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Biomedical subjects

Tomoko Suzuki

Publications and source records attributed to Tomoko Suzuki.

49 records · Page 3Linked to original sources
PubMed2003

Geometrically selective synthesis of functionalized beta,beta-disubstituted vinylic sulfoxides by Cu-catalyzed conjugate addition of organozinc reagents to 1-alkynyl sulfoxides.

[reaction: see text] A new synthetic method of chiral beta,beta-disubstituted vinylic sulfoxides bearing various functionalities has been developed by employing Cu-catalyzed conjugate addition of an organozinc reagent to chiral 1-alkynyl sulfoxide. Since the reaction proceeds with very high syn-selectivity, both geometric beta,beta-disubstituted vinylic sulfoxides were stereoselectively synthesized by changing the combination of 1-alkynyl sulfoxide and the organozinc reagent.

Journal Article↗
PubMed2003

Why is otosclerosis of low prevalence in Japanese?

OBJECTIVE: This study aimed to clarify the reasons why clinical otosclerosis, a very common disease among Caucasians, is not prevalent among Japanese. STUDY DESIGN: The incidence, site, activity, and volume of otosclerotic foci were examined in 1011 temporal bone sections from 507 Japanese individuals. SETTING: This study was prepared at the temporal bone laboratory, Fukushima Medical University, Fukushima. RESULTS: Otosclerotic foci were observed in 2.56% of individuals and in 1.48% of the ears. The most common site of involvement was anterior to the oval window region, but this was only in 38.9% of the ears with otosclerotic foci. The otosclerotic foci were not involved in the stapediovestibular articulation or the endosteal layer of the otic capsule in any ears. An active change of the otosclerotic focus was seen in 33.3% of ears with otosclerosis. The volume of otosclerotic foci at the site anterior to the oval window region was less than 0.8 mm3 in 5 out of 7 ears. CONCLUSION: The incidence of histologic otosclerosis among Japanese seemed to be almost the same as that among Caucasians. Three reasons why clinical otosclerosis was not as prevalent among Japanese as among Caucasians are suggested: low incidence of involvement of foci anterior to the oval window, low activity, and small lesion without involvement of the footplate and/or membranous labyrinth of the inner ear.

Aged↗
PubMed2003

Retinoic acid inhibits elastase-induced injury in human lung epithelial cell lines.

The protective effects of retinoic acid on elastase-induced lung epithelial cell injury were studied using elastase extracted from purulent human sputum, the BEAS-2B human bronchial epithelial cell line, A549 human type II lung cell line, and primary cultures of human tracheal epithelial cells. Elastase decreased viability of BEAS-2B cells, A549 cells, and human tracheal epithelial cells in concentration- and time-dependent fashions. Elastase also induced apoptosis of BEAS-2B cells, A549 cells, and the tracheal epithelial cells detected with cell death detection enzyme-linked immunosorbent assay and terminal deoxyribonucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL) methods. Retinoic acid alone did not affect the viability of BEAS-2B cells, A549 cells, or the tracheal epithelial cells, and did not induce apoptosis of the cells. However, retinoic acid prevented the decreases in the viability and reduced apoptosis of BEAS-2B cells, A549 cells, and the tracheal epithelial cells induced by elastase. Likewise, retinoic acid inhibited caspase 3 activity in BEAS-2B cells and A549 cells induced by elastase, as well as proteolytic activity of elastase. Furthermore, caspase 3 inhibitor inhibited the elastase-induced apoptosis of the cells. These findings suggest that retinoic acid may inhibit elastase-induced lung epithelial cell injury partly through the inhibition of proteolytic activity of elastase and through the inhibition of caspase 3 activity by elastase. Retinoic acid may, therefore, have protective effects against the elastase-induced lung injury and subsequent development of pulmonary emphysema.

Apoptosis↗
PubMed2002

Cholinergic inhibition of electrogenic sodium absorption in the guinea pig distal colon.

Submucosal cholinergic and noncholinergic neurons in intestines have been shown to be involved in regulating epithelial transport functions, particularly stimulating Cl(-) secretion. This study investigates the role of submucosal cholinergic neurons in regulating electrogenic Na(+) absorption in distal colon. Amiloride-sensitive short-circuit current (I(sc)) and (22)Na(+) flux were measured in mucosal and mucosal-submucosal preparations mounted in Ussing chambers. In the mucosal preparation, carbachol (CCh) added to the serosal side inhibited amiloride-sensitive I(sc) and amiloride-sensitive (22)Na(+) absorption. The inhibitory effect of CCh was observed at approximately 0.1 microM, and maximum inhibition of approximately 70% was attained at approximately 30 microM (IC(50) = approximately 1 microM). CCh-induced inhibition of amiloride-sensitive I(sc) was almost totally abolished by 10 microM atropine. Treatment of the tissue with ionomycin markedly reduced amiloride-sensitive I(sc), but a subsequent addition of CCh further decreased it. Also, CCh still had an inhibitory effect, although significantly attenuated, after the tissue had been incubated with a low-Ca(2+) solution containing ionomycin and BAPTA-AM. Applying electrical field stimulation to submucosal neurons in the mucosal-submucosal preparation resulted in inhibition of amiloride-sensitive I(sc), approximately 33% of this inhibition being atropine sensitive. Physostigmine inhibited amiloride-sensitive I(sc), this effect being abolished by atropine. In conclusion, submucosal cholinergic and noncholinergic neurons were involved in inhibiting electrogenic Na(+) absorption in colon. This inhibition by cholinergic neurons was mediated by muscarinic receptor activation.

Acetylcholine↗
PubMed2002

Hypoxia diminishes toll-like receptor 4 expression through reactive oxygen species generated by mitochondria in endothelial cells.

Hypoxia and inflammation often occur simultaneously due to prevention of adequate gas exchange. Understanding the influence of hypoxia on the inflammatory response is important because hypoxia directly regulates expression of many genes, including those regulating inflammation, and plays a role in modulating the resolution of an inflammatory response. LPS is a major mediator of cellular injury and inflammation that induces its effects through Toll-like receptor 4 (TLR4). The aim of this study was to evaluate the effect of hypoxia on TLR4 expression. Hypoxia decreased TLR4 expression on cultured endothelial cells. Furthermore, LPS-induced ICAM-1 up-regulation was decreased by hypoxia. Because reactive oxygen species (ROS) generated from mitochondria are one of the signaling molecules induced by hypoxia, the role of ROS in hypoxia-induced TLR4 down-regulation was evaluated. Our data showed that hypoxia increased ROS generation and that hypoxia-induced TLR4 down-regulation was inhibited by myxothiazol, a mitochondrial site III electron transport inhibitor. Hypoxia also inhibited AP-1 translocation. Since the TLR4 promoter has a binding site for AP-1, hypoxia-induced TLR4 down-regulation may be due to an ROS-mediated decrease in AP-1-binding activity. We conclude that hypoxia decreases TLR4 expression in endothelial cells and that this change is mediated by mitochondrial ROS leading to attenuation of AP-1 transcriptional activity.

Cell Hypoxia↗
PubMed2002

Effects of rhinovirus infection on histamine and cytokine production by cell lines from human mast cells and basophils.

To understand the biochemical events that occur in the airways after rhinovirus (RV) infection, we developed for the first time a model in which the cell lines from human mast cells (HMC-1) and basophils (KU812) can be infected with RV14, a major group RV. Viral infection was confirmed by demonstrating that viral titers in culture supernatants, and RV RNA increased with time. RV14 infection alone and a combination of PMA plus calcium ionophore A23187, did not increase histamine production by these cells, although IgE plus anti-IgE increased the histamine production. However, histamine content in the supernatants increased in response to PMA plus A23187, or IgE plus anti-IgE after RV14 infection. PMA plus A23187 or IgE plus anti-IgE induced the production of IL-8 and GM-CSF in supernatants of HMC-1 cells and IL-4 and IL-6 in supernatants of KU812 cells. RV14 infection further increased the production of the cytokines, whereas RV14 infection alone did not alter the production of the cytokines by these cells. An Ab to ICAM-1 inhibited RV14 infection of the cells and decreased the production of cytokines and histamine after RV14 infection. RV14 infection enhanced the increases in intracellular calcium concentration and activation of NF-kappaB by PMA plus A23187 in the cells. These findings suggest that RV14 infection may prime the cytokine and histamine production from mast cells and basophils and may cause airway inflammation in asthma.

Basophils↗
PubMed2002

Erythromycin inhibits rhinovirus infection in cultured human tracheal epithelial cells.

To examine the effects of erythromycin on rhinovirus (RV) infection in airway epithelium, primary cultures of human tracheal epithelial cells were infected with the RV major subgroup, RV14, and the minor subgroup, RV2. Infection was confirmed by increases in viral RNA of the infected cells and viral titers of the supernatants. RV14 upregulated the expression of the mRNA and protein of intercellular adhesion molecule-1 (ICAM-1), the major RV receptor, and it increased the cytokine production. Erythromycin reduced the supernatant RV14 titers, RV14 RNA, the susceptibility to RV14 infection, and the production of ICAM-1 and cytokines. Erythromycin also reduced the supernatant RV2 titers, RV2 RNA, the susceptibility to RV2 infection, and cytokine production, although the inhibitory effects of erythromycin on the expression of the low-density lipoprotein receptor, the minor RV receptor, were small. Erythromycin reduced the nuclear factor-kappaB activation by RV14 and decreased the number of acidic endosomes in the epithelial cells. These results suggest that erythromycin inhibits infection by the major RV subgroup by reducing ICAM-1 and infection by both RV subgroups by blocking the RV RNA entry into the endosomes. Erythromycin may also modulate airway inflammation by reducing the production of proinflammatory cytokines and ICAM-1 induced by RV infection.

Anti-Bacterial Agents↗
PubMedDate not supplied

Efficacy of fluticasone propionate compared with beclomethasone dipropionate in bronchial asthma: improvement in compliance and symptoms by fluticasone.

Recent studies have shown that fluticasone propionate (FP) was more effective than beclomethasone dipropionate (BDP) inhalation even at a dose reduced by twofold or more in the treatment of bronchial asthma. Here, we further compared the effectiveness of FP and BDP, including rates of drug compliance. Forty-two symptomatic patients were treated by BDP (1000 +/- 345; mean +/- SD; microgram/day) for 8 weeks, followed by FP at one-half the respective dose, and peak expiratory flow and forced expiratory volume in 1 second were investigated. In addition, the patients were asked about drug compliance and factors related to compliance (expressed using a visual analogue scale). Significant increases of peak expiratory flow (from 316 +/- 96 L/minute to 345 +/- 86 L/minute) and forced expiratory volume in 1 second (from 1.7 +/- 0.5 L to 1.9 +/- 0.4 L) were found. Furthermore, significantly higher scores were obtained for compliance and various factors related to compliance. These data indicate that FP is more effective than a twofold higher dosage of BDP and that better compliance with the use of FP, probably because of improved various factors associated with FP compliance, contributes to FP efficacy.

Adult↗