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Biomedical subjects

I Akiguchi

Publications and source records attributed to I Akiguchi.

At least 127 records · Page 7Linked to original sources
PubMed1996

[The value of F-waves in an early electrodiagnosis of the lower cervical cord infarction].

In a case of infarction in the lower cervical spinal cord, F-waves were lost in the paralyzed hand muscles 48 hours after the onset, in spite of normal compound muscle action potentials (CMAP). Subsequently the amplitude of CMAP decreased markedly in size 14 days later, when needle EMG revealed acute denervation. At 11 days after the onset MRI demonstrated a linear lesion in the ventral portion of the lower cervical spinal cord suggesting ischemia. Thus, the loss of F-waves is useful in early diagnosis of the lower cervical spinal cord infarction, which reflects the decrease in the excitability of the anterior horn cells taking place soon after ischemic insult.

Action Potentials↗
PubMed1996

[A case of familial juvenile dystonia-parkinsonism: 18F-6-fluorodopa and 18F-fluoro-2-deoxyglucose PET study].

A 27-year-old Japanese woman was admitted to Kyoto University Hospital because of gait disturbance since age 25. Her elder sister had been suffering from childhood-onset dystonia-parkinsonism with diurnal fluctuation which initially responded well to levodopa therapy, but later larger dose of levodopa was needed because of severe treatment-related fluctuation of the clinical symptoms. Physical examination revealed left foot dystonia, mild parkinsonism with kinesie paradoxale and dyskinesia of lower limbs. Symptoms were relieved by sleep and worsened by walking. Laboratory data including serum ceruloplasmin, serum and urinary amino acid analysis, and hexosaminidase and beta-glucosidase activity in leukocytes were all normal. Homovanillic acid (HVA) in cerebrospinal fluid was normal (68 ng/ml) at 8 pm but markedly decreased (7 ng/ml) at 4 pm. Cranial MRI was normal. 18F-6-fluorodopa PET demonstrated decreased dopa uptake in the bilateral striatum, especially in the putamen. 18F-fluoro-2-deoxyglucose PET showed decreased regional glucose metabolism in the bilateral putamen. Levodopa therapy rendered equivocal effects while trihexyphenydil was effective. This case indicated that some cases of dopa-unresponsive dystonia with parkinsonism might be a clinical variant of juvenile parkinsonism. 18F-6-fluorodopa PET is useful in evaluating juvenile dystonia-parkinsonism, though it may not predict levodopa effectiveness. 18F-fluoro-2-deoxyglucose PET study will be helpful in predicting the effect of levodopa therapy, because decreased regional glucose metabolism in the putamen probably indicates poor response to levodopa. Further study including dopaminergic receptor imaging study is needed to clarify the physiological mechanism of co-existing dystonia and parkinsonism in patients with juvenile parkinsonism and related disorders.

Adult↗
PubMed1995

A novel point mutation in the mitochondrial tRNA(Ser(UCN)) gene detected in a family with MERRF/MELAS overlap syndrome.

We found a new point mutation in the mitochondrial tRNA(Ser(UCN)) gene in a family with MERRF/MELAS overlap syndrome by screening for heteroplasmy by means of chemical cleavage of mismatch (CCM). Our strategy was based on the previous observations that most pathogenic mtDNA mutations in mitochondrial encephalomyopathies are heteroplasmic, whereas almost all neutral mitochondrial polymorphisms are homoplasmic. CCM followed by nucleotide sequencing of the corresponding region of the mitochondrial genome revealed a heteroplasmic mutation at nt 7512 in the tRNA(Ser(UCN)) gene. The 7512 (T to C) mutation disrupts a highly conserved base pair in the acceptor stem, and this mutation was not found in any of 120 normal controls, or in 43 patients with mitochondrial diseases. The proportion of the mutant mtDNA was 93% in muscle, 76 and 87% in the blood of the patients. A family member without apparent neuromuscular symptoms carried less mutant mtDNA. These findings support the view that this mutation is pathogenic in this family. Detection of heteroplasmy by CCM is an efficient means of screening pathogenic mtDNA point mutations.

Adult↗
PubMed1995

Ultrastructural localization of amyloid protein precursor in the normal and postischemic gerbil brain.

Intracellular localization of amyloid protein precursor (APP) in the normal and postischemic gerbil brain was examined by immunoelectron microscopy. In the normal brain, APP immunoreactivity was localized to the multivesicular body, the nuclear membrane, Golgi apparatus and rough endoplasmic reticulum. After ischemia for 5 min and reperfusion for 24 h, some neurons became intensely immunoreactive for APP in the subiculum and CA3 region of the hippocampus and layers III and V/VI of the cerebral cortex. No intense labeling occurred in glial cells. Intensely labeled neurons were characterized by eccentric nuclei and accumulation of cellular organelles in the center of the neuronal perikarya, as well as a strongly immunoreactive nuclear membrane and cisternal structures, which were presumed to be dispersed Golgi apparatus and/or fragmented rough ER. APP immunoreactivity in the multivesicular body suggests re-internalization of APP and its degradation in the endosomal-lysosomal pathway. The ultrastructural features of neurons with intense APP immunoreactivity suggested mild neuronal damage, similar to those found in central chromatolysis. This indicates that accumulation of APP in these neurons is caused by disturbance of axonal transport, although the information does not allow us to exclude the possibility of an increase in APP production.

Amyloid beta-Protein Precursor↗
PubMed1995

Topographic distributions of monoamine oxidase-B-containing neurons in the mouse striatum.

We have recently documented the presence of cholinergic neurons containing monoamine oxidase (MAO)-B activity in the striatum of C57BL/6 mouse. In the present study, we have mapped the topographical distributions of MAO-containing neurons in the mouse striatum. Positive neurons were located in the striatum of the entire rostralcaudal extent. However, the distribution of MAO-containing neurons was not uniform in the striatum. The larger number of positive neurons were located in the dorsal region of the C57BL/6 mouse striatum, in contrast to the uniform distributions of choline acetyltransferase-immunoreactive neurons in the mouse striatum. The present results suggest that cholinergic neurons are functionally heterogenous in the mouse striatum.

Animals↗
PubMed1995

Age-related decrease of nerve growth factor-like immunoreactivity in the basal forebrain of senescence-accelerated mice.

The senescence-accelerated mouse P10 (SAMP10) is a murine model of accelerated senescence characterized by the deterioration of learning and memory with advancing age. In the present study, we examined the distribution of nerve growth factor (NGF) immunohistochemically in SAMP10 mice and its control strain, SAMR1. In both strains, NGF-like immunoreactivity (NGF-IR) was observed in neurons throughout the entire forebrain and in glial cells in a particular location. In aged SAMP10 mice, each layer of the cerebral cortex retained its NGF-IR, although the thickness of the cortical mantle was markedly decreased in comparison with younger animals. There was an age-related decline in NGF-IR in the substantia innominata of SAMP10 mice at the age of 10 months, when compared to 2-month-old SAMP10. These results indicate age-related decrease of NGF in the basal forebrain in SAMP10 mice.

Age Factors↗
PubMed1995

Immunohistochemical study of apolipoprotein E in human cerebrovascular white matter lesions.

In the brains of ine cases with cerebrovascular disease, one with mixed dementia, one with amyloid angiopathy and two non-neurological controls, we found three cases with focal accumulation of apolipoprotein E (apo-E) in dystrophic axons and accompanying macrophages. Since amyloid precursor protein (APP) and chromogranin A (CgA) accumulate after axonal damages, and are sensitive markers of the white matter lesions, the regional distribution of apo-E was compared to that of APP and CgA. apo-E-immunoreactive axons were present in the periphery of an infarction with neighboring macrophages, but not in mild white matter lesions that contained APP- or CgA-immunoreactive fiber bundles. The results suggest a role of apo-E in recycling cholesterol and other membrane components via macrophages into remodeling neurites in the brain, but this phenomenon is restricted to the periphery of infarction and may be less prominent than in the peripheral nervous system.

Aged↗
PubMed1995

Monoamine oxidase-B-positive granular structures in the hippocampus of aged senescence-accelerated mouse (SAMP8).

We examined the histochemical localization of monoamine oxidase in the hippocampus of young and old senescence-accelerated mouse (SAM). We found a monoamine oxidase-B-positive granular structure (MGS) in the hippocampus of old SAMP8, an accelerated senescence-prone line of SAM. The MGS was a round-shaped granular structure of 0.5 to 5 microns diameter and usually formed a cluster, the largest diameter of which ranged from 50 to 150 microns. No MGS were found in the hippocampus of young SAMP8 or of young SAMR1, an accelerated senescence resistant line of SAM, and only few, if any, were seen in old SAMR1. A monoamine oxidase-positive astrocyte was usually observed in the central area of each cluster of MGS. Furthermore, the MGS was in close anatomical relationship with monoamine oxidase-positive astrocytic processes. The enzyme inhibition experiments showed that monoamine oxidase activities localized in the MGS and astrocytes were both predominantly of type B. These findings suggest MGS occurs at least partly in monoamine oxidase-B-positive astrocytes. Furthermore, the MGS was similar to a periodic acid-Schiff-positive granular structure, a polyglucosan body previously documented in the brains of old SAMP8 and some other aged mice strains including C57BL/6 and nude mice, in terms of their size, morphological appearances and topographical distribution in the hippocampus. Thus, the present results suggest that monoamine oxidase type B is a proteinaceous component of the periodic acid-Schiff-positive granular structure in aged mice brains, and might provide some clues for clarifying the mechanisms of age-related occurrence of periodic acid-Schiff-positive granular structures in mice brains.

Aging↗
PubMed1995

Localization in impaired spatial vision.

The present study provides clear clinico-anatomical evidence for localization of the spatial vision pathway. We report the case of a 29-year-old woman with severe spatial vision impairment. Magnetic resonance imaging revealed distinct bilateral and symmetrical occipito-parietal damage. The right lesion affected the superior parietal lobule, the dorsolateral portion of the occipital lobe, the precuneus, and the cuneus. The left lesion affected the superior parietal lobule, the dorsolateral portion of the occipital lobe, the precuneus, an upper part of the cuneus, and the posterior portion of the middle and inferior temporal gyri.

Adult↗
PubMed1995

Lectin binding to Renaut bodies.

Localization of sugar residues of Renaut bodies in human sural nerves was studied using lectin histochemistry. Lens culinaris specific to mannose and Triticum vulgaris specific to glcNAc bound to the capsular and core portions of Renaut bodies strongly. Arachis hypogaea specific to galb(1-3)galNAc and Ulex europaeus I specific to L-fucose bound to Renaut bodies granularly. Lectins specific to galactose or terminal galNAc bound to nowhere. The perineurium showed similar lectin binding to Renaut bodies. Our result suggests that Renaut bodies are rich in mannose and glcNAc. Renaut bodies may be originated from the perineurium.

Aged↗
PubMed1995

Diminished nocturnal blood pressure decline and lesion site in cerebrovascular disease.

BACKGROUND AND PURPOSE: Many studies have suggested that diminished nocturnal blood pressure decline in hypertensive cardiovascular disease is associated with the extent of hypertensive vascular disease. In our previous observation of cerebrovascular disease, however, we found reduced nocturnal blood pressure decline to be associated not only with the extent of hypertensive vascular disease but also with the specific location of cerebrovascular lesions. The purpose of this study was to elucidate the mechanism of nocturnal blood pressure decline in cerebrovascular disease. Moreover, to clarify whether reduced nocturnal blood pressure decline occurs before cerebrovascular disease, we examined patients with recurring episodes. METHODS: Ambulatory blood pressure monitoring was carried out every 30 minutes in 14 control subjects, 15 hypertensive subjects, 90 patients with cerebrovascular disease (16 single lacunar infarctions, 15 multiple lacunar infarctions, 10 putaminal hemorrhages, 14 thalamic hemorrhages, 11 pontine base infarctions, 15 pontine tegmentum infarctions, 8 pontine hemorrhages, 13 wide cortical infarctions), and 7 patients with recurring stroke episodes. The percentage of nocturnal blood pressure decline and the correlations for systolic blood pressure and heart rate were calculated. RESULTS: The percentage of nocturnal blood pressure decline was significantly smaller in the groups with multiple lacunar infarction (systolic, P < .001; diastolic, P < .01), thalamic hemorrhage (P < .01, P < .05), pontine tegmentum infarction (P < .01, P < .05), and pontine hemorrhage (both P < .05). The correlation between systolic blood pressure and heart rate was not significant for almost all the groups with diminished blood pressure decline. CONCLUSIONS: Diminished nocturnal blood pressure decline in cerebrovascular disease is thought to be caused by specific injury to the central autonomic nervous system such as the striatum, diencephalon, midbrain, and pontine tegmentum and their connecting fibers.

Aged↗
PubMed1995

Protective effect of cyclosporin A on white matter changes in the rat brain after chronic cerebral hypoperfusion.

BACKGROUND AND PURPOSE: Activation of glial cells and rarefaction of the white matter have been reported in rat brain after bilateral permanent occlusion of the common carotid arteries. Using this model, we investigated the effects of the immunosuppressant cyclosporin A on the activation of glial cells and the white matter rarefaction. METHODS: Both common carotid arteries were ligated bilaterally in 40 male Wistar rats. Twenty-two of these rats received an intraperitoneal injection of cyclosporin A, and the remaining 18 received a vehicle-solution injection. Microglia/macrophages were investigated with immunohistochemistry for the major histocompatibility complex class I and II antigens as well as for leukocyte common antigen. Astroglia were examined with glial fibrillary acidic protein as a marker. Activation of glial cells and white matter rarefaction were then investigated from 7 to 30 days after the ligation. RESULTS: In vehicle-treated animals, there was a persistent and extensive activation of both microglia/macrophages and astroglia in the white matter, including the optic nerve, optic tract, corpus callosum, internal capsule, and traversing fiber bundles of the caudoputamen. In cyclosporin A-treated rats, the number of activated microglia/macrophages was significantly reduced (P < .01) to approximately one fifth of that in vehicle-treated animals. Similarly, rarefaction of the white matter was much less intense in cyclosporin A-treated rats (P < .01). CONCLUSIONS: Cyclosporin A suppressed both glial activation and white matter changes after chronic cerebral hypoperfusion. These results suggest that immunologic reaction may play a role in the pathogenesis of the white matter changes and that the present model may be useful in investigating the pathophysiology of white matter changes induced by chronic cerebral hypoperfusion.

Animals↗
PubMed1995

[A case with hereditary motor and sensory neuropathy with multiple cranial nerves involvement].

We described a 62-year-old man presenting motor and sensory neuropathy with multiple cranial nerve involvement. He was admitted to our hospital for visual loss and gait disturbance. Visual disturbance appeared at age of 32 and have slowly progressed until admission. At age of 55, he noticed walking difficulty, which has progressed. On neurological examinations we found cranial nerve disturbance including the 2nd, 3rd, 4th, 5th, 6th, 7th and 12th nerves. Muscle atrophy and sensory disturbance were observed in four limbs, most strikingly at the distal lower limbs. The electromyographic study indicated chronic denervation in four limbs. The histological examination on sural nerve biopsy specimens showed neuronal type degeneration accompanied with a severe loss of myelinated fibers and proliferation of perineurial cells in this nerve. We diagnosed the present case as HMSN type 6 documented by Dyck. To our knowledge, the present case has been the initial case accompanied with multiple cranial nerve involvements.

Biopsy↗
PubMed1995

Immunocytochemical characterization of glial fibrillary tangles in Alzheimer's disease brain.

Neurofibrillary tangle is a major cytoskeletal pathology in Alzheimer's disease brains, and has been considered to develop exclusively in neuronal cells. We examined brains with Alzheimer's disease and observed argyrophilic fibrillary tangles not only in cortical neurons but also in subcortical glial cells in the frontal and temporal white matter. The tangles in glial cells were immunolabeled by antibodies against tau and ubiquitin, and double immunocytochemistry analyzed by confocal laser scanning microscopy demonstrated that the cytoplasms of tangle-bearing glia were labeled by antibodies against transferrin and 2'3'-cyclic nucleotide 3'-phosphohydrolase. Ultrastructurally, they were made up of bundles of straight filaments 16 nm in diameter and constricted filaments. These results indicate that fibrillary tangles resembling neurofibrillary tangles may develop in oligodendrocytes in brains with Alzheimer's disease and are distinguishable from glial cytoplasmic inclusions observed in multiple system atrophy brains. We referred to them as glial fibrillary tangles. Glial fibrillary tangles commonly occurred in this disease condition, and glial cells might be involved under the pathological processes similar to neuronal cells.

Aged↗
PubMed1995

[A case of rigid spine syndrome with congenital cardiac abnormality of sinus venosus defect].

A 28-year-old male with a rigid spine syndrome who had congenital cardiac abnormality of sinus venosus defect was described. The patient was admitted to our hospital because of easy fatigability and palpitation. At the age of 4 years, he had an operation for his congenital cardiac abnormality and developed persistent atrial fibrillation thereafter. On neurological examination, he had average mentality, rigid spine with joint contractures, especially in the left elbow joint, and winged scapulae. He had marked muscle weakness and atrophy, predominantly in the left half of the extremities and trunk. Electromyographic studies demonstrated myopathic with partial neurogenic changes. Motor and sensory nerve conduction velocity was normal. A muscle biopsy specimen obtained from the right rectus femoris showed some marked hypertrophic and atrophic muscle fibers, with prominent internal nuclei, fiber splitting and pyknotic nuclear clump. ATP-ase stain showed type 2B fiber deficiency, increased number of type 2C fibers and fiber type grouping.

Adult↗
PubMed1994

Histochemical demonstration of membranous localization of endothelial nitric oxide synthase in endothelial cells of the rat brain.

We examined cellular and subcellular localization of endothelial nitric oxide synthase by using immunoelectron microscopy. The results showed that immunoreaction products were associated with membranous structure, likely the endoplasmic reticulum and cytoplasmic vesicles. These membranous localization of immunoreactivities at electron microscopic level corresponded to the perinuclear granular structures observed by light microscopic immunohistochemistry for endothelial nitric oxide synthase as well as NADPH diaphorase histochemistry.

Amino Acid Oxidoreductases↗
PubMed1994

Microtubules stability in human peripheral nerves.

We examined the cold stability of microtubules (MT) in biopsied sural nerves. In control nerves, cold treatment reduced the density of MT in unmyelinated axons. The proportion of cold-insoluble MT was approximately 30% by morphological study. By contrast, the extraction study using essentially the same nerves showed that the ratio of cold-insoluble tubulin was 60-75%. These findings suggest the existence of a subpopulation of cold-stable tubulin which may not make up MT. However, in 2 patients with acute dysautonomia the proportion of cold-stable MT or tubulin was decreased compared to that in controls in both the morphological and extraction study. This suggests the altered local process involving MT in primary axonal degeneration.

Adult↗