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T Shohmori

Publications and source records attributed to T Shohmori.

At least 19 recordsLinked to original sources
PubMed2001

Fractal dimension analysis of static stabilometry in Parkinson's disease and spinocerebellar ataxia.

The static stabilometry patterns associated with Parkinson's disease (PD, n = 15) and spinocerebellar ataxia (SCA, n = 15) were compared with those of normal control (n = 15) by measuring the fractal dimensions. Fractal dimensions were estimated using the modified pixel dilation (mPD) method. The fractal dimensions with closed eyes showed a significant correlation with Environmental area for SCA group (p < 0.05). The fractal dimension for SCA group was significantly higher with closed eyes than that with open eyes (p < 0.05). The fractal dimension with closed eyes was significantly higher in PD and SCA groups than that in normal group (p < 0.05). The fractal dimension with closed eyes was higher when the clinical stage was more severe with PD and SCA group while Environmental and Longitude/Environmental areas were not. These findings suggest that the fractal dimension is more sensitive than traditional stabilometric analysis in an evaluation of postural instability in PD and SCA.

Aged↗
PubMed1999

Motor neglect following left thalamic hemorrhage: a case report.

We present a report on a patient who developed unilateral motor neglect of the right hemibody after a left thalamic hemorrhage. He presented with pure motor neglect without aphasia, ideomotor apraxia, or unilateral spatial neglect due to a lesion in the centromedian parafascicular (CMPF) and ventrolateral (VL) nuclei of the left thalamus. Although unilateral motor neglect is usually associated with right hemispheric lesions, a left thalamic lesion may also result in isolated motor neglect.

Adult↗
PubMed1999

Circadian rhythm sleep disorder associated with pontine lesion.

A 55-year-old man presented with excessive daytime sleepiness and a circadian rhythm sleep disorder. Magnetic resonance imaging of the brain revealed a pontine lesion distinguishable from major cerebrovascular disease, demyelination and neoplasm. Benzodiazepines, antidepressants, methylcobalamine and thyroxine failed to synchronize the circadian rhythm. Antiepileptic drugs aggravated the condition, while melatonin and protireline partially relieved the patient from poorly controlled sleep disorder. A pontine lesion appeared to be related to the circadian rhythm sleep disorder of the patient.

Circadian Rhythm↗
PubMed1999

Enhanced Fos expression in rat lumbar spinal cord cultured with cerebrospinal fluid from patients with amyotrophic lateral sclerosis.

The etiology of amyotrophic lateral sclerosis (ALS) remains unknown although an existence of neurotoxic substances in cerebrospinal fluid (CSF) from ALS patients have been postulated. In order to investigate a possible effect of CSF from ALS patients on cellular signaling in spinal neurons, we compared Fos-like immunoreactivity (Fos-LI) in organotypic cultures of rat lumbar spinal cord after addition of CSF from ALS patients or another neurologic disease. Fos-LI was normally present predominantly in dorsal horn neurons, whereas only a few ventral horn neurons were positive for Fos-LI. The number of Fos-LI positive neurons significantly increased in dorsal horn with addition of CSF from ALS patients as well as glutamate at 100 microM. However, the increase was not observed with addition of CSF from other neurologic diseases. The increase in Fos-LI positive neurons in dorsal horn was reversed by a further supplement of MK801, an N-methyl-D-aspartate (NMDA) receptor antagonist, but not of CNQX, an alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA)/kainate antagonist. These results indicate that there may be substances in CSF from ALS patients that stimulate Fos expression in certain populations of spinal neurons via the NMDA receptors.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1998

Genomic structure and sequence of a human homologue (NTHL1/NTH1) of Escherichia coli endonuclease III with those of the adjacent parts of TSC2 and SLC9A3R2 genes.

Genomic cloning and sequencing of a human homologue (the gene name, endonuclease III-like 1; gene symbol, NTHL1 or NTH1) for Escherichia coli endonuclease III, that is involved in pyrimidine base excision repair, were performed. The sequence covered the entire NTHL1 gene consisting of six exons and five introns spanning 8kb with 5' flanking (8kb) and 3' flanking (3.8kb) regions. Southern blot analysis suggested that the NTHL1 gene exists as a single copy in a haploid genome. The sequenced 5' flanking region lacks typical TATA and CAAT boxes, but contains a CpG island having putative binding sites for several transcription factors such as Ets1 and Sp1. The NTHL1 gene lies immediately adjacent to the tuberous sclerosis 2 (TSC2) gene on chromosome 16p13.3 in a 5'-to-5' orientation. Transcription initiation sites of both NTHL1 and TSC2 genes were suggested to be multiple by 5' RACE experiments. The northern hybridization experiment suggested that both genes are expressed in all tissues, but at different levels. Downstream of the NTHL1 gene, the gene for the regulatory factor 2 (SLC9A3R2/E3KARP; also called OCTS2, TKA-1 and SIP-1) of the solute carrier family 9 (sodium/hydrogen exchanger), isoform A3, lies in a 3'-to-3' orientation. This paper demonstrates for the first time the spatial relationship of these three genes (TSC2, NTHL1 and SLC9A3R2) at the nucleotide level, and the presence of multiple transcription initiation sites of the NTHL1 and TSC2 genes.

Base Sequence↗
PubMed1998

L-DOPA does not facilitate nitric oxide production in the rat striatum and substantia nigra: in vivo microdialysis study.

Using in vivo microdialysis and flow-injection, we evaluated the production of nitric oxide (NO) in the striatum and substantia nigra of freely moving rats in response to challenge doses of L-dihydroxyphenylalanine (L-DOPA) by measuring the NO metabolite levels of nitrate and nitrite. The dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) concentrations also were determined in the same perfusates. Intraperitoneal injection of L-DOPA produced a significant, dose-dependent increase in the extracellular levels of dopamine and DOPAC in these areas, but did not modify the extracellular levels of the NO metabolites. An acute dose of L-DOPA does not appear to facilitate NO production in the rat striatum and substantia nigra.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1998

Kainic acid may enhance hippocampal NO generation of awake rats in a seizure stage-related fashion.

Temporal changes in kainate-induced seizure activity and hippocampal NO generation were evaluated simultaneously in conscious rats by using in vivo microdialysis and by determining the concentrations of nitrite and nitrate in perfusates. Intraperitoneal injection of kainic acid produced 'wet dog shake', focal seizure of the limbs and neck, hypersalivation, or generalized convulsion. These behavioral changes peaked at 120 min after the drug challenge and lasted for about 100 min. In contrast, the concentrations of NO metabolites, nitrite and nitrate, in the hippocampal perfusates increased rapidly and reached a plateau level at 40 min after the injection, and the level remained high for over 220 min. The increase was more marked in animals presenting severe seizures than those presenting mild ones. Pre-treatment with 25 mg/kg N(G)-nitro-L-arginine methyl ester promoted the severity of kainate-induced seizures, but it suppressed the increase in NO metabolites. These results suggest that kainic acid enhances hippocampal NO generation in a severity-related manner of the induced seizures. The enhanced NO generation upon kainate challenge appears mainly to be involved in seizure suppression.

Animals↗
PubMed1998

Reversible pitch perception deficit due to carbamazepine.

Carbamazepine (CBZ) is a drug frequently used to treat variety of neurological diseases or symptoms. Among its adverse effects, auditory disturbance is described rarely. In the present report, we describe an 18-year-old girl who noted false lowering of perceived pitch after starting CBZ treatment for epilepsy, and review the literature reporting CBZ-associated abnormal pitch perception.

Adolescent↗
PubMed1998

Hyperintense basal ganglia on T1-weighted MR images in a patient with central nervous system lupus and chorea.

We describe a patient with central nervous system lupus and choreatic movements in whom both basal ganglia showed high signal intensity on T1-weighted MR images, while the signal on T2-weighted images remained low. Within 8 months after onset, the choreatic movements had disappeared, with a corresponding decrease in the hyperintense T1 signal. The emergence of the choreatic movement disorder in this patient might have been related to the T1 hyperintensity of the basal ganglia, which, in turn, might have resulted from a vascular insult associated with central nervous system lupus.

Adult↗
PubMed1998

Presumed venous infarction in spinal decompression sickness.

We describe the serial MR imaging findings in a patient with spinal decompression sickness. In the acute phase, the spinal cord was swollen, with increased T2 signal in the posterior part of the column; 1 month later, marked contrast enhancement was noted in the same location; and 2 months later, the swelling and T2 signal had decreased. MR imaging may facilitate the early diagnosis of spinal decompression sickness.

Decompression Sickness↗
PubMed1997

AMPA receptors modulate dopamine release in the striatum, as measured by brain microdialysis.

The effect of 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(f) quinoxaline (NBQX), a potent and selective antagonist of alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) receptors, on the release of dopamine from the striatum was investigated in freely moving rats using an in vivo microdialysis technique. Perfusion with 1.0 mM AMPA increased the concentration of striatal extracellular dopamine. After systemic administration of NBQX (40 mg/kg, i.p.), dopamine levels in the striatal perfusate decreased. The AMPA-induced increase in dopamine levels was suppressed significantly by the systemic administration of NBQX (40 mg/kg, i.p.). Perfusion with tetrodotoxin (TTX, 5 microM) alone reduced the basal level of dopamine by 80%. Perfusion with 1.0 mM AMPA together with TTX produced a 3.9-fold increase in dopamine efflux from the TTX reduced basal level. However, the maximum dopamine level obtained thereby was close to the basal level of dopamine seen prior to perfusion with TTX. The present results demonstrate that AMPA receptors participate in tonic facilitative modulation of striatal extracellular level of dopamine. In addition, the results support the view that glutamatergic neurons modulate the release of dopamine via subtypes of excitatory amino acid receptors in the central nervous system.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1997

Noninsulin-dependent diabetes mellitus-related encephalopathy presenting with amnesia, personality change, and autonomic seizure.

We describe a patient with noninsulin-dependent diabetes mellitus presenting with an amnestic disorder, personality change, and autonomic seizure. Magnetic resonance images of the brain showed T2-high signal lesion in the hippocampi bilaterally and nonspecific white matter disease, while single photon emission computed tomography revealed a diffuse reduction of cerebral blood flow. Sensory and auditory evoked potentials revealed delayed impulse conduction velocities in the central nervous system. Degenerative changes caused by a microvascular angiopathy related to noninsulin-dependent diabetes mellitus may underlie the central nervous system manifestations in our patient.

Action Potentials↗
PubMed1997

[A man with systemic lupus erythematosus presenting with spastic paraplegia].

We report a 38-year-old man systemic lupus erythematosus who presented with an acute onset of paraplegia and urinary retention. The man had a 12-year history of nodular cutaneous mucinosis and arthralgia. In 1994, he was admitted to our hospital with a sudden onset of weakness and numbness of the right leg followed by an emergence of similar symptoms in the left leg. His elder sister had died at 16 years of age after suffering from systemic lupus erythematosus for 6 years. On examination, the patient had skin rash on his chest, back, head, forehead, and extremities. The neurological examination revealed that his tongue deviated to the right on protrusion. The muscle power was reduced to 2-3/5 in the right leg and to 4/5 in the left leg. The sensory disturbance was noted in the lower extremities with predominant involvement of the right leg. Reflexes were increased in the right biceps, triceps, both patellas, and Achilles tendons. Babinski sign was noted bilaterally. Urinary retention and constipation were also noted. The results of the blood cell count and hepatic and renal function tests were normal. Serum levels of C-reactive protein and complements (C3, C4, CH50) were also normal. Serological examinations showed increased anti-DNA antibody (14 U/ml, [normal, < 6]). Antinuclear antibody was positive at a titer of 1:1380. CSF study showed an increased protein concentration of 83 mg/dl and an IgG level of 14 mg/dl with a normal number of cells. MR images revealed a T1-low, T2-high signal lesion at the upper part of the left ventral medulla. MR images of the brain and spinal cord were normal. The patient was diagnosed as having SLE. High-dose intravenous methylprednisolone (1 g/day) pulse treatment that was started 25 days after the onset of neurological symptoms, produced partial relief. Our case presented with paraplegia with a focal lesion in the left upper ventral part of the medulla on MR images. The incidence of male SLE is low, and paraplegia is a rare complication of SLE. Thus, the medullary lesion in SLE observed in our case appears to be rare. SLE should be considered as a cause of acute onset paraplegia or myelopathy.

Adult↗
PubMed1997

[A case of idiopathic orthostatic hypotension with selective involvement of postganglionic noradrenergic neurons].

A 44-year-old man had a 30-year history of orthostatic hypotension and diarrhea. One month before admission, he suddenly lost consciousness by defecation, and was hospitalized. He became alert within two days, but he could not sit up due to severe orthostatic hypotension. At that point, he was transferred to our hospital. On admission, talipes and microdactylia were noted. Neurological examination revealed brisk patellar tendon reflexes. Anhidrosis or impotence was not present. Analyses of blood and urine yielded normal results. Cardiological examination revealed no abnormality that could be responsible for the hypotension. MR images of the brain were also normal. However, single photon emission tomography revealed diffuse hypoperfusion of the brain. A head-up tilt (50 degrees) test induced a remarkable fall in systolic blood pressure from 149 (heart rate; 65/min) to 64 mmHg (83). Immersion of hand in ice-cold water failed to increase blood pressure. Heart rate variation and cystometry results, which represent the function of parasympathetic nerves, were normal. Warming of his body caused normal sweating. Intravenous injection of low doses of norepinephrine and methoxamine increased blood pressure while isoproterenol remarkably increased heart rate, suggesting that both alpha- and beta-receptors developed supersensitivity. Instillation of 5% cocaine and 5% tyramine into the conjunctival sac failed to cause pupillary dilation. Clinical findings and pharmacological challenge test results suggested that the main lesion of his autonomic nervous system was selectively confined to the postganglionic sympathetic nerves and noradrenergic (not cholinergic) neurons. The autonomic failure of our patient can be classified as idiopathic orthostatic hypotension. However, most patients with idiopathic orthostatic hypotension or pure autonomic failure complain of anhidrosis and impotence, which were not noted in our patient. These symptomatic differences may be the result of the highly selective involvement of noradrenergic neurons in the postganglionic sympathetic system in our patient.

Adult↗
PubMed1996

Subdomain structure of the matrix attachment region located within the mouse immunoglobulin kappa gene intron.

Using the matrix attachment region (MAR) derived from Ig kappa gene intron, we assessed the importance of internal subregions required for the specific binding to the nuclear matrix. Relative affinities of MAR subfragments were compared in an in vitro binding reaction with isolated matrix. Cleavage at the near-centric MboII site generated two subfragments retaining a significant binding affinity. Dimerization of these subfragments greatly increased the affinity. Only a partial segment (130 bp) of the 3' fragment was necessary to restore the binding. The dimerization effect was lost when the monomer units were separated by nonMAR spacers of 500 bp <. This bipartite organization of Ig kappa MAR could be a general feature of AT-rich MARs, regardless of their genomic locations.

Animals↗
PubMed1996

Levodopoa but not bromocriptine induces AP-1 and creb DNA-binding activity in the dopamine-depleted striatum of the rat.

To elucidate the neurochemical mechanism that underlies the effect of anti-parkinsonian agents on motor activities in the dopamine-depleted striatum, we evaluated AP-I and CREB DNA-binding activity in the striatum of 6-hydroxydopamine-lesioned rats by use of a gel mobility-shift assay. Rats with a unilateral lesion of the nigrostriatal dopamine pathway were injected i.p. with either SKF38393 (a DI receptor agonist), bromocriptine (a D2 receptor agonist), or levodopa (a Dl/D2 receptor agonist). Each treatment increased the number of rotational responses of rats contralateral to the lesioned side. However, only SKF38393 and levodopa increased AP-I and CREB DNA-binding activity in the dopamine-depleted striatum. As with the expression of c-fos, supersensitive DI receptors may play a key role in the enhanced induction of AP-I and CREB DNA-binding activity in the dopamine-depleted striatum. Supershift analysis revealed that c-Fos; and Jun family proteins are the main components for AP-1 induced in the dopamine-depleted striaturn by SKF38393 or levodopa.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1996

Synergistic effect of D1 and D2 dopamine receptors on AP-1 DNA-binding activity in the striatum and globus pallidus of the rat with a unilateral 6-OHDA lesion of the medical forebrain bundle.

The synergistic effect of D1 and D2 dopamine receptors on transcription factor AP-1 was studied in the striatum and globus pallidus of rats with unilateral 6-OHDA lesions of the medial forebrain bundle. Contralateral rotational behavior in response to a challenge dose of D1 agonist with and without D2 agonist was determined by behavioral observation, and AP-1 induction was studied by a gel mobility-shift assay. Single administration of vehicle and of a low dose of the D1 agonist (SKF38393, 0.5 mg/kg, i.p.) failed to induce rotational behavior, while the D2 agonists bromocriptine (2.5 mg/kg, i.p.) and quinpirole (1 mg/kg. i.p.) induced low rate rotations. High dose of SKF38393, 10 mg/kg, i.p., and low dose D1 and D2 agonists administered together induced a higher rate of rotation. The gel mobility-shift assay also suggested a synergistic interaction between D1 and D2 receptors on AP-1 induction in both the striatum and globus pallidus ipsilateral to the 6-OHDA lesioned nigrostriatal pathway. However, the mode of AP-1 induction via each dopamine receptor subtype appeared to differ between these brain structures. Thus, in the striatum of the lesioned side, single administration of a high dose of D1 agonist, and combined administration of D1 agonist with either of the D2 agonists resulted in AP-1 induction, while in the globus pallidus, AP-1 binding was induced by the D2 agonist bromocriptine and combined administration of a low dose D1 agonist with D2 agonists, but not by D1 agonist alone, even at a high dose. These results demonstrate that a D1/D2 dopamine receptor synergism is involved is the induction of AP-1 both in the striatum and globus pallidus of the rat with ipsilateral dopamine depletion. The induction of AP-1 via each receptor subtype appears, however, to be differently regulated in these two structures.

Animals↗