Biomedical subjects
Publications and source records attributed to T Urano.
Pseudomonas aeruginosa infection in laboratory mice was successfully eradicated by oral treatment of gentamicin, 1.0 g per liter of drinking water for 3 days.
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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.
The aim of this study was to investigate the relationship of Interleukin-8 (IL-8) with vascular endothelial growth factor (VEGF) and plasminogen activator system (PA system) in the progression of colorectal cancer (CRC). In eighty-seven patients with CRC, the levels of IL-8, and VEGF as representative angiogenic factors and urokinase-type plasminogen activator (uPA), uPA receptor (uPAR), plasminogen activator inhibitor-1 (PAI-1), and PAI-2 as representative invasive factors were quantitatively assayed in tumor and adjacent normal tissues. The levels of IL-8, VEGF, and PA system factors in tumor tissues were all significantly higher than those in normal tissues. The IL-8 level was significantly associated with tumor size, depth of infiltration, Dukes stage, and liver metastasis, and also significantly correlated with the levels of VEGF, uPAR, uPA, and PAI-1. The VEGF level was significantly associated with tumor size, vascular involvement. The levels of uPAR and PAI-1 were significantly associated with tumor size and depth of infiltration, and the uPAR level was associated with liver metastasis. The VEGF level was significantly correlated with the levels of uPAR and PAI-1. These results reveal that IL-8, VEGF, and PA system factors are contributed to tumor growth, invasion, and metastasis in CRC. Univariate analysis revealed that high levels of IL-8, VEGF, and uPAR were significantly associated with a shorter overall survival time; however, multivariate analysis identified only liver metastasis as an independent prognostic factor. In conclusion, IL-8 is responsible to tumor progression and liver metastasis of CRC, and the activation of PAS induced by IL-8 as well as VEGF may play an important role in the progression of CRC.
The effects of water immersion restraint stress on collagen-induced platelet aggregation in whole blood, and on the fibrinolytic and serotonergic systems in rats have been studied. One hour long stress caused a release of tissue plasminogen activator (tPA) into the blood and a shortening of euglobulin clot lysis time (ECLT), whereas restraint of longer duration was responsible for a reduction in platelet aggregation, an elevation in the activity of plasminogen activator inhibitor with a concomitant fall in tPA and a prolongation of ECLT relative to controls. Whole-blood and plasma serotonin and its metabolite 5-hydroxyindoleacetic acid were also higher in the stressed rats and whole-blood serotonin level showed a negative correlation with tPA in the stressed rats. Either stress and/or its duration are responsible for changes in both fibrinolytic and serotonergic systems.
In order to investigate a possible relationship between serotonergic and fibrinolytic systems, serotonin (5-hydroxytryptamine, 5-HT) metabolism was modified by the use of a monoamine oxidase inhibitor (tranylcypromine: 10 mg/kg body weight) and its effect on the fibrinolytic system was analyzed. Tranylcypromine caused a rise in whole blood 5-HT with a simultaneous fall in 5-hydroxyindoleacetic acid. Euglobulin clot lysis time was significantly prolonged 1 and 4 h after injection and tissue plasminogen activator (tPA) activity declined 4 h following administration with a simultaneous increase in its inhibitor (PAI) activity. Blood 5-HT was negatively related to tPA (r = -0.48; p < 0.05) and positively to PAI activities (r = 0.43; p < 0.05) in tranylcypromino-treated rats, whereas there were no such correlations in solvent-treated rats.
The rate of the conversion of Lys78 plasminogen (Lys78-plg) to Lys78 plasmin by tissue plasminogen activator (tPA) was directly quantitated by SDS-PAGE. The apparent second-order rate constant (Kapp) was (0.27 +/- 0.07) x 10(3)/M/s for single-chain tPA and Lys78-plg, and was enhanced approximately 5-fold by fibrinogen and 17-fold by polymerized fibrin. Kapp was (1.57 +/- 0.46) x 10(3)/M/s for two-chain tPA and Lys78-plg, and was enhanced approximately 2.6-fold by fibrinogen and 3.6-fold by fibrin. The factor of the enhancement by polymerized fibrin was far less than in previous reports in which chromogenic substrate was commonly employed.
Postprandial triglyceridemia and 'remnantemia' may better reflect the atherosclerotic risk than triglyceride (TG) levels in the fasting state. Recently, a new method was developed based on a monoclonal antibody recognizing an epitope distal to the carboxyl end of apo B48 which allows easy measurement of remnant-like lipoproteins (RLP). This study was performed in order to investigate RLP response to a standardized fat meal and establish a normal diurnal pattern of RLP in blood and compare it to platelet aggregation and fibrinolysis in healthy young men. We investigated 7 male volunteers (age range 18-23 years) who received a standardized fat meal (Othsuka Pharmaceutical Company, Japan) containing 32.9% lipids, 2.5% protein, 2.5% carbohydrate, 0.3% calcium and 0.1% phospholipids, and 74 mg/100 g cholesterol (C) at 7:30. The energetic value of this cocktail was 341 kcal/100 g. Area under curve (AUC) responses in TG, RLP-TG and RLP-C after the meal were as follows: for TG 28.66 +/- 8.94; for RLP-TG 17.54 +/- 5.55; for RLP-C 1.27 +/- 0.42 mg x dl-1 x h-1. These responses were correlated to each other. Surprisingly, collagen-induced platelet aggregation in whole blood was negatively related to RLP-C AUC. Fluctuation patterns of TG, RLP-TG and RLP-C concentrations during the day were remarkably similar, peaking in this particular group of subjects at 10:00-12:00 and at about 23:00, whereas cholesterol was decreasing late in the night and very early in the morning. This pattern was different from those of platelet aggregation and fibrinolysis parameters.