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Peter, D.

Publications and source records attributed to Peter, D..

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Exploring midwives understanding of respectful and non-abusive maternal care in Kumasi, Ghana: Qualitative Inquiry

BackgroundVarious aspects of disrespect and abusive maternity care have received scholarly attention because of frequent reports of the phenomenon in most healthcare facilities globally, especially in low- and middle-income countries. However, the perspectives of skilled providers on respectful maternal care have not been extensively studied. Midwives knowledge of respectful maternity care is critical in designing any interventive measures to address the menace of disrespect and abuse in maternity care. Therefore, the present study sought to explore the views of midwives on respectful maternity care at a Teaching Hospital in Kumasi, Ghana.\n\nMethodsPhenomenological qualitative research design was employed in the study. Data were generated through individual in-depth interviews, which were audio-recorded and transcribed verbatim. Data saturation was reached with fifteen midwives. Open Code 4.03 was used to manage and analyse the data.\n\nFindingsThe midwives understanding of respectful maternity care was comprised of the following components: non-abusive care, consented care, confidential care, non-violation of childbearing womens basic human rights, and non-discriminatory care. Probing questions to solicit midwives opinions on an evidenced-based component of respectful maternity care generated little information, suggesting that the midwives have a gap in knowledge regarding this component of respectful maternity care.\n\nConclusionMidwives reported an understanding of most components of respectful maternity care, but their gap in knowledge on evidenced-based care requires policy attention and in-service training. To understand the extent to which this gap in knowledge can be generalized for midwives across Ghana to warrant a redesign of the national midwifery curriculum, the authors recommend a nationwide cross-sectional quantitative study.

scientific communication and education

A role for EP3 and its associated G protein, Gz, in negatively regulating beta-cell function and mass in the context of insulin resistance and obesity

When homozygous for the LeptinOb mutation (Ob), Black-and-Tan Brachyury (BTBR) mice become morbidly obese and severely insulin resistant, and by 10 weeks of age, frankly diabetic. Previous work has shown Prostaglandin EP3 Receptor (EP3) expression and activity is up-regulated in islets from BTBR-Ob mice as compared to lean controls, actively contributing to their beta-cell dysfunction. In this work, we aimed to test the impact of beta-cell-specific EP3 loss on the BTBR-Ob phenotype by crossing Ptger3 floxed mice with the Rat insulin promoter (RIP)-CreHerr driver strain. Instead, germline recombination of the floxed allele in the founder mouse - an event whose prevalence we identified as directly associated with underlying insulin resistance of the background strain - generated a full-body knockout. Full-body EP3 loss provided no diabetes protection to BTBR-Ob mice, but, unexpectedly, significantly worsened BTBR-lean insulin resistance and glucose tolerance. This in vivo phenotype was not associated with changes in beta-cell fractional area or markers of beta-cell replication ex vivo. Instead, EP3-null BTBR-lean islets had essentially uncontrolled insulin hypersecretion. The selective up-regulation of constitutively-active EP3 splice variants in islets from young, lean BTBR mice as compared to C57BL/6J, where no phenotype of EP3 loss has been observed, provides a potential explanation for the hypersecretion phenotype. In support of this, high islet EP3 expression in Balb/c females vs. Balb/c males was fully consistent with their sexually-dimorphic metabolic phenotype after loss of EP3-coupled Gz protein. Taken together, our findings provide a new dimension to the understanding of EP3 as a critical brake on insulin secretion. New and NoteworthyIslet Prostaglandin EP3 receptor (EP3) signaling is well-known as up-regulated in the pathophysiological conditions of type 2 diabetes, contributing to beta-cell dysfunction. Unexpected findings in mouse models of non-obese insulin sensitivity and resistance provide a new dimension to our understanding of EP3 as a key modulator of insulin secretion. A previously-unknown relationship between mouse insulin resistance and the penetrance of Rat insulin promoter-driven germline floxed allele recombination is critical to consider when creating beta-cell-specific knockouts. For Table of Contents Use Only O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=121 SRC="FIGDIR/small/671289v3_ufig1.gif" ALT="Figure 1"> View larger version (37K): org.highwire.dtl.DTLVardef@15cf1d5org.highwire.dtl.DTLVardef@108f565org.highwire.dtl.DTLVardef@126e479org.highwire.dtl.DTLVardef@61fdf8_HPS_FORMAT_FIGEXP M_FIG C_FIG

molecular biology