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R Kaji

Publications and source records attributed to R Kaji.

At least 19 recordsLinked to original sources

Electronic band structure and Fermi surface of CaB6 studied by angle-resolved photoemission spectroscopy.

We report high-resolution angle-resolved photoemission spectroscopy (ARPES) on CaB6. The band structure determined by ARPES shows a 1 eV energy gap at the X point between the valence and the conduction bands. We found a small electron pocket at the X point, whose carrier number is estimated to be (4-5) x 10(19) cm(-3), in good agreement with the Hall resistivity measurement with the same crystal. The experimental results are discussed in comparison with band structure calculations and theoretical models for the high-temperature ferromagnetism.

Journal Article↗

Factors influencing the therapeutic effect of muscle afferent block for oromandibular dystonia and dyskinesia: implications for their distinct pathophysiology.

Oromandibular dystonia (OMD) is a focal dystonia manifested by involuntary masticatory and/or lingual muscle contractions. Muscle afferent block (MAB) by injecting anaesthetic and alcohol intramuscularly is recently used for the treatment of OMD. To study the factors affecting the efficacy of MAB, 44 patients with OMD were treated by local injection of lidocaine and ethanol. They were divided into four groups (spastic, rhythmic, dyskinetic, and task-specific) according to the pattern of incisal movement and involuntary contraction. We used a clinical scaling protocol in terms of four parameters (mastication, speech, pain, and discomfort) to evaluate the change of symptoms objectively. The relationship of improvement in clinical scores with various parameters was assessed statistically. The overall objective improvement was 60.2 +/- 29.5%. The scores decreased significantly (P<0.0001, paired t-test) after MAB. The maximal incisal velocity significantly correlated inversely with the clinical improvement, and MAB was particularly effective for spastic contraction. Dyskinetic and rhythmic groups showed variable and significantly less improvements than the spastic group. MAB is highly effective for OMD, but not for the patients with dyskinetic symptoms. The jaw movement pattern is an important factor for predicting the outcome. The difference in the response to MAB in OMD and oral and/or orofacial dyskinesia suggests the distinct pathophysiology between the two.

Adolescent↗

Abnormal cortical mechanisms of voluntary muscle relaxation in patients with writer's cramp: an fMRI study.

Although it is hypothesized that there is abnormal motor inhibition in patients with dystonia, the question remains as to whether the mechanism related to motor inhibition is specifically impaired. The objective of the present study was to clarify the possible abnormalities of the mechanisms underlying voluntary muscle relaxation during motor preparation and execution in patients with writer's cramp, using event-related functional MRI. Eight patients with writer's cramp and 12 age-matched control subjects participated in the study. Two motor tasks were employed as an experimental paradigm. In the relaxation task, subjects were asked to hold their right wrist in the horizontal plane by maintaining moderate contraction of wrist extensor muscles in the premotor phase; they relaxed those muscles voluntarily just once during each fMRI scanning session. In the contraction task, subjects extended the right wrist voluntarily from the same premotor state as for the relaxation task. Five axial images covering the primary sensorimotor cortex (SMC) and supplementary motor area (SMA) were obtained once every second. Activated volumes in the left SMC and the SMA were significantly reduced in patients for both muscle relaxation and contraction tasks. These data suggest that there is impaired activation in both SMC and SMA in voluntary muscle relaxation and contraction in patients with writer's cramp. This implies that abnormalities of both inhibitory and excitatory mechanisms in motor cortices might play a role in the pathophysiology of focal dystonia.

Adult↗

Acidic fibroblast growth factor (FGF-1) in the anterior horn cells of ALS and control cases.

The expression and localization of acidic fibroblast growth factor (aFGF; FGF-1) were examined in the spinal cord of patients with amyotrophic lateral sclerosis (ALS) and controls by reverse transcription-polymerase chain reaction (RT-PCR) method and immunohistochemistry. The RT-PCR experiments demonstrated that aFGF amplification products were clearly detected in all control cases but could be scarcely seen in ALS patients. aFGF immunoreactivity was detected in the anterior horn cells of the spinal cord. Double immunostaining for aFGF and choline acetyltransferase revealed that the majority (95.9%) of cholinergic neurons expressed aFGF. In ALS cases, the number and the staining intensity of aFGF-positive neurons were markedly decreased. These results suggest that aFGF is involved in ALS pathology.

Acetylcholine↗

Tumor necrosis factor gene polymorphisms in patients with sporadic Parkinson's disease.

We studied promoter region polymorphisms in the tumor necrosis factor (TNF) gene at position -1031, -863, and -857, in 172 Japanese patients with sporadic Parkinson's disease (PD). The frequency of the -1031C allele, a high producer of TNF, increased significantly in early onset PD patients compared with controls. In addition, PD patients with the -1031C allele showed a significantly earlier onset than those without -1031C allele, after stratification of the data by an interleukin-1beta gene polymorphism. Our findings suggest that TNF might have a toxic effect in PD.

Adult↗

Sensorimotor demyelinating neuropathy with IgM antibody against gangliosides GD1a, GT1b and GM3.

We report a patient with sensorimotor demyelinating neuropathy with high-titer IgM antibody against gangliosides GD1a, GT1b and GM3. The patient was a 65-year-old male who was hospitalized with chief complaints of muscular weakness of all limbs and numbness of the hands and feet. Nerve-conduction studies revealed reduced conduction velocities of the motor nerves with increased temporal dispersion and loss of sensory nerve action potentials. Treatment with steroids was ineffective. IgM antibody against GD1a, GT1b and GM3, which are known to be the ligands for myelin-associated glycoprotein (MAG), might have played a role in the demyelination in this patient by inhibiting adhesion between myelin and axonal membrane.

Aged↗

Influence of interleukin-1beta gene polymorphism on age-at-onset of spinocerebellar ataxia 6 (SCA6) in Japanese patients.

An inverse correlation is observed between the expanded CAG repeat number and age-at-onset of spinocerebellar ataxia 6 (SCA6). To detect another modifying genetic factor for SCA6, we studied polymorphisms in the genes for interleukin (IL)-1beta and tumor necrosis factor in 122 Japanese patients with SCA6. No contribution of these polymorphisms to the variance in disease onset was observed by regression analysis or by ANOVA. The IL-1beta promoter polymorphism, however, significantly affected the age-at-onset, when adjusted for the CAG repeat number as a covariate (P=0.0004, by ANCOVA), suggesting that IL-1beta may be a genetic factor other than the SCA6 gene that modifies the age-at-onset of the disease.

Age of Onset↗

DYT1 mutation in Japanese patients with primary torsion dystonia.

A GAG deletion at position 946 in the DYT1 gene has been identified as one of the gene mutations responsible for autosomal dominant primary torsion dystonia. We examined 178 Japanese patients with various forms of dystonia, and found the mutation in six patients (3.4%) from three families. Five of them had early clinical onset (before age 12) with initial involvement of a limb. To our knowledge, this is the first report of the frequency and the clinical features of DYT1 mutation in oriental patients, and the clinical presentation of the mutation in these patients was similar to that of Jewish or non-Jewish Caucasian patients.

Adult↗

Up-regulation of cyclooxygenase-2 in inflammatory demyelinating neuropathy.

To clarify the role of prostaglandins in peripheral nerve demyelination, we examined the expression of cyclooxygenase-2 (COX-2) using selected nerve specimens from patients with chronic inflammatory demyelinating polyneuropathy. COX-2 protein was up-regulated in macrophages causing active demyelination. In situ hybridization revealed that COX-2 mRNA signals were strongly expressed on macrophages adhering to the demyelinating nerve fibers at the endoneurium. This observation may provide a rationale for application of neuroprotective strategies employing COX-2 inhibitors in inflammatory demyelinating neuropathies.

Adolescent↗

Abnormal axonal inward rectifier in streptozocin-induced experimental diabetic neuropathy.

In order to explore the pathophysiology of diabetic neuropathy, we studied serial changes of axonal excitability in 20 adult Wistar rats with streptozocin-induced diabetes using the technique of threshold electrotonus (TE). After persistent hyperglycaemia had developed, rats were divided into two groups: nine were fed a diet containing aldose reductase inhibitor (Epalrestat 30 mg/kg/day) (ARI(+) group) and 11 were fed a diet without the inhibitor (ARI(-) group). Eight normal control rats of similar age (NC group) were also studied. We monitored membrane properties of motor axons in the tail for 3 months using TE to measure the changes in excitability induced by subthreshold polarizing currents while recording compound muscle action potentials (CMAPs) in the tail muscle. The ARI(-) group showed a significant increase in CMAP latency 1 month after streptozocin injection, and by 3 months there was significantly lower excitability after hyperpolarization for 100 ms compared with the NC group. A similar change in TE was reproduced by injection of caesium chloride, an inhibitor of inward rectification. By contrast, the ARI(+) group exhibited no significant change in TE or latency at 3 months, although they showed significant body weight loss and hyperglycaemia. These findings indicate that inward rectification is reduced in an experimental model, as in human diabetes, and that blocking the polyol pathway with an ARI prevents this reduction. Reduced inward rectification potentiates conduction block caused by activity-dependent hyperpolarization and may underlie the decreased vibratory sensation seen in the early stage of diabetic neuropathy.

Action Potentials↗

[Botulism].

Explore the source record for details and available documents.

Acetylcholine↗

Basal ganglia as a sensory gating devise for motor control.

Basal ganglia lie between the cerebral cortex and the thalamus, and have dense fiber connections between them. These connections form 4-5 distinct loops or circuits to allow parallel processing of information. Among them, the most intensively studied is the motor loop, which comprises 2 distinct direct and indirect pathways. The direct pathway disinhibits the powerful inhibition of the internal segment of the globus pallidus/substantia nigra pars reticulata upon thalamic ventrolateral nuclei with a net result of facilitatory influence upon the motor cortex. By contrast, the indirect pathway exerts an inhibitory effect. Overall this dual system provides a center (excitatory)-surround (inhibitory) mechanism to focus its effect on selected cortical neurons. Although putative transmitters, inhibitory or excitatory nature of these projections and their receptors are mostly known, the functional role of the loop in motor control is not precisely understood. Several lines of evidence have recently been presented to support the view that this center-surround mechanism is used to focus the output to a specific group of muscles required for performing a specific task. This operation is made possible through opening the sensory channel for the expected sensory feed-back afferents during movement. Thus one of the important functions of basal ganglia seems to be the gating of sensory input for motor control.

Animals↗

[Sensory-motor disintegration in the basal ganglia disorders].

Basal ganglia lie between the cerebral cortex and the thalamus, and have dense fiber connections between them. These connections form 4-5 distinct loops to allow parallel processing of information. Among them, the most intensively studied is the motor loop, which comprises 2 distinct direct and indirect pathways. The direct pathway disinhibits the powerful inhibition of Gpi/SNr upon the thalamic VL nuclei with a net result of facilitatory influence upon the motor cortex. By contrast, the indirect pathway exerts an inhibitory effect. Overall this dual system provides a center-surround mechanism to focus its effect on selected cortical neurons. The functional role of the loop in motor control has not been precisely understood. Several lines of evidence have recently been presented to support the view that this mechanism is used to focus the output to a specific group of muscles required for performing a specific task. Recent observations in dystonia and Parkinsonism suggest that this operation is made possible through opening the sensory channel for the expected sensory feed-back afferents during movement. Thus one of the important functions of basal ganglia seems to be the gating of sensory input for motor control.

Basal Ganglia↗

High-frequency SEP components generated in the somatosensory cortex of the monkey.

To investigate the origin of high-frequency somatosensory evoked potential (SEP) components, we recorded median nerve SEPs from the scalp and the depth in six monkeys. Laminar field potentials were analyzed in area 3b (N10; corresponding to human N20) and area 1 (P12; corresponding to human P25). After digital filtering (300-900 Hz), 4-6 components were identified, and the 1st to 4th peaks in area 3b (7-11 ms in latency) and the 3rd to 5th in area 1 (9-13 ms) showed clear polarity reversals between the surface and the depth of the cortex. These results provide direct evidence for intracortical origin of early high-frequency components in area 3b and of late ones in area 1.

Action Potentials↗