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Biomedical subjects

H Shinkawa

Publications and source records attributed to H Shinkawa.

At least 73 records · Page 4Linked to original sources

Nucleotide sequence of the gene for cholesterol oxidase from a Streptomyces sp.

The nucleotide sequence of a 2.1-kilobase-pair fragment containing the Streptomyces choA gene, which codes a secreted cholesterol oxidase, was determined. A single open reading frame encodes a mature cholesterol oxidase of 504 amino acids, with a calculated Mr of 54,913. The leader peptides extend over 42 amino acids and have the characteristics of a signal sequence, including basic amino acids near the amino terminus and a hydrophobic core near the signal cleavage site. Analyses of the total amino acid composition and amino acid sequencing of the first 21 amino acids from the N terminus of the purified extracellular enzyme agree with the values deduced from nucleotide sequencing data.

3-Hydroxysteroid Dehydrogenases↗

Effect of external auditory canal pressure upon the hearing threshold in patients with Menière's disease.

Fluctuation of hearing at low frequencies is one of the most characteristic findings in Meniere's disease and seems to be a phenomenon closely related to changes of endolymphatic pressure and volume. In the present study, pressure was applied to the external auditory canal of patients with Meniere's disease, and the effect on the bone conduction threshold was examined at times of depressed and improved hearing. In more than half of these cases, it was found that the pressure effect was marked at the time of improved hearing acuity, but not at the time of depressed hearing. This effect was also confirmed in more objective experiments with guinea pigs. It is concluded that the fluctuation of hearing in Meniere's disease seems to be a phenomenon accompanying the endolymphatic pressure change in the scala media.

Animals↗

[Middle ear dynamic characteristics of patients obtained by a newly developed measuring apparatus].

A tympanometer is well known to be a valuable apparatus for the diagnosis of secretory otitis media (SOM). However, it is insufficient for the diagnosis of ossicular chain disorders. Therefore, an attempt was made to develop a new measuring apparatus, which had a function of sweeping both frequency and pressure and was measurable the absolute sound pressure variations at the external auditory canal, owing to the carefully designed probe. In the previous papers, the middle ear dynamical characteristics of normal subjects were measured by this apparatus, and the measurement results were compared with the theoretical analysis. In this paper, the middle ear dynamical characteristics of patients were measured, and the effects of various kinds of middle ear diseases upon its dynamical characteristics were examined. The measurement results of the patients with ossicular chain separation, ossicular chain fixation, SOM and tympanic membrane perforation had their own distinctive patterns, and were also clearly different from those of normal subjects. Therefore, this apparatus seems to have a high degree of the clinical applicability to the diagnosis of these diseases.

Adolescent↗

The nucleotide sequence of a streptomycin streptomycin phosphotransferase (streptomycin kinase) [corrected] gene from a streptomycin producer.

The nucleotide sequence of the DNA fragment containing the streptomycin phosphotransferase (streptomycin kinase) [corrected] gene from the streptomycin-producer Streptomyces griseus strain HUT 6037 was determined. Analysis of the sequence revealed an open reading frame which could encode 325 amino acid residues. A biased codon usage pattern, reflecting the high G + C composition (approximately 74%) of Streptomyces DNA, was observed in the gene.

Amino Acid Sequence↗

Serial section reconstruction of the guinea pig outer hair cells as studied with a high-voltage electron microscope and a computer-graphic display.

The fine structural arrangement of the nerve endings on the guinea pig outer hair cells (OHCs) was studied by a serial sectioning technique by means of a high-voltage electron microscope and computer-graphic three-dimensional reconstruction. Sixty-nine series of consecutive sections were observed. Fifteen OHCs were located about 0.5 mm from the basal end (hook portion of basal turn) and 4 OHCs were seen at 6.0 mm, 20 OHCs at 8.0 mm (basal turn), 13 at 12.8 mm (second turn), 8 at 14.8 mm, 7 OHCs at 15.9 mm (third turn), and 2 OHCs at 17.5 mm (apical turn). Of 69 OHCs, 31 cells were from the first row, 22 from the second and 16 from the third row. The total number of nerve terminals on each OHC varied between 5 and 36. The OHCs with the least number of terminals were found in the hook portion, while the OHCs with the most numerous innervation were observed in the third row of the upper third turn. The afferent/efferent ratio (A/E ratio) of each OHC was evaluated and the OHCs were divided into two groups: Type A and Type B, depending upon the range of the A/E ratio. Thirty-five OHCs (50.7%) out of 69 were identified as being type A with an A/E ratio range of 0.5-1.5, while the remaining 34 OHCs (49.3%) were Type B cells with a greater A/E ratio than Type A cells. The detailed distribution of both types of cells was also studied along the entire length of the basilar membrane.

Animals↗

Positive intratympanic pressure in the morning and its etiology.

Intratympanic pressures were measured by tympanometer in forty ears free from disease. In the recumbent position, the first tympanogram was obtained in the morning at awakening, before swallowing. The second pressure measurement was performed in the upright position after swallowing and chewing. Twenty-two ears showed positive pressure in the middle ear before swallowing and decreased pressure after swallowing. The present results revealed no evidence of continuous gas absorption from the middle ear during sleep. The other experiment demonstrated that raising of the PCO2 level by hypoventilation increased the pressure in the middle ear. The results suggested indirectly a diffusion of carbon dioxide to the middle ear cavity from its surrounding tissue. The intratympanic pressure seems limited in part to the partial pressure gradient of gases between the middle ear cavity and its surrounding tissue when ventilation through the Eustachian tube is impaired.

Acoustic Impedance Tests↗

Molecular cloning and expression in Streptomyces lividans of a streptomycin 6-phosphotransferase gene from a streptomycin-producing microorganism.

The gene encoding streptomycin 6-kinase involved in the self-resistance of the streptomycin-producing Streptomyces griseus HUT 6037 was cloned in the plasmid vector pIJ703. The resulting plasmid, pSP6, contained 2.5 kb inserts of S. griseus DNA. When streptomycin-susceptible S. lividans 1326 was retransformed with pSP6, all transformants produced streptomycin 6-kinase. Addition of streptomycin to the culture medium of S. lividans carrying pSP6 plasmid brought about a remarkable increase in streptomycin 6-kinase activity in the cell extracts. It is suggested from the results that the production of streptomycin 6-kinase in streptomycin producer was induced by streptomycin accumulated during cultivation.

Cloning, Molecular↗

Bone destruction due to the rupture of a cholesteatoma sac: a pathogenesis of bone destruction in aural-cholesteatoma.

Severe bone destruction in a cholesteatoma is one of the characteristic clinical features. To clarify the mechanism of bone destruction in cholesteatoma, the matrix of cholesteatoma and the attached bone, obtained during middle ear surgery, was observed by light microscope. Rupture of the epithelial lining in a cholesteatoma and the escaping contents (keratin), which gave rise to intense characteristic granulations in subepithelial tissue, were found. Furthermore bone destruction was always found at the site of subepithelial tissue of cholesteatoma. From these facts, the escape of contents from the sac of cholesteatoma into the subepithelial layer is considered to be an important factor in the mechanism of bone destruction.

Bone Resorption↗

Sensorineural hearing loss caused by mitochondrial DNA mutations: special reference to the A1555G mutation.

Mutations in mitochondrial DNA, which are maternally inherited, have been thought to be one of the causes of sensorineural hearing loss. Two mitochondrial mutational sites (A1555G, A7445G) have been reported to be responsible for non-syndromic hearing impairments. The A1555G mutation causes increased susceptibility to aminoglycoside antibiotic-induced hearing loss as well as non-syndromic sensorineural hearing loss. Our wide screening study showed that there may be a great number of subjects within the Japanese population who have the A1555G mutation. Recent reports suggest that high-risk populations may exist throughout the world. The aminoglycoside-induced hearing loss associated with a mitochondrial mutation is commonly bilateral, symmetric, high frequency involved, and is sometimes associated with progressive sensorineural hearing loss.

Adult↗

Phylogenetic analysis of mitochondrial DNA in Japanese pedigrees of sensorineural hearing loss associated with the A1555G mutation.

Thirteen Japanese families (ten of which were from the northern part of Japan), with sensorineural hearing loss associated with the 1555 A to G (A1555G) mitochondrial mutation, a known cause of non-syndromic hearing loss, were phylogenetically analysed using data obtained by restriction fragment length polymorphism (RFLP) and D-loop sequencing of mitochondrial DNA (mtDNA). Various types of mtDNA polymorphism were detected by restriction enzymes and D-loop sequence. No common polymorphic pattern throughout the 13 families was found, though three families exhibited the same restriction patterns and the same sequence substitution in the D-loop. To find where each of the 13 families are situated in the phylogenetic tree, the 482-bp of D-loop sequence were compared with those of 62 normal Japanese subjects. Despite the three families mentioned above appearing to be clustered, the remaining 10 families were scattered along the phylogenetic tree. This indicates that there was no common ancestor for the 13 Japanese families bearing the A1555G mutation except three families, and that the A1555G mutation occurred sporadically and multiplied through evolution of the mtDNA in Japan. The present results showed that the common pathogenicity (hearing loss associated with the A1555G mutation) can occur sporadically in families which have different genetic backgrounds, even in the Japanese population.

DNA, Mitochondrial↗

Isepamicin sulfate-induced sensorineural hearing loss in patients with the 1555 A-->G mitochondrial mutation.

A mitochondrial mutation at nucleotide 1555 has been reported to be susceptible to aminoglycoside antibiotics as well as one of the causes of nonsyndromic sensorineural hearing loss. We herewith report 2 cases bearing the 1555 A-->G mitochondrial mutation who had hearing loss after short-term exposure to the new aminoglycoside antibiotic, isepamicin sulfate. Even when using aminoglycoside antibiotics with milder side effects, careful attention should be paid in applying them to patients with particular genetic backgrounds.

Adult↗

Different clinical characteristics of aminoglycoside-induced profound deafness with and without the 1555 A-->G mitochondrial mutation.

Recent genetic studies have shown that hereditary susceptibility to aminoglycoside antibiotics is caused by the 1555 A-->G mitochondrial mutation. We found the 1555 mutation in 4 out of 68 postlingual deaf patients who were candidates for cochlear implantation. All 4 patients developed bilateral profound hearing loss following administration of aminoglycosides. The pedigree of the family shows exclusively maternal transmission of hearing impairment in each case. On comparison with neuro-otological findings from aminoglycoside-induced deaf patients without the 1555 mutation, four distinct characteristics were noted: (1) a progressive nature of hearing loss; (2) better residual pure-tone thresholds; (3) lower thresholds for electrical promontory stimulation, and (4) well-preserved vestibular function. Although other factors such as differing dosages and/or administration routes may also be involved, profound hearing loss associated with the 1555 mutation may be due to a different pathogenic mechanism, i.e., strial dysfunction rather than a direct insult to the hair cells.

Aged↗

Primary chondrosarcoma arising in the parotid gland.

We report an extremely rare case of chondrosarcoma arising in the left parotid gland in a 45-year-old man who complained of painless swelling of the postauricular region. Computed tomography revealed a well-circumscribed tumor in the parotid area with a rim of scattered calcification. Under the diagnosis of benign parotid tumor, the tumor mass was removed with adequate margin. Histologic features were consistent with a low-grade chondrosarcoma showing lobular growth but clearly separated from adjacent glandular tissue of the parotid gland. Entire examination of the tumor disclosed no component of pleomorphic adenoma. There has been no evidence of recurrence for 2 months after the operation. The current case indicates that the parotid gland could be the site of occurrence of de novo primary chondrosarcoma.

Chondrosarcoma↗