During the latter half of the twentieth century, an explosion of research elucidated a growing number of causes of disease and contributors to health. Biopsychosocial models that accounted for the wide range of factors influencing health began to replace outmoded and overly simplified biomedical models of disease causation. More recently, models of lifecourse health development (LCHD) have synthesized research from biological, behavioral and social science disciplines, defined health development as a dynamic process that begins before conception and continues throughout the lifespan, and paved the way for the creation of novel strategies aimed at optimization of individual and population health trajectories. As rapid advances in epigenetics and biological systems research continue to inform and refine LCHD models, our healthcare delivery system has struggled to keep pace, and the gulf between knowledge and practice has widened. This paper attempts to chart the evolution of the LCHD framework, and illustrate its potential to transform how the MCH system addresses social, psychological, biological, and genetic influences on health, eliminates health disparities, reduces chronic illness, and contains healthcare costs. The LCHD approach can serve to highlight the foundational importance of MCH, moving it from the margins of national debate to the forefront of healthcare reform efforts. The paper concludes with suggestions for innovations that could accelerate the translation of health development principles into MCH practice.
Preterm birth represents the most significant problem in maternal-child health. The ongoing search to elucidate its underlying causes and pathophysiological mechanisms has identified maternal stress as a variable of interest. Based on emerging models of causation of complex common disorders, we suggest that the effects of maternal stress on risk of preterm birth may, for the most part, vary as a function of context. In this paper we focus on select key issues and questions that highlight the need to develop a better understanding of which particular subgroups of pregnant women, under what circumstances, and at which stage(s) of gestation, may be especially vulnerable to the potentially detrimental effects of maternal stress. Our discussion addresses issues related to the characterization and assessment of maternal stress and candidate biological (maternal-placental-fetal endocrine, immune, vascular and genetic) mechanisms. We propose the adoption of newer approaches (ecological momentary assessment) and a life-course perspective to further our understanding of the contribution of maternal stress to preterm birth.
An important step in the herpesvirus life cycle is the switch from latency to lytic reactivation. In order to study the life cycle of Kaposi's sarcoma-associated herpesvirus (KSHV), we developed a gene expression system in KSHV-infected primary effusion lymphoma cells. This system uses Flp-mediated efficient recombination and tetracycline-inducible expression. The Rta transcriptional activator, which acts as a molecular switch for lytic reactivation of KSHV, was efficiently integrated downstream of the Flp recombination target site, and its expression was tightly controlled by tetracycline. Like stimulation with tetradecanoyl phorbol acetate (TPA), the ectopic expression of Rta efficiently induced a complete cycle of viral replication, including a well-ordered program of KSHV gene expression and production of infectious viral progeny. A striking feature of Rtamediated lytic gene expression was that Rta induced KSHV gene expression in a more powerful and efficient manner than TPA stimulation, indicating that Rta plays a central, leading role in KSHV lytic gene expression. Thus, our streamlined gene expression system provides a novel means not only to study the effects of viral gene products on overall KSHV gene expression and replication, but also to understand the natural viral reactivation process.
Future research on racial disparities in birth outcomes needs to examine differential exposures to risk and protective factors not only during pregnancy, but over the life course of women. Eliminating disparities requires interventions and policy development that are more longitudinally and contextually integrated than currently prevail.
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