A well-documented and accepted explanation of the origins of diseases that occur with a high frequency in adulthood is the relationship between an adverse intrauterine environment during fetal life and development of diseases including hypertension, diabetes, obesity, insulin resistance, and metabolic syndrome. Several epidemiological studies have served as the basis for investigating actual studies determining cell and molecular mechanisms behind these alterations. However, these mechanisms are at present partially described. It is expected that continuation of these studies will yield further evidence regarding potential aspects such as timing in pregnancy and consequences of these alterations in the intrauterine life on the appearance and management of adulthood diseases. In addition, few studies have addressed concerning whether the preconceptional period is also involved in this phenomenon.

We invite investigators to contribute original research articles as well as review articles that will stimulate ongoing efforts for a better understanding of the cell and molecular mechanisms underlying fetal programming of adult diseases. We will be looking for contributions over a wide area of expertise but particularly those studying the vascular physiology/pathophysiology of diseases of pregnancy that could result in programming of the fetus. The areas of systemic physiology, cell physiology, molecular physiology, epigenetics, proteomics, and metabolomics are welcomed. Specific studies using animal models and cell lines are acceptable. Potential topics include, but are not limited to:

• Placenta angiogenesis and vasculogenesis
• Placental vascular dysfunction
• Placental microvascular and macrovascular endothelial dysfunction
• Preconception care of pregnancy and programming of adult diseases
• Fetal evidence for programming of adult diseases (early evidence)
• Newborn evidence for programming of adult diseases (early evidence)
• Epigenetics and placenta programming
• Proteomics and metabolomics as tools in programming
• Lipid signalling in the placenta
• Insulin signalling in the placenta
• Nucleoside and nucleotide signalling in the placenta
• Obesity in pregnancy
• Oxidative stress in pregnancy
• Gestational diabetes mellitus
• Preeclampsia
• Intrauterine growth restriction
• Premature rupture of membranes (PROM)
• Fetal hypoxia

Before submission authors should carefully read over the journal’s Author Guidelines which are located at http://www.hindawi.com/journals/bmri/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/submit/journals/bmri/physiology/preg/ according to the following timetable: