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Biomedical subjects

A Terada

Publications and source records attributed to A Terada.

At least 19 recordsLinked to original sources

Enhancement of biofilm formation onto surface-modified hollow-fiber membranes and its application to a membrane-aerated biofilm reactor.

Surface-modified hollow-fiber membranes were prepared by radiation-induced grafting of an epoxy-group-containing monomer, glycidylmethacrylate (GMA), onto a polyethylene-based fiber (PE-fiber). The epoxy ring of GMA was opened by introduction of diethylamine (DEA). The bacterial adhesivity to this material (DEA-fiber) was tested by immersion into a nitrifying bacterial suspension. The initial adhesion rates and the amount of attached bacteria of the DEA-fiber were 6-10-fold and 3-fold greater than those of the PE fiber, respectively. A membrane-aerated biofilm reactor (MABR) composed of DEA fibers was developed for partial nitrification with nitrite accumulation. Prior to the nitrification test, it was confirmed that the oxygen supply rate (OSR) was proportional to air pressure up to 100 kPa, allowing easy control of oxygen supply. Stable nitrite accumulation was observed in the partial nitrification test at a fixed oxygen supply throughout the operation period, indicating that oxygen was consumed only by ammonia oxidizers. Furthermore, it was demonstrated that oxygen utilization efficiency (OUE) in the ammonia oxidation process was nearly 100% after 300 h incubation.

Ammonia↗

Exhaled nitric oxide decreases during exercise-induced bronchoconstriction in children with asthma.

Nitric oxide (NO) produced in the airways can be either detrimental or protective to the host. To investigate the role of NO in the pathogenesis of exercise-induced bronchoconstriction (EIB), we measured exhaled NO (ENO) after exercise challenge in 39 asthmatic and six normal children. FEV(1) and ENO were measured before and at 0, 5, 10, and 15 min after exercise performed on a treadmill for 6 min. EIB was defined as a decrease in FEV(1) of more than 15% after the exercise. Normal children (control group) did not have EIB. Twenty-one patients with asthma had EIB (EIB group) whereas the remaining 18 patients did not (non-EIB group). The baseline ENO value was significantly higher in the asthmatic children than in the normal children, and there was a positive correlation between the maximal percent decrease in FEV(1) and the baseline ENO value (r = 0.501, p = 0.012). At the end of the exercise, ENO had decreased in all the subjects. In the non-EIB and control groups, ENO rebounded to above the baseline at 5 min after the exercise and thereafter. In contrast, ENO remained at a decreased level in the EIB group. The change in ENO did not correlate with the change in minute ventilation, and beta-agonist inhalation at the peak of EIB that accelerated the recovery of FEV(1) did not affect the depressed level of ENO, demonstrating that the reduction of ENO is not a simple consequence of increased ventilation nor airway obstruction. Among the EIB group, steroid-treated patients showed sooner recovery in ENO after the exercise than steroid-naive patients. Our study suggests that NO production in response to exercise may be impaired in patients with EIB, and that ENO represents not only airway inflammation but also a protective function of NO in EIB.

Administration, Inhalation↗

Chemokine production by the BEAS-2B human bronchial epithelial cells: differential regulation of eotaxin, IL-8, and RANTES by TH2- and TH1-derived cytokines.

BACKGROUND: Bronchial epithelial cells produce many types of chemokines and may contribute to lung inflammation by recruiting inflammatory cells. The CC chemokine eotaxin is a potent, eosinophil-specific chemoattractant that has been detected in the bronchial epithelium of patients with asthma. OBJECTIVES: The aim of this study was to investigate the regulatory mechanisms of chemokine production from bronchial epithelium by inflammatory cytokines, especially T(H)2- and T(H)1-derived cytokines, in bronchial asthma. METHODS: BEAS-2B human bronchial epithelial cells were cultured with TNF-alpha, IL-4, IL-13, and IFN-gamma alone or in combination, after which supernatants were assayed for eotaxin, IL-8, and RANTES proteins with ELISA. Reverse transcription-PCR was also performed. RESULTS: TNF-alpha induced production of eotaxin, IL-8, and RANTES in a concentration-dependent manner. Both IL-4 and IL-13 synergistically enhanced TNF-alpha-induced eotaxin production, whereas IL-8 production induced by TNF-alpha was significantly down-regulated by the T(H)2-derived cytokines. IFN-gamma, a T(H)1 cytokine, counteracted the enhancing effects of IL-4 and IL-13 on eotaxin production. RANTES production by TNF-alpha was not affected by IL-4 and IL-13 but was markedly enhanced by IFN-gamma. CONCLUSIONS: These results suggest that T(H)2 cytokines are involved in preferential recruitment of eosinophils in bronchial asthma by enhancing eotaxin and reducing IL-8 production from bronchial epithelial cells and that T(H)1 cytokines counteract the effects of T(H)2 cytokines by reducing eotaxin production.

Bronchi↗

Chemokines induce eosinophil degranulation through CCR-3.

BACKGROUND: Such CC chemokines as eotaxin and RANTES induce preferential eosinophil recruitment in allergic inflammation. They also elicit proinflammatory effector functions of eosinophils, such as enhanced adhesion and superoxide generation. Eosinophil degranulation by chemokines, however, has not been studied in detail. OBJECTIVE: The purpose of this study was to identify chemokines and their corresponding receptors that induce eosinophil degranulation by using a panel of chemokines and blocking antibodies to candidate receptors. METHODS: Highly purified eosinophils were preloaded with Fura-2 and stimulated with a panel of chemokine ligands for 14 known chemokine receptors: CCR1 to CCR8, CXCR1 to CXCR4, CX3CR1, and XCR1. Calcium influx was measured with fluorescence spectrometry. Eosinophils were also stimulated with the chemokines in the presence or absence of IL-5, and levels of eosinophil-derived neurotoxin were measured in the supernatant with RIA. Specific antibodies to chemokine receptors were used to block degranulation. RESULTS: Calcium influx was induced by monocyte chemotactic protein (MCP) 1, MCP-3, MCP-4, RANTES, eotaxin, IL-8, and stromal cell-derived factor 1alpha, which are chemokines that bind several chemokine receptors. However, degranulation was induced only by CCR3 ligands, including MCP-3, MCP-4, RANTES, and eotaxin. Priming of eosinophils with IL-5 enhanced CCR3 ligand-induced degranulation but did not cause non-CCR3 ligands to induce eosinophil-derived neurotoxin release. An antibody against CCR3 significantly inhibited degranulation induced by CCR3 ligands, eotaxin, or RANTES. CONCLUSION: These results suggest that chemokine-induced eosinophil degranulation, a major effector of eosinophil functions, is mediated through only CCR3, although some non-CCR3 ligands induce calcium influx in eosinophils. CCR3 may be an important target in the treatment of eosinophilic inflammation.

Calcium↗

Age affects hibernation in Syrian hamsters (Mesocricetus auratus).

In this study, we aimed to show how age affects hibernation in the Syrian hamster. Experimentally, we used 30 male animals differing in age. The old animals were 20 months of age and the adults were 8 months of age at the end of the test. The young animals were 3 weeks old at the start of testing and 5 months old at the end of the testing period. The torpor observation started October 15, 1996, and ended March 11, 1997, in the laboratory colony maintained under natural photoperiod and outdoor air. Observations were performed around noon daily. Three measures (i.e., prehibernation period [hibernation latency], proportion of hibernation spent in torpor, and proportion of animals in torpor), all of which reflect the strength of occurrence of hibernation, indicated that the older hamsters (1) started hibernation earlier, (2) spent more time in torpor, and (3) had a higher chance of being in torpor than the younger ones during the hibernation season.

Aging↗

Prevention of nephrotoxicity of cisplatin by repeated oral administration of ebselen in rats.

The ability of ebselen, which exhibits glutathione peroxidase (GSH-Px)-like activity, to prevent cisplatin (CDDP)-induced nephrotoxicity was examined in rats. CDDP (6 mg/kg [20 micromol/kg] body weight) was injected intraperitoneally. In subgroups, daily ebselen doses of 2.75 (10 micromol), 5.5 (20 micromol), or 11.0 mg (40 micromol)/kg body weight were administrated orally 1 hour prior to CDDP treatment. Treatment with CDDP alone resulted in significantly increased plasma creatinine (Cr) and blood urea nitrogen (BUN) levels. Repeated administration of 5.5 and 11.0 mg/kg ebselen prevented the CDDP-induced elevation of plasma Cr and BUN levels and protected against kidney damage. Relative to controls, rat that received CDDP treatment displayed a decreased ratio of reduced glutathione (GSH) to oxidized glutathione (GSSG), an indicator directly related to oxidative stress, and elevated malondialdehyde (MDA) levels in the kidney. In comparison with controls, activity of GSH-Px activity, which antioxidant enzyme, was also reduced in the kidney of rats treated with CDDP. Repeated administration of 5.5 or 11.0 mg/kg ebselen prevented CDDP-induced alteration of GSH/GSSG ratios, MDA levels, and GSH-Px activity; however, no protection against CDDP was observed with administration of 2.75 mg/kg ebselen. Effective protection of CDDP-induced nephrotoxicity with ebselen was observed only when the molar amount of each daily ebselen treatment equaled or exceeded

Administration, Oral↗

[Distribution of intraglandular metastatic foci in the contralateral lobe of papillary thyroid carcinoma].

The distribution of metastatic foci in the opposite lobe has not been studied in detail despite of several reports on the high incidence of contralateral metastasis. Whether foci spread to the upper one-third of the contralateral lobe influences the choice of total or subtotal thyroidectomy. Metastasis was studied in 66 patients 11 men and 55 women aged 24-73 years (mean; 51.3), undergoing primary total thyroidectomy from 1988 to 1996. Serial blocks of the opposite lobe, approximately 5 mm thick were sliced and stained by hematoxylin-eosin. Metastases were found in 44 patients (67%). Based on the size of the primary focus, these patients were divided into group A (smaller than one-third of the lobe) and group B (greater than that of group A). The average size of the primary focus was 21 mm in group A and 36 mm in group B. The contralateral metastatic rate was 64% (14/22) in group A and 68% (30/44) in group B. The distribution of metastatic foci in the opposite lobe was studied in 44 positive patients. The spread to the upper one third occurred in 61% (27/44); 29% (4/14) in group A and 76% (23/30) in group B a significant difference (p < .003). We thus concluded that the larger the primary focus, the wider the spread of metastatic foci to the opposite lobe.

Adult↗

[Japanese cedar pollinosis in infants in the allergy clinic].

Recently, the number of patients with Japanese cedar (Cryptomeria japonica) pollinosis has increased, especially in children. However, little is known about the incidence in infants. We studied on the rate of sensitization and the onset of pollinosis in children under 6 years old. The percentage of positive CAP-RAST to Japanese cedar pollen was 27.6%, in 76 infants (51 male and 25 female, 2 months-5 years old) who visited National Mie Hospital pediatric allergy clinic due to bronchial asthma and/or atopic dermatitis. The youngest child who has been sensitized to pollen was 1 year 8 month old boy. The percentage of positive rate of CAP-RAST to house dust mite was 61.8%. Twenty-seven infants (20 male and 7 female, 2-5 years of age) were diagnosed as Japanese cedar pollinosis in National Mie Hospital Otorhinolaryngology clinic in 1999 and 2000. The youngest child with pollinosis was 2 year 5 month old boy. Most of the 27 infants complained of rhinorrhea and/or eye symptoms and some of them complained cough, snoring, or epistaxis. About 40% were sensitized to Japanese cedar and/or cupressaceae pollen alone, 60% were also sensitized to house dust mite. In conclusion, it is possible that the sensitization to Japanese cedar pollen occurs after 2 season of pollen exposure and pollinosis occurs in 2 years old. Japanese cedar pollen has been an important allergen not only in school children, but also in infants.

Ambulatory Care↗

Active oxygen species generation and cellular damage by additives of parenteral preparations: selenium and sulfhydryl compounds.

We investigated the relationship between active oxygen species (AOS) generation and cultured vascular endothelial cellular damage caused by simultaneous exposure to selenium compounds and sulfhydryl compounds such as cysteine (Cys) or reduced glutathione (GSH). Selenium compounds, selenite, selenate or selenomethionine (SeMet), are added to total parenteral nutrition (TPN) and intravenously administered. We confirmed by luminol dependent chemiluminescence, an indicator of AOS generation, that selenite generates AOS in the presence of clinical concentrations of sulfhydryl compounds, 0.5 mM Cys or 0.5 mM GSH, and that the amount of AOS generated reaches the maximum when their mole ratio is 1:50. However, AOS generation was not observed after simultaneous administration of various concentrations of selenate or SeMet with sulfhydryl compounds. Moreover, simultaneous exposure to 10 microM selenite and sulfhydryl compounds was found to result in significant increases in the [3H]-adenine and lactate dehydrogenase (LDH) release rates from cells, a significant decrease in the amount of cellular protein, and enhancement of cellular damage as compared with after exposure to selenite alone. However, simultaneous exposure to 10 microM selenate or 10 microM SeMet together with sulfhydryl compounds did not induce cellular damage. These findings revealed that selenite generates AOS and causes cellular damage in the presence of sulfhydryl compounds. Accordingly, it seems better to choose selenate or SeMet instead of selenite when a selenium compound is to be added to TPN.

Adenine↗

Effects of intestinal bacteria on the development of colonic neoplasm: an experimental study.

Effects of intestinal microflora on the development of colonic neoplasm induced by 1,2-dimethylhydrazine (DMH) were observed using conventionalized and gnotobiotic mouse models. The incidence of colonic adenoma in germ-free mice (IQI/jic) (GF), mice conventionalized after DMH injection (Cvz-post-DMH) and conventionalized mice (Cvz, conventionalized before DMH injection) was 74%, 69% and 58%, respectively. The mean number of adenomas per mouse in the three groups was 2.6, 2.0 and 1.4, respectively. However, the adenoma in Cvz was larger than in GF. The incidence of adenoma in mice mono-associated with Mitsuokella multiacida, Clostridium butyricum, Bifidobacterium longum, Clostridium paraputrificum, Escherichia coli and Lactobacillus acidophilus was 68%, 68%, 63%, 50%, 50% and 30%, respectively. However, the adenoma in the Cl. paraputrificum group and the Cl. butyricum group was larger than in GF. Faecal pH in Cvz and the L. acidophilus group was significantly lower than in GF. The deconjugation rate of faecal bile acids in Cvz, the Cl. paraputrificum group and the Cl. butyricum group was significantly higher than in GF. These findings suggested two different effects of microflora on the development of DMH-induced adenoma: either an inhibition of the incidence of adenoma or a promotion of tumour growth. Effects of L. acidophilus may be mediated by faecal pH and effects of Cl. paraputrificum and Cl. butyricum by deconjugated bile acids.

1,2-Dimethylhydrazine↗

Mechanisms of eosinophil cationic protein release in the serum: role of adhesion molecules.

BACKGROUND: Measurement of eosinophil cationic protein (ECP) in serum has been utilized as a marker for allergic inflammation. The serum level of ECP represents the level found in vivo plus additional proteins released in vitro from peripheral blood eosinophils during the coagulation period. The mechanisms of release, however, are unclear. We investigated a possible involvement of adhesion molecules in the ECP release. MATERIALS AND METHODS: Venous blood was drawn in the presence of EDTA from allergic donors. The blood was incubated with neutralizing monoclonal antibodies to CD18, CD11a, CD11b, CD29, CD49d, CD54, alpha4beta7, or isotype-matched control antibodies, respectively, at 4 degrees C for 30 min. Calcium gluconate (calcium) was then added to induce coagulation. The blood was further incubated for 90 min and centrifuged to obtain the serum. ECP in the serum was measured with RIA. In some experiments, purified eosinophils were incubated with plasma and calcium, then ECP in the supernatants was assayed. RESULTS: ECP in the samples with calcium was significantly higher than in those without calcium. Purified eosinophils released ECP upon plasma coagulation. Anti-CD18, CD49d, and alpha4beta7 antibodies significantly suppressed ECP levels in the serum. CONCLUSIONS: These results suggest that ECP release in the serum is calcium and plasma coagulation-dependent and that cell adhesion through alphaLbeta2, alphaMbeta2, alpha4beta1 and alpha4beta7 integrins is at least in part responsible for ECP release.

Antigens, CD↗

Matrix metalloproteinase-9 in peripheral blood eosinophils.

BACKGROUND: Matrix metalloproteinases (MMPs) are major contributors to tumor invasion, remodeling of connective tissue and infiltration of inflammatory cells and may be important mediators in developing allergic inflammation. Overexpression of MMP-9 mRNA by eosinophils in the asthmatic airways has been reported. To clarify the relative significance of MMP as an inflammatory mediator from eosinophils, we determined the content of MMP-9 in the peripheral blood eosinophils and compared it with the other leukocyte fractions. METHODS: Peripheral blood eosinophils, neutrophils, and mononuclear cells were purified from normal and allergic donors with Percoll gradient centrifugation and CD16 negative selection. Cell lysate and culture supernatants stimulated with IL-5, PAF, and PMA were tested for MMP-9 with gelatin zymography and ELISA. RESULTS: The amount of MMP-9 in highly purified eosinophils, neutrophils, and mononuclear cells was 2.5 +/- 0.9, 4,073 +/- 581, and 7.6 +/- 1.4 ng/5 x 10(6) cells, respectively. There was no difference in MMP-9 content of eosinophils between normal donors and patients with asthma. Culture of peripheral blood eosinophils with IL-5 for 4 days did not induce MMP-9 production. The stimulation of eosinophils with PMA and other secretogogues caused only small amounts of MMP-9 secretion as compared with neutrophils. CONCLUSIONS: These findings suggest that circulating eosinophils normally have only small amounts of MMP-9 and that eosinophils may need complex activation signals to produce significant amounts of MMP as seen in tissues of allergic inflammation.

Asthma↗

DT-diaphorase-like quinone reductase in rat plasma.

The present study provides the evidence that DT-diaphorase-like quinone reductase exists in rat plasma. The quinone reductase activity toward menadione was found in rat plasma in the presence of NADH or NADPH. The enzyme activity was induced by pretreatment with 3-methylcholanthrene, but was not affected by phenobarbital. The 3-methylcholanthrene-induced quinone reductase activity was separated into three fractions (F1, F2, and F3) by gel filtration, which showed NAD(P)H-linked, NADH-linked, and NAD(P)H-linked activities, respectively. F1, which was induced by 3-methylcholanthrene, was inhibited by dicumarol, and cross-reacted with rat liver DT-diaphorase antibody.

Animals↗

[Exhaled nitric oxide of childhood asthma].

Chronic airway inflammation is a central feature of pathology of bronchial asthma. In order to evaluate inflammatory status in asthma, examinations such as bronchoscope or induced sputum test can be done. Because of difficulty of those examinations we need non-invasive and simple measures for childhood asthma. Here we investigated eNO in childhood asthma. Twenty-six of atopic asthma, 13 non-asthmatic atopic children and 12 normal children were enrolled in this study. eNO was measured by chemiluminescence analyzer. eNO was significantly collerated with % FEV 1.0 and blood eosinophil counts (R = -0.494, R = 0.416, respectively). Geometrical mean of eNO in normal, non-asthmatic atopic, asthma without inhaled corticosteroid (ICS) and asthma with ICS was 16.3, 23.7, 71.6, 43.6 ppb, respectively. eNO was significantly higher in asthma than in normals. eNO in patients without ICS were significantly higher than in non-asthmatic atopic. We concluded that eNO might be useful marker for evaluation of airway inflammation in asthmatic children.

Asthma↗

Effect of a probiotic formula on intestinal immunoglobulin A production in healthy children.

The anti-infectious effect of probiotics has recently been reported and one mechanism may be the non-specific stimulation of immunity. This study was performed to elucidate the influence of a probiotic formula on intestinal microflora and local immunity in healthy children. A follow-up formula containing viable bifidobacteria was given to seven healthy Japanese children (15 to 31 months old) for 21 days. During intake of the formula, the administered strain was detected in feces from five subjects (71%) and total fecal bifidobacteria slightly increased. Fecal levels of total IgA and anti-poliovirus IgA during intake of the formula were significantly higher than those before intake (P < 0.05). The increase in local IgA levels resulting from ingestion of the probiotic formula may contribute to enhancement of the mucosal resistance against gastrointestinal infections.

Antibodies, Viral↗

Effects of high-lipase pancreatin on fecal fat, neutral sterol, bile acid, and short-chain fatty acid excretion in patients with pancreatic insufficiency resulting from chronic pancreatitis.

CONCLUSIONS: Steatorrhea was almost completely stopped and malabsorption of neutral sterols and short-chain fatty acids was reduced by treatment of high-lipase pancreatin in Japanese patients with pancreatic insufficiency whose dietary fat consumption is low. METHODS: Fifteen patients with chronic pancreatitis complicated by steatorrhea who consumed an average of 48 g of dietary fats a day were selected as subjects and given 3 g of high-lipase pancreatin (lipase, 379,800 USP U/g), at each meal (total daily dose is 9 g) for a mean duration of 28.5 d. Fecal output and fecal fat neutral sterol, bile acid, and short-chain fatty acid excretion were determined before and after the course of pancreatin therapy. RESULTS: Pancreatin administration resulted in significant reductions (P < 0.01) in fecal output (from 243.2 to 149.1 g), excretion of fecal fat, (from 12.3 to 3.9 g), animal sterols (from 816.3 to 604.6 mg), and short-chain fatty acids (from 52.6 to 18.5 mM). In contrast, no marked changes were recorded in fecal excretion of beta-sitosterol (a plant sterol), bile acids, or the hydroxy fatty acid fraction. Fecal fat and short-chain fatty-acid excretion showed strong correlations with fecal output.

Adult↗

Clinical utility of serum levels of eosinophil cationic protein (ECP) for monitoring and predicting clinical course in childhood asthma.

BACKGROUND: The concentration of ECP in serum has been proposed as a marker of airway inflammation in asthma. However, its clinical significance is still to be determined. OBJECTIVES: This study was performed to determine whether concentration of ECP in serum reflects clinical status in asthma and can serve as a predictive parameter. METHODS: Cross-sectional analysis was performed in 28 children with asthma. A total of 91 blood samples was obtained to determine levels of ECP in serum and eosinophil counts. Forced expiratory volume in 1 s was also determined at the time of the sampling. Data were analysed on the basis of asthma symptoms in the 4 weeks before and the 4 weeks after sampling. RESULTS: Serum levels of ECP were significantly lower in patients who had been asymptomatic for 3 or 4 weeks before sampling than in patients who had been symptomatic or asymptomatic for only 1 or 2 weeks. In the former group, serum levels of ECP were higher when patients became symptomatic after sampling than when they remained stable, a finding that suggests that serum levels of ECP may have a predictive value in certain situations. Although the concentration of ECP in serum was not proved to be predictive in the latter symptomatic group, the concentration of ECP was significantly lower when measured again 4 weeks later when the patients' symptoms had resolved. In contrast, levels of ECP were unchanged when patients remained symptomatic, a finding that suggests serum levels of ECP may reflect the clinical response to therapy. CONCLUSIONS: Serum ECP may be a useful marker for monitoring and predicting the clinical course in asthma.

Adolescent↗