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Biomedical subjects

E Ohama

Publications and source records attributed to E Ohama.

At least 91 records · Page 5Linked to original sources

Comparative immunohistochemical study on the expression of alpha B crystallin, ubiquitin and stress-response protein 27 in ballooned neurons in various disorders.

This report deals with a comparative study on the expression of alpha B crystallin, ubiquitin, stress-response protein 27 (srp 27), srp 72 and phosphorylated neurofilament protein (pNFP) by ballooned neurons in Pick's disease, Creutzfeldt-Jakob disease (CJD), amyotrophic lateral sclerosis (ALS), leptomeningeal carcinomatosis, anterior spinal artery syndrome and pellagra. Immunohistochemical techniques were used. alpha B Crystallin was expressed by the majority of ballooned neurons of Pick's disease and CJD, but not by those of the other disorders. Ubiquitin and srp 27 expression was also restricted to abnormal neurons of Pick's disease and CJD, but the proportion of stained cells was less than that expressing alpha B-crystallin. There was no evidence of ballooned neurons expressing srp 72. Except for those of pellagra patients, phosphorylated neurofilament protein (pNFP) was detected in most abnormal neurons. Our results suggest that the mechanisms involved in formation and maintenance of swollen neurons in Pick's disease and CJD may be different than those of ballooned neurons in the other entities studied.

Aged↗

Topographic relationship between senile plaques and cerebrovascular amyloidosis in the brain of aged dogs.

The distributions of senile plaques (SP) and cerebrovascular amyloidosis (CA) were studied by employing thioflavin S and modified Bielschowsky stains, and beta-protein immunohistochemistry on serial sections of the brains of aged dogs older than 10 years. Mature and perivascular plaques, both of which contained compact amyloid deposits, always showed a close topographic relationship to CA. In contrast, the majority of diffuse plaques showed no topographic relationship to CA. Cell bodies of neurons and/or glia were almost always involved in the diffuse plaques. In addition, beta-protein immunohistochemistry demonstrated amyloid deposits on the periphery of occasional neurons. These findings suggest that different mechanisms may be involved in the development of the different subtypes of SP in the brains of aged dogs.

Aging↗

[A case of intracranial multiple nonspecific granulomas related to rheumatic disease: with special reference to magnetic resonance imaging].

We encountered a rare case of a 48-year-old man with intracranial multiple granulomas secondarily caused by rheumatic disease. This was proven surgically after an 11-year course of remissions and deteriorations. In 1980, at the age of 32 years, the patient was first seen at the clinic of Neurology of the University Hospital, complaining of swelling and arthralgia of the joints of the knee, ankle, and wrist and with remittent fever and visual disturbance. The patient was diagnosed as having possible rheumatoid arthritis, and treated with administration of 30mg/day of prednisolone, which greatly improved the symptoms. The administration of 5 to 10mg/day of prednisolone had been continued after discharge from hospital. In 1985, visual acuity of the left eye decreased, and left facial hypesthesia developed. The patient was rehospitalized at the same clinic, and treated with 100mg/day of prednisolone, which again diminished the symptoms. Computed tomography(CT) on admission showed a high density mass with contrast enhancement in the left cavernous region. In addition to the left cavernous mass, a high density mass was detected by CT in the left parietal lobe, in 1987. Visual acuity of the left eye deteriorated in 1989. Because his response to prednisolone had decreased, the visual symptom was treated with gold sodium, which acted effectiveness. Symptoms deteriorated again in 1990. Early in 1991, CT and magnetic resonance imaging showed a new mass at the right frontal lobe, while the mass in the left cavernous region had increased in size. The patient was transferred to the clinic of Neurosurgery for surgical treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[Interhemispheric choroidal epithelial cyst associated with partial agenesis of the corpus callosum: case report and review of the literature].

A case of interhemispheric choroidal epithelial cyst is reported. The patient is a 9-month-old female who was transadmitted to our hospital for further examination because of the enlargement of her head. She had no neurological deficits nor symptoms of increased intracranial pressure. CT scanning performed on admission showed multiple cystic lesions in the right frontoparietal interhemispheric space, whose circumference was partially enhanced with contrast medium. Metrizamide CT cisternography demonstrated no communication between the lesions and the ventricular system. The signal intensity of the cysts was higher than that of cerebrospinal fluid on both T1-weighted and T2-weighted MR images. Sagittal T1-weighted images showed partial agenesis of the corpus callosum. The surgical exploration was performed via interhemispheric approach. The cyst wall was found to be white, relatively rich in vascular components, and was removed as much as possible. The examination of the cyst fluid showed total protein levels of 1250 to 3440 mg/dl, and sugar contents of 43 to 99mg/dl. Callosal agenesis was confirmed at operation. The light microscopic examination revealed that the cyst wall was composed of a single layer of columnar or cuboidal epithelium with occasional papillary configuration and thick collagenous connective tissue. The epithelial cells contained PAS-positive granules in the cytoplasm. Electron microscopy showed numerous club-shaped microvilli with no coating materials, continuous basement membrane, tight junction, interdigitation, and multiple fenestrations of endothelium of stromal vessels. On the basis of these findings, the lesion was diagnosed as choroidal epithelial cyst. In the literature, interhemispheric choroidal epithelial cyst associated with partial callosal agenesis, confirmed ultrastructurally, has not, to out knowledge, been reported.

Agenesis of Corpus Callosum↗

[The rupture of cedar pollens in nasal secretions].

Allergic rhinitis caused by pollen of Japanese cedar (Cryptomeria japonica) is found in Japan. These pollens, when inhaled into the nasal cavity, contact the nasal mucus membrane, and the allergens separate from the pollens, and pass through the nasal mucosa to interact with the mast cell-bound IgE. Patients with allergic rhinitis produce a great volume of nasal secretion from the mucosa. The morphological transformation of the cedar pollens when mixed with nasal secretion was studied. Nasal secretion was collected from two patients with allergic rhinitis. Cedar pollen gathered from a Japanese cedar tree was mixed with distilled water, and the cedar pollen suspension was mixed with a drop of nasal secretion on a slide glass at the room temperature (23 degrees C), and examined by phase-contrast microscopy. Of the pollen 20.6% were ruptured after 3 min, and 52.9% after 10 min, 84.9% after 40 min, and 81.3% after 60 min respectively. Further changes in shape of the ruptured pollens were observed with continued incubation. A hole opened in the cytoplasmic membrane through which the nucleus escaped, and crinkling of the residual cytoplasmic membrane was observed. The escaped nucleus separated into many small granules. In order to determine possible causes of the pollen rupture in nasal secretion, the relationship between pH of the nasal secretion and rupture rate was examined. The pH of the nasal secretion from two patients was 8.95 and 9.15 respectively. Salt solutions of 0.1 M NaCl, (NH4) 2SO4, NaNO3, CaCl2, Na2SO4, KCl, MgSO4, had pH range from 5.13 to 6.40.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Syringomyelia. A neuropathological study of 18 autopsy cases.

Eighteen autopsy cases of syringomyelia were studied neuropathologically. In six cases associated with Chiari II malformation, the central canal was patent from the fourth ventricle to the syrinx, and the syrinx was simply a dilated central canal. In four cases associated with Chiari I malformation, the syrinx was irregularly shaped and communicated with the subarachnoid space at the entry zone of the posterior nerve roots. In six cases associated with spinal cord or posterior fossa tumors, the syrinx was located adjacent to the tumor tissues, and occupied the medullary gray matter or the spinal intermediate zone and the ventral part of the posterior horn. With regard to the pathogenesis of syringomyelia, we concluded that in cases associated with Chiari II malformation, vermian protrusion and direct continuity between the fourth ventricle and the syrinx were essential. In cases associated with Chiari I malformation, in addition to tonsillar protrusion, communication between the syrinx and the subarachnoid space was thought to play an important role, and in cases associated with tumors, the circulatory disturbance due to the presence of the tumors caused the syrinx.

Aged↗

[Clival chordoma in an infant; case report and review of the literature].

Skull base chordoma in infants is a very rare entity in spite of its congenital origin; only 11 clinical cases can be found in the literature so far. Here we report such a case and review the literature. The case is that of a 3.5-year old boy suffering from left abducent nerve palsy for 5 months. CT scan revealed an isodense mass lesion with bone destruction involving the clivus and left petrous apex, and was homogeneously enhanced on post-contrast study. MRI disclosed the clival tumor as a long T1 and long T2 mass. Angiogram showed no tumor stain. The tumor was preoperatively diagnosed as clival chordoma, and was partially removed via left transpetrosal-transtentorial approach. The tumor was found to extend into the subdural space through Dorrello's canal and compress the abducent nerve. Histological examination with H & E, PAS, mucicarmine, and reticulin stainings led us to a diagnosis of "typical chordoma". Electron microscopy demonstrated the mitochondria-endoplasmic reticulum complexes (MERC), glycogen granules, and vacuoles in the tumor cells. Postoperative irradiation (total dose 55 Gy) was performed. At present, 30 months after the operation, no evidence of tumor regrowth nor hypothalamus-pituitary deficiency is recognizable and the patient is free from left abducent nerve palsy. It is concluded that skull base chordoma in infants should be postoperatively irradiated in an appropriate manner.

Child, Preschool↗

Modified Bielschowsky and immunohistochemical studies on senile plaques in aged dogs.

Aged dogs developed senile plaques (SP) in the brain which were similar to those occurring in aged humans. These SP were studied with a modified Bielschowsky stain and immunohistochemical methods using polyclonal antibodies raised against beta-protein and glial fibrillary acidic protein (GFAP). Serial sections stained by immunohistochemical and modified Bielschowsky stains showed that all areas of slight beta-protein immunoreactivity were intensely stained by the modified Bielschowsky stain. Most SP were observed in the neocortex of the cerebrum. Plaque densities were highest in the cingulate and temporal cortices. There were occasional SP in the subcortical nuclei including the caudate nucleus and putamen, and hippocampus. Based on the morphological characteristics demonstrated by the modified Bielschowsky stain, SP in the brains of the dogs were grouped into 3 types: diffuse, mature and perivascular plaques, of which diffuse plaques were predominant. Various degrees of astroglial reaction were observed in all subtypes of SP except diffuse plaques. These findings indicate that dog may serve as a model for study of the pathogenesis of SP.

Aging↗

Galactosialidosis: neuropathological findings in a case of the late-infantile type.

The neuropathological findings in a 13-year-old Japanese male showing decrease of sialidase and beta-galactosidase activities are reported. The patient was the product of normal pregnancy to consanguineous parents. He started to sit at 8 months, stand at 20 months and walk at age of 2; mental retardation, visual disturbance, cerebellar ataxia, myoclonus and epilepsy developed by the age of 10, and he died at 13. Neuropathological investigation revealed neuronal loss and storage. Severe loss of neurons was observed in the thalamus, globus pallidus, lateral geniculate body, gracile nucleus, Purkinje and retinal ganglion cells. Marked ballooning was seen in the Betz cells and neurons in the basal forebrain, the motor neurons in the cranial nerve nuclei and spinal cord, and in the trigeminal and spinal ganglia. The storage material varied in staining from region to region and from neuron to neuron. Electron microscopic investigation revealed a variety of intracytoplasmic and intranuclear inclusions: membranous cytoplasmic bodies, parallel, wavy-lamellar or tortuous tubular structures, lipofuscin-like irregular-shaped pleomorphic bodies, and cytoplasmic vacuoles with fine granules and lamellar materials. The severity of the neuronal loss did not seem to correlate with the amount of the storage materials, but with the presence of tortuous tubular inclusion.

Brain↗

Are bunina bodies of endoplasmic reticulum origin? An ultrastructural study of subthalamic eosinophilic inclusions in a case of atypical motor neuron disease.

We carried out an electron microscopic study of eosinophilic intracytoplasmic inclusions in the subthalamic neurons in a case of atypical motor neuron disease. These inclusions were identical in light microscopic morphology and staining characteristics to Bunina bodies. Ultrastructurally, most of the intracytoplasmic inclusions observed were divisible into two different types (I and II). Type I inclusions had features essentially identical to those of Bunina bodies demonstrated previously in the anterior horn cells in cases of motor neuron disease; they consisted of electron-dense, granular material without a particular limiting membrane and often contained a number of translucent areas with entrapped cell organelle-like structures. Type II inclusions were very similar to structures known as multilaminated bodies; at their margin, they sometimes showed continuity with the cisternae of endoplasmic reticulum. The remainder of the inclusions were considered to be transitional forms between these two types, and some of them showed the respective features of both types I and II. These findings suggest that Bunina bodies are of endoplasmic reticulum origin.

Adult↗

An autopsy case of atypical motor neuron disease with Bunina bodies in the lower motor and subthalamic neurons.

We report a 37-year-old male without any family history of neurological disease who suffered progressive muscular atrophy and sensory impairment of 4 years' duration. Autopsy revealed neuronal loss in the anterior horns of the spinal cord and in the hypoglossal and facial nuclei of the brain stem. The corticospinal tracts of the spinal cord showed only mild degeneration. In addition, there were obvious degenerative lesions manifested by loss of neurons, myelin and axons in the spinal posterior columns, Clarke's column, spinocerebellar tracts and dorsal root ganglia as well as in the subthalamic nucleus, globus pallidus, substantia nigra and cerebellar dentate nucleus. Furthermore, we frequently encountered Bunina bodies not only in the lower motor neurons but also in the subthalamic neurons. We consider this case to be an atypical example of motor neuron disease with features of multisystem degeneration. The fact that Bunina bodies were observed in both lower motor and subthalamic neurons in this case suggests a common etiology of neuronal degeneration in these two different systems.

Adult↗

Parkinson's disease: an immunohistochemical study of Lewy body-containing neurons in the enteric nervous system.

We performed immunohistochemical analysis of specimens from three autopsied patients with Parkinson's disease, using antibodies to tyrosine hydroxylase (TH), vasoactive intestinal polypeptide (VIP), somatostatin, met-enkephalin, leu-enkephalin and substance P in an attempt to reveal the types of neurons that contain Lewy bodies (LBs) in the paravertebral and celiac sympathetic ganglia and in the enteric nervous system of the alimentary tract. In the sympathetic ganglia, almost all LB-containing neuronal cell bodies and processes were immunoreactive for TH. In the alimentary tract, however, most LBs were found in the VIP-immunoreactive (VIP-IR) neuronal cell bodies and processes. In spite of the significant presence of TH-IR neuronal cell bodies and processes in the alimentary tract, LB-containing TH-IR neuronal elements were rarely encountered. These findings indicate that in the alimentary tract, the VIP neuron system is mainly involved in the disease process of Parkinson's disease.

Aged↗

Lewy bodies in the lower sacral parasympathetic neurons of a patient with Parkinson's disease.

Lewy bodies were observed incidentally in the neurons of the dorsal group of nucleus intermediolateralis of the 3rd sacral segment of the spinal cord in a 74-year-old male with Parkinson's disease. The findings indicate the degeneration of the preganglionic parasympathetic neurons innervating the internal anal sphincter. The correlation between the findings and the mechanism of constipation in this disease are discussed.

Aged↗

Dural arteriovenous malformation with abnormal parenchymal vessels: an autopsy study.

A 48-year-old man with dural arteriovenous malformation (AVM) is reported. Radiologically, the dural AVM was demonstrated mainly in the region of the left transverse sinus. Postmortem examination revealed dural AVM involving the bilateral transverse, superior sagittal and straight sinuses. In addition, numerous malformed venous vessels and extensive necrosis were observed mainly in the parenchyma of the brain stem and cerebellum. The present case suggests that dural AVMs may be associated with malformed venous vessels in the brain parenchyma.

Adult↗

Involvement of extraocular muscle in mitochondrial encephalomyopathy.

We carried out a histological examination of the extraocular muscles (EOMs) in a case of myoclonus epilepsy associated with ragged-red fibers (MERRF) and two cases of mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS), which did not manifest external ophthalmoplegia clinically. By light microscopy, many granular and vesicular fibers were seen associated with endomysial fibrosis. Electron microscopy revealed that the fibers showed prominent accumulation of abnormal mitochondria, extensive loss of myofibrils, proliferation of free sarcoplasmic reticulum and an increased amount of lipid vacuoles. These changes were more pronounced in MELAS than in MERRF. Hirano bodies were often seen in the subsarcolemmal area of muscle fibers and also in the intramuscular myelinated nerve fibers and axon terminals. These findings suggest the presence of mitochondrial myopathy of the EOMs in cases of MELAS and MERRF.

Actin Cytoskeleton↗

Demyelination and remyelination in spinal cord lesions of human lymphotropic virus type I-associated myelopathy.

We describe postmortem findings in a patient with human T lymphotropic virus type I (HTLV-I)-associated myelopathy (HAM). The patient developed the disease 8 years after blood transfusion and showed good response to corticosteroid treatment but died of cardiac failure. Histologically, chronic, mild meningoencephalomyelitis was noted predominantly involving the bilateral lateral and anterior columns of the middle to lower thoracic segments. The spinal cord lesions showed obvious loss of myelinated nerve fibers and fibrillary gliosis with minimal inflammatory cell infiltration. Electron microscopy of the lesion revealed disintegration of the myelin sheaths, regular separation of the minor dense line of the myelin sheaths, and completely demyelinated axons. In addition, remyelinated fibers with thin central myelin sheaths and disproportionately large axons were seen frequently. These findings indicate that primary demyelination and remyelination by oligodendrocytes occur in the spinal cord lesions of HAM.

Aged↗

Abnormal glycosphingolipid metabolism in the nervous system of galactosialidosis.

In an autopsy case of galactosialidosis, GM3, GM2, GM1, and GD1a were accumulated in sympathetic and spinal ganglia and grey matter of the spinal cord. Especially, the accumulations of GM3 and GM2 amounted to 41- and 86-fold increases in sympathetic ganglia, respectively, as compared to normal controls. In addition LacCer, GA2 and GA1 were accumulated in sympathetic and spinal ganglia. The accumulations of GM3 and GD1a are considered to be the result of defective lysosomal sialidase activity and the accumulation of GM1, LacCer and GA1 is also considered to be due to decreased beta-galactosidase activity in this disorder. To better understand the possible mechanism of GM2 accumulation, we determined the activity of GM2 synthesizing enzyme (GM3:UDP-GalNAc transferase), as well as hexosaminidase activity, in sympathetic ganglia, but they did not change. Abnormal ganglioside and neutral glycosphingolipid metabolism, as well as sialyloligosaccharide and sialylglycoprotein metabolism, may be involved in the pathogenesis of this disorder.

Biomechanical Phenomena↗