Biomedical subjects

I Akiguchi

Publications and source records attributed to I Akiguchi.

At least 145 records · Page 8Linked to original sources

PubMed1994

Synaptophysin and chromogranin A immunoreactivities of Lewy bodies in Parkinson's disease brains.

Lewy bodies commonly observed in brains with Parkinson's disease (PD) histochemically contain both protein and lipid as chemical components. Ultrastructurally, they are composed of filamentous, vesicular and granular structures. We investigated PD brains with light and electron microscopic immunohistochemistry using antibodies against two marker proteins for neuronal secretory vesicles, synaptophysin and chromogranin A. Both antibodies immunolabeled the peripheral zones and occasionally central cores of Lewy bodies of the classical and intraneuritic types. In addition, the diffuse immunolabeling was observed in Lewy bodies of the cortical type. Furthermore, the ultrastructural immuno-decoration was found mainly in the vesicular structures, and also in the filamentous and granular structures of Lewy bodies. Immuno-blot analysis of each antibody showed no difference between PD and normal control brains. The present observations suggest that vesicular profiles of Lewy bodies represent presynaptic and dense core secretory vesicles, and therefore that the lipid elements of Lewy bodies are derived from membrane lipids of these vesicles.

Aged↗

PubMed1994

Isolated acalculia due to left parietal lesion.

OBJECTIVE: To clarify the characteristics and the localization of isolated calculation disturbances due to left parietal lesions. DESIGN: Case series. SETTING: Tertiary care hospital. PATIENTS AND OTHER PARTICIPANTS: Three referred patients with isolated calculation disturbances due to stroke in the left parietal region. Sixteen volunteers for age and education constituted the control group. OUTCOME MEASURES: Neuropsychological tests, including a battery of tests for acalculia and the Wechsler Adult Intelligence Scale, and magnetic resonance imaging were performed. RESULTS: Three patients made calculation errors in the process where a number of steps were carried out simultaneously. The patients showed no aphasic components in number operations. They understood the basic processes of calculation. They showed little difficulty in the retrieval of table values. The patients had no impairment in aligning arithmetic problems or in assigning and maintaining place-holding values. They did not show any deficit of immediate memory for calculation problems. Overlapping lesions were located along the left intraparietal sulcus. CONCLUSION: The area lying along the left intraparietal sulcus is critical for isolated parietal acalculia. The profile of isolated acalculia suggests that it results from the disruption of the working memory for calculation.

Brain Diseases↗

PubMed1994

Elevated serum levels of endothelial leukocyte adhesion molecules in Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy.

We determined the serum concentrations of the soluble form of endothelial leukocyte adhesion molecule-1 (sELAM-1) in 25 patients with Guillain-Barré syndrome, 14 patients with chronic inflammatory demyelinating polyneuropathy, 15 patients with amyotrophic lateral sclerosis, 15 patients with other polyneuropathies, 10 patients with acute stroke, and 12 healthy control subjects. The patients with Guillain-Barré syndrome in the acute stage had a higher sELAM-1 serum level compared with the control subjects (p < 0.001). In 7 of the 9 patients the elevated level returned to normal by 14 days after the onset of neurological symptoms. In addition, a significantly elevated serum level of sELAM-1 was found in patients with chronic inflammatory demyelinating polyneuropathy (p < 0.01). These findings suggest a role for ELAM-1 in the inflammatory process of these disorders.

Cell Adhesion↗

PubMed1994

Differential localization of lectin binding sites and neuropeptides in human dorsal root ganglia.

The subpopulations were compared of neurons in human dorsal root ganglia (DRG), as substance P, identified by somatostatin, Glycine max lectin (SBA) specific to terminal N-acetylgalactosamine, and Ulex europaeus I agglutinin (UEA-I) specific to L-fucose. The lectins and neuropeptides all bound to neurons of small diameter. Furthermore, the majority of the SBA binding neurons or somatostatin positive neurons were also UEA-I binding neurons. However, SBA binding neurons were not colocalized with somatostatin or substance P. Less than 20% of substance P positive neurons showed colocalization with L-fucosyl residues, and approximately 10% of L-fucosyl residues showed colocalization with substance P. Our results suggest that both L-fucose and terminal N-acetylgalactosamine containing neurons in the human DRG are subjected to different subpopulations from substance P or somatostatin positive neurons.

Acetylgalactosamine↗

PubMed1994

Bundles of amyloid precursor protein-immunoreactive axons in human cerebrovascular white matter lesions.

Cerebral white matter lesions commonly observed in Binswanger's disease, multi-infarct encephalopathy and elderly people are neuropathologically characterized by diffuse incomplete demyelination and considered to be ischemic in nature. Arteriolosclerosis in the white matter is a common feature in these white matter lesions. To investigate a possible alteration of the distribution of amyloid precursor protein (APP), chromogranin A (CgA) and synaptophysin (Syn) in such white matter lesions, we examined 15 cases with white matter lesions and 5 without white matter lesions. Many bundles of axons with APP-like immunoreactivity (LI) were observed particularly in mild white matter lesions. Such bundles of axons showed similar but less intense CgA-LI and Syn-LI. They appeared to occur in areas with many ameboid or ramified microglia labeled with anti-leukocyte common antigen and few astrocytes labeled with anti-glial fibrillary acidic protein. In the center of moderate of severe white matter lesions bundles of axons with APP-LI were never observed. Since APP, CgA and Syn undergo fast axonal transport, and since following ischemic insults to central nervous system microglial reaction occurs earlier than astroglial changes, our results suggest that axonal damage, which induces disturbance of fast axonal transport, can occur even in the early stage of white matter lesions.

Aged↗

PubMed1994

Glial activation and white matter changes in the rat brain induced by chronic cerebral hypoperfusion: an immunohistochemical study.

Activation of glial cells and white matter changes (rarefaction of the white matter) induced in the rat brain by permanent bilateral occlusion of the common carotid arteries were immunohistochemically investigated up to 90 days. One day after ligation of the arteries, expression of the major histocompatibility complex (MHC) class I antigen in microglia increased in the white matter including the optic nerve, optic tract, corpus callosum, internal capsule, anterior commissure and traversing fiber bundles of the caudoputamen. After 3 days of occlusion, MHC class I antigen was still elevated and in addition MHC class II antigen and leukocyte common antigen were up-regulated in the microglia in these same regions. Astroglia, labeled with glial fibrillary acidic protein, increased in number in these regions after 7 days of occlusion. A few lymphocytes, labeled with CD4 or CD8 antibodies, were scattered in the neural parenchyma 1 h after occlusion. Activation of glial cells and infiltration of lymphocytes persisted after 90 days of occlusion in the white matter and the retinofugal pathway. However, cellular activation and infiltration in microinfarcts of the gray matter was less extensive and was substantially diminished 30 days after occlusion. The white matter changes were most intense in the optic nerve and optic tract, moderate in the medial part of the corpus callosum, internal capsule and anterior commissure, and slight in the fiber bundles of the caudoputamen. These results indicated that chronic cerebral hypoperfusion induced glial activation preferentially in the white matter. This activation seemed to be an early indicator of the subsequent changes in the white matter.

Animals↗

PubMed1994

Abnormal glycosylation of motor neurons with N-acetyl-D-galactosamine in a case of subacute motor neuronopathy associated with lymphoma.

Lectins, glycine max (SBA) and Vicia villosa (VVA), which identify terminal N-acetyl-D-galactosamine (GalNAc), stained the motor neurons of a patient with subacute motor neuronopathy associated with neoplastic angioendotheliosis. In normal controls and in patients with other neurological disorders including amyotrophic lateral sclerosis, neither lectin stained motor neurons. Abnormal glycosylation of motor neurons with terminal galNAc may be associated with the pathogenesis of subacute motor neuronopathy in this patient.

Acetylgalactosamine↗

PubMed1994

Cheiro-oral-pedal syndrome in the lesion of thalamocortical projections.

Unilateral sensory disturbance in the hand and mouth (cheiro-oral syndrome) is well known, but one in the hand, mouth and foot region (cheiro-oral-pedal syndrome) has been reported only in 2 patients with brainstem lesion and in 2 patients with thalamic infarction. We report the first case of cheiro-oral-pedal syndrome due to involvement of thalamocortical projections, which favors somatotopy in thalamocortical projections.

Brain Mapping↗

PubMed1994

Anosodiaphoria for dressing apraxia: contributory factor to dressing apraxia.

We report 2 patients with bilateral dressing apraxia. One patient had prominent bilateral dressing apraxia without severe constructional apraxia together with anosodiaphoria for dressing apraxia. The other patient had mild dressing apraxia with severe constructional apraxia and was aware of her disabilities. This dissociation implies that anosodiaphoria for dressing apraxia is an important factor in the severity of bilateral dressing apraxia. This also explains why automatic acts in dressing are more severely affected than when patients are asked to put clothing on in dressing examination.

Adult↗

PubMed1994

Immunohistochemical localization in the rat brain of an epitope corresponding to the fibroblast growth factor receptor-1.

The localization of fibroblast growth factor receptor-1 was investigated in rat brain by immunohistochemistry using a polyclonal antibody against an acidic peptide sequence of chicken fibroblast growth factor receptor-1. For raising the antisera in rabbits, we synthesized the oligopeptide EDDDDEDDSSSEEKEAD which is a highly acidic region of chicken fibroblast growth factor receptor-1. The oligopeptide was used as a haptenic antigen by conjugating with poly-L-glutamate as a carrier protein. On immunospot assay, the best antiserum was capable of detecting 15.7 pmols of both the chicken and its analogous human oligopeptides but failed to react even with up to 1 nmol of poly-L-glutamate. When rat brain homogenate was examined by Western blots, the antiserum revealed two bands with molecular weights of 145,000 and 75,000 corresponding to known sizes of the membrane-bound and secreted forms of the rat receptor, respectively. Immunohistochemistry in rat brain demonstrated that putative fibroblast growth factor receptor-1 immunoreactivity sites were present mainly in neurons but also in tanycytes and ependymal cells. Positive neurons were distributed widely in various brain regions, but were particularly abundant in such regions as the lateral hypothalamus, substantia nigra, locus coeruleus and raphe nuclei. The present study suggests that fibroblast growth factor receptor-1 is expressed preferentially in certain neuronal systems that appear to be under the influence of fibroblast growth factors in the normal brain. The result should facilitate study of the functional significance of fibroblast growth factors in these brain neurons.

Amino Acid Sequence↗

PubMed1994

Cellular localization of nerve growth factor-like immunoreactivity in adult rat brain: quantitative and immunohistochemical study.

To elucidate the role and the mechanism of action of nerve growth factor in the adult central nervous system, we investigated the localization of nerve growth factor-like immunoreactivity in adult rat brain, both quantitatively and immunohistochemically, using polyclonal anti-nerve growth factor immunoglobulin G. We raised rabbit polyclonal anti-mouse nerve growth factor antibody with an extremely high titer as 10(-9) determined by an enzyme immunoassay. The affinity-purified anti-nerve growth factor immunoglobulin G specifically recognized nerve growth factor with no cross-reaction to recombinant brain-derived neurotrophic factor and neurotrophin-3 evaluated by an enzyme immunoassay. We quantified nerve growth factor content in each layer of the adult rat cerebral cortex and in each small piece (0.225 mg wet weight tissue) of the diencephalon, brainstem and cerebellum with a highly sensitive two-site enzyme immunoassay. Nerve growth factor content was unevenly distributed in the cerebral cortex (dense in layers II/III and V/VI and sparse in layers I and IV). Moderate to high levels of nerve growth factor were registered in the habenular nuclei, zona incerta, ventral tegmental area, substantia nigra, locus coeruleus, ventral cochlear nucleus, trapezoid body, lateral vestibular nucleus, cerebellar nuclei and paraflocculus. Immunohistochemically, the nerve growth factor-like immunoreactivity was found in the cell bodies, dendrites and axons of adult rat central neurons, not only in the cerebral cortex, hippocampus and basal forebrain, but also in the diencephalon, brainstem and cerebellum. The population of neurons with nerve growth factor-like immunoreactivity was limited, but unexpectedly widespread, and the density of these cells correlated well with the content determined by an enzyme immunoassay in the present and a previous study [Nishio T. et al. (1992) Expl Neurol. 116, 76-84]. The monoamine neurons, including dopaminergic, noradrenergic and serotonergic neurons, showed intense nerve growth factor-like immunoreactivity, indicating that the central monoaminergic neuronal system may also be involved in the nerve growth factor trophic system. To visualize nerve growth factor transported in the axons and to enhance the immunostaining in the nerve growth factor-producing cells, we injected colchicine, a potent inhibitor of microtubule polymerization and a blocker of axoplasmic transport, into the lateral ventricle of adult Wistar rat brain. Colchicine treatment enhanced the intensities of nerve growth factor-like immunoreactivity in the axons and cell bodies, especially in the axon hillocks and the proximal axons of the nerve growth factor-producing neurons. This observation may suggest the existence of an orthograde axonal transport system for nerve growth factor in the central neurons.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1994

Localization of atrophy-prone areas in the aging mouse brain: comparison between the brain atrophy model SAM-P/10 and the normal control SAM-R/1.

Mouse inbred strain "SAM-P/10" (Senescence Accelerated Mouse) is a model of age-related brain atrophy. In this strain there is an earlier and more severe age-related deterioration in the conditional avoidance learning than the normal control inbred SAM-R/1 strain. The present study analysed age-related changes in brain area size using a computerized morphometric method. The region most vulnerable to age-related atrophy in SAM-P/10 was the frontal region of the cerebral cortex, including the prefrontal cortex. Other neocortical regions underwent diffuse atrophy. Posterior piriform cortex, entorhinal cortex, anterior olfactory nucleus, amygdala, caudate-putamen, nucleus accumbens and cerebellar cortex were atrophy-prone regions. The septum also underwent atrophy but other basal forebrain structures were intact. The hippocampus, diencephalon and brainstem structures showed no atrophic change. White matter structures did not change in size with aging except for the forceps minor of the corpus callosum, which showed age-related atrophy. On the contrary, SAM-R/1 showed a significant age-related atrophy only in a restricted part of the cerebral cortex, mainly in the parietal region. Other cortical regions, subcortical structures, diencephalon, brainstem structures, cerebellum and white matter were atrophy-resistant in SAM-R/1. The prefrontal cortex, entorhinal cortex, piriform cortex and striatum are closely interconnected and also connect with the amygdala which plays a key role in conditioning in the rodent. Age-related atrophy in all these structures in SAM-P/10 presumably accounts for the age-related deficits in conditional avoidance learning in this strain of mouse. Comparison between SAM-P/10 and SAM-R/1 or other well-known rodents indicates that SAM-P/10 is a unique rodent that spontaneously and rapidly develops progressive generalized cerebral atrophy, which is considered to be a pathological process rather than an accelerated aging process.

Aging↗

PubMed1994

Distribution of nitric oxide synthase in the human cerebral blood vessels and brain tissues.

The distribution of nitric oxide synthase was investigated in human cerebral blood vessels and brain tissues. NADPH-diaphorase histochemistry, which is a marker for nitric oxide synthase in neurons and endothelial cells, revealed periadventitial nerve fibers in the arteries of the circle of Willis and their cortical branches, as well as the common carotid and subclavian arteries. The fibers were mostly nonvaricose in the periadventitial nerve trunk and were varicose within the adventitia. Patchy reaction products were distributed in the perinuclear region of each endothelial cell. Smooth muscle cells in the tunica media were weakly stained. Staining was particularly intense in regions with atherosclerotic changes, which consist of macrophage infiltration and proliferation of fibroblasts. In the neural parenchyma, two types of NADPH-diaphorase reactive neurons were differentiated. Type I neurons were intensely stained, medium-sized, and bipolar or multipolar. They were distributed in the cerebral cortex and white matter, mostly in the subcortical white matter. Type II neurons were lightly stained, small oval neurons with fine processes and were distributed in the cerebral cortex. Endothelial cells were intensely reactive for NADPH-diaphorase in the arteries, arterioles, and capillaries but weakly in veins. Immunohistochemistry for neural nitric oxide synthase labeled perivascular nerves in the larger arteries and those in the neural parenchyma. Both type I and type II neurons were labeled. Nitric oxide synthase in endothelial cells and the nerve encircling blood vessels further suggests a dual control of cerebral circulation by nitric oxide in human brain.

Aged↗

PubMed1994

Temporal profiles of accumulation of amyloid beta/A4 protein precursor in the gerbil after graded ischemic stress.

The neurons that accumulate beta/A4 amyloid protein precursor (APP) after transient cerebral ischemia were characterized by comparing their distribution with those destined to suffer delayed neuronal death or those with induction of 72-kDa heat-shock protein. With immunohistochemistry of APP in gerbil brains, no alterations were detected after ischemia for 2 min and subsequent reperfusion for up to 7 days, whereas after ischemia for 3 min and reperfusion for 48 h, a small number of neurons, intensely immunoreactive for APP, were found to be scattered in the CA1 subfield of the hippocampus and the layer V/VI of the frontoparietal cortex. After reperfusion for 24 h following ischemia for 5 or 15 min, a large number of densely stained neurons appeared in the subiculum, and CA3 subfield of the hippocampus, and layers III and V/VI of the frontoparietal cortex. The majority of these neurons did not undergo delayed neuronal death after reperfusion for 72 h and thereafter. APP and heat-shock protein were upregulated in the same regions, but mostly in distinct neurons. These results indicate that APP accumulates in the neurons marginating the regions destined to die, and the majority of these neurons seem to survive after ischemic insult.

Amyloid beta-Peptides↗

PubMed1994

CAG expansions in a novel gene for Machado-Joseph disease at chromosome 14q32.1.

We have identified a novel gene containing CAG repeats and mapped it to chromosome 14q32.1, the genetic locus for Machado-Joseph disease (MJD). In normal individuals the gene contains between 13 and 36 CAG repeats, whereas most of the clinically diagnosed patients and all of the affected members of a family with the clinical and pathological diagnosis of MJD show expansion of the repeat-number (from 68-79). Southern blot analyses and genomic cloning demonstrates the existence of related genes. These results raise the possibility that similar abnormalities in related genes may give rise to diseases similar to MJD.

Adult↗

PubMed1994

Accumulation of blood-borne horseradish peroxidase in medial portions of the mouse hippocampus.

The intracerebral distribution of intravenously injected horseradish peroxidase (HRP) in young adult DDD mice was examined. HRP-tetramethylbenzidine reaction products were observed in the medial portions of the hippocampus, particularly the medial CA1 region and medial dentate gyrus. Reaction products were observed in the subfornical organ in mice decapitated 5 min after HRP injection, and then also progressively more caudally in the medial portions of the hippocampus as postinjection survival time increased. These findings suggest that blood-borne macromolecules have ready access to the medial portions of the hippocampus, particularly the medial CA1 region and medial dentate gyrus.

Animals↗

PubMed1994

Impaired stereoacuity due to a lesion in the left pulvinar.

A right-handed patient with a haematoma in the left pulvinar showed impaired stereoacuity. In contrast with previous reports, he did not show peripheral visual extinction or prolonged reaction times for targets on the side contralateral to the lesion.

Cerebral Hemorrhage↗

PubMed1994

Expression of endothelial leukocyte adhesion molecule-1 (ELAM-1) in chronic inflammatory demyelinating polyneuropathy.

We used immunocytochemical methods to identify activated endothelial cells and the ligands of infiltrating cells in sural nerve biopsies from 30 patients with peripheral neuropathy. In chronic inflammatory demyelinating polyneuropathy (CIDP), the endothelial leukocyte adhesion molecule (ELAM-1; E-selectin) was detected in the epineurial vessels of five of the 10 patients. CD68-positive monocytes were usually at ELAM-1-positive endothelial sites and in perivascular tissues, while sialyl-Lewis x-positive cells were detected mostly in the lumina adherent to ELAM-1-positive endothelial cells. The location of activated T cells was not correlated with activated endothelial cells, and endoneurial vessels were not immunostained for ELAM-1. In view of the transient expression of ELAM-1 in response to cytokine stimulation, these findings suggest that endothelial cells play a role in the extravasation of infiltrating cells in CIDP.

Adolescent↗