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Is perinatal neuroendocrine programming involved in the developmental origins of metabolic disorders?  [cached]
David IW Phillips,Stephen G Matthews
World Journal of Diabetes , 2011, DOI: 10.4239/wjd.v2.i12.211
Abstract: The discovery that small size at birth and during infancy are associated with a higher risk of diabetes and related metabolic disease in later life has pointed to the importance of developmental factors in these conditions. The birth size associations are thought to reflect exposure to adverse environmental factors during early development but the mechanisms involved are still not fully understood. Animal and human work has pointed to the importance of changes in the set-point of a number of key hormonal systems controlling growth and development. These include the IGF-1/GH axis, gonadal hormones and, in particular, the systems mediating the classical stress response. Several studies show that small size at birth is linked with increased activity of the hypothalamic-pituitary-adrenal axis and sympathoadrenal system in adult life. More recent human studies have shown associations between specific adverse experiences during pregnancy, such as famine or the consumption of adverse diets, and enhanced stress responses many decades later. The mediators of these neuroendocrine responses are biologically potent and are likely to have a direct influence on the risk of metabolic disease. These neuroendocrine changes may also have an evolutionary basis being part of broader process, termed phenotypic plasticity, by which adverse environmental cues experienced during development modify the structure and physiology of the adult towards a phenotype adapted for adversity. The changes are clearly advantageous if they lead to a phenotype which is well-adapted for the adult environment, but may lead to disease if there is subsequent overnutrition or other unexpected environmental conditions.
Perinatal Programming of Asthma: The Role of Gut Microbiota
Meghan B. Azad,Anita L. Kozyrskyj
Clinical and Developmental Immunology , 2012, DOI: 10.1155/2012/932072
Abstract: Perinatal programming, a dominant theory for the origins of cardiovascular disease, proposes that environmental stimuli influence developmental pathways during critical periods of prenatal and postnatal development, inducing permanent changes in metabolism. In this paper, we present evidence for the perinatal programming of asthma via the intestinal microbiome. While epigenetic mechanisms continue to provide new explanations for the programming hypothesis of asthma development, it is increasingly apparent that the intestinal microbiota plays an independent and potentially interactive role. Commensal gut bacteria are essential to immune system development, and exposures disrupting the infant gut microbiota have been linked to asthma. This paper summarizes the recent findings that implicate caesarean delivery, breastfeeding, perinatal stress, probiotics, and antibiotics as modifiers of infant gut microbiota in the development of asthma.
OOASP: Connecting Object-oriented and Logic Programming  [PDF]
Andreas Falkner,Anna Ryabokon,Gottfried Schenner,Kostyantyn Shchekotykhin
Computer Science , 2015,
Abstract: Most of contemporary software systems are implemented using an object-oriented approach. Modeling phases -- during which software engineers analyze requirements to the future system using some modeling language -- are an important part of the development process, since modeling errors are often hard to recognize and correct. In this paper we present a framework which allows the integration of Answer Set Programming into the object-oriented software development process. OOASP supports reasoning about object-oriented software models and their instantiations. Preliminary results of the OOASP application in CSL Studio, which is a Siemens internal modeling environment for product configurators, show that it can be used as a lightweight approach to verify, create and transform instantiations of object models at runtime and to support the software development process during design and testing.
Fetal Programming of the Neuroendocrine-Immune System and Metabolic Disease  [PDF]
R. E. Fisher,M. Steele,N. A. Karrow
Journal of Pregnancy , 2012, DOI: 10.1155/2012/792934
Abstract: Adverse uterine environments experienced during fetal development can alter the projected growth pattern of various organs and systems of the body, leaving the offspring at an increased risk of metabolic disease. The thrifty phenotype hypothesis has been demonstrated as an alteration to the growth trajectory to improve the survival and reproductive fitness of the individual. However, when the intrauterine environment does not match the extrauterine environment problems can arise. With the increase in metabolic diseases in both Westernized and developing countries, it is becoming apparent that there is an environmental disconnect with the extrauterine environment. Therefore, the focus of this paper will be to explore the effects of maternal malnutrition on the offspring’s susceptibility to metabolic disorders such as obesity, cardiovascular disease, and diabetes with emphasis on programming of the neuroendocrine-immune system. 1. Introduction Early life events such as those experienced in utero have the ability to shape the phenotype of an individual in an effort to prepare the fetus for extrauterine life. This is typically referred to as developmental or fetal programming and suggests that adverse uterine environments can “permanently” alter the metabolic, endocrine, and immune function parameters of individuals well into adulthood. There appear to be critical windows during development in which the fetus is most sensitive to environmental cues, altering the projected plan of growth. For instance, maternal adversity experienced during gestation will convey signals to the fetus that the environment in which it is to live is less than optimal, altering the developmental programming of the various organs and systems in the body to better match life outside the uterus. As various tissues and systems in the body mature and differentiate at different rates during fetal development, there appear to be critical periods in development when they are most sensitive to this adversity. The hypothalamic-pituitary-adrenal axis (HPAA), for example, undergoes much growth and differentiation during early and late gestation in species such as humans, primates, and sheep, and these are the periods when it is most sensitive to developmental programming alterations [1–3]. Alterations in metabolic function such as glucose tolerance and insulin sensitivity are greatly affected during mid- and late gestation as metabolic parameters are undergoing much differentiation during this period [4]. The alterations in developmental programming trajectories are assumed to provide an
Perinatal nutritional programming of health and metabolic adult disease  [cached]
Didier Vieau
World Journal of Diabetes , 2011, DOI: 10.4239/wjd.v2.i9.133
Abstract: Data indicate that perinatal nutritional insults not onlyhave short-term consequences on the growth velocity of the fetus/neonate but also sensitize to the development of metabolic adult diseases. The pathophysiological mechanisms involved in the so-called “Developmental Origin of Health and Adult Diseases” are still largely unknown and depend on the type of alteration (nutritional, psychological, endocrine disruptors, etc.), its intensity and duration, species, sex and the time during which it is applied. Perinatal stress, via disturbances of both hypothalamo-pituitary-adrenal (HPA) axis and sympatho-adrenal-system (SAS), as well as brain-adipose axis and pancreas alterations could play a crucial role. Interestingly, it has been demonstrated that perinatal insults may be transmitted transgenerationally, suggesting that these long-term consequences may be inherited via epigenetic mechanisms. Finally, since the placenta has been demonstrated to be sensitive to perinatal nutritional manipulations, the identification of placental markers may thus represent an important new avenue to identify the more susceptible babies prone to developing metabolic diseases.
Hyperactive Neuroendocrine Secretion Causes Size, Feeding, and Metabolic Defects of C. elegans Bardet-Biedl Syndrome Mutants  [PDF]
Brian H. Lee,Jason Liu,Daisy Wong,Supriya Srinivasan,Kaveh Ashrafi
PLOS Biology , 2012, DOI: 10.1371/journal.pbio.1001219
Abstract: Bardet-Biedl syndrome, BBS, is a rare autosomal recessive disorder with clinical presentations including polydactyly, retinopathy, hyperphagia, obesity, short stature, cognitive impairment, and developmental delays. Disruptions of BBS proteins in a variety of organisms impair cilia formation and function and the multi-organ defects of BBS have been attributed to deficiencies in various cilia-associated signaling pathways. In C. elegans, bbs genes are expressed exclusively in the sixty ciliated sensory neurons of these animals and bbs mutants exhibit sensory defects as well as body size, feeding, and metabolic abnormalities. Here we show that in contrast to many other cilia-defective mutants, C. elegans bbs mutants exhibit increased release of dense-core vesicles and organism-wide phenotypes associated with enhanced activities of insulin, neuropeptide, and biogenic amine signaling pathways. We show that the altered body size, feeding, and metabolic abnormalities of bbs mutants can be corrected to wild-type levels by abrogating the enhanced secretion of dense-core vesicles without concomitant correction of ciliary defects. These findings expand the role of BBS proteins to the regulation of dense-core-vesicle exocytosis and suggest that some features of Bardet-Biedl Syndrome may be caused by excessive neuroendocrine secretion.
Hyperactive Neuroendocrine Secretion Causes Size, Feeding, and Metabolic Defects of C. elegans Bardet-Biedl Syndrome Mutants  [PDF]
Brian H. Lee,Jason Liu,Daisy Wong,Supriya Srinivasan,Kaveh Ashrafi
PLOS Biology , 2011, DOI: 10.1371/journal.pbio.1001219
Abstract: Bardet-Biedl syndrome, BBS, is a rare autosomal recessive disorder with clinical presentations including polydactyly, retinopathy, hyperphagia, obesity, short stature, cognitive impairment, and developmental delays. Disruptions of BBS proteins in a variety of organisms impair cilia formation and function and the multi-organ defects of BBS have been attributed to deficiencies in various cilia-associated signaling pathways. In C. elegans, bbs genes are expressed exclusively in the sixty ciliated sensory neurons of these animals and bbs mutants exhibit sensory defects as well as body size, feeding, and metabolic abnormalities. Here we show that in contrast to many other cilia-defective mutants, C. elegans bbs mutants exhibit increased release of dense-core vesicles and organism-wide phenotypes associated with enhanced activities of insulin, neuropeptide, and biogenic amine signaling pathways. We show that the altered body size, feeding, and metabolic abnormalities of bbs mutants can be corrected to wild-type levels by abrogating the enhanced secretion of dense-core vesicles without concomitant correction of ciliary defects. These findings expand the role of BBS proteins to the regulation of dense-core-vesicle exocytosis and suggest that some features of Bardet-Biedl Syndrome may be caused by excessive neuroendocrine secretion.
Developmental Immunotoxicity, Perinatal Programming, and Noncommunicable Diseases: Focus on Human Studies  [PDF]
Rodney R. Dietert
Advances in Medicine , 2014, DOI: 10.1155/2014/867805
Abstract: Developmental immunotoxicity (DIT) is a term given to encompass the environmentally induced disruption of normal immune development resulting in adverse outcomes. A myriad of chemical, physical, and psychological factors can all contribute to DIT. As a core component of the developmental origins of adult disease, DIT is interlinked with three important concepts surrounding health risks across a lifetime: (1) the Barker Hypothesis, which connects prenatal development to later-life diseases, (2) the hygiene hypothesis, which connects newborns and infants to risk of later-life diseases and, (3) fetal programming and epigenetic alterations, which may exert effects both in later life and across future generations. This review of DIT considers: (1) the history and context of DIT research, (2) the fundamental features of DIT, (3) the emerging role of DIT in risk of noncommunicable diseases (NCDs) and (4) the range of risk factors that have been investigated through human research. The emphasis on the human DIT-related literature is significant since most prior reviews of DIT have largely focused on animal research and considerations of specific categories of risk factors (e.g., heavy metals). Risk factors considered in this review include air pollution, aluminum, antibiotics, arsenic, bisphenol A, ethanol, lead (Pb), maternal smoking and environmental tobacco smoke, paracetamol (acetaminophen), pesticides, polychlorinated biphenyls, and polyfluorinated compounds. 1. Introduction Early-life environmental insults affecting the developing immune system can have significant health ramifications not only for the exposed offspring but also potentially extending to additional generations. Developmental immunotoxicity (DIT) appears to play a significant role in the current global epidemic of non-communicable diseases (NCDs) [1, 2]. This review of DIT begins with the history of DIT placed in the context of the area of immunology known as immunotoxicology and charts the emergence of recent concepts concerning early developmental programming as it impacts later-life health. It also describes the current state of the science for DIT and the likely applications of DIT assessment as it may impact both human health and environmental protection. In particular, the paper discusses (1) the history of DIT research, (2) the role of critical windows of vulnerability for the developing immune system, (3) frequent outcomes of DIT, (4) consideration of the microbiome in DIT, (5) the role of prenatal epigenetic alterations in immunotoxicity, and (6) the connection between DIT,
The Formation of Uranus and Neptune in Solid-Rich Feeding Zones: Connecting Chemistry and Dynamics  [PDF]
Sarah E. Dodson-Robinson,Peter Bodenheimer
Physics , 2009, DOI: 10.1016/j.icarus.2009.11.021
Abstract: The core accretion theory of planet formation has at least two fundamental problems explaining the origins of Uranus and Neptune: (1) dynamical times in the trans-Saturnian solar nebula are so long that core growth can take > 15 Myr, and (2) the onset of runaway gas accretion that begins when cores reach 10 Earth masses necessitates a sudden gas accretion cutoff just as the ice giant cores reach critical mass. Both problems may be resolved by allowing the ice giants to migrate outward after their formation in solid-rich feeding zones with planetesimal surface densities well above the minimum-mass solar nebula. We present new simulations of the formation of Uranus and Neptune in the solid-rich disk of Dodson-Robinson et al. (2009) using the initial semimajor axis distribution of the Nice model (Gomes et al. 2005; Morbidelli et al. 2005; Tsiganis et al. 2005), with one ice giant forming at 12 AU and the other at 15 AU. The innermost ice giant reaches its present mass after 3.8-4.0 Myr and the outermost after 5.3-6 Myr, a considerable time decrease from previous one-dimensional simulations (e.g. Pollack et al. 1996). The core masses stay subcritical, eliminating the need for a sudden gas accretion cutoff. Our calculated carbon mass fractions of 22% are in excellent agreement with the ice giant interior models of Podolak et al. (1995) and Marley et al. (1995). Based on the requirement that the ice giant-forming planetesimals contain >10% mass fractions of methane ice, we can reject any solar system formation model that initially places Uranus and Neptune inside the orbit of Saturn. We also demonstrate that a large population of planetesimals must be present in both ice giant feeding zones throughout the lifetime of the gaseous nebula.
Perinatal Programming of Childhood Asthma: Early Fetal Size, Growth Trajectory during Infancy, and Childhood Asthma Outcomes
Steve Turner
Clinical and Developmental Immunology , 2012, DOI: 10.1155/2012/962923
Abstract: The “fetal origins hypothesis” or concept of “developmental programming” suggests that faltering fetal growth and subsequent catch-up growth are implicated in the aetiology of cardiovascular disease. Associations between reduced birth weight, rapid postnatal weight gain, and asthma suggest that there are fetal origins to respiratory disease. The present paper first summarises the literature relating birth weight and post natal growth trajectories to asthma outcomes. Second, issues regarding the interpretation of antenatal fetal ultrasound measurements are discussed. Finally, recent reports linking antenatal measurement and growth trajectory to early childhood asthma outcomes are discussed. Understanding the nature and timing of factors which influence antenatal growth may give important insight into the antecedents of early-onset asthma with implications for interventions.
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