Study was conducted to investigate the synthesis of nascent peptide chains (NPC) on polyribosomes which was reported to be the final destinity of the cell in post-ischemic liver as described by BernelliZazzera, A. (1980).
In D-Galactosamine hepatitis rats, the effects of Glucagon-Insulin (G-I) and prednisolone (PSL) on the synthesis of NPC on free and membrane-bonud polyribosomes were determined, as well as the DNA synthesis and c-AMP contents in liver tissues.
A single dose of G-I elevated maximally the synthesis of NPC on both membrane-bound and free ribosomes 12 and 24 hour after the treatment, respectively. Following the increase in the synthesis of NPC, G-I produced a markedly increase in DNA synthesis in liver tissues 24 hour after the administration.
On the other hand, PSL caused a increase in the synthesis of NPC on polyribosomes only 12 hour after the treatment. However, DNA synthesis was markedly inhibited by PSL.
The administration of G-I produced also a prominent increase in the c-AMP levels of liver tissues as early as 6 hour after the treatment.
These results strongly suggest that synthesis of NPC on polyribosomes plays an important role in repair of cell damage caused by D-Gal and that c-AMP may regulate the synthesis of NPC on polyribosomes and DNA synthesis in liver tissues. Hence, G-I and PSL will prevent the progression of hepatic cell necrosis through increased Synthesis of the NPC on polyribosomes.

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For detection and characterization of the binding-sites on HB surface antigen (HBsAg)-particles associated with HBe antigen (HBeAg) against soluble polymerized human serum albumin (pHSA), namely albumin receptor, the new enzyme-liked immunosorbent assay (EHSA) using an anti-HBs-coated well of polystyrene microplates and horseradish peroxidase-labelled pHSA was used as an inhibition test using various specific antibodies against human serum components, HB virus (HBV)-associated antigens and liver cell membrane-associated antigens. As the characterization of the bindingsites, all of rabbit antibodies against human serum components, human sera with anti-HBs, human sera with anti-HBe and rabbit antibody against soluble liver specific lipoprotein (anti-LSP) could not bound to the sites, but rabbit anti-HBs, human antibody against non-soluble liver specific membrane antigen (antiLM) and human sera containing both anti-HBs and anti-LM bound to the binding-sites against pHSA.
Rabbit antibody against circulating immune complexes preparated from a patient serum with chronic active hapatitis (CAH) type B (anti-CIC) also bound to the binding-sites. The results of immunofluorescence using FITC-lebelled pHSA and human liver specimens were the same above such as the pHSA could bound to liver cell membranes.
These results indicate that the binding-sites on HBV-particles against pHSA may be associated with LMAg against anti-LM detected in HBsAg-negatve CAH patient sera differed from anti-LSP in both HBsAg-positive and-negative CAH patient sera.

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For selection of effective cases in hepatitis B patients for treatments by anti-viral agent and immunopotentiator, the binding-activity of albumin receptor on hepatitis B virus (HBV) (pHSA-BA) assay was used. The patient sera at 3, 6, 12, 24, 48 hours after one shot of adenine arabinoside (Ara-A: 5 mg/kg) or bacterial immunopotentiator (OK-432: 2.0KE) were tested. On the otherhand, the sera from 3 groups of Ara-A administration, OK-432 administration and combination administration with Ara-A and Ok-432 for 3 to 10 weeks were tested. As the results, one shot of Ara-A was no effective against the titers of HBeAg and pHSA-BA, and on the contrary indicated to decrease the titers of anti-HBe. On the other hand, one shot of OK-432 was effective against the titers of both HBeAg and pHSA-BA. In the 3 groups, the combination group with Ara-A and OK-432 was most effective against pHSA-BA. These results indicated that the pHSA-BA assay was useful for selection of effective cases in hepatitis B patients before administration of anti-viral agent or immunopotentiator in place of the conventional tests for HBV infectious markers (e.g. DNA polymerase activity, HBeAg, Dane particles).

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Eight patients with chronic HBsAg positive hepatitis were treated with human leucocyte interferon. Interferon was given as a daily dose of 6-10×106 international units for 10 to 14 days on alternate days. The total per patients varied between 38 and 75×106 international units. In all eight patients the level of DNA-polymerase fell during therapy. After treatment four patients remained persistently DNA polymerase negative, whereas relapse to initial values occured in others. In three patients HBeAg became undetectable and anti-HBe appeared in two patients. Although the data suggest that responses may be more frequent in interferon treated patients, spontanous remission must make us cautions in our interpretation. The data obtained in these studies showed an effect of interferon administration on indices of hepatitis-B virus infection in chronic hepatitis.

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To clarify metabolic abnormalities in serum lipoproteins we have studied the changes of chemical and apoprotein compositions of very low density lipoproteins in liver cirrhosis.
1) Serum VLDL levels were significantly decreased in liver cirrhosis.
2) With respect to the chemical compositions of VLDL, patients with liver cirrhosis had an increase in cholesterol and protein and a decrease in triglycerides. Surface/core ratio of VLDL was significantly elevated in liver cirrhosis.
3) In cirrhotics, apoprotein C was decreased while apoprotein E was increased according to the VLDL apoprotein compositions by 10% PAGE in 1% SDS.
4) The VLDL of patients with liver cirrhosis was slowly migrated on 1% agarose film electrophoresis as compared with that of controls.
5) In cirrhotics, VLDL with small size was increased on the elution steps of Biogel A-15m column chromatography.
6) On the basis of previous reports and our present studies, an increase in VLDL-apoprotein E is probably due to a low activity of hepatic triglyceride lipase which may convert IDL into LDL, but the mechanism remains to be clarified.

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Four normal subjects and 18 patients with esophageal varices with hepatic cirrhosis were catheterized into the portal vein using the technics of percutaneous transhepatic portography. Plasma levels of glucose, IRI and IRG of portal and peripheral blood were measured immediately after the beginning of intravenous administration of L-arginine (8g/5min).
A relative low level of portal IRI and a considerably high level of portal IRG were shown in patients with liver cirrhosis compared with the normal subjects.
It seemed to be likely that peripheral hyperinsulinemia reflected diminished hormone metabolism and that the high plasma glucagon levels observed in our cirrhotic patients were the result of pancreatic hypersecretion of glucagon.

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A 36-year-old woman had been pointed out of hypergammaglobulinemia without any biochemical evidence of liver dysfunction was admitted for the complaint of general fatigability. Serological findings revealed acute hepatitis. After a year of the onset, she proved the state of "subacute massive hepatic necrosis of the liver". In her clinical course, nuclear and smooth-muscle antibodies revealed positive and Liver-Specific-antigen was also detected with the depletion of suppressor T cell function.
Serological findings of her mother also showed hypergammaglobulinemia and high IgG level.
The pathogenesis of lupoid hepatitis is suggested to be correlated with the genetic predisposition to immunologic abnormalities.
This case suggested that hypergammaglobulinemia, one of the criteria of lupoid hepatitis described by Mackay, was not the result of liver injury but the possibility of genetic predisposition to immunologic abnormalities.

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We report a case of progressive systemic sclerosis (PSS) complicated with chronic active hepatitis and esophageal ulcer. This 42 year-old male patient was admitted to our hospital because of oppressive sensation on swallowing. His present illness disclosed edema of the 4 extremities 17 years ago, Raynaud's phenomenon 12 years before, sclerotic change of the fingers 7 years ago and hematemesis 1 year previously. He had masked face, sclerotic change of the skin and arthralgia of the left wrist with morning stiffness.
Laboratory studies revealed positive RA test, increased γ-globulin levels, negative HBsAg and Ab, K_ICG 0.12, serum compliment 45.4 CH50 u, negative anti-mitochondrial antibody, T-cells 80.2%, B-cells 14.2%, urinary 4-hydroxyproline 42.96mg/day, etc. The histology of the biopsied skin disclosed marked fibrosis in the true skin, which was consistent with PSS. Two esophageal ulcers were demonstrated in endoscopic examination. The surface of the liver showed slight unevenness, increased white network patterns and moderate splenomegaly on peritoneoscopic examination.
The histology of the biopsied liver disclosed chronic active hepatitis (CAH, 2A according to the European classification) and the relation with autoimmune mechanism was conjectured.

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A very rare case of coexistence of hepatocellular carcinoma and rhabdomyosarcoma in the liver was reported.
A 55 year old man was admitted to our hospital for high fever and right hypochondrial pain. Liver scintigram and CT scanning revealed enlargement of the right lobe with a large space occupying lesion. Hepatic angiography showed large hypovascular area with some hypervascular portion in the right lobe.
Alphafetoprotein in the serum remained positive. The liver enlarged rapidly and he died of intraperitoneal bleeding from the tumor. At autopsy, the liver weighed 3700g and a large, soft hemorrhagic and necrotic tumor occupied almost entire right lobe. The left lobe showed a feature of micronodular cirrhosis. In section, an another tumor, 5cm in diameter, was noted adjacent the major tumor. Microscopically, the large tumor was embruonal rhabdomyosarcoma and the smaller one hepatocellular carcinoma, Edmondson type III.

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A 56 year old man with hepatocellular carcinoma was treated by transcatheter arterial embolization with gelatin sponge (Spongel).
The patient was dead 10 days after embolization because of the rupture of esophageal varices. Necrosis were noted extensively throughout the tumor nodule and a few vialbe tumor cells remain at the periphery or solitarily in the center of nodules. In order to evaluate the effect of embolization, 746 pieces of serial section of embolized liver were examined. Spongel form networks with erythrocytes and fibers, making complete obstruction of a large vessel. In the branch vessels only the fibrin fibers occlude and no Spongel are noted in the periphery in one place, while frangments of Gelfoam are observed even in the smaller vessels without forming any networks with fibrin fibers, in the other.

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A 32-year-old woman admitted for pancytoprnia and splenomegaly, and diagnosed as idiopathic portal hypertension. Then, transthracic esophageal transection and paraesophageal devasculization were carried out, and moreover, through incision of diaphragm, splenctomy and devasculization of lesser curvature of stomach were done. At 40 days after sutgery, ascites and left flank continuous murmur were noticed. And 40 days later, she fell into henatic coma of grade IV. and serum ammonia concentration was 203μg/dl, and typical triphasic waves were showed on EEG. Selective celliac arteriogram demostrated rapid filling of dilated splenic vein via a fistula. Splenic arterio-venous fistulectomy with distal pancreatectomy was performed.
Splenic arterio-venous fistula is very rare, only 30 cases being reported in the world literatures. Rupture of splenic arterial aneurysm into splenic vein is thought to be causative for the fistula formation. Celiac arteriogram of our case on admission showed multiple splenic arterial aneurysm, so we think aneurysms ruptured into splenic vein. Usually, ascites, continuous murmur in the left flank, splenomegaly and rupture of esophageal varices are reported as symptoms of splenic arterio-venous fistula, but hepatic coma is uncommon.
It is, we thought, reason for hyperammoniemia in this case that, for the proximal collaterals were shut off at the first surgery, superior and inferior mesenteric vein altered to main collaterals, and ammonia originated from intestine flow mainly into systemic circulation, and finally resulted in portal systemic encephalopathy.

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A 51-year-old man was diagnosed as segmental obstruction of the intrahepatic bile duct in posterior segment by CT scan and percutaneous contrast study, and confirmed operatively. He had an episode of relapsing attacks of the right upper abdominal pain and back pain from childhood, and had cholecystectomy for cancer of the gallbladder and papilloplasty for primary bile duct stone before the diagnosis. He had quite relief of the attacks since rihgt hepatic lobectomy for removal of cholestasis in the occluded intrahepatic bile ducts. We consider the segmental obstruction as congenital origin.

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A 63-year-old female patient with Cruveilhier-Baumgarten disease is reported.
She had an episode of hematemesis due to a rupture of the esophageal varices. She showed splenomegaly with hypersplenism, dilatation of the abdominal vein, and venous hum in the right upper quadrant. A Celiac angiography demonstrated a marked dilatation of the umbilical vein and the portal vein, and splenomegaly. On laparoscopy, the liver was atrophic and its surface was smooth. A histological finding of the biopsied liver showed that there was mild fibrosis with minimal infiltration of the lylnphocyte in the portal area. There was no evidence of liver cirrhosis. A dilated umbilical vein seemed to be congenital. The definition of Creveilhier-Baumgarten disease and tis etiology were discussed.

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