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  1. Goh LC, Arvin B, Zulkiflee AB, Prepageran N
    Otolaryngol Head Neck Surg, 2018 10;159(4):783-788.
    PMID: 30126325 DOI: 10.1177/0194599818795852
    Objective To objectively compare the nasal decongestion potency of lidocaine/phenylephrine when delivered with a nasal nebulizer and a nasal spray before a rigid nasoendoscopic examination. Study Design Open-label randomized controlled trial. Setting Multicenter study. Methods This prospective clinical trial involved 106 participants with untreated chronic rhinitis. Fifty-three participants had 400 μL of lidocaine/phenylephrine administered into the right nostril with a nasal nebulizer, while the remaining 53 participants had 400 μL administered with a nasal spray. The control was the left nostril. Nasal resistance at 150-Pa fixed pressure was evaluated with an active anterior rhinomanometry at 5, 10, 15, and 30 minutes postintervention. Pain score was assessed subjectively by applying pressure to the inferior turbinate 30 minutes after intervention. Results There was an overall reduction in nasal resistance of the right nostril when lidocaine/phenylephrine was administered with the nasal nebulizer in comparison with the nasal spray. However, a statistically significant difference in nasal resistance was seen only at 5 minutes ( P = .047), 15 minutes ( P = .016), and 30 minutes ( P = .036). The examining endoscopist further supported the degree of nasal decongestion via subjective assessment of the nasal cavity ( P = .001). Pain scores obtained after the intervention showed a significant decrease in pain threshold when the nasal nebulizer was used instead of the nasal spray ( P = .040). Conclusions This study suggests that the delivery of lidocaine/phenylephrine to the nasal cavity by the nasal nebulizer provides better decongestive and analgesic potency as compared with the delivery by nasal sprays.
    Matched MeSH terms: Nasal Mucosa/drug effects*
  2. Tan SN, Sim SP
    BMC Cancer, 2018 04 12;18(1):409.
    PMID: 29649994 DOI: 10.1186/s12885-018-4327-4
    BACKGROUND: Chronic rhinosinusitis (CRS) increases the risk of developing nasopharyngeal carcinoma (NPC) while nasopharyngeal reflux is known to be one of the major aetiological factors of CRS. Bile acid (BA), the component of gastric duodenal contents, has been recognised as a carcinogen. BA-induced apoptosis was suggested to be involved in human malignancies. Cells have the potential and tendency to survive apoptosis. However, cells that evade apoptosis upon erroneous DNA repair may carry chromosome rearrangements. Apoptotic nuclease, caspase-activated deoxyribonuclease (CAD) has been implicated in mediating translocation in leukaemia. We hypothesised that BA-induced apoptosis may cause chromosome breaks mediated by CAD leading to chromosome rearrangement in NPC. This study targeted the AF9 gene located at 9p22 because 9p22 is one of the most common deletion sites in NPC.

    METHODS: We tested the ability of BA at neutral and acidic pH in inducing phosphatidylserine (PS) externalisation, reactive oxygen species (ROS) production, mitochondrial membrane potential (MMP) disruption, and caspase 3/7 activity in normal nasopharyngeal epithelial (NP69) and NPC (TWO4) cells. Inverse-PCR (IPCR) was employed to detect AF9 gene cleavages. To investigate the role of CAD in mediating these cleavages, caspase inhibition was performed. IPCR bands representing AF9 cleaved fragments were sequenced.

    RESULTS: BA-treated cells showed higher levels of PS externalisation, ROS production, MMP loss and caspase 3/7 activity than untreated control cells. The effect of BA in the induction of these intracellular events was enhanced by acid. BA at neutral and acidic pH also induced significant cleavage of the AF9 gene. These BA-induced gene cleavages were inhibited by Z-DEVD-FMK, a caspase-3 inhibitor. Intriguingly, a few chromosome breaks were identified within the AF9 region that was previously reported to participate in reciprocal translocation between the mixed lineage leukaemia (MLL) and AF9 genes in an acute lymphoblastic leukaemia (ALL) patient.

    CONCLUSIONS: These findings suggest a role for BA-induced apoptosis in mediating chromosome rearrangements in NPC. In addition, CAD may be a key player in chromosome cleavages mediated by BA-induced apoptosis. Persistent exposure of sinonasal tract to gastric duodenal refluxate may increase genomic instability in surviving cells.

    Matched MeSH terms: Nasal Mucosa/drug effects
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