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Notes: Luminescence spectra and their variation with temperature have been investigated for solid films of poly(methylphenylsilane) and its branched analogs. Introduction of branching points to the polymers enhances the broad luminescence band in the visible region while suppressing the sharp UV luminescence band due to the resonant recombination of the exciton. The intensity of the visible luminescence is observed to keep on increasing with decreasing temperature in contrast with the nearly temperature-independent intensity of the resonant luminescence. The behavior is interpreted in terms of phonon-assisted tunneling between luminescence centers and nonradiative ones. © 1995 American Institute of Physics.

Notes: Optical properties of silicon- and germanium-based network copolymers, [Si(C6H13)]1−x- [Ge(C6H13) ]x, have been investigated for various Si/Ge compositions (x). The backbone Si/Ge atoms are coordinated by the three other Si/Ge backbone atoms in the polymers. These Si/Ge copolymers show the absorption spectra which are typical of amorphous semiconductors. Their color continuously traverses the visible range with x, which is due to the change of the band gap (Tauc gap) energy as well as to the presence of localized subgap states. The Si/Ge copolymer shows a broad band of luminescence in the visible region. The luminescence band maximum was observed to shift by ∼0.5 eV with change of the Si/Ge ratio.

Notes: Increased sensitivity of cough reflex is a fundamental feature of bronchodilator resistant non-productive cough associated with eosinophilic tracheobronchitis. Our hypothesis is that cough sensitivity is increased by airway allergic reaction characterized by airway eosinophilic inflammation. The aim of this study was to elucidate the hypothesis and clarify the characteristics of the increased cough sensitivity.Number of coughs elicited by inhalation of increasing concentrations of capsaicin (10−8, 10−6 and 10−4 m) was counted 24 h after an aerosolized antigen or saline in actively sensitized or non-sensitized (naive) conscious guinea pigs and then bronchoalveolar lavage was performed. The cough response was also measured 1 day before and 1, 2, 3, 5 and 7 days after an aerosolized antigen challenge in sensitized or naive animals. In addition, effect of procaterol (0.1 mg/kg), atropine (1 or 10 mg/kg), phosphoramidon (2.5 mg/kg) given intraperitoneally 30 min before the capsaicin challenge or capsaicin desensitization on the cough response was examined. Furthermore, the thromboxane A2 (TXA2) receptor antagonist S-1452 in a dose of 0.01 or 0.1 mg/kg or vehicle (saline) was given intraperitoneally at 24 and 1 h before the measurement of cough response.Number of coughs caused by capsaicin was extremely increased 24 h after an antigen challenge in sensitized guinea pigs compared with a saline or an antigen challenge in naive animals or a saline challenge in sensitized animals. The increased cough response disappeared at 3–7 days after the antigen challenge. Eosinophils in bronchoalveolar lavage fluid obtained after the measurement of capsaicin-induced coughs, which was performed 24 h after the antigen challenge, were significantly increased in sensitized guinea pigs. The eosinophil count was significantly correlated to the number of capsaicin-induced coughs. Procaterol or atropine did not alter the antigen-induced increase of cough sensitivity, whereas atropine did reduce the cough response in naive animals. Phosphoramidon increased the number of capsaicin-induced coughs in naive guinea pigs but not in sensitized and antigen-challenged animals. Capsaicin desensitization decreased the cough response in both antigen-challenged sensitized guinea pigs and naive animals. S-1452 reduced the antigen-induced increase of cough response in sensitized guinea pigs, but not in naive animals.Airway allergy accompanied with airway eosinophilia induces transient increase in cough sensitivity, which is not mediated by bronchoconstriction. The increased cough sensitivity may result in part from inactivation of neutral endopeptidase and TXA2, one of the inflammatory mediators.

Notes: Background Cough receptor hypersensitivity is a fundamental feature of some conditions presenting with chronic non-productive cough. Suplatast tosilate, an anti-allergic agent, is a T helper (Th)2 cytokine inhibitor that inhibits the synthesis of interleukin (IL)-4, IL-5, immunoglobulin (Ig)E production, and local eosinophil accumulation.Objective The purpose of this study was to investigate the effect of suplatast on antigen-induced airway cough hypersensitivity and eosinophil infiltration into the airway.Methods Number of coughs elicited by inhalation of increasing concentrations of capsaicin (10−8, 10−6 and 10−4 M) was counted 24 h after an antigen challenge in conscious guinea-pigs and then bronchoalveolar lavage was performed. We investigated the effect of single (before antigen challenge or capsaicin provocation) or repetitive treatment with intraperitoneal suplatast at a dose of 10 or 30 mg/kg on antigen-induced cough hypersensitivity.Results Twenty-four hours after antigen challenge, guinea-pigs developed an increase in cough receptor sensitivity to inhaled capsaicin and eosinophil infiltration in the airways. After a 2-week treatment with suplatast, but not after only a single treatment before antigen challenge or capsaicin provocation, the antigen-induced early phase bronchoconstriction, cough hypersensitivity, and airway eosinophilia were inhibited in a dose-dependent manner.Conclusion These results indicate that suplatast inhibits airway cough hypersensitivity underlying allergic eosinophilic inflammation.

Notes: Background We previously reported that inhaled acetaldehyde, a metabolite of ethanol atid a maiti factor in alcohol-induced asthma, causes bronchial hyper-responsiveness (BHR) in asthmatics. However, the mechanisms are unclear.Objective The purpose of this study was to investigate a role of a peptide leukotriene (LT) in acetaldehyde-induced BHR.Methods Effects of LT antagonists, ONO-1078 (O.l-l.Omg/kg) and ICI-198, 615 (0.03–0.3 mg/kg), on acetaldehyde-induced bronchoconstriction and BHR to inhaled methacho-line were examined using a modified Konzett-Rössler method in guinea pigs.Results Aeetaldehyde at 0.8mg/ml, which failed to induce significant changes in Pao (pressure at the airway opening), enhanced an increase in Pao induced by subsequent inhalations of ascending doses (50–200 μg/ml) of methacholine. suggesting a potentiating effect of acetaldehyde oti bronchial responsiveness. Although ONO-1078 had no inhibitory effect on bronchoconstriction caused by ascending doses (5.0–20 mg/ml) of acetaldehyde, ONO-1078 and ICI-198, 615 reduced the acetaldehyde-induced BHR.Conclusion Acetaldehyde causes BHR via LT release in guinea-pigs.