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Fetal alcohol spectrum disorders

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https://www.readbyqxmd.com/read/29146504/minocycline-protects-developing-brain-against-ethanol-induced-damage
#1
Xin Wang, Kai Zhang, Fanmuyi Yang, Zhenhua Ren, Mei Xu, Jacqueline A Frank, Zun-Ji Ke, Jia Luo
Fetal alcohol spectrum disorders (FASD) are caused by ethanol exposure during the pregnancy and is the leading cause of mental retardation. Ethanol exposure during the development results in the loss of neurons in the developing brain, which may underlie many neurobehavioral deficits associated with FASD. It is important to understand the mechanisms underlying ethanol-induced neuronal loss and develop appropriate therapeutic strategies. One of the potential mechanisms involves neuroimmune activation. Using a third trimester equivalent mouse model of ethanol exposure, we demonstrated that ethanol induced a wide-spread neuroapoptosis, microglial activation, and neuroinflammation in C57BL/6 mice...
November 13, 2017: Neuropharmacology
https://www.readbyqxmd.com/read/29138110/neuronal-loss-in-the-developing-cerebral-cortex-of-normal-and-bax-deficient-mice-effects-of-ethanol-exposure
#2
Sheena M Britton, Michael W Miller
Fetal alcohol spectrum disorder is associated with defects in neuronal generation, migration, and differentiation. The present study tested the hypothesis that ethanol exposure during the period of naturally occurring neuronal death causes a time- and Bax-dependent neuronal loss. Wild-type and Bax knockout mice were given a pair of injections (two hours apart) of ethanol (2.5 g/kg) or saline on postnatal day (P) 4, P7, P10, or P13. Mean blood ethanol concentration was 435 mg/dl one hour after the second injection...
November 11, 2017: Neuroscience
https://www.readbyqxmd.com/read/29120886/comparison-of-alcohol-related-neurodevelopmental-disorders-and-neurodevelopmental-disorders-associated-with-prenatal-alcohol-exposure-diagnostic-criteria
#3
Sean Johnson, Chelsie Leigh Moyer, Marilyn G Klug, Larry Burd
OBJECTIVE: Recently, increased attention has been focused on the diagnosis of the most prevalent category of fetal alcohol spectrum disorders, alcohol-related neurodevelopmental disorders (ARNDs). In 2013, proposed criteria for neurodevelopmental disorders associated with prenatal alcohol exposure (ND-PAE) were included in the appendix of the latest revision of the Diagnostic and Statistical Manual of Mental Disorders. The concordance of the 2 sets of criteria is unknown. This study examines the overlap in diagnostic criteria for ND-PAE and the ARND Behavioral Checklist in children...
November 8, 2017: Journal of Developmental and Behavioral Pediatrics: JDBP
https://www.readbyqxmd.com/read/29120314/ethical-challenges-in-fasd-prevention-scientific-uncertainty-stigma-and-respect-for-women-s-autonomy
#4
Natalie Zizzo, Eric Racine
Fetal alcohol spectrum disorder (FASD) is a leading form of neurodevelopmental delay in Canada, affecting an estimated 3000 babies per year. FASD involves a range of disabilities that entail significant costs to affected individuals, families, and society. Exposure to alcohol in utero is a necessary factor for FASD development, and this has led to FASD being described as "completely preventable". However, there are significant ethical challenges associated with FASD prevention. These challenges revolve around 1) what should be communicated about the risks of alcohol consumption during pregnancy, given some ongoing scientific uncertainty about the effects of prenatal alcohol exposure, and 2) how to communicate these risks, given the potential for stigma against women who give birth to children with FASD as well as against children and adults with FASD...
November 9, 2017: Canadian Journal of Public Health. Revue Canadienne de Santé Publique
https://www.readbyqxmd.com/read/29109170/l1-coupling-to-ankyrin-and-the-spectrin-actin-cytoskeleton-modulates-ethanol-inhibition-of-l1-adhesion-and-ethanol-teratogenesis
#5
Xiaowei Dou, Carrie Menkari, Rei Mitsuyama, Tatiana Foroud, Leah Wetherill, Peter Hammond, Michael Suttie, Xiaopan Chen, Shao-Yu Chen, Michael E Charness
Ethanol causes fetal alcohol spectrum disorders (FASD) partly by inhibiting cell adhesion mediated by the L1 neural cell adhesion molecule. Ethanol interacts with an alcohol binding pocket in the L1 extracellular domain (ECD), and dephosphorylation of S1248 in the L1 cytoplasmic domain (CD) renders L1 adhesion insensitive to inhibition by ethanol (L1 insensitive). The mechanism underlying this inside-out signaling is unknown. Here we show that phosphorylation of the human L1-CD at S1152, Y1176, S1181, and S1248 renders L1 sensitive to ethanol by promoting L1 coupling with ankyrin-G and the spectrin-actin cytoskeleton...
November 6, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/29106518/prenatal-ethanol-exposure-and-neocortical-development-a-transgenerational-model-of-fasd
#6
Charles W Abbott, David J Rohac, Riley T Bottom, Sahil Patadia, Kelly J Huffman
Fetal Alcohol Spectrum Disorders, or FASD, represent a range of adverse developmental conditions caused by prenatal ethanol exposure (PrEE) from maternal consumption of alcohol. PrEE induces neurobiological damage in the developing brain leading to cognitive-perceptual and behavioral deficits in the offspring. Alcohol-mediated alterations to epigenetic function may underlie PrEE-related brain dysfunction, with these changes potentially carried across generations to unexposed offspring. To determine the transgenerational impact of PrEE on neocortical development, we generated a mouse model of FASD and identified numerous stable phenotypes transmitted via the male germline to the unexposed third generation...
July 6, 2017: Cerebral Cortex
https://www.readbyqxmd.com/read/29104501/in-utero-alcohol-exposure-and-the-alteration-of-histone-marks-in-the-developing-fetus-an-epigenetic-phenomenon-of-maternal-drinking
#7
REVIEW
Chanchal Mandal, Debasish Halder, Kyoung Hwa Jung, Young Gyu Chai
Ethanol is well known for its teratogenic effects during fetal development. Maternal alcohol consumption allows the developing fetus to experience the detrimental effects of alcohol exposure. Alcohol-mediated teratogenic effects can vary based on the dosage and the length of exposure. The specific mechanism of action behind this teratogenic effect is still unknown. Previous reports demonstrated that alcohol participates in epigenetic alterations, especially histone modifications during fetal development. Additional research is necessary to understand the correlation between major epigenetic events and alcohol-mediated teratogenesis such as that observed in fetal alcohol spectrum disorder (FASD)...
2017: International Journal of Biological Sciences
https://www.readbyqxmd.com/read/29094891/fetal-alcohol-syndrome-and-fetal-alcohol-spectrum-disorders
#8
LeeAnne Denny, Sarah Coles, Robin Blitz
Fetal alcohol syndrome (FAS) and fetal alcohol spectrum disorders (FASD) result from intrauterine exposure to alcohol and are the most common nonheritable causes of intellectual disability. The percentage of women who drink or binge drink during pregnancy has increased since 2012. FAS is commonly missed or misdiagnosed, preventing affected children from receiving needed services in a timely fashion. Diagnosis is based on the presence of the following clinical features, all of which must be present: prenatal and/or postnatal growth retardation, facial dysmorphology, central nervous system dysfunction, and neurobehavioral disabilities...
October 15, 2017: American Family Physician
https://www.readbyqxmd.com/read/29091741/skeletal-muscle-and-fetal-alcohol-spectrum-disorder
#9
Semone B Myrie, Mark A Pinder
Skeletal muscle is critical for mobility and many metabolic functions integral to survival and long-term health. Alcohol can affect skeletal muscle physiology and metabolism, which will have immediate and long-term consequences on health. While skeletal muscle abnormalities, including morphological, biochemical and functional impairments are well documented in adults consuming excessive alcohol, there is a scarcity of information about skeletal muscle in the prenatal alcohol exposure (PAE) offspring. This review examines the available studies addressing skeletal muscle abnormalities due to PAE...
November 1, 2017: Biochemistry and Cell Biology, Biochimie et Biologie Cellulaire
https://www.readbyqxmd.com/read/29075360/turnover-of-histones-and-histone-variants-in-postnatal-rat-brain-effects-of-alcohol-exposure
#10
Nadia Rachdaoui, Ling Li, Belinda Willard, Takhar Kasumov, Stephen Previs, Dipak Sarkar
BACKGROUND: Alcohol consumption during pregnancy is a significant public health problem and can result in a continuum of adverse outcomes to the fetus known as fetal alcohol spectrum disorders (FASD). Subjects with FASD show significant neurological deficits, ranging from microencephaly, neurobehavioral, and mental health problems to poor social adjustment and stress tolerance. Neurons are particularly sensitive to alcohol exposure. The neurotoxic action of alcohol, i.e., through ROS production, induces DNA damage and neuronal cell death by apoptosis...
2017: Clinical Epigenetics
https://www.readbyqxmd.com/read/29069573/sulforaphane-restores-acetyl-histone-h3-binding-to-bcl-2-promoter-and-prevents-apoptosis-in-ethanol-exposed-neural-crest-cells-and-mouse-embryos
#11
Fuqiang Yuan, Xiaopan Chen, Jie Liu, Wenke Feng, Lu Cai, Xiaoyang Wu, Shao-Yu Chen
Sulforaphane (SFN) is an isothiocyanate derived from cruciferous vegetables. SFN's cytoprotective properties have been demonstrated in several models associated with a variety of disorders. Our recent studies have shown that SFN protects against ethanol-induced oxidative stress and apoptosis in neural crest cells (NCCs), an ethanol-sensitive cell population implicated in Fetal Alcohol Spectrum Disorders (FASD). This study is designed to test the hypothesis that SFN can prevent ethanol-induced apoptosis in NCCs by inhibiting HDAC and increasing histone acetylation at the Bcl-2 promoter...
October 22, 2017: Experimental Neurology
https://www.readbyqxmd.com/read/29069552/-i-xenopus-i-embryos-to-study-fetal-alcohol-syndrome-a-model-for-environmental-teratogenesis
#12
Abraham Fainsod, Hadas Kot-Leibovich
Vertebrate model systems are central to characterize the outcomes of ethanol exposure and the etiology of Fetal Alcohol Spectrum Disorder (FASD), taking advantage of their genetic and morphological closeness and similarity to humans. We discuss the contribution of amphibian embryos to FASD research, focusing on <i>Xenopus</i> embryos. The <i>Xenopus</i> experimental system is characterized by external development and accessibility throughout embryogenesis, large clutch sizes, gene and protein activity manipulation, transgenesis and genome editing, convenient chemical treatment, explants and conjugates and many other experimental approaches...
October 25, 2017: Biochemistry and Cell Biology, Biochimie et Biologie Cellulaire
https://www.readbyqxmd.com/read/29056979/a-critique-of-the-new-canadian-fetal-alcohol-spectrum-disorder-guideline
#13
John D McLennan, Peter Braunberger
A new Fetal Alcohol Spectrum Disorder (FASD) guideline was published in the Canadian Medical Association Journal in 2016. This is relevant to the mental health field as mental health symptoms and psychiatric disorders are often identified as associated with and/or part of FASD presentations. Unfortunately, the new guideline has not advanced understanding of the interface between FASD and mental health problems; rather it may contribute to additional confusion. For example, a new recommendation to include additional mental health symptoms, such as anxiety and affect dysregulation, as manifestations contributing to a diagnosis of FASD is particularly concerning given the paucity of evidence supporting this assertion and the potential to distort delivery of mental health interventions for mental health problems...
2017: Journal of the Canadian Academy of Child and Adolescent Psychiatry
https://www.readbyqxmd.com/read/29048755/nifedipine-prevents-apoptosis-of-alcohol-exposed-first-trimester-trophoblast-cells
#14
Alan D Bolnick, Jay M Bolnick, Hamid-Reza Kohan-Ghadr, Brian A Kilburn, Michael Hertz, Jing Dai, Sascha Drewlo, D Randall Armant
BACKGROUND: Maternal alcohol abuse leading to fetal alcohol spectrum disorder (FASD) includes fetal growth restriction (FGR). Ethanol induces apoptosis of human placental trophoblast cells, possibly disrupting placentation and contributing to FGR in FASD. Ethanol facilitates apoptosis in several embryonic tissues, including human trophoblasts, by raising intracellular Ca(2+) . We previously found that acute ethanol exposure increases trophoblast apoptosis due to signaling from both intracellular and extracellular Ca(2+) ...
October 19, 2017: Alcoholism, Clinical and Experimental Research
https://www.readbyqxmd.com/read/29040815/the-role-of-folic-acid-and-selenium-against-oxidative-ethanol-damage-in-early-life-programming-a-review
#15
Mª Luisa Ojeda Murillo, Fatima Nogales Bueno, Mª Luisa Murillo Taravillo, Olimpia Carreras Sánchez
Several disorders in children, called Fetal Alcohol Spectrum Disorders (FASD), occur as result of alcohol consumption during pregnancy and lactation. They appear, at least in part, to be related to the oxidative stress that this drug generates. Ethanol metabolism generates reactive oxygen species and causes a depletion of the antioxidant molecule glutathione (GSH) leading to oxidative stress and lipid and protein damage which are related to growth retardation and neurotoxicity, increasing the incidence of FASD...
October 17, 2017: Biochemistry and Cell Biology, Biochimie et Biologie Cellulaire
https://www.readbyqxmd.com/read/29024604/the-avian-embryo-as-a-model-for-fetal-alcohol-spectrum-disorders
#16
Susan M Smith, George R Flentke
Prenatal alcohol exposure (PAE) remains a leading preventable cause of structural birth defects and permanent neurodevelopmental disability. The chick (Gallus gallus domesticus) is a powerful embryological research model and was possibly the first (Fere, 1895) in which alcohol's teratogenicity was demonstrated. Pharmacologically relevant alcohol exposures in the range of 20-70 mM (20-80 mg/egg) disrupt chick embryo growth, morphogenesis, and behavior, and the resulting phenotypes strongly parallel those of mammalian models...
October 12, 2017: Biochemistry and Cell Biology, Biochimie et Biologie Cellulaire
https://www.readbyqxmd.com/read/29023818/commentary-on-montag-et%C3%A2-al-2017-the-importance-of-cbpr-in-fasd-prevention-with-american-indian-communities
#17
Jessica D Hanson, Tess L Weber
Prenatal alcohol consumption is a public health concern due to potential lifelong physical and cognitive effects in offspring, often presenting in the form of fetal alcohol syndrome (FAS) or other fetal alcohol spectrum disorders (FASD). FASD is the continuum of lifelong outcomes in those born prenatally exposed to alcohol and includes a diagnosis of fetal alcohol syndrome (FAS), which is diagnosed through facial abnormalities, growth retardation, and delayed brain growth (Hoyme et al., 2016), as well as secondary disabilities such as conduct disorders, mental illness, and psychosocial functioning...
October 10, 2017: Alcoholism, Clinical and Experimental Research
https://www.readbyqxmd.com/read/29017910/developmental-ethanol-exposure-alters-the-morphology-of-mouse-prefrontal-neurons-in-a-layer-specific-manner
#18
Emma L Louth, Hanna D Luctkar, Kayla A Heney, Craig D C Bailey
Chronic developmental exposure to ethanol can lead to a wide variety of teratogenic effects, which in humans are known as fetal alcohol spectrum disorders (FASD). Individuals affected by FASD may exhibit persistent impairments to cognitive functions such as learning, memory, and attention, which are highly dependent on medial prefrontal cortex (mPFC) circuitry. The objective of this study was to determine long-term effects of chronic developmental ethanol exposure on mPFC neuron morphology, in order to better-understand potential neuronal mechanisms underlying cognitive impairments associated with FASD...
October 7, 2017: Brain Research
https://www.readbyqxmd.com/read/29017023/maternal-iron-nutriture-as-a-critical-modulator-of-fasd-risk-in-alcohol-exposed-pregnancies
#19
Kaylee K Helfrich, Nipun Saini, Pamela J Kling, Susan M Smith
Alcohol consumption during pregnancy places the fetus at risk for permanent physical, cognitive, and behavioral impairments, collectively termed fetal alcohol spectrum disorders (FASD). However, prenatal alcohol exposure (PAE) outcomes vary widely, and growing evidence suggests that maternal nutrition is a modifying factor. Certain nutrients, such as iron, may modulate FASD outcomes. Untreated gestational iron deficiency (ID) causes persistent neurodevelopmental deficits in the offspring that affect many of the same domains damaged by PAE...
October 10, 2017: Biochemistry and Cell Biology, Biochimie et Biologie Cellulaire
https://www.readbyqxmd.com/read/28988969/fetal-alcohol-spectrum-disorders-zebrafish-in-the-analysis-of-the-milder-and-more-prevalent-form-of-the-disease
#20
REVIEW
Diane Seguin, Robert Gerlai
Fetal Alcohol Spectrum Disorders (FASD) represent a large unmet medical need. Exposure of the developing human embryo to alcohol can lead to life-long suffering. Despite the well documented deleterious effects of alcohol on the developing fetus, pregnant women continue to drink alcohol, and FASD remains the leading cause of preventable mental retardation and other behavioral abnormalities. Particularly prevalent are the milder forms of the disease cluster, representing children who do not show obvious physical signs and who may be undiagnosed or misdiagnosed...
October 5, 2017: Behavioural Brain Research
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