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Context:Heavy menstrual bleeding (HMB) is common and incapacitating. Aberrant menstrual endometrial repair may result in HMB. The transforming growth factor (TGF)-β superfamily contributes to tissue repair, but its role in HMB is unknown.Objective:We hypothesized that TGF-β1 is important for endometrial repair, and women with HMB have aberrant TGF-β1 activity at menses.Participants/Setting:Endometrial biopsies were collected from women, and menstrual blood loss objectively measured [HMB >80 mL/cycle; normal menstrual bleeding (NMB) <80 mL].Design:Immunohistochemistry and reverse transcription polymerase chain reaction examined endometrial TGF-β1 ligand, receptors, and downstream SMADs in women with NMB and HMB. The function and regulation of TGF-β1 were examined using cell culture.Results: TGFB1 mRNA was maximal immediately prior to menses, but no differences detected between women with NMB and HMB at any cycle stage. Histoscoring of TGFB1 revealed reduced staining in the stroma during menses in women with HMB (P < 0.05). There were no significant differences in TGFBR1/2 or TGFBR1/2 immunostaining. Cortisol increased activation of TGFB1 in the supernatant of human endometrial stromal cells (HES; P < 0.05) via thrombospondin-1. Endometrial SMAD2 and SMAD3 were lower in women with HMB during menstruation (P < 0.05), and decreased phosphorylated SMAD2/3 immunostaining was seen in glandular epithelial cells during the late secretory phase (P < 0.05). Wound scratch assays revealed increased repair in HES cells treated with TGF-β1 versus control (P < 0.05).Conclusions:Women with HMB had decreased TGF-β1 and SMADs perimenstrually. Cortisol activated latent TGF-β1 to enhance endometrial stromal cell repair. Decreased TGF-β1 activity may hinder repair of the denuded menstrual endometrium, resulting in HMB.TGF-β1 and downstream SMADs were decreased in perimenstrual endometrium from women with heavy menstruation versus controls. TGF-β1 was activated by cortisol in endometrial cells and enhanced repair.

Governmental efforts to strengthen marriage through a variety of approaches have become increasingly common in the last decade. Societal trends related to family formation, marriage, and divorce have shaped interest in marriage and its stability as a social institution. The public sector has targeted efforts at key stages in the life history of the family system, including preparation for marriage, formation of marriage, rights and responsibilities within marriage, and dissolution of marriage. Particular governmental approaches to preserving and promoting marriage in these contexts are reviewed and discussed, and implications for practitioners and policymakers are outlined.

In a weekly radio address in 2004, President George W. Bush said: \"If courts create their own arbitrary definition of marriage as a mere legal contract and cut marriage off from its cultural, religious, and natural roots, then the meaning of marriage is lost and the institution is weakened.\"

Abstract Heavy menstrual bleeding (HMB) is common and incapacitating. Aberrant menstrual endometrial repair may result in HMB. The transforming growth factor (TGF)-β superfamily contributes to tissue repair, but its role in HMB is unknown. We hypothesized that TGF-β 1 is important for endometrial repair, and women with HMB have aberrant TGF-β 1 activity at menses. Endometrial biopsies were collected from women, and menstrual blood loss objectively measured [HMB >80 mL/cycle; normal menstrual bleeding (NMB) <80 mL]. Immunohistochemistry and reverse transcription polymerase chain reaction examined endometrial TGF-β 1 ligand, receptors, and downstream SMADs in women with NMB and HMB. The function and regulation of TGF-β 1 were examined using cell culture. TGFB1 mRNA was maximal immediately prior to menses, but no differences detected between women with NMB and HMB at any cycle stage. Histoscoring of TGFB1 revealed reduced staining in the stroma during menses in women with HMB (P < 0.05). There were no significant differences in TGFBR1/2 or TGFBR1/2 immunostaining. Cortisol increased activation of TGFB1 in the supernatant of human endometrial stromal cells (HES; P < 0.05) via thrombospondin-1. Endometrial SMAD2 and SMAD3 were lower in women with HMB during menstruation (P < 0.05), and decreased phosphorylated SMAD2/3 immunostaining was seen in glandular epithelial cells during the late secretory phase (P < 0.05). Wound scratch assays revealed increased repair in HES cells treated with TGF-β 1 versus control (P < 0.05). Women with HMB had decreased TGF-β 1 and SMADs perimenstrually. Cortisol activated latent TGF-β 1 to enhance endometrial stromal cell repair. Decreased TGF-β 1 activity may hinder repair of the denuded menstrual endometrium, resulting in HMB. TGF-β 1 and downstream SMADs were decreased in perimenstrual endometrium from women with heavy menstruation versus controls. TGF-β 1 was activated by cortisol in endometrial cells and enhanced repair.