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Biomedical subjects

N Oka

Publications and source records attributed to N Oka.

At least 91 records · Page 5Linked to original sources
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↗
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

Anti-GM1 antibodies and impaired blood-nerve barrier may interfere with remyelination in multifocal motor neuropathy.

Multifocal motor neuropathy has pure motor manifestation and nonremittent clinical courses. Antiganglioside antibodies, though variable in titers, are characteristically elevated in the majority of these patient. In our cases, pathological findings at the site of conduction block suggested impaired remyelination and disruption of blood-nerve barrier. These findings lead us to postulate that antibodies toward gangliosides or toward unknown antigens containing gangliosides initiate motor-specific demyelination. The lesion, once produced, may persist as a result of impaired remyelination caused by disrupted blood-nerve barrier. The antibodies bound to denuded axons may also interfere with a remyelinative process. If so, antibodies may not always be circulating, thus accounting for variable levels of titers.

Antibodies↗
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

Intracranial hemorrhage due to rupture of an arteriovenous malformation in a full-term neonate.

A case of neonatal intracerebral hemorrhage (ICH) secondary to rupture of an arteriovenous malformation (AVM) is reported. The baby began to vomit frequently 9 h after birth. Computed tomographic scan revealed the presence of an ICH. Intravenous digital subtraction angiography (IVDSA) demonstrated an AVM, which was successfully excised on the 2nd day after birth. It is stressed that IVDSA is safe and noninvasive in comparison with conventional angiography and is useful for diagnosis of cerebral vascular disease in neonates.

Angiography, Digital Subtraction↗
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

Ultra-high dose methylcobalamin promotes nerve regeneration in experimental acrylamide neuropathy.

Despite intensive searches for therapeutic agents, few substances have been convincingly shown to enhance nerve regeneration in patients with peripheral neuropathies. Recent biochemical evidence suggests that an ultra-high dose of methylcobalamin (methyl-B12) may up-regulate gene transcription and thereby protein synthesis. We examined the effects of ultra-high dose of methyl-B12 on the rate of nerve regeneration in rats with acrylamide neuropathy, using the amplitudes of compound muscle action potentials (CMAPs) after tibial nerve stimulation as an index of the number of regenerating motor fibers. After intoxication with acrylamide, all the rats showed equally decreased CMAP amplitudes. The animals were then divided into 3 groups; rats treated with ultra-high (500 micrograms/kg body weight, intraperitoneally) and low (50 micrograms/kg) doses of methyl-B12, and saline-treated control rats. Those treated with ultra-high dose showed significantly faster CMAP recovery than saline-treated control rats, whereas the low-dose group showed no difference from the control. Morphometric analysis revealed a similar difference in fiber density between these groups. Ultra-high doses of methyl-B12 may be of clinical use for patients with peripheral neuropathies.

Acrylamide↗
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

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↗
PubMed1994

Isolated adrenocorticotrophin deficiency associated with anti-pituitary antibodies, pituitary cyst, sphenoidal cyst and pineal tumor.

This paper reports a rare case of isolated ACTH deficiency associated with anti-pituitary antibodies, pituitary cyst, sphenoidal cyst and pineal tumor. A 68-year-old man consulted our clinic for general fatigue. Laboratory data showed low plasma adrenocorticotrophin (ACTH) and cortisol levels with blunted responses to insulin-induced hypoglycemia and corticotrophin releasing factor (CRF). Urinary 17-OHCS was low but responded to ACTH-Z administration. No other pituitary functions were impaired. Antibodies to the cytoplasm of rat pituitary and the surface of GH3 cells were detected in the serum. The magnetic resonance imaging (MRI) showed a high signal intensity mass in the anterior pituitary and in the sphenoidal sinus in both T1 and T2 weighted images as well as a low signal intensity mass in a T1 weighted image of the pineal region. Transsphenoidal surgery was performed to resect the mass in the sphenoid sinus and in the pituitary. Pathological studies showed a benign cyst in the sphenoid sinus, and fibrous degeneration and decreased basophils in the pituitary. No infiltrative mononuclear cells were detected in the pituitary. Immunohistochemical studies revealed a decrease in the number of ACTH-producing cells in the pituitary. The patient was well maintained by glucocorticoid replacement without any growth of a possibly benign pineal tumor.

Adrenocorticotropic Hormone↗
PubMed1994

[Clinical study of total prostatectomy for prostatic cancer].

Total retropubic prostatectomy was performed on 31 patients with prostatic cancer (median age; 70 years). The accuracy of staging was 55% (17 patients). In 11 patients (35%) the staging had been underestimated, and in 3 patients (10%) overestimated. The pathological stage and grade were stage B in 14 patients, stage C in 4 patients, stage D1 in 13 patients (pN1; 8 patients, pN2; 5 patients), well differentiated adenocarcinoma (WDA) in 8 patients moderately differentiated adenocarcinoma (MDA) in 7 patients, and poorly differentiated adenocarcinoma (PDA) in 16 patients. The WDA were all stage B, and 85% of the PDA were stage D1. The positive surgical margin rate was 21% in stage B, 50% in stage C, 85% in stage D1, 13% in WDA, 43% in MDA, and 75% in PDA. Five of the patients died, and the causes of death were prostatic cancer in 2 patients (pN2/PDA), and others in 3 patients (1 patient; stage B/PDA, 2 patients; pN2/PDA). The 5-year survival rate (Kaplan-Meier) was 84% on the whole, 83% for stage B, 100% for stage C, 83% for stage D1, 100% for WDA, 100% for MDA, 71% for PDA, 86% for pN0, 100% for pN1, and 38% for pN2.

Adenocarcinoma↗
PubMed1993

Ulex europaeus I and glycine max bind to the human olfactory bulb.

The distribution of binding sites for the fucose-selective lectin Ulex europaeus I and the terminal N-acetylgalactosamine-selective lectin glycine max in the human olfactory bulb were studied. These lectins bound to primary olfactory axons in the olfactory nerve layer and the glomerular layer. They also bound to fibers located in the deeper layers such as the external plexiform layer and the granular layer. Furthermore they projected to the olfactory stalk but not in the cerebrum. The deeper projections of the lectin binding fibers may affect the function of the olfactory bulb in humans.

Aged↗
PubMed1993

Pathological findings at the site of conduction block in multifocal motor neuropathy.

We report on 2 patients with multifocal motor neuropathy with focal conduction block involving motor but not sensory fibers at the site of nerve swelling. A nerve biopsy specimen from adjacent to the enlargement in 1 patient showed a perivascular area containing scattered demyelinated axons surrounded by small onion bulbs. The observed pathological findings are consistent with the conduction block considered characteristic of this neuropathy, although the underlying immunological mechanisms for selectivity and persistence remain undetermined.

Action Potentials↗
PubMed1993

Altered spectrum of retrogradely transported axonal proteins in p-bromophenylacetylurea neuropathy.

The composition of retrogradely transported axonal proteins was examined by acrylamide gel electrophoresis and gel autoradiography in the experimental neuropathy induced in rats by p-bromophenylacetylurea (BPAU). Protein composition was normal during the early phase of retrograde transport but showed significant abnormalities during a later phase. The early phase consisted of proteins collected distal to a mid-thigh ligature of sciatic nerve between 15 and 24 hours after injection of [35S] methionine into lumbar ventral horn of the spinal cord. In terms of their relative labeling and electrophoretic mobility, these proteins were almost identical in experimental and control rats. Most of the labeled protein bands were also identical in the later phase, collected between 24 and 48 hours, but there were some consistent omissions and additions. Present in controls but missing in BPAU treated rats were three bands at 42, 41, and 25 KDa. In contrast, 4 bands (63, 56, 50, 26 KDa) were more prominent in the experimental rats than in controls. We suspect abnormal post-translational modification or proteolysis of rapidly transported proteins in the terminal or preterminal portion of the neurons exposed to BPAU. This abnormality, in addition to a previously reported premature processing of transported organelles, may underlie the development of peripheral neuropathy.

Animals↗
PubMed1993

Death of intermediolateral spinal cord neurons follows selective, complement-mediated destruction of peripheral preganglionic sympathetic terminals by acetylcholinesterase antibodies.

Systemically injected anti-acetylcholinesterase antibodies in rats cause selective lesions of preganglionic sympathetic neurons. Adult rats were examined up to four months after a single i.v. injection of murine monoclonal acetylcholinesterase antibodies or normal immunoglobulin G (1.5 mg). Within 4 h, antibody-treated rats developed ptosis, a sign of sympathetic dysfunction that was never reversed. Persistent pupillary constriction reflected preserved and unopposed parasympathetic function. Weight gain was depressed, but locomotor activity, excitability, and sensorimotor responses were normal, and gross neuromuscular performance was near normal. These findings were supported by biochemical evidence for selective sympathetic damage. Acetylcholinesterase activity was reduced for the whole period of observation in sympathetic ganglia and adrenal glands but fell only transiently in muscle and serum. At all times, choline acetyltransferase activity (a marker of presynaptic terminals) was unaffected in muscle but grossly depleted in ganglia. Light and electron microscopy showed that preganglionic sympathetic terminals of superior cervical ganglia were severely damaged while parasympathetic ganglia were less affected and motor endplates of skeletal muscle were apparently spared. Immunocytochemistry revealed punctate deposits of murine immunoglobulin G and complement component C3 in ganglionic neuropil 12 h after antibody injection. This finding was consistent with complement-mediated lysis of preganglionic terminals. Morphometric analysis of preganglionic neurons in the intermediolateral nucleus of the spinal cord showed progressive loss of cholinergic perikarya over several months. We conclude that antibody-induced destruction of ganglionic terminals leads to death of preganglionic sympathetic neurons and, hence, permanent dysautonomia.

Acetylcholinesterase↗
PubMed1993

Beta/A4 proteinlike immunoreactive granular structures in the brain of senescence-accelerated mouse.

The immunohistochemical localization of amyloid beta/A4 protein in the senescence-accelerated mouse brain was studied using six different antisera against human amyloid precursor protein peptides. beta/A4 proteinlike immunoreactivity was observed in the form of granular structures (beta-LIGS) in various regions, including the medial septum, cerebral cortex, hippocampus, cerebellum, and some cranial nerve roots. beta-LIGS were 1.5 to 2.5 mu in diameter and irregularly shaped. They increased significantly in number with aging, predominantly in animals with a phenotype of age-related deterioration of memory and learning abilities. Congo red and thioflavine S did not stain the granules. On immunoblots, the main immunoreactive bands were observed at 14 to 18 kd. The staining intensities of these bands also increased with advancing age. We consider that beta-LIGS are not only a new morphological manifestation of senescence in mice, but also a pertinent clue in understanding the mechanisms of amyloid deposition.

Aging↗
PubMed1992

[A case of type 1 diabetes mellitus with hypothalamic amenorrhea: successful pregnancy following subcutaneous pulsatile administration of LHRH].

A 27-year-old woman with type 1 diabetes mellitus was admitted to the Shimane Medical University Hospital because of secondary amenorrhea. She had been treated with insulin since July, 1986. Fasting plasma glucose and HbA1c levels were controlled within normal limits. However, body weight gradually decreased and amenorrhea started in 1988. Physical examination revealed emaciation with BMI of 17.3. Basal levels of plasma T3, somatomedin C, LH, FSH and estradiol levels were low, whereas HGH levels were slightly elevated. Plasma LH markedly increased in response to LHRH administration. She was diagnosed as having weight loss-related hypothalamic amenorrhea. Induction of ovulation was not obtained with clomiphene citrate. Treatment with subcutaneous pulsatile administration of LHRH (20 micrograms every 120 min) resulted in an increase in plasma levels of LH, FSH and estradiol, which was accompanied by ovulation and corpus luteum formation. Further treatment with pulsatile LHRH administration was followed by conception. Two gestational sacs were detected by ultrasonography. One of them was absorbed at the early stage of pregnancy. She was delivered of one healthy female infant without complications. These findings suggest that it is important not only to control plasma glucose levels but to keep the appropriate weight and support the psychological aspects of the subject in the treatment of diabetes mellitus. Subcutaneous pulsatile LHRH therapy may be effective for the induction of ovulation in clomiphene-resistant hypothalamic amenorrhea; however, it will be necessary to solve the problem of dosage and the interval of LHRH administration in the future.

Adult↗