The eosinophilic CRSwNP phenotype is clinically characterized by serum eosinophilia, atopy, extensive disease, and poor prognosis compared to the neutrophilic and the noneosinophilic nonneutrophilic groups. We clearly demonstrated that all three subgroups of CRSwNP had characteristic differences in those inflammatory markers, which allows for pathophysiologically meaningful differentiations with likely therapeutic consequences.

This study suggests that type 1 diabetes mellitus can cause cochlear microangiopathy and subsequently degeneration of cochlear lateral walls and OHCs.

Background: Interleukin (IL)-17A is a highly inflammatory cytokine with a robust effect on stromal cells in many tissues. Although IL-17A is known to be associated with inflammatory lung disorders by triggering an accumulation of neutrophils, the effect of IL-17A on the upper airway is still uncertain. The expression of IL-17A and its role were investigated in the nasal polyps of chronic rhinosinusitis associated with asthma. Methods: IL-17A was detected by immunohistochemistry and quantitative real-time RT-PCR. The cellular source of IL-17A was examined by double staining with EG2, CD4 and neutrophil elastase. The tissue remodeling of the nasal polyps was evaluated by assessing the epithelial damage and basement membrane thickness. Results: Both the immunoreactivity and mRNA of IL-17A were significantly detected in the nasal polyps in comparison with control normal sinus mucosa. The localization of IL-17A expression predominantly coincided with eosinophils and CD4-positive lymphocytes. Furthermore, the number of IL-17A-positive cells correlated with tissue eosinophils, but not with neutrophils. The degree of epithelial damage and basement membrane thickness was dependent on the number of infiltrated IL-17A-positive cells. Conclusion: The present study suggests, for the first time, that IL-17A plays an important role in the eosinophil accumulation in the nasal polyps and the remodeling of the nasal polyps of chronic rhinosinusitis associated with asthma.

The present study shows that GLUT-1 served as a marker indicating that tumors with deep invasion tended to result in a worse prognosis in patients due to either lymph node metastasis, a recurrence of the primary lesion or distant metastasis.

Major causes of olfactory disorders are sinonasal disease, viral upper respiratory tract infection, head trauma and old age. Olfactory testing is an important part of objective assesment of the severity of the disease in chronic rhinosinusitis and nasal polyposis. The aim of this study was to correlate results of objective smell testing with subjective scores on olfaction and other nasal symptoms in different subgroups of patients with smell impairment.Data were extracted from questionnaires filled by patients sent to smell testing by the ENT specialist. For the analysis data were divided in subgroups: 20 with chronic rhinosinusitis (CRS), 24 patients operated for nasal polyps, 7 patients with nasal polyps on medical treatment, 7 with hyposmia after common cold, 4 with anosmia and 11 controls with no smell impairment. Smell testing was done by using the Sniffin Sticks 12 complete odorant. This test is based on the assessment of odor identification abilities for 12 standard odors with forced choice. Subjective scores on (0-4) were taken for olfaction, nasal obstruction, hypersecretion and headache.The correlation between subjective score for olfaction and olfactometry score was significant for the whole group (r 0.682), and was similar when anosmic and controls were excluded. Subjective olfaction and olfactometry score did not correlate with any other symptom. Comparing correlation coefficients between the subgroups, it seems that patients with CRS and nonoperated nasal polyp patients have better correlation between subjective and objective smell assesment than patients operated for nasal polyps and those who had olfactory lesion following viral infection.Although correlation between subjective and objective smell assesment is significant, some subgroups of patients overrate their ability to recognize odors. STRESS EFFECTS ON ALLERGIC INFLAMMATION OF THE AIRWAYS Pontus Stierna and Susanna GeorenDepartment of Otorhinolaryngology, Karolinska University Hospital, Stockholm, SwedenWe have used a mouse model to investigate the effects of endogenous GC synthesis and GC receptor inhibition, as well as acute stress, and different doses of exogenous administered GCs on inflammatory cells in different cellular compartments in allergic airway inflammation. including nerve growth factor (NGF) in the airways, during allergic inflammation.First we investigated the effects of endogenous GCs on eosinophilic airway inflammation. Inhibition of GC release with metyrapone (ME) induced an increase of bone marrow eosinophilia and when the ME treatment was combined with a GC receptor antagonist (RU 486) the allergen-induced bone marrow eosinophilia was further enhanced.The second study was focused on the effects of timing of a short acute stress on allergic airway inflammation in upper and lower airways. Short stress applied before an allergen challenge decreased the allergen-induced eosinophilia in bronchoalveolar lavage fluid and lungs and also the inflammation in the nasal tissue. No effects on eosinophilia or inflammation were seen...