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Biomedical subjects

K Okuda

Publications and source records attributed to K Okuda.

At least 883 records · Page 49Linked to original sources
PubMed1985

Study of cellular immunity in experimental autoimmune hepatitis in mice: transfer of spleen cells sensitized with liver proteins.

This study was based on our model of experimental autoimmune hepatitis produced by immunizing C57BL/6 (B6) mice with syngeneic liver proteins and Freund's complete adjuvant. Spleen cells obtained from these hepatitis mice were transferred to syngeneic normal recipient mice, and histological changes occurring in the liver and the role of cellular immunity in producing liver damages in recipient mice were investigated. Sensitized spleen cells from these immunized (donor) mice were fractionated by a nylon wool column and injected intravenously into normal B6 mice. Histology of the liver of the recipient mice showed mild infiltration of mononuclear cells around the periportal area 7 days after the transfer of sensitized spleen cells, and changes were most prominent in the mice injected with the fraction of nylon wool column adherent spleen cells. Induction of these liver lesions in the recipient mice was blocked by treatment of sensitized donor spleen cells with anti-Thy 1,2 monoclonal antibody and guinea pig complement before injection. Lymphocyte reactivity to liver-specific lipoprotein (LSP) in recipient mice was studied by a lymphocyte transformation system, and a high immune response was demonstrated with the fraction of nylon wool column non-adherent (T-enriched) spleen cells. These data seem to indicate T-cell interactions between donor and recipient mice in the transfer study using our experimental autoimmune hepatitis model.

Animals↗
PubMed1985

[Episode secretion of LH releasing hormone and LH in peripheral plasma of women with and without ovulatory disturbances].

We studied the secretory dynamics of plasma luteinizing hormone releasing hormone (LHRH) and luteinizing hormone (LH) in 5 normal ovulatory women during the early follicular phase, and 29 cases of ovuluatory disturbances using radioimmunoassay methods. All of the normal ovulatory women demonstrated one or two pulsatile LHRH releases in 3 or 4 hours. The height of LHRH secretory spikes was observed to be between 1.4 and 9.2 pg/ml. Plasma LH episodic secretion was related to LHRH episodic secretion. In 15 out of 27 cases of of ovulatory disturbances except cases with primary ovarian dysfunction, the LH episodic secretion revealed a significant decrease in pulse frequency. In 13 out of 16 cases of ovulatory disturbances, the height of LHRH secretory spikes was not greater than 1.3 pg/ml. This study indicates that the main causes of ovulatory disturbances are decrease in LHRH and LH episodic secretion. In all cases treated with clomphene, the plasma LHRH pulse increased after treatment. But in the cases where ovulation was not induced by clomiphene citrate, the plasma LH pulse did not increase as the LHRH pulse increased.

Anovulation↗
PubMed1985

Effects of cimetidine and ranitidine on splanchnic hemodynamics in patients with chronic liver disease.

Effects of two histamine H2 receptor antagonists, cimetidine and ranitidine, on systemic and splanchnic hemodynamics were studied in patients with chronic liver disease by simultaneous catheterization of the portal vein and the right hepatic vein and measurement of portal venous flow using the ultrasound doppler system or cineangiography. Neither infusion of 200 mg of cimetidine nor 50 mg of ranitidine reduced cardiac output, portal venous pressure, the gradient between wedged hepatic venous pressure and free hepatic venous pressure, hepatic blood flow, and portal venous flow. It is unlikely that histamine is an important modulator of flow via the H2 receptor.

Chronic Disease↗
PubMed1985

Interrelationship between type of spontaneous portal systemic shunt and portal vein pressure in patients with liver disease.

The interrelationship between the type and degree of spontaneous portal systemic shunting, and portal vein pressure was studied in 155 patients with liver disease by catheterizing the portal vein. The degree of portal vein shunting was measured in 100 patients and that of splenic vein shunting in 50 and that of total portal systemic shunting in 52, using macroaggregated radioalbumin. Increasing portal vein pressures were associated with progressively higher indices of portal vein shunt, splenic vein shunt, and total portal systemic shunt up to a certain level. Beyond this level, portal vein pressure did not increase further, and rather it decreased with further increasing degrees of splenic vein shunt and total portal systemic shunt. These results indicate that spontaneous portal systemic shunt keeps the portal vein pressure within certain limits or decreases it.

Catheterization↗
PubMed1985

Hepatic encephalopathy associated with extensive portal-hepatic venous shunts: a case report.

Extensive intrahepatic portal-hepatic venous anastomosis is very rare. This report describes a 47-year-old man with cirrhosis who presented with mental confusion and flapping tremor, and in whom percutaneous transhepatic portography and superior mesenteric angiography demonstrated shunting between the portal vein branches and the right hepatic vein. Measurements of pressure, ammonia, and immunoreactive insulin in blood of the portal and right hepatic veins clearly indicated that a large amount of portal vein blood was being shunted into the right hepatic vein. These findings suggest that hepatic encephalopathy in this patient is accounted for at least in part by an intrahepatic portal-hepatic venous shunting.

Angiography↗
PubMed1985

Early events in duck hepatitis B virus infection. Sequential appearance of viral deoxyribonucleic acid in the liver, pancreas, kidney, and spleen.

Early events in duck hepatitis B virus infection were studied in 1-day-old ducklings following inoculation. Group A ducklings (n = 26) were inoculated intraperitoneally with 10 microliter of infective serum, and group B ducklings (n = 29) were inoculated with 50 microliter. Samples of the serum, liver, pancreas, kidney, and spleen were taken, starting 3 h after inoculation and continuing through the 14th day. In group A, relaxed circular double-stranded deoxyribonucleic acid (DNA) did not appear in serum until day 10, whereas single-stranded DNA, indicative of active replication of the virus, was already demonstrable in the liver on day 6. In group B, single-stranded DNA was first detected in the liver on day 3, and relaxed circular double-stranded DNA became detectable in the liver and serum on day 6. The pancreas started to have single-stranded DNA on day 10 in group A and on day 6 in group B, suggesting active viral replication in this organ soon after it occurred in the liver. In the spleen, relaxed circular double-stranded DNA was detectable when serum became positive for viral DNA, probably due to contamination by serum DNA. However, single-stranded DNA became detectable on day 14 in group A and on day 6 in group B, suggesting a delayed but active viral replication in the constituent tissues of the spleen. These results have demonstrated that active replication of duck hepatitis B virus starts in the liver after infection, and is followed by the pancreas, the kidney, and the spleen. The incubation period is shortened when larger amounts of virus are inoculated, but the sequential occurrence of viral replication in these organs remains the same.

Animals↗