Biomedical subjects

I Akiguchi

Publications and source records attributed to I Akiguchi.

333 records · Page 19Linked to original sources

PubMedDate not supplied

Role of central aminergic fibers in experimental cerebral ischemia in stroke-prone SHR. Relation to anesthetic effect.

Dopamine and norepinephrine fluorescence in the nucleus caudatus and putamen and cerebral cortex was markedly depleted along with rCBF reduction in symptomatic stroke-prone spontaneously hypertensive rats (SHRSP) with bilateral carotid artery ligation under light pentobarbital anesthesia. An accumulation of fluorescence at the intima of blood vessels, especially in the nucleus caudatus and putamen, was noted in some SHRSP under the same experimental conditions. These changes were hardly seen in deeply anesthetized SHRSP, as well as in normotensive Wistar-Kyoto (WK) rats. It may be possible, therefore, that released cerebral amines in acute brain ischemia accelerate the vasoconstriction and permeability of cerebral arteries, which further decreases the blood supply to these areas. Also, a barbiturate protective effect against the release of central dopamine and norepinephrine during acute brain ischemia was noted in deeply anesthetized SHRSP.

Animals↗

PubMedDate not supplied

Sympathetic nerve terminals in the tunica media of human superficial temporal and middle cerebral arteries: wet histofluorescence.

In specimens from the superficial temporal artery (STA) and middle cerebral artery (MCA), obtained during STA-MCA anastomosis, green fluorescent varicose fibers of sympathetic nerves were clearly visible with both formaldehyde-glutaraldehyde and sucrose-potassium phosphate-glyoxylic acid wet-histofluorescent techniques. These fibers were fairly thick, were densely packed and had a meshwork-like arrangement. Fluorescent terminals were seen both in the adventitia and in the outer muscular layer of the media in both STA and MCA specimens. They were more often observed in patients with prominent atherosclerosis in these vessels. The present study suggests the possible role of sympathetic nerve terminals in the development of vasospasm and occlusive lesions in cerebral vessels. It may also help to explain the marked constriction and transient occlusion following a STA-MCA bypass procedure.

Adrenergic Fibers↗

PubMedDate not supplied

Density of sympathetic nerve terminals in human superficial temporal arteries: potassium permanganate fixation and monoamine oxidase histochemistry.

The density of sympathetic nerve terminals in human superficial temporal arteries from 5 cases at intra- and extracranial bypass surgery was examined with two histochemical methods, one with potassium permanganate fixation and the other with the new monoamine oxidase staining technique. By potassium permanganate fixation, small cored vesicles containing fibers of noradrenergic nerve terminals made up 29.2% of all nerve fibers in the adventitia. The monoamine oxidase-containing nerves in the adventitia made up 31.4%. According to this study, sympathetic nerve terminal density in human superficial temporal arteries was assumed to consist of approximately 30% of all adventitial nerve terminals. In periadventitial nerve bundles, some unmyelinated axons contained monoamine oxidase activity. Thus, staining is considered to be useful in demonstrating the periadventitial and intervaricose fibers as well as the nerve terminals of sympathetic nerves in human cerebral arteries.

Fixatives↗

PubMedDate not supplied

Expression of the endocytosis regulatory proteins Rab5 and Rabaptin-5 in glial cytoplasmic inclusions from brains with multiple system atrophy.

BACKGROUND: Glial cytoplasmic inclusions (GCIs) occur specifically in oligodendrocytes in brains with multiple system atrophy (MSA). Oligodendrocytes in MSA appear to be functionally altered in their nature in terms of the occurrence of GCIs and aberrant expression of various proteins such as neuron specific protein, MAP2 or pre-synaptic protein, ct-synuclein. The present study examined whether or not aberrant expression of the endocytosis regulatory proteins Rab5 and Rabaptin-5 occcur in oligodendrocytes of brains with MSA. MATERIALS AND METHODS: We examined immunohistochemically the post-mortem brain tissues from 5 patients with MSA and 5 controls. Immunohistochemistry was done using monoclonal anti-Rab5 and anti-Rabaptin-5 antibodies based on ABC method. RESULTS: We have observed Rab5 and Rabaptin-5 immunoreactivity in the neuronal somata and axons of the controls, suggesting that Rab5 and Rabaptin-5 are involved in the regulation of the endocytosis in neurons of the human central nervous system. In the brain tissues from patients with MSA, we have found Rab5 and Rabaptin-5 immunoreactivity in GCIs. CONCLUSION: Rab5, in association with Rabaptin-5, has been demonstrated in the early endosome and regulates the endocytosis. Since Rab5 and Rabaptin-5 have been immunolocalized to neurons in the human brains, we propose that oligodendrocytes may ectopically express Rab5 and Rabaptin-5 in MSA. Thus, the oligodendrocytes in MSA brains appear to be functionally significantly altered, which may be associated with the formation of GCIs in the oligodendrocytes.

Aged↗

PubMedDate not supplied

A case of frontotemporal dementia and parkinsonism of early onset with progressive supranuclear palsy-like features.

We report a patient with frontotemporal degeneration and parkinsonism with mental retardation. The patient was a 54-year-old man who had parkinsonism that resembled progressive supranuclear palsy, frontotemporal degeneration and myoclonus. His family included many affected members. Neuropathologically, there was degeneration of the frontal and temporal cortices, the basal ganglia, the brainstem and the cerebellum. Microscopically, neuronal loss was severe in the frontal and temporal cortex, the globus pallidus, substantia nigra, red nucleus and dentate nucleus. Fibrillary changes were found in neurons and glia that were immunostained for tau. Although we could not define the genetic abnormalities, we thought that this case might have involved frontotemporal dementia and parkinsonism linked to chromosome 17.

Brain↗

PubMedDate not supplied

[A patient with Crow-Fukase syndrome associated with pulmonary plasmacytoma].

We here reported a 54-year-old female patient with Crow-Fukase syndrome associated with pulmonary plasmacytoma. She was found to have scattered tumor in 1990. Although the tumor had slowly grown for the last 10 years, she showed no clinical symptoms. Numbness and weakness of lower extremities began in June 1999, and she was referred to Kyoto University Hospital on Oct. 21 1999 for evaluation of progressive symptoms. She had skin pigmentation, edema of the lower extremities, lymphadenopathy, muscle weakness and sensory disturbance in a glove-and-stocking distribution. Serological examination showed monoclonal IgG-lambda gammopathy. Serum vascular endothelial growth factor (VEGF) was markedly elevated. Microscopic studies on biopsied sural nerve demonstrated mild decrease of myelinated fibers. Immunohistochemically, the pulmonary tumor was defined as an IgG (lambda type) plasmacytoma. After treatment with melphalan-prednisolone therapy, the neurological symptoms improved along with decrease of serum VEGF levels as well as the size of pulmonary plasmacytoma. This is the first report of a patient with Crow-Fukase syndrome associated with pulmonary plasmacytoma. This case suggests that growth of pulmonary plasmacytoma might have played an important role in the overproduction of VEGF and thus development of Crow-Fukase syndrome.

Antineoplastic Agents, Alkylating↗

PubMedDate not supplied

Immunohistochemical localization of phosphoinositide 3-kinase in brains with multiple system atrophy.

Oligodendrocytes have been shown to display some morphological characteristics of apoptosis in MSA. The accumulated evidence shows that phosphoinositide 3-kinase (PI3K) is closely associated with the regulation of apoptosis. Thus, we examined immunohistochemically PI3K in the cerebellum and pons from autopsy samples with MSA. In control tissues, PI3K was immunostained in some neurons and a few oligodendrocytes. In MSA samples, the larger number of oligodendrocytes was observed in the pons and cerebellum. Furthermore, some neurons were strongly immunolabeled in MSA samples. The recent study has shown that PI3K phosphorylates PKB/Akt which phosphorylates BAD resulting in the cessation of apoptotic process. The present results suggest that PI3K is upregulated in oligodendrocytes and some neurons in MSA, possibly in response to the apoptotic signals to these cells.

Aged↗

PubMedDate not supplied

Myofibrillar (desmin-related) myopathy: clinico-pathological spectrum in 3 cases and review of the literature.

Myofibrillar or desmin-related myopathies encompass neuromuscular disorders with abnormal deposits of desmin and myofibrillar alterations. We report 3 unrelated patients presenting with proximal and distal myopathy, and, as a unique congenital syndrome, diffusely distributed myopathy, osteoporosis and myopia. Muscle biopsies shared cytoplasmic inclusions, rimmed vacuoles, and ragged-red-like fibers. Sarcoplasmic inclusions, either plaque-like or amorphous, strongly immunoreacted on dystrophin and variably for desmin, alphaB crystallin and ubiquitin. Cyclin-dependent kinases CDK1, CDK2 and CDK5 were overexpressed in affected fibers. Ultrastructurally, focal myofibrillar disruption was accompanied by tubulo-filamentous inclusions in one case and abundant glycogen and enlarged mitochondria displaying respiratory chain dysfunction at biochemistry in another case. Molecular analysis of the alphaB crystallin gene coding sequence and exons 4, 5 and 6 of the desmin gene did not reveal any mutation. The morphologic denominator of hyaline structures and areas of myofibrillar destruction occurs in heterogeneous conditions and may overlap with features of inclusion body myopathy and mitochondrial myopathy.

Adult↗

PubMedDate not supplied

Spinocerebellar degeneration: qualitative and quantitative MR analysis of atrophy.

Magnetic resonance imaging at 1.5 T was performed in 27 patients with either the cerebellar or spinocerebellar form of spinocerebellar degeneration and in 10 control subjects. Neither T1- nor T2-weighted images (T1WIs and T2WIs) of the patients showed any abnormal intensity areas within the cerebellum or in any other structures of the brain. The T2WIs delineated normal configurations of symmetrical dentate and red nuclei. On T1WIs two patterns of atrophy were detected: (a) moderate to severe shrinkage of the basis pontis and the middle cerebellar peduncles associated with atrophy of the cerebellum, and (b) moderate atrophy of the cerebellum with a preserved basis pontis. The former morphological changes are consistent with the pathology of pontocerebellar atrophy (PCA) and the latter with those of cerebellar cortical degeneration (CCD). In 11 patients, only after a quantitative analysis of the images were we able to classify them in one of the two morphological categories (PCA or CCD). There was a significant correlation between atrophy of the cerebellum and atrophy of the basis pontis. Furthermore, in the PCA group the anterior portion of the body of the corpus callosum was significantly smaller in comparison with the control subjects.

Adult↗