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BackgroundPreterm birth (birth before 37 weeks of gestation) and its complications are the leading contributors to neonatal and under-5 mortality. The majority of neonatal deaths in Kenya and Uganda occur during the intrapartum and immediate postnatal period. This paper describes our study protocol for implementing and evaluating a package of facility-based interventions to improve care during this critical window.Methods/designThis is a pair-matched, cluster randomized controlled trial across 20 facilities in Eastern Uganda and Western Kenya. The intervention facilities receive four components: (1) strengthening of routine data collection and data use activities; (2) implementation of the WHO Safe Childbirth Checklist modified for preterm birth; (3) PRONTO simulation training and mentoring to strengthen intrapartum and immediate newborn care; and (4) support of quality improvement teams. The control facilities receive both data strengthening and introduction of the modified checklist. The primary outcome for this study is 28-day mortality rate among preterm infants. The denominator will include all live births and fresh stillbirths weighing greater than 1000 g and less than 2500 g; all live births and fresh stillbirths weighing between 2501 and 3000 g with a documented gestational age less than 37 weeks.DiscussionThe results of this study will inform interventions to improve personnel and facility capacity to respond to preterm labor and delivery, as well as care for the preterm infant.Trial registrationClinicalTrials.gov, ID: NCT03112018. Registered on 13 April 2017.Electronic supplementary materialThe online version of this article (10.1186/s13063-018-2696-2) contains supplementary material, which is available to authorized users.

The genetic basis of hypertension is well established, yet very few genes that cause common forms of hypertension are known. Quantitative trait locus (QTL) analyses in rodent models can guide the search for human hypertension genes, but the excellent genetic resources for mice have been underutilized in this regard. To address this issue, we surveyed blood pressure variation in mice from 37 inbred strains and generated 2,577 mice in eight intercross populations to perform QTL analyses of blood pressure. We identified 14 blood pressure QTL in these populations, including at least 7 regions of the mouse genome not previously linked to blood pressure. Many QTL were detected in multiple crosses, either within our study or in previously published studies, which facilitates the use of bioinformatics methods to narrow the QTL and focus the search for candidate genes. The regions of the human genome that correspond to all but one of the 14 blood pressure QTL in mice are linked to blood pressure in humans, suggesting that these regions contain causal genes with a conserved role in blood pressure control. These results greatly expand our knowledge of the genomic regions underlying blood pressure regulation in mice and support future studies to identify the causal genes within these QTL intervals.