Background: Excess mucus production and hypersecretion characterize upper airway diseases. The primary mechanisms leading to mucus hypersecretion in chronic rhinosinus inflammation are not well understood. Mucus hypersecretion is commonly accompanied by goblet cell and submucosal gland cell hyperplasia. It is important to identify which mucin gene messenger RNAs (mRNAs) are expressed in the sinus mucosa. Objectives: To investigate the expression of MUC5AC and MUC5B mRNAs and localization of these proteins in human sinus mucosa and to compare the expression of MUC5AC and MUC5B mRNAs in normal and in chronic sinus mucosa. Design: Twenty chronic maxillary sinusitis mucosa samples and 20 normal maxillary sinus mucosa samples were obtained; RNAs were extracted from sinus mucosa, and semiquantitative reverse transcriptionpolymerase chain reaction was performed for MUC5AC and MUC5B. Localization of these proteins was sought by using immunohistochemical analysis. Results: The levels of MUC5AC and MUC5B mRNA in chronic rhinosinusitis were significantly increased compared with those in normal sinus mucosa (P=.02). In inflammed sinus mucosa, MUC5AC protein was expressed in the cytoplasm of the goblet cell in the surface epithelium, and MUC5B expression was restricted to mucous cells of the submucosal glands and to the epithelium of sinus mucosa. However, in the normal sinus mucosa, MUC5AC and MUC5B proteins were expressed at low levels in the sinus epithelium and submucosal glands, respectively. Conclusion: These results suggest that up-regulation of MUC5AC and MUC5B, which are major components of respiratory secretion in chronic rhinosinusitis, may play important roles in the pathogenesis of sinus hypersecretion in chronic rhinosinusitis.

Nasolabial cysts are rare but easily identifiable when they do occur. They are thought to arise f rom the remnants of the nasolacrimal ducts, but most ofthe available inf ormati on on these cysts is limited to isolated case reports. The pur p ose of our study was to examine the clinical and path ologic fea tures of nasolab ial cysts in order to p rovide a basis fo r their correct diagnosis and treatment. Eighteen patients with nasolabial cysts were

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DJ-1, a Parkinson's disease (PD)–associated gene, has been shown to protect against oxidative stress in Drosophila. However, the molecular mechanism underlying oxidative stress-induced phenotypes, including apoptosis, locomotive defects, and lethality, in DJ-1-deficient flies is not fully understood. Here we showed that Daxx-like protein (DLP), a Drosophila homologue of the mammalian Death domain-associated protein (Daxx), was upregulated under oxidative stress conditions in the loss-of-function mutants of Drosophila DJ-1β, a Drosophila homologue of DJ-1. DLP overexpression induced apoptosis via the c-Jun N-terminal kinase (JNK)/Drosophila forkhead box subgroup O (dFOXO) pathway, whereas loss of DLP increased resistance to oxidative stress and UV irradiation. Moreover, the oxidative stress-induced phenotypes of DJ-1β mutants were dramatically rescued by DLP deficiency, suggesting that enhanced expression of DLP contributes to the DJ-1β mutant phenotypes. Interestingly, we found that dFOXO was required for the increase in DLP expression in DJ-1β mutants and that dFOXO activity was increased in the heads of DJ-1β mutants. In addition, subcellular localization of DLP appeared to be influenced by DJ-1 expression so that cytosolic DLP was increased in DJ-1β mutants. Similarly, in mammalian cells, Daxx translocation from the nucleus to the cytosol was suppressed by overexpressed DJ-1β under oxidative stress conditions; and, furthermore, targeted expression of DJ-1β to mitochondria efficiently inhibited the Daxx translocation. Taken together, our findings demonstrate that DJ-1β protects flies against oxidative stress- and UV-induced apoptosis by regulating the subcellular localization and gene expression of DLP, thus implying that Daxx-induced apoptosis is involved in the pathogenesis of DJ-1-associated PD.

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