Notes: LO phonon-overdamped plasmon coupled modes in n-type epitaxial films of β-SiC have been measured in the carrier concentration range from 6.9×1016 to 2×1018 cm−3. The carrier concentrations and damping constants are determined by line-shape fitting of the coupled modes and compared with the values derived from Hall measurements. The concentrations obtained from the two methods agree fairly well. The Faust–Henry coefficient determined from the fitting is 0.35. The line-shape analysis of the coupled mode has shown that the dominant scattering mechanisms in β-SiC are deformation-potential and electro-optic mechanisms.

Notes: The temperature dependence of the band gap in InAsyP1−y (y=0–0.67) has been determined by photoluminescence, x-ray diffraction, and absorption spectra measurements. We found that the measured data within the temperature range of 77–300 K can be expressed by the equation proposed by O'Donnell and Chen. The band gap at 77 K is given by Eg=1.407−1.073y+0.089y2, while the compositional dependence of the band gap observed at 300 K, agrees with the values previously reported. We confirmed that changes in temperature caused a slight change in the bowing parameters, and hence found that the band gap temperature dependence of InAsyP1−y (y=0–1) varies very little with changes in composition (2.5–3.5×10−4 eV/K). © 2000 American Institute of Physics.

Notes: Effects of substance P on cultured neurons of the locus coeruleus of the rat were studied using the whole-cell patch clamp technique. In some cells substance P produced a decrease in a K conductance which showed an inwardly rectifying property. In other cells substance P produced an initial inward current which was accompanied by a conductance increase. The rest of the cells showed responses which were mixtures of the above two responses. The measurement of the reversal potential of the initial inward current after suppressing the voltage-gated Ca and K conductances suggests that it is caused by an increase in a non-selective ionic conductance. In cells loaded with 260 μM GTPγS, application of substance P produced an irreversible reduction of the K conductance, while the initial inward current could still be recorded, suggesting that the former is mediated by a G protein, whereas the latter may be activated by a different signal transduction mechanism. The initial inward current was not eliminated by external application of high concentrations of tetrodotoxin, d-tubocurarine or amiloride. Nor was it affected by the intracellular application of cyclic GMP or cyclic AMP.

Notes: Lesions of trachea cuticles are a pathological histological characteristic of bronchial asthma. Furthermore, collected tracheal cuticles desquamated from the respiratory tract are found in patients’ sputum when asthma attacks occur or after the induction of allergen inhalation. From these facts, it is assumed that desquamation of trachea cuticle cells is a pathological symptom of bronchial asthma. However, there has not been any chronological report of desquamation of trachea cuticles through the process of bronchial asthma attacks.For this report, we made an experimental bronchial asthma model using guinea pigs, and conducted chronological examinations of trachea cuticle lesions related to pathological symptoms of bronchial asthma using a transmission electron microscope and a scanning electron microscope.The experimental asthma models were made by injection of ovalbumin into the abdominal cavity of guinea pigs. Then the airway responses to inhaled aerosolized ovalbumin were induced. The trachea were enucleated and examined under an optical microscope, a transmission electron microscope (hereafter abbreviated as TEM), and a scanning electron microscope (hereafter abbreviated as SEM) after 1, 2, 4, 8, 12, 24 h and 7 days after the immediate airway responses.Intercellular oedema of ciliated epithelium was observed in the sensitization groups immediately after the immediate airway response. SEM observation revealed increased mucus secretion and shortening of cilium. A slight case of desquamation or deciduation of ciliated epithelium was also beginning to appear. TEM observation revealed a dilation of ciliated epithelium intervals. Infiltration of eosinophilic leucocytes was already detectable beneath the ciliated epithelium. The degree of ciliated epithelium desquamation and infiltration of eosinophilic leucocytes progressed with time. When the late airway response occurred 4 hours later, eosinophilic leucocytes had increased drastically, and ciliate epithelium had desquamated to the extent that basal cells were exposed. Seven days after the immediate airway response, epithelium intercellular oedema had improved, and cilium had been reproduced.These results suggest that desquamation of epithelium caused by trachea cuticle lesions appears at an early stage of an asthma attack, owing to the contraction of the trachea, and that the damage is intensified by the infiltration of eosinophilic leucocytes.

Notes: Background Oral leukotriene receptor antagonists have been shown to have efficacy in chronic asthma.Objective To determine whether the addition of montelukast could lead to a reduction in inhaled corticosteroid dose without a significant decrease in peak expiratory flow rate (PEFR).Methods After a 4-week run-in period, 191 moderate-to-severe asthmatic patients whose asthma had been well controlled with daily inhaled corticosteroid therapy (beclometasone dipropionate 800 to 1600 µg/day), were randomly assigned to one of two treatments – placebo (n = 98) or montelukast 10 mg once daily (n = 93) – for a 24-week, multicentre, double-blind, treatment period. At the beginning of the active treatment period, the daily dose of inhaled corticosteroid was halved in all of the patients. In addition, the inhaled corticosteroid dose was subsequently titrated every 8 weeks, based on PEFR, asthma symptoms and β-agonist use.Results After 8 weeks of a 50% reduction in inhaled corticosteroid use, morning PEFR increased by 5.3 ± 32.3 L/min from baseline in patients receiving montelukast and significantly decreased by 6.9 ± 29.0 L/min in those receiving placebo (P = 0.035). In addition, evening PEFR significantly decreased by 9.8 ± 28.5 L/min (P = 0.003) in the placebo group, but was maintained in the montelukast group. In spite of a subsequent 50% reduction in the inhaled corticosteroid dose every 8 weeks, morning and evening PEFRs were maintained over the 24-week treatment period in the montelukast group; PEFR significantly decreased in the placebo group. There was a significant difference between the two groups with regard to morning PEFR, therapy score and asthmatic score at weeks 8, 16 and 24, as well as evening PEFR at week 8. However, the symptom scores were not significantly different between the two groups or within each group.Conclusion These data suggest that montelukast reduces the need for inhaled corticosteroids while maintaining asthma control over a 24-week period. Therefore, montelukast may be useful for long-term treatment in patients with asthma who require high doses of inhaled corticosteroids.

Notes: Background TMK688 is being developed as ati anti-allergic drug having both 5-lipoxygenasc inhibitory activity atid anti-histaminc activity.Method We compared the inhibition ol the late asthmatic rcsponses by TMK688 with that by other anti-allergic agents in actively sensitized guinea pigs, and examined the relationship between 5-lipoxygetiase inhibition and the late asthmatic responsesResults At 1–3.2 mg/kg, TMK688 inhibited the increases in respiratory resistance, leukotriene (LT) B4 and C4 production in the lungs and eosinophil infiltralion into the alveoli during the late asthmatic response, whereas the eliects tended to lessen at the dose of 10mg/kg. These effects are thought to be caused by the 5-lipoxygenase inhibitory activity of TMK688 because Azelastine. an anti-allergic drug having potent antihistamine activity, exhibited no effect. ONO-1078. a peptide LT antagonist. inhibited the late-phase bronchoconstriction at a dose of 100mg/kg p.o., but not the increase in the infiltration of inflammatory cells into the alveoli, suggesting that the late-phase bronchoconstriction is induced, in part, by peptide LTs, i.e. LT C4, D4 and E4 atid that the inflammatory cell infiltration may be caused by LTB4, TMK688 inhibited the immediate bronchoconstriction dose-dependently, and the effect was significant at a dose of 10mg/kg orally. Since Azelastine, Ketotifen and Oxatomide suppressed the bronchoconstriction at far lower doses than did TMK688, the inhibitory effect was mainly caused by its antihistamine activity.Conclusions TMK688 appears to be a novel anti-allergic drug having inhibitory effects on both the bronchoconstriction and the infiltration of inflatnmutory cells during late asthmatic responses.

Notes: Background: In Japan in 1993, the Japanese Society of Allergology (JSA) developed guidelines for diagnosis and management of asthma (JGL), which were based on the concept that asthma is a chronic inflammatory disorder of the airway. Methods: This survey study was intended to investigate the recognition and utilization of JGL among physicians who had treated asthma. The survey comprised two methods: a quantitative mail survey and a qualitative door-to-door survey conducted by trained interviewers. Results: In the mail survey, a total of 1028 physicians responded; 552 members of the JSA and 476 nonmembers. Ninety-four percent of JSA members were aware of adult asthma management guidelines, while 53 nonmembers were aware of them. Although approximately half of the physicians, both member and nonmember, found differences between the asthma management policies in JGL and their previous policies, most of them utilized JGL, once they read it. In the qualitative door-to-door survey, 80–90% of physicians evaluated JGL as good after they read it. Conclusions: JGL was recognized and utilized by most JSA members, but only half of nonmember physicians were aware of JGL, although they utilized JGL after they read it. Further action to implement JGL among nonspecialist physicians is needed to improve management of asthma.

Notes: Background : As chronic atrophic gastritis is a precancerous condition for gastric cancer and the eradication of Helicobacter pylori infection halts chronic gastritis, eradication of infection may prevent gastric cancer. However, as chronic atrophic gastritis is a risk factor for reflux oesophagitis after eradication of infection, the risk of oesophageal adenocarcinoma may also increase.Methods : We systematically reviewed papers and estimated the expected annual incidence of oesophageal or gastric cancer with and without eradication of H. pylori infection in patients with chronic atrophic gastritis.Results : The expected annual incidence of gastric cancer in patients with corpus atrophy with persistent infection was at least 5.8-fold higher than that for oesophageal adenocarcinoma after the eradication of infection at all ages. Even for patients with accompanying reflux oesophagitis or Barrett's oesophagus, the expected incidence of either gastric or oesophageal adenocarcinoma with persistent infection was higher than that of oesophageal adenocarcinoma after eradication of infection.Conclusion : If eradication of infection lowers the incidence of gastric cancer, it should be recommended for patients with corpus atrophy at all ages irrespective of the presence of reflux oesophagitis or Barrett's oesophagus, especially in populations having a high prevalence of gastric cancer.