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Recent Endowment Fund Award Recipients

2016 Endowment Awardees



Angelo Furgiuele Young Investigator Technology Award

Winner: Janet Sangodele

Award Year: 2016
Current Degrees: BSc, MSc
Institution/Affiliation: Federal University of Technology Akure Nigeria

Reproductive toxicity is a hazard that is often associated with some chemical substances that interfere in some way with normal reproduction. Ms. Sangodele's research focuses on toxic effects of some selected environmental and occupational toxicants on key aspects of male reproduction, oxidative stress and fertility. The overall goal of her research is to evaluate the toxic effects and elucidate the mechanisms of toxicity of oral and dermal exposure of toxicants and better understand the toxicity in animal models. However, the knowledge of mechanisms underlying the effects of toxicants by oral and dermal exposure is an important way of protecting people exposed to toxicants, thereby reducing the health implications of toxicants exposure and providing means to eradicate the toxic effects of toxicants that can affect reproduction and influence fertility.

Carl C. Smith Student Mechanisms Award Fund

Winner: Rance Nault

Award Year: 2016
Current Degrees: BSc, MSc
Institution/Affiliation: Michigan State University

Mr. Nault's research examines the role of environmental contaminants of the development of fatty liver disease. In order to explore these questions he uses a combination of ‘omic’ techniques to examine changes in gene expression regulation, gene expression, and metabolites, and integrate these using a variety of computational tools. Consequently, by using these data together we can look at changes within the context of the whole system. In the future he will delve deeper into key features that were highlighted by these high-throughput evaluations, more specifically on the role of PKM2 in fatty liver caused by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) which is the research for which this award was given. They found that following TCDD exposure, a change in the PKM isoform is observed which reprograms metabolism similar to that of a cancer cell. Further evidence in metabolite and protein levels demonstrated that the livers of TCDD treated mice exhibit many features of cancer cells despite the absence of cancer. They conclude that this isoform switching likely plays a role in antioxidant defenses. Future work will examine this hypothesis in further depth using genetic models.

Carl C. Smith Student Mechanisms Award Fund

Winner: Bharat Bhushan

Award Year: 2016
Current Degrees: PhD
Institution/Affiliation: University of Kansas Medical Center

Acetaminophen (APAP) overdose is the foremost cause of acute liver failure (ALF) in the US. Despite decades of research, current treatment options after APAP-overdose are extremely limited. Liver injury after APAP-overdose is subsequently followed by compensatory liver regeneration, which promotes recovery. Preventing liver injury and stimulating liver regeneration are potential strategies to develop novel therapies for APAP-induced ALF. However, mechanisms of APAP-induced liver toxicity or subsequent liver regeneration are not completely understood. In the work that will be presented at the 2016 SOT annual meeting, they investigated role of EGFR (Epidermal Growth Factor Receptor) signaling in APAP-induced ALF. Role of EGFR signaling in APAP-induced liver toxicity and subsequent liver regeneration is completely unknown. In this extremely novel work, Dr. Bhushan and colleagues demonstrated that EGFR signaling plays a dual role in APAP overdose and is involved in both initiation of APAP-induced injury and in stimulating subsequent liver regeneration. They demonstrated, for the first time, that EGFR is rapidly activated after APAP overdose in both mice and primary human hepatocytes and translocated to mitochondria where it was involved in mitochondrial damage leading to liver injury. APAP-induced liver injury was almost completely abolished by early treatment with EGFR inhibitor. In fact, they demonstrated that an early EGFR inhibition as a therapeutic strategy may outperform treatment with NAC (N-acetyl cysteine), which is the current standard of care for not only APAP overdose but all suspected cases of ALF. Interestingly, they found that delayed activation of EGFR was crucial for compensatory liver regeneration response, such that delayed inhibition of EGFR in mice caused remarkable impairment of liver regeneration, resulting in substantial decrease of both recovery and survival. Thus, their work revealed an extremely novel and intriguing mechanisms about how a cell membrane receptor, EGFR, can translocate to mitochondria and cause both cell death or cell proliferation signaling in hepatocytes, in a time dependent manner, during APAP-induced ALF.

Carl C. Smith Student Mechanisms Award Fund

Winner: Nikita Joshi

Award Year: 2016
Current Degrees: MS, MSc
Institution/Affiliation: Michigan State University

Primary sclerosing cholangitis (PSC) is a type of fibrotic liver disease that can lead to liver failure and potentially cancer. It accounts for approximately 8% of all liver transplants in the United States and there is currently no established curative therapy for PSC. Ms. Joshi's exciting research characterizes a novel mechanism whereby the coagulation protein fibrinogen interacts with integrin aMß2 to reduce biliary fibrosis and suggests a novel putative therapeutic target for this difficult to treat fibrotic disease.

Dharm V. Singh Association of Scientists of Indian Origin Student Award Fund

Winner: Ratanesh Seth

Award Year: 2016
Current Degrees: PhD
Institution/Affiliation: University of South Carolina

With obesity becoming a global pandemic and more than a third are obese in this country, Dr. Seth's research focusing on the environmental toxins as potentiators of hepatotoxicity and disease has monumental significance. He has established the novel link between environmental toxin bromodichloromethane and Nonalcoholic Steatohepatitis (NASH). Though environmental contaminants and NASH development is known, the mechanisms remain unclear. His research has established that environmental toxin bromodichloromethane (BDCM), a disinfection byproduct of drinking water causes NASH and hepatic metabolic reprogramming, mediated by cytochrome P450 isoform CYP2E1 and adipokine leptin in an underline condition of obesity. In his current project, he investigated the molecular mechanism of transient receptor potential vanilloid channel 4 (TRPV4) regulating inflammation and Kupffer cell activation in nonalcoholic steatohepatitis by attenuation of CYP2E1-mediated oxidative stress. Nitric oxide regulates CYP2E1-mediated oxidative stress, inflammation and endothelial injury and attenuate NASH progression. Based on the above, targeting TRPV4 or its downstream signaling cascade might be a promising therapeutic strategy in NASH. He is sure that these findings are prooving to be very significant and novel to the field of liver disease research.

Dharm V. Singh Association of Scientists of Indian Origin Student Award Fund

Winner: Priyanka  Trivedi

Award Year: 2016
Current Degrees: PhD
Institution/Affiliation: Harvard Medical School

Dr. Trivedi's research focuses on discovering therapeutic targets for acute and chronic kidney diseases. Kidney fibrosis, the hallmark of the chronic kidney disease (CKD), is an irreversible process leading to the life-threatening end-stage renal failure. Unfortunately, no effective therapeutic strategies are available to cure this condition. This is due to lack of our understanding of the underlying mechanisms of fibrosis. Using RNA sequencing, we identified phospholipase D4 (PLD4) as one of the targets for the treatment of kidney fibrosis. Our research work deciphers a mechanistic role of PLD4 in the regulation of fibrosis. We observed that PLD4 was significantly increased in mechanistically different mouse models of kidney fibrosis as well as in patients with biopsy-proven kidney fibrosis. Further, we found that PLD4 knockout mice (PLD4-/-) showed less fibrosis compared to the wild type (PLD4+/+) mice after folic acid injection- as well as unilateral ureteral obstruction-induced kidney fibrosis. This was attributed to mainly two reasons, (i) PLD4-/- mice had increased level of anti-fibrotic cytokines compared to the PLD4+/+ mice and, (ii) sustained activation of the proteases, due to decreased level of serpina1 (a protease inhibitor) in PLD4-/- mice, led to an efficient degradation of collagen rescuing these mice from scar tissue formation in the kidney. Thus we identified that PLD4 is a central target that can be intervened in preventing fibrosis-associated organ dysfunction. Her future goal is to continue contributing to the mechanistic toxicological sciences, which can be translated clinically.

Dharm V. Singh Carcinogenesis Award Fund

Winner: Alisa Suen

Award Year: 2016
Current Degrees: BS
Institution/Affiliation: NIEHS/UNC Chapel Hill

Currently Ms. Suen is a 4th year PhD student in the Curriculum in Toxicology at the University of North Carolina-Chapel Hill. Her research is performed in the laboratory of Carmen Williams, a UNC-Chapel Hill adjunct faculty member who is a Clinical Investigator in the Reproductive and Developmental Biology Laboratory at the National Institute of Environmental Health Sciences in RTP, NC. She won the CSS Dharm V. Singh Carcinogenesis Endowment Award for her research on aberrant SIX1 expression in a developmental mouse model of hormonal carcinogenesis. During her dissertation research, she plans to investigate molecular mechanisms underlying the development of endometrial carcinoma following neonatal exposure to estrogenic chemicals. Her research will focus on the oncoprotein, sine oculis homeobox 1 (SIX1), a developmentally important and cancer-associated transcription factor that becomes overexpressed in the uteri of mice treated neonatally with the synthetic estrogen, diethylstilbestrol (DES), or the phytoestrogen, genistein. Her hypothesis is that persistent uterine SIX1 expression contributes to the cancer phenotype observed in this mouse model of hormonal carcinogenesis. To test this hypothesis, she designed a series of experiments to investigate the role of SIX1 in cancer development and the mechanisms by which neonatal estrogenic chemical exposure induces uterine SIX1 expression. She plans on pursuing an industry career focusing on drug discovery related to reproductive health, or reproductive/developmental toxicity testing.

Donald E. Gardner Inhalation Toxicology Education Award Fund

Winner: Katherine Zychowski

Award Year: 2016
Current Degrees: PhD
Institution/Affiliation: University of New Mexico

Dr. Zychowski studies how air pollution drives vascular disease. Her hope is to stay in an academic or government research setting. Additionally, she is very interested in toxicological implications pertaining to public health. Under the esteemed mentorship of Drs. Matt Campen(University of New Mexico) and Jim Wagner (Michigan State University) her plan is to use this award to travel to Michigan State University this summer to train on the state-of-the-art mobile air pollution laboratory, AirCARE 2.

Edward W Carney Trainee Award Fund

Winner: Kristin Bircsak

Award Year: 2016
Current Degrees: BS
Institution/Affiliation: Rutgers University

Ms. Bircsak's PhD research focuses on characterizing the regulation of a feto-protective protein and placental xenobiotic transporter, the breast cancer resistance protein (BCRP/ABCG2). The data presented in her 2016 SOT abstract describes transcription factor expression and genetic variants as contributors to the up to 6-fold variation in the BCRP mRNA expression between 109 ethnically-diverse placentas. Importantly, an exonic SNP was associated with reduced BCRP protein expression, but not mRNA of individuals that expressed one or two of the variant alleles. By understanding the factors that govern placental BCRP function, the hope is to identify at risk populations that require individualized prescribing of drugs during pregnancy. Submerging herself in the research and literature of her doctoral thesis project served as inspiration to seek a career in the field of reproductive and developmental toxicology. Ultimately, Ms. Bircsak aspires for a research career in which she will help expand the limited safety data available for drugs used in pregnancy, thereby ensuring the safety of future generations.

Edward W. Carney Trainee Award Fund

Winner: Deirdre Tucker

Award Year: 2016
Current Degrees: BS
Institution/Affiliation: UNC Chapel Hill

Overall, Ms. Tucker's research focuses on the effects of early life exposures to chemicals that have the potential to alter the developing mammary gland in a rodent model system. Her chemicals of interest include Bisphenol A and other analogues including BPAF and BPS. The goal is to determine if these chemicals may play a role in changing key morphological and cellular processes that are responsible for normal development. In turn she is also trying to determine if these chemicals have long term consequences that may increase the likelihood of developing later life diseases, including mammary carcinogenesis. The work for this award determined that following an in utero exposure to BPA, BPAF and BPS female CD-1 offspring developed multiple mammary phenotypes that included inflammation, hyperplasia, and adenocarcinoma that were present as early as 8-11 months of age. The severity of these phenotypes increased with age (14 mos.), especially in BPAF 5 mg/kg and BPS 0.5 mg/kg treated animals. Interestingly, estrogen receptor alpha and progesterone receptor mRNA expression were unchanged which may point to other mechanisms of action for these chemicals.

Endowment - Jean Lu Student Scholarship Award Fund

Winner: Xiao Xiao

Award Year: 2016
Current Degrees: BS
Institution/Affiliation: University of Massachusetts Amherst

The purpose of Mr. Xiao's research is to determine the role of permethrin, a pyrethroid insecticide, on development of obesity and type 2 diabetes. Permethrin is a structural analog of pyrethrin, a naturally occurring pyrethroid insecticide from Chrysanthemum flower heads, accounting 17% of the world insecticide uses in 2013 and more than 60% of pyrethroids. Human exposure to permethrin is very likely to occur through food chain contamination and direct application to control ectoparasites. Concurrently, the rising rate of obesity and type 2 diabetes cannot be explained fully by considering changes in diet, lifestyle or genetics of individuals, suggesting the need to investigate other factors that may be involved in this disease outbreak. An increasing number of scientific studies have suggested a potential link between insecticide exposure and the development of obesity and type 2 diabetes. His research will help to fill the current knowledge gap between insecticide exposure and alteration of glucose and lipid metabolism. The research that helped him win the Jean Lu student award was determination of the role of permethrin and its interaction with dietary fat on development of obesity and diabetes in mice. This will be the first in vivo study determining the role of permethrin and development of obesity and type 2 diabetes. We tested three doses of permethrin, between acceptable daily intake and chronic no observed effect levels, in low-fat fed and high-fat fed mice for 12 weeks. Our results showed that permethrin treatment significantly increased weight gain, fat mass, and insulin resistance in high-fat fed groups, but no significant effect were observed in low-fat fed animals. These results suggest that increased dietary fat may have contributed to effects of permethrin in altered lipid and glucose metabolism. His next goal is to investigate detailed mechanism of how permethrin exposure, interacting with dietary fat, caused weight gain and insulin resistance by using a cell culture model.

Frank C. Lu Food Safety Students Award Fund

Winner: Gopi Gadupudi

Award Year: 2016
Current Degrees: BS, MS
Institution/Affiliation: University of Iowa

Mr. Gadupudi's research involves understanding the toxicity of food-borne chemicals such as PCB126. Specifically, this work involves characterizing the dose and time dependent toxicity of PCB126 in causing metabolic disorders such as diabetes, fatty liver and metabolic syndrome. Moving forward, he and his colleagues would like to understand the mechanisms involved in the PCB or POP induced metabolic disruption. Understanding these mechanisms would definitely aid in identifying adverse effects on human health and risk characterization.

Gabriel L. Plaa Education Award

Winner: Nicole Olgun

Award Year: 2016
Current Degrees: BS, MS, PhD
Institution/Affiliation: CDC/NIOSH

Dr. Olgun's research has always focused on preterm birth, and various methods of prevention. She has worked with cells, pregnant mice, and human placental explants to study inflammation in pregnancy and cytokine expression and production. Upon becoming a post doc at NIOSH, she joined a lab that focuses on metal toxicity and free radicals. The abstract for which she won an award this year, looked at the toxicity that exists between sintered and unsintered indium tin oxide, and how these particles are cause damage to cells. Workers that are exposed to indium tin oxide in the occupational setting experience pulmonary problems, so it is important that these workers be properly protected.

Gabriel L. Plaa Education Award

Winner: Sridhar Jaligama

Award Year: 2016
Current Degrees: PhD
Institution/Affiliation: University of Tennessee Health Science Center

Dr. Jaligama's research is focused on understanding the mechanism of pulmonary immunosuppression during early-life exposure to radical containing ultrafine particulate matter (PM) and how such exposure during early stages of life would affect the infant pulmonary host response to lower respiratory tract infections such as influenza virus. His research findings reported the role of regulatory T cells and IL10 in mediating the immunosuppressive effects of PM and exacerbation of influenza disease severity. He and his colleagues observed a significant increase in regulatory T cells and IL10 in PM exposed mice. Specific depletion of Tregs in PM-exposed mice enhanced protection against influenza virus. Further, IL10 deficiency protected the mice by decreasing the morbidity and pulmonary viral load. Together, these findings demonstrated the role of Tregs and IL10 in mediating PM-induced exacerbation of morbidity and mortality associated with acute influenza infection. These finding were based on our earlier observations of pulmonary immunosuppression in neonatal mice after acute inhalation exposure to PM. A number of epidemiological studies indicate relation between exposure to elevated levels of PM and an increased rate of hospitalization of children with adverse pulmonary events. The research outcomes from my studies would provide valuable insights into understanding the underlying mechanism of these PM-induced adverse pulmonary events. Also, these studies would contribute to general understanding of infant immune responses to such similar PM. It is his belief that a deeper understanding of the mechanism of PM-induced adverse events is critical to protecting susceptible infant populations. He hopes his studies will provide important insights that are valuable for understanding the public health risks of exposure to PM and aid in developing therapeutic interventions for PM-induced respiratory illnesses.

Gabriel L. Plaa Education Award

Winner: Karilyn Sant

Award Year: 2016
Current Degrees: PhD, MPH
Institution/Affiliation: University of Massachusetts Amherst

Dr. Sant is a postdoctoral fellow in Dr. Alicia Timme-Laragy's laboratory at the University of Massachusetts. The lab uses a zebrafish model to better understand the effects of endocrine disrupting compounds on pancreatic organogenesis, and seeks to identify mechanisms by which these developmental exposures may lead to metabolic dysfunction throughout the lifecourse. Her current work used two transgenic zebrafish models to visualize dysmorphogenesis of the pancreas following exposure to perfluorooctane sulfonic acid (PFOS), characterized changes in the gene expression of pancreas hormones at several developmental time points, and identified perturbations of embryonic redox state following exposure.

Harihara Mehendale Association of Scientists of Indian Origin Student Award Fund

Winner: Bharat Bhushan

Award Year: 2016
Current Degrees: PhD
Institution/Affiliation: University of Kansas Medical Center

Acetaminophen (APAP) overdose is the foremost cause of acute liver failure (ALF) in the US. Despite decades of research, current treatment options after APAP-overdose are extremely limited. Liver injury after APAP-overdose is subsequently followed by compensatory liver regeneration, which promotes recovery. Preventing liver injury and stimulating liver regeneration are potential strategies to develop novel therapies for APAP-induced ALF. However, mechanisms of APAP-induced liver toxicity or subsequent liver regeneration are not completely understood.The major focus of Dr. Bhushan's research work is to study these mechanisms. In the work that will be presented at the 2016 SOT annual meeting, we investigated role of EGFR (Epidermal Growth Factor Receptor) signaling in APAP-induced ALF. Role of EGFR signaling in APAP-induced liver toxicity and subsequent liver regeneration is completely unknown. In this extremely novel work, we demonstrated that EGFR signaling plays a dual role in APAP overdose and is involved in both initiation of APAP-induced liver injury (via mitochondrial damage) and in stimulating subsequent liver regeneration (via controlling cell cycle). Our work revealed an extremely novel and intriguing mechanisms about how a cell membrane receptor, EGFR, can translocate to mitochondria and cause both cell death or cell proliferation signaling in hepatocytes, in a time dependent manner, during APAP-induced ALF.

Harihara Mehendale Association of Scientists of Indian Origin Student Award Fund

Winner: Alok Ranjan

Award Year: 2016
Current Degrees: BS
Institution/Affiliation: Texas Tech University Health Sciences Center

Mr. Ranjan started his project on brain cancer with a very rational approach. Glioblastoma (Brain cancer) is one of the most malignant and incurable brain cancers. The median survival rate of glioblastoma patients is only 12%. Although, there are several treatment options available but glioblastoma still claims thousands of lives each year. Existing obstacles with current treatment options are (a) Recurrence of tumor within six months after surgical removal (b) Development of resistance to the current chemotherapeutic options available and (c) Inability of the drugs to cross the blood brain barrier. Most of the antipsychotic drugs cross blood brain barrier and reach the brain to provide a relief to the patients with psychotic disorder. This gave us the rationale to test toxic effect of the antipsychotic drugs against glioblastoma. We examined several antipsychotic drugs for their toxic effects against glioblastoma and discovered that penfluridol had significant toxicity against brain cancer cells. His studies also established anti-metastatic potential of penfluridol in several brain metastasis of breast cancer (Alok Ranjan, Parul Gupta and Sanjay Srivastava “Penfluridol: An antipsychotic agent suppresses metastatic tumor growth in triple negative breast cancer by inhibiting integrin signaling axis” Cancer Research 2015). We also observed that chronic treatment of mice with penfluridol was not associated with any toxicity or behavioral side effect. Since penfluridol is an FDA approved drug, the pharmacology, formulation and potential toxicities are already known. Our preclinical studies can fasten the clinical trial and review by Food and Drug Administration. This could bring relief to the patients with highly lethal and resistant brain tumor He has short term and long term goals. His goals are listed below. Short term goals: 1. He wants to have in depth knowledge of cell signaling pathways involved in glioblastoma progression, in vivo models and different skills useful in the research related to glioblastoma. 2. Publish research work in high impact factor journals. Long term goal: 1.After completing his doctoral studies, he wants to establish myself as an independent cancer researcher especially in brain tumor. 2.He wants to open a cancer center where poor or needy people suffering from cancer, who cannot afford expensive bills can get counseling and care at no cost/very low cost.

Harihara Mehendale Association of Scientists of Indian Origin Student Award Fund

Winner: Gopi Gadupudi

Award Year: 2016
Current Degrees: BS, MS
Institution/Affiliation: University of Iowa

Mr. Gadupudi's research works involves understanding the toxicity of food-borne chemicals such as PCB126. Specifically, this work involves characterizing the dose and time dependent toxicity of PCB126 in causing metabolic disorders such as diabetes, fatty liver and metabolic syndrome. Moving forward, we would like to understand the mechanisms involved in the PCB or POP induced metabolic disruption. Understanding these mechanisms would definitely aid in identifying adverse effects on human health and risk characterization.

John Doull Award

Winner: Julia Tobacyk

Award Year: 2016
Current Degrees: BS Biology
Institution/Affiliation: University of Arkansas for Medical Sciences

In this project, Ms. Tobacyk investigated whether gene by environment interactions could contribute to obesity in the context of tributyltin (TBT) exposure. In these studies, she and her team exposed four different strains of mice prenatally to low concentrations of TBT in drinking water, a common route of exposure in human populations. Previous research reported that prenatal TBT exposure increases adipocyte size/number and leads to liver steatosis (Chamorro-Garcia et al. 2011). Their studies showed that there are chemicals such as obesogens that may alter lipid metabolism. Her lab became interested and excited about the outcome of their study and therefore, they decided to investigate the effect of genetic background on prenatal TBT exposure. They observed no TBT-dependent changes in bone or fat formation, hepatic steatosis, or hepatic glutathione levels, suggesting that TBT-induced obesogenic outcomes may be context-dependent with modifiers unrelated to gene sequence (such as diet, epigenetics, or yet unknown environmental modifiers). These data may therefore enrich the dialogue regarding how and whether chemicals with obesogenic potential ought to be regulated to protect human populations. She has always been fascinated with the concept of individual responses to xenobiotics within the human population. As a second year pharmacology student, she would love to pursue a career in academia or in industry where to further expand and develop her research interests.

Laxman S. Desai ASIO Student Award Fund

Winner: Kshama Doshi

Award Year: 2016
Current Degrees: MS
Institution/Affiliation: University of Maryland Baltimore

Ms. Doshi's research is focused to design novel treatment regimens for improving long-term clinical outcome of acute myeloid leukemia patients with FLT3-ITD mutation. While doing so, she is studying various means and mechanisms to sensitize FLT3-ITD expressing leukemic cells to conventional chemotherapy. This award from ASIO-SOT is for her project which illustrates the effect of modulating Pim kinase activity to enhances the anti-cancer effects of the most widely used chemotherapy drugs

Laxman S. Desai ASIO Student Award Fund

Winner: Prachi Borude

Award Year: 2016
Current Degrees: MTech BPT
Institution/Affiliation: University of Kansas Medical Center

The primary focus of Miss Borude's research is to study regulation of liver regeneration after Tylenol overdose, specifically to improve liver regeneration and save patient without liver transplant. In this awarded research work she found that DNA in our liver gets damaged after Tylenol overdose and if that damage is not repaired, the guardian of the genome/DNA (Cell cycle checkpoint) stops the liver regeneration and the recovery in mouse model. Improving the DNA repair and removing the checkpoint may have a therapeutic benefit.

Mary Amdur Student Award Fund

Winner: Matthew Marshall

Award Year: 2016
Current Degrees: BS in Nuclear Engineering
Institution/Affiliation: New York University

It has been well documented that World Trade Center (WTC) dust has contributed to health problems in First Responders (FR). However, the mechanisms for how WTC dust chronically affects FR are not well understood, because a majority of studies have only focused on the fine particle fraction (< 2.5 µm) of WTC dust when it consists primarily of coarse (2.5-10 µm) and supercoarse (> 10 µm) particles. The pH of coarse and supercoarse particles is 10–11 so they have more potential to induce damage by causing prolonged irritation due to their highly alkaline properties. Mr. Marshall's research explores an in vivo model that simulates a WTC dust exposure comparable to 9/11/01 for FR near or around Ground Zero to see the health effects that arise over time from the WTC dust. He used RNA Sequencing to analyze the transcriptome of lung and liver samples from Day 7 and Day 360 post-exposure rats to discover and identify differentially-expressed genes (DEGs). Following RNA Sequencing, he performed pathway analysis on his DEGs to find disparate differences between Day 7 and Day 360. The results illuminated that WTC dust exacerbates injury with time, and it revealed crucial genes that could be causing molecular dysfunctions and disease. When comparing rat Day 360 lung samples to Day 7 lung samples, he found a pathway activation for atherosclerosis, atherosclerotic lesions, and a dilation of the left ventricle. He has received this award specifically for his research on the rat lungs and demonstrating how WTC dust causes irritation to the pulmonary system. This irritation from the coarse fraction of WTC dust creates an inflammatory response, which could be responsible for the formation of atherosclerosis and atherosclerotic lesions. Additionally, when comparing Day 360 liver samples to Day 7 liver samples, pathway analysis revealed an increased inflammatory response, increased proliferation of hepatic stellate cells (HSC), and decreased apoptosis of HSCs. His future research goals for this project are to take the current research and see how it relates to human tissue samples from FR. To date, there have been few transcript studies done on FR so this could help in disease mitigation and better targeted treatment therapies. These findings could truly benefit FR and better their lives.

Mary Amdur Student Award Fund

Winner: Parker Duffney

Award Year: 2016
Current Degrees: MS
Institution/Affiliation: University of Rochester

People who are exposed to cigarette smoke are at an increased risk for viral lung infections, however the mechanism of how cigarette smoke affects the lung immune response to viral pathogens is not fully understood. Mr. Duffney's work investigates how cigarette smoke affects epithelial cells in the lung in the context of a viral challenge. His work shows that cigarette smoke impairs a proper antiviral response to a viral mimetic by disrupting the production of key antiviral molecules. Also he found that proteolytic processing of a key pathogen recognition receptor, TLR3, is necessary for proper anti-viral signaling. Furthermore, exposure to cigarette smoke alters proper TLR3 signaling resulting in a dampened response to a viral mimetic. Future aims of this project look to develop novel therapeutic strategies to resolve smoke-induced immune defects that can be used to treat smokers to lessen the risk of viral lung infections.

Molecular Biology Specialty Section Postdoctoral Fellow Research Award

Winner: Anna Kopec

Award Year: 2016
Current Degrees: PhD
Institution/Affiliation: Michigan State University

Overdose of acetaminophen (APAP) is the leading cause of drug-induced acute liver injury in the U.S. and other developed countries, because APAP is present in >600 over-the-counter and prescription medications, making accidental (as well as intentional) overdose a serious public concern. Current therapies for management of APAP overdose patients are very limited and are usually only effective when administered very early. Understanding the mechanisms of liver repair after APAP overdose is necessary to develop effective therapies to stimulate liver regeneration and re-establish liver function in patients after APAP overdose. Dr. Kopec's work focuses on understanding the role of fibrinogen in APAP-hepatotoxicity. Utilizing mice with a specific mutation in fibrinogen molecule that lacks a binding motif for an integrin expressed on leukocytes she identified key molecular events and a novel pathway of liver regeneration after APAP overdose in mice. Her studies are aimed at identifying existing knowledge gaps and are likely to reveal novel strategies to prevent liver failure after APAP overdose, even in patients presenting with extensive hepatotoxicity.

Molecular Biology Specialty Section Postdoctoral Fellow Research Award

Winner: Jenna Currier

Award Year: 2016
Current Degrees: PhD
Institution/Affiliation: ORISE at US EPA

As a current postdoctoral fellow at the U.S. EPA, Dr. Currier is studying the underlying mechanisms that differentiate cellular responses to oxidative exposures in human lung cells for the purpose of biomarker discovery and predictive model development using a systems biology approach. The work for which she won this award involved characterizing adverse effects in human lung cells and determining gene expression changes that can distinguish exposures at the tipping point of cell death.

Molecular Biology Specialty Section Postdoctoral Fellow Research Award

Winner: Priyanka  Trivedi

Award Year: 2016
Current Degrees: PhD
Institution/Affiliation: Harvard Medical School

Dr. Trivedi's research focuses on discovering therapeutic targets for acute and chronic kidney diseases. Kidney fibrosis, the hallmark of chronic kidney disease (CKD), is an irreversible process leading to the life-threatening end-stage renal failure. Unfortunately, no effective therapeutic strategies are available to cure this condition. This is due to lack of our understanding of the underlying mechanisms of fibrosis. Using RNA sequencing, she and her colleagues identified phospholipase D4 (PLD4) as one of the targets for the treatment of kidney fibrosis. Our research work deciphers a mechanistic role of PLD4 in the regulation of fibrosis. They observed that PLD4 was significantly increased in mechanistically different mouse models of kidney fibrosis as well as in patients with biopsy-proven kidney fibrosis. Furthermore, they found that PLD4 knockout mice (PLD4-/-) showed less fibrosis compared to the wild type (PLD4+/+) mice after folic acid injection- as well as unilateral ureteral obstruction-induced kidney fibrosis. This was attributed to mainly two reasons, (i) PLD4-/- mice had increased level of anti-fibrotic cytokines compared to the PLD4+/+ mice and, (ii) sustained activation of the proteases, due to decreased level of serpina1 (a protease inhibitor) in PLD4-/- mice, led to an efficient degradation of collagen rescuing these mice from scar tissue formation in the kidney. Thus they identified that PLD4 is a central target that can be intervened in preventing fibrosis-associated organ dysfunction. Her future goal is to continue contributing to the mechanistic toxicological sciences, which can be translated clinically.

Molecular Biology Student Award Fund

Winner: Vivekkumar Dadhania

Award Year: 2016
Current Degrees: MS (Pharm)
Institution/Affiliation: University of Louisiana at Monroe (ULM)

It is widely known that low to moderate doses of hepatotoxicants such as acetaminophen (APAP), carbon tetrachloride (CCl4), and thioacetamide (TA) cause minimal liver necrosis in mice and rats. At such low doses, the initiated injury does not expand to cause the organ failure and animal death due to the stimulated compensatory liver regeneration (CLR). At lethal doses however, the initiated injury expands uncontrollably causing liver failure and death of the animals. This expansion occurs even after the offending toxicant is completely eliminated from the body by 8 to 10 half-lives (10h for APAP in mice). This indicates that the continued progression of liver injury at lethal doses of toxicants is not dependent on the presence of toxicants in the body. So how does that injury expand? To the best of our knowledge, entire biomedical literature is silent on what causes the unabated expansion of toxicant-initiated liver injury in the absence of offending toxicant in the body. Therefore, it is worthwhile to identify such mechanisms of liver injury expansion. Moreover, finding out the mechanisms of liver regeneration that can potentially restore the damaged liver to its normal structure and function is equally important to rescue the toxicant-poisoned patients. Mr. Dadhania's thesis work addresses this area of toxicology. He and his colleagues found that Ca2+-dependant hydrolytic enzyme such as secretory phospholipase A2 (sPLA2) get spilt out of the dying cells after lethal dose exposure. The spilt sPLA2 is highly activated by the extracellular high Ca2+ (1.3mM), now termed as death protein, and causes the expansion of APAP-initiated liver injury in mice. This mechanism of injury expansion is independent of the presence of toxicant in the body. Our data indicate that hepatic expression of annexin A1 (ANX1) and annexin A2 (ANX2), the endogenous inhibitors of sPLA2, in the proliferating hepatocytes during the pre­placed CLR in response to liver injury induced by a small dose of TA affords protection against a lethal dose of APAP (TA+APAP treated mice). ANX1 and ANX2 expression on the plasma membrane of the hepatocytes strongly supports our hypothesis of the inhibition of spilt sPLA2-mediated unrestrained destruction of the hepatocytes. We also found that it is timely activation and appropriate termination of the Wnt/ß-catenin signaling that drives well-balanced liver regeneration in the TA+APAP treated mice. Their studies demonstrate that a novel life-saving strategy can be developed by targeting death protein sPLA2 and Wnt/ß-catenin pathway to rescue the APAP-overdosed patients. Mr. Dadhania feels that his graduate studies at the ULM have provided a solid toxicology background with exceptional research training. In particular, he found the hepatotoxicity and liver regeneration research of Dr. Mehendale and Dr. Apte highly intriguing and exhilarating. Soon after his PhD, he looks forward to have an outstanding opportunity to make a successful career as a toxicology scientist and continue his relationship with SOT in whatever manner he can.

Molecular Biology Student Award Fund

Winner: Gloria Garcia

Award Year: 2016
Current Degrees: BS
Institution/Affiliation: Oregon State University

Ms. Garcia's research uses the zebrafish model to understand unexplored mechanisms of gene expression. Specifically, she is trying to determine the relationship between a nuclear receptor (AHR), a transcription factor required for proper vertebrate development (Sox9b), and a regulatory RNA molecule (Sox9b-lncRNA) in the context of normal development and under chemical perturbation. Thus far, she and her colleagues have determined that Sox9b-lncRNA is expressed in distinct tissue-specific patterns adjacent to Sox9b, the expression levels and patterns of Sox9b-lncRNA are altered by strong AHR ligands in an AHR dependent manner, and normal Sox9b mRNA expression levels and in situ patterns require the presence of Sox9b-lncRNA. Our data has led to the following hypothesis: The conserved Sox9b-lncRNA is a direct AHR target gene that transcriptionally represses Sox9b upon induction by strong AHR ligands to produce target organ specific toxicity. Her long term career goal is to become an independent investigator running her own laboratory using the zebrafish model and systems biological approaches to identify mechanistic links between chemical exposures, lncRNA regulation, and pathology of disease.

Molecular Biology Student Award Fund

Winner: Jeffrey Willy

Award Year: 2016
Current Degrees: BS, BM, MS
Institution/Affiliation: Indiana University School of Medicine

Currently a Ph.D. candidate at Indiana University School of Medicine, Mr. Willy studies the role of the Unfolded Protein Response (UPR) in the progression of NASH. Specifically, he has shown that the UPR regulates both secretion and autophagy through a novel adapter protein IBTKa during the progression of NASH at both the cellular level and in human patient samples. It is his hope to apply his molecular and translational training to better understand preclinical and clinical risk assessment.

Molecular Biology Student Award Fund

Winner: Rance Nault

Award Year: 2016
Current Degrees: BSc, MSc
Institution/Affiliation: Michigan State University

Mr. Nault's research examines the role of environmental contaminants of the development of fatty liver disease. In order to explore these questions a combination of ‘omic’ techniques is used to examine changes in gene expression regulation, gene expression, and metabolites, and integrate these using a variety of computational tools. Consequently, by using these data together he and his colleagues can look at changes within the context of the whole system. In the future Mr. Nault will delve deeper into key features that were highlighted by these high-throughput evaluations, more specifically on the role of PKM2 in fatty liver caused by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) which is the research for which this award was given. They found that following TCDD exposure, a change in the PKM isoform is observed which reprograms metabolism similar to that of a cancer cell. Further evidence in metabolite and protein levels demonstrated that the livers of TCDD treated mice exhibit many features of cancer cells despite the absence of cancer. He concludes that this isoform switching likely plays a role in antioxidant defenses. Future work will examine this hypothesis in further depth using genetic models.

Perry J. Gehring Biological Modeling Student Award Fund

Winner: Rachel Worley

Award Year: 2016
Current Degrees: BS, MA
Institution/Affiliation: CDC/ATSDR, University of Georgia

Ms. Worley's research applies in vitro-to-in vivo extrapolation to develop a a PBPK model for perfluorooctanoic acid (PFOA) in the rat that includes physiological descriptions of transporter kinetics in the kidney. PFOA exhibits sex-specific clearance in the rat. This is thought to be primarily driven by hormonally regulated expression of organic anion transporters (OATs) on the apical and basolateral membranes of the proximal tubule cells. Her model includes in vitro-derived descriptions of these transporters and successfully simulates time-course serum, liver, and urine data for intravenous (IV) and oral exposures in both male and female rats. Thus, this work supports the hypothesis that sex-specific serum half-lives for PFOA are largely driven by expression of transporters in the kidney and contributes to the development of PBPK modeling as a tool for evaluating the role of transporters in renal clearance. Future work will apply this method to develop a PBPK model for PFOA exposure in humans that includes physiologically-based descriptions of kidney transporters.

Perry J. Gehring Diversity Student Travel Award

Winner: Lizbeth Perez-Castro

Award Year: 2016
Current Degrees: Undergraduate Student
Institution/Affiliation: University of Puerto Rico at Cayey

Perry J. Gehring Risk Assessment Best Postdoctoral Fellow Abstract Award

Winner: Marjory Moreau

Award Year: 2016
Current Degrees: PhD
Institution/Affiliation: Health Canada

The use of computational modeling can help interpret and integrate in vitro screening data and biomonitoring results to improve the prioritization of chemicals in risk assessment. There is still work needed to improve at making these toxicity screening results more relevant to human exposure and risk assessment. The work of Dr. Moreau and colleagues will be used to assist in developing predictive tools and informing the utility of non-traditional toxicity data for Health Canada assessment of chemicals. The general population is exposed to many chemicals that can have various possible health effects. Levels of exposure of a population to these chemical or their metabolites can be surveyed using biomonitoring data. Despite the usefulness of this data, it is sometimes difficult to interpret the levels of exposure in a risk assessment context. The past few years, advances in toxicity testing methods such as systems biology and high-throughput screening have brought new ways to assess the potential harm from chemicals. Margin of exposures between endpoints and exposure levels can be used to bridge the data generated from these new toxicity methods and effectively screen biological activities into a common measure. The purpose of my research is (1) to estimate exposure from biomonitoring levels in the population using physiologically-based pharmacokinetic (PBPK) model for flame retardants (hexabromocyclododecane, HBCD) and (2) to compare human equivalent dose metrics based on in vitro and in vivo endpoints from high throughput screening assays (HTS) results.

Perry J. Gehring Risk Assessment Student Award Fund

Winner: Brittany Weldon

Award Year: 2016
Current Degrees: BS
Institution/Affiliation: University of Washington School of Public Health

Ms. Weldon's research focuses on assessing the risk of adverse health effects from exposure to silver nanoparticles by various exposure routes. Additionally, her research investigates the potential for silver nanoparticles to interact with sensitive organ systems such as the developing central nervous system and reproductive system. This award will help her continue in these endeavors and with the broader goals of applying toxicological sciences to improve human and environmental health.

Regulatory and Safety Evaluation Specialty Section Student Award

Winner: Jasmine Brown

Award Year: 2016
Current Degrees: BS
Institution/Affiliation: US Environmental Protection Agency

Thousands of environmental compounds have not been characterized for their potential to cause developmental neurotoxicity (DNT). Due to the need for DNT hazard identification, efforts to develop alternative screening assays is a high priority. In an effort to address this issue, Ms. Brown's research focuses on developing a high-throughput in vitro method for screening compounds for DNT potential. This research evaluates the use of primary cortical neural cultures on microelectrode arrays (MEAs) to screen compounds for DNT hazard. The MEA platform utilizes an electrophysiological approach to identifying compounds as having the potential to cause DNT by measuring the changes in neural function of treated primary cortical cultures. Specifically, she discusses further evaluation of a set of known DNT compounds as well as compounds that show no evidence of DNT in vivo using the MEA platform discussed earlier. Near future goals include analyzing this content rich data to provide us with more information on how “hits” would be determined in this assay. Eventually, she and her colleagues hope to implement this method as an initial screen allowing for prioritization of these compounds for further testing, and providing support for regulatory decision making.

Regulatory and Safety Evaluation Specialty Section Student Award

Winner: Brittany Weldon

Award Year: 2016
Current Degrees: BS
Institution/Affiliation: University of Washington School of Public Health

Ms. Weldon's research focuses on assessing the risk of adverse health effects from exposure to silver nanoparticles by various exposure routes. Additionally, her research investigates the potential for silver nanoparticles to interact with sensitive organ systems such as the developing central nervous system and reproductive system. This award will help her continue in these endeavors and with the broader goals of applying toxicological sciences to improve human and environmental health.

Renal Toxicology Fellowship Award Fund

Winner: Ramya Kolli

Award Year: 2016
Current Degrees: MS
Institution/Affiliation: Interdisciplinary Toxicology Program

Ozonation is used for the disinfection of drinking water and one of its major byproducts is bromate. Bromate is a possible human carcinogen whose mechanism of action is not totally understood. Ms. Kolli and her colleagues study the effects of bromate on one of the cell cycle checkpoint proteins p21, which is protective against various nephrotoxic effects. However it is also hypothesized to drive carcinogenesis via its ability to inhibit apoptosis. They previously showed that bromate increased p21 expression in renal cells in vitro. She and her colleagues hypothesize that this occurs via epigenetic mechanisms. To test this hypothesis we analyzed DNA methylation and histone acetylation using high-throughput techniques like next-generation sequencing and chromatin immunoprecipitation assays, respectively. Understanding the effects of bromate on DNA methylation and histone acetylation of p21 would bridge the gaps-in-knowledge about the mechanisms of bromate-induced nephrotoxicity. This knowledge would further facilitate understanding the carcinogenic effects of bromate and mechanisms of action of other disinfection byproducts.

Renal Toxicology Fellowship Award Fund

Winner: Priyanka  Trivedi

Award Year: 2016
Current Degrees: PhD
Institution/Affiliation: Harvard Medical School

Dr. Trivedi's research focuses on discovering therapeutic targets for acute and chronic kidney diseases. Kidney fibrosis, the hallmark of the chronic kidney disease (CKD), is an irreversible process leading to life-threatening end-stage renal failure. Unfortunately, no effective therapeutic strategies are available to cure this condition. This is due to lack of our understanding of the underlying mechanisms of fibrosis. Using RNA sequencing, we identified phospholipase D4 (PLD4) as one of the targets for the treatment of kidney fibrosis. Her research deciphers a mechanistic role of PLD4 in the regulation of fibrosis. She and her colleagues observed that PLD4 was significantly increased in mechanistically different mouse models of kidney fibrosis as well as in patients with biopsy-proven kidney fibrosis. Further, they found that PLD4 knockout mice (PLD4-/-) showed less fibrosis compared to the wild type (PLD4+/+) mice after folic acid injection- as well as unilateral ureteral obstruction-induced kidney fibrosis. This was attributed to mainly two reasons, (i) PLD4-/- mice had increased level of anti-fibrotic cytokines compared to the PLD4+/+ mice and, (ii) sustained activation of the proteases, due to decreased level of serpina1 (a protease inhibitor) in PLD4-/- mice, led to an efficient degradation of collagen rescuing these mice from scar tissue formation in the kidney. Thus they identified that PLD4 is a central target that can be intervened in preventing fibrosis-associated organ dysfunction. Her future goal is to continue contributing to the mechanistic toxicological sciences, which can be translated clinically.

Renal Toxicology Fellowship Award Fund

Winner: Mira Pavkovic

Award Year: 2016
Current Degrees: PhD
Institution/Affiliation: Harvard Medical School - LSP

Drug-induced kidney injury is frequently encountered in hospitalized patients, but routinely used markers are insensitive and nonspecific. Dr. Pavkovic is evaluating a small class of RNAs, microRNAs, in urine as new biomarkers for this type of kidney injury. For the evaluation she is using urine samples from two cohorts of patients with acetaminophen- or cisplatin-induced kidney injury. Our results indicate that three specific microRNAs (miR-21, -200c and -423) in combination with the known protein biomarker KIM-1 could be non-invasive as well as specific biomarkers for the detection of drug-induced kidney injury in patients. Based on the kidney expression and target analysis of the three microRNAs they could add information about the affected molecular pathways in the injured kidney.

Robert J. Rubin Student Award Fund

Winner: Kristin Bircsak

Award Year: 2016
Current Degrees: BS
Institution/Affiliation: Rutgers University

Ms. Bircsak's dissertation research focuses on the regulation of the placental BCRP transporter, which is an efflux transporter that helps to protect the developing fetus from xenobiotic exposure by actively transporting chemicals out of the placenta. Previously, she and colleagues characterized the ability of soy dietary component, genistein, to inhibit the BCRP-mediated transport of the gestational diabetes medication, glyburide by two distinct mechanisms: 1) competitively inhibiting glyburide transport and 2) reducing BCRP protein expression in a placental cell model. More recently, we observed transcription factor expression and genetic variants to be associated with up to a 6-fold variation in BCRP mRNA expression between healthy, human term placentas. Importantly, two genetic variants in the non-coding region of the BCRP gene were associated with reduced BCRP mRNA expression in the placentas of Asian infants. This research aims to identify a population that may be vulnerable to fetal exposure to harmful chemicals, which in turn may help to improve the individualized prescribing of drugs during pregnancy.

Robert J. Rubin Student Award Fund

Winner: Dana Lauterstein

Award Year: 2016
Current Degrees: MS, PhD Candidate
Institution/Affiliation: New York University

The use of electronic cigarettes (e-cigarettes) during early life stages may pose a significant risk to the developing central nervous system, and Ms. Lauterstein's work seeks to examine potential adverse outcomes associated with exposure to these products throughout gestation and lactation. Furthermore, this work addresses the emerging need for studies examining early life exposure to environmental toxicants and later adult disease. She received this award for a portion of her doctoral work that was presented this year at the SOT Annual Meeting. She exposed pregnant mice to aerosols produced from e-cigarettes with and without nicotine via whole body inhalation. The mice were exposed throughout gestation, and after birth both mothers and offspring were exposed to e-cigarette aerosols together throughout the lactational period. Following lactational exposure a subset of male and female offspring were sacrificed (~1-month-old at time of sacrifice) and RNA Sequencing was preformed on frontal cortex samples to examine global genomic changes. Subsequently, pathway analyses enabled the prediction of downstream biological outcomes associated with the observed changes in levels of gene expression. Results from this study demonstrated that e-cigarettes, both with and without nicotine, induced sex-dependent gene expression changes associated with predicted adverse neurobiological and neurobehavioral outcomes similar to those associated with early life exposure to the smoke from conventional cigarettes. Another subset of mice was used for behavioral testing in adulthood (done in collaboration with Dr. Cory-Slechta at the University of Rochester). I wish to contribute much-needed research for the toxicological assessment of alternative tobacco products (ATPs). Many ATPs, including e-cigarettes, are being used widely in the U.S. and around the world today. Many, if not all of them pose sizeable health risks, but are not adequately studied and/or regulated and thus are perceived to have reduced harm when compared to conventional cigarettes. After she finishes her doctoral degree Ms. Lauterstein would like to have a career in risk assessment for a regulatory agency where her work directly influences public health policy decisions. She also wishes to play a role in communicating scientific findings with the general public to further their knowledge of potential toxicological dangers in their environment.

Roger O. McCellan Student Award Fund

Winner: Manushree Bharadwaj

Award Year: 2016
Current Degrees: BVSc
Institution/Affiliation: Oklahoma State University

Despite recent advances in therapy, heart failure is a major public health problem with persistently high morbidity and mortality rates and high health care costs. The background and preliminary data available today provide a strong rationale for our current study of the therapeutic strategy of augmentation of cardiac parasympathetic signaling in heart failure. Under normal conditions, the heart is involuntarily under the control of our nervous system which is called as the Autonomic nervous system. This autonomic nervous system has two limbs, sympathetic and parasympathetic nervous system. These two systems work antagonistically, for example, sympathetic system increases the heart rate and parasympathetic system decreases the heart rate. Under healthy conditions there exists a balance between these two systems. This balance is lost during the conditions of the failing heart. Sympathetic over-activity and parasympathetic withdrawal indicate profound dysregulation of autonomic control. Currently, high sympathetic tone is controlled by the administration of beta-blockers, such as atenolol. Additionally, activation of the parasympathetic tone improves autonomic balance and may lead to a better prognosis for heart failure patients (Adamopoulos et al., 1995). Pyridostigmine is an acetylcholinesterase inhibitors which increases the activity of the parasympathetic system in the heart. It is a quaternary ammonium compound which belongs to the class of carbamates. This drug is used by militaries as a prophylactic agent against organophosphate poisoning and is also indicated for the symptomatic treatment of Myasthenia gravis. Ms. Bharadwaj's overall hypothesis is that “pyridostigmine administration will improve autonomic regulation during congestive heart failure and enhance the rate of survival associated with this disease, as predicted by pharmacokinetic parameters and their associated covariates.” Her overall objective is to develop a population PK/PD model to predict the association between human PK/PD parameters and the covariates and establish an exercise model of rodent to determine the effects of pyridostigmine on heart rate recovery in rat. In order to test the above hypothesis, she and her colleagues have designed three specific aims. As their first aim, they are developing highly sensitive and specific analytical assays to be able to quantify the amount of pyridostigmine and its metabolite, 3-hydroxy-N-methylpyridinium, in plasma samples from heart failure patients. In the second specific aim, we will collect all available information about the pharmacodynamic and pharmacokinetic parameters tested in the patients, details of the covariates etc. Using this information, they will perform population pharmacokinetic (PK) and pharmacodynamic (PD) modelling to identify the covariates that affect the disposition of pyridostigmine. For this purpose we will use non-linear mixed effect modelling software, abbreviated as NONMEM. The third aim for this research was to develop an animal exercise model to be able to estimate post-exercise heart rate recovery in rats. She won the award for this section of her research. According to our hypothesis, administration of pyridostigmine in rats will enhance the heart rate recovery after submaximal exercise on a treadmill. To test this hypothesis, they investigated the effects of pyridostigmine administration on cardiac parasympathetic function in rats. Radiotelemetry device was surgically implanted in rats to record ECG and heart rates. The rats were treated with pyridostigmine and observed for any cholinergic signs. The rats followed an exercise protocol on treadmill, so that heart rate during rest and after exercise was recorded to calculate the heart rate recovery at 1 and 5 minute post-exercise. They found that HRR was significantly higher in the PYR rats on days 7, 14 and 28 (p=0.003, <0.001, 0.03). Vagal tone (measured as HR after atropine treatment) was increased in PYR rats which was shown by a 17% decrease in HR compared to only 3% in CTL rats (p<0.001). Together, these data supported the hypothesis that PYR enhances HRR by increasing cardiac vagal tone. Post-exercise HRR can be used in toxicology or pharmacology studies to assess parasympathetic tone in rats. Her future goal is to further confirm the stability and tolerability of pyridostigmine in congestive heart failure patients. It is also required to determine the effect or toxicity of pyridostigmine, if any, in patients who are already taking some prescription drugs to manage their heart conditions.

Ronald G. Thurman Student Travel Award

Winner: Bharat Bhushan

Award Year: 2016
Current Degrees: PhD
Institution/Affiliation: University of Kansas Medical Center

Acetaminophen (APAP) overdose is the foremost cause of acute liver failure (ALF) in the US. Despite decades of research, current treatment options after APAP-overdose are extremely limited. Liver injury after APAP-overdose is subsequently followed by compensatory liver regeneration, which promotes recovery. Preventing liver injury and stimulating liver regeneration are potential strategies to develop novel therapies for APAP-induced ALF. However, mechanisms of APAP-induced liver toxicity or subsequent liver regeneration are not completely understood. The major focus of my research work is to study these mechanisms. In the work that will be presented at the 2016 SOT Annual Meeting, Dr. Bhushan and colleagues investigated role of EGFR (Epidermal Growth Factor Receptor) signaling in APAP-induced ALF. Role of EGFR signaling in APAP-induced liver toxicity and subsequent liver regeneration is completely unknown. In this extremely novel work, they demonstrated that EGFR signaling plays a dual role in APAP overdose and is involved in both initiation of APAP-induced liver injury (via mitochondrial damage) and in stimulating subsequent liver regeneration (via controlling cell cycle). Their work revealed an extremely novel and intriguing mechanisms about how a cell membrane receptor, EGFR, can translocate to mitochondria and cause both cell death or cell proliferation signaling in hepatocytes, in a time dependent manner, during APAP-induced ALF.

Ronald G. Thurman Student Travel Award

Winner: Hui Li

Award Year: 2016
Current Degrees: MS
Institution/Affiliation: University of Arizona

Ms. Li's research is concentrating on adverse drug reactions (ADRs) associated with non-alcoholic fatty liver disease(NAFLD), the most common chronic liver disease across the world. Her lab has demonstrated that patients with NAFLD could experience higher risk of potential ADRs. They further observed that expression and activity of many enzymes involved in drug metabolism processes were significantly altered during NAFLD progression. Her research is focusing on one important category of those enzymes, called Cytochrome p450s (CYPs). They play very critical roles in the metabolism of majority of clinical drugs. In this present study, she evaluated the activity of a few major members from CYPs in the pediatric patients with non-alcoholic steatohepatitis, the most severe form of NAFLD. She reported significant alterations in these enzymes in pediatric NASH. These alterations could introduce unexpected ADRs in these pediatric patients. With this study, they intend to alert current clinical practice to recognize NAFLD and NASH as one potential risk factor of ADRs, and take this into consideration during dosage determinations.

Ronald G. Thurman Student Travel Award

Winner: Suvarthi Das

Award Year: 2016
Current Degrees: MS
Institution/Affiliation: University of South Carolina

CYP2E1 has been found to play a key role in the development of nonalcoholic fatty liver disease. CYP2E1-mediated oxidative stress leads to hepatocellular necrosis and release of damage associated molecular patterns including NAD, ATP and HMGB1. Interestingly, DAMPs are known to act as ligands to pattern recognition receptors like P2X7r and toll like receptors. Our previous results showed a clear role of TLR4 trafficking into lipid rafts that was dependent on NADPH oxidase induced peroxynitrite in NASH pathogenesis. Extending our previous findings we test the hypothesis that CYP2E1-mediated oxidative stress and its downstream HMGB1 release regulates Myd88 expression that is critical for innate immune activation in NASH. Using a high fat (60%kcal) induced NASH model where bromodichloromethane is used as a second hit, we show that there was a significant increase in MyD88 mRNA and protein in NASH mice while the levels were significantly decreased in a CYP2E1 KO and Diallyl sulfide-treated (CYP2E1 inhibitor) groups. HMGB1 levels were significantly higher in NASH group as compared to only high fat diet-treated group and CYP2E1 KO or DAS-treated group suggesting a strong correlation. Higher HMGB1 and higher MyD88 also correlated strongly with NASH progression, higher serum ALT, hepatocellular necrosis, ballooning and inflammation while MYd88 KO mice receiving identical treatment showed significant decrease in these symptoms. Mechanistically immortalized Kupffer cells treated with HMGB1 and leptin (represents strong leptin resistance) showed a significant increase in MyD88 and 3-nitrotyrosine formation while apocynin or Fetpps blocked the increase suggesting a possible role of NADPH oxidase mediated peroxynitrite. To show the role of oxidative stress and activation of PI3K pathway, HMGB1-primed cells were treated with PI3/AKT pathway inhibitor LY294002. Results showed that LY294002 significantly inhibited MyD88 levels, CD68 expression and MCP1 release suggesting a strong role of PI3/AKT pathway in redox stress mediated MyD88 expression and Kupffer cell activation. In conclusion Ms. Das and colleagues report a novel role of redox stress mediated MYD88 induction in NASH pathogenesis that might be complementary to the TLR4 pathway.

Sheldon D. Murphy Award Fund

Winner: Mary Francis

Award Year: 2016
Current Degrees: BA
Institution/Affiliation: Rutgers University

Ms. Francis is currently studying a nuclear receptor, farnesoid x receptor (FXR), that is involved in bile acid synthesis in the liver. This nuclear receptor is not well studied in the lung, however,FXR activation is known to attenuate the inflammatory response. To evaluate the contribution of FXR to ozone-induced lung injury and repair, FXR-/- mice were used. This research suggests that FXR plays a role in anti-inflammatory activities that counters ozone injury. Identification of the FXR activity may be important in the development of novel therapeutics aimed at reducing lung inflammatory diseases.

Sheldon D. Murphy Award Fund

Winner: Leah Norona

Award Year: 2016
Current Degrees: BS
Institution/Affiliation: University of North Carolina at Chapel Hill

Ms. Norona's research interests involve understanding the fundamental mechanisms underlying drug- and chemical-induced liver injury leading to fibrosis. Fibrosis is essentially an abnormal wound healing response to chronic insult and involves multiple cell types. In order to better understand the early events leading to fibrosis, she and colleagues turned to a three-dimensional approach which has a number of advantages over some of the simple and short-lived conventional model systems. They were able to demonstrate compound-induced fibrosis in this 3D model system which recapitulated some key features of fibrotic disease giving us confidence in the model system to study the series of early and adaptive events and a better understanding of fibrosis development. Her future goals are to better understand and develop more physiologically relevant in vitro model systems useful for toxicity risk assessment.

Sheldon D. Murphy Award Fund

Winner: Ludwik Gorczyca

Award Year: 2016
Current Degrees: BA
Institution/Affiliation: Rutgers University

Currently Mr. Gorczyca is working on determining the regulation of various transporters in the placenta and whether or not it can be affected by changes in oxygen tension, a common phenomenon during the placental development. Specifically, compared to atmospheric levels (20% O2), the early placenta develops under hypoxic conditions (3% O2) and by the second trimester the oxygen tension rises to 8% O2. He has shown that exposure of BeWo human choriocarcinoma cells and term human placental explants (n=6) to 3, 8, and 20% oxygen for 24 h alters the mRNA, protein, and function of uptake and efflux transporters (BCRP, MRP1-3,5, MDR1, OATP4A1). Exploring the potential transcriptional regulatory factors of BCRP down-regulation he found a significant reduction of mRNA expression of nuclear receptors PPAR gamma and RXR alpha as well as transcription factors AhR and NRF2 under hypoxic conditions. Together, these data suggest that placental expression of transporters is differentially regulated by hypoxia, and that the fetus may be at higher risk of exposure to some xenobiotics early in pregnancy and during fetal diseases associated with hypoxia such as preeclampsia.

Sheldon D. Murphy Award Fund

Winner: Aram Cholanians

Award Year: 2016
Current Degrees: BS
Institution/Affiliation: The University of Arizona

Parkinson's Disease is the second most common neurodegenerative disorder, belonging to a larger family of diseases collectively known as synucleinopathies. This family of diseases is characterized by accumulation of a small prion-like neuronal protein, alpha-synuclein. Mr. Cholanians and his colleagues currently show that exposure to environmentally relevant concentrations of Arsenic, induces accumulation of alpha-synuclein and other stress markers. Moreover, in their animal model, animals that were exposed transiently to arsenic show signs of increase in alpha-synuclein and other stress markers. Their research suggests that low level arsenic exposure, even for a short period of time, may increase the risk of developing synucleinopathy and/or neurodegeneration.

Sheldon D. Murphy Award Fund

Winner: Natalie Holman

Award Year: 2016
Current Degrees: BS Biology
Institution/Affiliation: University of North Carolina Chapel Hill

Ms. Holman's research focuses on mechanisms of drug-induced liver injury, specifically the role of small extracellular vesicles known as exosomes in early liver stress. This award was granted based on her work establishing alterations in hepatocyte-derived exosome content prior to overt hepatocellular toxicity in rats and humans. She and her colleagues are currently expanding on these findings to understand the signaling capacity of exosomes released after drug exposure. Her goal is to utilize this knowledge to better understand the mechanisms underlying drug-induced liver injury and ultimately improve its prediction and treatment.

Toshio Narahashi Neurotoxicology Fellowship Award Fund

Winner: Jasmine Brown

Award Year: 2016
Current Degrees: BS
Institution/Affiliation: US Environmental Protection Agency

Thousands of environmental compounds have not been characterized for their potential to cause developmental neurotoxicity (DNT). Due to the need for DNT hazard identification, efforts to develop alternative screening assays is a high priority. In an effort to address this issue, Ms. Brown's research focuses on developing a high-throughput in vitro method for screening compounds for DNT potential. This research evaluates the use of primary cortical neural cultures on microelectrode arrays (MEAs) to screen compounds for DNT hazard. The MEA platform utilizes an electrophysiological approach to identifying compounds as having the potential to cause DNT by measuring the changes in neural function of treated primary cortical cultures. Specifically, my poster discusses further evaluation of a set of known DNT compounds as well as compounds that show no evidence of DNT in vivo using the MEA platform discussed earlier. Near future goals include analyzing this content rich data to provide us with more information on how “hits” would be determined in this assay. Eventually, their hope is to implement this method as an initial screen allowing for prioritization of these compounds for further testing, and providing support for regulatory decision making.

Toshio Narahashi Neurotoxicology Fellowship Award Fund

Winner: Dana Lauterstein

Award Year: 2016
Current Degrees: MS, PhD Candidate
Institution/Affiliation: New York University

The use of electronic cigarettes (e-cigarettes) during early life stages may pose a significant risk to the developing central nervous system, and Ms. Lauterstein's work seeks examine potential adverse outcomes associated with exposure to these products throughout gestation and lactation. Furthermore, this work addresses the emerging need for studies examining early life exposure to environmental toxicants and later adult disease. She has received this award for a portion of her doctoral work that is being presented this year at the SOT Annual Meeting. Her project involved exposing pregnant mice to aerosols produced from e-cigarettes with and without nicotine via whole body inhalation. The mice were exposed throughout gestation, and after birth both mothers and offspring were exposed to e-cigarette aerosols together throughout the lactational period. Following lactational exposure a subset of male and female offspring were sacrificed (~1-month-old at time of sacrifice) and RNA Sequencing was preformed on frontal cortex samples to examine global genomic changes. Subsequently, pathway analyses enabled the prediction of downstream biological outcomes associated with the observed changes in levels of gene expression. Results from this study demonstrated that e-cigarettes, both with and without nicotine, induced sex-dependent gene expression changes associated with predicted adverse neurobiological and neurobehavioral outcomes similar to those associated with early life exposure to the smoke from conventional cigarettes. Another subset of mice was used for behavioral testing in adulthood (done in collaboration with Dr. Cory-Slechta at the University of Rochester). Her wish is to contribute much-needed research for the toxicological assessment of alternative tobacco products (ATPs). Many ATPs, including e-cigarettes, are being used widely in the U.S. and around the world today. Many, if not all of them pose sizeable health risks, but are not adequately studied and/or regulated and thus are perceived to have reduced harm when compared to conventional cigarettes. After she receives her doctoral degree she would like to have a career in risk assessment for a regulatory agency where her work will directly influence public health policy decisions. She also wishes to play a role in communicating scientific findings with the general public to further their knowledge of potential toxicological dangers in their environment.

Toshio Narahashi Neurotoxicology Fellowship Award Fund

Winner: Katriana Popichak

Award Year: 2016
Current Degrees: BS
Institution/Affiliation: Colorado State University

Ms. Poichak is a PhD candidate in the Cell and Molecular Biology Program at Colorado State University in Dr. Ronald Tjalkens' laboratory. Together they research neurodegenerative disease, such as Parkinson's disease and manganism. Her research involves the identification of what causes these diseases and how we can halt their progression. I hope to determine what environmental factors and exposures, as well as genetics and cellular pathways, are involved in the death of neurons. The research for which she was awarded is to identify the cellular mechanism that a novel anti-inflammatory drug is able to inhibit cellular injury and death in a Parkinson's disease model in astrocytes, brain cells needed to support neurons. She hopes to be a professor at the university level so that she may encourage and inspire young researchers to achieve greatness.

Toshio Narahashi Neurotoxicology Fellowship Award Fund

Winner: Kimberly Keil

Award Year: 2016
Current Degrees: PhD
Institution/Affiliation: University of California Davis

Neurodevelopmental disorders affect 1 in 10 children in the US and rates are increasing. Environmental factors are implicated in these disorders and are thought to interact with genetic susceptibilities. However, mechanisms by which environmental chemicals interact with genetic factors to confer individual risk remain a current knowledge gap in our understanding of these diseases. Epigenetic changes, which are modifications to DNA that alter gene expression without altering the DNA sequence, are one mechanism by which genes and environment may interact to influence individual neurodevelopmental disease risk; however, there is a paucity of experimental data in direct support of this mechanism. The goal of Dr. Keil's current research is to address this gap, yielding novel mechanistic data regarding not only the developmental neurotoxicity of polychlorinated biphenyls (PCBs), which are a current risk to the developing human brain, but also the role of the epigenome, specifically DNA methylation, in gene-environment interactions that confer risk for adverse neurodevelopmental outcomes. Collectively, her results presented at the 2016 SOT meeting suggest that enzymes responsible for DNA methylation regulate basal dendritic growth in vitro and that their expression can be modified by PCB 95. These observations suggest DNA methyltransferase enzymes as a target of PCB developmental neurotoxicity that may represent a convergence point for gene-environment interactions that influence the risk and/or severity of neurodevelopmental disorders. This information is urgently needed to inform rational strategies for minimizing neurodevelopmental risk by mitigating relevant exposures and for identifying novel therapeutic targets and is an area she intends to pursue in her career goal of becoming a tenure track faculty member.

Toshio Narahashi Neurotoxicology Fellowship Award Fund

Winner: Marissa Sobolewski

Award Year: 2016
Current Degrees: PhD
Institution/Affiliation: University of Rochester

Recent research has shown that developmental exposure to low-dose endocrine disrupting chemical (EDC) mixtures can produce enhanced male reproductive disease, yet, little is known about the extension of such cumulative effects to the central nervous system (CNS). As a key target of EDCs, multiple hits, even small ones, along a hormonal cascade may overwhelm the neuroendocrine system’s ability to compensate, altering pathways that converge downstream on a single disease phenotype. To address this possibility, Dr. Sobolewski's research aims to understand how exposure to relatively low doses of four EDCs, all with different modes of action, but common downstream consequences on mesocorticolimbic (MESO) neurotransmitter function and behavior: Atrazine, Perfluorooctanoic acid, Bisphenol-A, 2,3,7,8- tetrachlorodibenzo-p-dioxin and their mixture (MIX), can disrupt neurobehavioral development. Preliminary data revealed male-specific enhanced responses to MIX, including increased postnatal testosterone (T), life-long endocrine and neurotransmitter deficits, reproductive malformations and adult behavioral deficits. The male-specific, enhanced behavioral deficits occurred across behavioral domains mediated by MESO function, including reduced attention/memory, increased risk-taking, implusitivity, and reduced sociality. In contrast, no enhanced MIX effects were observed in females, despite single EDCs producing deficits. Altered attention, impulsivity, decreased sociality, increased developmental testosterone with concomitant reproductive alterations have all been associated with the etiology of male-biased neurobehavioral diseases, such as ADHD and autism spectrum disorders. Given that humans are chronically exposed to mixtures and the highly sex-specific nature of our findings, the proposed studies provide an ideal platform to study the role of EDC mixtures in the etiopathology of behavioral disorders with sex-biased prevalence rates. Her future goals are to continue this research to unveil the complicated systems-level changes that occur with early disruption of endocrine signaling during development.

Toshio Narahashi Neurotoxicology Fellowship Award Fund

Winner: Miles Bryan

Award Year: 2016
Current Degrees: BS Marine Biology
Institution/Affiliation: Vanderbilt University

Mr. Bryan's research is focused on understanding how disruptions in manganese homeostasis may contribute to Huntington's Disease (HD) pathology. In particular, he is interested in how Mn deficiency might disrupt critical cell signaling pathways which give rise to HD symptoms and phenotypes. The work presented this year at SOT is focused on how PI3K and autophagy might regulate Mn homeostasis and also how Mn uptake might be able to stimulate and rescue autophagy pathways which are defective in HD.

Toshio Narahashi Neurotoxicology Fellowship Award Fund

Winner: Shivani Ghaisas

Award Year: 2016
Current Degrees: BS, MS
Institution/Affiliation: Iowa State University

Broadly, Ms. Ghaisas's focus on comprehending the impact of environmental toxins on the enteric nervous system and its downstream effects on the central nervous system (CNS) via the gut-brain axis. In conjunction with this project, she is also assessing the effect of metal toxicity on the gut physiology and gut-brain axis. Another project deals with the development of a nano-vaccine platform to effectively deliver drugs protecting the CNS from traumatic brain injury induced neuro-inflammation and neuro-degeneration.

Toshio Narahashi Neurotoxicology Fellowship Award Fund

Winner: Marshall Edwards

Award Year: 2016
Current Degrees: BS Microbiology
Institution/Affiliation: The University of Texas Health Science Center at San Antonio

The focus of Mr. Edward's research involves investigating the role of serotonin and how it modulates social behavior. The lab he currently work in measures preference for social interaction in mouse models. His work that won the NTSS Toshio Narahashi Neurotoxicology Fellowship Award, he and colleagues decided to characterize the cytokine profile (immune response), following injection with acetaminophen, in mice shown to exhibit an autistic-like phenotype. These mice were then allowed to mature to postnatal day 80 in which their behavior was observed and measured. They aimed at investigating the effect such a challenge would elicit in these mice in regards to their social behavior. After he graduates with his MS in Immunology & Infection, he plans on entering a PhD program to further my education.

Toshio Narahashi Neurotoxicology Fellowship Award Fund

Winner: Briana De Miranda

Award Year: 2016
Current Degrees: PhD
Institution/Affiliation: University of Pittsburgh

Dr. De Miranda's research is focused on using gene therapy to mitigate the death of dopamine neurons, and the underlying pathology of Parkinson’s disease. Using the pesticide rotenone, a mitochondrial toxin, she and her colleagues can recapitulate several of the features of human Parkinson’s disease, including the loss of dopamine producing neurons. This study focuses on injecting a lentivirus (containing the human protein DJ-1) into the rodent brain that is targeted for astrocytes, the most abundant cell type in the central nervous system. They have found that astrocyte-specific expression of human DJ-1 protein is protective against the neurotoxicity of rotenone. This study has shown that targeting non-neuronal cells is a possible mechanism for successful mitigation of the underlying pathology of Parkinson’s disease. The next phase of this project will begin to look at the mechanisms behind astrocyte-specific DJ-1 protection of dopamine neurons in the rotenone model of Parkinson's disease.

Toxicologists of African Origin Endowment Fund

Winner: Chiagoziem Otuechere

Award Year: 2016
Current Degrees: MSc
Institution/Affiliation: Redeemer's University

Mr. Otuechere is working on a remedy for liver diseases by screening potential medicinal plants. He is also elucidating the molecular mechanisms for their protective action. He aims to win grants to further this line of research and also to be an authority/mentor in the field of molecular toxicology. His research, which won this award, for the first time, demonstrated the hepatoprotective effects of a locally consumed vegetable in Nigeria, Pterocarpus mildbraedii on pesticide-induced liver injury.

Toxicologists of African Origin Endowment Fund

Winner: Motunrayo Akande

Award Year: 2016
Current Degrees: DVM, MVM, PhD
Institution/Affiliation: University of Abuja

Dr. Akande lectures and conducts research in Veterinary Pharmacology and Toxicology at the University of Abuja in Nigeria. Her research focus is the alleviation of cases of poisoning caused by pesticides and heavy metals through the use of functional amino acids that have antioxidant and bioprotective effects. Her future goals are to develop additional antidotes for the abrogation of pesticides and heavy metals toxicities in biological systems. She also intends to mentor students and professional colleagues in Veterinary Toxicology. The specific research for which she won this award entailed the attenuation of neuromuscular dysfunction by taurine (a semi essential functional amino acid)in male Wistar rats exposed to chronic chlorpyrifos (an organophosphate insecticide) toxicity.The results of the research indicated that chlorpyrifos might have induced deficits in neuromuscular coordination through oxidative stress and inhibition of acetylcholinesterase. It was deduced that taurine might be beneficial for the protection of animals against the toxic effects of chlorpyrifos through its antioxidative and acetylcholinesterase restorative properties.

Toxicologists of African Origin Endowment Fund

Winner: Salmon Adebayo

Award Year: 2016
Current Degrees: PhD
Institution/Affiliation: Tshwane University of Technology

The use of herbal remedies for therapeutic purpose is widely considered to be safe due to its long history of use and anecdotal claim of efficacy. However, some plant species are known to synthesize poisonous chemical that are capable of adversely impacting on the health of consumers. Unfortunately, thorough evaluation of herbal products for safety is rare and manufacturers are not mandated to proof the safety of their products before making them available to the public. Dr. Adebayo's research is focused on the evaluation of herbal products for safe use, and the potential impact on the health and well being of consumers. In addition, assessments of possible interaction occurring as a result of concurrent use of herbal products and conventional drugs is of great interest to him. According to the WHO, more than 80% of the people in developing countries rely on traditional medicare systems for their primary health care needs. Therefore, assessments of herbal remedies for safety is vital for the protection of public health and possibly the quality of life of consumers. The TAO award is a testament to the interests of the award committee in the promotion of the quality of life of users of herbal products in developing countries.

Toxicologists of African Origin Endowment Fund

Winner: Ashley Jordan

Award Year: 2016
Current Degrees: BS Chemistry
Institution/Affiliation: New York University Sackler Institute

Ms. Jordan's lab (Dr. Max Costa) focuses mainly on the toxic and carcinogenic effects of various metals. Her thesis work as been specifically focused on the carcinogenic effects of nickel. Her ultimate goal is to conduct relevant and meaningful research that will advance the field of environmental toxicology. It is imperative to the health of humans and animals alike that we understand the effects and mechanisms of action of environmental toxins that we are exposed to. With regard to the work she is presenting this year, her lab found that a particular gene, SATB2 may play a key role in metal (specifically nickel) induced carcinogenesis. Understanding the induction of the SATB2 gene could potentially lead to new diagnostic tests and treatments for those living with the effects of metal induced toxicity and/or cancer.

Toxicologists of African Origin Endowment Fund

Winner: Olalekan Ogunsakin

Award Year: 2016
Current Degrees: MD, MPH, PhD
Institution/Affiliation: Tulane University

In the last couple of years, Dr. Ogunsakin has had the opportunity and rare privilege of learning from and working closely with my Research Advisor and Principal Investigator, Dr. Michael McCaskill. Thier research is focused on understanding the mechanisms by which excessive alcohol affect vitamin D metabolism and the subsequent effects (chronic and acute) on anti-microbial peptides in human lung. Specifically, in the award-winning abstract, his poster will show our research findings that chronic over-consumption of alcohol reduces the levels of anti-microbial peptides in different human samples and tissues (BALF, monocytes and alveolar epithelial cells. This reduction has a potential adverse effect on human health as it predisposes vulnerable individuals to severe forms of associated lung infection, especially bacteria pneumonia, which has been widely documented to be highly prevalent and severe among patients diagnosed with Alcohol Use Disorder (AUD). His future goal is to pursue a career as a toxicologist in academia or industry and work extensively on projects in the field of toxicology (translational), especially as it relates to human exposure and health.

Toxicologists of African Origin Endowment Fund

Winner: Gbedolo Honesty Tohon

Award Year: 2016
Current Degrees: MPH, MSC
Institution/Affiliation: University of Montreal

The work described in Mr. Tohon's poster presentation consists in reconstructing the toluene concentrations in residential indoor air concordant with the blood measurements reported by the Canadian Health Measures Survey using reverse dosimetry modeling. The overall aim of his research is to improve the toxicological risk assessment by providing new tools for estimating external exposure to VOCs (alone or combinations)from their biomonitoring data increasingly available in national health surveys. These tools will help us to use human biological data to estimate the relevant environmental concentrations that reflect the real human exposure conditions (e.g.: multiple exposures, differences between exposure levels in human populations). Comparisons can then be made with guidance values which are derived from the traditional toxicological method using animal models and with the qualitative values from epidemiological surveys. A very important aspect taken into account in this work concerns the physiological inter-individual variability that is integrated into his models.

Toxikon, a Preclinical Tox Organization, & Dr. Dharm Singh ASIO Award Fund

Winner: Siva Prasad Bitragunta

Award Year: 2016
Current Degrees: MSc, PhD
Institution/Affiliation: Birla Institute of Technology and Science Pilani, Hyderabad Campus, India

Applications of nanotechnology led to the intentional and unintentional release of nanomaterials into various compartments of environment. It raised the concerns about environmental health impacts of nanomaterials. In this regard, one of the new dimensions of toxicology in 21st Century inheres in assessing the environmental health impacts of nanomaterials. In this context, outcomes of Dr. Bitragunta's research in the field of nanoecotoxicology assist in codifying the influence of nanomaterial properties on their fate and behavior in environment. The study also paraphrases the importance of invertebrate sentinels in divulging the basis nanoparticle toxicity. In future, he is planning to pursue post-doc research in nanotoxicology and allied areas. After his post-doc, he wants to focus career trajectory into the line of academics or research. He won the award for encompassing the principle of ‘omics’ to unravel biomarkers of TiO2 nanomaterial toxicity in coelomic fluid of invertebrate, earthworm. In conclusion, his research definitely aids in interpreting nanomaterial toxicity thereby designing innovative approaches to environmental monitoring of nanomaterials. Consequently, he is interested in unifying the outcomes of current toxicology research in disseminating the knowledge of environmental nanotoxicology in 21st Century.

Toxikon, a Preclinical Tox Organization, & Dr. Dharm Singh ASIO Award Fund

Winner: Indarchand Gupta

Award Year: 2016
Current Degrees: MSc
Institution/Affiliation: Institute of Science

Now a days Silver nanoparticles are getting more attention in nanotechnology. Through several methods they are being synthesized and are used for many applications. Our lab has expertise in synthesizing silver nanoparticles by using fungi. This technique is called as Mycosynthesis of silver nanoparticles. This method of synthesis is preferred over other methods of synthesis such as Chemical and Physical methods.It is because this method is biocompatible and does not uses any toxic material for the synthesis. Such mycosynthesised silver nanoparticles are finding many applications. But the possible harm/toxicity associated with their overuse has been less studied. Therefore, Mr. Gupta's aim is to study the toxicity of these mycosynthesised silver nanoparticles on animal cell lines and soil beneficial bacterium. The award winning paper describes the toxicity of mycosynthesised silver nanoparticles to Pseudomonas putida which is the bacteria beneficial for soil environment. After analysing the obtained data through this study we concluded that if such nanoparticles get accumulated in the soil, it will disturb the soil ecosystem and therefore their use should be controlled.

Vera W. Hudson and Elizabeth K. Weisburger Scholarship Fund

Winner: Kyla Walter

Award Year: 2016
Current Degrees: BA
Institution/Affiliation: University of California Davis

Ms. Walter's research focuses on developing a better understanding of the impacts of exposure to thyroid hormone disrupting compounds. Thyroid hormones (THs) are known to be important for multiple cellular processes from development through adulthood and play an especially critical role in fetal neurodevelopment. There are a number of environmental contaminants that are known to disrupt TH-mediate signaling, thus they are suspected to cause developmental neurotoxicity. However the identification of mechanisms linking TH disruption to adverse impacts on neurodevelopment have been limited by major gaps in the understanding of how THs influence specific neurodevelopmental processes and the identification of endpoints that are sensitive to TH. Her project aims to develop a better understanding of how THs contribute to neurodevelopment, using larval zebrafish as a model, and to identify endpoints that are sensitive to TH disruption. By establishing TH-sensitive neurodevelopmental endpoints in larval zebrafish, her research project will facilitate the future development of mechanism based in vivo screening tools to identify TH disrupting chemicals that cause developmental neurotoxicity and pose a risk to human, animal, and environmental health.

Vera W. Hudson and Elizabeth K. Weisburger Scholarship Fund

Winner: Logeswari Ponnusamy

Award Year: 2016
Current Degrees: DVM, MVSc
Institution/Affiliation: The Institute of Environmental and Human Health, Texas Tech University

Ms. Ponnusamy's current doctoral research focus on the role of epigenetic mechanisms in oxidant/pro-oxidants induced oxidative stress mediated resistance to chemotherapeutic drugs in cancer cells. Chemotherapy is the only treatment of choice for advanced-stage cancer while resistance to chemotherapy accounts 90% of treatment-failure that remains major hurdle for clinical management. Mounting evidences strongly associates the role of environmental-toxicants and oxidative stress in both cancer development and chemotherapeutic resistance. Thus the interaction between gene-environment (epigenetic regulation) is crucial event in chemotherapeutic response. As limited knowledge exists on epigenetic regulation of acquired chemoresistance, fathoming epigenetic mechanisms in relevant resistance cell model resembles the clinical resistance could advance mechanistic basis to understand drug resistance. Bringing together her multifaceted scholarship (DVM and Masters in Veterinary Pharmacology and Toxicology), she wants to become an interdisciplinary cancer researcher incorporating toxicology elements. Specific research for which she has won the award focuses on the role of chronic oxidative stress and associated epigenetic mechanisms in chemoresistance development. Her novel research findings have provided direct evidence for role of chronic oxidative stress in acquired resistance for doxorubicin in renal carcinoma cells, and for the first time revealed that oxidative stress induced acquired resistance is mechanistically mediated by DNA hypermethylation mediated silencing of mismatch repair (MMR) gene MSH2 and loss of MMR-dependent apoptosis. These findings are highly significant clinically, as they may open a new avenue for application of epigenetic and/or anti-oxidant therapy in renal cell carcinoma patients.

Women in Toxicology SIG Celebrating Women in Toxicology Award

Winner: Kristin Licko

Award Year: 2016
Current Degrees: BS
Institution/Affiliation: Water Quality Association

As the Toxicology Manager for the Water Quality Association, Ms. Licko collaborates with other members of the Joint Peer Review Steering Committee (JPRSC) which is comprised of representatives from competing ANSI accredited product certification bodies working together to reconcile and develop safe levels for chemicals found in drinking water treatment products. It is a delicate balance of sharing expenses, directives, and producing defensible criteria – in addition to all of our individual organizational priorities. We have made exceptional progress toward making sure all products are evaluated to the same safe levels, no matter where product certification is sought. In choosing this profession and expanding upon her education, she hopes to work to continue the directive of the JPRSC and improve her skills in order to develop risk assessments for chemicals we are exposed to that have not yet been evaluated.

Women in Toxicology SIG Celebrating Women in Toxicology Award

Winner: Dana Lauterstein

Award Year: 2016
Current Degrees: MS
Institution/Affiliation: New York University

The use of electronic cigarettes (e-cigarettes) during early life stages may pose a significant risk to the developing central nervous system, and Ms. Lauterstein's work seeks examine potential adverse outcomes associated with exposure to these products throughout gestation and lactation. Furthermore, this work addresses the emerging need for studies examining early life exposure to environmental toxicants and later adult disease. She has received this award for a portion of her doctoral work that she is presenting this year at SOT. For her project she exposed pregnant mice to aerosols produced from e-cigarettes with and without nicotine via whole body inhalation. The mice were exposed throughout gestation, and after birth both mothers and offspring were exposed to e-cigarette aerosols together throughout the lactational period. Following lactational exposure a subset of male and female offspring were sacrificed (~1-month-old at time of sacrifice) and RNA Sequencing was preformed on frontal cortex samples to examine global genomic changes. Subsequently, pathway analyses enabled the prediction of downstream biological outcomes associated with the observed changes in levels of gene expression. Results from this study demonstrated that e-cigarettes, both with and without nicotine, induced sex-dependent gene expression changes associated with predicted adverse neurobiological and neurobehavioral outcomes similar to those associated with early life exposure to the smoke from conventional cigarettes. Another subset of mice was used for behavioral testing in adulthood (done in collaboration with Dr. Cory-Slechta at the University of Rochester). She wishes to contribute much-needed research for the toxicological assessment of alternative tobacco products (ATPs). Many ATPs, including e-cigarettes, are being used widely in the U.S. and around the world today. Many, if not all of them pose sizeable health risks, but are not adequately studied and/or regulated and thus are perceived to have reduced harm when compared to conventional cigarettes. After she finishes her doctoral degree she would like to have a career in risk assessment for a regulatory agency where her work directly influences public health policy decisions. She also wishes to play a role in communicating scientific findings with the general public to further their knowledge of potential toxicological dangers in their environment.

Women in Toxicology SIG Celebrating Women in Toxicology Award

Winner: Kimberly Keil

Award Year: 2016
Current Degrees: PhD
Institution/Affiliation: University of California Davis

Neurodevelopmental disorders affect 1 in 10 children in the US and rates are increasing. Environmental factors are implicated in these disorders and are thought to interact with genetic susceptibilities. However, mechanisms by which environmental chemicals interact with genetic factors to confer individual risk remain a current knowledge gap in our understanding of these diseases. Epigenetic changes, which are modifications to DNA that alter gene expression without altering the DNA sequence, are one mechanism by which genes and environment may interact to influence individual neurodevelopmental disease risk; however, there is a paucity of experimental data in direct support of this mechanism. The goal of Dr. Keil's current research is to address this gap, yielding novel mechanistic data regarding not only the developmental neurotoxicity of polychlorinated biphenyls (PCBs), which are a current risk to the developing human brain, but also the role of the epigenome, specifically DNA methylation, in gene-environment interactions that confer risk for adverse neurodevelopmental outcomes. Collectively, her results presented at the 2016 SOT meeting suggest that enzymes responsible for DNA methylation regulate basal dendritic growth in vitro and that their expression can be modified by PCB 95. These observations suggest DNA methyltransferase enzymes as a target of PCB developmental neurotoxicity that may represent a convergence point for gene-environment interactions that influence the risk and/or severity of neurodevelopmental disorders. This information is urgently needed to inform rational strategies for minimizing neurodevelopmental risk by mitigating relevant exposures and for identifying novel therapeutic targets and is an area she intends to pursue in her career goal of becoming a tenure track faculty member.

Women in Toxicology SIG Celebrating Women in Toxicology Award

Winner: Samantha Snow

Award Year: 2016
Current Degrees: BS, PhD
Institution/Affiliation: US EPA

Dr. Snow's research focuses on investigating the adverse pulmonary, cardiovascular, and metabolic effects associated with exposure to gaseous pollutants in susceptible animal models, and determining the role stress hormones may play in these adverse responses. This current research explores the notion that dietary supplementation with fish oil or olive oil would attenuate ozone-induced metabolic impairments.

Young Soo Choi Student Scholarship Award Fund

Winner: Yoonjeong Jang

Award Year: 2016
Current Degrees: DVM, BS
Institution/Affiliation: Seoul National University

As a research vet, Miss Jang performs not only in vivo experiments for cancer therapy but also in vitro studies for alternative toxicity test. The purpose of her research is to benefit both human and animals. By bringing out the strong point of research vet, she is eager to be a distinguished worldwide toxicologist who contributes to development of our society. She has a dream to become a global scholar and heighten Korean status in the world. She hopes that her achievements will contribute to the enhancement of scientific technology.

SOT/AstraZeneca/SOT Endowment Fund/IUTOX Travel Awards

Khaled Abdou, PhD, Beni Suef University, Beni Suef, Egypt
Amos O. Abolaji, PhD, University of Ibadan, Ibadan, Oyo State, Nigeria
Motunrayo G. Akande, PhD, University of Abuja, Abuja, Nigeria
Huawei Duan, PhD, National Institute of Occupational Health and Poison Control, Beijing, China
Patient Guedenon, PhD, University of Abomey-Calavi, Cotonou, Littoral, Benin
Jin Hongtao, PhD, New Drug Safety Evaluation Center of Chinese Academy of Medical Sciences, Beijing, China
Carine J. Marks, MSc, Tygerberg Hospital Poison Centre, Stellenbosch University, Cape Town, South Africa
Davaadorj Rendoo, MD, National Institute for Public Health, Ulaanbaatar, Mongolia
Palanisamy Sankar, PhD, Tamil Nadu Veterinary and Animal Sciences University, Thanjavur, Tamil Nadu, India
Tawit Suriyo, PhD, Chulabhorn Research Institute, Laksi, Bangkok, Thailand

Go to: Historical Archive of Endowment Fund Award Recipients