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Publisher: Routledge
Date: 06-10-2015
Publisher: Springer Publishing Company
Date: 06-2015
Publisher: Informa UK Limited
Date: 1998
DOI: 10.3109/13697139809085527
Abstract: The aim of this study was to test the hypothesis that increased dietary intake of phytoestrogens reduces the health impact of the menopause. To test this hypothesis, a double-blind, randomized, entry-exit, cross-over study was conducted to assess the effects of three dietary manipulations--soy and linseed diets (high in phytoestrogens) and a wheat diet (low in phytoestrogens). Postmenopausal women were recruited and randomly assigned to one of the three dietary regimens. Urinary phytoestrogen concentrations, hot flush rate, vaginal smears, bone mineral density and bone mineral content were assessed for two 12-week periods. Comparative analysis showed no significant differences, but, when analyzed separately, groups consuming high phytoestrogen diets had between 10 and 30 times higher urinary excretion of phytoestrogens compared to those consuming the low phytoestrogen diet (p < 0.01). Study participants consuming soy, linseed and wheat diets had a 22% (not significant, n.s.), 41% (p < 0.009) and 51% (p < 0.001) reduction in hot flush rate a 103% (p < 0.04), 5.5% (n.s.) and 11% (n.s.) increase in vaginal cytology maturation index and a 5.2% (p < 0.04), 5.2% (n.s.) and 3.8% (n.s.) increase in bone mineral content, respectively. No changes were detected in bone mineral density. The differential effects of high phytoestrogen dietary manipulations on outcomes may represent tissue-specific responses to isoflavones and lignans contained in soy and linseed, respectively. Whilst health outcome measures were not significantly different between groups, the data obtained from separate analysis suggest that phytoestrogens in soy and linseed may be of use in ameliorating some of the symptoms of menopause. Furthermore, the significant decrease in hot flush rate in the wheat group cannot be attributable to phytoestrogens measured in this study. Due to subject variability, larger studies are still needed to evaluate population benefit.
Publisher: Informa UK Limited
Date: 14-07-2015
Publisher: Elsevier BV
Date: 12-2005
DOI: 10.1086/316888
Publisher: Elsevier BV
Date: 02-2001
Abstract: We investigated maternal versus fetal genetic causes of preecl sia and ecl sia by assessing concordance between monozygotic and dizygotic female co-twins, between female partners of male monozygotic and dizygotic twin pairs, and between female twins and partners of their male co-twins in dizygotic opposite-sex pairs. Two large birth cohorts of volunteer Australian female twin pairs (N = 1504 pairs and N = 858 pairs) were screened and interviewed, and available medical and hospital records were obtained and reviewed where indicated, with diagnoses assigned according to predetermined criteria. With strict diagnostic criteria used for preecl sia and ecl sia, no concordant female twin pairs were found. Collapsing diagnoses of definite, probable, or possible preecl sia or ecl sia resulted in very low genetic recurrence risk estimates. Results from these two cohorts of female twin pairs do not support clear, solely maternal genetic influences on preecl sia and ecl sia. Numbers of parous female partners of male twins were too low for conclusions to be drawn regarding paternal transmission.
Publisher: Informa UK Limited
Date: 1999
DOI: 10.3109/10641959909009613
Abstract: To investigate the endothelial cell nitric oxide synthase (eNOS) gene as a candidate for susceptibility to preecl sia. Twenty-six Australian families containing 11 ecl tics, 59 severe preecl tics, and 27 mild preecl tics were used to test for linkage between the eNOS gene region and preecl sia. Two microsatellite markers (D7S483 and D7S505) in the proximity of the eNOS gene were used. Logarithm of odds (LOD) scores were used to examine the cosegregation of alleles with the disease under a variety of inheritance models. Model-independent analysis, affected pedigree member method (AFFPED), and pairwise haplotype sharing between affected sibs were also used. Two-point LOD score analysis gave no evidence of linkage between preecl sia and two markers in close proximity to the eNOS gene (LOD scores 0.05). This study provides no evidence for linkage between two markers in close proximity to the eNOS gene and preecl sia in these families. These results do not support the recent suggestion that eNOS could be a familial pregnancy-induced hypertension gene (Arngrimsson R, et al., Am J Hum Genet 1997 :354-62). Distinguishing preecl sia from other hypertensive disorders in pregnancy is difficult. Hypertension appears to be a consequence, rather than a primary cause of preecl sia. Given the vasodilatory role of the eNOS gene product, it is possible that the linkage recently reported for eNOS reflects its relationship with hypertension rather than preecl sia.
Publisher: Canadian Association of Schools of Nursing
Date: 17-09-2020
Publisher: Wiley
Date: 24-08-2004
Publisher: S. Karger AG
Date: 2004
DOI: 10.1159/000076689
Abstract: The genetic background predisposing pregnant women to the disorder pre-ecl sia/ecl sia (PE/E) is still unknown. There is compelling evidence to suspect involvement of the immune system in the development of PE/E. The aim of this current study was to investigate whether there is an association between the tumor necrosis factor (TNF)-α –307 polymorphism and PE or ecl sia. In this study, 51 cases of ecl sia, 122 cases of PE and 100 normotensive control cases were genotyped for the TNF-α –307 polymorphism. We found a significant difference between the TNF2 allele frequencies of ecl tic and normotensive controls (χ sup /sup = 6.3 and p = 0.025), but not of pre-ecl tic and normotensive controls (χ sup /sup = 0.5 and p = 1.0). We conclude from this study that the TNF2 allele contributes to the occurrence of ecl sia in our population.
Start Date: 2019
End Date: 2020
Funder: University of Virginia, Eleanor Crowder Bjoring Centre for Nursing Historical Inquiry
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