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Frontmatter -- Contents -- Preface -- Introduction -- Chapter One. The Japanese-Canadian Community: From Relocation to Redress -- Chapter Two. Social Mobility: The Sansei Style -- Chapter Three. Sansei Socialization: The Way They Were Brought Up -- Chapter Four. Sansei Identity: Subjectively Defined -- Chapter Five. Sansei Behaviour: With a Focus on Intermarriage -- Chapter Five. Sansei Behaviour: With a Focus on Intermarriage -- Chapter Seven. Conclusion -- Appendix 1. Myth of a 'Model Minority'?: Social Mobility and Integration Achieved by Canadian Nisei in a Metropolitan Community (1991) -- Appendix 2. Interview Questions -- Notes -- References -- Index

La nature et la durée de la survie de l'identité culturelle du groupe ethnique des Canadiens d'origine japonaise dépendent de deux facteurs principaux: la répartition géographique de la population, puis la mobilité qu'elle a eu à subir dans les décades suivant la guerre. Ce rapport analyse les éléments de l'identité culturelle nippo‐canadienne au sein de la seconde génération, dans Toronto, au moyen d'une échelle d'identité. II apporte, de plus, une preuve empirique de l'hypothése généralement admise que l'identité culturelle d'un groupe est affaiblie par la mobilité sociale. L'analyse statistique de nos données confirme cette hypothèse: il existe une corrélation négative significative entre l'importance de l'identité culturelle et l'indice de mobilité des individus.The geographic dispersal of the Japanese population and the subsequent mobility experienced by Japanese Canadians in the postwar decades are considered as critical factors in explaining the nature and the extent of the group's ethnic identity maintenance. The present report explores the components of Japanese‐Canadian identity as revealed by the second‐generation Japanese in Metropolitan Toronto through the work of identity‐scale construction. It further provides empirical evidence supporting the commonly conceived hypothesis that ethnic group identity is weakened with social mobility. The statistical analysis of our data supports the hypothesis: there is a significant correlation between the strength of ethnic identity and the rate of mobility experienced by individuals.

Objective: The aim of this study was to clarify the expression of Ninj1 in endometriosis and adenomyosis lesions, and its inductive factor in human endometriotic stromal cells (ESCs). Background: Nerve injury-induced protein 1 (Ninj1) is a molecule originally identified in dorsal root ganglion neurons and Schwann cells after nerve injury and promotes neurite outgrowth. The aim of this study was to clarify the expression of Ninj1 in endometriosis and adenomyosis lesions, and its inductive factor in human endometriotic stromal cells (ESCs). Materials and Methods: Tissues were obtained with consent from patients diagnosed with ovarian endometrioma (n = 15 in total), peritoneal endometriosis (n = 5), adenomyosis (n = 5), and other gynecological disorders (n = 5, control) during surgery. Immunohistochemistry was conducted in order to detect Ninj1 protein expression in the lesion of endometriosis, adenomyosis, and eutopic endometrium. Nerve fibers in the ovarian endometrioma were detected by positive staining of PGP-9.5. To evaluate the effects of IL-1β on Ninj1 gene expression in endometriosis, ESCs isolated from ovarian endometrioma (n = 5) were treated with IL-1β (5 ng/mL) for 3 or 6 hours. Messenger RNA (mRNA) expression for Ninj1 was examined using quantitative RT-PCR. Results: The Ninj1 protein was expressed by ovarian endometrioma, peritoneal endometriotic, and adenomyotic tissue. Nerve fibers were found in the areas of positive staining for Ninj1 in ovarian endometrioma. IL-1β, an indicator of inflammation in endometriosis, significantly increased Ninj1 mRNA expression by ESC. Conclusion: Our study demonstrates that Ninj1 is expressed in endometriosis and adenomyosis and is induced by the inflammatory stimuli. Given the neurogenetic property of Ninj1, our results imply that Ninj1, induced by inflammation in endometriosis lesion, may contribute to the pathogenesis of pain symptoms characteristic of endometriosis.