[Rapid and non-irritable analysis of basal tear volumes by an electronic resistance measuring method].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to K Kono.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
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.
Explore the source record for details and available documents.
To study the effects of intra- and extrahepatic portal-systemic shunts on insulin degradation, 11 patients with liver cirrhosis and 7 noncirrhotic patients with liver disease were studied with percutaneous transhepatic catheterization. Insulin levels in portal and peripheral blood were measured simultaneously for 1-2 hr after intravenous administration of glucose. The degrees of intra- and extrahepatic portal-systemic shunting were measured with this technique using 131I-macroaggregated albumin and 99mTc-macroaggregated albumin. The amount of insulin secreted and insulin degraded were assessed from the areas under blood concentration curves for portal and peripheral blood. Insulin degradation was significantly reduced in cirrhotics compared to noncirrhotics with liver disease, although there was no difference in the amount of insulin secreted between these two groups. It was also correlated significantly with the degree of intrahepatic shunting but not with the degree of extrahepatic shunting. These results suggest that intrahepatic shunting plays an important role in the reduction of insulin degradation in cirrhosis.
This study reports the use of radiolabeled antibody to AFP and CEA for the detection and localization of AFP- or CEA-producing tumors. Thirty-one patients received 131I-labeled anti-AFP or anti-CEA antibodies. Photoscans were taken at 24 and 48 hours after injection of radioantibodies. In three of six patients with CEA-producing tumors, radioimmunodetection with anti-CEA antibody showed positive scans. In AFP-producing tumors, 7 of 15 patients had positive findings on immunoscintigraphy using polyclonal anti-AFP antibody, and two of nine patients had positive findings when monoclonal antibodies were used. Analysis of radioantibody in the blood after injection showed both complex and free antibody with immunoreactivity in the circulation, and smaller complexes were seen to form after administration of monoclonal antibodies.
Sera from patients with collagen diseases, chronic liver diseases and hepatocellular carcinoma were analysed for alphafetoprotein (AFP)-binding protein. The method used was a 125I-labeled AFP-binding assay with goat anti-human immunoglobulin G (IgG) as the precipitating antibody. AFP-binding IgG was found in the sera from one of 34 patients with systemic lupus erythematosus (SLE) and one of nine patients with hepatocellular carcinoma. This protein may interfere with the conventional radioimmunoassay of human AFP, and may be of interest because of its usefulness as a carrier of radioactivity or therapeutic agents to AFP-producing tumors.
Studies have been undertaken to clarify the localizing properties of radioactively labeled antibody to AFP using ascitic hepatoma cells which produce AFP. In the in vitro studies, radioantibodies to AFP were incorporated into the AFP-producing cells, even though excess antigen existed in the medium and the antibodies remained on the cell surface for a long time. In the in vivo studies, the radioantibodies to AFP bound to the AFP-producing cells, especially those producing high levels of AFP (AH66). Tumor localization by scintigraphy was clearer with the AH66 hepatoma than with the AH41C hepatoma, which produces less AFP. The presence of large amounts of AFP in the circulation did not prevent the tumor radioimmunodetection. It is suggested that radioantibodies to AFP bind to the AFP-producing cells despite the presence of large amounts of AFP in the circulation or in ascitic fluid.
14 patients with hepatocellular carcinoma and one with a hepatoblastoma were given AFP antibodies and changes in serum AFP levels and clinical courses were observed. Anti-human AFP horse IgG was purified by immunoadsorbent column chromatography. 1 mg of the purified antibody was able to bind 100-150 micrograms of AFP. 200-800 mg were given to each patient, according to their AFP levels. Also, conventional anti-cancer agents were administered consecutively. In all cases, the serum AFP levels measured by RIA decreased rapidly to undetectable levels within 24-48 h after the infusion. Then, in seven of 15 cases, the relatively low level was maintained for periods of 10-96 weeks. In the remaining eight cases, the serum AFP level increased again after 1-2 weeks and rose further with clinical deterioration. Since the antibody administered was undetectable in the serum within 2 weeks after its infusion, it is suggested that the AFP antibody had an inhibitory effect on the production or the release of AFP in some patients.
To determine the effect of hypothermic pulsatile and nonpulsatile cardiopulmonary bypass (CPB) with hemodilution on adrenocortical function we measured plasma levels of adrenocorticotropic hormone (ACTH), cortisol, aldosterone, and renin in two groups of patients. Group I, comprising 11 patients had routine CPB (nonpulsatile), and Group II, comprising 12 patients, had pulsatile flow during CPB (pulsatile). Both groups demonstrated comparable increases in cortisol, ACTH, and aldosterone with operation. Levels for all three hormones appeared to decline during CPB and then rose again in the post-CPB period. There were no significant differences between groups. Plasma renin activity gradually declined in a comparable manner in both groups. In the post-CPB period, renin activity was slightly higher in the nonpulsatile group (1.7 +/- 0.5 versus 0.8 +/- 0.2 ng/ml/hr, p less than 0.05). Correction for the effect of hemodilution demonstrated no decrease in cortisol and a slight increase in ACTH in both groups during CPB. Significant increases occurred in both groups during CPB in urinary Na+ excretion rate and urinary Na+/K+ ratio, more so for the nonpulsatile group. There was no correlation between urinary Na+/K+ ratios and either plasma cortisol or aldosterone levels. Thus routine CPB demonstrates no evidence of adrenocortical hypofunction and the addition of pulsatile flow produces little improvement.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
To study the effects of habitual alcohol intake on the latency period for the development of liver cirrhosis and hepatocellular carcinoma (HCC), 158 patients with cirrhosis and 79 with HCC were analyzed with respect to age at the time of diagnosis. They were classified into four groups based on hepatitis B surface antigen (HBsAg) in serum, and the history of intake of more than one small bottle of Japanese "sake" or an equivalent per day for more than 10 years. The average age of HBsAg positive male cirrhotics with a drinking habit (n = 10) was 38.8 years, 10.5 years younger than that of those without a drinking habit (n = 8) (P less than 0.05). The average age of HBsAg negative cirrhotics with a drinking habit (n = 97) was 47.9 years, eight years younger than that of those not drinking (n = 36) (P less than 0.001). There was no significant difference in the laboratory data between these groups. The average age of the HBsAg positive HCC patients with a drinking habit (n = 20) was 48.9 years, nine years younger than that of those without a drinking habit (n = 12) (P less than 0.05). The average age of HBsAg negative male HCC cases with habitual intake of more than 126 ml of ethanol per day was 51.0 years (n = 8), ten years younger than that of nondrinking male HCC cases (n = 11) (P less than 0.05). These data suggest that habitual alcohol intake may promote the development of liver cirrhosis and HCC, especially in HBsAg carriers.
Explore the source record for details and available documents.
Nonpulsatile cardiopulmonary bypass, in patients with coronary artery disease, produces a significant increase in thromboxane, a potent platelet aggregant and putative coronary vasoconstrictor. Pulsatile flow may decrease the incidence of perioperative infarction and the hormonal stress response to bypass. This study assessed the effect of pulsatile blood flow on plasma thromboxane and prostacyclin profiles during cardiopulmonary bypass by serial measurement of their stable metabolites, thromboxane B2 (TxB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha). Two groups of eight patients each were studied before, during, and after cardiopulmonary bypass. Eight patients had routine (nonpulsatile) bypass and eight had pulsatile flow. In the nonpulsatile group, the TxB2 concentration significantly increased during bypass (65 +/- 39 to 1,224 +/- 306 pg/ml, p less than 0.01) and rapidly returned to control. Prostacyclin also rose (53 +/- 20 to 613 +/- 132 pg/ml, p less than 0.01). In the pulsatile group, TxB2 rose during bypass (53 +/- 18 to 693 +/- 130 pg/ml, p less than 0.01), but peak concentration was significantly lower than in the nonpulsatile group (1,224 +/- 306 versus 693 +/- 130 pg/ml, p less than 0.05). Prostacyclin rose sharply during cardiopulmonary bypass in the pulsatile group (53 +/- 22 to 1,033 +/- 136 pg/ml, p less than 0.01) and was higher than in the nonpulsatile group (1,033 +/- 136 versus 325 +/- 33 pg/ml, p less than 0.01). There were no intragroup differences of plasma hemoglobin, hematocrit, or platelet count. These data demonstrate that pulsatile flow significantly alters prostacyclin and thromboxane profiles during cardiopulmonary bypass and favors production of the coronary vasodilator and platelet disaggregant prostacyclin. This may be an important factor in some of the clinical advantages previously reported with this modality.
Explore the source record for details and available documents.