211 research outputs found

    The Empower Nudge lottery to increase dual protection use: a proof-of-concept randomised pilot trial in South Africa

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    The objective of this study is to measure the preliminary efficacy of a pilot intervention, grounded in behavioural economics, increasing adherence of dual protection (simultaneous use of effective modern contraception and a barrier method, such as a condom) to protect against HIV, other sexually transmitted infections, and unintended pregnancy. Between 2015 and 2016, 100 women aged 18–40 years, seeking post-abortion care in Cape Town, South Africa were recruited to Empower Nudge, a randomised controlled trial to test a lottery incentive intervention designed to increase dual protection. At baseline, the mean age of participants was 27 years; 82% of them were from South Africa; 58% self-identified as Black African; average education completed was 11.7 years. At three months, assignment to the lottery intervention was associated with higher odds of returning for study visits (OR: 6.0; 95%CI: 2.45 to 14.7, p < 0.01), higher condom use (OR: 4.5; 95%CI: 1.43 to 14.1; p < 0.05), and higher use of dual protection (OR: 3.16; 95%CI: 1.01 to 9.9; p < 0.05). Only 60% of the study population returned after three months and only 38% returned after six months. Women who receive post-abortion care represent a neglected population with an urgent need for HIV and pregnancy prevention. Dual protection is a critically important strategy for this population. Lottery-based behavioural economics strategies may offer possible ways to increase dual protection use in this population. Further research with larger samples, longer exposure time, and more sites is needed to establish fully powered efficacy of lottery incentives for dual protection; using objective verification for monitoring

    Estrogen Receptor Beta rs1271572 Polymorphism and Invasive Ovarian Carcinoma Risk: Pooled Analysis within the Ovarian Cancer Association Consortium

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    The association of ovarian carcinoma risk with the polymorphism rs1271572 in the estrogen receptor beta (ESR2) gene was examined in 4946 women with primary invasive ovarian carcinoma and 6582 controls in a pooled analysis of ten case-control studies within the Ovarian Cancer Association Consortium (OCAC). All participants were non-Hispanic white women. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using unconditional logistic regression adjusted for site and age. Women with the TT genotype were at increased risk of ovarian carcinoma compared to carriers of the G allele (ORβ€Š=β€Š1.10; 95%; CI: 1.01–1.21; pβ€Š=β€Š0.04); the OR was 1.09 (CI: 0.99–1.20; pβ€Š=β€Š0.07) after excluding data from the center (Hawaii) that nominated this SNP for OCAC genotyping A stronger association of rs1271572 TT versus GT/GG with risk was observed among women aged ≀50 years versus older women (ORβ€Š=β€Š1.35; CI: 1.12–1.62; pβ€Š=β€Š0.002; p for interactionβ€Š=β€Š0.02) that remained statistically significant after excluding Hawaii data (ORβ€Š=β€Š1.34; CI: 1.11–1.61; pβ€Š=β€Š0.009). No heterogeneity of the association was observed by study, menopausal status, gravidity, parity, use of contraceptive or menopausal hormones, tumor histological type, or stage at diagnosis. This pooled analysis suggests that rs1271572 might influence the risk of ovarian cancer, in particular among younger women

    Teaching About Health Care Disparities in the Clinical Setting

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    Clinical teachers often observe interactions that may contribute to health care disparities, yet may hesitate to teach about them. A pedagogical model could help faculty structure teaching about health care disparities in the clinical setting, but to our knowledge, none have been adapted for this purpose. In this paper, we adapt an established model, Time-Effective Strategies for Teaching (TEST), to the teaching of health care disparities. We use several case scenarios to illustrate the core components of the model: diagnose the learner, teach rapidly to the learner’s need, and provide feedback. The TEST model is straightforward, easy to use, and enables the incorporation of teaching about health care disparities into routine clinical teaching

    Evaluation of Candidate Stromal Epithelial Cross-Talk Genes Identifies Association between Risk of Serous Ovarian Cancer and TERT, a Cancer Susceptibility β€œHot-Spot”

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    We hypothesized that variants in genes expressed as a consequence of interactions between ovarian cancer cells and the host micro-environment could contribute to cancer susceptibility. We therefore used a two-stage approach to evaluate common single nucleotide polymorphisms (SNPs) in 173 genes involved in stromal epithelial interactions in the Ovarian Cancer Association Consortium (OCAC). In the discovery stage, cases with epithelial ovarian cancer (nβ€Š=β€Š675) and controls (nβ€Š=β€Š1,162) were genotyped at 1,536 SNPs using an Illumina GoldenGate assay. Based on Positive Predictive Value estimates, three SNPsβ€”PODXL rs1013368, ITGA6 rs13027811, and MMP3 rs522616β€”were selected for replication using TaqMan genotyping in up to 3,059 serous invasive cases and 8,905 controls from 16 OCAC case-control studies. An additional 18 SNPs with Pper-allele<0.05 in the discovery stage were selected for replication in a subset of five OCAC studies (nβ€Š=β€Š1,233 serous invasive cases; nβ€Š=β€Š3,364 controls). The discovery stage associations in PODXL, ITGA6, and MMP3 were attenuated in the larger replication set (adj. Pper-alleleβ‰₯0.5). However genotypes at TERT rs7726159 were associated with ovarian cancer risk in the smaller, five-study replication study (Pper-alleleβ€Š=β€Š0.03). Combined analysis of the discovery and replication sets for this TERT SNP showed an increased risk of serous ovarian cancer among non-Hispanic whites [adj. ORper-allele 1.14 (1.04–1.24) pβ€Š=β€Š0.003]. Our study adds to the growing evidence that, like the 8q24 locus, the telomerase reverse transcriptase locus at 5p15.33, is a general cancer susceptibility locus

    Transcription Factors Mat2 and Znf2 Operate Cellular Circuits Orchestrating Opposite- and Same-Sex Mating in Cryptococcus neoformans

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    Cryptococcus neoformans is a human fungal pathogen that undergoes a dimorphic transition from a unicellular yeast to multicellular hyphae during opposite sex (mating) and unisexual reproduction (same-sex mating). Opposite- and same-sex mating are induced by similar environmental conditions and involve many shared components, including the conserved pheromone sensing Cpk1 MAPK signal transduction cascade that governs the dimorphic switch in C. neoformans. However, the homeodomain cell identity proteins Sxi1Ξ±/Sxi2a encoded by the mating type locus that are essential for completion of sexual reproduction following cell–cell fusion during opposite-sex mating are dispensable for same-sex mating. Therefore, identification of downstream targets of the Cpk1 MAPK pathway holds the key to understanding molecular mechanisms governing the two distinct developmental fates. Thus far, homology-based approaches failed to identify downstream transcription factors which may therefore be species-specific. Here, we applied insertional mutagenesis via Agrobacterium-mediated transformation and transcription analysis using whole genome microarrays to identify factors involved in C. neoformans differentiation. Two transcription factors, Mat2 and Znf2, were identified as key regulators of hyphal growth during same- and opposite-sex mating. Mat2 is an HMG domain factor, and Znf2 is a zinc finger protein; neither is encoded by the mating type locus. Genetic, phenotypic, and transcriptional analyses of Mat2 and Znf2 provide evidence that Mat2 is a downstream transcription factor of the Cpk1 MAPK pathway whereas Znf2 functions as a more terminal hyphal morphogenesis determinant. Although the components of the MAPK pathway including Mat2 are not required for virulence in animal models, Znf2, as a hyphal morphology determinant, is a negative regulator of virulence. Further characterization of these elements and their target circuits will reveal genes controlling biological processes central to fungal development and virulence
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