Biomedical subjects

Nobuhiro Hakuba

Publications and source records attributed to Nobuhiro Hakuba.

17 recordsLinked to original sources

PubMed2006

Storage of the incus in the mastoid bowl for use as a columella in staged tympanoplasty.

OBJECTIVE: To evaluate whether the incus of the cholesteatomatous ear preserved in the mastoid bowl during the first stage of planned two-stage tympanoplasty can tolerate long-term implantation and be used in ossicular reconstruction during the second stage. METHODS: The study group included 24 ears of 23 patients who underwent staged tympanoplasty for the treatment of middle ear cholesteatoma. At the first stage, after removing the incus to eradicate the middle ear disease, it was returned to the mastoid bowl and stored there until use at the second stage. The average interval between the two stages was 8.3 months (range 6-12 months). RESULTS: The incus was identified in all cases at the second stage: 10 incudes were found to be covered with a thin mucosa layer, 12 were buried in fibrous or granulation tissue, and 2 were joined to the surrounding bone. Residual cholesteatoma was found in six ears, either in the attic (three ears) or tympanic sinus (three ears). It never occurred in the mastoid bowl where the incus had been preserved. In 19 cases, the incus was available as a short columella for ossicular reconstruction. The remaining five cases were reconstructed using a hydroxyapatite ossicle as a long columella, since the stapes superstructure was missing at the second stage. In one case, the stored incus underwent remarkable absorption between stages. CONCLUSION: Preservation of the incus in the mastoid bowl is an effective option in planned two-stage tympanoplasty, when the incus is considered useful for ossicular reconstruction at the second stage.

Cholesteatoma, Middle Ear↗

PubMed2006

A new tool for testing ossicular mobility during middle ear surgery: preliminary report of four cases.

OBJECTIVE: We developed an ossicular vibration tester for the objective and quantitative assessment of ossicular mobility, which is one of the most critical factors affecting postoperative hearing after tympanoplasty. METHODS: Our device consists of three components: a probe shaft with a curved tip to be attached to the target ossicle, a vibration exciter to activate the probe, and a piezoelectric sensor to detect vibrations of the probe. These components are encased in a stainless steel holder, allowing easy hand manipulation during ear surgery. The probe is activated with an electric signal at around 1,600 Hz. The system is controlled with a laptop computer, and the results are presented as the ratio of the ossicular resistance (ROR) to a reference value as a percentage. One measurement takes 10 ms. The device was applied in four selected patients during ear surgery. RESULTS: Several measurements in two of the cochlear implantees showed a greater difference in the RORs of the stapes (15-20% in Case 1 and 35-45% in Case 2), whereas the RORs of the malleus and incus were within the same range. This was thought to correspond to the partial cochlear calcification noted in Case 2. In Case 3, who underwent surgery because of otosclerosis, the ROR of the stapes was high, ranging from 70 to 80%. When measured for the malleus-incus fixation anomaly (Case 4), the ROR of the malleus and incus was in the range of 60 to 70%. Owing to the limited surgical view, the ROR of the stapes could not be measured. No problems related to the measurements with this device were noted. CONCLUSION: The design, principles, measuring procedures, and preliminary results of our new tool for testing ossicular mobility are reported. Measuring the ossicular mobility during surgery may provide important information for deciding the surgical procedures.

Adolescent↗

PubMed2005

Neural stem cells suppress the hearing threshold shift caused by cochlear ischemia.

Neural stem cells are multipotent progenitor cells that show self-renewal activity. In this study, we assessed the use of neural stem cells for ameliorating ischemia-reperfusion injury of the gerbil cochlea. Neural stem cells were injected into one inner ear through the round window 1 day after ischemic insult. Immunostaining for nestin showed that the distribution of neural stem cells was concentrated within the organ of Corti. Seven days after ischemia, the injury-induced auditory brainstem response threshold shift and progressive inner hair cell damage were markedly less on the neural stem cell-transplanted side. These results suggest that the transplantation of neural stem cells is therapeutically useful for preventing damage to hair cells that occurs after transient ischemia of the cochlea.

Animals↗

PubMed2005

Irinotecan (CPT-11) combined with cisplatin for small cell carcinoma of the nasal cavity.

We describe a case of small cell carcinoma arising in the nasal cavity using combined chemotherapy with irinotecan (CPT-11)/cisplatin followed by surgical salvage which successfully avoided a radical operation. In a follow-up no local recurrence was observed over 3 years after the operation. Ours is the first report of the use of combined irinotecan (CPT-11)/cisplatin chemotherapy in small cell carcinoma of the nasal cavity.

Aged↗

PubMed2005

Ischemic damage increases nitric oxide production via inducible nitric oxide synthase in the cochlea.

The present study was designed to elucidate the dynamic changes of nitric oxide (NO) production in the perilymph and to investigate the immunostaining for inducible nitric oxide synthase (iNOS) in the cochlea for 7 days after transient cochlear ischemia. Moreover, aminoguanidine, which is a selective iNOS inhibitor, was administrated immediately following ischemia and every 24h thereafter for 7 days to investigate whether the production of NO is dependent on the iNOS pathway. Significant increases in the oxidative NO metabolites, nitrite (NO(2)(-)) and nitrate (NO(3)(-)), were measured on day 1 using an in vivo microdialysis and on-line high performance liquid chromatography (HPLC) system. The immunostaining for iNOS was strongly expressed on days 1 and 4 and returned to normal on day 7 after the ischemia. The administration of aminoguanidine reduced the oxidative NO metabolites on day 1 and suppressed the expression of iNOS. These findings suggest that transient ischemia causes a remarkable increase in NO production in the perilymph, which might be attributable to the iNOS pathway.

Animals↗

PubMed2005

Transient cochlear ischemia and its effects on the stria vascularis.

The effects of transient cochlear ischemia on the stria vascularis were studied. Fifteen minutes of ischemia decreased the endocochlear potential by up to 17.5 mV on day 1; it returned to normal on day 7. Immunostaining for Na+,K+-ATPase, a marker for the Na+/K+-pump, and for connexin 26, a marker for gap junctions, was inhibited on days 1 and 4, and returned to normal on day 7. Electron microscopy showed expansion of the intercellular space with abundant vacuolar formation in the stria vascularis. These morphological changes disappeared completely by day 7. The results indicate that transient ischemia causes a reversible functional disorder of the stria vascularis with fine structural changes, which may be owing to dysfunction of Na+/K+-pump or gap junctions.

Animals↗

PubMed2005

Kanamycin ototoxicity in glutamate transporter knockout mice.

Glutamate-aspartate transporter (GLAST), a powerful glutamate uptake system, removes released glutamate from the synaptic cleft and facilitates the re-use of glutamate as a neurotransmitter recycling system. Aminoglycoside-induced hearing loss is mediated via a glutamate excitotoxic process. We investigated the effect of aminoglycoside ototoxicity in GLAST knockout mice using the recorded auditory brainstem response (ABR) and number of hair cells in the cochlea. Kanamycin (100 mg/mL) was injected directly into the posterior semicircular canal of mice. Before the kanamycin treatment, there was no difference in the ABR threshold average between the wild-type and knockout mice. Kanamycin injection aggravated the ABR threshold in the GLAST knockout mice compared with the wild-type mice, and the IHC degeneration was more severe in the GLAST knockout mice. These findings suggest that GLAST plays an important role in preventing the degeneration of inner hair cells in aminoglycoside ototoxicity.

Amino Acid Transport System X-AG↗

PubMed2004

Chondroma of the bony external auditory canal attached to the short process of the malleus.

A chondroma located in the external auditory canal is a rare finding. Here, we report the case of a 12-year-old girl who attended our clinic with complaints of a rustling sound in her left ear. Otoscopic examination revealed a tiny bone-like tumor protruding from the anterior wall of the bony external auditory canal, attached to the short process of the malleus. An audiogram revealed a conductive hearing loss in her left ear, although she did not notice it. After excision of the tumor through the ear canal, her complaints disappeared and her hearing recovered. Histologically, the tumor proved to be a chondroma.

Child↗

PubMed2004

Reconstruction of mastoid cortex defect using bone morphogenetic protein: an experimental study in the guinea pig.

OBJECTIVE: The aim of this experimental study was to examine whether recombinant human bone morphogenetic protein-2 (rhBMP-2) could induce new bone formation in a small hole drilled through the temporal bone near the external auditory canal wall in guinea pigs. MATERIAL AND METHODS: A 4-mm diameter hole was made in the center of the temporal bone and a piece of collagen sheet infiltrated with rhBMP-2 was placed in the hole. New bone formation was confirmed by means of X-ray examination and the bone mineral density was quantified using dual-energy X-ray absorptiometry 1, 2 and 4 weeks after treatment. RESULTS: The bone mineral density in the rhBMP-2-treated group was significantly increased compared to the control group. CONCLUSION: These results suggest that rhBMP-2 induces remarkable new bone formation in the temporal bone and will be useful in clinical ear surgery.

Animals↗

PubMed2003

Free radical scavenger protects against inner hair cell loss after cochlear ischemia.

We investigated the protective effects of edaravone, a free radical scavenger, against ischemic damage of inner hair cells (IHCs) in gerbils. Cochlear ischemia was induced in the animals by occluding the vertebral arteries bilaterally for 15 min. Edaravone (1 mg/kg, i.v.) or saline was administered 1 h after ischemia. Hearing was assessed by auditory brain response (ABR). In animals treated with saline, the ABR threshold shift was 24.1 dB and there was a 26.5% decrease in the number of IHCs. By contrast, in animals treated with edaravone, the threshold shift was 7.5 dB and only 8.8% of IHCs was lost. These results suggest that edaravone protects against damage to the inner ear following transient ischemia.

Analysis of Variance↗

PubMed2003

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↗

PubMed2003

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↗

PubMed2003

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↗

PubMed2003

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↗

PubMed2003

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↗

PubMed2002

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↗

PubMed2002

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↗