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Tatsuya Yamasoba

Publications and source records attributed to Tatsuya Yamasoba.

At least 19 recordsLinked to original sources
PubMed2007

Methimazole-induced cell death in rat olfactory receptor neurons occurs via apoptosis triggered through mitochondrial cytochrome c-mediated caspase-3 activation pathway.

The administration of methimazole is known to induce cell death in rat olfactory receptor neurons (ORNs). We investigated whether this injury occurs via apoptosis or through necrosis and whether it involves the extrinsic or intrinsic pathway. Rats were intraperitoneally injected with vehicle (control) or 300 mg/kg methimazole. The experimental animals were also administered vehicle or a caspase-3 or caspase-9 inhibitor 30 min earlier. The administration of methimazole induced cell death predominantly in the mature ORNs and partially reduced olfactory sensitivity in the rats; the injured cells were TUNEL-positive and showed a nuclear staining pattern. This insult induced cytochrome c release from the mitochondria and a significant increase in the immunoreactivity of activated caspase-3 and caspase-9 as well as that of cleaved poly-ADP-ribose-polymerase; in addition, it caused a significant increase in the fluorogenic activity of caspase-3 and caspase-9. However, it did not affect the immunoreactivity of activated caspase-8 or the fluorogenic activity of caspase-8. Pretreatment with a caspase-3 or caspase-9 inhibitor nearly completely prevented the morphologic, biochemical, and functional changes induced by methimazole. These findings suggest strongly that methimazole-induced cell death in rat ORNs is predominantly apoptosis; moreover, the majority of this apoptotic cell death is triggered through mitochondrial cytochrome c-mediated caspase-3 activation pathway, and both caspase-3 and caspase-9 inhibitors can prevent methimazole-induced cell death in the ORNs.

Animals↗
PubMed2007

Influence of chronic middle ear diseases on gustatory function: an electrogustometric study.

OBJECTIVE: We aimed to quantitatively determine whether middle ear inflammation associated with unilateral chronic otitis media (COM), cholesteatoma, or otosclerosis affects gustatory function. STUDY DESIGN: Prospective study. SETTING: University Hospital, Department of Otolaryngology. PATIENTS: Forty-two patients had unilateral COM (22 men, 20 women; mean age, 54.2 yr), 57 had unilateral cholesteatoma (35 men, 22 women; mean age, 42.1 yr), and 19 had unilateral otosclerosis (10 men, 9 women; mean age, 49.3 yr). MAIN OUTCOME MEASURES: Patients underwent taste testing using electrogustometry (EGM) and sensation thresholds were compared in the affected and unaffected ears among groups and between affected and unaffected ears in each group. RESULTS: Patients with COM and cholesteatoma exhibited an increase in taste threshold in the affected ears compared to the unaffected ears (p < 0.05), whereas otosclerosis patients did not. The extent of the increase of the sensation thresholds in the affected ears was very similar between patients with COM and those with cholesteatoma (p = 0.548). CONCLUSION: Our EGM study showed that cholesteatoma and chronic middle ear inflammation affected gustatory function to a similar degree.

Adult↗
PubMed2006

Mechanisms of noise-induced hearing loss indicate multiple methods of prevention.

Recent research has shown the essential role of reduced blood flow and free radical formation in the cochlea in noise-induced hearing loss (NIHL). The amount, distribution, and time course of free radical formation have been defined, including a clinically significant late formation 7-10 days following noise exposure, and one mechanism underlying noise-induced reduction in cochlear blood flow has finally been identified. These new insights have led to the formulation of new hypotheses regarding the molecular mechanisms of NIHL; and, from these, we have identified interventions that prevent NIHL, even with treatment onset delayed up to 3 days post-noise. It is essential to now assess the additive effects of agents intervening at different points in the cell death pathway to optimize treatment efficacy. Finding safe and effective interventions that attenuate NIHL will provide a compelling scientific rationale to justify human trials to eliminate this single major cause of acquired hearing loss.

Animals↗
PubMed2006

Caloric restriction suppresses apoptotic cell death in the mammalian cochlea and leads to prevention of presbycusis.

Presbycusis is characterized by an age-related progressive decline of auditory function, and arises mainly from the degeneration of hair cells or spiral ganglion (SG) cells in the cochlea. Here we show that caloric restriction suppresses apoptotic cell death in the mouse cochlea and prevents late onset of presbycusis. Calorie restricted (CR) mice, which maintained body weight at the same level as that of young control (YC) mice, retained normal hearing and showed no cochlear degeneration. CR mice also showed a significant reduction in the number of TUNEL-positive cells and cleaved caspase-3-positive cells relative to middle-age control (MC) mice. Microarray analysis revealed that CR down-regulated the expression of 24 apoptotic genes, including Bak and Bim. Taken together, our findings suggest that loss of critical cells through apoptosis is an important mechanism of presbycusis in mammals, and that CR can retard this process by suppressing apoptosis in the inner ear tissue.

Aging↗
PubMed2006

Role of mitochondrial dysfunction and mitochondrial DNA mutations in age-related hearing loss.

Mitochondrial DNA (mtDNA) mutations/deletions are considered to be associated with the development of age-related hearing loss (AHL). We assessed the role of accumulation of mtDNA mutations in the development of AHL using Polg(D257A) knock-in mouse, which exhibited increased spontaneous mtDNA mutation rates during aging and showed accelerated aging primarily due to increased apoptosis. They exhibited moderate hearing loss and degeneration of the hair cells, spiral ganglion cells and stria vascularis by 9 month of age, while wild-type animals did not. We next examined if mitochondrial damage induced by systemic application of germanium dioxide caused progressive hearing loss and cochlear damage. Guinea pigs and mice given germanium dioxide exhibited degeneration of the muscles and kidney and developed hearing loss due to degeneration of cochlear tissues, including the stria vascularis. Calorie restriction, which causes a metabolic shift toward increased energy metabolism in some organs, has been shown to attenuate AHL and age-related cochlear degeneration and to lower quantity of mtDNA deletions in the cochlea of mammals. Together these findings indicate that decreased energy metabolism due to accumulation of mtDNA mutations/deletions and decline of respiratory chain function play an important role in the manifestation of AHL.

Animals↗
PubMed2006

Supporting cell proliferation after hair cell injury in mature guinea pig cochlea in vivo.

In cold-blooded animals, lost sensory hair cells can be replaced via a process of regenerative cell proliferation of epithelial supporting cells. In contrast, in mammalian cochlea, receptor (hair) cells are believed to be produced only during embryogenesis; after maturity, sensory or supporting cell proliferation or regeneration are thought to occur neither under normal conditions nor after trauma. Using bromodeoxyuridine (BrdU) as a proliferation marker, we have assessed cell proliferation activity in the mature organ of Corti in the cochlea of young guinea pigs following severe damage to the outer hair cells induced by kanamycin sulfate and ethacrynic acid. Although limited, we have found BrdU-labeled nuclei in the regions of Deiters cells when BrdU is given for 3 days or longer. When BrdU is given for 10 days, at least one labeled nucleus can be observed in the organ of Corti in approximately half of the ears; proliferating cells typically appear as paired daughters, with one nucleus being displaced away from the basement membrane to the position expected of the hair cells. Double-staining with antibodies to cytokeratin, vimentin, and p27 have shown that the BrdU-labeled nuclei are located in cells phenotypically similar to Deiters cells. Most of the uptake of BrdU occurs 3-5 days following ototoxic insult, and the number of BrdU-labeled cells does not decrease until 30 days following insult. These findings indicate that Deiters cells in the mature mammalian cochlea maintain a limited competence to re-enter the cell cycle and proliferate after hair cell injury, and that they can survive at least for 1 month.

Animals↗
PubMed2005

Cochlear damage due to germanium-induced mitochondrial dysfunction in guinea pigs.

This investigation addressed the effect of germanium dioxide (GeO(2))-induced mitochondrial dysfunction on hearing acuity. Guinea pigs were fed chow that contained 0%, 0.15%, or 0.5% GeO(2). The animals that were fed 0.5% GeO(2) for 2 months developed hearing impairment chiefly due to degeneration of stria vascularis and cochlear supporting cells, which exhibited electron-dense mitochondrial inclusions. Cytochrome c oxidase activity was decreased in the skeletal muscles and kidney, which also exhibited electron-dense mitochondrial inclusions. No apparent pathological changes were observed in the utricle, semicircular canal, or among the vestibular nerve fibers, or in the liver or heart. The untreated animals and those treated with 0.15% GeO(2) did not exhibit hearing impairment or pathological changes in any organs. These findings suggest that administration of 0.5% GeO(2) induces mitochondrial dysfunction in the stria vascularis and supporting cells in the cochlea, as in the skeletal muscles and kidney, thereby causing hearing impairment in the guinea pigs.

Animals↗
PubMed2005

Alteration of frequency range for binaural beats in acute low-tone hearing loss.

The effect of acute low-tone sensorineural hearing loss (ALHL) on the interaural frequency difference (IFD) required for perception of binaural beats (BBs) was investigated in 12 patients with unilateral ALHL and 7 patients in whom ALHL had lessened. A continuous pure tone of 30 dB sensation level at 250 Hz was presented to the contralateral, normal-hearing ear. The presence of BBs was determined by a subjective yes-no procedure as the frequency of a loudness-balanced test tone was gradually adjusted around 250 Hz in the affected ear. The frequency range in which no BBs were perceived (FRNB) was significantly wider in the patients with ALHL than in the controls, and FRNBs became narrower in the recovered ALHL group. Specifically, detection of slow BBs with a small IFD was impaired in this limited (10 s) observation period. The significant correlation between the hearing level at 250 Hz and FRNBs suggests that FRNBs represent the degree of cochlear damage caused by ALHL.

Acute Disease↗
PubMed2005

Ebselen prevents noise-induced excitotoxicity and temporary threshold shift.

This investigation tested the hypothesis that a noise-induced temporary threshold shift (TTS) can be attenuated by a peroxynitrite scavenger, ebselen (2-phenyl-1,2-benzisoselenazol-3(2H)-one). Guinea pigs received an oral dose of the vehicle or 10 mg/kg ebselen 1h before exposure to 115 dB SPL 4-kHz octave band noise for 3 h. In controls, auditory brainstem response (ABR) thresholds increased by 25-45 dB immediately after noise and returned to pre-exposure baseline thresholds 7 days later. Ebselen eliminated this ABR threshold shift following noise exposure. In controls, swelling of the afferent dendrites beneath the inner hair cells was evident immediately after noise, whereas ebselen significantly reduced this pathology. These findings suggest that scavenging peroxynitrite can attenuate noise-induced excitotoxicity and, thereby, TTS.

Animals↗
PubMed2005

Correlation between microtia and temporal bone malformation evaluated using grading systems.

OBJECTIVE: To evaluate the relationships between temporal bone abnormalities and the severity of microtia in Japanese patients using objective grading systems. DESIGN: Retrospective case series study conducted between 1992 and 2003. SETTING: Academic, tertiary care, referral medical center. PATIENTS: One hundred forty-two ears of 109 Japanese patients (85 male and 24 female patients; mean age, 12.8 years [range, 2-36 years]) with microtia. MAIN OUTCOME MEASURES: The severity of microtia was classified according to Marx classification. Developmental abnormalities of the temporal bone were evaluated by a computed tomographic (CT) scoring system modified after the system used by Jahrsdoerfer and colleagues, using high-resolution CT scans of the temporal bone. Correlations between the scores obtained from these 2 grading systems were evaluated using a nonparametric statistical method. RESULTS: Male preponderance and incidence of bilateral cases of approximately 30% were observed in our Japanese patients with microtia. There was no significant difference in the severity of microtia between unilateral and bilateral cases. The mean +/- SEM total points in the CT scoring system (full marks, 10) was 7.9 +/- 0.4 for grade I microtia, 6.6 +/- 0.6 for grade II, and 6.4 +/- 0.3 for grade III; the total points correlated inversely with the microtia grade. Development of the auricle correlated significantly with aeration in the middle ear spaces but not with ossicular development or formation of the oval/round windows. Proportion of acceptable surgical candidates according to the CT scoring system (>5 points) was 79% for grade I microtia, 52% for grade II microtia, and 65% for grade III microtia. CONCLUSION: The principle "the better developed the auricle, the better developed middle ear" was confirmed in Japanese patients with microtia; however, even with grade II/III microtia, more than half of the patients were considered suitable for atresia surgery.

Abnormalities, Multiple↗
PubMed2005

Acquired atrophy of the long process of the incus.

Various lesions can cause conductive hearing loss in a patient with a normal tympanic membrane. These include congenital ossicular anomaly, otosclerosis, and congenital or acquired ossicular fixation and discontinuity. We had an experience with a patient who presented with a conductive hearing loss in both ears, in which small pieces of the long process of the incus were absent and had been replaced with fibrous tissues in both ears. No other abnormalities, such as postinflammatory changes or fixation of the ossicles, were found. Because the long process of the incus undergoes remodeling through resorption and rebuilding throughout life, failure of the remodeling or impaired vascular supply to the long process of the incus may have been the cause of the conductive hearing loss in this patient.

Atrophy↗
PubMed2005

Cyclooxygenase-2 regulates the degree of apoptosis by modulating bcl-2 protein in pleomorphic adenoma and mucoepidermoid carcinoma of the parotid gland.

CONCLUSION: These results suggest that COX-2 and bcl-2 protein were overexpressed and that apoptosis was reduced in MEC compared to PMA, and that COX-2 may regulate the degree of apoptosis by modulating bcl-2 protein in PMA and MEC. OBJECTIVE: Cyclooxygenase (COX)-2 plays a crucial role in tumorigenesis and overexpression of COX-2 in vitro accompanied by overexpression of bcl-2 protein has been shown to reduce apoptosis. The purpose of this study was to verify that COX-2 regulates the degree of apoptosis by modulating bcl-2 protein in benign and malignant parotid gland tumors. : We examined archival formalin-fixed, paraffin-embedded tissue sections of 10 pleomorphic adenomas (PMAs) and 10 mucoepidermoid carcinomas (MECs) by immunostaining with anti-COX-2, anti-bcl-2 and anti-single-stranded DNA (ssDNA) antibodies. Labeling indices of the three antibodies were calculated using computer-assisted image analysis. RESULTS: Labeling indices (mean+/-SD) of anti-COX-2 antibody in PMA and MEC were 2.05+/-1.30 and 11.2+/-2.95, respectively (p < 0.001), those of anti-bcl-2 antibody were 2.00+/-1.28 and 9.68+/-4.05, respectively (p < 0.001) and those of anti-ssDNA antibody were 8.06+/-2.54 and 2.08+/-1.47; respectively (p <0.001). Correlation coefficients between the labeling indices of anti-COX-2 antibody and anti-bcl-2 antibody, anti-bcl-2 antibody and anti-ssDNA antibody and anti-COX-2 antibody and anti-ssDNA antibody were 0.88, -0.75 and -0.76, respectively (p <0.001).

Adenoma, Pleomorphic↗
PubMed2005

Are vestibular sensory cells preserved after destruction of Scarpa's ganglion? A study based on metastatic tumors of temporal bone.

OBJECTIVE: The contribution of nerve fibers to the maintenance of vestibular sensory cells is a controversial issue in previous studies using animals and has not yet been studied in humans. The authors investigated this issue by observing vestibular end organs in the temporal bone of three patients in whom the internal auditory canal was infiltrated with tumor cells, and Scarpa's ganglion cells showed complete degeneration. STUDY DESIGN: Retrospective case review. SETTING: University Hospital, Department of Otolaryngology. PATIENTS: Three patients with malignant metastatic temporal bone tumors. INTERVENTION: We investigated the preservative state of vestibular sensory hair cells with the Scalpa's ganglion was destructed. MAIN OUTCOME MEASURES: Maintenances of vestibular sensory hair cells. RESULTS: We found that sensory cells were intact despite the severe destruction of Scarpa's ganglion cells in two of the patients. CONCLUSION: The findings suggest that human vestibular sensory cells can be maintained for an indefinite period after denervation.

Adolescent↗
PubMed2004

Cortical activation shortly after cochlear implantation.

We evaluated the cortical activations in postlingually deaf cochlear implant (CI) users in the early period (0-2 months) of CI usage. The subjects were 8 early CI users and 8 normal subjects. With tone burst stimuli (1 kHz) delivered to the right side, strong and broad activation of the ipsilateral (right) primary auditory cortex with 2 peaks and weaker activation of the contralateral (left) temporal lobe were observed in early CI users, in a clear contrast with the normal subjects in whom activation was observed in a small area of the contralateral (left) primary cortex. With word stimuli, activation of the superior frontomedian cortex presumably including the supplementary motor area and the neighboring cingulate gyri was observed in early CI users, which was absent in normal subjects. The activation in the immediate association cortices near the primary area was lower in early CI users, while the periphery of the association cortex seemed to be more mobilized.

Acoustic Stimulation↗
PubMed2004

The role of the external auditory canal in the development of the malleal manubrium in humans.

OBJECTIVE: To determine if the external auditory canal (EAC) plays a role in the induction and proper positioning of the malleal manubrium in humans. STUDY DESIGN: Retrospective study between 1994 and 2002. SETTING: Academic, tertiary care referral medical center. Patients Fifty-five ears of 50 patients with congenital atresia (n = 47) or stenosis (n = 8) of the EAC, for which meatoplasty was performed at the University hospital between 1994 and 2002. MAIN OUTCOME MEASURES: The presence of the manubrium was examined during surgery, and the corre-lation between the presence of the manubrium and the grade of the microtia was evaluated. RESULTS: The manubrium was identified in all ears with EAC stenosis, whereas it was absent in all ears with EAC atresia. No correlation was observed between manubrium formation and auricular deformity. CONCLUSIONS: Our results demonstrated a close relationship between the formation of the EAC and that of the malleal manubrium in humans. This is consistent with the recent findings in knockout mice. This information is useful for surgical intervention in cases of congenital EAC anomalies.

Adolescent↗