Birth Defects Research Part C-Embryo Today-Reviews最新文献

{"title":"Fetal programming of neuropsychiatric disorders.","authors":"G. Faa, M. Manchia, R. Pintus, C. Gerosa, M. A. Marcialis, V. Fanos","doi":"10.1002/bdrc.21139","DOIUrl":"https://doi.org/10.1002/bdrc.21139","url":null,"abstract":"Starting from the Developmental Origins of Health and Disease (DOHaD) hypotheses proposed by David Barker, namely fetal programming, in the past years, there is a growing evidence of the major role played by epigenetic factors during the intrauterine life and the perinatal period. Furthermore, it has been assessed that these factors can affect the health status in infancy and even in adulthood. In this review, we focus our attention on the fetal programming of the brain, analyzing the most recent literature concerning the epigenetic factors that can influence the development of neuropsychiatric disorders such as bipolar disorders, major depressive disorders, and schizophrenia. The perinatal epigenetic factors have been divided in two main groups: maternal factors and fetal factors. The maternal factors include diet, smoking, alcoholism, hypertension, malnutrition, trace elements, stress, diabetes, substance abuse, and exposure to environmental toxicants, while the fetal factors include hypoxia/asphyxia, placental insufficiency, prematurity, low birth weight, drugs administered to the mother or to the baby, and all factors causing intrauterine growth restriction. A better comprehension of the possible mechanisms underlying the pathogenesis of these diseases may help researchers and clinicians develop new diagnostic tools and treatments to offer these patients a tailored medical treatment strategy to improve their quality of life. Birth Defects Research (Part C) 108:207-223, 2016. © 2016 Wiley Periodicals, Inc.","PeriodicalId":55352,"journal":{"name":"Birth Defects Research Part C-Embryo Today-Reviews","volume":"1 1","pages":"207-223"},"PeriodicalIF":0.0,"publicationDate":"2016-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72908756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effect of maternal exposure to endocrine disrupting chemicals on fetal and neonatal development: A review on the major concerns.","authors":"M. Mallozzi, G. Bordi, Chiara Garò, D. Caserta","doi":"10.1002/bdrc.21137","DOIUrl":"https://doi.org/10.1002/bdrc.21137","url":null,"abstract":"There is a widespread exposure of general population, including pregnant women and developing fetuses, to the endocrine disrupting chemicals (EDCs). These chemicals have been reported to be present in urine, blood serum, breast milk, and amniotic fluid. Endocrine disruptions induced by environmental toxicants have placed a heavy burden on society, since environmental exposures during critical periods of development can permanently reprogram normal physiological responses, thereby increasing susceptibility to disease later in life-a process known as developmental reprogramming. During development, organogenesis and tissue differentiation occur through a continuous series of tightly-regulated and precisely-timed molecular, biochemical, and cellular events. Humans may encounter EDCs daily and during all stages of life, from conception and fetal development through adulthood and senescence. Nevertheless, prenatal and early postnatal windows are the most critical for proper development, due to rapid changes in system growth. Although there are still gaps in our knowledge, currently available data support the urgent need for health and environmental policies aimed at protecting the public and, in particular, the developing fetus and women of reproductive age. Birth Defects Research (Part C) 108:224-242, 2016. © 2016 Wiley Periodicals, Inc.","PeriodicalId":55352,"journal":{"name":"Birth Defects Research Part C-Embryo Today-Reviews","volume":"11 1","pages":"224-242"},"PeriodicalIF":0.0,"publicationDate":"2016-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87820647","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fine particle-induced birth defects: Impacts of size, payload, and beyond","authors":"Chuanfeng Teng,&nbsp;Zhiping Wang,&nbsp;Bing Yan","doi":"10.1002/bdrc.21136","DOIUrl":"10.1002/bdrc.21136","url":null,"abstract":"<p>Worldwide epidemiological studies have shown that exposures to particulate matters (PMs), such as PM_2.5 or PM₁₀, during pregnancy cause birth defects in the newborn. Although mechanistic understanding of such effects are not available, recent research using murine models highlights some key progress: (1) toxicity caused by PMs is a combined effects of particles and the adsorbed toxic pollutants, such as heavy metals, persistent organic pollutants, bacteria, and virus. Fine particles may hold on to pollutants and, therefore, reduce their toxicity or enhance the toxicity by carrying pollutants crossing the placental barrier; (2) smaller size, certain particle surface chemistry modifications, early developmental stage of placenta, and maternal diseases all aggravate PM-induced birth defects; (3) molecular events involved in such toxicity are begin to emerge: induction of oxidative stress, DNA damage, and alteration of molecular signaling or epigenetic events are some possible causes. Despite this progress, a clear understanding of PM-induced birth defects awaits further breakthroughs on many fronts, including epidemiological studies, animal models, nanotoxicity, and molecular mechanism investigations. Birth Defects Research (Part C) 108:196–206, 2016. © 2016 Wiley Periodicals, Inc.</p>","PeriodicalId":55352,"journal":{"name":"Birth Defects Research Part C-Embryo Today-Reviews","volume":"108 3","pages":"196-206"},"PeriodicalIF":0.0,"publicationDate":"2016-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/bdrc.21136","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34351709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prenatal exposure: The effects of prenatal cocaine and methamphetamine exposure on the developing child","authors":"Lynne M. Smith,&nbsp;Lucinda S. Santos","doi":"10.1002/bdrc.21131","DOIUrl":"10.1002/bdrc.21131","url":null,"abstract":"<p>Prenatal substance use remains a significant issue in the United States. Initial reports regarding prenatal cocaine and methamphetamine exposure suggested profound adverse effects on child development. However, subsequent prospective, longitudinal investigations have found more subtle effects. What follows is a brief review of the health, growth, behavioral, and intellectual outcomes for children exposed to prenatal cocaine and prenatal methamphetamine. Factors that may mitigate or intensify subtle adverse effects manifested in exposed children will also be discussed. Birth Defects Research (Part C) 108:142–146, 2016. © 2016 Wiley Periodicals, Inc.</p>","PeriodicalId":55352,"journal":{"name":"Birth Defects Research Part C-Embryo Today-Reviews","volume":"108 2","pages":"142-146"},"PeriodicalIF":0.0,"publicationDate":"2016-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/bdrc.21131","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34677096","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prenatal substance use and developmental disorders: Overview and highlights","authors":"Rocky S. Tuan","doi":"10.1002/bdrc.21133","DOIUrl":"10.1002/bdrc.21133","url":null,"abstract":"This issue of Birth Defects Research Part C: Reviews – EMBRYO TODAY, “Prenatal Substance Use and Developmental Disorders”, features contemporary reviews of the health challenges to the conceptus resulting from prenatal substance use, including methamphetamine, cocaine, alcohol, and smoking, and associated long-term developmental disorders. This topical issue complements the WileyBlackwell Symposium, “Neurodevelopmental Deficits from Fetal Exposure to Methamphetamine, Cocaine, and Alcohol: Emerging Mechanisms and Human Consequences”, jointly hosted by the Teratology Society and the Developmental Neurotoxicology Society and held at the 2016 Teratology Society Annual Meeting, San Antonio, Texas. Substance use or abuse represents an increasingly significant health concern worldwide. The 2014 U.S. National Survey on Drug Use and Health (Center for Behavioral Health Statistics and Quality, 2015) reported that over 27 million individuals aged 12 and older used an illicit drug in the preceding 30 days. Among females, 7.4% of those over age of 12 and 5.3% of pregnant women 15 to 44 years of age reported current illicit drug use. Substance use among women of reproductive age is particularly concerning, as it is well documented that children of drug abusing parents are at an increased risk for Child Protective Services involvement, child abuse, and neglect, and there is a higher likelihood of caregiver depression and other co-occurring mental health disorders. In addition to drugs such as methamphetamine and cocaine, alcohol consumption and smoking during pregnancy represent additional challenges to developmental health of the fetus. In their manuscript entitled “Fetal Oxidative Stress Mechanisms of Neurodevelopmental Deficits and Exacerbation by Ethanol and Methamphetamine”, Wells et al. reviewed research findings that support oxidative stress as a principal mechanism of the effects of methamphetamine and ethanol on developmental and brain functions, specifically the formation of reactive oxygen species (ROS), resulting in altered signal transduction, and/or oxidative damages to cellular macromolecules, including lipids/proteins and DNA, the latter leading to altered gene expression, likely via non-mutagenic mechanisms. Free radicals such as ROS are highly reactive and short-lived, and antioxidative enzymes and DNA repair proteins normally serve as the body’s protective agents. Understanding the balance between oxidative and anti-oxidative mechanisms and the role of repair enzyme is critical to the development of future treatments. In “Mechanisms Involved in the Neurotoxic and Cognitive Effects of Developmental Methamphetamine Exposure”, Vorhees and colleagues pointed out that 42% of pregnant women using methamphetamine continue to use throughout gestation, with the third trimester as the most susceptible period for the developing brain to prenatal exposure, resulting in a variety of higher-order cognitive deficits, such as decreased attention and working,","PeriodicalId":55352,"journal":{"name":"Birth Defects Research Part C-Embryo Today-Reviews","volume":"108 2","pages":"106-107"},"PeriodicalIF":0.0,"publicationDate":"2016-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/bdrc.21133","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34677094","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fetal oxidative stress mechanisms of neurodevelopmental deficits and exacerbation by ethanol and methamphetamine","authors":"Peter G. Wells,&nbsp;Shama Bhatia,&nbsp;Danielle M. Drake,&nbsp;Lutfiya Miller-Pinsler","doi":"10.1002/bdrc.21134","DOIUrl":"10.1002/bdrc.21134","url":null,"abstract":"<p><i>In utero</i> exposure of mouse progeny to alcohol (ethanol, EtOH) and methamphetamine (METH) causes substantial postnatal neurodevelopmental deficits. One emerging pathogenic mechanism underlying these deficits involves fetal brain production of reactive oxygen species (ROS) that alter signal transduction, and/or oxidatively damage cellular macromolecules like lipids, proteins, and DNA, the latter leading to altered gene expression, likely via non-mutagenic mechanisms. Even physiological levels of fetal ROS production can be pathogenic in biochemically predisposed progeny, and ROS formation can be enhanced by drugs like EtOH and METH, via activation/induction of ROS-producing NADPH oxidases (NOX), drug bioactivation to free radical intermediates by prostaglandin H synthases (PHS), and other mechanisms. Antioxidative enzymes, like catalase in the fetal brain, while low, provide critical protection. Oxidatively damaged DNA is normally rapidly repaired, and fetal deficiencies in several DNA repair proteins, including oxoguanine glycosylase 1 (OGG1) and breast cancer protein 1 (BRCA1), enhance the risk of drug-initiated postnatal neurodevelopmental deficits, and in some cases deficits in untreated progeny, the latter of which may be relevant to conditions like autism spectrum disorders (ASD). Risk is further regulated by fetal nuclear factor erythroid 2-related factor 2 (Nrf2), a ROS-sensing protein that upregulates an array of proteins, including antioxidative enzymes and DNA repair proteins. Imbalances between conceptal pathways for ROS formation, versus those for ROS detoxification and DNA repair, are important determinants of risk. Birth Defects Research (Part C) 108:108–130, 2016. © 2016 Wiley Periodicals, Inc.</p>","PeriodicalId":55352,"journal":{"name":"Birth Defects Research Part C-Embryo Today-Reviews","volume":"108 2","pages":"108-130"},"PeriodicalIF":0.0,"publicationDate":"2016-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/bdrc.21134","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34677095","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cocaine-induced neurodevelopmental deficits and underlying mechanisms","authors":"Melissa M. Martin,&nbsp;Devon L. Graham,&nbsp;Deirdre M. McCarthy,&nbsp;Pradeep G. Bhide,&nbsp;Gregg D. Stanwood","doi":"10.1002/bdrc.21132","DOIUrl":"10.1002/bdrc.21132","url":null,"abstract":"<p>Exposure to drugs early in life has complex and long-lasting implications for brain structure and function. This review summarizes work to date on the immediate and long-term effects of prenatal exposure to cocaine. In utero cocaine exposure produces disruptions in brain monoamines, particularly dopamine, during sensitive periods of brain development, and leads to permanent changes in specific brain circuits, molecules, and behavior. Here, we integrate clinical studies and significance with mechanistic preclinical studies, to define our current knowledge base and identify gaps for future investigation. Birth Defects Research (Part C) 108:147–173, 2016. © 2016 Wiley Periodicals, Inc.</p>","PeriodicalId":55352,"journal":{"name":"Birth Defects Research Part C-Embryo Today-Reviews","volume":"108 2","pages":"147-173"},"PeriodicalIF":0.0,"publicationDate":"2016-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/bdrc.21132","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34611345","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of fetal alcohol exposure on body systems: A systematic review","authors":"Courtney Caputo,&nbsp;Erin Wood,&nbsp;Leila Jabbour","doi":"10.1002/bdrc.21129","DOIUrl":"10.1002/bdrc.21129","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <p>Review of published manuscripts on fetal alcohol exposure on several body systems.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Method</h3>\u0000 \u0000 <p>Articles in this review were found online using databases such as Medline, Medline Complete, PubMed, and Health Source: Nursing/Academic Edition. The following terms were searched: fetal alcohol spectrum disorders, fetal alcohol syndrome, prenatal alcohol exposure, and alcohol related birth defects.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Thirteen articles were gathered, five original investigations and eight reviews. This review identified several abnormalities in the body systems discussed and their associations to fetal alcohol syndrome.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Evidence shows that the brain was the most severely impacted organ of the body systems discussed. However, prenatal alcohol exposure causes several abnormalities within the heart, kidney, liver, gastrointestinal tract, and the endocrine systems. In addition, preventative measures need to be taken by mothers during pregnancy. Birth Defects Research (Part C), 2016. © 2016 Wiley Periodicals, Inc. Birth Defects Research (Part C) 108:174–180, 2016. © 2016 Wiley Periodicals, Inc.</p>\u0000 </section>\u0000 </div>","PeriodicalId":55352,"journal":{"name":"Birth Defects Research Part C-Embryo Today-Reviews","volume":"108 2","pages":"174-180"},"PeriodicalIF":0.0,"publicationDate":"2016-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/bdrc.21129","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34637917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effects of nicotine on human fetal development","authors":"Bradley D. Holbrook","doi":"10.1002/bdrc.21128","DOIUrl":"10.1002/bdrc.21128","url":null,"abstract":"<p>Maternal smoking during pregnancy continues to represent a major public health concern. Nicotine is extremely harmful to the developing fetus through many different mechanisms, and the harms increase with later gestational age at exposure. Pregnancies complicated by maternal nicotine use are more likely to have significant adverse outcomes. Nicotine-exposed children tend to have several health problems throughout their lives, including impaired function of the endocrine, reproductive, respiratory, cardiovascular, and neurologic systems. Poor academic performance and significant behavioral disruptions are also common, including ADHD, aggressive behaviors, and future substance abuse. To diminish the adverse effects from cigarette smoking, some women are turning to electronic cigarettes, a new trend that is increasing in popularity worldwide. They are largely perceived as being safer to use in pregnancy than traditional cigarettes, although there is not adequate evidence to support this claim. At this time, electronic cigarette use during pregnancy cannot be recommended. Birth Defects Research (Part C) 108:181–192, 2016. © 2016 Wiley Periodicals, Inc.</p>","PeriodicalId":55352,"journal":{"name":"Birth Defects Research Part C-Embryo Today-Reviews","volume":"108 2","pages":"181-192"},"PeriodicalIF":0.0,"publicationDate":"2016-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/bdrc.21128","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34574960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanisms involved in the neurotoxic and cognitive effects of developmental methamphetamine exposure","authors":"Sarah A. Jablonski,&nbsp;Michael T. Williams,&nbsp;Charles V. Vorhees","doi":"10.1002/bdrc.21130","DOIUrl":"10.1002/bdrc.21130","url":null,"abstract":"<p>Methamphetamine exposure in utero leads to a variety of higher-order cognitive deficits, such as decreased attention and working, and spatial memory impairments in exposed children (Piper et al., 2011; Roussotte et al., 2011; Kiblawi et al., 2011). As with other teratogens, the timing of methamphetamine exposure greatly determines its effects on both neuroanatomical and behavioral outcomes. Methamphetamine exposure in rodents during the third trimester human equivalent period of brain development results in distinct and long-lasting route-based and spatial navigation deficits (Williams et al., 2003; Vorhees et al., 2005, 2008, 2009;). Here, we examine the impact of neonatal methamphetamine-induced neurotoxicity on behavioral outcomes, neurotransmission, receptor changes, plasticity proteins, and DNA damage. Birth Defects Research (Part C) 108:131–141, 2016. © 2016 Wiley Periodicals, Inc.</p>","PeriodicalId":55352,"journal":{"name":"Birth Defects Research Part C-Embryo Today-Reviews","volume":"108 2","pages":"131-141"},"PeriodicalIF":0.0,"publicationDate":"2016-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/bdrc.21130","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34574984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}