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Biomedical subjects

M Suda

Publications and source records attributed to M Suda.

At least 109 records · Page 6Linked to original sources
PubMed1993

In vitro oxidation of pyrazinamide and allopurinol by rat liver aldehyde oxidase.

Aldehyde oxidase was purified about 120-fold from rat liver cytosol by sequential column chromatography using diethylaminoethyl (DEAE) cellulose, Benzamidine-Sepharose 6B and gel filtration. The purified enzyme was shown as a single band with M(r) of 2.7 x 10(5) on polyacrylamide gel electrophoresis (PAGE) and M(r) of 1.35 x 10(5) on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Using this purified enzyme, in vitro conversion of allopurinol, pyrazinamide and pyrazinoic acid was investigated. Allopurinol and pyrazinamide were oxidized to oxypurinol and 5-hydroxy-pyrazinamide, respectively, while pyrazinoic acid, the microsomal deamidation product of pyrazinamide, was not oxidized to 5-hydroxypyrazinoic acid. The apparent Km value of the enzyme for pyrazinamide was 160 microM and that for allopurinol was 1.1 mM. On PAGE, allopurinol- or pyrazinamide-stained band was coincident with Coomassie Brilliant Blue R 250-stained band, respectively. These results suggest that aldehyde oxidase may play a role in the oxidation of allopurinol to oxypurinol and that of pyrazinamide to 5-hydroxypyrazinamide with xanthine dehydrogenase which can oxidize both allopurinol and pyrazinamide in vivo. The aldehyde oxidase may also play a major role in the oxidation of allopurinol and pyrazinamide in the subgroup of xanthinuria patients (xanthine oxidase deficiency) who can oxidize both allopurinol and pyrazinamide.

Aldehyde Oxidase↗
PubMed1993

Purification and immunohistochemical tissue localization of human xanthine oxidase.

Xanthine oxidase was purified 1600-fold from human liver cytosol. The purified enzyme was shown as a single band of 300 kDa on polyacrylamide gel electrophoresis and 150 kDa on SDS-PAGE. Using this purified enzyme, polyclonal antibody against xanthine oxidase was raised in a rabbit. On Ouchterlony's double immunodiffusion method, the raised antibody and the human liver cytosol made a precipitation line stained by activity stain and protein stain, respectively. With the raised anti-xanthine oxidase sera, the immunohistochemical localization of xanthine oxidase in human tissues was examined. Immunostaining of frozen hepatic tissue section showed that the cytoplasm of hepatocytes and endothelial lining cells were stained. In a number of other tissues, the xanthine oxidase antigen was detected only in the endothelial lining cells from heart, kidney, brain, aorta, lung and mesentery, except for the duodenal mucosa cells. A possible role for xanthine oxidase in the endothelial cells from various human tissues in the pathogenesis of reperfusion injury was suggested.

Antibody Specificity↗
PubMed1993

Cell differentiation of alveolar epithelium in the developing rat lung: ultrahistochemical studies of glycoconjugates on the epithelial cell surface.

Glycoconjugates on the surface of pulmonary epithelial cells were ultrahistochemically examined in the fetal, neonatal and adult rat lung. Lectin and colloidal iron staining procedures were performed in combination with digestion using carbohydrate-degrading enzymes or methylation. The glycoconjugate composition of columnar cells at 16 days gestation was similar to that of cuboidal cells at 19 days gestation. Glycoconjugate differentiation on the cell surface occurred at 20 days gestation, and especially the loss of soybean agglutinin (SBA) binding sites could be detected on type II cells. The contents of Ricinus communis agglutinin-I (RCA-I) and Concanavalin A (Con A) binding sites on type II cells also began to decrease. On the contrary, the content of sulfated saccharides decreased on the surface of type I cells during development. Glycoconjugate differentiation on both type I and II cells was completed with the disappearance of hyaluronic acid and peanut agglutinin (PNA) binding sites; type I and II cells acquired a similar histochemical composition to that on adult type I and II cells at 5 days after birth. Both type I and II cells share a common early precursor cell, that is, the cuboidal epithelial cell at the canalicular stage.

Animals↗
PubMed1993

Degradation of methyl and ethyl mercury by singlet oxygen generated from sea water exposed to sunlight or ultraviolet light.

Photodegradation of methyl mercury (MeHg) and ethyl Hg (EtHg) in sea water was studied by sunlight or ultraviolet (UV) light exposure, and by determining inorganic Hg produced by degradation. Sea water containing 1 microM MeHg or EtHg was exposed to sunlight or UV light. N-Acetyl-L-cysteine was added to the solution for preventing Hg loss during the light exposure. MeHg and EtHg in sea water were degraded by sunlight (> 280 nm), UV light A (320-400 nm) and UV light B (280-320 nm), though the amounts of inorganic Hg produced from MeHg were 1/6th to 1/12th those from EtHg. Inorganic Hg production was greater with increasing concentration of sea water. Degradation of MeHg and EtHg by the UV light A exposure was inhibited by singlet oxygen (1O2) trappers such as NaN3, 1,4-diazabicyclo[2,2,2]octane, histidine, methionine and 2,5-dimethylfuran. On the other hand, inhibitors or scavengers of superoxide anion, hydrogen peroxide or hydroxyl radical did not inhibit the photodegradation of alkyl Hg. These results suggested that 1O2 generated from sea water exposed to sunlight, UV light A or UV light B was the reactive oxygen species mainly responsible for the degradation of MeHg and EtHg.

Ethylmercury Compounds↗
PubMed1993

Effect of ethanol ingestion on nucleotides and glycolytic intermediates in erythrocytes and purine bases in plasma and urine: acetaldehyde-induced erythrocyte purine degradation.

The effect of ethanol on nucleotides and glycolytic intermediates in erythrocytes and purine bases in plasma and urine was investigated. Ethanol ingestion (0.45 mL/kg body weight) increased plasma concentrations and urinary excretion of oxypurines (hypoxanthine and xanthine) and concentrations of adenosine monophosphate (AMP), adenosine diphosphate (ADP), and glyceraldehyde 3-phosphate+dihydroxyacetonephosphate in erythrocytes. In an in vitro incubation study using erythrocytes, acetaldehyde increased the concentrations of AMP, ADP, and glyceraldehyde 3-phosphate+dihydroxyacetonephosphate in erythrocytes as well as the concentration of hypoxanthine in the incubation medium. These results suggest that acetaldehyde (a metabolite of ethanol) induces an increase in purine degradation by erythrocytes and then contributes to the ethanol-induced enhanced purine degradation in vivo.

Acetaldehyde↗
PubMed1993

Preoperative assessment and prediction of postoperative results in an artificial arterial network using computer simulation.

A computer model has been developed that can be used to describe the human arterial system mathematically. It simulates the complex relationship of morphology and hydraulics in the vessel network. After entering patient data into a standard vessel model, the mean flow velocity, the flow direction, and the blood pressure at each specified point of the flow network can be calculated. The vessel picture can be altered and modified with the help of a graphic editor. Localized or diffuse stenoses, bypasses with simple or multiple anastomoses, end-to-end anastomoses, end-to-side anastomoses, etc., can be studied in terms of the hydraulic effects on the local situation or on the entire vessel system. Experimental results of ultrasonic mean flow data in vessel systems of leg and cerebral arteries of patients are compared with calculated values. The predicted and measured flow velocities show a mean difference of about 10% indicating that such a computer model may be successfully used in the optimal planning of bypass operations.

Arteries↗
PubMed1993

Scavenger macrophages and central macrophages of erythroblastic islands in liver hemopoiesis of the fetal and early postnatal mouse: a semithin light- and electron-microscopic study.

The livers of 12-day mouse embryos contain many hemopoietic cells in the hepatic cords and macrophages which are laden with large heterophagosomes in the sinusoids. Macrophages, as scavengers, engulfed circulating primitive erythroblasts from the yolk sac, as well as nuclei expelled from erythroblasts. At the 14th day of gestation, scavenger macrophages in mitosis were seen, extending long and thin cytoplasmic projections from their cell surface. At the 13-14 day of gestation, macrophages migrated from sinusoids into hepatic cords, and erythroblasts gathered around them, thus forming cell clusters designated as erythroblastic islets. Central macrophages formed a cell-socket-like structure on their cell surface for surrounding erythroblasts, reflecting the close association between macrophages and erythroblasts. In the erythroblastic islands, contained in late fetal and neonatal livers, erythroblasts have dissociated from the central macrophages having a starfish-shaped cell profile. The macrophage-erythroblastic association in the islands became less marked rapidly after birth.

Animals↗
PubMed1993

Studies on abnormal lipid metabolism in experimental nephrotic syndrome.

The specific lipid alterations in plasma and four different tissues, as well as the activities of plasma lecithin-cholesterol acyltransferase (LCAT) and tissue lipolytic enzymes were determined in experimental nephrotic and control rats. In nephrotic rats, the cholesterol level in the heart was significantly increased, while the kidney level was decreased. When expressed per unit protein, the cholesterol level in the adrenal was also increased. The respective triglyceride and phospholipid levels were similar in both groups, except for the significant increase in the adrenal triglyceride of nephrotic rats when expressed per unit protein. The tissue lipolytic activities were significantly reduced in the heart and adrenals of the nephrotic rats. The plasma LCAT was increased, and electron-microscopically heterogenous lipoproteins (very-low density and high-density lipoproteins) were demonstrated in the nephrotic rats. These results suggest that an excess of abnormal lipoproteins in the circulation may contribute to an increased uptake of cholesterol by circulatory organs like the heart and that an accumulation of cholesterol in the circulatory organs may accelerate atherosclerosis in nephrotic syndrome.

Animals↗
PubMed1993

Elevated serum fucose levels in idiopathic nephrotic syndrome.

We measured serum fucose concentrations in 34 children with idiopathic nephrotic syndrome (INS), 23 with chance proteinuria and/or hematuria (CPH), and 20 healthy children as controls. The serum fucose levels in the patients with INS were significantly elevated at onset (14.0 +/- 3.7 mg/dl, n = 4, p < 0.02), in relapses (19.1 +/- 3.7 mg/dl, n = 10, p < 0.001), and in remission (13.9 +/- 7.0 mg/dl, n = 30, p < 0.01) as compared with CPH patients (10.6 +/- 3.2 mg/dl, n = 23) and controls (9.1 +/- 3.1 mg/dl, n = 20). Those in remission were further divided into 2 groups and the mean fucose concentrations were significantly different in the two remission groups: 20.1 +/- 4.6 mg/dl in 14 patients whose blood samples were taken within one week of remission and 9.0 +/- 2.9 mg/dl in the other 16 patients whose samples were taken at 1 to 6 months of remission. The mean value in the latter remission group was significantly lower in comparison with the former group, but not different from the controls. Gel-chromatography of serum samples from patients with INS revealed a single peak of fucose in the high molecular fraction, and this was also found in the same fractions of serum inhibitor of lymphocyte blastogenesis in INS. We concluded that serum fucose concentrations are elevated in INS patients and that, because of the large molecular weight, the fucose is probably in a form bounded to some glycoproteins in the serum. Considering various reports on fucose, serum fucose may be associated with immunodepression in INS patients.

Child↗
PubMed1993

Cell death and phagocytosis of haematopoietic elements at the onset of haematopoiesis in the mouse spleen: an ultrastructural study.

The spleen in fetal and early postnatal mice contains a variety of proliferating haematopoietic cells as well as 2 kinds of phagocytes, scavenger macrophages and mast cells, laden with large heterogeneous inclusions. Their phagocytotic activity is directed towards extruded erythrocyte nuclei, erythrocytes and dying haematopoietic cells. The splenic cords after 18 d of gestation become filled with proliferating haematopoietic cells, and the cords contain a small number of free haematopoietic cells undergoing degeneration. The early signs of cell death can be observed in the nuclear structures: hyperchromasia of the nuclear membrane or nuclear dissolution. Erythroblast nuclei are amongst the most frequent elements engulfed. Phagocytes also take up and digest degenerating blood cells, i.e. erythrocytes, erythroblasts and neutrophil granulocytes. Since the digestion processes are ultrastructurally different for the various haematopoietic elements, the origins of heterolysosomes enclosed by phagocytes can be identified by electron microscopy. Mast cells, originally classified as secretory cells, phagocytose erythroid line cells in the spleen. Cell death in several haematopoietic cell lines is discussed in relation to programmed cell death in the developing spleen.

Animals↗
PubMed1993

Inflammatory cytokines in virus-associated hemophagocytic syndrome. Interferon-gamma as a sensitive indicator of disease activity.

PURPOSE: We assayed serum interleukin-1 beta (IL-1 beta), tumor necrosis factor alpha (TNF-alpha) and interferon gamma (IFN-gamma) levels in children with virus-associated hemophagocytic syndrome (VAHS) to evaluate the relationship of these cytokines to other laboratory parameters. We also studied the role of IFN-gamma as a macrophage activator in hemophagocytic syndrome (HPS). PATIENTS AND METHODS: Interleukin-1 beta, TNF-alpha, and IFN-gamma were measured in 42 serial sera from six children with VAHS using a sensitive radioimmunoassay. RESULTS: The cytokine IFN-gamma or TNF was detected in 19/19 (100%) or 11/19 (69%) samples, respectively, during the active febrile phase, at much higher levels than during the remission phase of the disease (IFN: p < 0.00001; TNF: p < 0.01). In contrast, IL-1 could be detected in only two sera obtained from a patient during severe relapse. Serial cytokine examination revealed that the elevated TNF and IFN-gamma levels decreased rapidly to an undetectable level in concert with clinical improvement after an effective treatment, and that IFN-gamma, but not TNF, was detected just before a relapse marked by spiking fever. In the active phase, the CD4/8 ratio was depressed, and the total number of CD3+ HLA-DR+ cells was increased. Of the activated T cells, CD8+ cells outnumbered CD4+ T cells. By the Spearman's rank sum test, the IFN-gamma level correlated positively with the peripheral leukocyte count [Correlation coefficient (CC): 0.585, p < 0.05] and serum lactate dehydrogenase level (CC: 0.538, p < 0.05) and negatively with the CD4/8 ratio (CC: -0.618, p < 0.05), but not with any other parameter including ferritin and C-reactive protein. Although TNF and IL-1 were not statistically linked to these parameters, TNF levels were related to IFN-gamma levels (product moment CC: 0.546, p < 0.05). CONCLUSIONS: These results suggest that circulating IFN-gamma is one of the most sensitive indicators of disease activity; it may act as a potent macrophage activator during the hypercytokinemic state of childhood VAHS.

Adolescent↗
PubMed1993

[A study of trientine therapy in Wilson's disease with neurological symptoms].

D-penicillamine, an orally-administered chelating agent, is effective for Wilson's disease (WD). However 25% of WD patients showed serious adverse reactions to D-penicillamine cause this drug to be discontinued after months or years of treatment. For these cases, trientine-2HCl and trientine-4HCl, less toxic agents, are investigated. Three patients with WD, associated with neurological symptoms, were given either trientine-2HCl or trientine-4HCl. These patients had been on therapy with D-penicillamine. Severe adverse reactions had developed during the course of therapy, and D-penicillamine was discontinued, pancytopenia in case 1, nephrotic syndrome in case 2, and myasthenia gravis in case 3. Trientine-2HCl for case 1, and trientine-4HCl for cases 2 and 3 were instituted and continued. The neurological findings in all patients were extremely improved without side effects by trientine therapy. Though the chelating action on copper is weaker than that of D-penicillamine, it is efficient in improvement of the clinical neurological symptoms.

Adolescent↗
PubMed1993

Xylitol-induced increase in purine degradation: a role of erythrocytes.

We administered xylitol intravenously to normal subjects to investigate the mechanism of xylitol-induced increase in the purine degradation in humans. Xylitol increased the plasma concentrations of hypoxanthine, xanthine and uric acid but decreased the blood concentration of pyruvic acid. The erythrocyte concentrations of IMP, AMP, ADP, glyceraldehyde 3-phosphate and fructose 1,6-diphosphate as well as the urinary excretion of hypoxanthine and xanthine were increased, while the erythrocyte concentration of ATP was decreased. In addition, the in vitro incubation studies using erythrocytes demonstrated that both xylitol-induced purine degradation and xylitol-induced inhibition of the conversion of glyceraldehyde 3-phosphate to 1,3-bisphosphoglycerate were protected by pyruvic acid. These results indicate that xylitol-induced impairment of glycolysis in erythrocytes contributes to the observed xylitol-induced increase in the purine degradation in the body.

Adult↗
PubMed1992

An immunoreactive xanthine oxidase protein-possessing xanthinuria and her family.

The presence of immunoreactive xanthine oxidase protein was proven in a xanthinuric patient, using a polyclonal antibody against xanthine oxidase. The antibody was raised against purified human liver xanthine oxidase in a rabbit. Double immunodiffusion method demonstrated the existence of an immunologically reactive xanthine oxidase which did not possess xanthine oxidase activity. In addition, urinary excretion of oxypurines in the patient and her family was investigated. The results indicated that a brother and a sister had xanthinuria.

Adult↗
PubMed1992

Two cases in whom pyrazinamide does not inhibit the uricosuric action of benzbromarone.

The 2 subjects were a diabetic male with renal hypouricemia and a healthy male with normouricemia. In these subjects, 200 mg of benzbromarone increased fractional uric acid clearance (FUa) and 3.0 g of pyrazinamide decreased FUa. However, pyrazinamide did not inhibit the uricosuric action of benzbromarone at all on the administration of 3.0 g of pyrazinamide together with 200 mg of benzbromarone. These results indicated that in these cases, the relative role of each component could not be determined on the basis of the hypothetical four-component model.

Adult↗
PubMed1992

Tissue distribution of intraperitoneally administered (1-->3)-beta-D-glucan (SSG), a highly branched antitumor glucan, in mice.

Distribution of metabolically 3H-labeled (1-->3)-beta-D-glucan (3H-SSG) obtained from the culture filtrate of Sclerotinia sclerotiorum IFO 9395, in various tissues after intraperitoneal administration into ICR mice (250 micrograms/mouse) was examined. 3H-SSG was mainly detected in liver, spleen, and blood, and a negligible amount was excreted into the feces and excrement within 2 d. The significant amount of 3H-SSG remained in liver and spleen after 1 month. On the other hand, SSG was not incorporated effectively in vivo and in vitro by peritoneal exudate macrophages (0.5 microgram/1 x 10(6) M phi) Similarly in vivo, the majority of 3H-SSG distributed in spleen and liver were recovered from the non-cellular fraction and not from splenic macrophage and Kupffer cell fractions. These results suggested that (1-->3)-beta-D-glucans would not be easily incorporated by the host cells to degrade and exclude from the body even after the onset of the biological response modifier activity.

Animals↗
PubMed1991

Chromatosomes are not produced from Tetrahymena chromatin by micrococcal nuclease digestion.

The subnucleosomal organization of Tetrahymena chromatin, which has an unusual H1 histone, was investigated by NaCl extraction and micrococcal nuclease digestion of nuclei. It was found that Tetrahymena histone H1 is extracted with 0.35 M NaCl, whereas bovine thyroid H1 is not. Micrococcal nuclease digestion of Tetrahymena nuclei did not yield chromatosomes as a stable intermediate, whereas digestion of bovine thyroid nuclei did.

Animals↗