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Nobuhiro Hakuba

Publications and source records attributed to Nobuhiro Hakuba.

7 recordsLinked to original sources

AMPA/kainate-type glutamate receptor antagonist reduces progressive inner hair cell loss after transient cochlear ischemia.

We investigated the effect of glutamate receptor antagonists on progressive inner hair cell (IHC) loss following transient cochlear ischemia in gerbils. Transient cochlear ischemia was induced by 15-min bilateral vertebral artery occlusion. An alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA)/kainate-type glutamate receptor antagonist, 6-7-dinitroquinoxaline-2,3-dione (DNQX), or an N-methyl-D-aspartate (NMDA)-type receptor antagonist, MK-801, was administered 10 min before the ischemic insult. Hearing was assessed by sequentially recording compound action potentials (CAPs) before, during, and after the ischemia. The degree of hair cell loss in the organ of Corti was evaluated in specimens stained with rhodamine-phalloidin and Hoechst 33342. On the seventh day after ischemia, the increases in the CAP threshold and the progressive IHC loss were significantly reduced in cochleae treated with DNQX, while MK-801 was ineffective. These results suggest that the AMPA receptor plays a critical role in the development of the progressive IHC loss induced by ischemia/reperfusion injury in the cochlea.

Acoustic Stimulation↗

Transient cochlear ischemia causes delayed cell death in the organ of Corti: an experimental study in gerbils.

To elucidate whether ischemia-reperfusion can cause delayed cell death in the cochlea, the effects of transient cochlear ischemia on hearing and on neuronal structures in the cochlea were studied in Mongolian gerbils. Ischemia was induced by bilaterally occluding the vertebral arteries for 5 minutes in gerbils, which lack posterior cerebral communicating arteries. In gerbils, the labyrinthine arteries are fed solely by the vertebral arteries. Occlusion of the vertebral arteries caused a remarkable increase in the threshold of compound action potentials (CAPs), which recovered over the following day. However, 7 days after the onset of reperfusion, the threshold began to increase again. Morphologic changes in the hair cell stereocilia were revealed by electron microscopy. The number of nuclear collapses was counted in cells stained for DNA and F-actin to evaluate the degree of cell death in the organ of Corti. Changes in spiral ganglion cell (SGC) neuron number were detected, whether or not progressive neuronal death occurred in the SGC. These studies showed that sporadic fusion of hair cells and the disappearance of hair cell stereocilia did not begin until 4 days after ischemia. On subsequent days, the loss of hair cells, especially inner hair cells (IHCs), and the degeneration of SGC neurons became apparent. Ten days after ischemia, the mean percentage cell loss of IHCs was 6.4% in the basal turn, 6.4% in the second turn, and 0.8% in the apical turn, respectively, and the number of SGC neurons had decreased to 89% of preischemic status. These results indicate that transient ischemia causes delayed hearing loss and cell death in the cochlea by day 7 after ischemia.

Action Potentials↗

A new method for closing tympanic membrane perforations using basic fibroblast growth factor.

OBJECTIVE: To present a new method for closing tympanic membrane perforations using basic fibroblast growth factor (bFGF) combined with an atelocollagen/silicone bilayer membrane as a patch material. STUDY DESIGN: Closure of tympanic membrane perforations was attempted using bFGF, which is thought to facilitate the growth of fibroblasts and collagen fibers at the margin of the perforation. METHODS: Under an operating microscope, the margin of the perforation was trimmed, and a piece of an atelocollagen/silicone bilayer membrane infiltrated with 0.2 mL Trafermin (0.1% solution) (bFGF group) or saline (control group) was then placed in the perforation with the silicon layer facing outward. Nine patients were treated with bFGF, and five were treated with saline. Data obtained from patient records included patient age, perforation size, and duration of treatment, with a focus on hearing improvement and complete tympanic membrane closure. RESULTS: The mean perforation size before treatment was 16.5% in the bFGF group and 9.6% in the control group. Closure of the tympanic membrane perforation was achieved in all cases in the bFGF group, whereas it was achieved in only two of five cases in the control group. With bFGF treatment, the tympanic membrane perforations closed completely within 3.7 weeks, and hearing improved by 13.3 dB in the bFGF group. CONCLUSION: The study demonstrated that bFGF combined with an atelocollagen/silicone bilayer membrane is effective for the conservative treatment of tympanic membrane perforation.

Adult↗

Lateralization of the tympanic membrane as a complication of canal wall down tympanoplasty: a report of four cases.

OBJECTIVE: To describe the pathophysiology and treatment of the lateralized tympanic membrane that occurs after canal wall down tympanoplasty. STUDY DESIGN: Retrospective case review. SETTING: Tertiary referral hospital. PATIENTS: Four patients in whom lateralization of the tympanic membrane developed as a complication of canal wall down tympanoplasty. RESULTS: The patients had undergone middle ear surgery 20 to 34 years before their first visit to the authors. A Bondy operation with soft-wall reconstruction of the ear canal had been performed in three patients and a modified radical mastoidectomy in one patient. They all had severe conductive hearing loss. Common findings were anterior canal sulcus blunting, good tubal function, normal middle ear mucosa, and mobile stapes. At revision surgery, the lateralized tympanic membrane was removed, and the temporalis fascia was grafted medial to the malleus manubrium. The exposed bony surface in the ear canal was covered with a split-thickness skin graft, and the ear canal and the mastoid cavity were tightly packed to secure the graft. All the patients regained good hearing after the revision. Although deterioration of the anterior tympanic ring was presumed to be the primary cause of the graft lateralization, the lack of a posterior bony ear canal might have facilitated this condition. CONCLUSION: Lateralization of the tympanic membrane can occur even in an ear with a radicalized mastoid cavity, especially when the anterior tympanic ring is torn and the posterior ear canal is reconstructed with soft tissue.

Bone Conduction↗

Synchronous bilateral mucoepidermoid carcinoma of the parotid gland.

It is rare for a parotid gland tumour to arise bilaterally, the most common example being Warthin's tumour. Furthermore, it is rare for a parotid gland cancer to occur bilaterally. Here, we describe a case of synchronous bilateral mucoepidermoid carcinoma arising in the parotid gland. A case of bilateral facial nerve dysfunction is presented in which aggressive surgery failed to save the life of a 48-year-old man. This is the first such case reported in the available English literature.

Carcinoma, Mucoepidermoid↗

Apoptotic hair cell death after transient cochlear ischemia in gerbils.

The mechanisms of cochlear hair cell death following exposure to transient inner ear ischemia were investigated in gerbils histologically. The animals were subjected to ischemic insult by occluding both vertebral arteries for 15 min. Hoechst 33342 nuclear staining showed that inner hair cells (IHCs) underwent sporadic degeneration via nuclear condensation, which peaked 12 hours after the ischemia. Furthermore, nuclear DNA fragmentation was noted by the terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate (dUTP)-biotin nick end labeling method. Transmission electron microscopy revealed morphological changes in the IHCs characteristic of apoptosis, including karyopyknosis, chromatin condensation. These findings suggest that apoptotic cell death is the major process in hair cell degeneration in this animal model.

Animals↗

Labyrinthine fistula as a late complication of middle ear surgery using the canal wall down technique.

OBJECTIVES: To evaluate the clinical features of labyrinthine fistulae occurring as a late complication of middle ear surgery using the canal wall down technique. STUDY DESIGN: This was a retrospective study of the past 23 years, conducted at a single tertiary care center. The authors evaluated the backgrounds, clinical features, and surgical findings in 25 patients with labyrinthine fistulae, who had a history of ear surgery using the canal down technique and who underwent a second operation at their hospital. INTERVENTIONS: All the patients underwent revision surgery because of persistent or recurrent vertigo caused by labyrinthine fistulae, circumscribed labyrinthitis, or suppurative labyrinthitis. MAIN OUTCOME MEASURES: The clinical features of this disease entity were assessed by history, surgical findings, and the results of audiovestibular testing. RESULTS: The patients had a long history of repetitive postoperative aural discharge before experiencing vertigo, which initially occurred 4 to 64 years (average, 20.2 years) after the previous operation. At the first visit to the authors' clinic, the results of a fistula test conducted with a Politzer's bulb were positive in 14 patients and negative in 5 patients. In the remaining 6 ears, pressure loading of the ear canal induced the sensation of vertigo without accompanying nystagmus. Surgical intervention showed that the fistulae were located at the lateral semicircular canal in 19 ears, at the footplate of the stapes in 4 ears, and at the promontory in 2 ears. Labyrinthine fistulae were closed with conchal cartilage, bone paste (bone dust mixed with fibrin glue), and/or temporalis fascia. In some patients, the fistulae were further covered with pedicled temporalis muscle. In 2 cases complicated by acute suppurative labyrinthitis, the mastoid cavity was obliterated after completion of the labyrinthectomy. The postoperative courses in all patients were uneventful. CONCLUSIONS: A labyrinthine fistula may be created by repeated and insidious infection of a mastoid cavity that has been exposed to the outside during canal wall down surgery. Intensive care of the opened mastoid cavity is essential to avoid this late complication.

Adolescent↗