Biomedical subjects

Sousuke Takeuchi

Publications and source records attributed to Sousuke Takeuchi.

3 recordsLinked to original sources

PubMed2006

[Case of Fisher syndrome with impairment of taste].

A 38-year-old man developed dysesthesia, diplopia, and an unsteady gait following an upper respiratory infection. IgG anti-GQ1b antibody was detected in his serum and he was diagnosed as Fisher syndrome. The patient also complained of loss of taste sensation, and it resolved along with improvement of other neurological manifestations. In Guillain-Barré syndrome, cranial nerve involvement is very common, though taste disturbance is a rare complaint. Impairment of taste has been reported in association with severe facial nerve involvement, but taste disturbance developed without facial nerve palsy in the present case and taste sensation was diminished in the area of all four nerves involved in taste sensation. These findings suggest that the impaired taste sensation in the present patient was not a complication of facial nerve palsy as in previous cases, but rather due to taste sensory specific involvement.

Adult↗

PubMed2004

Diffusion-weighted MR imaging in acute spinal cord ischemia.

We report diffusion-weighted (DW) MR findings for acute spinal cord ischemia in a 56-year-old patient. MR imaging obtained approximately 3 h after symptom onset demonstrated an area of hyperintensity on DW images, but no conspicuous signal abnormality on T2-weighted images in the conus medullaris. DW imaging of the spinal cord can contribute to the early detection of spinal cord vascular compromise.

Acute Disease↗

PubMed2003

PQBP-1 transgenic mice show a late-onset motor neuron disease-like phenotype.

A body of experimental evidence indicates that transcription and/or mRNA processing factors interacting with the polyglutamine disease gene products play crucial roles in the pathology. PQBP-1 is one of these factors and it has been shown to interact with the spinocerebellar ataxia type-1 (SCA1) disease gene product, ataxin-1. Our previous data suggested that relatively high expression of PQBP-1 in the cerebellum might explain the selective neuronal degeneration of SCA1. To further test whether PQBP-1 expression level regulates neuronal death, we generated transgenic mice of human PQBP-1 driven by a regulatory element for ubiquitous gene expression. The mice showed a late-onset and gradually progressive motor neuron disease-like phenotype, which might be related to neurogenic muscular atrophy observed in SCA1 patients. Ataxia could not be discriminated from predominant progressive weakness. Pathological examinations of the transgenic mice revealed loss of Purkinje and granular cells in the cerebellum as well as that of spinal motor neurons, corresponding to the pathology of human SCA1. These findings show that excessive action of PQBP-1 causes neuronal dysfunction and support PQBP-1 being involved in the pathology of SCA1.

Animals↗