No abstract

This study explored the factorial structure of the Parental Bonding Instrument (PBI) in the Japanese population. Several differences between the structure model in the current study and Parker et al.'s original model were identified. We also examined the adaptability of the inventory to children currently being raised by parents. We also developed a structural equation model that takes into account the impacts of the respondents' generation and gender and the caregivers' gender. The cultural, developmental, generational, and gender influences on the factorial structure of the PBI as well as the implications for clinical settings were discussed.

In order to examine the relationships between parenting styles and personality traits over generations, a cross-sectional questionnaire study was conducted for fathers and mothers of school-age children of grades 5-9. The parenting styles measured by the Parental Bonding Instrument (PBI) and the personality traits measured by the Temperament and Character Inventory (TCI) were correlated within and between the consecutive generations (the grandparents and the parents for the PBI and the parents and the children for the TCI). A series of structural equation modeling showed that (1) while the parenting styles were transmitted directly from the grandparents to the parents, it was partly mediated by the fathers' Co-operativeness (C) but not so for the mothers, (2) while the personality traits were transmitted directly from the parents to the children, it was only the fathers' parenting styles that mediated C, and (3) the parents' parenting styles had independent effects upon the children's personality traits.

Our data support the fact that homozygosity for the SAA1.3 allele is a univariate predictor of survival in addition to a risk factor for the association of AA amyloidosis adversely influencing the outcome in Japanese RA patients. Renal involvement is a pivotal clinical manifestation in the development of AA amyloidosis, as is likely to be cardiac involvement in AA amyloidosis secondary to RA.