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Biomedical subjects

K Oyanagi

Publications and source records attributed to K Oyanagi.

At least 37 records · Page 2Linked to original sources
PubMed1999

Pursuit of the origin of the large myelinated fibers of the anterolateral funiculus in the spinal cord in humans in relation to the pathomechanism in amyotrophic lateral sclerosis.

To determine the origin of the large myelinated fibers in the anterolateral funiculus (ALF) in the spinal cord of humans, myelinated fibers in the ALF of the mid-cervical spinal cord were examined quantitatively. Five groups of subjects were examined, consisting of control subjects, patients with cerebral lesions and showing complete degeneration of the unilateral/bilateral pyramis of the medulla oblongata, those with lesions of the pontine tegmentum, those with lesions of the lower cervical spinal cord, and those with thoracic/lumbar lesions. The results indicate that the large myelinated fibers in the ALF of the mid-cervical spinal cord of humans originate from the tegmentum of the brain stem and the lower cervical spinal cord, and not from the cerebrum, or the thoracic or lumbar spinal cord. Thus, they are descending fibers from the brain stem tegmentum and ascending fibers from the lower cervical cord, and not corticospinal tracts or long-ascending fibers from the thoracic or lumbar spinal cord. The origin of the large myelinated fibers in the ALF of the spinal cord in humans, the number of which was severely decreased in patients with amyotrophic lateral sclerosis, is considered to be the long-descending neurons in the brain stem tegmentum and the propriospinal neurons in the spinal cord.

Adult↗
PubMed1999

Expression of protective protein in human tissue.

The authors investigated by immunohistochemistry the distribution of protective protein in human tissues. Immunoreactivity was observed in the cytoplasm, revealing a granular pattern and cell type specificity. The most intense staining was observed in the large neurons of brain, distal and collecting tubular cells of kidney, epithelial cells of bronchus, and Leydig cells of testis. In a patient with galactosialidosis type IIa, all these stains were absent. The neurons that were most strongly stained in the control group, such as the Betz cells, neurons in the basal forebrain, motor neurons in the cranial nerve nuclei, and ventral horn cells of the spinal cord, were markedly ballooned in the patient with galactosialidosis.

Adolescent↗
PubMed1999

A non-familial Huntington's disease patient with grumose degeneration in the dentate nucleus.

We report a non-familial Huntington's disease (HD) patient presenting with increased levels of protein and IgG in his cerebrospinal fluid (CSF), antineuronal antibody in his serum and CSF, Purkinje cell and granule cell degeneration in the cerebellum, and grumose degeneration in the dentate nucleus, in addition to typical HD findings. This patient showed an expanded CAG repeat in the HD gene, and provides new information on the clinical and neuropathologic varieties of HD.

Aged↗
PubMed1998

Process of repair in the neuroepithelium of developing rat brain during neurogenesis: chronological and quantitative observation of DNA-replicating cells.

The neuroepithelium (NE) of the cerebrum of the developing brain has been reported to 'regenerate' within a certain period after being injured. To clarify the process of repair of the NE during neurogenesis, we chronologically examined the number of cells in the neocortex, and the rate of DNA-replicating cells and the mitotic figure ratio in the NE of rats after injury. The injury was induced by transplacental administration of ethylnitrosourea (ENU), which is cytotoxic immediately after administration, to the pregnant rats on embryonic day 16. The number of living and pyknotic cells in a 220-micron width of the neocortex was evaluated in each of three groups, such as NE, subventricular zone (SVZ) + intermediate zone (IMZ) + subplate (SP), and cortical plate (CP). The 5-bromo-2-deoxyuridine (BrdU)-labeling index and the mitotic index were examined 4, 8, 16, 24, 36, and 48 h after ENU administration. Up to 16 h after ENU administration, the number of living cells per 220 microns width in the NE and SVZ + IMZ + SP decreased, but increased in CP. From 16 to 24 h, the living cell number per 220 microns width in the NE and CP was unchanged, but increased in the SVZ + IMZ + SP. From 24 to 36 h, the living cell number per 220 microns width increased in all the groups, NE, SVZ + IMZ + SP and CP. From 36 to 48 h, the living cell number per 220 microns width in the NE was unchanged, but increased in the SVZ + IMZ + SP and CP. The BrdU-labeling index reached its nadir at 8 h, but markedly increased by 16 h, and then decreased to the control level by 36 h. No mitotic figures were observed at 16 h after administration, but a significant increase in mitotic index was noted at 24 h, and after which it decreased to almost the control value by 36 h. These findings indicate: (i) that temporary arrest of neuroepithelial cell cycle occurs in the G1-phase from 4 to 8 h after ENU administration, (ii) that the cell synchronizes in the S-phase at 16 h, (iii) that a proportion of neuroepithelial cells of rat fetal neocortex at the neurogenesis stage return to neuroepithelial cell proliferation stage, to repair the NE, and (iv) that regulation of the cell kinetics of neuroepithelial cells depends on the number of cells in a certain width of NE during regeneration.

Alkylating Agents↗
PubMed1998

Suprachiasmatic nucleus in a patient with multiple system atrophy with abnormal circadian rhythm of arginine-vasopressin secretion into plasma.

We performed a quantitative investigation of arginine-vasopressin (AVP) immunopositive neurons in the suprachiasmatic nucleus (SCN), which is the endogenous clock of the brain of a patient with multiple system atrophy (MSA) who exhibited nocturnal polyuria associated with decreased urinary specific gravity and depression of nocturnal AVP secretion. Eleven age- and sex-matched subjects were used as controls. Although, the number of AVP-positive neurons was decreased in neither the supraoptic nucleus nor the paraventricular nucleus, the number of AVP-positive neurons in the SCN was decreased and gliosis was present in the SCN. The cytoplasmic area of AVP-immunopositive neurons in the SCN was smaller in the patient than in the control subjects. These findings raise the possibility that SCN is involved in MSA and the neurodegeneration in the SCN results in altered circadian rhythm of AVP secretion and nocturnal polyuria.

Adult↗
PubMed1997

Familial lethal inheritance of a mutated paternal gene in females causing X-linked ornithine transcarbamylase (OTC) deficiency.

A Leu148Phe substitution of the ornithine transcarbamylase (OTC) gene was identified in a 2-year-old girl with OTC deficiency (14% of control). Her two elder sisters died in childhood of hyperammonemia, and the patient also died of OTC deficiency. Enzyme activity in Cos1 cells transfected by the mutant cDNA was undetectable, thereby indicating a definite pathogenic mutation. Familial gene analysis showed that the mother had wild-type OTC alleles on both X-chromosomes and the father was a mosaic for the mutant allele in his lymphocytes and spermatozoa. This clinical case shows that a somatic and germline mosaicism for a single-gene disorder led to an unusual pattern of X-linked inheritance in the family, and all three daughters in the family died of OTC deficiency. The possibility that inherited factors will lead to skewed X-inactivation needs to be considered.

Fatal Outcome↗
PubMed1997

Solitary plasmacytomas of the occipital bone: a report of two cases.

The radiological appearances of two cases of solitary plasmacytoma in the occipital bone are described. One arose in the lateral part and the other in the squama. They showed characteristic radiological features on CT, MRI and angiography. Bone scintigraphy and gallium scintigraphy were also available. Solitary plasmacytoma of the skull is a rare condition and usually occurs in the calvarium. The skull base is an extremely rare site and only four cases have been reported. The literature of solitary plasmacytoma of the skull is reviewed.

Aged↗
PubMed1997

Traumatic spinal cord injury: a neuropathological study on the longitudinal spreading of the lesions.

Eight patients died after traumatic spinal cord injuries. At autopsy, neuropathological examination revealed longitudinal spreading of cord lesions in two of these patients. One developed progressive paralysis 43 h after fracture of the fifth cervical (C5) vertebra and died 38 days after injury. Necrotic lesions extended upward to the medulla oblongata and downward to the C7 cord segment. Pencil-shaped necrosis (C7-T4) and marginal spongiosis (C7-T2) were also found. A second patient died 5 months after C5 subluxation with tetraplegia. His spinal cord was severely compressed at C4/5 and pencil-shaped necrosis, which had become partially cystic, extended upward to C3 and downward to T1; marginal spongiosis was also found in C4-C5. In both cases, complete necrosis without cell reaction was found in several cord segments, including the initially impacted segment. These findings suggest that intra- and extramedullary circulatory impairment occurred not only at the initial impact level, but also in the adjacent levels. Increased intramedullary pressure, resulting from this circulatory disturbance, in combination with a narrowed spinal canal, may induce the upward and downward spreading of the lesion.

Adolescent↗
PubMed1997

Eosinophilic intranuclear inclusions in the hippocampal pyramidal neurons of a patient with amyotrophic lateral sclerosis.

We report the presence of round eosinophilic intranuclear inclusions in a patient with sporadic amyotrophic lateral sclerosis (ALS). The inclusions were limited to the hippocampal pyramidal neurons; they were frequently encountered in the CA1 and CA2 regions and much less frequently in the CA3 and CA4 regions and in the subiculum. Ultrastructurally, they consisted of randomly oriented straight filaments, each about 8-14 nm in diameter, some of which had a tubular appearance in cross-section. Electron-dense, granular material was intermingled with the filaments. Immunohistochemically, all the inclusions were positive for ubiquitin, but were negative for several kinds of cytoskeletal protein, including actin, glial fibrillary acidic protein, vimentin, neurofilament polypeptides, keratin, tubulin, tau protein and microtubule-associated protein 2. To our knowledge, this type of neuronal intranuclear inclusion has not so far been reported in ALS, and its distribution limited to the hippocampal formation is of great interest.

Amyotrophic Lateral Sclerosis↗
PubMed1997

Distinct pathological features of the gallyas- and tau-positive glia in the Parkinsonism-dementia complex and amyotrophic lateral sclerosis of Guam.

We examined 50 patients with parkinsonism-dementia complex of Guam (Guam PDC), 10 Guamanian patients with amyotrophic lateral sclerosis (ALS), 5 patients with combined PDC and ALS (PDC-ALS), and 20 non-PDC non-ALS Guamanians, who had been autopsied between 1979 and 1982, paying special attention to glial inclusions. Gallyas-positive and tau-immunopositive intracytoplasmic inclusions were observed in many of the glial cells, in addition to extensive neurofibrillary tangles (NFTs) in the brains of Guam PDC and PDC-ALS patients. Granular hazy inclusions were seen in the astrocytes, and some crescent/coiled inclusions were observed in the oligodendroglia. Many granular hazy inclusions were observed in the amygdaloid nucleus, inferior olivary nucleus, and lateral funiculus of the spinal cord. The crescent/coiled inclusions were observed predominantly in the anterior nucleus of the thalamus, motor cortex, midbrain tegmentum, pyramids of the medulla oblongata, and lateral funiculus of the spinal cord. The granular hazy inclusions have never been reported previously, and the topographic distribution of the crescent/coiled inclusions in Guam PDC and PDC-ALS differs from those reported previously in other NFT-forming diseases. These findings indicate that Guam PDC and PDC-ALS involve not only neurons but also glia, and that their morphological and topographic differences from other NFT-forming diseases may provide further insights into their distinct etiopathogenesis, and thus prove useful for diagnosis.

Adult↗
PubMed1997

Genetic analysis of isolated persistent hypermethioninemia with dominant inheritance.

We describe a type of mild hypermethioninemia due to a point mutation in the MATA1 gene, which was inherited dominantly in a family. Three patients coming from the same family pedigree were detected by the presence of isolated hypermethioninemia on a mass-screening program. The measurement of methionine adenosyltransferase (MAT) activity in a patient's liver revealed a partial deficiency of hepatic MAT with a reduction in the Km for methionine. Single strand conformation polymorphism (SSCP) analysis and direct sequencing of the patients' genomic DNA revealed a G to A mutation at nucleotide 791 that converts Arg-264 to His (R264H) in one allele of MATA1 gene. The other allele was normal in all the patients examined. Gene tracking in the family revealed that the hypermethioninemia is associated with heterozygosity for the R264H mutation in the MATA1 gene.

Adult↗
PubMed1996

Cervical spondylotic myelopathy. Clinicopathologic study on the progression pattern and thin myelinated fibers of the lesions of seven patients examined during complete autopsy.

STUDY DESIGN: This study was designed to reveal the progression pattern and essential histological findings of the lesions in the spinal cord affected by cervical spondylotic myelopathy. OBJECTIVES: The purpose of this study was to gain new information about symptom progression and recovery in cervical spondylotic myelopathy. SUMMARY OF BACKGROUND DATA: The characteristics of the distribution and the progression pattern of the lesions and whether demyelination and remyelination processes actually occur in cervical spondylotic myelopathy remain unclear. METHODS: Tissues from seven patients with cervical spondylotic myelopathy were taken during autopsy and examined macroscopically and microscopically. An ultrastructural examination of spinal cord from two patients was also performed. RESULTS: The anterior horn and intermediate zone of the gray matter in the compressed segments showed atrophy in all the cases and in one, atrophy was limited to these areas. Atrophy and myelin pallor in the lateral and posterior funiculi were observed in six patients, and the lateral funiculi of two were severely affected. Many thin myelinated fibers and denuded axons were demonstrated ultrastructurally in the damaged white matter of two patients. CONCLUSIONS: There appears to be a common pattern of lesion progression in cervical spondylotic myelopathy: atrophy and neuronal loss in the anterior horn and intermediate zone develop first, followed by degeneration of the lateral and posterior funiculi. Eventually, marked atrophy develops throughout the entire gray matter and severe degeneration occurs in the lateral funiculus. Furthermore, the existence of thin myelinated fibers in the white matter suggests focal demyelinating and remyelinating processes occur in cervical spondylotic myelopathy.

Aged↗
PubMed1996

Development of fat within a meningioma.

We report a tentorial meningioma containing fat. Multiple areas of fatty density or intensity in the tumour were seen on CT and MRI, which corresponded histologically to lipomatous components. CT 10 years previously had demonstrated a smaller tumour without evidence of fatty components. We found only five cases in the literature in which fatty density was demonstrated within a meningioma on CT and a lipomatous component histologically proved. Xanthomatous change, with lipid in tumour cells, causes decrease in density on CT, but not to the levels of fat. As both lipomatous components and xanthomatous change show similar intensity on MRI, CT can be helpful in differentiating these two conditions. To our knowledge, our case is the only one in which the advent of fatty tissue was confirmed during follow-up.

Adipose Tissue↗
PubMed1996

Cystic acoustic neurinomas: studies of 14 cases.

Cystic acoustic neurinomas (ANs) are less frequent and are different from solid ANs in clinical and radiological features. We had 14 cystic ANs (13.5% of 104 cases) in the last 17 years. Computerized tomographic or magnetic resonance images allowed for the classification of these cystic ANs into three types: Type A being large single cysts with a thin tumourous wall (7 cases); type B single cysts with a thick tumourous wall (3 cases); type C multicystic (4 cases). Half of the cystic ANs were not accompanied by enlargement of the internal auditory canal, despite the largeness of the cysts. The mean size of the tumours was 29 mm in diameter. Type A cysts had a shorter clinical history than types B and C. One patient had intact hearing. In five cases, an atypical initial symptom such as facial pain, dysgeusia, facial palsy, unsteadiness or vertigo presented. The trigeminal nerve was involved in 12 cases, the facial nerve in nine. The characteristic features of cystic ANs are largeness of the tumour, a short clinical history, an atypical initial symptom, facial nerve involvement, and/or no enlargement of the internal auditory canal. In addition, the histological features are a lobular growth pattern, high nuclear atypia, and numerous macro phages.

Adult↗