Editorial: saving mothers and babies for the new world

First, where or what is the New World? Historically, this refers to the region of the Americas. In this context, the New World is the future of humankind, an ambiguous borderless phenomenon that is informed and built upon from lessons of its past and from stories of triumph and regrets; of innovations, experiences of the pandemic, economic successes, and failures; of those unwanted wars; and of great science. The New World we envision emphasizes the quintessential of actions to ensure human survivability, by prioritizing equitable care to mothers and babies regardless of their region. Positive outcomes for mothers and babies can only be achieved by ensuring that healthcare professionals are knowledgeable, holistic, ethical, and safe and that effective execution of ethically robust healthcare policies and guidelines for equitable perinatal healthcare is adequately supported. These aims need to be at the forefront of policies of governments across all countries in the New World despite all setbacks. With this in mind, the research topic Saving Mothers and Babies for the New World accepted 16 diverse full-length articles and collected abstracts presented at the 21st Federation of Asia Oceania Perinatal Societies (FAOPS) Congress that provided a wealth of information and science that can help carve future research and inform policies

Comparison of the Mycoplasma Duo Test with PCR for Detection of Ureaplasma Species in Endotracheal Aspirates from Premature Infants

We compared the Mycoplasma Duo kit (Sanofi Diagnostics Pasteur) with PCR for detection of Ureaplasma spp. in endotracheal aspirates from 60 premature neonates. The overall agreement between the two tests was 96%. The Mycoplasma Duo assay is a useful alternative to culture and PCR for detection of neonatal Ureaplasma infection

Antimicrobial stewardship and targeted therapies in the changing landscape of maternal sepsis.

Pregnant and postnatal women are a high-risk population particularly prone to rapid progression to sepsis with significant morbidity and mortality worldwide. Moreover, severe maternal infections can have a serious detrimental impact on neonates with almost 1 million neonatal deaths annually attributed to maternal infection or sepsis. In this review we discuss the susceptibility of pregnant women and their specific physiological and immunological adaptations that contribute to their vulnerability to sepsis, the implications for the neonate, as well as the issues with antimicrobial stewardship and the challenges this poses when attempting to reach a balance between clinical care and urgent treatment. Finally, we review advancements in the development of pregnancy-specific diagnostic and therapeutic approaches and how these can be used to optimize the care of pregnant women and neonates

Studying the Effects of Granulocyte-Macrophage Colony-Stimulating Factor on Fetal Lung Macrophages During the Perinatal Period Using the Mouse Model.

Background: Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a pro-inflammatory cytokine that is increased in the amniotic fluid in chorioamnionitis and elevated in the fetal lung with endotoxin exposure. Although GM-CSF has a pivotal role in fetal lung development, it stimulates pulmonary macrophages and is associated with the development of bronchopulmonary dysplasia (BPD). How antenatal GM-CSF results in recruitment of lung macrophage leading to BPD needs further elucidation. Hence, we used a transgenic and knock-out mouse model to study the effects of GM-CSF focusing on the fetal lung macrophage. Methods: Using bitransgenic (BTg) mice that conditionally over-expressed pulmonary GM-CSF after doxycycline treatment, and GM-CSF knock-out (KO) mice with no GM-CSF expression, we compared the ontogeny and immunophenotype of lung macrophages in BTg, KO and control mice at various prenatal and postnatal time points using flow cytometry and immunohistology. Results: During fetal life, compared to controls, BTg mice over-expressing pulmonary GM-CSF had increased numbers of lung macrophages that were CD68+ and these were primarily located in the interstitium rather than alveolar spaces. The lung macrophages that accumulated were predominantly CD11b+F4/80+ indicating immature macrophages. Conversely, lung macrophages although markedly reduced, were still present in GM-CSF KO mice. Conclusion: Increased exposure to GM-CSF antenatally, resulted in accumulation of immature macrophages in the fetal lung interstitium. Absence of GM-CSF did not abrogate but delayed the transitioning of interstitial macrophages. Together, these results suggest that other perinatal factors may be involved in modulating the maturation of alveolar macrophages in the developing fetal lung