[Clinical studies on the obstructive uropathy--cystometry, uroflometry and renal function test].
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Biomedical subjects
Publications and source records attributed to K Jinnouchi.
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The aim of the present study was to establish an animal model of autoimmune labyrinthitis using heterologous inner ear antigen (IEAg) and to elucidate whether the experimentally induced labyrinthitis could be passively transferred. Cochlear and vestibular membranous labyrinthine tissues from bovine temporal bones were used as IEAg. Donor mice were inoculated intracutaneously at multiple sites with an emulsion consisting of equal parts of IEAg and complete Freund's adjuvant. After 10 days, mononuclear cells were collected from lymph nodes, spleen and blood of the donor mice and injected intravenously into naive recipient mice. Cellular infiltration was observed in the perilymphatic space of the cochlea of all donor and recipient mice. Endolymphatic hydrops was also observed in 63% of donor and 42% of recipient mice. These findings suggest that the experimentally induced labyrinthitis observed in this animal model was probably due to an autoimmune reaction to the IEAg and was passively transferred by a cell-mediated immune reaction.
The purpose of this study was to elucidate the mechanism of endothelin 1 (ET1) production in the cochlea of rats. Animals were anesthetized with pentobarbital sodium intraperitoneally and sacrificed by cardiac perfusion with warm saline followed by periodate-lysine-paraformaldehyde. The temporal bones and kidneys were fixed overnight in the same fixative, decalcified with 5% EDTA and embedded in paraffin. Immunohistochemical staining was performed using the labeled streptavidin biotin method to detect the localization of big endothelin 1 (BET1), ET1 and endothelin-converting enzyme 1 (ECE1). Immunoreactivity for BET1, ET1 and ECE1 was localized to the small vessels of the bony labyrinth adjacent to the spiral ligament. Immunohistochemistry for ET1 and BET1 was also localized to the spiral ligament. These results suggest that ET1 may be produced in the small vessels of the bony labyrinth adjacent to the spiral ligament and may play an important role in the cochlear function.
Immunohistochemical study for inducible nitric oxide synthase (iNOS or NOS II) in the cochlea of guinea pigs was performed after the injection of keyhole limpet hemocyanin (KLH) into the endolymphatic sac. Morphological changes were observed in the cochlea of all animals after the injection of KLH. Increased iNOS expression was detected in the lateral wall, organ of Corti and ganglion cells. It is known that high levels of nitric oxide can lead to inner ear dysfunction. Our results suggest that iNOS may mediate the inner ear disturbance as seen in endolymphatic hydrops.
This study has investigated immune injuries to the inner ear auditory system of guinea pigs. Following secondary antigen challenge to the endolymphatic sac, the mean hearing threshold significantly increased in the early phase from day 1 to day 3 and thereafter recovered. In the early phase, hearing threshold significantly increased simultaneously to the elevation of perilymph antibody levels. The size of hydrops was not the only factor that causes an increase in hearing loss as well as in AP/SP ratio. Scale-out hearing loss was seen in 2 animals with severe degeneration of the stria vascularis as well as the organ of Corti associated with the inflammatory cellular infiltration especially in the perilymphatic space, even in the absence of keyhole limpet hemocyanin antigen in the cochlea. On the other hand, control animals did not suffer hearing loss. These results suggest that an immune reaction in the endolymphatic sac is a possible pathogenic etiology of Ménière's disease or sudden deafness.
Endothelin (ET) has been revealed to be a local hormonal regulator of pressure, fluid, ions and neurotransmitters. In order to investigate the mechanism of homeostasis within the microenvironment of the inner ear, the present study has examined the distribution of ET in the vestibule of normal guinea pigs, by immunohistochemistry using mouse antihuman ET IgG1 monoclonal antibody. ET-like activity was identified in the sensory epithelial cells, supporting cells, dark cells, transitional cells, vestibular membrane, semicircular wall cells and vestibular ganglion cells. These findings suggest that ET may play an important role in maintaining homeostasis of the vestibule.
BACKGROUND: Cisplatinum (CDDP) has a toxic effect on the inner ear. CDDP reacts with DNA and leads to apoptotic cell death. In this study, the presence of single-stranded DNA (ssDNA) was examined immunohistochemically. MATERIALS AND METHODS: CDDP (10 mg/kg b.w.) was injected into the guinea pigs intra-peritoneally. Animals were sacrificed three days after the injection. The temporal bones were fixed via cardiac infusion. The tissues were embedded in paraffin and then used for immunohistochemical examination. RESULTS: That ssDNA was detected in the CDDP treated vestibule. The sensory epithelium, transitional area, dark cells and vestibular ganglion cells exhibited a positive immunoreactivity to ssDNA. CONCLUSIONS: DNA fragmentation is a characteristic feature of apoptosis. Fragmented DNA is detected as ssDNA. Our results indicate that CDDP involves the apoptosis in the inner ear and this is the cause of the ototoxicity of CDDP.
BACKGROUND: During the process of apoptosis, double-stranded DNA is broken into single-stranded DNA by the action of caspases and caspase-activated deoxyribonuclease. We immunohistochemically examined the apoptotic changes induced by cisplatin in the vestibule of guinea pigs. MATERIALS AND METHODS: Cisplatin (10 mg/kg b.w.) was intraperitoneally injected into guinea pigs and, 3 days after the injection, the animals were sacrificed by intracardiac perfusion of fixative. The temporal bones were then removed and immunohistochemically stained for caspase-activated deoxyribonuclease or caspase 3. RESULTS: Both caspase-activated deoxyribonuclease and caspase 3 were observed in the dark cell area, transitional area and the sensory epithelium. CONCLUSION: These findings suggest that apoptosis is involved in the vestibular dysfunction of the CDDP-treated patients.