffbrences in ICG concentration per lipid concentration of each lipoprotein fraction. During acute phase in acute hepatitis cholesterol concentration of HDL2 and HDL3 subfractions was about half a value compared with that of control group and esterified ratio of cholesterol was also decreased.

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A case of asymptomatic primary biliary cirrhosis was reported. She presented high serum immunoglobulin M, and portal hypertension, and liver histology revealed chronic non-suppurative destructive cholangitis without septal fibrosis. Antinuclear (IgM) and antismooth muscle antibodies (IgM and/or IgG) were clustered in all her family members, her parents, one sister, two brothers and one daughter. Their mitochondrial antibodies however, were not demonstrated except patient, and liver function and serum immunoglobulin were within normal limits in her family. Such a case with familial clustering of antinuclear antibodies of IgM has not been reported in the literature up to date.

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Obstruction of the biliary tree by large amounts of mucinous substance was reported in two patients with mucin-producing cholangiocarcinoma. The tumor graw intralumenally and they were histologically papillary adenocarcinoma showing excessive mucin production. No metastasis was found in both cases. Although mucin-producing cholangiocarcinoma is ocassionally associated with clonorchiasis, no evidence was noted that two cases had a history of clonorchis infection. Mucinous obstruction of the biliary tree is extremely rare, however, in cases representing peculiarly shaped abnormal defects of the bile duct by cholangiography, mucinous obstruction should be remainded despite of its rarity.

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