Angiolipoma of internal auditory canal presenting repeated sudden hearing loss.
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Biomedical subjects
Publications and source records attributed to N Yanagihara.
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We developed two types of implantable hearing aids, a totally implantable hearing aid (TIHA) and a partially implantable hearing aid (PIHA) in 1983. In both types a piezoelectric ceramic bimorph was used as an ossicular vibrator which was coupled to the stapes to transmit sound signals to the inner ear efficiently. Due to technological immaturities, clinical application of the TIHA has not yet been realized. But the PIHA is available for clinical use at present. In the PIHA only the ossicular vibrator is implanted with inner link coil. The rest of components such as microphone, amplifier, battery, and outer link coil remain in their usual location behind the auricle. Since 1984, we have applied the PIHA to 37 patients with mixed deafness. Careful follow-up studies have been conducted on all of them to assess clinical and audiological results. We have confirmed that the device could function safely for more than 10 years affording natural quality of hearing without howling and wearing discomforts. Our studies suggest that the PIHA can be a choice of rehabilitation for mixed deafness due to middle ear diseases which cannot be rehabilitated satisfactorily by either surgical means or a conventional hearing aid. Functional principle of device, indications and surgical methods of implantation were described. Failures and delayed problems we experienced were also presented together with the preventive measures. We believe that an implantable hearing aid of this type will be an otologic breakthrough if substantial technological difficulties are cleared.
PTH and PTH-related peptide (PTHrP) bind to a type I PTH/PTHrP receptor expressed in bone and kidney or a type II receptor in nonclassical target tissue with equal affinity and similar bioactivities. PTHrP is abundant in the central nervous system, but its physiological role remains unknown. Herein, we examined the role of PTHrP-(1-34) on arginine vasopressin (AVP) release from the rat supraoptic nucleus (SON). Application of PTHrP-(1-34) to SON slices caused an increase in AVP release in a concentration-dependent manner. Neither PTHrP-(7-34) nor PTH-(1-34) had any effect on AVP release from the SON. PTHrP-(1-34)-induced AVP release was antagonized by a large excess of PTHrP-(7-34) and by H89, an inhibitor of cAMP-dependent protein kinase (A kinase), but not by PTH-(1-34) or PTH-(13-34). PTHrP-(1-34), but not PTH-(1-34), also dose-dependently increased the levels of cAMP in the SON. 125I-Labeled PTHrP-(1-34) bound specifically to crude membranes isolated from the SON. Scatchard analysis showed a single class of binding sites for PTHrP-(1-34) with a Kd of 36.4 nM and a maximum binding capacity of 3.94 pmol/mg protein. No specific binding for 125I-labeled PTH-(1-34) was noted. The binding of 125I-labeled PTHrP-(1-34) was displaced by unlabeled PTHrP-(1-34) and unlabeled PTHrP-(7-34), but not by unlabeled PTH-(1-34). These findings suggest that PTHrP-(1-34), but not PTH-(1-34), causes the release of AVP from the SON through a novel receptor distinct from type I or II PTH/PTHrP receptors.
The relationship of paranasal sinusitis to optic neuritis remains controversial. One of the major sources of this controversy is that there are some reports of rhinogenic optic neuritis (RON) in patients with mild paranasal sinusitis or with almost normal paranasal sinuses. The Onodi cell is a posterior ethmoid cell which pneumatized far laterally and to some degree superiorly to the sphenoid sinus and is intimately associated with the optic nerve. Coronal CT scanning is requisite to detect the Onodi cell; when it is present, an image of the sphenoid sinus just as if it were divided into top and bottom is characteristic. In our material from 200 patients (direct coronal CT scans 10 mm in width), the Onodi cell was observed in 7%. A case of RON whose pathogenesis was considered to be a direct spread of inflammation from the localized infection of the Onodi cell is reported. Ethmoiditis localized to the Onodi cell seems to play an important role in the pathogenesis of RON. Continued careful documentation of the localized posterior paranasal sinus lesion around the optic canal by detailed diagnostic imaging and endoscopic sinus surgery is necessary to resolve the disease entity of RON.
The removal of a functioning cochlear implant in order to upgrade to a more advanced device is a critical issue to many otologists, since we currently have no means to predict the results preoperatively. This paper reports on two patients who successfully upgraded from a single-channel to a multichannel implant. The new implants outperformed the original devices in both the live-voice test and the videotaped test. The patients stated that the hearing quality afforded by the multichannel implant was much better than that provided by the original implant.
Based on the analysis of the operative findings in 97 temporal bone fractures with respect to location, site of injury to the facial nerve and associated damage, we propose a new classification of the temporal bone fracture, using types 1, 2, 3 and 4, as previously described. Three-dimensional helical CT is valuable for assessment of fracture type. The incidence of each fracture type and the site of the injury to the facial nerve are described and the surgical significance of the classification is discussed.
Protrusion of the receiver-stimulator of a cochlear implant or a piezoelectric implantable hearing aid (IHA) was masked using bone dust applied in the gap between the receiver and the surrounding bone, making a smooth transitional border. The bone dust was then fixed with fibrin glue. Bone pâté (a mixture of bone dust and fibrin glue) was also used to fix the lead wire of a cochlear implant at the region of the posterior tympanotomy and to fasten an IHA vibrator holder to the temporal bone. Over the past two years, the use of these techniques in six patients with cochlear implants and two patients with IHAs has resulted in gratifying results; the edge of the receiver remained flush in all cases. They have been free from problems such as infection of the wound, necrosis of the overlying skin, and protrusion or migration of the receiver.
We have recently isolated a new endogenous substrate of 70 kDa for Ca2+/calmodulin-dependent protein kinase II (CaM kinase II) from bovine adrenal medullary cells (Yanagihara, N., Toyohira, Y., Yamamoto, H., Ohta, Y., Tsutsui, M., Miyamoto, E., and Izumi, F. (1994) Mol. Pharmacol. 46, 423-430). Here we report the sequence analysis of the 70-kDa protein and examine its phosphorylation by various protein kinases in vitro and by depolarization of the cultured cells. Protein sequencing and immunoblotting revealed that the 70-kDa protein is chromogranin A (CgA) or a closely related protein. Partially purified CgA was phosphorylated by cyclic AMP-dependent protein kinase and protein kinase C as well as CaM kinase II. Tryptic phosphopeptide mapping patterns of CgA differed among these protein kinases. In 32P-labeled bovine adrenal medullary cells, 56 mM K+ increased the phosphorylation of CgA and catecholamine secretion in similar time- and concentration-dependent manners, both of which were inhibited by 20 mM MgSO4, an inhibitor of voltage-dependent Ca2+ channels. These findings suggest that CgA serves as a substrate for several multifunctional protein kinases and that the elevation of the intracellular Ca2+ stimulates the phosphorylation of CgA associated with catecholamine secretion in cultured adrenal medullary cells.
OBJECTIVE: To determine whether herpes simplex virus type 1 (HSV-1) causes Bell palsy. DESIGN: Prospective study. SETTING: University inpatient service. PATIENTS: 14 patients with Bell palsy, 9 patients with the Ramsay-Hunt syndrome, and 12 other controls. MEASUREMENTS: Viral genomes of HSV-1, varicella-zoster virus, and Epstein-Barr virus were analyzed in clinical samples of facial nerve endoneurial fluid and posterior auricular muscle using polymerase chain reaction (PCR) followed by hybridization with Southern blot analysis. RESULTS: Herpes simplex virus type 1 genomes were detected in 11 of 14 patients (79%) with Bell palsy but not in patients with the Ramsay-Hunt syndrome or in other controls. The nucleotide sequences of the PCR fragments were identical to those of the HSV-1 genome. CONCLUSIONS: Herpes simplex virus type 1 is the major etiologic agent in Bell palsy.
In the central and peripheral noradrenergic neurons, the balance between noradrenaline release and reuptake determines the level of noradrenaline at the synaptic cleft or the nerve ending. In the present study, we examined the effects of propofol, an intravenous general anaesthetic, on catecholamine secretion and noradrenaline uptake in cultured bovine adrenal medullary cells and on the serum noradrenaline and blood pressure in rats. In cultured adrenal medullary cells, propofol (10-50 mumol/l) concentration-dependently inhibited catecholamine secretion stimulated by carbachol. Propofol suppressed carbachol-evoked 22Na+ influx as well as 45Ca2+ influx at concentrations similar to those which suppressed the catecholamine secretion. Propofol (10-50 mumol/l) also inhibited veratridine-evoked 22Na+ influx, 45Ca2+ influx and catecholamine secretion, whereas it had little effect on the 45Ca2+ influx and catecholamine secretion induced by 56 mmol/l K+. Cultured adrenal medullary cells show [3H] noradrenaline uptake which is sensitive to imipramine. Propofol (10-50 mumol/l) significantly inhibited the imipramine-sensitive uptake of [3H] noradrenaline. In rats, intravenous administration of propofol (2.5 mg/kg) lowered serum noradrenaline and arterial blood pressure. From these findings, in spite of inhibiting noradrenaline uptake, propofol at anaesthetic concentrations (10-30 mumol/l) seems to reduce catecholamine secretion by interfering with Na+ influx through voltage-dependent Na+ channels as well as nicotinic acetylcholine receptor-associated ion channels in the adrenal medulla and, probably, in the sympathetic nervous system. This may explain the propofol-induced hypotension during anaesthesia.
It has been recently reported that proadrenomedullin N-terminal 20 peptide (PAMP), which is secreted with adrenomedullin and catecholamines from the adrenal medulla, inhibits catecholamine release stimulated with nicotine. In the present study, to elucidate anticholinergic mechanisms of PAMP we employed the whole-cell patch-clamp and the intracellular Ca2+ imaging techniques in cultured bovine adrenal medullary cells. PAMP inhibited nicotinic currents and [Ca2+]i rises induced by nicotine in a dose-dependent manner (10(-9)-10(6) M). These inhibitions were selective, since PAMP alone did not induce any ionic currents, moreover it did not affect voltage-dependent Ba2+ currents or high K+ (50 mM)-induced [Ca2+]i rises. The onset of the inhibitory effect of PAMP (10(-6) M) was very rapid and reached a steady-state level within 10 sec. The effect of PAMP (10(-6) M) lasted for about 10-15 min. Desensitization process of the nicotinic current fitted to a single exponential function with a time constant of 6.4 +/- 0.3 sec. When PAMP (10(-6) M) simultaneously added with nicotine (10(-5) M), the desensitization process was facilitated and fitted to two exponentials with time constants of 0.46 +/- 0.08 and 2.5 +/- 0.8 sec. From the present results, the inhibition by PAMP of nicotinic currents which was well associated with that of nicotine induced [Ca2+]i rises leads to the attenuation of catecholamine release probably, at least in part, due to the facilitation of the desensitization process of the nicotinic currents.
In surgical treatment of ears with chronic discharge, pathogenic microorganisms may remain in the middle ear even after meticulous tympanomastoidectomy, and cause recurrent infection unless an appropriate antimicrobial agent is administered. The present study was conducted to determine the incidence of residual bacterial infection in the tympanic cavity by examining secretions from a drainage tube placed there via the mastoid cavity during surgery. Comparison of the bacterial flora before and after surgery demonstrated that some of the microorganisms continued to be present in the tympanic cavity for up to 2 weeks despite medication, and that the incidence of Pseudomonas aeruginosa and Staphylococcus epidermidis remained fairly high.
A large vagal neurilemmoma in a 33-year-old man is reported. He complained of slowly progressive palsy of the tongue on the left side. Weakness of soft palate movement was also noted. Magnetic resonance imaging (MRI) revealed a tumour in the left parapharyngeal space with partial extension to the posterior cranial fossa through the jugular foramen. Carotid angiography revealed avascularity of the tumour and anterior shift of the left internal carotid artery. The venous phase showed no blood flow in the internal jugular vein. The tumour was successfully extirpated via a transmandibular transpterygoid approach. Although vagus nerve dysfunction was not observed pre-operatively, the tumour was identified as a neurilemmoma arising from the vagus nerve. The surgical approach should be selected according to the lesion in individual patients. Since neurilemmoma is benign in nature, minimal post-operative sequelae should be expected.
KN-62, an inhibitor of Ca2+/calmodulin-dependent protein kinase II (CaM kinase II), inhibited significantly catecholamine secretion and tyrosine hydroxylase activity stimulated by acetylcholine in cultured bovine adrenal medullary cells. KN-62, however, showed an additional inhibitory effect on acetylcholine-induced 45Ca2+ influx, which is essential for functional responses. Carbachol-stimulated 22Na+ influx, veratridine-induced 22Na+ influx, and 56 mM K(+)-evoked 45Ca2+ influx were also attenuated by KN-62. Inhibitions by KN-62 of these ion influxes were correlated closely with those of catecholamine secretion. KN-04, which is a structural analogue of KN-62 but does not inhibit CaM kinase II activity, elicited inhibitory effects on the three kinds of stimulant-evoked ion influxes with an inhibitory potency similar to KN-62. These results suggest that KN-62 inhibits catecholamine secretion and tyrosine hydroxylase activation due to mainly its ion channel blockade on the plasma membrane rather than the inhibition of CaM kinase II activity in the cells.
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To clarify the role and site of herpes simplex virus (HSV) infection in the pathogenesis of facial paralysis, we examined the viral genome by the polymerase chain reaction and the neutralization antibody titer using microplates in an animal model. Following inoculation with HSV type 1 of the KOS strain into mouse auricles, HSV DNA appeared in the ipsilateral facial nerve on the 3rd day, and in bilateral facial nerves and the brain stem on the 10th day only in animals with facial paralysis. In animals without facial paralysis, no HSV DNA was detected in these tissues. The neutralization antibody titer was elevated between 4 and 20 days in all animals, with or without facial paralysis. Facial paralysis developed only on the inoculated side, even though HSV DNA was also present in the contralateral facial nerve. We conclude that HSV infection in the facial nerve and brain stem is prerequisite for facial paralysis, and suggest that an immunologic reaction following viral infection plays a key role in the pathogenesis.
The rate of residual disease after surgery for acquired middle ear cholesteatoma was investigated in 167 ears of 164 patients who had undergone planned second-look tympanoplasty by the intact canal wall technique. Overall, operative findings at the second stage revealed 65 cases of residual disease in 48 ears (29%). These consisted of 50 squamous pearls, 11 cases of the flat, open type, and 4 cases of the extensive type. The configuration of residual disease is closely related to the technical difficulty of eradication, since en bloc removal is much easier in the squamous pearl than in the open or extensive type, mainly because of the unclear margin with the surrounding tissues. The proportion of cases of the open type was greater in children than in adults, in pars tensa cholesteatoma than in pars flaccida cholesteatoma, and in severe primary middle ear disease than in moderate or mild disease, although these differences were not statistically significant. The extensive type occurred in 4 ears with severe primary disease, 3 of which were in children. These results support the value and importance of the staged procedure for middle ear cholesteatoma, particularly when operated on by the intact canal wall technique.
Blood patch is a therapeutic procedure that uses a perilymphatic fistula to repair an inner ear window rupture by filling the tympanic cavity with autologous blood. The experimental study was conducted in 13 guinea pigs. Autologous blood or commercially available fibrin glue was poured into the otic bulla after artificial rupture of the round window. The animals were sacrificed immediately, or 1 to 7 days after the operation. The results showed that the blood or the fibrin glue successfully closed the window rupture by closing directly and by facilitating the formation of granulation at the margin of the rupture. Fibrin glue seemed to be preferable to autologous blood due to its non-toxic nature in the inner ear.