19 research outputs found

    Early Detection of Nasopharyngeal Carcinoma

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    Nasopharyngeal carcinoma (NPC) is a unique disease with a clinical presentation, epidemiology, and histopathology differing from other squamous cell carcinomas of the head and neck. NPC is an Epstein-Barr virus-associated malignancy with a marked racial and geographic distribution. Specifically, it is highly prevalent in southern China, Southeast Asia, and the Middle East. To date, most NPC patients have been diagnosed in the advanced stage, but the treatment results for advanced NPC are not satisfactory. This paper provides a brief overview regarding NPC, with the focus on the early detection of initial and recurrent NPC lesions

    Ischemia-Reperfusion Injury of the Cochlea: Pharmacological Strategies for Cochlear Protection and Implications of Glutamate and Reactive Oxygen Species

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    A large amount of energy produced by active aerobic metabolism is necessary for the cochlea to maintain its function. This makes the cochlea vulnerable to blockade of cochlear blood flow and interruption of the oxygen supply. Although certain forms of human idiopathic sudden sensorineural hearing loss reportedly arise from ischemic injury, the pathological mechanism of cochlear ischemia-reperfusion injury has not been fully elucidated. Recent animal studies have shed light on the mechanisms of cochlear ischemia-reperfusion injury. It will help in the understanding of the pathology of cochlear ischemia-reperfusion injury to classify this injury into ischemic injury and reperfusion injury. Excitotoxicity, mainly observed during the ischemic period, aggravates the injury of primary auditory neurons. On the other hand, oxidative damage induced by hydroxyl radicals and nitric oxide enhances cochlear reperfusion injury. This article briefly summarizes the generation mechanisms of cochlear ischemia-reperfusion injury and potential therapeutic targets that could be developed for the effective management of this injury type

    Ceramide/sphingomyelin cycle involvement in gentamicin-induced cochlear hair cell death

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    Ceramide, a sphingolipid metabolite, regulates diverse cellular processes including apoptosis, cell senescence, the cell cycle, and cellular differentiation. Exogenously administered ceramide reportedly increased cochlear hair cell death due to gentamicin-induced ototoxicity. Ceramide is mainly generated via a ceramide/sphingomyelin cycle by sphingomyelinase and sphingomyelin synthase or via de novo synthesis by serine palmitoyltransferase and ceramide synthase. This study was designed to investigate the possible involvement of neutral sphingomyelinase, sphingomyelin synthase, or serine palmitoyltransferase in hair cell death due to gentamicin. The basal turns of the organ of Corti of Sprague–Dawley rats were dissected on postnatal days 3–5. Cochlear cultures were exposed to media containing 35 μM gentamicin for 48 h to assess the effects of GW4869 (a neutral sphingomyelinase inhibitor), 2-hydroxyoleic acid (a sphingomyelin synthase activator), and myriocin (a serine palmitoyltransferase inhibitor). Hair cell loss was significantly decreased in the presence of GW4869 or 2-hydroxyoleic acid. Myriocin had no significant effects against gentamicin-induced hair cell loss. In addition, neutral sphingomyelinase was activated by gentamicin exposure. The present findings strongly suggest that the ceramide/sphingomyelin cycle plays an important role in the protection of hair cells against gentamicin-induced ototoxicity

    Protective role of Nrf2 in age-related hearing loss and gentamicin ototoxicity

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    Expression of antioxidant enzymes is regulated by transcription factor NF-E2-related factor (Nrf2) andinduced by oxidative stress. Reactive oxygen species contribute to the formation of several types ofcochlear injuries, including age-related hearing loss and gentamicin ototoxicity. In this study, we examinedthe roles of Nrf2 in age-related hearing loss and gentamicin ototoxicity by measuring auditory brainstemresponse thresholds in Nrf2-knockout mice. Although Nrf2-knockout mice maintained normalauditory thresholds at 3 months of age, their hearing ability was significantly more impaired than thatof age-matched wild-type mice at 6 and 11 months of age. Additionally, the numbers of hair cells andspiral ganglion cells were remarkably reduced in Nrf2-knockout mice at 11 months of age. To examinethe importance of Nrf2 in protecting against gentamicin-induced ototoxicity, 3-day-old mouse organof Corti explants were cultured with gentamicin. Hair cell loss caused by gentamicin treatment wasenhanced in the Nrf2-deficient tissues. Furthermore, the expressions of some Nrf2-target genes were activatedby gentamicin treatment in wild-type mice but not in Nrf2-knockout mice. The present findingsindicate that Nrf2 protects the inner ear against age-related hearing injuries and gentamicin ototoxicityby up-regulating antioxidant enzymes and detoxifying proteins
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