• Journal of Life Science
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• v.11 no.3
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• pp.259-265
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• 2001

Mercury vapor inhalation-induced acute respiratory failure(ARF) has been reported to be fatal. This study was designed to observe the possible mechanism of inhaled mercury vapor poisoning in the respiratory system. Sixty percent of rats(12/20) exposed to mercury vapor were dead within 72 hours of exposure whereas all the rats(20/20) exposed to mercury vapor combined with dithiothreitol(DTT) vapor survived. The histological observation showed that ARF was a direct cause of the death induced by mercury vapor inhalation, which was significantly circumvented by DTT vapor. Cyclic AMP mediated chloride secretion was inhibited by luminal side but not serosal side sulfhydryl blocking agents (Hf$^{2+}$ $\rho$-chloromercuribenzoic acid or $\rho$-chloromercuriphenyl sulfonic acid) in a dose-dependent manner in a primary cultured rat airway monolayer. The inhibitory component of cAMP induced chloride secretion was completely restored by luminal side DTT(0.5mM). these results suggest that the oxidized form(Hg$^{2+}$) of mercury vapor(Hg0) contribute to ARF and subsequent death. The finding is important as it can provide important information regarding emergency manipulation of ARF patients suffering from by mercury vapor poisoning.ing.

• IMMUNE NETWORK
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• v.16 no.4
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• pp.201-210
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• 2016

Allergic inflammation requires the orchestration of altered gene expression in the target tissue and in the infiltrating immune cells. The transcription factor STAT6 is critical in activating cytokine gene expression and cytokine signaling both in the immune cells and in target tissue cells including airway epithelia, keratinocytes and esophageal epithelial cells. STAT6 is activated by the cytokines IL-4 and IL-13 to mediate the pathogenesis of allergic disorders such as asthma, atopic dermatitis, food allergy and eosinophilic esophagitis (EoE). In this review, we summarize the role of STAT6 in allergic diseases, its interaction with the co-factor PARP14 and the molecular mechanisms by which STAT6 and PARP14 regulate gene transcription.

• International Journal of Oral Biology
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• v.37 no.2
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• pp.57-62
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• 2012

The nasal cavity encounters various irritants during inhalation such as dust and pathogens. To detect and remove these irritants, it has been postulated that the nasal mucosa epithelium has a specialized sensing system. The oral cavity, on the other hand, is known to have bitter taste receptors (T2Rs) that can detect harmful substances to prevent ingestion. Recently, solitary chemosensory cells expressing T2R subtypes have been found in the respiratory epithelium of rodents. In addition, T2Rs have been identified in the human airway epithelia. However, it is not clear which T2Rs are expressed in the human nasal mucosa epithelium and whether they mediate the removal of foreign materials through increased cilia movement. In our current study, we show that human T2R receptors indeed function also in the nasal mucosa epithelium. Our RT-PCR data indicate that the T2R subtypes (T2R3, T2R4, T2R5, T2R10, T2R13, T2R14, T2R39, T2R43, T2R44, T2R 45, T2R46, T2R47, T2R48, T2R49, and T2R50) are expressed in human nasal mucosa. Furthermore, we have found that T2R receptor activators such as bitter chemicals augments the ciliary beating frequency. Our results thus demonstrate that T2Rs are likely to function in the cleanup of inhaled dust and pathogens by increasing ciliary movement. This would suggest that T2Rs are feasible molecular targets for the development of novel treatment strategies for nasal infection and inflammation.