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N Yazaki

Publications and source records attributed to N Yazaki.

23 records · Page 2Linked to original sources
PubMed1983

Influence of temperature and relative humidity on human rotavirus infection in Japan.

A climatologic analysis of human rotavirus infection in inpatients with acute diarrhea was conducted over a seven-year period. The infection frequency appeared to be related to temperature, but not to relative humidity. Human rotavirus infection was found to appear abruptly when the mean temperature of any 10-day period became less than 5 C (November or December), reached a peak when it was less than 0 C (January and February), and waned when it became greater than 20 C (June and July) in the city of Yamagata in northern Japan.

Adolescent↗
PubMedDate not supplied

Severe bleeding tendency in a patient with Bernard-Soulier syndrome associated with a homozygous single base pair deletion in the gene coding for the human platelet glycoprotein Ibalpha.

PURPOSE: The genetic basis of Bernard-Soulier syndrome (BSS) was studied to clarify a relationship between severe clinical manifestations and gene abnormality. PATIENT AND METHODS: A patient with BSS had a severe bleeding tendency that was sometimes life threatening. Flow cytometric analysis of the patient's and normal control platelets was performed to study which glycoprotein (GP) was impaired in glycoprotein Ib/V/IX complex. The genes encoding GPIbalpha from the patient's and control genomic DNA were amplified and directly sequenced. RESULTS: Flow cytometric analysis revealed a defect of GPIbalpha on the surface of the patient's platelets. A homozygous single base pair deletion was identified in seven repeats of adenine at positions 1932 to 1938 in the GPIbalpha gene. This mutation, which has been previously reported, results in a frameshift and predicts a premature stop codon leading to a truncated peptide that cannot fix on the platelet membrane. CONCLUSION: This patient's severe clinical phenotype would be explained by this mutation in the GPIbalpha gene.

Adolescent↗
PubMedDate not supplied

Mutant p53 mediated induction of cell cycle arrest and apoptosis at G1 phase by 9-hydroxyellipticine.

Wild-type p53 causes cell-cycle arrest at late G1 phase and induction of apoptosis by up- regulation of waf1 and bax, respectively. Although in many cancer cells p53 is frequently mutated and loses its functions, we have proposed that mutant p53 may be involved in the anticancer mechanism of 9-hydroxy ellipticine (9HE). It was shown using flow cytometry that 9HE (10 microM) caused induction of apoptosis in G1 phase of the cell cycle in mutant p53 (p53ala143, p53his175, orp53his273) transfected Saos-2 cells, but not in p53-deficient parental Saos-2 cells. Similar induction of apoptosis was observed 24-48 h after treatment with 9HE in mutant p53-containing SW480, SK-BR-3 and MKN-1, but not in p53-deficient KATO m cells. Using G1 phase cells isolated by centrifugal elutriation, it was confirmed that 9HE caused cell cycle arrest at G1 phase and subsequently induced G1 phase-restricted apoptosis. In accordance with the induction of arrest and apoptosis in G1 phase, 9HE caused up-regulation of waf1 and bax mRNA in mutant p53-containing cells, but not in p53-deficient parental Saos-2 cells. In control experiments, adriamycin (ADR) showed neither G1-restricted apoptosis nor elevation of bax mRNA. It is suggested that 9HE may cause G1 arrest and induction of G1 phase-restricted apoptosis by restoring the wild-type function of mutant p53 protein.

Apoptosis↗