PIP: 43 determinants of low birth weight were analyzed from 895 published papers in the English and French literature from 1970-1984 The assessment was limited to singleton births of women living at sea level with no chronic illness; rare factors and complications of pregnancy were excluded The 43 factors were categorized as genetic and constitutional, demographic and psychosocial, obstetric, nutritional, maternal morbidity during pregnancy, toxic exposure and antenatal care The existence and magnitude of a causal effect on birth weight, gestational age, prematurity and intrauterine growth retardation were determined by a set of methodological standards In developed countries, the most important factor was cigarette smoking, followed by nutrition and pre-pregnancy weight In developing countries the major determinants were racial origin, nutrition, low pre-pregnancy weight, short maternal stature, and malaria Pre-pregnancy weight, prior premature birth or miscarriage, diethylstilbestrol exposure and smoking were major determinants of gestational duration, but the majority of prematurity was unexplained in both developed and developing countries There is a need for future research on the effect of maternal work, prenatal care, and certain vitamin and mineral deficiencies on intrauterine growth, and the effect of genital tract infection, prenatal care, maternal employment, stress and anxiety on prematurity

Determinants of low birth weight: Methodological assessment and meta-analysis

Prolactin is a protein hormone of the anterior pituitary gland that was originally named for its ability to promote lactation in response to the suckling stimulus of hungry young mammals. We now know that prolactin is not as simple as originally described. Indeed, chemically, prolactin appears in a multiplicity of posttranslational forms ranging from size variants to chemical modifications such as phosphorylation or glycosylation. It is not only synthesized in the pituitary gland, as originally described, but also within the central nervous system, the immune system, the uterus and its associated tissues of conception, and even the mammary gland itself. Moreover, its biological actions are not limited solely to reproduction because it has been shown to control a variety of behaviors and even play a role in homeostasis. Prolactin-releasing stimuli not only include the nursing stimulus, but light, audition, olfaction, and stress can serve a stimulatory role. Finally, although it is well known that dopamine of hypothalamic origin provides inhibitory control over the secretion of prolactin, other factors within the brain, pituitary gland, and peripheral organs have been shown to inhibit or stimulate prolactin secretion as well. It is the purpose of this review to provide a comprehensive survey of our current understanding of prolactin's function and its regulation and to expose some of the controversies still existing.

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Prolactin: Structure, Function, and Regulation of Secretion

Since the first identification of renin by Tigerstedt and Bergmann in 1898, the renin-angiotensin system (RAS) has been extensively studied. The current view of the system is characterized by an increased complexity, as evidenced by the discovery of new functional components and pathways of the RAS. In recent years, the pathophysiological implications of the system have been the main focus of attention, and inhibitors of the RAS such as angiotensin-converting enzyme (ACE) inhibitors and angiotensin (ANG) II receptor blockers have become important clinical tools in the treatment of cardiovascular and renal diseases such as hypertension, heart failure, and diabetic nephropathy. Nevertheless, the tissue RAS also plays an important role in mediating diverse physiological functions. These focus not only on the classical actions of ANG on the cardiovascular system, namely, the maintenance of cardiovascular homeostasis, but also on other functions. Recently, the research efforts studying these noncardiovascular effects of the RAS have intensified, and a large body of data are now available to support the existence of numerous organ-based RAS exerting diverse physiological effects. ANG II has direct effects at the cellular level and can influence, for example, cell growth and differentiation, but also may play a role as a mediator of apoptosis. These universal paracrine and autocrine actions may be important in many organ systems and can mediate important physiological stimuli. Transgenic overexpression and knock-out strategies of RAS genes in animals have also shown a central functional role of the RAS in prenatal development. Taken together, these findings may become increasingly important in the study of organ physiology but also for a fresh look at the implications of these findings for organ pathophysiology.

Physiology of local renin-angiotensin systems.

Oxidative stress and gene regulation.

Indoor air quality and health

The biological effects of carbon monoxide on the pregnant woman, fetus, and newborn infant☆

Mercury toxicity in the pregnant woman, fetus, and newborn infant. A review.

Objective: Maternal protein malnutrition during pregnancy can lead to significant alterations in the systemic renin-angiotensin system (RAS) in the fetus. All components of the RAS are present in brain and may be altered in many disease states. Importantly, these disorders are reported to be of higher incidence in prenatally malnourished individuals. In the current study, we tested the hypothesis that antenatal maternal low protein diet (MLPD) leads to epigenetic changes and alterations in gene expression of brain RAS of the mouse fetus. Methods: Mice dams were given control and 50% MLPD during second half of the gestation. We analyzed messenger RNA (mRNA), microRNA (miRNA), promoter DNA methylation, and protein expression of various RAS genes in the fetal offspring. Results: As a consequence of 50% MLPD, fetal brains showed increased mRNA expression of angiotensinogen and angiotensin converting enzyme-1 (ACE-1), with a decrease in mRNA levels of angiotensin II type-2 (AT2) receptors. In contrast, while a...

Brain renin-angiotensin system: fetal epigenetic programming by maternal protein restriction during pregnancy.

Successful placental development is crucial for optimal growth, development, maturation and survival of the embryo/fetus into adulthood. Numerous epidemiologic and experimental studies have demonstrated the profound influence of intrauterine environment on life, and the diseases to which one is subject as an adult. For the most part, these invidious influences, whether maternal hypoxia, protein or caloric deficiency or excess, and others, represent types of maternal stress. In the present review, we examine certain aspects of gene expression in the placenta as a consequence of maternal stressors. To examine these issues in a controlled manner, and in a species in which the genome has been sequenced, most of these reported studies have been performed in the mouse. Although each individual maternal stress is characterized by up- or down-regulation of specific genes in the placenta, functional analysis reveals some patterns of gene expression common to the several forms of stress. Of critical importance, these genes include those involved in DNA methylation and histone modification, cell cycle regulation, and related global pathways of great relevance to epigenesis and the developmental origins of adult health and disease.

http://www.ijdb.ehu.es/web/descarga/paper/082770cg

Gene expression in the placenta: maternal stress and epigenetic responses

In order to determine the relative roles of O2 tension and content, CO2 tension, hydrogen ion concentration, arterial blood pressure, and cardiac output in the regulation of fetal cerebral blood flow (CBF), we used radioactively labeled microspheres to measure flow to 20 major brain regions in 24 chronically catheterized fetal lambs. We continually monitored fetal heart rate and blood pressure, and periodically measured arterial Po2, Pco2, pH, and hematocrit. In addition to CBF measurements during control periods, we measured CBF during: 1) hypoxia (O2 content 50 torr) induced by increasing the maternal inspired CO2, 3) acidosis and alkalosis (7.60 > pH > 6.60) induced by infusing lactic acid or bicarbonate into the fetus, and 4) hypotension (blood pressure 55 mm Hg) induced by rapidly phlebotomizing or transfusing the fetus. We used multiple regression analysis and analysis of covariance to examine the dependence of total cerebral blood flow on arterial O2 tension and content, CO2 tension, pH, blood pressure, and cardiac output. The results demonstrated that 1) fetal CBF increased linearly as oxygen tension or content decreased and a hierarchy of responsivity occurred (brainstem > subcortex and cortex), 2) fetal CBF increased as carbon dioxide tension increased with a different hierarchy of responsivity (brainstem > subcortex > cortex), and 3) autoregulation of fetal CBF over a wide range of blood pressure or cardiac output was maintained for both total CBF and the various brain regions examined.

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Lawrence D. Longo

Papers

The biological effects of carbon monoxide on the pregnant woman, fetus, and newborn infant☆

Mercury toxicity in the pregnant woman, fetus, and newborn infant. A review.

Brain renin-angiotensin system: fetal epigenetic programming by maternal protein restriction during pregnancy.

Gene expression in the placenta: maternal stress and epigenetic responses

Regional Cerebral Blood Flow: Studies in the Fetal Lamb during Hypoxia, Hypercapnia, Addosis, and Hypotension