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Biomedical subjects

Y Hashizume

Publications and source records attributed to Y Hashizume.

At least 199 records · Page 11Linked to original sources
PubMed1989

Spinal pencil-shaped softening. Report of an autopsy case studied using a three-dimensional model.

The pathologic features of a case of spinal pencil-shaped softening (PS) were studied by detailed step-sectioning and reconstruction using a three-dimensional (3D) model. The spinal cord was obtained at autopsy from a patient who had developed paraplegia due to extradural involvement of lung cancer. Above and below the area of transverse necrosis were PSs containing necrotic debris. They compressed the surrounding tissue and extended longitudinally over several segments. The PS was continuous with the area of transverse necrosis. These findings support the hypothesis that PS is formed by penetration of necrotic debris. The 3D model revealed that the PS was cylindrical to spindle-shaped. It showed a remarkable change in width along its course, with an unusual expanding shape. The PS was mainly located in the ventral part of the posterior column but was also observed in other locations in the segment near the transverse necrosis. Detailed step-sectioning showed that the PS changed in width mainly in response to intrapial pressure, and that it occurred where the parenchymal tissue was fragile. The expansion produced by penetration of necrotic debris may thus play an important role in the morphogenesis of this unusual lesion. Furthermore, the condition of the surrounding tissue may also be an important factor influencing the width and location of PS.

Aged↗
PubMed1989

Redundant nerve roots of the cauda equina: clinical aspects and consideration of pathogenesis.

In order to investigate the clinical significance of redundant nerve roots of the cauda equina (RNR) and their pathogenesis, the following studies were performed: 1) examination of 1,256 myelograms of patients with lumbar disease; 2) clinical analysis of 55 patients with RNR and 75 without RNR; 3) electrophysiological examination of 9 patients with RNR; and 4) anatomical and histopathological examination of 6 autopsy cases. RNR were found in 42% of patients with severely constricted spinal canals. In comparing patients with RNR and those without RNR, RNR were found in older patients, these patients exhibited a longer period from the onset of the symptoms to the time of myelographic manifestation, and they caused more severe signs and symptoms. The spatial distribution of redundant nerve roots and the extent of degeneration of nerve fibers in redundant nerve roots indicated the close causal relationship between RNR and constriction of the spinal canal. As the pathogenesis of RNR, the authors suggest a squeezing force from the constricted spinal canal acting on the nerve roots.

Adolescent↗
PubMed1989

[An autopsy case of pallido-nigro-luysian atrophy associated with OPLL].

Clinical and neuropathological studies of a case of pallido-nigro-luysian atrophy with thalamic degeneration and ossification of the posterior longitudinal ligament (OPLL) is reported. The patient was a 72-year-old man, suffering from gait disturbance caused by OPLL for about 3 years. The clinical features were characterized by gradual development of disorientation in place, time and person, memory disturbance, vertical gaze palsy and rigidity of extremities. Dysarthria, dysphagia, bradykinesia, masked face and neck dystonia appeared at the advanced stage of his illness. There was no tremor or other involuntary movements. A clinical diagnosis of parkinsonism was suspected. The main neuropathological findings were neuronal loss and gliosis in globus pallidus, substantia nigra, subthalamic nucleus and thalamus. In addition, neuronal loss of the anterior horn of the cervical spinal cord due to compression by OPLL (C4-C7) was recognized. The neuropathological findings of the present case were consistent with systemic degenerative disorder of the nervous system affecting the pallido-nigro-luysian tract. This rare disorder should be considered in the differential diagnosis of parkinsonism in old people.

Aged↗
PubMed1989

[Expression of nerve growth factor receptor in human benign peripheral nerve sheath tumor].

We examined in vivo and in vitro expression of nerve growth factor (NGF) receptors in 13 dermal and 9 plexiform neurofibromas, 28 schwannomas, and 4 traumatic neuromas with an immunohistochemical method using a monoclonal antihuman NGF receptor antibody (ME20-4) and anti S-100 beta protein antibody. Immunoreactivity for NGF receptor and S-100 beta protein was universally observed on the principal cells of both neurofibroma and schwannoma in vivo. Moreover, we examined the NGF receptor and S-100 beta protein immunoreactivity in the culture system of the neurofibroma and schwannoma with an immunofluorescent double staining method. The principal cells of both tumors were positively stained by both ME20-4 and anti S-100 beta protein antibodies. These cells also express the ability for 125I-NGF binding, which was examined with an autoradiographic technique. These results suggest that NGF receptors are universally expressed on the S-100 beta protein positive Schwann-like cells composing of these tumors both in vivo and in vitro. In traumatic neuroma, however, a positive staining of NGF receptor was more strongly observed in the perineurium rather than in the endoneurial cells.

Adolescent↗
PubMed1989

[Pathology of the peripheral nervous system in polyarteritis nodosa: a clinico-pathological study of two autopsy cases].

Peripheral nerves from the two autopsied cases with polyarteritis nodosa were pathologically examined. Case 1 was a seventy-year-old female, complaining of numbness and weakness of the extremities. Sensory deficits in all modality with induced dysesthesia were distributed as a mode of overlapping mononeuritis multiplex in the distal portion of extremities. Motor involvement was also noted in extremities in disarray-accentuated pattern. Extensive steroid hormone therapy was performed and remarkable improvement in clinical sign was temporarily obtained. Relapse with bowel involvement was a cause of the death. In the post-mortem examination, central fascicular degeneration with the loss of large myelinated fibers were seen at the middle portion of upper limbs in median nerve and at the lower mid-thigh in sciatic nerve. In the distal portion of those nerves, diffuse extensive loss of large myelinated fibers in the fasciculus were observed. Some of small thin myelinated fibers in the central fasciculus or distal portion of nerves were thought to be regenerated in nature. Accumulation of cell organelles in the axonal swellings were frequently occurred in the proximal to the ischemic site. Case 2 was a seventy five-year-old female with a both motor and sensory involvement in the distal extremities. Right pulmonary effusion and extensive subcutaneous hemorrhage and necrotic gangrene in the leg was also noted. Post-mortem examination of peripheral nerves revealed a presence of central fascicular degeneration in the distal sciatic nerves and nearly complete loss of myelinated fibers in the distal nerves. Ventral and dorsal roots and dorsal root ganglia were well preserved.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

[Immunotherapy for lung cancer by streptococcal preparation OK-432].

To evaluate the clinical efficacy of OK-432 immunotherapy, patients admitted between 1975 and 1982 were randomized into two groups: An immunochemotherapy (IM-C) group and a chemotherapy (control) group. For each group, a fixed chemotherapy was administered using a combination of three drugs. The survival rates of cases with non-small cell carcinoma were evaluated at the end of 1987. One hundred and fifty-seven cases in the IM-C group and 148 in the control group were eligible for evaluation of long-term survival rates. Statistically significant improvement of the survival rates in the IM-G group were noted in the following items: All cases, resected cases, non-resected cases, resected stage I + II cases, resected stage III cases, completely resected cases, incompletely resected cases, and cases with epidermoid carcinoma. However, in comparison of adenocarcinoma there was no significant difference between the two groups. SU-polysaccharide skin test and natural killer activity were the best immunological parameters during the OK-432 therapy. To intensify the effects of immunotherapy, a possibility of regional immunotherapy was studied following some experimental works. Regional infusion of LAK cells (induced by incubation of patient's lymphocytes with rIL-2) through bronchial artery after regional infusion of OK-432 and chemotherapeutics showed favorable effect for advanced lung cancer. Future prospect of these regional adoptive immunotherapy was discussed.

Biological Products↗
PubMed1989

[A nosological study of a patient showing ataxia & lower motor neuron involvement].

A sporadic case of spinocerebellar degeneration with prominent involvement of the motor system has recently been encountered. A 54-year-old man without family history noticed speech disturbance at the age of 46 and weakness in his right hand the following year. The muscle weakness and atrophy were slowly progressive and made walk impossible at the age of 50, when his dysphagia increased. At the age of 54, he was admitted to our hospital when neurological findings revealed marked amyotrophy of general skeletal muscle and tongue with fasciculation. Deep tendon reflexes were decreased. Cerebellar ataxia was impossible to evaluate because of profound muscle weakness. And sensory disturbance was suspected in the distal portion of the lower extremities. CT scan revealed progressive atrophy of the brain stem and cerebellum. The patient died at the age of 54 due to CO2 narcosis. The clinical course was 8 years. A summary of the pathological findings was as follows: 1) Marked neuronal loss of the anterior horn of the spinal cord and motor cranial nerve nuclei except for oculomotor nuclei, with mild degeneration of pyramidal tract below lumbosacral level. 2) Degeneration of cerebellipetal system, spinocerebellar tract, Clarke's column and the middle root zone and cerebellifugal system, dentate nucleus, superior cerebellar peduncles, and red nucleus. 3) Mild degeneration of pontine nuclei, inferior olivary nuclei, pontine transverse fibers, the middle and inferior cerebellar peduncles, cerebellar white matter and Purkinje cells as in OPCA.(ABSTRACT TRUNCATED AT 250 WORDS)

Amyotrophic Lateral Sclerosis↗
PubMed1989

[Two cases of Creutzfeldt-Jakob disease with high neuron-specific enolase level in cerebrospinal fluid].

Because neuron-specific enolase (NSE), one of the distal branch enzyme of Embden-Myerhof glycolytic pathway is abundant in the neuronal cytoplasm and axons, the measurement of its level in cerebrospinal fluid (CSF) would be useful in diagnosis and consideration of pathophysiology in various neurological diseases. The Creutzfeldt-Jakob disease (CJD) in which neuronal destruction is usually prominent pathologically, has so far been thought to reveal no abnormalities in CSF. In the two cases of CJD, we conducted the time sequential measurement of NSE level in CSF and compared it with serum NSE and CSF lactate levels. We found that the CSF NSE level was high in the early stage of this disease, at which time the brain CT showed no or minimal abnormalities, followed by gradual increase up to the maximum level when myoclonus and periodic synchronous discharge appeared in electroencephalogram. Then, the CSF NSE level decreased in parallel with the progression of brain atrophy in CT scan and finally on the late stage, the CSF NSE level fell within normal range. Serum NSE and CSF lactate levels were mildly elevated in all stages of this disease, but were not parallel to the disease activity. This implies that the CSF NSE level can serve as a marker for the presence of active process in neuronal destruction. Again the CSF NSE level was elevated in both cases even from the very early stage when the typical clinical manifestations of this disease were absent. Therefore, the results of this study provided us with an important indicator for the early stage diagnosis of CJD.

Aged↗
PubMed1989

[An autopsied case of type II citrullinemia--transient effectiveness with either citrate or benzoate to the consciousness disturbance].

A 44-year-old man suffered from repeated impairment of consciousness associated with flapping tremor, myoclonus and generalized convulsions, and died in coma 6 months after admission. He had had a psychosomatically underdeveloped childhood, with a propensity for legumes without a family history of the same or a record of consanguinity. On admission, he had disturbed consciousness and emaciation without other physical abnormalities. The EEG revealed diffuse slow waves with occasional appearance of triphasic waves. A high level of serum citrulline (534.7 nmol/ml) was recognized and the assay of urea cycle enzymes in the liver demonstrated decreased argininosuccinate synthetase (ASS) activity (0.062 U/g liver, 7.4% of that in normal liver), although no kinetic abnormality was found. Accordingly he was diagnosed as having type II citrullinemia. In addition, this case could be classified as cluster type of localization of the ASS in the liver by immunohistochemical study. There were characteristic findings concerning his clinical picture and laboratory data, such as a significant correlation between the grade of disturbed consciousness and arterial blood gas pH (r = 0.61, p less than 0.01). However, the blood ammonia level did not always correlate with the severity of disturbed consciousness. Oral treatment with sodium citrate and sodium benzoate was very effective, though transiently, for disturbed consciousness in this case. Pathological findings of the autopsied liver were fatty change and fibrosis. Neuropathologically, characteristic findings were brain edema with cerebellar tonsilar herniation, laminar necrosis with spongy formation in cerebral cortex, and Alzheimer type II glia. The relationship between citrullinemia and other hepatic encephalopathy was also discussed.

Adult↗
PubMed1988

Purification and characterization of human liver beta-galactosidase from a patient with the adult form of GM1 gangliosidosis and a normal control.

beta-Galactosidases were purified to homogeneity from livers of a normal control and a patient with the adult form of GM1 gangliosidosis. The purification was achieved by chromatography on DEAE-Sepharose fast flow, Con A-Sepharose, p-aminophenyl-1-thio-beta-D-galactopyranoside-Sepharose, and QAE-Mono Q. The normal and mutant enzymes were purified about 5000-fold with a yield of 10% and 1800-fold with a yield of 34%, respectively, and could hydrolyze 4-methylumbelliferyl-beta-D-galactoside, GM1 ganglioside, and asialofetuin. The purified normal enzyme was eluted from a TSK gel G-4000SW column as three symmetrical peaks of protein which were coincident with the three peaks of enzyme activity. The enzyme in these three peaks had apparent molecular weights of 800,000 (polymer), 140,000 (dimer), and 65,000 (monomer), whereas the mutant enzyme was eluted as two symmetrical peaks of protein and enzyme activity. The apparent molecular weight of a major monomeric form of the enzyme (beta-galactosidase A) was 60,000, and no dimeric form of the enzyme existed. Normal and mutant purified enzyme preparations migrated as a single major protein band with apparent molecular weights of 65,000 or 60,000, respectively, by SDS-polyacrylamide gel electrophoresis after treatment with mercaptoethanol. On isoelectric focussing, the mutant enzyme migrated more anodally than the normal enzyme. The mutant enzyme also had altered enzyme properties, such as pH optimum, Km values, substrate specificity and heat-stability. These data on the characteristics of the purified enzyme preparations provide the first direct evidence that patients with the adult form of GM1 gangliosidosis have a structurally altered beta-galactosidase.

Adult↗
PubMed1988

Chronic progressive sensory ataxic neuropathy with polyclonal gammopathy and disseminated focal perivascular cellular infiltrations.

One autopsied case of chronic progressive sensory-ataxic neuropathy with polyclonal elevation of serum and CSF IgG and IgA and without malignancy is reported. A marked loss of large myelinated fibers was universal in both the central and peripheral rami of primary sensory neurons. Fiber loss showed a multifocal patchy pattern in the proximal nerve trunks. The posterior root ganglion cell bodies were moderately atrophic and loss of large cells was observed. Unmyelinated axons were well preserved. The ventral spinal roots, ventral spinal horn cells, and muscles showed minimal involvement. There were focal perivascular mononuclear inflammatory cells without necrotizing vasculitis around the endoneurial and epineurial vessels. Similar perivascular cellular invasions were observed in the visceral organs, occasionally forming germinal follicle centers. This case suggested that this neuropathy has a unique background with a possible immune-mediated basis.

Ataxia↗
PubMed1987

High neuron-specific enolase level of cerebrospinal fluid in the early stage of Creutzfeldt-Jakob disease.

The measurement of neuron-specific enolase level in serum and cerebrospinal fluid was conducted time-sequentially in an autopsy confirmed patient with Creutzfeld-Jakob disease. The level was markedly high in the early stage of the disease at which time the brain CT showed no or minimal abnormalities, while falling into the normal range in the advanced stage. This is the first report of the elevated level of neuron-specific enolase in Creutzfeldt-Jakob disease.

Aged↗
PubMed1987

Presence of tetrahydroisoquinoline and 2-methyl-tetrahydroquinoline in parkinsonian and normal human brains.

1,2,3,4-Tetrahydroisoquinoline (TIQ) and 2-methyl-1,2,3,4-tetrahydroquinoline (2-Me-TQ) were identified for the first time by gas chromatography-mass spectrometry in the parkinsonian and normal human brains. TIQ, an analogue of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), was markedly increased in the parkinsonian brain and could be an endogenous neurotoxin to induce Parkinson's disease.

Autopsy↗