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Biomedical subjects

A Takada

Publications and source records attributed to A Takada.

At least 433 records · Page 24Linked to original sources
PubMed1984

N-Acetyl-L-tyrosine ethyl ester (ATEe) hydrolytic activities of diseased human palatine tonsils. Possible pathogenesis of recurrent acute tonsillitis.

The N-acetyl-L-tyrosine ethyl ester (ATEe)-hydrolysing activities of tonsillar extracts in cases of recurrent acute tonsillitis decreased more than those in less severe cases of chronic tonsillitis and in cases of obstructive enlargement of the palatine tonsil. Since ATEe is hydrolysed by C1-esterase, the ATEe hydrolytic activity of the tonsil might be related to the C1-activating system of the tonsil. This indicates that tonsils in which ATEe hydrolytic activities are low, repeatedly and severely, become infected, possibly due to easy invasion of micro-organisms.

Acute Disease↗
PubMed1983

The activation of two isozymes of glu-plasminogen (I and II) by urokinase and streptokinase.

Glu-plasminogen (Glu-plg) was eluted through lysine-Sepharose by using a gradient of 6 aminohexanoic acid, and two peaks corresponding to Glu-plg I and II were obtained. Glu-plg I has a molecular weight of 93,000 and Glu-plg II has a molecular weight of 89,000. When these plgs were activated by urokinase (UK) or streptokinase (SK) in the presence of S-2251 (H-D-Val-Leu-Lys-pNA0, the hydrolysis of S-2251 by Glu-plg I activated by UK or SK was larger than that by Glu-plg II activated by UK or SK. The results of SDS-PAGE indicate that the conversion of Glu-plg I to plasmin by UK was faster than that of Glu-plg II. It may be concluded that Glu-plg I is activated better to plasmin by activators than Glu-plg II.

Electrophoresis, Polyacrylamide Gel↗
PubMed1983

Chronic hepatitis induced by alcohol.

Fifteen heavy drinkers with the histological features of chronic hepatitis were studied. Chronic hepatitis observed in heavy drinkers can be divided into two categories. One is caused by alcohol, and the other is not etiologically related to alcohol. Chronic hepatitis caused by alcohol showed a definite improvement of clinical features following abstinence, as well as significantly high serum GOT/GPT ratios and high glutamate dehydrogenase activities on admission. These clinical features are distinctly different from chronic hepatitis without etiological relation to alcohol and resemble the other types of alcoholic liver injury. The leukocyte migration inhibition test by ethanol was more frequently positive in chronic hepatitis induced by alcohol than in the other types of alcoholic liver injury except for alcoholic hepatitis. Histological characteristics of the liver in chronic hepatitis induced by alcohol included the coexistence of features of both chronic hepatitis and alcoholic fibrosis. Three of four cases of chronic hepatitis induced by alcohol developed cirrhosis during the follow-up period. These results suggest that chronic hepatitis induced by alcohol is a type of alcoholic liver disease with an immunopathological etiology. It is a step toward the development of liver cirrhosis.

Adult↗
PubMed1983

Changes of hepatic microtubules and secretory proteins in human alcoholic liver disease.

It has been shown that alcohol consumption disrupts liver microtubules, impairs protein secretion and leads to ballooning of the hepatocytes in rats. Ethanol-induced hepatomegaly was accounted for by an increase of the hepatocytes volume. To study whether these changes occur in human alcoholic liver disease, hepatic tubular protein and export protein content were measured in 29 cases of alcoholic liver disease and were compared with those of 37 cases of non-alcoholic liver disease and 5 cases of non-hepatobiliary disease. Hepatic polymerized tubulin was significantly decreased in alcoholic liver disease compared to non-alcoholic liver disease (p less than 0.01), while free tubulin was increased in alcoholic liver disease. Hepatic transferrin (one of the export proteins) content was significantly higher (p less than 0.01) and serum transferrin level was significantly lower (p less than 0.05) in alcoholic liver disease than in non-alcoholic liver disease. These findings indicated that even in humans, chronic alcohol consumption decreased hepatic microtubules by impairing polymerization of tubular protein and increased hepatic export protein content. This decrease in hepatic microtubules by chronic alcohol consumption may play an important role in the development of human alcoholic liver disease.

Albumins↗
PubMed1983

Plasminogen activator in rat ovary during the ovulatory process: independence of prostaglandin mediation.

To elucidate the possible roles of increased plasminogen activator (PA) in follicular rupture and to investigate whether prostaglandins participate in ovarian PA synthesis in vivo, enzyme activities were sequentially measured by a method using the chromogenic substrate S-2251 in immature rat ovaries primed with pregnant mare serum gonadotrophin (PMSG) followed by human chorionic gonadotrophin (hCG) either alone or with a concurrent injection of indomethacin. Before hCG injection PA activity was 0.006 +/- 0.006 (S.D.) mumol/1.6 mg ovarian tissue (wet wt) per 30 min: PA activity of a saline-treated group remained at low levels (less than 0.018 +/- 0.003 mumol/l X 6 mg tissue per 30 min). In contrast, PA activity of animals given hCG alone increased after the treatment, reaching a peak value of 0.112 +/- 0.071 mumol/l X 6 mg tissue per 30 min 12h later, before decreasing to 0.023 +/- 0.014 mumol/l X 6 mg tissue per 30 min at 32 h. Contrary to expectations, a dose of indomethacin which completely blocked ovulation had no effect on either the magnitude or the time-course of PA synthesis after hCG administration (P greater than 0.05). These results indicate that prostaglandins are not involved in the preovulatory synthesis of PA induced by hCG in rat ovaries and that PA is not a primary proteolytic enzyme for follicular rupture. It is suggested that PA has possible roles in cumulus detachment and/or proliferation of granulosa cells during the ovulatory process.

Animals↗
PubMed1983

Gentamicin ototoxicity dissociated from glucose uptake and utilization.

The hypothesis was tested that gentamicin causes loss of cochlear microphonic potentials by interfering with glucose transport or metabolism in cochlear structures. Gentamicin (3 or 10 mM), applied by perilymphatic perfusion in the guinea pig, reduced cochlear microphonics in a dose-dependent manner. The presence of 5 mM glucose lowered the initial rate but not the final (60 min) loss of cochlear microphonics. Glucosamine (2-deoxy-2-aminoglucose), a reported inhibitor of glucose transport, had no effect at concentrations as high as 20 mM. Glucose utilization was measured by introducing radiolabeled deoxyglucose into the perfusate and determining its uptake into inner ear tissues. Concentrations of deoxyglucose-6-phosphate in organ of Corti and in stria vascularis increased linearly with time and remained unaffected by the presence of 3 mM gentamicin. Ten mM gentamicin reduced deoxyglucose uptake by 30% in the lateral wall tissues but not in the organ of Corti preparation. The lack of correlation between loss of microphonics and glucose utilization does not support interference with glucose metabolism as a primary mechanism of aminoglycoside ototoxicity.

Animals↗
PubMed1982

Activation pathway of glu-plasminogen to Lys-plasmin by urokinase.

When Glu-plasminogen (Glu-plg) was incubated with plasmin for various time intervals, and the mixture was activated by urokinase (UK), the activation rate increased gradually as incubation time increased. The presence of fibrin not only enhanced the activation rate of Glu-plg but also that of proteolytically modified form to some extent. The results of SDS-PAGE indicated that the release of N-terminal peptides from Glu-plg or Glu-plasmin takes place gradually when the concentration of plg was about 1 microM, and that Glu-plasmin I of larger molecular weight is more slowly converted to Lys-plasmin than Glu-plasmin II of smaller molecular weight. The amounts of carbohydrate moieties on the heavy chain of plasmin may influence the release of N-terminal peptide from Glu-plasmin. Kinetic studies indicate that Lys-plasmin has smaller km than Glu-plasmin, thus the former being better enzymatically than the latter.

Electrophoresis, Polyacrylamide Gel↗
PubMed1982

Potentiation of the activation of Glu-plasminogen by streptokinase and urokinase in the presence of fibrinogen degradation products.

When Glu-plasminogen was activated by streptokinase (SK), the presence of early degradation products of fibrinogen (FgDP) enhanced the rate of activation. When various fragments of FgDP were fractionated, FgDP-Y and E fragments had a potentiating activity while D fragment did not. When Glu-plasminogen was activated by urokinase (UK), the activation rate was enhanced by every fragment of FgDPs, i.e. X, Y, D and E. Although both D and E fragments seem to be able to bind with lysine binding sites of Glu-plasminogen, and to enhance the activation rate by UK, only binding of E fragment with plasminogen can result in enhancement of the activation of Glu-plasminogen by SK.

Drug Synergism↗
PubMed1982

Sulfonated poly(vinylidene fluoride) as a biomaterial: immobilization of urokinase and biocompatibility.

The adsorption of urokinase (UK) on sulfonated poly(vinylidene fluoride) (PVDF) films was examined. The amount of adsorbed UK on sulfonated PVDF films increased linearly with the degree of the ion exchange capacity (IEC) of sulfonated film. Moderately sulfonated PVDF film (IEC = 0.25 meq/g) adsorbed 3 IU/cm2 UK, and highly sulfonated film (IEC = 0.54 meq/g) adsorbed 5 IU/cm2 UK. All UK-immobilized PVDF films were active for ten weeks. The presence of the sulfonated films in the culture of rat lymphocytes did not result in any change of their viability. The implant of the film (IEC greater than 0.48 meq/g) into the subcutaneous layer of rats resulted in the cell infiltration composed of lymphocytes and plasma cells or the blastogenesis within the surrounding tissues of the implant and the regional lymph nodes. On the contrary, the implant of the films (IEC less than 0.27 meq/g) did not exert any visible changes, indicating that the lightly sulfonated films may be applicable in the sense of biocompatibility in vivo.

Animals↗
PubMed1982

Lysine and polylysine: correlation of their effects on polyphosphoinositides in vitro with ototoxic action in vivo.

Low concentrations of poly-L-lysine, a polycationic hydrophilic molecule, caused a large expansion of polyphosphoinositide monolayers and produced a significant loss of cochlear microphonic potentials in perilymphatic perfusions in the guinea pig. In contrast, the monomeric L-lysine had only slight effects on polyphosphoinositide monolayers and did not affect cochlear microphonic potentials even at concentrations as high as 10 mM. These data substantiate the hypothesis that the expansion of polyphosphoinositide monolayers by a drug is an indicator of its ototoxicity.

Animals↗
PubMed1982

Studies on the pathogenesis of the constitutional excretory defect of indocyanine green.

Constitutional excretory defect of indocyanine green (ICG) is characterized by the selective impairment of plasma ICG clearance. We studied binding patterns of ICG to plasma proteins and plasma ICG kinetics in three patients and one relative. Binding patterns of ICG to plasma proteins were modified in subjects with the ICG excretory defect. However, plasma disappearance rates of ICG bound to various protein fractions were not significantly different from each other, except for one case. In the kinetic study of ICG hepatic uptake rates (a values) were decreased, and hepatic reflux rates (b values) were increased in ICG excretory defect and liver cirrhosis. However, a values were unchanged and b values were clearly increased in ICG excretory defect, while a values decreased and changes in b values were slight in liver cirrhosis after loading with a large dose of ICG. These results suggest that active transport of ICG in the hepatic cell membrane is selectively lost in the ICG excretory defect.

Adult↗
PubMed1982

Calcium antagonism and reversibility of gentamicin-induced loss of cochlear microphonics in the guinea pig.

The perilymphatic space of the guinea pig cochlea was perfused with various concentrations of Ca2+, Mg2+ and gentamicin. Cochlear microphonic potentials (CM) were essentially stable when solutions contained 1 mM Ca2+ plus 2 mM Mg2+, 1 mM Ca2+ and no Mg2+ or when both Ca2+ and Mg2+ were omitted. In the absence of Ca2+, the presence of 2 mM Mg2+ or 1 mM EGTA markedly decreased CM. Addition of 3 mM gentamicin lowered CM, the magnitude of the effect depending on the concentration of Ca2+ present. Ten mM Ca2+ eliminated the action of the drug. In the absence of Ca2+, the effects of Mg2+ and gentamicin were additive. When the application of gentamicin was followed by perfusion with drug-free medium, suppression of CM by 3 mM drug could be reversed with 10 mM Ca2+ but not with 1 mM Ca2+. Loss of CM was irreversible when administration of 10 mM Ca2+ was delayed or when the drug concentration was increased to 10 mM. The results are consistent with our previous hypothesis of a biphasic mechanism of aminoglycoside toxicity: an initial action competitive with calcium ions and reversible and a second step, non-competitive and irreversible.

Aminoglycosides↗
PubMed1982

The inhibition by lysine of the activation of the first component of complement, C1.

Lysine prevented the activation of Cl at low ionic strength or by heat aggregated IgG (aggIgG) measured by the hydrolysis of acetyl tyrosine ethyl ester (ATEe) by Cls. When serum was mixed with aggIgG, complement was activated and consumed. If lysine was present in the serum containing aggIgG, the activation of complement, thus its consumption, was inhibited in a dose-response manner. Cl haemolysis assay which measures the Cl activity to interact with EA (erythrocytes bound with antibody) was used to study the effects of lysine. The results indicate that 50% of Cl haemolysis was inhibited at 3 mM of lysine. Crossed immunoelectrophoresis indicates that Cl in the serum was activated by aggIgG, but Cls thus formed seemed to be soon complexed with Cl inactivator. The presence of lysine prevented the conversion of Cls to Cls completely. It might be possible that lysine binds with the binding sites on Clq, thus preventing the interaction of Clq and C gamma 2.

Complement Activation↗
PubMed1982

Clinicopathological study of alcoholic fibrosis.

Among 112 patients with alcoholic liver injury, 45 had alcoholic fibrosis. The incidence of alcoholic fibrosis was 40.2% which was the highest among various types of alcoholic liver injury (fatty liver; 3.6%, alcoholic hepatitis; 2.7% and liver cirrhosis; 31.3%). Clinical features of alcoholic fibrosis were milder than those of liver cirrhosis and more severe than those of fatty liver. The mean laboratory values in alcoholic fibrosis were significantly different from those in fatty liver and liver cirrhosis. The laboratory data were well correlated with the presence of pericellular fibrosis and thickening of the terminal hepatic venule, but only partially with hepatic cell necrosis and not with fatty metamorphosis. Two patients with alcoholic fibrosis who developed cirrhosis without any clinical and histological features of hepatitis were observed during 5-yr follow-up. These results indicate that alcoholic fibrosis is the most common type of alcoholic liver injury in Japan and is an independent clinicopathological entity distinct from the classical types of alcoholic liver injury. Pericellular fibrosis and thickening of the terminal hepatic venule which are the main histological features of alcoholic fibrosis may play an important role in its transition to liver cirrhosis.

Aged↗