Jennifer Freeman

Dr. Jennifer Freeman

Purdue University, W. Lafayette, IN 47907, USA
orcid

Research Focus & Metrics

Academic Career Length

23Years (2004-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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23 November 2006 in Nature
Verified
Journal Article
Closed access
PDF file
RRRichard Redon
Richard Redon
SIShumpei Ishikawa
Shumpei Ishikawa
KFKaren R. Fitch
Karen R. Fitch
LFLars Feuk
Lars Feuk
GPGeorge H. Perry
George H. Perry
MHMatthew E. Hurles
Matthew E. Hurles

29 June 2006 in Genome Research
Verified
Journal Article
Open access
PDF file
Jennifer FreemanJennifer Freeman
Jennifer Freeman
GPGeorge H. Perry
George H. Perry
LFLars Feuk
Lars Feuk
RRRichard Redon
Richard Redon
SMSteven A. McCarroll
Steven A. McCarroll
CLCharles Lee
Charles Lee
DNA copy number variation has long been associated with specific chromosomal rearrangements and genomic disorders, but its ubiquity in mammalian genomes was not fully realized until recently. Although our understanding of the extent of this variation is still developing, it seems likely that, at least in humans, copy number variants (CNVs) account for a substantial amount of genetic variation. Since many CNVs include genes that result in differential levels of gene expression, CNVs may account for a significant proportion of normal phenotypic variation. Current efforts are directed toward a more comprehensive cataloging and characterization of CNVs that will provide the basis for determining how genomic diversity impacts biological function, evolution, and common human diseases.

18 October 2019 in Chemical Research in Toxicology
Verified
Journal Article
Open access
SCSteven Cassar
Steven Cassar
IAIsaac Adatto
Isaac Adatto
Jennifer FreemanJennifer Freeman
Jennifer Freeman
JGJoshua T. Gamse
Joshua T. Gamse
IIIñaki Iturria
Iñaki Iturria
LZLeonard I. Zon
Leonard I. Zon
Unpredicted human safety events in clinical trials for new drugs are costly in terms of human health and money. The drug discovery industry attempts to minimize those events with diligent preclinical safety testing. Current standard practices are good at preventing toxic compounds from being tested in the clinic; however, false negative preclinical toxicity results are still a reality. Continual improvement must be pursued in the preclinical realm. Higher-quality therapies can be brought forward with more information about potential toxicities and associated mechanisms. The zebrafish model is a bridge between in vitro assays and mammalian in vivo studies. This model is powerful in its breadth of application and tractability for research. In the past two decades, our understanding of disease biology and drug toxicity has grown significantly owing to thousands of studies on this tiny vertebrate. This Review summarizes challenges and strengths of the model, discusses the 3Rs value that it can deliver, highlights translatable and untranslatable biology, and brings together reports from recent studies with zebrafish focusing on new drug discovery toxicology.

19 February 2018 in Toxicological Sciences
Verified
Journal Article
Open access
PDF file
KHKatharine A Horzmann
Katharine A Horzmann
Jennifer FreemanJennifer Freeman
Jennifer Freeman
The laboratory zebrafish (Danio rerio) is now an accepted model in toxicologic research. The zebrafish model fills a niche between in vitro models and mammalian biomedical models. The developmental characteristics of the small fish are strategically being used by scientists to study topics ranging from high-throughput toxicity screens to toxicity in multi- and transgenerational studies. High-throughput technology has increased the utility of zebrafish embryonic toxicity assays in screening of chemicals and drugs for toxicity or effect. Additionally, advances in behavioral characterization and experimental methodology allow for observation of recognizable phenotypic changes after xenobiotic exposure. Future directions in zebrafish research are predicted to take advantage of CRISPR-Cas9 genome editing methods in creating models of disease and interrogating mechanisms of action with fluorescent reporters or tagged proteins. Zebrafish can also model developmental origins of health and disease and multi- and transgenerational toxicity. The zebrafish has many advantages as a toxicologic model and new methodologies and areas of study continue to expand the usefulness and application of the zebrafish.

27 August 2016 in Toxics
Verified
Journal Article
Open access
PDF file
KHKatharine Horzmann
Katharine Horzmann
Jennifer FreemanJennifer Freeman
Jennifer Freeman
Neurotransmission is the basis of neuronal communication and is critical for normal brain development, behavior, learning, and memory. Exposure to drugs and chemicals can alter neurotransmission, often through unknown pathways and mechanisms. The zebrafish (Danio rerio) model system is increasingly being used to study the brain and chemical neurotoxicity. In this review, the major neurotransmitter systems, including glutamate, GABA, dopamine, norepinephrine, serotonin, acetylcholine, histamine, and glutamate are surveyed and pathways of synthesis, transport, metabolism, and action are examined. Differences between human and zebrafish neurochemical pathways are highlighted. We also review techniques for evaluating neurological function, including the measurement of neurotransmitter levels, assessment of gene expression through transcriptomic analysis, and the recording of neurobehavior. Finally examples of chemical toxicity studies evaluating alterations in neurotransmitter systems in the zebrafish model are reviewed.

2 November 2015 in Toxics
Verified
Journal Article
Open access
PDF file
SWSara E. Wirbisky
Sara E. Wirbisky
Jennifer FreemanJennifer Freeman
Jennifer Freeman
Endocrine disrupting chemicals (EDC) are exogenous agents that alter endogenous hormone signaling pathways. These chemicals target the neuroendocrine system which is composed of organs throughout the body that work alongside the central nervous system to regulate biological processes. Of primary importance is the hypothalamic-pituitary-gonadal (HPG) axis which is vital for maintaining proper reproductive function. Atrazine (2-chloro-4-ethylamino-6-isopropylamino-1,3,5-triazine) is a pre-emergent herbicide used to prevent the growth of weeds on various crops. This herbicide is reported to widely contaminate potable water supplies everywhere it is applied. As such, the European Union banned the use of atrazine in 2004. Currently the United States Environmental Protection Agency regulates atrazine at 3 parts per billion (ppb; μg/L) in drinking water, while the World Health Organization recently changed their drinking water guideline to 100 ppb. Atrazine is implicated to be an EDC that alters reproductive dysfunction by targeting the HPG axis. However, questions remain as to the human health risks associated with atrazine exposure with studies reporting mixed results on the ability of atrazine to alter the HPG axis. In this review, the current findings for atrazine’s effects on the HPG axis are examined in mammalian, anuran, and fish models and in epidemiological studies.