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Biomedical subjects

A Takada

Publications and source records attributed to A Takada.

At least 325 records · Page 18Linked to original sources
PubMed1990

A diagnostic approach to different types of non-A non-B acute hepatitis through the evaluation of the lobular distribution of hepatocytic damage.

The activity in the serum of three hepatic mitochondrial enzymes, glutamate dehydrogenase (GDH), ornithine carbamyl transferase (OCT) and mitochondrial glutamic oxaloacetic transaminase (m-GOT), all of which show different lobular distribution in the liver, was investigated in order to clarify the usefulness of determinations of these enzymes for the diagnosis of different types of acute non-A non-B (NANB) hepatitis. In NANB hepatitis, there were two different histological types: portal and non-portal. In most portal cases, the GDH/OCT ratios were lower than 0.35, but the ratios were higher than 0.36 in all non-portal cases. The prognosis of the portal group and the short incubation group of NANB hepatitis was better than that of the non-portal and the long incubation group, respectively. The cases showing GDH/OCT ratios of less than 0.35 clearly displayed better prognoses than the cases showing high GDH/OCT ratios. These findings implied that the low GDH/OCT group may have been infected by particular viruses and that ratio determination is useful for the diagnosis of NANB hepatitis caused by different viruses.

Acute Disease↗
PubMed1990

Clinical significance of plasminogen activator inhibitor activity in patients with exercise-induced ischemia.

To assess the fibrinolytic system in patients with exercise-induced ischemia and its relation to ischemia and severity of coronary artery disease (CAD), 47 patients with CAD confirmed by results of coronary angiography underwent symptom-limited multistage exercise thallium-201 emission computed tomography. All patients with CAD had exercise-induced ischemia as assessed from thallium-201 images. Pre- and peak exercise blood samples from each patient and preexercise blood samples from control subjects were assayed for several fibrinolytic components and were also assayed for plasma adrenaline. The extent of ischemia was defined as delta visual uptake score (total visual uptake score in delayed images minus total visual uptake score in initial images) and the severity of CAD as the number of diseased vessels. In the basal condition, plasminogen activator inhibitor (PAI) activity was significantly higher in patients with exercise-induced ischemia as compared to control subjects (p less than 0.01), although there were no significant differences in other fibrinolytic variables between the two groups. Moreover, PAI activity in the basal condition displayed a significantly positive correlation with the extent of ischemia (r = 0.47, p less than 0.01). Patients with exercise-induced ischemia were divided into two groups (24 with single-vessel disease and 23 with multivessel disease). There were no significant differences in coronary risk factors, hemodynamics, or plasma adrenaline levels during exercise between single-vessel and multivessel disease except that delta visual uptake score was significantly higher in multivessel disease (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

A new method to measure brain serotonin synthesis in vivo. II. A practical autoradiographic method tested in normal and lithium-treated rats.

We describe here a practical autoradiographic method to estimate the rate of serotonin synthesis in brain. A two-time point method (60 and 150 min after injection of alpha-[14C]methyl-L-tryptophan) was first evaluated in 14 normal rats (7 at each time point). After this the method was tested in lithium-treated rats. In normal rats the rate of serotonin synthesis measured by the two-time point method generally correlated with known concentrations of tryptophan hydroxylase. The rate of synthesis in lithium-treated rats was compared with that in sham-treated rats (NaCl treatment). The results showed a significant increase in the synthesis rate in some cerebral structures. The greatest increases in the serotonin synthesis rate, attributable to the lithium treatment, were observed in the parietal cortex (52%) and caudate nucleus (47%). This is the first investigation to demonstrate, with autoradiographic resolution (approximately 100 microns), the differential changes in the rate of serotonin synthesis in the brain. Lithium had no significant effect on the rate of synthesis in the pineal gland.

Animals↗
PubMed1990

Changes in plasminogen activator inhibitor 1 and tissue-type plasminogen activator during exercise in patients with coronary artery disease.

As depressed fibrinolysis is implicated in the pathogenesis of coronary artery disease, we have studied the activation of fibrinolysis during maximal, symptom-limited exercise in a group of 68 men. After exercise they were divided, according to their coronary angiography and exercise 201Tl emission computed tomography results, into three groups. Group 1: persons with normal exercise 201Tl emission computed tomography results and no underlying diseases who served as controls; group 2: patients with coronary artery disease without exercise-induced myocardial ischemia, and group 3: patients with coronary artery disease with transient, exercise-induced myocardial ischemia. Before and at peak exercise we measured the plasminogen activator activity (PAA) in the euglobulin fraction of plasma by an amidolytic method and the concentrations of tissue plasminogen activator (t-PA), activator-inhibitor complex - plasminogen activator inhibitor 1 (PAI-1) complexed with t-PA - and total PAI-1 by enzyme immunoassay. The concentration of free PAI-1 in plasma was calculated by subtraction of the concentration of activator-inhibitor complex from that of total PAI-1. Under basal conditions, group 3 had significantly higher free and total PAI-1 levels than group 1. There were no statistically significant differences between the three groups in PAA, t-PA, and activator-inhibitor complex levels. At peak exercise, group 1 showed the highest release of t-PA accompanied with highest increases in PAA as well as in activator-inhibitor complex, the proportion of released t-PA antigen not bound to PAI-1 being highest in group 1. Free PAI-1 decreased significantly, but there were no differences between individual groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

[A case of icteric hepatoma with laryngeal metastasis and coexisting pancreatic cancer].

An autopsy case of a hepatocellular carcinoma with an omental mass, a laryngeal metastasis, and a coexisting pancreatic head carcinoma is reported and the diagnostic problems it presented is discussed. An obstructive jaundice was treated by transhepatic drainage, and was proved to be caused by the invasion into the bile duct of the hepatocellular carcinoma and not the pancreatic head tumor. An asymptomatic, papillomatous growth from the metastasis of the hepatocellular carcinoma was found in subglottic region, an extremely rare type of metastasis .

Adenocarcinoma↗
PubMed1989

Urinary UK, t-PA and urinary trypsin inhibitor in health and glomerular diseases.

The concentrations of two different plasminogen activators(PAs), urokinase (UK), tissue-type plasminogen activator (t-PA) and urinary trypsin inhibitor (UTI) were determined in the urine and blood from 48 normal subjects and 92 patients with glomerulonephritis using highly sensitive enzyme immunoassay (EIA). The values of UK clearance were approximately 1.5-fold larger than those of creatinine clearance and at least 60.8% of UK was reabsorbed in the renal tubules, which suggest that one of major secretion site of UK is located in the outer region of the glomerular basement membrane (GBM), that is glomerular epithelium. Decreased urinary excretion of UK was observed in the glomerular disease depending on their severity and correlated with the increasing degree of FDP D-dimer excretion. On the other hand, the values of t-PA clearance were quite smaller than those of creatinine clearance, which suggest that urinary t-PA originated from the blood circulation or the inner side of the GBM (possibly glomerular endothelium) and filtrated from the GBM. Like UK, urinary t-PA also decreased in glomerular diseases. UTI which is highly anionic and has a comparable size with albumin was excreted increasingly in glomerulo-nephritis due to loss of the anionic charge barrier of the GBM. No significant correlations were noted between UTI excretion and UK or t-PA excretion.

Adolescent↗
PubMed1989

Stimulation of plasmin catalyzed conversion of single-chain to two-chain urokinase-type plasminogen activator by sulfated polysaccharides.

Influence of heparin, chondroitin sulfate C and dextran sulfate (MW 3,500 and 7,000) on plasmin catalyzed conversion of single-chain (scu-PA) to two-chain (u-PA) urokinase-type plasminogen activator and generation of plasmin in mixtures of scu-PA and Glu-plasminogen (Glu-plg) was investigated. Conversion of scu-PA to u-PA catalyzed by plasmin was enhanced by chondroitin sulfate C and heparin, maximally by 10-fold and 3-fold, respectively. Sulfated polysaccharides potentiated generation of plasmin in mixtures of Glu-plg and scu-PA, as well as enhanced plasminogenolytic activity of u-PA. The possible role of these interactions is discussed.

Catalysis↗
PubMed1989

Inhibition by tranexamic acid of the conversion of single-chain tissue plasminogen activator to its two chain form by plasmin: the presence on tissue plasminogen activator of a site to bind with lysine binding sites of plasmin.

The addition of tranexamic acid inhibited the conversion of single chain tissue plasminogen activator (sct-PA) to its two chain form (tct-PA) by plasmin. Increase in the concentrations of tranexamic acid resulted in more inhibition of the conversion, with 50% inhibition being obtained at 0.251 mM of the concentration of tranexamic acid. The addition of the fragments of plasminogen such as kringle 1 to 3 (K1-3), and K4 resulted in the facilitation of the conversion of sct-PA to tct-PA by plasmin. The addition of tranexamic acid to the mixture of sct-PA and K4 inhibited the rate of the conversion of sct-PA by plasmin. These results suggest that binding of lysine binding sites of plasmin or plasminogen with sct-PA enhanced its conversion to tct-PA by plasmin, and that there is a site on a t-PA molecule to bind to plasminogen or plasmin.

Animals↗
PubMed1989

Plasma levels of t-PA free PAI-1 and a complex of t-PA with PAI-1 in human males and females at various ages.

The concentration of tissue plasminogen activator (t-PA), plasminogen activator inhibitor 1 (PAI-1) and the complex of t-PA and PAI-1 (t-PA-PAI-1 complex) were measured using an enzyme immunoassay, where the first antibody was monoclonal antibody against PAI-1 and the second one was polyclonal anti-t-PA Fab' antibody. Plasma levels of t-PA and t-PA-PAI-1 complex increased with increase in age in the total population of males and females, but there was no age related change in free and total PAI-1. Plasma levels of t-PA antigen were higher in males than in females, and those in females gradually increased with increase in age, reaching the same levels as those of males at their 60s. Plasma levels of t-PA-PAI-1 complex were also higher in males than in females, but the difference was low at their 50s and no difference was observed at their 60s. Plasma levels of free PAI-1 were higher in males than in females, but those of males declined at age group higher than their 50s. At their 60s plasma levels of free PAI-1 were higher in females than in males. These results indicate that fibrinolytic parameters such as t-PA and PAI-1 were balanced at higher levels in plasma in males than in females.

Adult↗
PubMed1989

Source of increased plasminogen activators during pregnancy and puerperium.

We investigated the increase of plasminogen activators (tPA and uPA) in the plasma during pregnancy. Both tPA and uPA antigens were found to increase after the third trimester of pregnancy and high levels of PAs persisted through the first stage of labor. The tPA antigen levels rose further for the first few hours post-partum, while the level of uPA antigen returned to normal immediately following childbirth. To clarify whether the uterus and/or placenta are involved in the increased levels of plasma PAs, the levels were measured in uterine venous blood in cases of caesarean sections. During the ante-partum period, the level of uPA antigen in the uterine venous blood was higher than that in the peripheral venous blood, while there was no significant difference between the levels of tPA antigen in peripheral blood and uterine venous blood. The level of tPA antigen in the uterine venous blood rose after delivery. In contrast, the level of uPA antigen declined immediately after delivery. These results suggest that (1) the placenta is the major source of the increased uPA antigen during pregnancy, (2) entire vascular system is involved in the increased tPA antigen during pregnancy, (3) a further increase in tPA after delivery is due to the release of this enzyme from the involuting uterus.

Antigens↗
PubMed1989

The conversion of streptokinase-plasminogen complex to SK-plasmin complex in the presence of fibrin or fibrinogen.

When equimolar amounts of Glu-plasminogen (Glu-plg) and streptokinase (SK) were mixed in the presence of S-2251, SK-plg complex was formed and only gradually converted to SK-plasmin complex. When equimolar amounts of Glu-plg and SK were mixed with fibrinogen or fibrin, Glu-plg was converted faster to plasmin suggesting that Glu-plg molecule in the complex was converted to plasmin. It is thus concluded that SK-plg complex is converted to SK-plasmin complex slowly in the absence of fibrin or fibrinogen. When SK-plg-fibrin(ogen) complex was formed, plasminogen moiety was converted to plasmin faster inside a trimolecular complex of SK, plasminogen and fibrin(ogen).

Autoradiography↗
PubMed1989

Absence of synergism between tissue-type plasminogen activator and urokinase on plasminogen activation rate in plasma.

Effects of tissue-type plasminogen activator (t-PA), urokinase (u-PA) and their combinations on plasminogen activation rate (PAR) in plasma, in vitro were investigated. T-PA and u-PA over concentrations range of 10 U/ml to 50 U/ml induced a linear, concentration dependent increase in PAR. Combinations of t-PA and u-PA in ratios of 3/1, 1/1 and 1/3 induced additive but not synergistic effect in the activation of plasminogen. We conclude, therefore, that t-PA and u-PA do not act synergistically in the activation of plasminogen in plasma in vitro.

Chromogenic Compounds↗