Mandibular advancement appliances (MAAs) are accepted as a treatment option for snoring and mild obstructive sleep disorders. In the present clinical study two differently designed devices were examined for their effectiveness in treating obstructive sleep apnoea (OSA). The study was based on an assessment of 26 patients with a polysomnographic diagnosis of mild OSA [22 men, four women; mean body mass index 27.3 kg/m2 (SD 3.1); mean age 56.8 years (SD 5.2); mean respiratory disturbance index (RDI): 16.0 events/hour (SD 4.4)]. After insertion of the first MAA and a 6-8-week habituation period, a cardio-respiratory home-sleep study was carried out. Following a 2-3-week period with no treatment, the second appliance was inserted. The sequence of the devices was randomized. Once the patients had become accustomed to the second appliance, another somnographic registration was carried out. Daytime sleepiness, snoring, and sleep quality were assessed subjectively on a visual analogue scale. The results showed that a statistically significant improvement in the respiratory parameters was achieved with both appliances (P < 0.01). However, the activator [RDI: 5.5 events/hour, SD 3.3; apnoea index (AI): 3.4 events/hour, SD 2.1] was significantly more effective (P < 0.01) than the Silencor (RDI, 7.3 events/hour, SD 5.3; AI: 5.8 events/hour, SD 3.2). No difference was recorded in the subjective assessment of the therapeutic effects. Both appliances reduced daytime sleepiness and snoring and improved sleep quality, and both influenced the treatment outcome.

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Growing evidence suggests that eosinophils play an important role as proinflammatory cells in asthma, possibly by releasing toxic cationic proteins. In this study concentrations of serum and sputum eosinophil cationic protein (ECP) from 134 patients with productive cough and a history suggestive of airflow obstruction were measured by radioimmunoassay. Small sputum volumes were suspended in saline, vortexed, and centrifuged and ECP measured in the supernatant. Serum ECP levels ranged from 0.002 to 0.095 mg/L (0.016 +/- 0.0014), whereas sputum ECP concentrations were between 0.024 and 5.66 mg/L ECP per g sputum (0.878 +/- 0.092). Only 17 of the 134 patients (14 asthma, one cystic fibrosis, one bronchiectasis, and one bronchitis) had not been pretreated with corticosteroids. Sputum but not serum ECP levels of the 14 patients with asthma were inversely correlated with impairment of FEV1 (r = -0.73). Airway resistance (Raw) (r = 0.71) as well as the change in FEV1 (r = 0.79) and Raw (r = 0.84) after inhalation of 0.2 mg albuterol were positively correlated. This relationship was not observed in the remaining 117 patients on topical and/or systemic corticosteroids, suggesting that corticosteroid treatment influences sputum ECP levels. Also, sputum ECP levels and the degree of sputum eosinophilia were not correlated in any of the patient groups. Neither did serum ECP levels predict sputum ECP concentrations. We conclude that sputum ECP concentrations serve as a marker of eosinophil degranulation in the sputum, and this marker correlates with airflow obstruction. Sputum ECP levels are more closely related to lung function parameters than serum ECP concentrations and/or microscopic sputum analysis.

1 Extracellular nucleotides are the focus of increasing attention for their role as extracellular mediators since they are released into the extracellular environment in a regulated manner and/or as a consequence of cell damage. 2 Here, we show that human eosinophils stimulated with different nucleotides release eosinophil cationic protein (ECP) and the chemokine interleukin 8 (IL-8), and that release of these two proteins has a different nucleotide requirement. 3 Release of ECP was triggered in a dose-dependent manner by ATP, UTP and UDP, but not by 2 0 -&3 0 -o-(4-benzoyl-benzoyl)adenosine 5 0 -triphosphate (BzATP), ADP and a,b-methylene adenosine 5 0 triphosphate (a,b-meATP). Release of IL-8 was triggered by UDP, ATP, a,b-meATP and BzATP, but not by UTP or ADP. Pretreatment with pertussis toxin abrogated nucleotide-stimulated ECP but not IL-8 release. 4 Release of IL-8 stimulated by BzATP was fully blocked by the P2X 7 blocker KN-62, while release triggered by ATP was only partially inhibited. IL-8 secretion due to UDP was fully insensitive to KN-62 inhibition. 5 Priming of eosinophils with GM-CSF increased IL-8 secretion irrespectively of the nucleotide used as a stimulant. 6 It is concluded that extracellular nucleotides trigger secretion of ECP by stimulating a receptor of the P2Y subfamily (possibly P2Y 2 ), while, on the contrary, nucleotide-stimulated secretion of IL-8 can be due to activation of both P2Y (P2Y 6 ) and P2X (P2X 1 and P2X 7 ) receptors.

SUMMARYSputum from sympioinauc asihmaiics is a rich source of eosinophils Irom the respiratory tract. Foliowing liquefaction ofsputuin with dithioerythritol (DTE), a cell suspension suitable for indirect double immunofiuorescence with fiow cytometry was obtained. Eosinophiis were identilicd using anti-CD9 fluoreseein conjugate, and particular surface maritcrs measured with Ihe relevant mouse MoAb foilowed by goat anti-mouse immunogiobuiin phycoerythrin conjugate. Blood and sputum eosinophil surfacemarkers were determined in paraiiel from asthmatics nol receiving steroid therapy. Sputum eosinophiis were found to have considerabiy eievated levels of CDlib, a refleetion of eosinophii activation. Sputum but not blood eosinophils were Ibund to express ICAM-I (nine out of ! 1 eases) and HLA-DR (eight out of 11 cases). Furthermore, following culture of normal blood eosinophiis with pooled T ceil supernatants. ICAiV1-l and HLA-DR could be induced in vitro. The induction of eosinophil adhesion molecules such as ICAM-l and HLA-DR may inliucnce eosinophil iocaiization and function in asthma.