Seminar: Nov. 3, Dr. Andrew Whitehead, UC Davis

Our speaker this Friday, November 3, is Dr. Andrew Whitehead from UC Davis. We be in Field Auditorium, Environment Hall, on Duke’s West Campus, for his talk from 12:00 pm – 1:20 pm. Please join us!

Dr.  Whitehead will be speaking about “The Solution to Pollution is … Evolution? The Genomic Basis of Rapid Adaptation in Killfish.” The abstract for his talk is below:

A hallmark of biological systems is their ability to evolve and adapt to changing environmental conditions. In particular, species have been successfully evolving adaptations to chemical poisons for billions of years. They key challenge in the anthropocene is the severity and pace of change of the chemical environment. What are the attributes of species that contribute to their adaptive potential in the face of such environmental change, and what kinds of genetic changes are necessary to rescue species from extinction? Killifish are abundant in estuaries along the Atlantic coast of North America, including in sites polluted with common and persistent organic pollutants. Rapid adaptive evolution has increased the frequency of genetic variants that contribute to heritable chemical tolerance in polluted sites. We present an analysis of 400 whole genome sequences and transcriptomics to reveal the genes and pathways that affect chemical sensitivity in these populations. Importantly, this evolutionary process, coupled with our analysis, has revealed the types of sensitivity-affecting mutations that remain fit in nature. We also present some preliminary QTL mapping that links sensitivity to particular classes of chemicals to particular genes. We propose a comparative QTL mapping program to link sensitivity to specific chemicals (dioxins, PCBs, PAHs) and resistance to particular developmental phenotypes (cardiovascular system and craniofacial developmental abnormalities) in multiple genetic backgrounds. This program should reveal the types of mutations, and the genes and pathways in which they may occur, that affect sensitivity to multiple developmental syndromes upon exposure to environmental pollution while maintaining animal fitness in the real world

Reminder – if you are coming from off-campus, we can help you with parking. Please email Sarah Phillips for more info.

HELP US BEING GREEN – bring your personal drinkware and/or plates!

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Seminar: October 27, Laura Maurer, PhD, MPH, ExxonMobil Biomedical Sciences, Inc.

A friendly reminder about the upcoming Friday, October 27, UPEH/ITEHP Seminar from 12:00 pm – 1:20 pm in Love Auditorium, LSRC B101, on Duke’s West Campus. Laura Maurer, PhD, MPH, will be speaking about “Applying toxicological data to regulatory decision making.”

Dr. Maurer was postdoc in the Nicholas School from 2014-2016 in Joel Meyer’s lab. Prior to her time in Durham, she did her thesis work in toxicology at the University of Michigan. Following her time at Duke, Laura took a position in industry as a toxicologist with ExxonMobil Biomedical Sciences, Inc. which involves multiple toxicology-related roles and a few non-toxicology-related ones.

Reminder: if you are coming from off-campus, we can help you with parking. Please contact Sarah Phillips at sarah.anne.phillips@duke.edu for more information.

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Seminar: Oct. 20, Robert Tighe, MD, Duke University Medical Center

Please join us on Friday, October 20, at 12:00 pm in Field Auditorium, Environment Hall, to hear Dr. Robert Tighe speak about “Links between pulmonary macrophage function and environmental exposures.”

Dr. Tighe is an Assistant Professor of Medicine at the Duke University School of Medicine within the Pulmonary, Allergy and Critical Care unit.

See abstract below for specific information regarding his talk on Friday.

The research focus of our laboratory is to identify susceptibility factors and candidate pathways, relevant to host biological responses to environmental pollutants. By carefully dissecting these links, his lab is gaining insight into how environmental pollutants acutely induce respiratory symptoms and exacerbate chronic lung diseases. This can lead to targeted therapeutics and/or identify susceptible populations. We focus on macrophages as central mediators of pulmonary responses to environmental pollutants. To do this, we have developed advanced techniques using flow cytometry to define macrophages and immune cells in the lung of rodents and humans. In the present talk, I will discuss the use of flow cytometry techniques to define immune populations in the lung and also discuss ways that air pollution modifies macrophage functions.

Seminar: Oct. 13, Dr. Christopher Kassotis, PhD

Please join us on Friday, October 13, at 12:00 pm in Field Auditorium, Environment Hall, to hear Dr. Chris Kassotis speak about “Mechanisms of adipogenic activity of environmental contaminants and mixture.” Dr. Kassotis is currently an NRSA postdoctoral research fellow in the Nicholas School of the Environment. He works in Dr. Heather Stapleton’s lab and is researching the ability of and mechanisms through which various indoor contaminants and house dust may promote adipogenesis (lipid accumulation in fat cells and/or fat cell proliferation) and contribute to potential adverse metabolic health in children.

See abstract below for specific information regarding his talk on Friday. 

Obesity and metabolic disorders are a large societal concern and generate significant human health care costs. Recently, attention has focused on the potential for environmental contaminants to act as metabolic disruptors through disruption of nuclear hormone receptors. Our work has sought to evaluate the potential for diverse environmental contaminants to promote fat cell development, using an in vitro model of adipogenesis. These mouse pre-adipocytes, when exposed to “active” chemicals, differentiate into adipocytes, undergo morphological changes, accumulate triglycerides, and eventually come to resemble a mature human white fat cell. Our recent work has found that numerous indoor semivolatile organic contaminants can promote fat cell differentiation, and that mixtures of these chemicals present in house dust are also sufficient to drive differentiation at low, environmentally relevant levels. Our next steps are digging deeper into mechanisms, causative chemicals, and potential health impacts from exposure.

Seminar: October 6, Dr. Rebecca Fry, UNC

On Friday, October 6, at 12:00 pm in Environment Hall’s Field Auditorium, Dr. Rebecca Fry will present a talk entitled “The Placental Epigenome as a Driver of the Developmental Origins of Health and Disease.“

Dr. Fry serves as the Director of the UNC Superfund Research Program and is a professor with the Department of Environmental Sciences and Engineering. The abstract for her talk is below:

The placenta serves as a transient organ that is responsible for the regulation of the prenatal environment and is critical for optimal fetal development. It acts as a nutrient transporter and produces critical hormones to maintain pregnancy and support the fetus. In contrast to these essential functions, the placenta may also serve as a source of exposure for toxic substances, dysregulated hormone signaling and immune-related proteins. Such exposures including maternal stress, excess hormones, cytokines or environmental toxicants impact fetal health and influence later-life health outcomes. An increasing body of literature supports sex-specific birth and later-life outcomes in relation to adverse in utero environments. For example, sex-specific perinatal and later life outcomes have been linked to toxic substance exposure, maternal stress and maternal immune status. It is likely that sexdependent health outcomes in infants may be associated with sexual dimorphism of the placenta. In support of this, physiologic differences between placentas obtained from male or female pregnancies have been observed. While key physiological differences have been observed in male and female placentas, the underlying mechanisms are not well established. Epigenetic regulation may underlie not only the physiologic differences observed between male and female placentas but later life health outcomes. For instance, key differences in chromatin structure have been observed between male and female placentas, suggesting that there is a role for epigenetic regulation in placental sexual dimorphism. Understanding epigenetic regulation in the placenta is important given the modifiability of its epigenome in response to prenatal stressors, and its role as a mediator of the developmental origins of health and disease. Additionally, because certain epigenomic marks are stable over time, it is possible that changes to the fetal placenta methylome explain the sex-based differences in later-life disease risks. These data provide key insights into sexual dimorphism of the placental methylome as a driver of differential susceptibility to adverse prenatal environmental conditions and later life health.