Notes: We have performed several band structure calculations on 2H–, 4H–, and 6H–SiC, using different lattice constants and basis atom positions in order to investigate the sensitivity of the electronic structure and explain the discrepancies in band structure results between different authors. It is shown that even small changes in the basis atom positions have a strong impact on the crystal-field splitting, whereas the relative changes in the fundamental band gap, the spin-orbit splitting, and the effective electron and hole masses are practically negligible. The computational method was based on the local density approximation within the density functional theory. © 1999 American Institute of Physics.

Notes: Doping-induced energy shifts of the conduction band minimum and the valence band maximum have been calculated for n-type and p-type 3C-, 2H-, 4H-, 6H-SiC, and Si. The narrowing of the fundamental band gap and of the optical band gap are presented as functions of ionized impurity concentration. The calculations go beyond the common parabolic treatments of the ground state energy dispersion by using energy dispersion and overlap integrals from band structure calculations. The nonparabolic valence band curvatures influence strongly the energy shifts especially in p-type materials. The utilized method is based on a zero-temperature Green's function formalism within the random phase approximation with local field correction according to Hubbard. We have parametrized the shifts of the conduction and the valence bands and made comparisons with recently published results from a semi-empirical model. © 1999 American Institute of Physics.

Notes: Densities of states for the hexagonal polytypes 2H, 4H, and 6H of SiC have been derived for energies within a few hundred meV around the band gaps. The nonparabolic energy dispersions of the valence bands have been taken into consideration, as well as the camel's back structure of the lowest conduction band in 6H–SiC. The nonparabolicities of the energy bands are shown to strongly influence the densities of states in these polytypes. © 1998 American Institute of Physics.

Notes: A full-potential band structure calculation, within the local density approximation to the density functional theory, has been performed for the polytypes 3C, 2H, 4H, and 6H of SiC. The calculated effective electron masses are found to be in very good agreement with experimental values. The electron-optical phonon coupling has been estimated and the polaron masses are calculated to be 3%–13% larger than the corresponding bare masses. The effective electron masses of the second lowest conduction band minima are also presented and the calculated energy difference between the two lowest minima in 4H–SiC is only 0.12 eV. The lowest conduction band in 6H–SiC is found to be very flat and to have a double-well-like minimum along the ML line. The top of the valence bands has been parametrized according to the k⋅p approximation, whereupon the effective hole masses have been determined. The spin-orbit interaction was found to have a strong influence on the value of the effective hole masses. Furthermore, total and partial densities of states are presented. © 1997 American Institute of Physics.

Notes: We have investigated the photoluminescence emission energy of InP dots as a function of cap layer thickness. We find a strong blue-shift with increasing cap layer thickness. The strain tensor in the dot as well as in the surrounding matrix has been modeled using finite element methods and the band gap has been calculated using deformation potential theory. We find good agreement between calculation and experiment. For uncapped dots we find that the emission energy is lower than for biaxially strained InP, and is indeed close to unstrained InP. © 1995 American Institute of Physics.

Notes: Allergic contact dermatitis is often caused by solid products such as rubber gloves. Patch testing with the product as is often gives negative results. Extraction of the haptens into an organic solvent is commonly performed to achieve a more correct investigation. The technique used for extraction of haptens from solid materials is only sporadically described. In this study, we investigated and optimized the yields of dithiocarbamates obtained by extraction from rubber gloves. The influence of solvent, extraction time and the procedures for extraction are evaluated. The delivery of zinc dibutyldithiocarbamate from the patch test preparation to the skin is determined.

Notes: This study compares the effects of two topical nasal treatments for allergic rhinitis, budesonide and levocabastine, on symptom development during seasonal pollen exposure. Additionally, the protective effects of drug treatments on allergen-challenge-induced responses (symptoms and microvascular exudation of plasma) are examined late into the pollen season. Forty-four patients with seasonal allergic rhinitis to birch pollen participated in this single-blind, randomized, and placebo-controlled study. Topical nasal treatment with either levocabastine (200 p.g b.i.d.: n = 16), budesonide (200 μg b.i.d.; n = 16), or placebo (n= 12) was instituted before the start of the pollen season and continued for 5 weeks until the end of the birch pollen season. The participants kept diaries for scores of nasal and ocular symptoms. Nasal allergen challenges with increasing doses of a birch pollen extract (102, 103 and lC SQ-U) were carried out both before, when patients were asymptomatic and without treatment, and late into the pollen season. A nasal lavage followed each challenge, and the lavage fluid levels of albumin were measured as an index of the acute inflammatory response of the allergic mucosa. The birch pollen season was rather mild, producing only small increases in nasal symptoms. Budesonide treatment reduced the total nasal symptoms compared to placebo (P〈0.01) and to levocabastine (P〈0.05), while levocabastine treatment did not differ significantly from placebo. Ocular symptoms and use of rescue medication did not differ between placebo and the active treatments. At the end of the pollen season, both treatments reduced allergen-challenge-induced nasal symptoms compared to placebo (P〈0.01). Only budesonide reduced allergen-challenge- induced increments of albumin levels in postchallenge nasal lavage fluids (P〈0.05, in comparison with placebo). The results suggest that budesonide reduces both seasonal and allergen-challenge-induced nasal symptoms, while levocabastine is effective against allergen-challenge-induced symptoms also during the season. In addition, the topical steroid treatment, but not the antihistamine, inhibits the inflammatory exudation evoked by allergen challenge in patients with active seasonal disease.

Notes: Studies of the nasal permeation of small molecules (〈 1000 Da) have yielded important information about the integrity of the human airway mucosa in health and disease. In this study, we used a much larger tracer molecule, polysucrose (PS) 15000 (approx. 14700 Da), to predict the mucosal permeation of inhalational allergens. PS 15000 (50 mg/ml; 15 ml), with or without a detergent type of permeation enhancer (dioctyl sodium sulfosuccinate 10 mg/ml), was maintained for 15 min in one nasal cavity of 12 healthy nonatopic subjects by employment of a nasal-pool device. Permeation as determined by the 24-h urine recovery of PS (micro-ELISA analysis assay) was expressed as percentage of nasal instillate. Mean baseline permeation was 0.044% (range 0.009–0.250%). In the presence of the detergent, permeation increased to 0.600% (range 0.007–2.260%) (P〈0.01). After oral intake of 750 mg of PS 15 000 (50 μg/ml; 15 ml), the 24-h urinary recovery was 0.013% (range 0.004–0.023%). Our study thus demonstrates a measurable baseline permeation of PS 15 000, an elevated permeation rate in the presence of an epithelium-damaging detergent molecule, and a negligible permeation by the oral route. These properties support the utility of PS 15 000 as a nasal airway permeation tracer. Its size further suggests that its permeation may reflect mucosal perviousness to many allergens.

Notes: In subjects not developing allergy, inhalation of nonpathogenic protein antigens causes no harm and is associated with tolerance induction. Repeated exposure to aerosolized ovalbumin (OVA) likewise does not evoke airway inflammation and induces inhalation tolerance in experimental animals. The present study explored the role of the inhibitory T-cell receptor CTLA-4, in preventing inflammation and in establishing inhalation tolerance in response to a protein antigen. Naive BALB/c mice were injected intraperitoneally with anti-CTLA-4 monoclonal antibody or control immunoglobulin G (IgG) and exposed daily to aerosolized saline or OVA over 10 or 20 consecutive days. OVA-specific IgE levels and the inflammatory response in airway tissues were assessed 2 days after last exposure. The OVA-specific IgE response was also evaluated in mice subjected to a subsequent immunogenic OVA challenge 18 days after last aerosol exposure. Additional mice were made tolerant by 10 days of OVA aerosol exposure and were then subjected to an immunogenic OVA challenge combined with CTLA-4 blockade or control IgG treatment. Repeated inhalation of aerosolized OVA alone did not cause a pulmonary inflammatory response. In contrast, 10 days of OVA exposure combined with blockade of CTLA-4 led to development of eosinophilic lung infiltrates, BAL fluid eosinophilia, goblet cell hyperplasia and increased OVA-specific IgE. By 20 days of OVA exposure and blockade of CTLA-4, the inflammatory response remained. Mice exposed to aerosolized OVA for 10 days exhibited greatly reduced OVA-specific IgE responses to subsequent immunogenic OVA challenge. Blockade of CTLA-4 during the period of OVA aerosol exposure did not prevent this suppression of the OVA-specific IgE response. Neither did blockade of CTLA-4 during immunogenic OVA challenge alter the allergen-specific IgE response. Our results indicate that in vivo blockade of CTLA-4 modulates the initial immune response to a protein antigen allowing the development of allergen-induced airway inflammation in naive mice. However, this initial exaggerated immune response is followed by the induction of inhalation tolerance, demonstrating that CTLA-4 signalling is not decisive in this process. Our findings also show that once inhalation tolerance is established it may not be disrupted by blockade of CTLA-4.

Notes: Coronavirus-induced common cold and allergen-induced rhinitis are characterized by nasal mucosal exudation of bulk blood plasma. The mucosal exudation process involves ‘flooding’ of the lamina propria with plasma-derived binding proteins and it is possible that subepithelial inflammatory cytokines and mediators may be moved by the exudate to the mucosal surface. In this study, we have analysed cytokine levels in nasal lavage (NAL) fluids from non-allergic subjects inoculated with coronavirus (n= 20) and from subjects with allergic (birch pollen) rhinitis subjected to additional allergen challenge (samples were obtained 35min post challenge) in the laboratory (n= 10). Ten of the 20 inoculated subjects developed common cold and 10 remained healthy. Interferon-γ (IFN-γ), interleukin-1β (IL-1β), granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-4, and IL-6 were analysed in unprocessed NAL fluids using immunoassays. The subjects who developed common cold had increased NAL fluid levels of IFNγ (P 〈 0.05) that correlated well with the symptoms (P 〈 0.001). IFNγ did not increase in subjects with allergic rhinitis. IL-1β levels were similar in NAL fluids obtained from all inoculated subjects. In the subjects with allergic rhinitis NAL fluid levels of both IL-1β and GM-CSF were increased (P 〈 0.05). GM-CSF was not detected in common cold. IL-4 and IL-6 were not detectable in any of the NAL fluids. The present cytokines may not only emanate from superficial mucosal cells. By aiding plasma exudation subepithelial cytokines may potentially also be retrieved on the mucosal surface. Our study provides original in vivo data supporting the notion that a TH-1 profile of cytokines, notably IFNγ, is present in viral infection and further supporting the view that GM-CSF is an important cytokine in allergic airways disease.