A5100686467- Prenatal Substance Exposure Effects
- Birth, Development, and Health
- Folate and B Vitamins Research
- Gestational Diabetes Research and Management
- Pregnancy and preeclampsia studies
- Fatty Acid Research and Health
- Epigenetics and DNA Methylation
- Iron Metabolism and Disorders
- Peroxisome Proliferator-Activated Receptors
- Adipose Tissue and Metabolism
- Rangeland and Wildlife Management
- Cancer-related Molecular Pathways
- Insect and Pesticide Research
- Toxic Organic Pollutants Impact
- Diet and metabolism studies
- Insect Pest Control Strategies
- Metabolism and Genetic Disorders
- Anesthesia and Sedative Agents
- Pharmaceutical studies and practices
- Wildlife Ecology and Conservation
- Health Systems, Economic Evaluations, Quality of Life
- Medical Research and Practices
- Prenatal Screening and Diagnostics
- Fibromyalgia and Chronic Fatigue Syndrome Research
- Inflammatory Biomarkers in Disease Prognosis
David H. Murdock Research Institute
2018-2025
University of North Carolina at Chapel Hill
2008-2025
Trinity College Dublin
2022-2025
LAC+USC Medical Center
2022
Case Western Reserve University
2022
Royal College of Surgeons in Ireland
2022
University School
2022
University of Wisconsin–Madison
1987-2019
Cheltenham General Hospital
2016
CABI Kenya
1999
Abstract Background Identifying clusters of multiple long-term conditions (MLTCs), also known as multimorbidity, and their associated burden may facilitate the development effective cost-effective targeted healthcare strategies. This study aimed to identify MLTCs associations with health-related quality life (HRQoL) in two UK population-based cohorts. Methods Age-stratified were identified at baseline Biobank ( n = 502,363, 54.6% female) UKHLS 49,186, 54.8% using latent class analysis (LCA)....
Background Prenatal alcohol exposure ( PAE ) is a leading cause of significant neurobehavioral and neurocognitive deficits. Its potential consequences for eating behaviors, nutritional status, other issues in childhood have received little attention. Methods Nineteen children (11 boys, 8 girls) mean age 9.6 years, referred fetal spectrum disorder FASD screening assessment, were analyzed with physical exams caregiver questionnaires to identify possible abnormalities food behaviors. Fourteen...
Fetal alcohol spectrum disorder (FASD) is a leading cause of neurodevelopmental disability. Individuals with FASD may exhibit characteristic facial appearance that has diagnostic utility. The mechanism by which disrupts craniofacial development incompletely understood, as are the genetic factors can modify individual vulnerability. Using an established avian model, we characterized cranial transcriptome in response to inform underlying these cells' Gallus gallus embryos having 3-6 somites...
Prenatal alcohol exposure (PAE) is a leading cause of neurodevelopmental disability through its induction neuronal growth dysfunction incompletely understood mechanisms. Ribosome biogenesis regulates cell cycle progression p53 and the nucleolar stress response. Whether those processes are targeted by unknown. Pregnant C57BL/6J mice received 3 g alcohol/kg daily at E8.5–E17.5. Transcriptome sequencing was performed on E17.5 fetal cortex. Additionally, primary neural stem cells (NSCs) were...
Background: Prenatal alcohol exposure (PAE) can reduce fetal growth and cause neurodevelopmental disability. choline supplements attenuate PAE-induced behavioral deficits; however, the underlying mechanisms are unknown. Alcohol alters nutrient metabolism potentially increases needs. Here, we investigate how affects in maternal–fetal dyad role of supplemental choline. Methods: Pregnant C57BL/6J mice were assigned to one four groups: alcohol-exposed (3 g/kg alcohol/day) or control +/− 100...
Background Fetal alcohol spectrum disorders (FASD) is a leading cause of neurodevelopmental disability. Genetic factors can modify vulnerability to FASD, but these elements are poorly characterized. Methods We performed high-throughput transcriptional profiling identify gene candidates that could potentially ethanol's (EtOH's) neurotoxicity. interrogated unique genetic resource, neuroprogenitor cells from 2 closely related Gallus gallus lines having well-characterized robust or attenuated...
Abstract Prenatal alcohol exposure (PAE) causes permanent cognitive disability. The enteric microbiome generates microbial-dependent products (MDPs) that may contribute to disorders including autism, depression, and anxiety; it is unknown whether similar alterations occur in PAE. Using a mouse PAE model, we performed untargeted metabolome analyses upon the maternal–fetal dyad at gestational day 17.5. Hierarchical clustering by principal component analysis Pearson’s correlation of maternal...
Abstract Background Individuals exposed to gestational stressors such as alcohol exhibit a spectrum of growth patterns, suggesting individualized responses the stressors. We hypothesized that intrauterine are modified not only by stressor’s severity but fetal sex and placenta’s adaptive capacity. Methods Pregnant C57BL/6J mice were assigned one three groups. Group 1 consumed normal protein diet (18% weight) received 4.5 g alcohol/kg body weight (NP-Alc-8) or isocaloric maltodextrin (NP-MD-8)...
Prenatal alcohol exposure (PAE) causes cognitive impairment and a distinctive craniofacial dysmorphology, due in part to apoptotic losses of the pluripotent cranial neural crest cells (CNCs) that form facial bones cartilage. We previously reported PAE rapidly represses expression >70 ribosomal proteins (padj = 10-E47). Ribosome dysbiogenesis nucleolar stress activates p53-MDM2-mediated apoptosis. Using primary avian CNCs murine CNC line O9-1, we tested whether p53-MDM2 signaling mediates...
The use of hydrogenated rapeseed oil as a carrier for conidia the entomopathogenic fungus Beauveria bassiana (Bals) Vuill was investigated part research programme on control larger grain borer, Prostephanus truncatus (Horn). Melting oil, which is solid at temperatures below 32 °C, allows incorporation materials such aggregation pheromones and conidia; sudden cooling produces fat pellets. In attraction tests conducted with pellets containing P pheromone, significantly higher numbers beetles...
Although prenatal alcohol exposure (PAE) reduces offspring growth, it may increase obesity risk at adolescence. Animal models of PAE display glucose intolerance and increased adiposity, suggesting that causes metabolic reprogramming. We tested this hypothesis in a mouse model binge PAE, wherein pregnant C57Bl/6J females received 3 g/kg (ETOH) daily from gestational day 12.5 to 17.5; maltodextrin (MD) medium chain triglycerides (MCT) served as isocaloric nutritional controls, sham (H2O)...
Abstract Background Prenatal alcohol exposure causes distinctive craniofacial anomalies that arise, in part, from the apoptotic elimination of neural crest (NC) progenitors form face. This vulnerability NC to is puzzling as they normally express transcriptional repressor Snail1/2 (in chick Snai2), which suppresses apoptosis and promotes their migration. Here, we investigate alcohol's impact upon Snai2 function. Methods Chick cranial cells were treated with acute (52 mM, 2 hr). We evaluated...
People that experience prenatal alcohol exposure (PAE) may have behavioral and metabolic impairments, it is unclear whether these remain stable or change with age. We assessed endpoints across the lifespan in a mouse model of fetal spectrum disorder (FASD). Pregnant C57BL/6J mice received (ALC; 3 g/kg) maltose-dextrin (control, CON) daily from embryonic day 8.5 to 17.5. Offspring were tested on accelerating rotarod, Y-maze, novel object recognition, fear conditioning at 6 weeks 10 17 months;...