Background: Although questionnaires have demonstrated an association between impairment of quality of sleep and symptoms in allergic rhinitis (AR) patients, to date there is no report of an objective assessment of sleep in patients with persistent allergic rhinitis (PER) as defined by ARIA guidelines. The aim of the present study was therefore to assess sleep disturbance in PER patients by polysomnography (PSG). Methods: Ninety-eight PER patients with moderate-to-severe nasal obstruction and 30 healthy volunteers were included in the study. All patients underwent PSG during nocturnal sleep to assess the presence and severity of sleep disorders. Peak nasal inspiratory flow (PNIF) was also measured to assess nasal resistance. Results: There were statistically significant, though clinically modest, differences between PER patients and healthy controls in most PSG parameters including sleep efficiency, arousal index, average SaO₂, lowest SaO₂, time spent with a saturation below 90%, and snoring time. Although the apnea-hypopnea index (AHI) was not significantly different between the 2 groups, 17 subjects (17.3%) in the PER group but none of the control subjects had an AHI >5. Patients with higher T5SS scores (12 ≤ T5SS ≤ 15) had a greater tendency to snore than did patients with lower scores (8 ≤ T5SS ≤ 11). Finally, PNIF in the PER group was significantly lower than in the control group. Weak correlations between the arousal index and PNIF, average SaO₂, and PNIF were found. Conclusion: PSG showed modest changes in PER patients versus control subjects.

The regulating gene of femA was studied in methicillin-resistant Staphylococcus aureus (MRSA). High-level MRSA, low-level MRSA and methicillin-sensitive S. aureus (MSSA) were identified by agar diffusion. Beta-lactamases were detected by nitrocephin and the presence of the mecA gene was determined by polymerase chain reaction (PCR). Only isolates that were both beta-lactamase-negative and mecA-positive were used. The femA gene and its 250 base pair (bp) upstream sequence were amplified by PCR and expression was determined by real-time fluorescent quantitative PCR. The 250 bp upstream sequence was labelled by BrightStar Psoralen-Biotin and detected by electrophoretic mobility shift assay (EMSA). Expression levels of femA in MSSA, low-level MRSA and high-level MRSA were 3.53 x 10(-3)% - 29.91%, 5.54 x 10(-3)% - 3.1 x 10(2)% and 13.88 - 5.50 x 10(4)%, respectively. EMSA detected a signal shift in 57 high-level MRSA isolates but not in four low-level MRSA and four MSSA strains. Expression of femA in high-level MRSA (non-beta-lactamase-producing) was higher than in low-level MRSA and MSSA. The femA regulating gene probably lies in the 250 bp upstream sequence in MRSA and high-level expression is essential for high-level methicillin resistance.

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