Screening for Antepartum Depression Through Community Health Outreach in Swaziland.

Maternal depression, including antepartum and postpartum depression, is a neglected public health issue with potentially far-reaching effects on maternal and child health. We aimed to measure the burden of antepartum depression and identify risk factors among women in a peri-urban community in Swaziland. We conducted a cross-sectional study within the context of a community outreach peer support project involving "Mentor Mothers". We used of the Edinburgh Postnatal Depression Scale (EPDS) to screen women for depression during the third trimester of pregnancy, using a cut-off score of ≥13 to indicate depression. We also collected demographic and socioeconomic factors, and assessed the association of these factors with EPDS score using logistic regression models. A total of 1038 pregnant women were screened over a period of 9 months. Almost a quarter (22.7 %) had EPDS scores ≥13 and 41.2 % were HIV positive. A fifth, 17.5 % were teenagers and 73.7 % were unemployed. Depression was not associated with HIV status, age or employment status. However, women with multiple socioeconomic stressors were found to be more likely to score highly on the EPDS. Depression was common among pregnant women in the peri-urban areas of Swaziland. Screening for depression using the EPDS is feasible and can be included in the community health worker standard tool box as a way to improve early detection of depression and to highlight the importance of maternal mental health as a core public health concern.

Prolonged Exclusive Breastfeeding Through Peer Support: A Cohort Study From a Community Outreach Project in Swaziland.

Swaziland faces great public health challenges, including suboptimal breastfeeding practices and the world's highest prevalence of HIV. The objective of this study was to estimate neonatal and infant mortality rate and rate of exclusive breastfeeding for clients enrolled in a community-based peer support project in peri-urban areas of Swaziland. The intervention builds on the so called "Philani-model" with Mentor Mothers in the community under high level of supervision. Cohort data was collected from journals kept by the Mentor Mothers. Kaplan-Meier and Cox regression were used to analyse data. Neonatal and infant mortality were estimated to 15 respectively 57 per 1000 live births. High level of social vulnerability was associated with risk of neonatal mortality (HR 1.12, CI 95 % 1.01-1.24) while the mother's positive HIV status was associated with infant mortality (HR 2.05, CI 95 % 1.15-3.65). More visits by a Mentor Mother could not be shown to result in lower mortality. The chance to practice exclusive breastfeeding for 6 months was estimated to 50 %. The risk of discontinuing exclusive breastfeeding before 6 months was lower for mothers being unemployed (HR 0.55, CI 95 % 0.44-0.69) or socially vulnerable (HR 0.95, CI 95 % 0.92-0.99) and higher for mothers being HIV positive (HR 1.22, CI 95 % 1.01-1.48). Receiving at least four visits by a Mentor Mother during pregnancy decreased the risk of discontinuing exclusive breastfeeding prematurely (HR 0.82, CI 95 % 0.67-0.99). Peer support with Mentor Mothers thus had a positive impact on exclusive breastfeeding rates in this disadvantaged population.

Drosophila Ebi mediates Snail-dependent transcriptional repression through HDAC3-induced histone deacetylation.

The Drosophila Snail protein is a transcriptional repressor that is necessary for mesoderm formation. Here, we identify the Ebi protein as an essential Snail co-repressor. In ebi mutant embryos, Snail target genes are derepressed in the presumptive mesoderm. Ebi and Snail interact both genetically and physically. We identify a Snail domain that is sufficient for Ebi binding, and which functions independently of another Snail co-repressor, Drosophila CtBP. This Ebi interaction domain is conserved among all insect Snail-related proteins, is a potent repression domain and is required for Snail function in transgenic embryos. In mammalian cells, the Ebi homologue TBL1 is part of the NCoR/SMRT-HDAC3 (histone deacetylase 3) co-repressor complex. We found that Ebi interacts with Drosophila HDAC3, and that HDAC3 knockdown or addition of a HDAC inhibitor impairs Snail-mediated repression in cells. In the early embryo, Ebi is recruited to a Snail target gene in a Snail-dependent manner, which coincides with histone hypoacetylation. Our results demonstrate that Snail requires the combined activities of Ebi and CtBP, and indicate that histone deacetylation is a repression mechanism in early Drosophila development.

Wollknauel is required for embryo patterning and encodes the Drosophila ALG5 UDP-glucose:dolichyl-phosphate glucosyltransferase.

N-linked glycosylation is a prevalent protein modification in eukaryotic cells. Although glycosylation plays an important role in cell signaling during development, a role for N-linked glycosylation in embryonic patterning has not previously been described. In a screen for maternal factors involved in embryo patterning, we isolated mutations in Drosophila ALG5, a UDP-glucose:dolichyl-phosphate glucosyltransferase. Based on the embryonic cuticle phenotype, we designated the ALG5 locus wollknäuel (wol). Mutations in wol result in posterior segmentation phenotypes, reduced Dpp signaling, as well as impaired mesoderm invagination and germband elongation at gastrulation. The segmentation phenotype can be attributed to a post-transcriptional effect on expression of the transcription factor Caudal, whereas wol acts upstream of Dpp signalin by regulating dpp expression. The wol/ALG5 cDNA was able to partially complement the hypoglycosylation phenotype of alg5 mutant S. cerevisiae, whereas the two wol mutant alleles failed to complement. We show that reduced glycosylation in wol mutant embryos triggers endoplasmic reticulum stress and the unfolded protein response (UPR). As a result, phosphorylation of the translation factor eIF2alpha is increased. We propose a model in which translation of a few maternal mRNAs, including caudal, are particularly sensitive to increased eIF2alpha phosphorylation. According to this view, inappropriate UPR activation can cause specific patterning defects during embryo development.