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1.
Nihon Rinsho ; 72(2): 333-40, 2014 Feb.
Article in Japanese | MEDLINE | ID: mdl-24605537

ABSTRACT

This study aimed to investigate the influences of menorrhagia, premenstrual syndrome and perimenopausal syndrome on health-related quality of life (HR QOL) of working women. HR QOL was assessed using the SF-36 questionnaire. Menorrhagia and premenstrual syndrome significantly decreased the scales of HR QOL, respectively. Perimenopausal symptoms significantly decreased the scales of HR QOL of working women.


Subject(s)
Women, Working , Adolescent , Adult , Female , Humans , Menorrhagia/therapy , Menstruation Disturbances/therapy , Middle Aged , Premenstrual Syndrome/therapy , Quality of Life
2.
Int J Oncol ; 23(3): 657-63, 2003 Sep.
Article in English | MEDLINE | ID: mdl-12888901

ABSTRACT

Menstrual cycle-dependent expressions of activin A in normal human endometrial tissues have been reported. Expression of activin receptor mRNAs and increased activin A production were also observed in human endometrial adenocarcinoma tissues, suggesting that activin A might enhance cell proliferation and inhibit apoptotic signaling in endometrial cancer cells. In this study, we have examined the effects of activin A on cell proliferation, anticancer drug-induced apoptosis and Fas-mediated apoptosis in 3 differentiated human endometrial adenocarcinoma cell lines, namely HEC-1, HHUA and Ishikawa. Flow cytometric analyses revealed moderate expressions of all 4 types of activin receptor subunits on the cell surfaces of the 3 cell lines. The proliferations of the 3 endometrial cancer cells were completely unaffected by activin A, whereas it suppressed the cell proliferation of a human ovarian endometrioid adenocarcinoma cell line, OVK-18, in a dose-dependent manner. Moreover, activin A did not affect the apoptotic changes in the 3 endometrial adenocarcinoma cells treated with 4 different anticancer drugs, namely CDDP, paclitaxel, etoposide and SN38. The apoptotic changes in HHUA cells treated with anti-Fas IgM were also unaffected by activin A. These results indicate that the increased activin A production in human endometrial adenocarcinoma tissues in vivo may not stimulate carcinoma cell proliferation or inhibit apoptotic signaling in carcinoma cells. Insensitivity to the usual growth suppression signals induced by activin A might be one of the mechanisms of immortality of human endometrial adenocarcinoma cells.


Subject(s)
Activin Receptors/biosynthesis , Activin Receptors/physiology , Adenocarcinoma/metabolism , Endometrial Neoplasms/metabolism , Endometrium/metabolism , Activins/metabolism , Apoptosis , Cell Division , Cell Line, Tumor , Cell Membrane/metabolism , Cell Survival , DNA Fragmentation , Dose-Response Relationship, Drug , Female , Flow Cytometry , Humans , Inhibin-beta Subunits/metabolism , RNA, Messenger/metabolism , fas Receptor/biosynthesis
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