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Purpose: To report a rare variant of the posterior septal artery (PSA), which supplies blood to the posterior mucosa of the contralateral nasal septum. Case report: A 31-year-old female patient underwent suture removal 14 days after septoplasty and developed left-sided epistaxis 6 h after suture removal. To safely and effectively relieve the patient from epistaxis, the cauterization of the left PSA was performed under general anesthesia. However, 24 h after the first surgical hemostasis, the patient experienced epistaxis again in the right nasal cavity. We have reviewed the patient's sinus computed tomography again and found a rare variant of PSA, which is the right-sided PSA passing through a bony canal in the left-sided nasal septum. Discussion: The variant of PSA well explained the failure of the first hemostatic surgery. Therefore, we again performed a cauterization of the right-sided PSA, after which the patient recovered and no further epistaxis occurred. Conclusion: When cauterization of PSA is used to manage posterior epistaxis, it is necessary to pay attention to the possible variation in PSA.
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OBJECTIVE: To investigate the necessity of subsequent dental treatment for patients with odontogenic sinusitis (OS) after endoscopic sinus surgery (ESS). METHODS: OS patients who received ESS from January 2018 to May 2022 were eligible. Demographic data, medical history, Lund-Mackay (LM) computed tomography (CT) score, Lund-Kennedy (LK) endoscopic score, and OS-specific CT score were recorded and analyzed. All patients were followed up for 6 months after surgery. RESULTS: A total of 48 patients (30 males and 18 females) were enrolled. A total of 35 cases (72.9%) were caused by dental diseases (periapical periodontitis), and 13 cases (27.1%) were caused by iatrogenic factors (including tooth extraction or implantation). The overall treatment success rate was 97.9%, and the success rates in the dental disease OS group (97.1%) and the iatrogenic OS group (100%) were not significantly different (X2 = 0.329, P = .729). None of the patients in the dental disease group received treatment of the causative teeth within 6 months after the operation, except for one patient who received tooth extraction treatment 6 months after the operation. CONCLUSION: Without considering the impact of dental disease on patients' oral health, OS can be completely alleviated by ESS alone, even if no dental treatment is carried out after surgery.
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Lysosomes contribute to cellular homeostasis via processes including macromolecule degradation, nutrient sensing, and autophagy. Defective proteins related to lysosomal macromolecule catabolism are known to cause a range of lysosomal storage diseases; however, it is unclear whether mutations in proteins involved in homeostatic nutrient sensing mechanisms cause syndromic sensory disease. Here, we show that SLC7A14, a transporter protein mediating lysosomal uptake of cationic amino acids, is evolutionarily conserved in vertebrate mechanosensory hair cells and highly expressed in lysosomes of mammalian cochlear inner hair cells (IHCs) and retinal photoreceptors. Autosomal recessive mutation of SLC7A14 caused loss of IHCs and photoreceptors, leading to presynaptic auditory neuropathy and retinitis pigmentosa in mice and humans. Loss-of-function mutation altered protein trafficking and increased basal autophagy, leading to progressive cell degeneration. This study implicates autophagy-lysosomal dysfunction in syndromic hearing and vision loss in mice and humans.
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Sistema de Transporte de Aminoácidos y+ , Pérdida Auditiva Central , Lisosomas , Retinitis Pigmentosa , Sistema de Transporte de Aminoácidos y+/genética , Animales , Pérdida Auditiva Central/metabolismo , Humanos , Lisosomas/metabolismo , Lisosomas/patología , Mamíferos , Ratones , Mutación , Retinitis Pigmentosa/genética , Retinitis Pigmentosa/metabolismoRESUMEN
Hearing loss is a debilitating disease that affects 10% of adults worldwide. Most sensorineural hearing loss is caused by the loss of mechanosensitive hair cells in the cochlea, often due to aging, noise, and ototoxic drugs. The identification of genes that can be targeted to slow aging and reduce the vulnerability of hair cells to insults is critical for the prevention of sensorineural hearing loss. Our previous cell-specific transcriptome analysis of adult cochlear hair cells and supporting cells showed that Clu, encoding a secreted chaperone that is involved in several basic biological events, such as cell death, tumor progression, and neurodegenerative disorders, is expressed in hair cells and supporting cells. We generated Clu-null mice (C57BL/6) to investigate its role in the organ of Corti, the sensory epithelium responsible for hearing in the mammalian cochlea. We showed that the deletion of Clu did not affect the development of hair cells and supporting cells; hair cells and supporting cells appeared normal at 1 month of age. Auditory function tests showed that Clu-null mice had hearing thresholds comparable to those of wild-type littermates before 3 months of age. Interestingly, Clu-null mice displayed less hair cell and hearing loss compared to their wildtype littermates after 3 months. Furthermore, the deletion of Clu is protected against aminoglycoside-induced hair cell loss in both in vivo and in vitro models. Our findings suggested that the inhibition of Clu expression could represent a potential therapeutic strategy for the alleviation of age-related and ototoxic drug-induced hearing loss.
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Clusterina/deficiencia , Células Ciliadas Auditivas/fisiología , Pérdida Auditiva Sensorineural/prevención & control , Presbiacusia/prevención & control , Animales , Umbral Auditivo , Secuencia de Bases , Sistemas CRISPR-Cas , Senescencia Celular , Clusterina/biosíntesis , Clusterina/genética , Clusterina/fisiología , Sinergismo Farmacológico , Potenciales Evocados Auditivos del Tronco Encefálico , Furosemida/administración & dosificación , Furosemida/toxicidad , Células Ciliadas Auditivas/efectos de los fármacos , Pérdida Auditiva Sensorineural/inducido químicamente , Kanamicina/administración & dosificación , Kanamicina/toxicidad , Ratones , Ratones Endogámicos C57BL , Ratones Noqueados , Técnicas de Cultivo de Órganos , Órgano Espiral/patología , Emisiones Otoacústicas Espontáneas , ARN Mensajero/biosíntesis , ARN Mensajero/genéticaRESUMEN
The mammalian inner ear has two major parts, the cochlea is responsible for hearing and the vestibular organ is responsible for balance. The cochlea and vestibular organs are connected by a series of canals in the temporal bone and two distinct extracellular fluids, endolymph and perilymph, fill different compartments of the inner ear. Stereocilia of mechanosensitive hair cells in the cochlea and vestibular end organs are bathed in the endolymph, which contains high K+ ions and possesses a positive potential termed endolymphatic potential (ELP). Compartmentalization of the fluids provides an electrochemical gradient for hair cell mechanotransduction. In this study, we measured ELP from adult and neonatal C57BL/6J mice to determine how ELP varies and develops in the cochlear and vestibular endolymph. We measured ELP and vestibular microphonic response from saccules of neonatal mice to determine when vestibular function is mature. We show that ELP varies considerably in the cochlear and vestibular endolymph of adult mice, ranging from +95 mV in the basal turn to +87 mV in the apical turn of the cochlea, +9 mV in the saccule and utricle, and +3 mV in the semicircular canal. This suggests that ELP is indeed a local potential, despite the fact that endolymph composition is similar. We further show that vestibular ELP reaches adult-like magnitude around post-natal day 6, ~12 days earlier than maturation of cochlear ELP (i.e., endocochlear potential). Maturation of vestibular ELP coincides with the maturation of vestibular microphonic response recorded from the saccular macula, suggesting that maturation of vestibular function occurs much earlier than maturation of hearing in mice.