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Biomedical subjects

H Iwamoto

Publications and source records attributed to H Iwamoto.

At least 235 records · Page 13Linked to original sources

Reaction of human myeloperoxidase with hydrogen peroxide and its true catalase activity.

The instability of human myeloperoxidase [EC 1.11.1.7] compound I, which was spontaneously reduced to compound II, and the abnormal stoichiometry of the reaction of myeloperoxidase with H2O2 were investigated. As to the former, a pretreatment of myeloperoxidase with H2O2 did not stabilize compound I, and no difference in its stability was observed between native (alpha 2 beta 2) and hemi (alpha beta) myeloperoxidase. From these results, it was thought that the instability of compound I was caused by neither the presence of endogenous donors nor the intramolecular reduction of compound I to compound II by the other heme in the native enzyme molecule. As for the latter, true catalase activity of myeloperoxidase was demonstrated by monitoring O2 evolution after the injection of H2O2 into the enzyme solution. Myeloperoxidase compound I reacted with H2O2 and returned to the ferric state with concomitant evolution of an O2 molecule. Accordingly, the abnormal stoichiometry of the reaction with H2O2 and a part of the instability of compound I can probably be ascribed to this true catalase activity.

Catalase↗

Immunohistochemical demonstration of peptide YY in gastrointestinal endocrine tumors.

Fourteen cases of gastrointestinal endocrine tumors were examined immunohistochemically for peptide YY, pancreatic polypeptide, glucagon, and somatostatin. Peptide YY cells were present in seven tumors, pancreatic polypeptide cells in eight tumors, glucagon cells in six tumors, and somatostatin cells in nine tumors. All 7 rectal endocrine tumors examined were found to contain peptide YY, while in the tumors of the other sites peptide YY cells were not detected. Peptide YY cell population in the rectal tumors was small to moderate in comparison with pancreatic polypeptide and glucagon cell population. This study suggests that peptide YY cells may be a common constituent of rectal endocrine tumors together with pancreatic polypeptide and glucagon cells, and that the peptide YY spectrum of gastrointestinal endocrine tumors may be closely related to the location of the tumors. Moreover, it can also be said that peptide YY may be used as one of the markers of rectal endocrine tumors.

Adolescent↗

Efficient transformation of phytopathogenic strains of Xanthomonas species.

Efficient transformation and conjugation systems for use in phytopathogenic strains of Xanthomonas species were developed with a dual-function plasmid vector, pBXC12, which was constructed from a newly isolated Xanthomonas citri plasmid, pXCL6, and pBR328. By using this system, pBR328 could also transform the same strains of Xanthomonas. The systems make useful cloning vectors for the study of genes involved in the plant pathogenesis of this species.

Cloning, Molecular↗

Diffuse intrapulmonary hemorrhage and renal failure in adult Henoch-Schönlein purpura.

A 53-year-old woman with Henoch-Schönlein purpura presented with massive intrapulmonary hemorrhage and renal failure. Renal pathology revealed diffuse proliferative glomerulonephritis with granular deposition of immunoglobulin on immunofluorescent staining. Therapy with oral prednisolone resulted in resolution of the pulmonary lesions and renal failure.

Acute Kidney Injury↗

Hypouricemia due to increased tubular urate secretion.

A 45-year-old woman had hypouricemia (serum uric acid, 1.0-2.3 mg/dl) with increased uric acid clearance (29.8 +/- 9.3 ml/min/1.73 m2). Uric acid clearance to creatinine clearance ratio (Cua/Ccr) was suppressed markedly by pyrazinamide to 2.3% and surprisingly enhanced by probenecid to 227.8%. No other renal tubular or metabolic abnormalities were detected. This previously unreported high postprobenecid Cua/Ccr suggests that markedly increased urate secretion by the renal tubule is responsible for hypouricemia in this patient.

Creatinine↗

Effect of a new H2-blocker, famotidine, in reflux esophagitis among severely handicapped children.

Vomiting, hematemesis, and esophagitis resulting from gastroesophageal reflux or hiatal hernia are frequently observed in severely handicapped children. This study was conducted to determine whether the use of a new H2-antagonist, famotidine, could prevent recurrence of reflux esophagitis among such children. Seventeen severely handicapped, bedridden children admitted to a children's medical center between April 1985 and September 1986 were studied. All had vomiting or hematemesis as a main symptom, and the cause of esophagitis was suggested to be gastroesophageal reflux in 13 cases and hiatal hernia in four. Six had been previously treated with cimetidine or other drugs or a combination thereof without relief. Famotidine was administered at about 1 to 2 mg/kg/day, two times daily to patients weighing more than 10 kg and three times daily to those weighing less than 10 kg. In 13 cases, famotidine was administered intravenously for between seven and ten days and then given orally, while the rest were given the drug orally from the outset. The following results were obtained: (1) improvement was seen within seven days after start of famotidine treatment, and reduction of vomiting or hematemesis or both was reached within two weeks in 70% of cases and within three weeks in 94%; (2) famotidine was markedly effective in 29% and moderately effective in 41%; in no case was the drug ineffective; (3) no side effects were observed; five patients had transient, mild elevation of SGOT . SGPT, but this was not attributable to the drug.

Adolescent↗

Hypouricemia due to subtotal defect in the urate transport.

Hypouricemia due to renal tubular defects is rarely reported. We report here our observations of two such patients who cannot be classified into any of the previously reported categories of renal hypouricemia. They showed no suppression of urate clearance to creatinine clearance ratio (Cua/Ccr) following the administration of pyrazinamide, and no increase of Cua/Ccr after probenecid. It is tempting to speculate upon the subtotal defect in the urate transport as a condition explaining the above results.

Adult↗

Diabetic renal hypouricemia.

In diabetes, the serum uric acid level is low due to increased urate clearance; however, its mechanism remains unknown. We examined seven maturity-onset diabetic patients with rarely reported hypouricemia due to renal tubular abnormality to better understand the renal handling of urate by the diabetic kidney. The results of studies indicate that the increase in urate clearance was entirely accounted for by increased pyrazinamide-suppressible urate clearance. The maximal uricosuric response to probenecid administration was exaggerated. The effects of drugs on urate clearance were similar to those we have previously reported in the syndrome of inappropriate secretion of antidiuretic hormone. In four patients, the family survey did not reveal anyone with hypouricemia. These observations suggest that hypouricemia due to hyperuricosuria, which responds markedly to pyrazinamide and probenecid, is actually an indicator of renal tubular abnormality in diabetics.

Adult↗

Crystallization and properties of myeloperoxidase from normal human leukocytes.

Myeloperoxidase was purified from normal human leukocytes in a crystalline state. Two types of crystals were obtained by the batchwise and dialysis crystallization methods, one of which had a bipyramidal shape belonging to the orthorhombic system. Three multiple forms of human myeloperoxidase were separated from the crystalline enzyme by CM-Sepharose chromatography with sodium chloride gradient elution. These three multiple forms were found to have very similar enzymatic, spectroscopic, and chemical properties. However, slight differences were observed in their amino acid compositions and the molecular weights of their large subunits determined by sodium dodecyl sulfate (SDS)-polyacrylamide gel electrophoresis. Hemi-myeloperoxidase was prepared from holo-myeloperoxidase by reduction with dithiothreitol and modification with iodoacetamide, and the molecular shapes of the holo- and hemi-enzymes were determined by analytical ultracentrifugation. The axial ratios were calculated to be 2.4-3.5 for the holo-enzyme and 2.9-3.1 for the hemi-enzyme. These results suggest that the shapes of the two enzymes are more spherical in solution than the proposed structural model previously reported.

Amino Acids↗

Structural changes during contraction in vertebrate skeletal muscle as studied by time-resolved X-ray diffraction technique.

To obtain information about the structural changes in vertebrate skeletal muscle during contraction, time-resolved X-ray diffraction studies were performed on the intensity changes of the 59 A and 51 A actin layer lines from bullfrog sartorius muscle during the isometric force development, and the intensity changes of the 143 A and 215 A myosin meridional reflections and of the 1.0 and 1.1 equatorial reflections when isometrically contracting muscle was subjected to sinusoidal length changes (1%, 5-10 Hz) with the following results. The integrated intensities of the 59 A and 51 A actin layer lines increased during the force development by 30-50% for the 59 A reflection, and by about 70% for the 51 A reflection compared to their respective resting values. These intensity changes were greater than those taking place during the transition from rest to rigor state, and observed to precede the intensity changes of the 429 A myosin off-meridional reflection and of equatorial reflections. When sinusoidal length changes were applied to the muscle generating steady isometric force, the resulting periodic intensity changes in the 1.0 and 1.1 equatorial reflections were in phase and in antiphase with the length changes respectively. On the other hand, the 143 A myosin reflection exhibited a characteristic periodic changes; its intensity reached a maximum at each boundary between the stretch and release phases of the length changes. These results are discussed in connection with the behaviour of the cross-bridges during contraction.

Actin Cytoskeleton↗