Biomedical subjects

Toshitaka Nabeshima

Publications and source records attributed to Toshitaka Nabeshima.

111 records · Page 7Linked to original sources

PubMed1999

Pain relief of oral ulcer by dibucaine-film.

A water-soluble three-layered oral mucosa-adhesive film made from hydroxypropyl cellulose containing dibucaine (0.25 mg of drug/cm(2)) was designed for alleviation of severe pain due to oral ulcers, caused by chemotherapy and/or radiotherapy. We report two patients with constant severe pain ulcers treated with the dibucaine film. Patients were asked to record the time that pain was relieved while chewing following first application of the film. Pain relief lasted for 2-5 h after application of the dibucaine film.

Adhesives↗

PubMedDate not supplied

Involvement of BDNF receptor TrkB in spatial memory formation.

The N-methyl-D-aspartate (NMDA) receptors are involved in long-term potentiation (LTP), and are phosphorylated by several tyrosine kinases including a Src-family tyrosine kinase Fyn. Brain-derived neurotrophic factor (BDNF) is a neurotrophin, which also enhances hippocampal synaptic transmission and efficacy by increasing NMDA receptor activity. Here, we show that Fyn is a key molecule linking the BDNF receptor TrkB with NMDA receptors, which play an important role in spatial memory formation in a radial arm maze. Spatial learning induced phosphorylation of TrkB, Fyn, and NR2B, but not NR2A, in the hippocampus. Fyn was coimmunoprecipitated with TrkB and NR2B, and this association was increased in well-trained rats compared with control animals. Continuous intracerebroventricular infusion of PP2, a tyrosine kinase inhibitor, in rats delayed memory acquisition in the radial arm maze, but PP2-treated animals reached the same level of learning as the controls. The phosphorylation of Fyn and NR2B, but not TrkB, was diminished by PP2 treatment. Our findings suggest the importance of interaction between BDNF/TrkB signaling and NMDA receptors for spatial memory in the hippocampus.

Animals↗

PubMedDate not supplied

Latent copper deficiency in patients receiving low-copper enteral nutrition for a prolonged period.

BACKGROUND: Copper deficiency has been reported in patients supported with long-term enteral nutrition. Occasionally, this leads to anemia and leukopenia. There is no detailed report relating to the onset time of copper deficiency and how the symptoms develop. This report describes the relation between copper deficiency symptoms and duration of enteral nutrition. METHODS: The study included 55 patients, with 82 measurements, at the neurologic ward of Nagoya Daini Red Cross Hospital. The mean age was 71 +/- 11 years. The daily average dosage of energy was 938 kcal/d. A commercial nutrient for enteral administration that contains 0.13 mg/1000 mL copper was used. Baseline measures on individual patients were taken every month. Blood was collected at 8 am before and after the start of enteral nutrition. Levels of copper, zinc, ceruloplasmin, hemoglobin, and white blood cells were measured. RESULTS: The serum level of copper in the patients was 94.0-181.0 microg/dL before the start of enteral nutrition. The level of serum copper remained within the normal range for about 3 months. The level of serum copper in the patients decreased gradually and was less than the normal level after 3 months, with the exception of 1 patient. The serum level of copper in the patients was 3.0-123.0 microg/dL 3 months after the start of enteral nutrition. The levels of serum copper were below normal in 25 cases out of 82 measurements. However, the number of patients with symptoms of copper deficiency was only 2. Copper deficiency symptoms appeared at 41 and 77 months, the average being 59 months. CONCLUSIONS: Almost all patients showed a latent copper deficiency about 3 months after the start of enteral nutrition. However, only a few patients developed overt symptoms of copper deficiency.

Adult↗