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Biomedical subjects

I Kanazawa

Publications and source records attributed to I Kanazawa.

At least 19 recordsLinked to original sources
PubMed1992

Dopaminergic stimulation up-regulates the in vivo expression of brain-derived neurotrophic factor (BDNF) in the striatum.

We investigated the effect of dopamine on the in vivo expression of brain-derived neurotrophic factor (BDNF) in the striatum of mouse. BDNF mRNA expression in the striatum, which was quantified with the reverse transcriptase polymerase chain reaction, was up-regulated from 2 h after oral administration of levodopa, a precursor of dopamine. The increase was sustained for 16 h. Co-administration of haloperidol partially inhibited dopamine-induced BDNF enhancement. These data suggest that dopaminergic stimulation directly promotes the expression of BDNF in the striatum in vivo.

Amino Acid Sequence↗
PubMed1992

Serum IgG antibody to ganglioside GQ1b is a possible marker of Miller Fisher syndrome.

We studied serum anti-glycolipid antibodies by enzyme-linked immunosorbent assay and thin-layer chromatography-enzyme immunoassay in six consecutive patients with typical Miller Fisher syndrome. In all six, increased activity of IgG antibody against ganglioside GQ1b was present in the early phase and reduced with time, whereas such activity was not detected in normal control subjects and disease control subjects including those with Guillain-Barré syndrome. Anti-GQ1b IgG antibody is a new possible diagnostic marker of Miller Fisher syndrome and could well be related to the disease process itself.

Adult↗
PubMed1992

Argentophilic intracytoplasmic inclusions in multiple system atrophy.

Argentophilic intracytoplasmic glial inclusions were recently reported in olivo-ponto-cerebellar atrophy (OPCA). We examined the brains of 3 cases of OPCA [2 with striato-nigral degeneration (SND) and 1 without SND], 1 case of pure autonomic failure (PAF) without pathology of OPCA or SND, as well as 36 controls including 2 cases of Holmes' type cerebellar cortical atrophy and 2 cases of Joseph's disease. Although the inclusions were tubulin-positive, the immunoreactivity was different from that of the dendrites. Electron microscopically, the microtubular structures composing the inclusion were fuzzy with granular material. These findings may indicate that the microtubules composing the inclusions are modified. Inclusion-bearing cells appeared to be oligodendrocytes while many of them had larger and lighter nuclei than those of normal-looking oligodendrocytes without the inclusions. The inclusions were widely distributed in a characteristic fashion beyond the typical lesions of OPCA, SND and PAF. The distribution pattern was essentially the same in the case of PAF and 3 cases of OPCA irrespective of the presence or absence of OPCA or SND lesions. In contrast, argentophilic inclusions were not observed in other types of spinocerebellar degeneration, in Holmes' type cerebellar cortical atrophy or in Joseph's disease. It is suggested, in line with other studies, that the inclusion may be specific to OPCA and related disorders which include PAF and a useful marker to distinguish OPCA from other neurodegenerative diseases.

Adult↗
PubMed1992

Rapid axonal transport velocity is reduced in experimental ethylene oxide neuropathy.

Chronic exposure of rats to ethylene oxide (EO) causes distal axonal neuropathy of lumbosacral primary sensory neurons. To study the pathogenesis of this neuropathy, we measured rapid axonal transport in peripheral nerves. Rats were exposed for 6 h to 500 ppm EO in a chamber three times a wk for 15 wk. Rapid axonal transport and quantitative histological alterations of peripheral nerves were studied. After [35S]methionine injection into the dorsal root ganglion, the velocity of rapid anterograde axonal transport of radioisotope-labeled protein was measured. The velocity in the rats exposed to EO was 33% less than that in control rats exposed to filtered room air. However, histological differences were slight. Morphometric studies showed that in EO-exposed rats, only the distal portions of the sural nerve had significantly greater incidental degeneration of myelinated fibers than did controls. There were significantly fewer large myelinated fibers only in the distals peroneal nerve. Therefore, a decrease in the velocity of anterograde axonal transport, related to these slight histological abnormalities of the peripheral nerve, may play a causative role in the development of the distal axonal neuropathy owing to chronic EO exposure.

Animals↗
PubMed1992

Cerebrospinal fluid endothelin-1 in Alzheimer's disease and senile dementia of Alzheimer type.

We have measured the endothelin-1 concentrations in the cerebrospinal fluid samples from 5 patients with Alzheimer's disease (AD), 6 patients with senile dementia of Alzheimer type (SDAT) and 7 patients with other diseases without dementia (disease control: DC). The cerebrospinal fluid endothelin-1 level was significantly lower in AD than in DC. No correlation was observed between cerebrospinal fluid endothelin-1 concentration and any other factors such as age, duration from onset, systolic blood pressure, cerebrospinal fluid protein level or plasma endothelin-1 concentration in AD or SDAT. These results suggest a possible alteration of the endothelin-1 system in the central nervous system in Alzheimer's disease.

Age Factors↗
PubMed1992

Developmental changes of fucosylated glycoconjugates in rabbit dorsal root ganglia.

Developmental changes of the fucosylated glycoconjugates in the dorsal root ganglia (DRG) of the rabbit were investigated histochemically using anti-fucosyl GM1 antibody and Ulex europaeus agglutinin 1 (UEA-1) lectin. Neither anti-fucosyl GM1 antibody nor UEA-1 lectin bound to the neural tubes or to the neural crest on embryonic day 14 (E14). Anti-fucosyl GM1 antibody binds diffusely to the DRG of E25. Large neurons unreactive with anti-fucosyl GM1 antibody appeared at 1 month and increased within 6 months after birth. Schwann cells immunoreactive with anti-fucosyl GM1 antibody came to be limited to the satellite cells surrounding the positive neurons. No staining with UEA-1 lectin was observed in the DRG of E25. Some small neurons became reactive with UEA-1 lectin within 1 month and remained to be so at 6 months after birth. Schwann cells including satellite cells were unreactive with this lectin. Since fucosyl GM1 was detected in the lipid fraction of DRGs from 1-month-old and 6-month-old rabbits, fucosyl GM1 itself should be the antigen molecule recognized by the anti-fucosyl GM1 antibody. Further study is necessary to elucidate the association between these developmental changes of the fucosylated glycoconjugates in DRG and their possible functional roles.

Animals↗
PubMed1992

Fast and slow depolarizations produced by substance P and other tachykinins in sympathetic neurons of rat prevertebral ganglia.

Using intracellular recording, we examined the effects of three mammalian tachykinins, substance P (SP), neurokinin A (NKA), and neurokinin B (NKB), on sympathetic neurons of isolated rat coeliac-superior mesenteric ganglia (C-SMG). The 3 tachykinins elicited two distinct depolarizing responses in ganglion cells: fast depolarization with time-to-peak of 1-2 sec and duration of 5-10 sec, and slow depolarization with time-to-peak of about 20 sec and duration of 120-140 sec. Both fast and slow responses persisted in a solution containing low Ca2+ and high Mg2+ or tetrodotoxin, which indicates that the tachykinins directly act on ganglion cells to produce fast and slow depolarizations. The two types of tachykinin-induced responses exhibited clearly distinguishable properties. The membrane conductance was increased during the fast response, but not significantly changed, slightly decreased or sometimes increased during the slow response. Within certain range of membrane potential, the amplitude of fast response increased upon membrane hyperpolarization and decreased upon depolarization of ganglion cells. In contrast, the amplitude of slow response associated with membrane conductance decrease was increased with membrane depolarization and decreased with hyperpolarization. The fast response was markedly suppressed in a Na(+)-deficient solution, a solution containing nominally zero Ca2+ (plus 0.1 mM EGTA in some cases), and in a solution containing Cd2+ or Mn2+, whereas the slow response was not affected in these solutions and was augmented in some cells in K(+)-free solution. Thus it seems that the increase in Ca(2+)-dependent cationic conductance underlies the fast response and that the slow response is produced at least in part by suppression of certain K+ channels. The fast response progressively decreased in amplitude upon repeated application of the peptides with short intervals, whereas the slow response was rather augmented by repeated application. Lowering the temperature markedly depressed the slow response, while the fast response remained almost unaffected. It is therefore likely that the fast and slow depolarizations are mediated by two different subtypes of tachykinin receptors or a single class of receptors linked with two different intracellular mechanisms. Measurement of tachykinins in several sympathetic ganglia by combined use of HPLC and radioimmunoassay revealed that the highest amount of SP occurs in the C-SMG where the content of SP (136.0 pmol/g protein) was higher than those of NKA (44.3) and NKB (18.7). SP thus appears to function as a major tachykinin in rat C-SMG.

Animals↗
PubMed1992

On chorea: possible neuronal mechanisms.

The mechanism of generation of choreic movements is a rather difficult issue to be elucidated, chiefly due to the lack of a good animal model. Recently we have succeeded to reproduce choreic movements in monkey by using kainic acid lesion of the striatum and the administration of L-dopa. Based on the morphological and biochemical findings of monkey brains, we proposed the hypothesis for the mechanism of choreic movements to be the presynaptic "activation" of the nigro-striatal dopaminergic pathways rather than the postsynaptic dopaminergic receptors in the striatum. This hypothesis coincide well with the clinical and clinico-pharmacological experience in Huntington's disease. The possible mechanisms of the dopaminergic "activation" are discussed.

Animals↗
PubMed1992

Stimulation of corticospinal pathways at the level of the pyramidal decussation in neurological disorders.

A newly developed technique of brainstem stimulation was applied in 14 normal subjects and 23 patients with various neurological disorders. The electromyographic (EMG) responses of limb muscles following cortical, brainstem and cervical stimulation were recorded. The cortical-brainstem conduction time and brainstem-cervical conduction time were then calculated from the difference in latency between the two sites of stimulation. From the regression lines of the relationship between the normal conduction times in the first dorsal interosseous muscle and the length of the descending tracts, the site of activation by brainstem stimulation was estimated to lie near the cervical-medullary junction. The most distal lesion causing prolongation of cortical-brainstem conduction time was a small cerebral infarction in the lower pons. Herniation of the third cervical spinal disc was the most rostral lesion resulting in delayed brainstem-cervical conduction time and normal cortical-brainstem conduction time. These observations suggest that activation occurs at the level of the cervical-medullary junction where the pyramidal decussation lies. The conduction velocities of the activated tracts estimated from the regression lines for normal individuals were 57-92 m/s. In patients with supratentorial lesions, the threshold for brainstem stimulation was abnormally high. The abnormal findings in this test were correlated significantly with the clinical pyramidal signs. This suggests that the EMG responses elicited by brainstem stimulation are mediated mainly by the corticospinal tract. We conclude that the brainstem stimulation technique would be clinically useful for localization of lesions in the corticospinal tract; the primary lesion can be localized whether above or below the pyramidal decussation.

Adult↗
PubMed1992

Kanji word reading process analysed by positron emission tomography.

Positron emission tomography, involving the H2(15)O injection technique, was used to study changes in regional cerebral blood flow during Japanese kanji word reading. Three-times intrasubject averaging analysis revealed that the main cortical responses occurred in the bilateral (left-side dominant) posterior inferior temporal area for visual input. We believe the left posterior inferior temporal area processes highly complex morphological features of kanji. For language output, left-side dominant activation of the posterior inferior frontal gyrus and the basal ganglia was found.

Adult↗
PubMed1992

Nation-wide collaborative study on the long-term effects of bromocriptine in the treatment of parkinsonian patients. Final report.

Final results of the 5-year multicentric collaborative study on the long-term effects of bromocriptine in the patients with Parkinson's disease are reported. This prospective study started in May 1985 in order to see whether the early combination therapy with bromocriptine and levodopa is really superior to the levodopa monotherapy with regard to the late side effects of levodopa in the treatment of parkinsonian patients. Another project of the study was to see the therapeutic efficacy of bromocriptine monotherapy without concomitant use of levodopa. For these purposes, a total of 702 patients with Parkinson's disease were enrolled into three groups: Group 1 (n = 286) with bromocriptine monotherapy, Group 2A (n = 216) with early combination of bromocriptine and levodopa, and Group 2B (n = 200) with levodopa alone. At the end of the 5-year study, 48 patients in Group 1 (16.8%) were still continuing bromocriptine monotherapy with satisfactorily good therapeutic effects. About half (49.1%) of the Group 2A patients remained on the combined therapy, and the comparable number of the Group 2B patients (46.0%) were also kept on the initial mode of therapy, while 13.5% of the latter group with levodopa monotherapy needed bromocriptine to be added in order to assure the good therapeutic effects. Moreover, significant differences were seen between group 2A and Group 2B with regard to the incidence of wearing-off phenomenon and dyskinesias. Disappearance rate of dyskinesias which were present at the time of enrollment was significantly higher in Group 2A than in Group 2B. No significant difference was noted as to the incidence of untoward symptoms and the death rate among all three therapeutic groups. These results support the view that the early combination of bromocriptine with levodopa is superior to levodopa alone in the treatment of Parkinson's disease.

Activities of Daily Living↗
PubMed1992

Nation-wide collaborative study on the long-term effects of bromocriptine in the treatment of parkinsonian patients: analysis on the maintenance and the change of the original mode of treatment.

A nation-wide collaborative study to evaluate the long-term effects of bromocriptine in patients with Parkinson's disease was completed as described in the accompanying paper. The present study analysed the same data by paying attention to a group of patients who maintained the original mode of therapy and to a group of patients who changed the mode of treatment by adding levodopa or bromocriptine to the original drug. Surprisingly, 48 among 286 patients in a group of bromocriptine monotherapy maintained the original mode of therapy. This group has particular features of a short duration of illness and a low grade of Hoehn-Yahr's scale. It is noteworthy that this group of patients did not show wearing-off phenomenon. The effects of additional bromocriptine to levodopa for a 5-year period were analysed by comparing two groups of combination therapy and levodopa alone therapy maintained for 5 years, with 106 and 92 patients, respectively. Results were essentially the same as those obtained from the accompanying paper, i.e., in general, treatment by combination with bromocriptine may be more suitable than treatment by levodopa alone. In order to find the best timing of the combination of levodopa and bromocriptine, results of 3 groups were compared, i.e. a group of patients who started with bromocriptine alone and later added with levodopa (82 patients), a group of patients who maintained the combination for 5 years (106 patients) and a group of patients who started with levodopa alone and later added bromocriptine (27 patients). The best results were obtained in the group of 5-year combination.(ABSTRACT TRUNCATED AT 250 WORDS)

Activities of Daily Living↗
PubMed1992

Accumulation of amyloid precursor protein and beta-protein immunoreactivities in axons injured by cerebral infarct.

To determine the distribution of amyloid precursor protein (APP), monoclonal antibodies against APP45-62 (APP1-28-9) and beta1-17 (4A18 and 4A61) were produced. In the sections of Alzheimer's disease (AD) brain, APP1-28-9 was reactive with neurites around senile plaques and a few neurons but not with amyloid cores. This antibody also immunostained the axons in the ischemic lesions of brain tissues from cases with cerebral infarct. 4A18 and 4A61 were reactive with amyloid plaques but not with neurites and neurons. The latter two antibodies also immunostained axons in ischemic lesions. These findings suggest that APP, transported by the fast axonal flows, accumulated in the injured axons in the central nervous system. The beta immunoreactivity appearing in those axons may provide a clue to the mechanism of amyloidogenesis.

Alzheimer Disease↗
PubMed1992

Lidocaine unmasks silent demyelinative lesions in multiple sclerosis.

Blockage of a small number of sodium channels may prevent impulse conduction in some demyelinated segments of nerve fibers with low safety factors, thereby unmasking subclinical demyelinative lesions. On the basis of this hypothesis, lidocaine, a sodium channel blocker, was administered intravenously to 28 MS patients and to 19 normal subjects and seven patients with nondemyelinating diseases. As predicted, lidocaine (mean plasma level, 2.7 micrograms/ml) elicited reversible subclinical symptoms in 23 of the MS patients, but it had not effect on the control subjects. We made a quantitative study of the visual functions (visual acuity, color vision, visual evoked potential [VEP]) that were impaired in 15 MS patients. Of the 23 affected eyes, nine showed normal VEPs, indicative of the test's sensitivity to focal lesions. This test should be useful in the diagnosis of MS and in the evaluation of the subclinical activity of MS as well.

Adult↗
PubMed1992

[A case of acid maltase deficiency (juvenile type)--immunohistochemical and biochemical study].

A 22-year-old housewife was referred to us for review of progressive proximal muscle weakness which started at 15 years of age. A biopsy of left rectus femoris muscle showed acid phosphatase positive vacuoles partly filled with PAS-positive material. Acid maltase activity of the cultured fibroblasts was pathologically low at 0.4 nmol/mg protein considering 161.0 +/- 32.4 nmol/mg protein as a normal range. A diagnosis was made of acid maltase deficiency (juvenile type). Western blot using anti-acid maltase polyclonal antibody revealed 115 and 70 kDa bands in control muscles, where as only the 115 kDa band, a presumable precursor of the enzyme, was visualized in the patient. By immunohistochemistry using the same antibody the epitope was localized to the acid phosphatase positive vacuoles and immunoelectron microscopy demonstrated the acid maltase immunoreactivity within lysosomes. We concluded that the protein precursor unable to proceed into mature enzyme can access to lysosomes from endoplasmic reticulum through Golgi complex in the present case.

Adult↗
PubMed1992

[Carcinomatous autonomic neuropathy and the autoantibodies in paraneoplastic neuropathy].

Carcinomatous autonomic neuropathy is a syndrome of autonomic dysfunction associated with malignant neoplasm. It is most often associated with small-cell lung cancer. Auto-immune mechanism is suspected to underlie this syndrome. Among the symptoms of autonomic dysfunction, intestinal pseudo-obstruction is most frequently seen. The autonomic dysfunction often precedes the discovery of the cancer. Several autoantibodies have been reported in paraneoplastic neuropathies. Anti-Hu antibody, which was originally reported in paraneoplastic sensory neuronopathy, has also been detected in some cases with autonomic failure. Anticarbohydrate antibody activity has been frequently shown in IgM M-proteins associated with peripheral neuropathies. These include anti-MAG, Po, and sulphated glucuronyl glycolipids in demyelinating neuropathy and anti-GM1 in motor dominant neuropathy or motor neuron disease. Further investigation should reveal more glycoconjugate antigens as targets of possible auto-immune attack in paraneoplastic neuropathies.

Autoimmune Diseases↗
PubMed1992

[Familial amyloidotic polyneuropathy type IV (Finnish type)--the first description of a large kindred in Japan].

Familial amyloidotic polyneuropathy type IV, one of the hereditary systemic amyloidoses with an autosomal dominant trait, is clinically characterized by cranial neuropathy and corneal lattice dystrophy. Recent biochemical studies have indicated that the amyloid fibril protein in FAP IV is related to gelsolin, an actin-modulating protein. Cases were clustered in the Finnish population and only a few cases have been reported from other populations. Here we described a large kindred with FAP IV as the first report in Japan. This family comprises 42 members in three generations with 14 affected individuals. We examined 7 patients at the age ranging from 43 to 80 years. All cases have corneal lattice dystrophy type II. The disease begins with slowly progressive facial weakness in the fifth or sixth decade of life and consequently the V, XII, IX and X cranial nerves become involved. Peripheral neuropathy of the extremities remained mild until late of life. Microscopy of skin biopsy samples showed deposits of amyloid around the eccrine glands, sebaceous glands, epidermal-dermal junction and blood vessel walls. Immunohistochemistry of the skin revealed the immunopositive material against a monoclonal antibody to gelsolin in the amyloid deposits. Molecular analysis of the gelsolin gene is now in progress.

Adult↗