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S Umeki

Publications and source records attributed to S Umeki.

At least 55 records · Page 3Linked to original sources
PubMed1992

[Structure, function and pathophysiology of mucociliary transport system].

There has been growing appreciation of the significant role played by the mucociliary transport system in the body. The mucociliary transport system is an important defense mechanism by which the human body usually maintains its "homeostasis" by protecting the body against invading particles, including bacteria. This system includes two major functional mechanisms; i.e., ciliary transport and mucous secretional systems, each of which is usually complimentary and cooperative. Three hereditary disorders, primary ciliary dyskinesia (immotile-cilia syndrome), cystic fibrosis and Young's syndrome, have been shown to be systemically associated with mucociliary transport failure, leading to male infertility and chronic sinopulmonary infections. Localized mucociliary transport failure, however, is observed in respiratory diseases, especially chronic sinusitis, chronic bronchitis, bronchiectasis and bronchial asthma. We aim, in this review, to draw together those developments in the study of ciliary transport and mucous secretion, the interactions between them and their pathophysiology that can provide a better understanding of the mucociliary transport system of the human body.

Cilia↗
PubMed1991

Flow cytometric measurements of somatic cell mutations in Thorotrast patients.

Exposure to ionizing radiation has long been well-recognized as a risk factor for cancer development. Since ionizing radiation can induce mutations, an accurate way of measuring somatic mutation frequencies could be a useful tool for evaluating cancer risks. In the present study, we have examined in vivo somatic mutation frequencies at the erythrocyte glycophorin A (GPA) and T-cell receptor (TCR) loci in 18 Thorotrast patients who have been continuously irradiated with alpha-particles emitted from the internal deposition of thorium dioxide and who thus have increased risks of certain malignant tumors. When compared with controls, the results showed a significantly higher frequency of mutants at the lymphocyte TCR loci but not at the erythrocyte GPA loci in the Thorotrast patients. The discrepancy between the results of the two assays is discussed.

Aged↗
PubMed1991

[Bronchial asthma associated with primary lung cancer--comparison of extrathoracic malignancies].

Regarding 249 bronchial asthma patients having been admitted to our division for the recent 9 years, clinical manifestations of 8 bronchial asthma with primary lung cancer (group A; squamous cell carcinoma--5 cases, adenocarcinoma--2 cases, small cell carcinoma--1 case; 3.2% of 249 cases) and 8 asthma patients with extrathoracic malignancy (group B; gastric cancer--3 cases, malignant lymphoma--2 cases, bladder cancer--1 case, laryngeal cancer--1 case, prostatic cancer--1 case) were investigated. In group A, the mean of asthmatic history was 19 years and all cases were associated with respiratory tract infections. Three of 8 patients, were mild type and other 5 were moderate type. In group B, the mean of asthmatic history was 20 years and all cases were involved with respiratory tract infections. Five of 8 patients were mild type and other 3 were moderate type. The mean smoking (Brinkmann) index (1194) in group A was significantly higher than that (166) in 241 asthmatic patients without lung cancer or that (169) in group B. The median survival duration (more than 26 months) of group A patients was significantly lower than that (more than 77 months) of group B. These results suggested that, in many bronchial asthma patients accompanied by primary lung cancer who have adult-typed infectious asthmatic history, smoking exposure and aging are deeply related to the development of lung cancer.

Adenocarcinoma↗
PubMed1991

[Biochemical study on anti-inflammatory action of anti-allergic drugs--with regard to NADPH oxidase].

The effects of anti-allergic drugs with or without H1-receptor antagonism on the NADPH oxidase from human neutrophils in both whole-cell and fully soluble (cell-free) systems were investigated. Three anti-allergic drugs with H1-receptor antagonism, azelastine, ketotifen and oxatomide, were found to inhibit the superoxide generation of human neutrophils exposed to phorbol myristate acetate in a whole-cell system and the activation of superoxide-generating NADPH oxidase by sodium dodecyl sulfate in a cell-free system. The concentrations of three drugs required for 50% inhibition of the oxidase (IC50) were as follows: azelastin--0.7 microM in the whole-cell system and 0.5 microM in the cell-free system, ketotifen--60 microM in the whole-cell system and 6.8 microM in the cell-free system, and oxatomide--25 microM in the whole-cell system and 9.7 microM in the cell-free system. In addition, in the cell-free system, these drugs did not change the Km values for the NADPH of the oxidase. However, micromoles of tranilast, an anti-allergic drug without H1-receptor antagonism, did not inhibit neutrophil NADPH oxidase in the whole-cell and cell-free systems. The IC50 of hydrocortisone in the cell-free system was 60 microM. These results suggest that anti-allergic drugs with H1-receptor antagonism inhibit reconstitution of the solubilized membrane-bound enzyme by sodium dodecyl sulfate in cell-free systems and that they have a strong anti-inflammatory action. Anti-allergic drugs are not the drugs of first choice for asthma, but these drugs, especially basic anti-allergic drugs, should be used more frequently for the treatment of chronic asthma, infectious-typed asthma and mixed-typed asthma closely associated with acute and chronic inflammation of the airways as well as atopic asthma.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1991

[A case of eosinophilic granuloma of the cervical lymph nodes associated with pulmonary cystic lesions].

A 33-year-old man was referred to our department because of left cervical lymphadenopathy for one month which did not respond to antibiotics. Histological examination of the lymph node biopsy revealed eosinophilic granuloma. However, repeated bronchoscopic examinations performed to evaluate the pulmonary lesions appearing on chest roentgenograms and chest CT scans revealed no evidence of eosinophilic granuloma. Steroid therapy resulted in resolution of the cervical lymphadenopathy, but the pulmonary lesions showed no response. The possible relationship between eosinophilic granuloma and pulmonary cystic lesions in our patient is discussed.

Adult↗
PubMed1991

[A case of oral gold tablet-induced interstitial pneumonitis].

A 76-year-old woman was admitted with exertional dyspnea and chest roentgenographical abnormal shadows appearing after oral gold therapy (total 720 mg) for rheumatoid arthritis. Based on the patient's clinical course, chest roentgenograms, chest CT and pathological findings of TBLB specimens, gold pneumonitis was diagnosed. Steroid therapy improved symptoms and pulmonary function and cotton-like shadows on chest roentgenograms and chest CT scanning. However, linear and large ringed shadows on chest roentgenograms and chest CT scan remained, even after steroid therapy. This case is the first case of oral gold tablet-induced pneumonitis. Although the mechanism of oral gold tablet-induced pneumonitis is considered to be almost the same that of gold injection therapy-induced pneumonitis, this case suggested that fibrotic changes in oral gold tablet-induced pneumonitis may be delayed over a long period.

Administration, Oral↗
PubMed1990

Effects of non-steroidal anti-inflammatory drugs on human neutrophil NADPH oxidase in both whole cell and cell-free systems.

The effects of non-steroidal anti-inflammatory drugs (NSAIDs) on the respiratory burst oxidase (NADPH oxidase, EC 1.6.99.6) from human neutrophils in both whole cell and fully soluble (cell-free) systems were investigated. Three NSAIDs, indomethacin, salicylic acid and acetylsalicylic acid (aspirin), were found to inhibit the superoxide generation by human neutrophils exposed to phorbol myristate acetate in a whole cell system and the activation of superoxide-generating NADPH oxidase by sodium dodecyl sulfate in a cell-free system. Concentrations of these NSAIDs required for 50% inhibition of the oxidase (IC50) were: indomethacin (180 microM in both systems), salicylic acid (1.30 mM in the cell-free system, and more than 3.0 mM in the whole cell system) and acetylsalicylic acid (1.35 mM in the cell-free system, and more than 3.0 mM in the whole cell system). In addition, in the cell-free system, these NSAIDs did not change the Km values for NADPH of the oxidase. These results suggest that these NSAIDs, especially indomethacin, concentration-dependently inhibit the reconstitution of the solubilized membrane-bound enzyme by sodium dodecyl sulfate in the cell-free system.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1990

Spontaneous loss and alteration of antigen receptor expression in mature CD4+ T cells.

The TCR/CD3 complex plays a central role in antigen recognition and activation of mature T cells, and, therefore, abnormalities in the expression of the complex should induce unresponsiveness of T cells to antigen stimulus. Using flow cytometry, we detected and enumerated variant cells with loss or alteration of the surface TCR/CD3 expression among human mature CD4+ T cells. The presence of variant CD4+ T cells was demonstrated by isolating and cloning them from peripheral blood, and their abnormalities can be accounted for by alterations in TCR expression such as defects of protein expression and partial protein deletion. The variant frequency in peripheral blood increased with aging in normal donors and was highly elevated in patients with ataxia telangiectasia, an autosomal recessive inherited disease with defective DNA repair and variable T cell immunodeficiency. These findings suggest that such alterations in TCR expression are induced by somatic mutagenesis of TCR genes and can be important factors related to age-dependent and genetic disease-associated T cell dysfunction.

Adult↗
PubMed1990

Hydrocortisone inhibits the respiratory burst oxidase from human neutrophils in whole-cell and cell-free systems.

The effects of hydrocortisone on the respiratory burst oxidase (NADPH oxidase, EC 1.6.99.6) from human neutrophils in both whole-cell and full soluble (cell-free) systems were investigated. In the whole-cell system, hydrocortisone inhibited the generation of superoxide by neutrophils exposed to phorbol myristate acetate, suggesting that steroids inhibit the bactericidal capacity of the body in an acute inflammatory phase. Hydrocortisone, which was added to the cuvette after the addition of NADPH and before the addition of sodium dodecyl sulfate, in a cell-free system, was found to inhibit the activation of superoxide-generating NADPH oxidase by sodium dodecyl sulfate. The concentration of hydrocortisone required for 50% inhibition of oxidase was 40 microM. Its inhibition was dose- and time-dependent in the cell-free system. However, hydrocortisone did not alter the Km of the oxidase for NADPH. These results suggest that steroids inhibit the reconstitution of NADPH oxidase by sodium dodecyl sulfate in the cell-free system, and that they do not alter the affinity to NADPH of the oxidase.

Cell-Free System↗
PubMed1990

Human neutrophil cytosolic activation factor of the NADPH oxidase. Characterization of activation kinetics.

The kinetics of sodium dodecyl sulfate-induced activation of respiratory burst oxidase (NADPH oxidase) in a fully soluble cell-free system from resting (control) or phorbol myristate acetate (PMA)-stimulated human neutrophils were investigated. In a cell-free system containing solubilized membranes and cytosol fractions (cytosol) derived from control neutrophils (control cell-free system), the values of Km and Vmax for NADPH of the NADPH oxidase from control neutrophils continuously increased with increasing concentrations of cytosol, but with increasing concentrations of solubilized membranes from the control neutrophils, Km values continuously decreased, suggesting cytosolic activation factor-dependent continuous changes in the affinity of NADPH oxidase to NADPH. In a cell-free system containing solubilized membranes and cytosol prepared from PMA-stimulated neutrophils, NADPH oxidase was not activated after the addition of NADPH. However, cytosol from control neutrophils activated the NADPH oxidase of PMA-stimulated neutrophils in a cell-free system. Cytosol from PMA-stimulated neutrophils did not activate the control neutrophil oxidase, although it contained no inhibitors of NADPH oxidase activation. The results suggest that, in PMA-stimulated neutrophils, cytosolic activation factors may be consumed or exhausted with an increasing period of time after the stimulation of neutrophils, and that the affinity of PMA-stimulated neutrophil NADPH oxidase to NADPH may almost be the same as that of control neutrophil oxidase. It was concluded that the affinity of NADPH oxidase to NADPH was closely associated with interaction between solubilized membranes and cytosolic activation factors, as indicated by the concentration ratio.

Cell Membrane↗
PubMed1990

Ampicillin serves as an electron donor.

1. The effect of ampicillin on cytochrome c reduction and on the superoxide production of human neutrophils stimulated by phorbol myristate acetate (PMA) was investigated. 2. Ampicillin did not stimulate the superoxide production of intact (resting) neutrophils and not amplify the superoxide production of neutrophils stimulated by phorbol myristate acetate (PMA). 3. However, ampicillin dose-dependently increased the reduction of cytochrome c. 4. In addition, 50 mM ampicillin stimulated a superoxide dismutase-inhibitable reduction of cytochrome c by 0.70 +/- 0.02 (mean +/- SD) nmol/min and a superoxide dismutase-noninhibitable reduction of cytochrome c by 2.08 +/- 0.03 (mean +/- SD) nmol/min. 5. These results suggest that ampicillin serves as an electron donor and/or a superoxide generator.

Ampicillin↗
PubMed1990

Activation of the NADPH oxidase in a cell-free system from human neutrophils stimulated by phorbol myristate acetate.

Kinetics of activation of the NADPH oxidase in a fully soluble cell-free system from phorbol myristate acetate (PMA)-stimulated human neutrophils were investigated. In a cell-free system in which Mg2+ and sodium dodecyl sulfate, an anionic detergent required for the activation of NADPH oxidase are contained, cytosol prepared from PMA-stimulated neutrophils failed to activate PMA-stimulated neutrophil oxidase. However, cytosol prepared from resting (control) neutrophils was capable of activating PMA-stimulated neutrophil oxidase in a cell-free system in which its Km for NADPH was almost similar to that of control neutrophil oxidase. Cytosol from PMA-stimulated neutrophils could not activate control neutrophil oxidase, although it did not contain any inhibitors of NADPH oxidase activation. These results suggest that, in PMA-stimulated neutrophils, cytosolic activation factors may be consumed or exhausted, and that the affinity for NADPH of PMA-stimulated neutrophil oxidase may be the same as that of control neutrophil oxidase.

Cell-Free System↗
PubMed1990

A microtechnique for neutrophil respiratory burst oxidase in a cell-free system--characterization of oxidase activation system.

1. A microtechnique for quantitating human neutrophil NADPH oxidase in a cell-free system is described. 2. This spectrophotometric discontinuous (fixed time) method is less material-consuming than existing methods and is more useful for experiments in which superoxide production by neutrophils must be measured in a large number of samples. 3. Measurement of NADPH oxidase using the new method can be accomplished in a final vol of 0.15 ml. 4. In the assay, neutrophil membranes solubilized with deoxycholate were incubated for 3 min with cytosolic fractions, magnesium, sodium dodecyl sulfate, and cytochrome c in the absence of NADPH to preincubate the oxidase before the addition of the reducing agent. 5. The reaction was started by adding NADPH and 2 min later terminated by adding superoxide dismutase. 6. The apparent Km for NADPH obtained by the new method was almost the same as that by the authorized method (39.2 +/- 3.1 SD vs 36.8 +/- 1.6). Activation of neutrophil NADPH oxidase was characterized using the new assay method.

Cell Membrane↗