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Biomedical subjects

Kiyokazu Kawabe

Publications and source records attributed to Kiyokazu Kawabe.

7 recordsLinked to original sources
PubMed2005

Cheiro-oral-pedal syndrome due to brainstem hemorrhage.

Cheiro-oral-pedal syndrome is characterized by specific sensory disturbance around the corner of the mouth, in the hand and in the foot on the same side. Lesions responsible for causing this syndrome vary. We report two cases of cheiro-oral-pedal syndrome due to midbrain and pontine hemorrhage, respectively. Pontine hemorrhage producing cheiro-oral-pedal syndrome has been reported in three cases, but this is the first case that midbrain hematoma exhibits this syndrome. Damage in the sensory pathway can cause cheiro-oral-pedal syndrome. Difference in the threshold may explain the specific sensory pattern in this syndrome. Cheiro-oral-pedal syndrome is caused by lacunar infarction in majority of the cases. However, it should be kept in mind that hematomas can cause cheiro-oral-pedal syndrome.

Cerebral Hemorrhage↗
PubMed2005

Cheiro-pedal syndrome following pontine infarction.

We report the case of a 64-year-old man with sudden onset of numbness in the right hand and foot. Neurological examinations were normal except for hypersthesia, and hyperalgesia of the right hand and foot. Brain MRI demonstrated a high signal intensity on T2-weighted image and a low signal intensity on T1-weighted image in the left tegmetum of the pons. He was diagnosed with pontine infarction presenting with cheiro-pedal syndrome (CPS). Damage in the sensory pathways can cause CPS. Difference in the threshold may explain the specific sensory pattern in this syndrome. Further examination of the relationship between sensory symptoms and localization on MRI is needed to clarify this syndrome.

Brain Stem Infarctions↗
PubMed2004

T-588 protects motor neuron death following axotomy.

R(-)-1-(benzo [b] thiophen-5-yl)-2-[2-(N,N-diethylamino)ethoxy] ethanol hydrochloride) (T-588) enhances acetylcholine release. This compound slows the motor deterioration of wobbler mouse motor neuron disease and enhances neurite outgrowth and choline acetyltransferase activity in cultured rat spinal motor neurons. We examined the ability of T-588 on axotomized spinal motor neuron death in the rat spinal cord. After the postnatal unilateral section of sciatic nerve, there was approximately a 50% survival of motor neurons in the fourth lumbar segment. In comparison with vehicle, intraperitoneal injection of T-588 for 14 consecutive days rescued spinal motor neuron death. Our results showing in vivo neurotrophic activity of T-588 for motor neurons support the applicability of T-588 for the treatment of motor neuron diseases, such as amyotrophic lateral sclerosis and motor neuropathies.

Animals↗
PubMed2003

Protein and gene analyses of dysferlinopathy in a large group of Japanese muscular dystrophy patients.

Mutations in the dysferlin gene cause muscular dystrophies called dysferlinopathy, which include limb-girdle muscular dystrophy type 2B (LGMD2B) and Miyoshi myopathy (MM). To clarify the frequency, clinicopathological and genetic features of dysferlinopathy in Japan, we performed protein and gene analyses of dysferlin. We examined a total of 107 unrelated Japanese patients, including 53 unclassified LGMD, 28 MM and 26 other neuromuscular disorders (ONMD). Expression of dysferlin protein was observed using immunohistochemistry (IHC) and mini-multiplex Western blotting (MMW), and mutation analysis was performed. We found a deficiency of dysferlin protein by both IHC and MMW in 19% of LGMD and 75% of MM patients, and mutations in the dysferlin gene were identified in this group alone. 19% of dysferlin-deficient patients had 3370G-->T missense mutation and 16% had 1939C-->G nonsense mutation. The patients with homozygous 3370G-->T mutation showed milder clinical phenotypes. Twenty-five percent of MM muscles had normal dysferlin protein contents that suggested the genetic heterogeneity of this disease. Altered immunolocalization of dysferlin was observed in not only primary dysferlinopathy, but also in the several diseased muscles with normal protein contents. This result implies the necessity of other protein(s) for proper membrane localization of dysferlin, or some roles of dysferlin in the cytoplasmic region.

Age of Onset↗