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Mihoko Nakamura

Publications and source records attributed to Mihoko Nakamura.

5 recordsLinked to original sources
PubMed2006

Ischemia promotes calpain-mediated degradation of p120-catenin in SH-SY5Y cells.

p120-catenin contributes to the cadherin-mediated adhesion and aggregation of cells. mu-Calpain was activated and p120-catenin was degraded after 36 h of ischemia in differentiated SH-SY5Y cells. Calpain inhibitors Cbz-Val-Phe-H (MDL28170, 20 microM) and N-acetyl-leucyl-leucyl-norleucinal (ALLN, 20 microM) increased the levels of dephosphorylated p120-catenin, aggregation, and cell survival as detected by reduced LDH release in ischemic cells. However, a proteasome inhibitor lactacystin had no such effects. This is the first report of the calpain-mediated degradation of p120-catenin and an association between the level of dephosphorylated p120-catenin and cell aggregation in ischemic neuronal cells.

Acetylcysteine↗
PubMed2006

A case of sudden death after intramuscular injection of butylscopolamine bromide.

A 40-year-old man experienced cardiopulmonary arrest after intramuscular injection of 20 mg of butylscopolamine bromide. No pathological changes were found at autopsy, and 1.19 microg/mL of butylscopolamine bromide was detected in his serum. Since he had taken no other drugs, his severe symptoms were thought to have been caused by an anaphylactic reaction to butylscopolamine bromide. Butylscopolamine bromide has been used for many years worldwide, and is considered to be a safe drug, with no reports of severe side effects following intramuscular injection. Since an anaphylactic reaction may not be related to a particular medication, the possibility of such a severe reaction must be considered, even during administration of an ostensibly safe drug such as butylscopolamine bromide.

Adult↗
PubMed2003

Mutations in the human homologue of Drosophila patched in Japanese nevoid basal cell carcinoma syndrome patients.

Mutations in the human homologue of Drosophila patched (PTCH) have been identified in patients with nevoid basal cell carcinoma syndrome (NBCCS; also called Gorlin syndrome) as well as sporadic basal cell carcinomas and medulloblastomas. However, using PCR-SSCP analysis, mutations in PTCH have been found in only a fraction (about one third to a half) of NBCCS patients. In this study, we determined the whole genomic organizations of the PTCHgene and developed a new set of more accurate primers for the analysis of mutations in PTCH. Using these primers, we examined 8 Japanese NBCCS patients for mutations in all PTCH exons by direct sequencing of the PCR products. As a result, we identified 5 novel PTCH mutations in 6 out of 8 patients including 2 sisters as well as 5 polymorphisms, two of them, 1704G>C and 2928G>C were novel. Four of these mutations, 900delC, 1247insT, 1999delC and 933+5G>T, cause protein truncation due to the insertion or deletion of a single nucleotide or aberrant splicing. The remaining mutation, 1514G>A was a missense alteration (G509D). Interestingly, the amino acid substitution, G509V, has been reported previously in an NBCCS patient, suggesting an important role of this amino acid residue in the function of PTCH protein. The difference in the detection rate of PTCH mutations among NBCCS between previous reports and ours is due to the difference either in ethnicity or in the detection methods.

Amino Acid Sequence↗
PubMed2002

[Alpers' syndrome].

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Child, Preschool↗