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Biomedical subjects

K Okuda

Publications and source records attributed to K Okuda.

At least 937 records · Page 52Linked to original sources
PubMed1984

Study of cellular immunity in experimental autoimmune hepatitis in mice.

This study was undertaken to produce experimental autoimmune hepatitis in mice, and to examine the role of liver specific lipoprotein (LSP), if any, and of cellular immunity in such a model. After immunization of three strains of mice (C57BL/6, C3H/He and BALB/c) with syngeneic crude liver proteins, most prominent liver changes histologically mimicking human hepatitis were produced in the liver of C57BL/6 (B6) mice. Antigenic and immunogenic activity of LSP in the crude liver proteins was decreased by the treatment of freezing and thawing, and the recovery of the antigenic activity seemed to correlate with the susceptibility of immunized mice to the induction of liver damage. Autoantibody against LSP was demonstrated in the serum of immunized B6 mice, but not in the sera of other strains after immunization. It was also found that EDTA contained in the buffer used for purification of LSP distinctly suppressed lymphocyte activity in vivo and in vitro. With the use of EDTA free LSP, it was shown that spleen cells of immunized B6 mice (especially of T cell enriched fraction) had a high reactivity studied by lymphocyte transformation test. Further examination showed that EDTA free LSP could induce mild liver lesions and lymphocyte reactivity against LSP, although neither histological change nor lymphocyte reactivity was found in the liver of B6 mice immunized with EDTA containing LSP.

Animals↗
PubMed1984

Cholangiographic features in hepatolithiasis.

The cholangiographic features of hepatolithiasis in 150 patients studied by PTC and ERC are described. On the basis of the findings, it is suggested that hepatolithiasis be divided into primary and the secondary groups, and the former into the major intrahepatic bile duct type and the peripheral intrahepatic bile duct type. There is certain correlation between these cholangiographic classifications and clinical features.

Adult↗
PubMed1984

Aneurysm of the intrahepatic branch of the portal vein. Report of two cases.

Two patients in whom real-time ultrasonography and percutaneous transhepatic portography or the venous phase of the arteriogram of the superior mesenteric artery demonstrated a localized saccular dilation of a peripheral branch of the portal vein are described. One patient subsequently died, and autopsy confirmed the diagnosis. A hypoechoic lesion continuous with a branch of the portal vein seems to be the characteristic sonographic picture. Radiologic evidence for portal vein aneurysm was obtained in only 2 of 300 patients with portal hypertension in whom percutaneous transhepatic portography was performed, and in 2 of 3000 patients who visited our unit and in whom ultrasonography for the liver was performed. Thus, aneurysm of the intrahepatic portal vein does occur, but very rarely.

Aneurysm↗
PubMed1984

Role of portal and splenic vein shunts and impaired hepatic extraction in the elevated serum bile acids in liver cirrhosis.

To study the mechanism for the elevation of serum bile acids in liver cirrhosis, bile acid concentrations were measured in the portal, superior mesenteric, and splenic veins, using percutaneous transhepatic catheterization, and compared with those of peripheral veins in 41 patients with mild to moderately advanced cirrhosis. The demonstrated gradient of bile acid concentration was superior mesenteric vein greater than portal vein greater than peripheral vein nearly equal to splenic vein, suggesting that the superior mesenteric vein is the main route of transport for the intestinally absorbed bile acids. Bile acid concentrations in peripheral vein were correlated with the measured portal and splenic vein shunt indexes. The ursodeoxycholic acid oral tolerance test carried out in 10 patients during portal vein catheterization demonstrated that hepatic extraction of this bile acid was correlated with indocyanine green clearance and that it was inversely correlated with portal vein shunt index. These findings are consistent with the view that distorted hepatic blood flow has a significant role in elevating serum bile acid, at least in patients with moderately advanced liver cirrhosis.

Adolescent↗
PubMed1984

Clinical study of eighty-six cases of idiopathic portal hypertension and comparison with cirrhosis with splenomegaly.

The clinical features of 86 cases of idiopathic portal hypertension, the equivalent of hepatoportal sclerosis in the United States and of noncirrhotic portal fibrosis in India, are presented. This disease is characterized by overt splenomegaly with pancytopenia, portal hypertension, and relatively mild abnormalities in liver function tests. Although differential diagnosis from liver cirrhosis is not always easy, liver histology, laparoscopy, portography, hepatic venography, and measurement of wedged hepatic vein pressure are useful in diagnosis. Prognosis is relatively benign if variceal bleeding is controlled or prevented, and the disease does not progress to cirrhosis. The etiology is still undetermined, but the liver pathology characterized by occlusive changes of the intrahepatic portal radicles, portal and periportal fibrosis, and irregularly distributed parenchymal atrophies suggests some sort of portal venopathy that causes decreased portal perfusion of peripheral liver parenchyma. These patients with idiopathic portal hypertension were compared with 63 cases of cirrhosis with splenomegaly and 80 cases of cirrhosis without splenomegaly. There was some similarity in hematologic findings between idiopathic portal hypertension and cirrhosis with splenomegaly, but the basic disease process seemed distinctly different. The cause of marked splenomegaly does not seem to be simply congestion, and remains an enigma.

Adolescent↗
PubMed1984

Renal tubular disturbances induced by tributyl-tin oxide in guinea pigs: a secondary Fanconi syndrome.

Painting of tributyl-tin oxide on the skin induced a secondary Fanconi syndrome in guinea pigs. In the urine of these animals, excretion of sodium, chloride, phosphate, glucose and many kinds of amino acids increased and reached a maximum between day 40 and 50. In sera, the concentrations of phosphate and certain amino acids were low due to excessive loss into urine. Histological examination of the kidney revealed damage to the tubular epithelium with no glomerular change. It was also found that cytochrome P-450 in the kidney and 1-25-dihydroxy vitamin D in serum were reduced in the tin-treated animals. It is most likely that tributyl-tin oxide caused a secondary Fanconi syndrome as defined by renal tubular disturbances represented by glucosuria, generalized amino aciduria, phosphaturia, and hypophosphatemia.

Administration, Topical↗
PubMed1983

[Production of antithyroid hormone antibodies. 2. Genetic control of the production of anti-human thyroglobulin and antithyroid hormone antibodies in mice immunized with human thyroglobulin].

Recently anti-thyroid hormone antibodies have been found in many cases of thyroidal and non-thyroidal disorders. However, the exact mechanism(s) of production of anti-thyroid hormone antibodies in these patients is so far obscure. Thyroxine (T4) and triiodothyronine (T3) are haptens and are not immunogenic in free form. In this respect, human thyroglobulin (HTg) has long been suggested as an antigen of the anti-thyroid hormone antibodies observed in them because it carries thyroid hormones on its surface. In our previous communication, we reported the production of anti-HTg antibodies and anti-thyroid hormone antibodies in two rabbits and various strains of mice immunized with HTg. In order to elucidate the gene(s) which controls the production of anti-HTg and anti-thyroid hormone antibodies, various strains of mice which have different H-2 and Igh allotypes were immunized with HTg. The titers of anti-HTg and anti-thyroid hormone antibodies were measured, and the locus (loci) which controls the immune response against them was determined. Our present investigation has revealed that the Ir-gene(s) which controls the production of anti-HTg and anti-T4 antibodies is located in the I-A subregion. Concerning the production of anti-T4 antibodies in mice, the presence of Ir-gene(s) outside of H-2 is also suggested. The significance of the genetic mechanisms controlling the immune response against thyroid hormones in various thyroidal disorders is discussed.

Animals↗
PubMed1983

Analysis of T cell hybridomas. IV. Characterization of inducible suppressor cell hybridomas.

The Ts3 subset of suppressor cells is generated after antigen priming, but, in order to express suppressor activity these cells require an additional activation step involving triggering with specific suppressor factors (TsF2). This report characterizes two cloned hybridoma cell lines (pTs3 hybridomas) that represent this stage of Ts3 cell differentiation. These hybridoma cells could be specifically activated with TsF2 to release another antigen-specific suppressor factor (TsF3) within 6 h. The inducible feature of these cells permitted analysis of the signals necessary for Ts3 activation. Antigen was not required for activation. Only TsF2 factors derived from antiidiotypic second-order suppressor cells could activate pTs3 hybridoma cells. There were stringent genetic restrictions on the ability of Ts2 to activate pTs3 cells. Triggering of pTs3 required corecognition of two determinants on the TsF2 molecular complex, i.e., the I-J and Igh-related idiotypic determinants. Thus, although pTs3 cells could absorb TsF2 from an I-J-mismatched source, these pTs3 were not activated by the allogeneic TsF2. For activation to occur, the H-2 (I-J) and Igh complexes of the TsF2 donor had to match those of the strain from which the pTs3 cells were derived. Mixing two distinct TsF2, one derived from an H-2-matched source and the other from an Igh-matched source, failed to activate pTs3 cells. Once activated, the pTs3 cells released a suppressive material that was indistinguishable from the TsF3 factors previously characterized in this system. Finally, the activation of the pTs3 cells apparently does not induce the de novo synthesis of TsF3 since the suppressive activity could be extracted from nonactivated pTs3 cells. Thus, the inducible pTs3 hybridomas represent a mature stage in the differentiation cycle of Ts3 cells and provide a means for studying the nature of the specific signals required for Ts3 activation.

Animals↗
PubMed1983

Physiological function and kinetic mechanism of human liver alcohol dehydrogenase as 5 beta-cholestane-3 alpha,7 alpha,12 alpha,26-tetrol dehydrogenase.

To test whether human liver alcohol dehydrogenase (alcohol:NAD+ oxidoreductase, EC 1.1.1.1) plays a role in the metabolism of cholesterol in man or not, a major isozyme of human liver alcohol dehydrogenase, beta 2 beta 2, was purified from homozygous atypical human livers, measuring both liver acetaldehyde reductase activity and that of 3 alpha,7 alpha,12 alpha-trihydroxy-5 beta-cholestan-26-al reductase (5 beta-cholestane-3 alpha,7 alpha,12 alpha,26-tetraol:NAD+ 26-oxidoreductase, EC 1.1.1.161) in the course of purification, and it was found that both enzyme activities were accompanied with each other at any step. Both enzyme activities of the highly purified isozyme, beta 2 beta 2, were inhibited by a chelating agent, 1,10-phenanthroline, for Zn which resides in the active site of the enzyme, the pKiapp value of which was 4.1 for both activities. They were also inhibited by a known competitive inhibitor, isobutyramide, in the same fashion and the Ki values calculated from both activities were the same (2.0 mM). From these results it was suggested that both enzyme activities are catalyzed by the same active site of the same enzyme protein. Kinetic studies of 5 beta-cholestane-3 alpha,7 alpha,12 alpha,26-tetrol dehydrogenase have shown that neither Theorell-Chance mechanism nor simple Ordered Bi Bi mechanism holds in the reaction; instead a mechanism which is asymmetric in both directions is operative.

Alcohol Dehydrogenase↗