Objective To analyse preterm birth rates worldwide to assess the incidence of this public health problem, map the regional distribution of preterm births and gain insight into existing assessment strategies. Methods Data on preterm birth rates worldwide were extracted during a previous systematic review of published and unpublished data on maternal mortality and morbidity reported between 1997 and 2002. Those data were supplemented through a complementary search covering the period 2003-2007. Region-specific multiple regression models were used to estimate the preterm birth rates for countries with no data. Findings We estimated that in 2005, 12.9 million births, or 9.6% of all births worldwide, were preterm. Approximately 11 million (85%) of these preterm births were concentrated in Africa and Asia, while about 0.5 million occurred in each of Europe and North America (excluding Mexico) and 0.9 million in Latin America and the Caribbean. The highest rates of preterm birth were in Africa and North America (11.9% and 10.6% of all births, respectively), and the lowest were in Europe (6.2%). Conclusion Preterm birth is an important perinatal health problem across the globe. Developing countries, especially those in Africa and southern Asia, incur the highest burden in terms of absolute numbers, although a high rate is also observed in North America. A better understanding of the causes of preterm birth and improved estimates of the incidence of preterm birth at the country level are needed to improve access to effective obstetric and neonatal care.Une traduction en français de ce résumé figure à la fin de l'article. Al final del artículo se facilita una traducción al español. ‫املقالة.‬ ‫لهذه‬ ‫الكامل‬ ‫النص‬ ‫نهاية‬ ‫يف‬ ‫الخالصة‬ ‫لهذه‬ ‫العربية‬ ‫الرتجمة‬

Summary Currently there are no approved vaccines or specific therapies to prevent or treat Zika virus (ZIKV) infection. We interrogated a library of FDA-approved drugs for their ability to block infection of human HuH-7 cells by a newly isolated ZIKV strain (ZIKV MEX_I_7). More than 20 out of 774 tested compounds decreased ZIKV infection in our in vitro screening assay. Selected compounds were further validated for inhibition of ZIKV infection in human cervical, placental and neural stem cell lines, as well as primary human amnion cells. Established anti-flaviviral drugs (e.g., bortezomib and mycophenolic acid) and others that had no previously known anti-viral activity (e.g., daptomycin) were identified as inhibitors of ZIKV infection. Several drugs reduced ZIKV infection across multiple cell types. This study identifies drugs that could be tested in clinical studies of ZIKV infection and provides a resource of small molecules to study ZIKV pathogenesis.

BackgroundGestational age is often used as a proxy for developmental maturity by clinicians and researchers alike. DNA methylation has previously been shown to be associated with age and has been used to accurately estimate chronological age in children and adults. In the current study, we examine whether DNA methylation in cord blood can be used to estimate gestational age at birth.ResultsWe find that gestational age can be accurately estimated from DNA methylation of neonatal cord blood and blood spot samples. We calculate a DNA methylation gestational age using 148 CpG sites selected through elastic net regression in six training datasets. We evaluate predictive accuracy in nine testing datasets and find that the accuracy of the DNA methylation gestational age is consistent with that of gestational age estimates based on established methods, such as ultrasound. We also find that an increased DNA methylation gestational age relative to clinical gestational age is associated with birthweight independent of gestational age, sex, and ancestry.ConclusionsDNA methylation can be used to accurately estimate gestational age at or near birth and may provide additional information relevant to developmental stage. Further studies of this predictor are warranted to determine its utility in clinical settings and for research purposes. When clinical estimates are available this measure may increase accuracy in the testing of hypotheses related to developmental age and other early life circumstances.Electronic supplementary materialThe online version of this article (doi:10.1186/s13059-016-1068-z) contains supplementary material, which is available to authorized users.

Preterm labor leading to preterm delivery (<37 weeks' gestation) affects approximately 5-7% of live births in developed countries, but significantly higher in developing countries. Prematurity due to preterm birth (PTB) accounts for around 28% of neonatal mortality worldwide. Approximately 45-50% of PTBs are idiopathic or spontaneous, 30% are related to preterm rupture of membranes, and another 15-20% are attributed to medically indicated or elective preterm deliveries. The rate of spontaneous PTB is also increasing and the exact cause is still unclear. Generalized approaches in screening for high risk status of preterm labor and interventions have failed to reduce PTB rates. PTB presents a clinical dilemma due to etiologic, pathophysiologic and genetic heterogeneities. Racial disparity in PTB rates observed in the US further complicates its understanding. PTB is a complex phenotype and is not initiated by a single etiologic agent. Etiologic factors operate through multiple pathophysiologic pathways, and these pathways include highly overlapping biomarkers and molecular factors creating pathophysiologic heterogeneities. In this article, the current understanding of PTB pathophysiology is reviewed and the need for a much broader approach in research, analysis and interpretation of data is explained, where environmental and race/ethnicity specific risk factors may dictate specific pathways leading to PTB. Recent data on amniotic fluid biomarkers and maternal and fetal genetic variants, which indicate huge disparity between races in the US, are also reviewed. These data suggest that gene-gene interactions and gene-environmental interactions produce distinct pathophysiologic pathways with respect to an individual's genetic make-up and environmental risk exposure. Current strategies of high risk screening and intervention measures may not be generalized, and a more individualized approach may be required to understand PTB and its prevention.