Search PubMed⌕ Search

Biomedical subjects

Y Shibayama

Publications and source records attributed to Y Shibayama.

103 records · Page 6Linked to original sources
PubMed1982

Creutzfeldt-Jakob disease with demonstration of virus-like particles.

Two kinds of virus-like particles, doughnut-shaped particles and particles with dense core, were discovered in a brain tissue from a patient with Creutzfeldt-Jakob disease. The two types of virus-like particles are similar to immature type C and type C particles. although no direct relationship between Creutzfeldt-Jakob disease and these virus-like particles can be established, these facts may suggest that viruses play some role in the pathogenesis of Creutzfeldt-Jakob disease.

Aged↗
PubMed1978

Electroncytochemical and biochemical demonstration of guanylate cyclase activity in the pancreatic islet.

With a cytochemical method using guanylyl imidodiphosphate as a substrate, the guanylate cyclase activity was localized on the plasma membrane of A, B and D cells of islets of Langerhans isolated from the rat. Adequate control experiments were performed by a double-blind method. Parallel biochemical assay showed that guanylate cyclase activity was not completely lost after fixation with 1% glutaraldehyde and incubation with 4 mM lead nitrate. Furthermore, the depressed activity was still stimulatable with acetylcholine.

Acetylcholine↗
PubMed1977

Sipple's syndrome with peculiar changes in pancreatic islets--an autopsy case.

A diagnosis of the heritable disorder Sipple's syndrome was made in a Japanese male aged 28 years. The coexistence of bilateral phenochromocytomas, bilateral medullary thyroid carcinomas and secondary hyperplasia of parathyroid was confirmed at the time of autopsy. Pancreatic islets were hyperplastic with marked proliferation of A and D cells. Transition of the ductal cell to the islet, i.e. "nesidioblatosis" was observed. There was no proliferation of B cells, but a retention of B cell granules, a manifestation of suppressed secretion of insulin attributed to the overproduction of catecholamines was evident. In the stomach, numerous petechial hemorrhages and proliferation of gastrin cells were found. The pathogenesis of changes in the pancreatic islets and stomach is discussed from the viewpoint of hormonal disorders induced by pheochromocytoma and medullary thyroid carcinoma such as are found in Sipple's syndrome.

Adult↗
PubMed1972

[Amnioscopy].

Explore the source record for details and available documents.

Amnion↗
PubMedDate not supplied

Localization of increased hepatic vascular resistance in liver cirrhosis.

To determine the localization of increased vascular resistance in cirrhotic liver, blood pressures were measured by a direct cannulation method at several key points in the hepatic vascular pathway in normal and cirrhotic rats. Cirrhosis was produced by feeding a choline-deficient diet. Blood pressures in normal rats were 110 mm H2O in the portal vein, 68 mm H2O in the terminal portal venule, 28 mm H2O in the terminal hepatic venule and 20 mm H2O in the inferior vena cava. In cirrhotic rats, blood pressures in the portal vein and the terminal portal venule were 173 and 100 mm H2O, respectively, while those in the terminal hepatic venule and the inferior vena cava were elevated only slightly above normal. These hemodynamic data suggest that an increase in vascular resistance in cirrhotic liver is present in the intrahepatic portal vein and sinusoids, but not in intrahepatic hepatic vein. In cirrhotic liver, stenosis and distortion were found in peripheral branches of the portal vein, and sinusoidal stenoses and a decrease in sinusoidal space were recognized. Accordingly, it is suggested that the increase in vascular resistance in the intrahepatic portal vein and sinusoids correlate with these structural changes. Although severe stenoses and distortion were found in hepatic vein branches, it was thought that they do not contribute to portal hypertension because of lack of increase in vascular resistance in the intrahepatic hepatic vein.

Animals↗
PubMedDate not supplied

Role of hepatic artery in haemodynamics in normal and cirrhotic livers in rats.

To examine the degree of influence of the hepatic artery on microcirculation in the liver, microscopic observation of blood flow in the hepatic minute blood vessels and the sinusoids and pressure measurements at key points in hepatic vascular pathways in vivo were performed before and after hepatic artery ligation in normal and cirrhotic rats. In normal rats, portal vein pressure (109 mmH2O) fell 10 mmH2O after hepatic artery ligation, but the pressures of the terminal portal venule, the terminal hepatic venule and the inferior vena cava did not change. In cirrhotic rats, portal vein pressure (206 mmH2O) and terminal portal venule pressure (106 mmH2O) fell 23 and 10 mmH2O after hepatic artery ligation respectively: the pressures in the terminal hepatic venule and the inferior vena cava did not change. These results suggests that the pressure transmitted from the hepatic artery was mostly supplied to the intrahepatic portal vein in normal rats and both to the intrahepatic portal vein and to the sinusoids in cirrhotic rats. In both normal and cirrhotic rats, however, the pressure transmitted from the hepatic artery was about 10 per cent of the initial portal vein pressure, and the blood flow in minute vessels and sinusoids did not change after hepatic artery ligation. Accordingly, it is believed that the hepatic artery plays only a small role in the haemodynamics of the liver in both normal and cirrhotic rats, irrespective of the distribution and manner of the hepatic arterial termination.

Animals↗
PubMedDate not supplied

Pathogenesis of centrilobular necrosis following congestion of the liver.

The exact pathogenesis of centrilobular necrosis following congestion of the liver is still unknown. We reviewed the clinical data related to systemic circulatory disturbance and histopathology of the liver and the gut in 320 autopsy subjects. Congestion of the liver alone was associated only with atrophy and loss of hepatocytes in centrilobular areas, but not with hepatocellular coagulative necrosis. In many patients with coagulative necrosis of centrilobular hepatocytes and congestion of the liver, fibrin thrombi and neutrophil infiltration in the sinusoids, which are the characteristic histopathological features of the liver in endotoxaemia, were found in and around the necrotic area. Congestion, erosion or haemorrhage of the intestinal mucosa, which may allow entrance of endotoxin into the liver through the portal vein, was seen in such patients. Prolonged hypotension or shock, which may lead to portal endotoxaemia, was present in half the patients with centrilobular necrosis and congestion of the liver. These results suggest that not only congestion of the liver but also portal endotoxaemia may be involved in the pathogenesis of centrilobular necrosis in patients with congestion of the liver.

Adult↗
PubMedDate not supplied

Activation of the plasma kinin forming cascade along cell surfaces.

Proteins of the plasma kinin-forming cascade bind to endothelial cells and activation of the cascade can be initiated along the surface. The light chain of high molecular weight kininogen (HK) (domain 5) and factor XII bind to gC1qR, the heavy chain of HK (domain 3) binds to cytokeratin 1 and the interactions are zinc dependent. Prekallikrein binds to domain 6 of HK. Antisera to gC1qR and cytokeratin 1 inhibit binding and activation. Incubation of normal plasma with endothelial cells leads to gradual conversion of prekallikrein to kallikrein, while plasma deficient in factor XII or HK are inactive within a 2-hour time frame. Thus factor XII is critical for activation to proceed. Augmentation of these reactions may occur when C1 inhibitor is functionally deficient or with ACE inhibitors which also inhibit kininases.

Carrier Proteins↗