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The goals of which are to divert the development of lung disease mood disorder characteristics buy on line bupropion, and alleviate the associated global health burdens. A broad range of environmental stressors (pre- and postnatal) have been shown to affect health outcomes. Stressors include nutrition, environmental stress and, important for this volume, toxic exposures. Disease outcomes following pre- and early postnatal exposures cover a broad range of physiologic processes; many of which constitute major public health concerns. Obesity, diabetes, hypertension, cardiovascular disease, immune and autoimmune diseases, neurodevelopmental and neurodegenerative diseases, fertility, cancers, depression, psychiatric disorders, and finally lung disease all have origins, at least in part, in early-life environmental exposures (reviewed in Heindel et al. The Fourth Conference on Prenatal Programming and Toxicity in Boston, in 2014, focused on the connections between early environmental exposures and later onset disease, as well as the substantial role that the placenta plays in influencing development and programming of disease (Grandjean et al. Developmental programming following adverse environmental exposures during development results in alterations in the normal developmental trajectory and "programs" changes in the structure or function of an organ. Alternatively, programming can be more subtle; producing effects not obvious until later in life, or producing effects not elicited until the organ is faced with an additional stressor (Table 1). Understanding of the developmental programming of lung disease is an important public heath directive which has gained momentum over the last decade (Stocks et al. The adverse environmental exposures best understood in the context of programming of lung disease occur during the second half of human gestation, or in the early postnatal periodda time collectively referred to as the perinatal period. The perinatal period corresponds to periods of ongoing development of a number of organs, including the lung (Burri, 1984). A wide range of adverse exposures have been studied in the context of programming of lung disease. Some adverse exposures affect the fetus/neonate directly, while some adverse exposures affect the fetus secondary to effects on the placenta. Table 1 Aspects of environment and chemical exposures on developmental programming Functional l Developmental Exposure act during specific windows of developmental plasticity l Exposures result in sex-divergent effects l Genetic l Exposure interacts with fixed genetic Exposures cause subtle functional changes which may not be apparent without a second components l Exposures act via alteration in epigenetic marks hit later in life l Latency between exposure and disease/ which may be irreversible l Exposure effects can be transmitted via the dysfunction germ line to future generations Adapted from Heindel, J. Endocrinology 156, 3416­3421 Environmental Exposures and Developmental Programming of the Lung 15. The placenta acts as the lifeline for the fetus, providing nutrients and oxygen to the fetus while removing waste products from the fetal circulation. Another important function of the placenta is to protect the fetus from potential toxic substances. Disruption of placental development and function by environmental exposures therefore effects fetal development; often quite profoundly. An understanding of basic placental biology is necessary to appreciate the effects of toxic exposures on placental function. The origins of the placenta are the trophoblast cells surrounding the blastocyst and early embryo. The trophoblasts facilitate implantation of the embryo into the maternal uterine wall, rupturing maternal capillaries and establishing an interface between maternal blood and the embryonic extracellular fluid. In normal placentation the embryonic vessels, covered by fetal stem cells called cytotrophoblasts, give rise to the fetal chorionic villi which further branch into smaller, terminal villi, and form the interface between maternal and fetal blood flow. When cytotrophoblasts invade the uterine wall, and disrupt the smooth muscle of maternal vessels, spiral arteries are formed in the uterine decidua. This invasion transforms the maternal vasculature to a low-resistance, high-capacitance system and permits increased blood flow to the fetal side. The projections are surrounded by multinucleated syncytiotrophoblasts which secrete hormones that protect the pregnancy and maintain the uterine lining until the syncytiotrophoblast is mature enough to support the pregnancy at approximately the 4th month of gestation. Maternal blood from the spiral arteries surrounds the terminal villi and syncytiotrophoblast layer, providing the primary location for maternal-fetal exchange of nutrients and oxygen (Burton and Fowden, 2015). Environmental exposures frequently result in alterations in placental vascularity and function. Maternal tobacco use contributes to programming of the fetus directly via effects of nicotine and other toxic metabolites, as well as indirectly via effects on the placenta. Notably, incidences of maternal smoking during the last 3 months of pregnancy are as high as 29% in some states. Maternal tobacco smoke exposure has been linked to a number of negative effects on the developing fetus. Evidence from epidemiological studies supports the link between maternal tobacco smoke exposure and negative effects on lung function, as well as increased wheezing and asthma (Cunningham et al.

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Animal models have also shed light on the effects of prenatal exposures on the response to postnatal second hit mood disorder lesson plans purchase bupropion 150 mg on-line. Mice exposed to second-hand smoke during the prenatal period were reexposed to second-hand smoke in adulthood. Compared to mice with no exposure, or exposure during either the prenatal period or the postnatal period (but not both), mice with prenatal and postnatal exposures had lung remodeling with increased collagen deposition, increased proinflammatory cytokines gene expression, and increased profibrotic gene expression (Xiao et al. Impaired alveolar formation, decreased alveolar number, and decreased internal surface area are evident in sheep and baboons born preterm and managed with mechanical ventilation (Albertine et al. Oxygen toxicity contributes, at least in part, to altered lung structure in preterm animals managed with mechanical ventilation. When the immature lungs of newborn mice are exposed to hyperoxia (65% O2) in the neonatal period, the lung in adulthood is altered and lung function is reduced. The severity and timing of perinatal exposures affects the response of the lung, both in terms of severity and lung phenotype (JossMoore and Lane, 2009; Harding and Maritz, 2012; Briana and Malamitsi-Puchner, 2012). These early changes in alveolar structure result in a lung with different inherent characteristics. Notably, the gene expression changes, and resulting gene characteristics altered by perinatal insults become the basis upon which additional growth and development, as well as response to injury are set. Gene expression and the regulation of gene expression are governed by epigenetics. Regulation of gene expression is maintained by epigenetic Environmental Exposures and Developmental Programming of the Lung 157 mechanisms. Throughout development, and beyond, genes may be turned on or off have expression that is increased or decreased in magnitude, and have expression localized to specific cells. This spatial and temporal regulation of gene expression is controlled by interactions between the transcription machinery, transcriptional coactivators and repressors, and the epigenetic code. Excellent reviews of the general mechanisms of transcription and epigenetic regulation of gene expression are available (Voss and Hager, 2014; Klose and Bird, 2006; Zentner and Henikoff, 2013). Because of this, each cell type has a unique epigenetic profile, or pattern of epigenetic marks. When perinatal insults alter that unique pattern, altered gene expression, and alterations in the cellular characteristics result. Spatial and temporal changes in the expression of genes that govern lung growth and development, as well as reprogramming of lung cells, alter the immediate response of the lung, and primes the lung for altered responses to future insults. While genetic susceptibility is also an important component of developmental programming here we will focus only on epigenetics because epigenetic regulation is responsive to environmental cues, such as toxin exposure. Within the developing lung, there are three major consequences of altered epigenetics and gene expression. First, lung structure and/or function may be altered secondary to changes in cell differentiation and cell-to-cell communications. The second effect of altered epigenetic profiles involves the concept that throughout development the epigenetic profile of the genome is dynamic and changes to produce a developmentally appropriate expression profile. When the epigenome of a cell is altered at a developmentally sensitive time point, the "new" epigenetic platform becomes the basis upon which subsequent epigenetic changes are built. The effect of altering the epigenome during development is an increasing deviation from "normal" during and after development. The third consequence of changing lung cell epigenetics during development is an epigenome that is primed to direct gene expression differently in response to a second hit. However, whether epigenetic phenomena are causative in the programming of lung disease, or a biomarker of an event, this is an important arena of study. CpG motifs may be clustered in dense regions known as CpG "islands," or dispersed at low density throughout the genome (Gardiner-Garden and Frommer, 1987). CpG islands are commonly found in promoter regions of mammalian genes, and are often unmethylated in transcriptionally active genes (Huh et al. Unlike promoter regions, coding regions and regions between genes contain a low density of CpGs. These intergenic and intragenic CpGs and are more frequently methylated, and may be associated with regulation of alternative splicing (Illingworth et al. The agouti gene encodes a peptide that stimulates production of a yellow pigment which normally is only transiently expressed in the hair follicle, producing a brown coat color. In the viable yellow agouti mouse the agouti gene contains a retrotransposon insertion with a promoter that drives ectopic expression of agouti, which results in a yellow coat color.

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Particulate matter exposure in cars is associated with cardiovascular effects in healthy young men anxiety rash bupropion 150 mg purchase with amex. Diesel exhaust particulate induces pulmonary and systemic inflammation in rats without impairing endothelial function ex vivo or in vivo. Inhalation of ultrafine and fine particulate matter disrupts systemic vascular function. Montelukast prevents vascular endothelial dysfunction from internal combustion exhaust inhalation during exercise. Identification of chemical components of combustion emissions that affect pro-atherosclerotic vascular responses in mice. Production of arrhythmias by elevated carboxyhemoglobin in patients with coronary artery disease. Long-term air pollution exposure and acceleration of atherosclerosis and vascular inflammation in an animal model. Nitrogen dioxide air pollution near ambient levels is an atherogenic risk primarily in obese subjects: A brief communication. Exposure to inhaled particulate matter impairs cardiac function in senescent mice. Effects of ozone and particulate matter on cardiac mechanics: Role of the atrial natriuretic peptide gene. C(6)(0) exposure augments cardiac ischemia/reperfusion injury and coronary artery contraction in Sprague Dawley rats. Differential regulation of the lung endothelin system by urban particulate matter and ozone. Differential cardiopulmonary effects of size-fractionated ambient particulate matter in mice. Evidence for an association between air pollution and daily stroke admissions in Kaohsiung, Taiwan. Surface area-dependence of gas-particle interactions influences pulmonary and neuroinflammatory outcomes. Effects of acute exposure to ozone on heart rate and blood pressure of the conscious rat. Ultrafine carbon particle mediated cardiovascular impairment of aged spontaneously hypertensive rats. Atherosclerotic plaque rupturedPathologic basis of plaque stability and instability. Associations between outdoor air pollution and emergency department visits for stroke in Edmonton, Canada. Autism spectrum disorder: Interaction of air pollution with the met receptor tyrosine kinase gene. Ambient air pollution is associated with increased risk of hospital cardiac readmissions of myocardial infarction survivors in five European cities. Specific phospholipid oxidation products inhibit ligand activation of Toll-like receptors 4 and 2. Effect of changes in ambient temperature on extrapulmonary physiological parameters. Cardiac arrhythmia induction after exposure to residual oil fly ash particles in a rodent model of pulmonary hypertension. Acute exposure to diesel exhaust impairs nitric oxide-mediated endothelial vasomotor function by increasing endothelial oxidative stress. Air pollution and hospital admissions for ischemic and hemorrhagic stroke among medicare beneficiaries. Particulate air pollution and hospital admissions for congestive heart failure in seven United States cities. Relation of long-term exposure to air pollution to brachial artery flow-mediated dilation and reactive hyperemia. Cardiovascular remodeling in response to long-term exposure to fine particulate matter air pollution. Retinal microvascular abnormalities and blood pressure in older people: the cardiovascular health study. Retinal microvascular abnormalities and 10-year cardiovascular mortality: A populationbased case-control study. Effect of early particulate air pollution exposure on obesity in mice: Role of p47phox.

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In such hypoxic locations depression diagnosis code purchase discount bupropion online, epithelial recovery is thought to be impaired through feedback effects involving tubule stress, interstitial pathology involving capillary endothelium and pericytes, and inflammation. Large scale physiological autophagy is the presumed explanation for this remarkable transformation. Dedifferentiation, migration, and proliferation of the surviving epithelium is driven and coordinated by complex and intricate signaling programs triggered soon after injury. These autocrine and paracrine signaling events include the production and secretion of a multitude of growth factors, cytokines and autacoids by surviving epithelium (Basile et al. Notably, the abnormal undifferentiated cells are growth arrested, morphologically atrophic, and display intense profibrotic signaling activity (Lan et al. In all the micrographs, well differentiated and atrophic epithelium are seen in whole tubules, or parts of tubules often as small clusters or single cells, with sharp contrasts between the two. The close association of undifferentiated atrophic epithelium showing persistently increased signaling activity and expression of profibrotic peptides with immediately adjacent or surrounding fibrosis (Lan et al. Furthermore, signaling intensities as well as signaling protein and growth factor expression in these abnormal tubules increases progressively with time to strikingly high levelsdfar higher than during the earlier stages of physiological regeneration (Geng et al. These findings and other data suggesting that pyruvate dehydrogenase activity may also become suppressed show that a profound shift from mitochondrial oxidative metabolism to glycolysis takes place in regenerating tubules and persists pathologically in tubules of the failed differentiation phenotype (Lan et al. Premature growth arrest of proliferating tubule epithelium has been invoked as a possible cause of the profibrotic tubule phenotype (Yang et al. Ischemia injures not only tubule epithelium but also capillary endothelium (Molitoris and Sutton, 2004; Sutton et al. Moreover, several studies have provided evidence for tubule paracrine effects that produce interstitial pathology. Additionally, during reperfusion after ischemia, endothelial cells become injured and activated independently of the actions of tubules. Regardless of whether endothelial activation occurs primarily or secondarily, it sets in motion cellular events that result in early neutrophil chemotaxis, adhesion, and infiltration followed by the recruitment of monocytes and lymphocytes. Monocytes undergo transformation to macrophages and these cells, lymphocytes and resident dendritic cells that also become activated, produce and secrete a multitude of cytokines, growth factors, and autacoids. These humoral factors and others released by regenerating tubule cells are candidate ligands for receptors in resident fibroblast progenitors that initiate and maintain the signaling that results in their activation, proliferation, and fibrosis. The majority of resident fibroblast precursors in the interstitium are pericytes (Duffield, 2014; Humphreys et al. Lineage analysis studies have shown that FoxD1 expressing embryonic progenitors give rise to adult pericytes (Humphreys et al. Signaling interactions between endothelial cells and pericytes are required to maintain capillary integrity on one hand and pericyte quiescence on the other. Normal endothelial­pericyte interactions are disrupted by activating signals from several sources that trigger intercellular proteolysis and dissociate pericytes from endothelial cells. The interstitium becomes widened by proliferating myofibroblasts and connective tissue, and the injured endothelium regresses, causing capillary rarefaction. Recent studies have yielded important information regarding endothelial­pericyte signaling that becomes perturbed to bring about fibrosis. These proteases cleave connective tissue molecules and disrupt cellular interactions to facilitate the movement of pericytes away from capillaries. Thus, specific inhibition of pericyte protease activity may prove to be one approach to promote normal pericyte­endothelial interactions and prevent fibrogenesis. Pericyte­endothelial cross-talk also includes bidirectional signaling between pairs of Ephrin B2 and Ephrin B4 receptors present in both types of cells. On the other hand, disruption of Ephrin B2 reverse signaling in pericytes increased their motility and decreased their ability to promote stability of endothelial microvessels in culture. A variety of other factors also affect fibrosis development after injury through their actions on pericytes. These actions appear to take place both in tubule epithelium and pericytes but it is as yet unclear which cell type is more critical. Other candidate pathways to fibrosis include hedgehog signaling in which interstitial cells are targeted by tubule epithelium derived hedgehog ligands (Fabian et al. These monocytes become activated through the classical pathway to become M1 macrophages that are proinflammatory and contribute to kidney injury.

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