14 research outputs found
May measurement month 2018: a pragmatic global screening campaign to raise awareness of blood pressure by the International Society of Hypertension (vol 40, pg 2006, 2019)
Biparental expression of ESX1L gene in placentas from normal and intrauterine growth-restricted pregnancies
Equivalent levels of X-linked gene products between males and females are reached by means of X chromosome inactivation (XCI). In the human and murine embryonic tissues, both the paternally and maternally derived X chromosomes (X P and X M) may be inactivated. In murine extra-embryonic tissues, X P is imprinted and always silenced; humans, unlike mice, can inactivate the X M in extra-embryonic lineages without an adverse outcome. This difference is probably due to the presence of imprinted placental genes on the murine X chromosome, but not on the human homologue, essential for placental development and function. An example is the paternally imprinted Esx1 gene; mice with a null maternally derived Esx1 allele show intrauterine growth restriction (IUGR) because of placental insufficiency. We investigated the imprinting status of the human orthologous Esx1 gene (ESX1L) in placental samples of four normal full-term and 13 IUGR female fetuses, in which we determined the XCI pattern. Our findings demonstrated that IUGR as well as normal placentas display XCI heterogeneity, thus indicating that the IUGR phenotype is not correlated with a preferential pattern of XCI in placentas. Moreover, ESX1L is equally expressed in IUGR and normal placentas, and shows the same methylation pattern in the presence of both random and skewed XCI. These findings provide evidence that ESX1L is not imprinted in human third-trimester placentas and there is no parent-of-origin effect of chromosome X associated with placental insufficiency
Biparental expression of ESX1L gene in placentas from normal and intrauterine growth-restricted pregnancies
Situs ambiguus in a female fetus with balanced (X;21) translocation – evidence for functional nullisomy of the ZIC3 gene?
Somatic segregation errors predominantly contribute to the gain or loss of a paternal chromosome leading to uniparental disomy for chromosome 15
Quantitative analysis of methylation status at 11p15 and 7q21 for the genetic diagnosis of Beckwith–Wiedemann syndrome and Silver–Russell syndrome
Income inequality and its implications for gendered conflict
We argue that inequality plays such an important role in shaping human behavior because of the strong effects it exerts on individual reproductive success and thus evolutionary fitness. Here we examine evidence of the relationship between economic inequality and reproductive incentives in men and women. Inequality has been shown to increase men’s competition for status and respect, particularly among men who are younger and poorer. This competition is an important explanatory variable in rates of accidental death, addiction, violence, and property crime. We then focus on parallel links in women, summarizing evidence that high economic inequality increases women’s investment of time and attention on competitive reproductive pursuits (such as improving physical and sexual attractiveness). We suggest that these behaviors are due to proximate desires to socially signal and socially climb, and may also reflect a concern with external approval. We show that these proximate mechanisms can be interpreted in terms of the ultimate function of achieving greater reproductive success via enhanced status, safety, and material well-being in economically unequal environments