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Recent Endowment Fund Award Recipients

2017 Endowment Awardees



Angelo Furgiuele Young Investigator Technology Award

Winner: Rachel Shaffer

Award Year: 2017
Current Degrees: BA
Institution/Affiliation: University of Washington School of Public Health

Ms. Shaffer thought it very exciting to receive news of the award, which will provide much needed assistance to help advance research in advanced in vitro techniques for testicular toxicity evaluation.

Under the direction of Dr. Elaine Faustman, she and colleagues have developed an in vitro 3D testicular co-culture system (3D-TCS) to evaluate male reproductive toxicants. Because testicular toxicity is often a driver for chemical and drug risk assessments, there is a great need for in vitro alternative models of the testes. The next step in the work described above will be to translate the 3D testes culture system from cell-culture plates to a microphysiologic system (MPS), also known as “organ on a chip” or “organotypic culture systems.” Our department is one of Environmental Protection Agency (EPA)’s Predictive Toxicology Centers, which is focused on developing and validating organotypic culture systems across multiple organs. The team is uniquely positioned to advance these technologies because of the presence of Nortis, Inc in the Seattle area. Faculty members in the department have developed MPS for liver and lung systems. They have yet to transition their testes model to the chip system because of funding limitations. With the receipt of this award, however, they will be able to move forward with plans to develop a “testis on a chip” model. The initial plan will be to demonstrate maintenance of healthy cell populations in the testis chip system for 14 -21 days. Next, they will validate the system through treatment with a known testicular toxicant, cadmium. Once the system is reliable and validated, they will be able to proceed with a variety of investigations that will significantly advance the field of reproductive toxicology. For example, they can explore the role of metabolizing enzymes and cytokines within the testes chip system, and will also be able to connect the liver chip system to the testes chip system to understand how biotransformation in the liver may affect testicular toxicity. The plan is to apply the findings of their work to elucidate adverse outcome pathways (AOPs) for testicular toxicity. Ms. Shaffer thought it very exciting to receive news of the award, which will provide much needed assistance to help advance research in advanced in vitro techniques for testicular toxicity evaluation. Under the direction of Dr. Elaine Faustman, she and colleagues have developed an in vitro 3D testicular co-culture system (3D-TCS) to evaluate male reproductive toxicants. Because testicular toxicity is often a driver for chemical and drug risk assessments, there is a great need for in vitro alternative models of the testes. The next step in the work described above will be to translate the 3D testes culture system from cell-culture plates to a microphysiologic system (MPS), also known as “organ on a chip” or “organotypic culture systems.” Our department is one of Environmental Protection Agency (EPA)’s Predictive Toxicology Centers, which is focused on developing and validating organotypic culture systems across multiple organs. The team is uniquely positioned to advance these technologies because of the presence of Nortis, Inc in the Seattle area. Faculty members in the department have developed MPS for liver and lung systems. They have yet to transition their testes model to the chip system because of funding limitations. With the receipt of this award, however, they will be able to move forward with plans to develop a “testis on a chip” model. The initial plan will be to demonstrate maintenance of healthy cell populations in the testis chip system for 14 -21 days. Next, they will validate the system through treatment with a known testicular toxicant, cadmium. Once the system is reliable and validated, they will be able to proceed with a variety of investigations that will significantly advance the field of reproductive toxicology. For example, they can explore the role of metabolizing enzymes and cytokines within the testes chip system, and will also be able to connect the liver chip system to the testes chip system to understand how biotransformation in the liver may affect testicular toxicity. The plan is to apply the findings of their work to elucidate adverse outcome pathways (AOPs) for testicular toxicity.

Carl C. Smith Student Mechanisms Award Fund

Winner: Kelly Fader

Award Year: 2017
Current Degrees: BSc
Institution/Affiliation: Michigan State University

Ms. Fader said it was an honor to learn that she had been selected as a finalist for the Carl C Smith Student Mechanisms Award. She immediately shared the news with her principal investigator, Dr. Timothy Zacharewski, as well as the postdoctoral researchers in the lab, who shared in the excitement. It is a great feeling to receive recognition for the research that she has been working on over the past three years from fellow scientists in the field of toxicology. She looks forward to attending the Mechanisms Specialty Section Reception in Baltimore at the 2017 Annual Society of Toxicology Meeting for the announcement of the winner.

Metabolic syndrome, a disease which consists of obesity, elevated blood lipids, high blood pressure and high blood sugar, is approaching epidemic levels in the United States. In the liver, MetS is first observed as fat accumulation which can develop into non-alcoholic fatty liver disease (NAFLD), a risk factor for diabetes, cardiovascular disease and liver cancer. Recently, several environmental contaminants including dioxin have been implicated in MetS development. In mice, dioxin causes accumulation of fat in the liver (fatty liver), primarily originating from the diet, which progresses to inflammation and fibrosis over time. Her research investigates dioxin-induced changes along the intestinal tract that promote the development of NAFLD and other complex metabolic disorders. Specifically, the manuscript she submitted for consideration of the Carl C Smith Award investigated the role of dioxin-elicited iron overloading in the progression of NAFLD. Upon completing her PhD at Michigan State University, she plans to obtain further postdoctoral training before pursuing an independent research career at either an academic institution or the Environmental Protection Agency (EPA). She would like to remain in the field of biomedical toxicology, investigating the effects of environmental contaminants, food ingredients, and drugs on human health and disease. In particular, she is interested in investigating the role of gene-environment interactions in the development and progression of complex multifactorial diseases such as metabolic syndrome and cancer. Ms. Fader said it was an honor to learn that she had been selected as a finalist for the Carl C Smith Student Mechanisms Award. She immediately shared the news with her principal investigator, Dr. Timothy Zacharewski, as well as the postdoctoral researchers in the lab, who shared in the excitement. It is a great feeling to receive recognition for the research that she has been working on over the past three years from fellow scientists in the field of toxicology. She looks forward to attending the Mechanisms Specialty Section Reception in Baltimore at the 2017 Annual Society of Toxicology Meeting for the announcement of the winner. Metabolic syndrome, a disease which consists of obesity, elevated blood lipids, high blood pressure and high blood sugar, is approaching epidemic levels in the United States. In the liver, MetS is first observed as fat accumulation which can develop into non-alcoholic fatty liver disease (NAFLD), a risk factor for diabetes, cardiovascular disease and liver cancer. Recently, several environmental contaminants including dioxin have been implicated in MetS development. In mice, dioxin causes accumulation of fat in the liver (fatty liver), primarily originating from the diet, which progresses to inflammation and fibrosis over time. Her research investigates dioxin-induced changes along the intestinal tract that promote the development of NAFLD and other complex metabolic disorders. Specifically, the manuscript she submitted for consideration of the Carl C Smith Award investigated the role of dioxin-elicited iron overloading in the progression of NAFLD. Upon completing her PhD at Michigan State University, she plans to obtain further postdoctoral training before pursuing an independent research career at either an academic institution or the Environmental Protection Agency (EPA). She would like to remain in the field of biomedical toxicology, investigating the effects of environmental contaminants, food ingredients, and drugs on human health and disease. In particular, she is interested in investigating the role of gene-environment interactions in the development and progression of complex multifactorial diseases such as metabolic syndrome and cancer.

Carl C. Smith Student Mechanisms Award Fund

Winner: Dahea You

Award Year: 2017
Current Degrees: PharmD, PhD Candidate
Institution/Affiliation: Rutgers University

Ms. You was very pleased and honored to receive the news that she was selected as the finalist for this prestigious award. It really reminded her of the importance of the research that she is pursuing and provided further motivation to drive her project.

She was really interested in research during her pharmacy program and thus decided to obtain deeper knowledge and skills in pursuing research to achieve her career goals as a clinical researcher. Toxicology was a very attractive field where she feels she could maximally incorporate her clinical knowledge with basic science. She was greatly interested in neurotoxicology and decided to pursue her current research. There are yet lots of aspects that need more extensive investigations in the field of neurotoxicology and with her clinical and scientific knowledge, it is her hope to play an unique role in expanding this subject area. Ms. You was very pleased and honored to receive the news that she was selected as the finalist for this prestigious award. It really reminded her of the importance of the research that she is pursuing and provided further motivation to drive her project. She was really interested in research during her pharmacy program and thus decided to obtain deeper knowledge and skills in pursuing research to achieve her career goals as a clinical researcher. Toxicology was a very attractive field where she feels she could maximally incorporate her clinical knowledge with basic science. She was greatly interested in neurotoxicology and decided to pursue her current research. There are yet lots of aspects that need more extensive investigations in the field of neurotoxicology and with her clinical and scientific knowledge, it is her hope to play an unique role in expanding this subject area.

Carl C. Smith Student Mechanisms Award Fund

Winner: Bryan Harder

Award Year: 2017
Current Degrees: BS
Institution/Affiliation: University of Arizona

Mr. Harder felt it was a terrific honor to be selected to receive the Mechanism Specialty Section's Carl C. Smith Graduate Student Award. His initial reaction to becoming a finalist was tremendous relief, because two members from my laboratory have previously won this prestigious award. Because of this, there is a large amount of pressure to conduct award-worthy science and he is extremely pleased to learn that his hard work has paid off. It is his hope to showcase this accomplishment on his CV and resume as he prepares to apply and interview for jobs in the coming months. He is confident that this award will attract excellent scientists, which will allow him to continue working on challenging research projects in the field of cancer pharmacology and cancer toxicology.

Under the supervision of Dr. Donna Zhang, his lab largely focuses on understanding cancer progression and finding ways to suppress this phenomenon. They have recently described how activation of a transcription factor called NRF2 is frequently observed in various cancers, and that inhibition of this factor can help chemotherapy work better. Typically, the events that lead to NRF2 overexpression are due to genetic mutations, but his research has pinpointed a novel mechanism of unwanted NRF2 activation via activation of the progesterone receptor. He has shown that women who take progestins for the treatment of Type 1 Endometrial cancer could be susceptible to activation of NRF2, potentially leading to acquired chemoresistance in their tumors. He has identified a novel progesterone receptor target gene, TSC22D4, that aberrantly activates the NRF2 pathway, providing a new link between hormone receptor signaling and NRF2 research and how they relate to cancer progression. He feels that his work is a good representation of the quality of science that typically comes out of the lab and hopes that future students can utilize this finding to continue to pursue this interesting story. It is his intent to publish this research soon after the SOT meeting and use it to showcase his intellectual abilities while applying to cancer research positions. Mr. Harder felt it was a terrific honor to be selected to receive the Mechanism Specialty Section's Carl C. Smith Graduate Student Award. His initial reaction to becoming a finalist was tremendous relief, because two members from my laboratory have previously won this prestigious award. Because of this, there is a large amount of pressure to conduct award-worthy science and he is extremely pleased to learn that his hard work has paid off. It is his hope to showcase this accomplishment on his CV and resume as he prepares to apply and interview for jobs in the coming months. He is confident that this award will attract excellent scientists, which will allow him to continue working on challenging research projects in the field of cancer pharmacology and cancer toxicology. Under the supervision of Dr. Donna Zhang, his lab largely focuses on understanding cancer progression and finding ways to suppress this phenomenon. They have recently described how activation of a transcription factor called NRF2 is frequently observed in various cancers, and that inhibition of this factor can help chemotherapy work better. Typically, the events that lead to NRF2 overexpression are due to genetic mutations, but his research has pinpointed a novel mechanism of unwanted NRF2 activation via activation of the progesterone receptor. He has shown that women who take progestins for the treatment of Type 1 Endometrial cancer could be susceptible to activation of NRF2, potentially leading to acquired chemoresistance in their tumors. He has identified a novel progesterone receptor target gene, TSC22D4, that aberrantly activates the NRF2 pathway, providing a new link between hormone receptor signaling and NRF2 research and how they relate to cancer progression. He feels that his work is a good representation of the quality of science that typically comes out of the lab and hopes that future students can utilize this finding to continue to pursue this interesting story. It is his intent to publish this research soon after the SOT meeting and use it to showcase his intellectual abilities while applying to cancer research positions.

Carl C. Smith Student Mechanisms Award Fund

Winner: Emma Bowers

Award Year: 2017
Current Degrees: MS
Institution/Affiliation: University of North Carolina Chapel Hill

Ms. Bowers is thrilled to have received the Carl C. Smith award. Many of the most successful scientists in SOT have received this award, and she is honored to be in their ranks. This award will help her to gain recognition as a leader in the toxicology field. Additionally this award will help offset travel costs associated with attending the annual meeting.

She is conducting research at the US EPA Human Studies facility under the direction of Dr. David Diaz-Sanchez and Dr. Shaun McCullough. In her dissertation research she uses a novel application of human primary cell culture to identify molecular mechanisms that mediate differential susceptibility to ozone exposure. She is examining two long-observed but poorly understood ozone inflammatory responses that may hold the key to understanding differences in susceptibility: response heterogeneity and adaptation. As air pollutant exposure causes inflammation which contributes to the leading cause of mortality- cardiopulmonary diseases- her research has the potential to make a significant public health impact. After her doctoral studies her plan is to obtain a post-doctoral position and eventually become a principal investigator. As a PI, she will continue investigating mechanisms of toxicity with a specific emphasis on toxicoepigenomics research. Ms. Bowers is thrilled to have received the Carl C. Smith award. Many of the most successful scientists in SOT have received this award, and she is honored to be in their ranks. This award will help her to gain recognition as a leader in the toxicology field. Additionally this award will help offset travel costs associated with attending the annual meeting.She is conducting research at the US EPA Human Studies facility under the direction of Dr. David Diaz-Sanchez and Dr. Shaun McCullough. In her dissertation research she uses a novel application of human primary cell culture to identify molecular mechanisms that mediate differential susceptibility to ozone exposure. She is examining two long-observed but poorly understood ozone inflammatory responses that may hold the key to understanding differences in susceptibility: response heterogeneity and adaptation. As air pollutant exposure causes inflammation which contributes to the leading cause of mortality- cardiopulmonary diseases- her research has the potential to make a significant public health impact. After her doctoral studies her plan is to obtain a post-doctoral position and eventually become a principal investigator. As a PI, she will continue investigating mechanisms of toxicity with a specific emphasis on toxicoepigenomics research.

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

Winner: Satya Achanta

Award Year: 2017
Current Degrees: DVM, PhD
Institution/Affiliation: Duke University School of Medicine

Dr. Achanta feels honored to receive this prestigious award. As an aspiring scientist, this award will be a feather in his hat and give him more enthusiasm to pursue toxicological research.

The treatment of chlorine gas induced acute lung injury (ALI) remains challenging because of the lack of mechanism-based therapeutic approaches. Chlorine gas is a severe chemical threat agent with frequent exposures in domestic and occupational environments and in transportation accidents (for example, train derailment in Graniteville, SC, 2005). Recent chlorine bomb attacks in Syria resulted in a death toll of several thousands. Despite its known chemical threat potencies since World War I, there is no specific antidote for chlorine gas. They examined the therapeutic effects of a novel transient receptor potential vanilloid 4 (TRPV4) inhibitor, GSK691, in pigs exposed to chlorine gas as a translational model of human chemically induced acute lung injury to meet the US FDA’s animal rule. Dr. Achanta feels honored to receive this prestigious award. As an aspiring scientist, this award will be a feather in his hat and give him more enthusiasm to pursue toxicological research. The treatment of chlorine gas induced acute lung injury (ALI) remains challenging because of the lack of mechanism-based therapeutic approaches. Chlorine gas is a severe chemical threat agent with frequent exposures in domestic and occupational environments and in transportation accidents (for example, train derailment in Graniteville, SC, 2005). Recent chlorine bomb attacks in Syria resulted in a death toll of several thousands. Despite its known chemical threat potencies since World War I, there is no specific antidote for chlorine gas. They examined the therapeutic effects of a novel transient receptor potential vanilloid 4 (TRPV4) inhibitor, GSK691, in pigs exposed to chlorine gas as a translational model of human chemically induced acute lung injury to meet the US FDA’s animal rule.

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

Winner: Priyanka Trivedi

Award Year: 2017
Current Degrees: PhD
Institution/Affiliation: Harvard Medical School

She was really excited and pleased when she received this award. She immediately shared the good news with her advisor and also thanked him for all his support and encouragement. This award will provide recognition to her work and complement my research in the field of renal toxicology. She will use this award as a springboard for my career in which she will make important contributions to advancing our understanding of toxicology research.

Her research focuses on discovering therapeutic targets for acute and chronic kidney diseases. In order to identify druggable targets, they performed RNA sequencing in mouse model of toxic kidney fibrosis and identified Phospholipase D4 (PLD4), a single pass transmembrane glycoprotein, as one of the highly up-regulated genes. Up-regulation of PLD4 was confirmed in three mechanistically distinct mouse models as well as in patients with biopsy-proven kidney fibrosis. Mechanistically, they show that PLD4 facilitates fibrogenesis by modulating innate and adaptive immune responses thereby promoting a TGF-β signaling pathway. Moreover, PLD4 induced the expression of α1-antitrypsin protein (a serine protease inhibitor) that resulted in subsequent down-regulation of a protease neutrophil elastase (NE) expression, thereby leading to the accumulation of extracellular matrix proteins. Interestingly, therapeutic targeting of PLD4 using specific siRNA also protected the mice from kidney fibrosis by inhibiting TGF-β signaling and inducing NE expression. In conclusion, their findings identified PLD4 as a novel therapeutic target for kidney fibrosis - an unmet medical need. Her future goal is to continue contributing to the toxicological science, which can be directly applied clinically to benefit the society.She was really excited and pleased when she received this award. She immediately shared the good news with her advisor and also thanked him for all his support and encouragement. This award will provide recognition to her work and complement my research in the field of renal toxicology. She will use this award as a springboard for my career in which she will make important contributions to advancing our understanding of toxicology research. Her research focuses on discovering therapeutic targets for acute and chronic kidney diseases. In order to identify druggable targets, they performed RNA sequencing in mouse model of toxic kidney fibrosis and identified Phospholipase D4 (PLD4), a single pass transmembrane glycoprotein, as one of the highly up-regulated genes. Up-regulation of PLD4 was confirmed in three mechanistically distinct mouse models as well as in patients with biopsy-proven kidney fibrosis. Mechanistically, they show that PLD4 facilitates fibrogenesis by modulating innate and adaptive immune responses thereby promoting a TGF-ß signaling pathway. Moreover, PLD4 induced the expression of a1-antitrypsin protein (a serine protease inhibitor) that resulted in subsequent down-regulation of a protease neutrophil elastase (NE) expression, thereby leading to the accumulation of extracellular matrix proteins. Interestingly, therapeutic targeting of PLD4 using specific siRNA also protected the mice from kidney fibrosis by inhibiting TGF-ß signaling and inducing NE expression. In conclusion, their findings identified PLD4 as a novel therapeutic target for kidney fibrosis - an unmet medical need. Her future goal is to continue contributing to the toxicological science, which can be directly applied clinically to benefit the society.

Dharm V. Singh Carcinogenesis Award Fund

Winner: Nehal Gupta

Award Year: 2017
Current Degrees: MPharm, BPharm
Institution/Affiliation: Texas Tech University Health Sciences Center

Ms. Gupta was very excited and enthusiastic after receiving Dharm V. Singh Carcinogenesis Graduate Student Award. She would like to thank SOT for selecting her for this award. This award would offer a tremendous financial support to attend the 2017 SOT Annual Meeting. It will be an excellent opportunity to meet scientists across the globe and share her work with them, which will provide novel insights to her work. Also, Recognition by award committee has boosted her morale to do better work in the field of toxicology as well as science.

She started her project on breast cancer, which is one of the most malignant carcinoma in women worldwide. Despite of currently available treatment options, breast cancer kills approximately 40,000 women every year, making it the second-leading cause of cancer related deaths. Resistance to current chemotherapeutics is the major obstacle in treating breast cancer patients. She and colleagues developed resistance towards paclitaxel in various breast cancer cell lines (MCF-7, 4T1, HCC1806). With extensive research, they are able to unravel the mechanism behind the resistance and based on previous publication (Ranjan et al. “Penfluridol: An antipsychotic agent suppresses metastatic tumor growth in triple negative breast cancer by inhibiting integrin signaling axis” Cancer Research 2015), they are able to develop penfluridol as a treatment option to overcome resistance. Their results showed that penfluridol treatment synergistically enhanced the growth suppressive effects of paclitaxel in vitro as well as in vivo. They also observed that chronic treatment of mice with penfluridol was not associated with any toxicity or behavioral side effect. Therefore, combining penfluridol with paclitaxel will reduce the dose as well as toxic side effects of current chemotherapy. Since penfluridol is an FDA approved drug, the pharmacology, formulation and potential toxicities are already known. Their 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 breast tumors. For her long term goals, she would like to develop her professional career as an academic scientist in the field of Oncology. She has been mentored by one student that gave her motivation to train new researchers in cancer field. Ms. Gupta was very excited and enthusiastic after receiving Dharm V. Singh Carcinogenesis Graduate Student Award. She would like to thank SOT for selecting her for this award. This award would offer a tremendous financial support to attend the 2017 SOT Annual Meeting. It will be an excellent opportunity to meet scientists across the globe and share her work with them, which will provide novel insights to her work. Also, Recognition by award committee has boosted her morale to do better work in the field of toxicology as well as science. She started her project on breast cancer, which is one of the most malignant carcinoma in women worldwide. Despite of currently available treatment options, breast cancer kills approximately 40,000 women every year, making it the second-leading cause of cancer related deaths. Resistance to current chemotherapeutics is the major obstacle in treating breast cancer patients. She and colleagues developed resistance towards paclitaxel in various breast cancer cell lines (MCF-7, 4T1, HCC1806). With extensive research, they are able to unravel the mechanism behind the resistance and based on previous publication (Ranjan et al. “Penfluridol: An antipsychotic agent suppresses metastatic tumor growth in triple negative breast cancer by inhibiting integrin signaling axis” Cancer Research 2015), they are able to develop penfluridol as a treatment option to overcome resistance. Their results showed that penfluridol treatment synergistically enhanced the growth suppressive effects of paclitaxel in vitro as well as in vivo. They also observed that chronic treatment of mice with penfluridol was not associated with any toxicity or behavioral side effect. Therefore, combining penfluridol with paclitaxel will reduce the dose as well as toxic side effects of current chemotherapy. Since penfluridol is an FDA approved drug, the pharmacology, formulation and potential toxicities are already known. Their 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 breast tumors. For her long term goals, she would like to develop her professional career as an academic scientist in the field of Oncology. She has been mentored by one student that gave her motivation to train new researchers in cancer field.

Donald E. Gardner Inhalation Toxicology Education Award Fund

Winner: Matthew McGraw

Award Year: 2017
Current Degrees: MD
Institution/Affiliation: University of Colorado School of Medicine

Dr. McGraw was honored to receive the Donald E. Gardner Inhalation Toxicology Award. This award will allow him to learn the entire process of induced pluripotent stem cell (iPSC) reprogramming from reprogramming methodologies, iPSC identification, isolation and characterization, and current approaches to their directed differentiation into endodermal and lung lineages. He will use the information learned at Dr. Kotton's lab in Boston to use cell-based therapy for repair of a damaged epithelium after sulfur mustard inhalation injuries and prevention of bronchiolitis obliterans.

His research is on inhalation injury after sulfur mustard. Sulfur mustard is a common warfare agent that causes both acute and chronic morbidity and mortality. One common long-term morbidity is bronchiolitis obliterans (BO). BO is defined as a progressive narrowing of the airway from fibroproliferation. One of the central pathways behind the development of BO is injury to the airway epithelium and aberrant repair. His research focuses on the contribution of the airway epithelium after inhalation injury. Additionally, he is interested in how an impaired epithelium after injury contributes to the development of BO. Recently, his lab has shown a lack of proliferation and differentiation of the airway epithelium weeks after exposure to sulfur mustard with the concurrent development of BO. The Donald Gardner Inhalation Toxicology Education Award will allow him to travel to Boston to study induced pluripotent stem cell programming. He hopes to use this education to identify, isolate, and re-program airway epithelium after sulfur mustard exposure to prevent the development of BO. Dr. McGraw was honored to receive the Donald E. Gardner Inhalation Toxicology Award. This award will allow him to learn the entire process of induced pluripotent stem cell (iPSC) reprogramming from reprogramming methodologies, iPSC identification, isolation and characterization, and current approaches to their directed differentiation into endodermal and lung lineages. He will use the information learned at Dr. Kotton's lab in Boston to use cell-based therapy for repair of a damaged epithelium after sulfur mustard inhalation injuries and prevention of bronchiolitis obliterans. His research is on inhalation injury after sulfur mustard. Sulfur mustard is a common warfare agent that causes both acute and chronic morbidity and mortality. One common long-term morbidity is bronchiolitis obliterans (BO). BO is defined as a progressive narrowing of the airway from fibroproliferation. One of the central pathways behind the development of BO is injury to the airway epithelium and aberrant repair. His research focuses on the contribution of the airway epithelium after inhalation injury. Additionally, he is interested in how an impaired epithelium after injury contributes to the development of BO. Recently, his lab has shown a lack of proliferation and differentiation of the airway epithelium weeks after exposure to sulfur mustard with the concurrent development of BO. The Donald Gardner Inhalation Toxicology Education Award will allow him to travel to Boston to study induced pluripotent stem cell programming. He hopes to use this education to identify, isolate, and re-program airway epithelium after sulfur mustard exposure to prevent the development of BO.

Edward W. Carney Trainee Award Fund

Winner: Karilyn Sant

Award Year: 2017
Current Degrees: PhD, MPH
Institution/Affiliation: University of Massachusetts

Dr. Sant is incredibly grateful for this award, and hopes to serve the developmental toxicology community throughout her career according to Dr. Carney's lead. This award will not only allow her to share her current work with the toxicology community, but will also give her opportunities to establish lasting professional relationships with the many excellent developmental toxicologists in RDTSS.

Her research investigates the consequences of embryonic exposures to endocrine disruptors, namely those which predispose to metabolic dysfunction later in the lifecourse. She and her colleagues are working to understand how these exposures influence embryonic nutrition, pancreas development, and glucoregulatory function. This project specifically probes the role of the Nrf2 antioxidant pathway in the response to perfluorooctanesulfonic acid (PFOS), a persistent compound previously used as a surfactant in products such as Teflon and Scotchgard. Dr. Sant is incredibly grateful for this award, and hopes to serve the developmental toxicology community throughout her career according to Dr. Carney's lead. This award will not only allow her to share her current work with the toxicology community, but will also give her opportunities to establish lasting professional relationships with the many excellent developmental toxicologists in RDTSS. Her research investigates the consequences of embryonic exposures to endocrine disruptors, namely those which predispose to metabolic dysfunction later in the lifecourse. She and her colleagues are working to understand how these exposures influence embryonic nutrition, pancreas development, and glucoregulatory function. This project specifically probes the role of the Nrf2 antioxidant pathway in the response to perfluorooctanesulfonic acid (PFOS), a persistent compound previously used as a surfactant in products such as Teflon and Scotchgard.

Edward W. Carney Trainee Award Fund

Winner: Edith Marie McKenzie

Award Year: 2017
Current Degrees: BS, MS
Institution/Affiliation: University of Georgia

Ms. McKenzie was honored and excited to receive the Edward W Carney Trainee Award. It provides an opportunity to attend and share at both the Society of Toxicology and Teratology Society 2017 Annual Meetings. The state of the art research presentations are an unparalleled learning experience. In addition, the prospect of networking with leading researchers and students, while receiving specific, on point feedback about her project is a fantastic opportunity. She looks forward to increasing her knowledge and building on developmental/reproductive toxicology concepts.

After a career of working with children with birth defects, her greatest accomplishment will be contributing to the science of prevention. The ultimate goal of her research is to create an alternative cell based model which predicts toxicity to the developing human brain. She is utilizing a systems approach to evaluate nerve cell responses to pesticides. The study objectives were 1) to compare the metabolomic profile of three pesticide groups; aldicarb (a carbamate), chlorpyrifos (an organophosphate) and lindane (an organochloride) in neural progenitor (hN2) cells, and 2) to determine whether the biological impact in hN2 cells would be affected by first exposing pesticides to C3A cells, an immortal liver cell line derived from hepG2 cells, and subsequently exposing the pre-conditioned media to hN2 cells. C3A cells were added to our model to mimic in vivo liver biotransformation of chemical exposures. To biotransform the pesticides, C3A cells were grown to confluency and treated with the same concentrations of pesticide in hN2 media for two hours. This pre-conditioned media was removed and added to hN2 cells. Afterwards, the media was analyzed by GC/MS. This study confirmed hN2 cells are responsive to pesticide exposure at doses less than 30uM, and pre-conditioning media results in biotransformation (i.e. chlorpyrifos forms chlorpyrifos-oxon). For parent pesticides, fluxes in the metabolomic profile increased with increasing doses and various metabolomic pathways were affected following exposure to biotransformed products. Independent of which pesticide was used in hN2 cells, some overlap occurred in metabolomic profiles; within each pesticide different profiles were observed for each dose. The introduction of the C3A pre-conditioned media affected the quantity of metabolites and biochemical pathways. In conclusion, addition of a metabolic component changed the metabolites affected and may be a better model for assessing risk. Ms. McKenzie was honored and excited to receive the Edward W Carney Trainee Award. It provides an opportunity to attend and share at both the Society of Toxicology and Teratology Society 2017 Annual Meetings. The state of the art research presentations are an unparalleled learning experience. In addition, the prospect of networking with leading researchers and students, while receiving specific, on point feedback about her project is a fantastic opportunity. She looks forward to increasing her knowledge and building on developmental/reproductive toxicology concepts. After a career of working with children with birth defects, her greatest accomplishment will be contributing to the science of prevention. The ultimate goal of her research is to create an alternative cell based model which predicts toxicity to the developing human brain. She is utilizing a systems approach to evaluate nerve cell responses to pesticides. The study objectives were 1) to compare the metabolomic profile of three pesticide groups; aldicarb (a carbamate), chlorpyrifos (an organophosphate) and lindane (an organochloride) in neural progenitor (hN2) cells, and 2) to determine whether the biological impact in hN2 cells would be affected by first exposing pesticides to C3A cells, an immortal liver cell line derived from hepG2 cells, and subsequently exposing the pre-conditioned media to hN2 cells. C3A cells were added to our model to mimic in vivo liver biotransformation of chemical exposures. To biotransform the pesticides, C3A cells were grown to confluency and treated with the same concentrations of pesticide in hN2 media for two hours. This pre-conditioned media was removed and added to hN2 cells. Afterwards, the media was analyzed by GC/MS. This study confirmed hN2 cells are responsive to pesticide exposure at doses less than 30uM, and pre-conditioning media results in biotransformation (i.e. chlorpyrifos forms chlorpyrifos-oxon). For parent pesticides, fluxes in the metabolomic profile increased with increasing doses and various metabolomic pathways were affected following exposure to biotransformed products. Independent of which pesticide was used in hN2 cells, some overlap occurred in metabolomic profiles; within each pesticide different profiles were observed for each dose. The introduction of the C3A pre-conditioned media affected the quantity of metabolites and biochemical pathways. In conclusion, addition of a metabolic component changed the metabolites affected and may be a better model for assessing risk.

Emil A. Pfitzer Drug Discovery Postdoc Award Fund

Winner: Xi Li

Award Year: 2017
Current Degrees: PhD
Institution/Affiliation: Texas A&M University

Dr. Li felt it was a great pleasure to participate in the Drug Discovery Toxicology Specialty Section's poster competition and receiving the award is a great encouragement to pursue his research and career in drug discovery.

His work is focused on cancer biology, specially antitumor drugs. He and colleagues have synthesized and identified several diindolylmethane analogs including the hydroxyphenyl-bisindole isomers that target NR4A nuclear receptors in several solid tumor cell lines. These bisindole compounds also exhibit low cytotoxicity in animal xenograft studies while exhibiting potent antitumor effects. They will continue to identify chemical structural features that are important for ligand-dependent antitumor effects in order to develop compounds that could be used for cancer chemotherapy. Dr. Li felt it was a great pleasure to participate in the Drug Discovery Toxicology Specialty Section's poster competition and receiving the award is a great encouragement to pursue his research and career in drug discovery. His work is focused on cancer biology, specially antitumor drugs. He and colleagues have synthesized and identified several diindolylmethane analogs including the hydroxyphenyl-bisindole isomers that target NR4A nuclear receptors in several solid tumor cell lines. These bisindole compounds also exhibit low cytotoxicity in animal xenograft studies while exhibiting potent antitumor effects. They will continue to identify chemical structural features that are important for ligand-dependent antitumor effects in order to develop compounds that could be used for cancer chemotherapy.

Emil A. Pfitzer Drug Discovery Postdoc Award Fund

Winner: Priyanka Trivedi

Award Year: 2017
Current Degrees: PhD
Institution/Affiliation: Harvard Medical School

Dr. Trivedi was really excited and pleased when she received this award. She immediately went to her advisor’s office to share this good news with him and also to thank him for all his support and encouragement. She is clearly committed to a career in toxicology research and this award will provide recognition to her work and complement her research in the field of toxicology. She will use this award as a springboard for her career in which she will make important contributions to advancing our understanding of toxicology research.

Kidney fibrosis, the hallmark of the chronic kidney disease, is an irreversible process leading to the life threatening end-stage renal failure. Unfortunately there is no effective therapeutic cure for this serious condition. Her research focuses on identifying and validating druggable targets for kidney fibrosis. Using RNA sequencing, she identified phospholipase D4 (PLD4) as one of the targets for the treatment of kidney fibrosis. Proposed project for this award was to decipher a mechanistic role of PLD4 in the regulation of fibrosis. Mechanistically, they show that PLD4 facilitates fibrogenesis by modulating innate and adaptive immune responses thereby promoting a TGF-β signaling pathway. Moreover, PLD4 induced the expression of α1-antitrypsin protein (a serine protease inhibitor) that resulted in subsequent down-regulation of a protease neutrophil elastase (NE) expression, thereby leading to the accumulation of extracellular matrix proteins. Further, PLD4 induced tyrosine receptor kinase A (TrkA)-mediated MAPK signaling. Interestingly, therapeutic targeting of PLD4 using specific siRNA also protected the mice from FA-induced kidney fibrosis by inhibiting TGF-β signaling and activating NE. In conclusion, their findings identified PLD4 as a novel therapeutic target for kidney fibrosis - an unmet medical need.Dr. Trivedi was really excited and pleased when she received this award. She immediately went to her advisor’s office to share this good news with him and also to thank him for all his support and encouragement. She is clearly committed to a career in toxicology research and this award will provide recognition to her work and complement her research in the field of toxicology. She will use this award as a springboard for her career in which she will make important contributions to advancing our understanding of toxicology research. Kidney fibrosis, the hallmark of the chronic kidney disease, is an irreversible process leading to the life threatening end-stage renal failure. Unfortunately there is no effective therapeutic cure for this serious condition. Her research focuses on identifying and validating druggable targets for kidney fibrosis. Using RNA sequencing, she identified phospholipase D4 (PLD4) as one of the targets for the treatment of kidney fibrosis. Proposed project for this award was to decipher a mechanistic role of PLD4 in the regulation of fibrosis. Mechanistically, they show that PLD4 facilitates fibrogenesis by modulating innate and adaptive immune responses thereby promoting a TGF-ß signaling pathway. Moreover, PLD4 induced the expression of a1-antitrypsin protein (a serine protease inhibitor) that resulted in subsequent down-regulation of a protease neutrophil elastase (NE) expression, thereby leading to the accumulation of extracellular matrix proteins. Further, PLD4 induced tyrosine receptor kinase A (TrkA)-mediated MAPK signaling. Interestingly, therapeutic targeting of PLD4 using specific siRNA also protected the mice from FA-induced kidney fibrosis by inhibiting TGF-ß signaling and activating NE. In conclusion, their findings identified PLD4 as a novel therapeutic target for kidney fibrosis - an unmet medical need.

Emil A. Pfitzer Drug Discovery Postdoc Award Fund

Winner: Sarah Thacker

Award Year: 2017
Current Degrees: BS, PhD
Institution/Affiliation: University of North Carolina Chapel Hill

Dr. Thacker was thrilled to receive this award. She said it feels great to have others excited about her research as well and have the support from the specialty section.

Her research is focused on exploring the biomarker potential of hepatocyte-derived exosomes to predict intrinsic and idiosyncratic drug-induced liver injury (DILI). Specifically, these studies aimed to optimize methods for hepatocyte-derived exosome enrichment as well as hepatocyte cell culture; methods that hadn't previously been optimized. They can now utilize these approaches to identify novel biomarkers for DILI and IDILI. A future goal is to use these biomarkers in the development of an in vitro screen of lead compounds to predict their DILI and IDILI potential.Dr. Thacker was thrilled to receive this award. She said it feels great to have others excited about her research as well and have the support from the specialty section. Her research is focused on exploring the biomarker potential of hepatocyte-derived exosomes to predict intrinsic and idiosyncratic drug-induced liver injury (DILI). Specifically, these studies aimed to optimize methods for hepatocyte-derived exosome enrichment as well as hepatocyte cell culture; methods that hadn't previously been optimized. They can now utilize these approaches to identify novel biomarkers for DILI and IDILI. A future goal is to use these biomarkers in the development of an in vitro screen of lead compounds to predict their DILI and IDILI potential.

Emil A. Pfitzer Drug Discovery Student Award Fund

Winner: Elijah Weber

Award Year: 2017
Current Degrees: BS
Institution/Affiliation: University of Washington

Mr. Weber was ecstatic when he received the award! He felt honored with the opportunity to be a selected finalist in the poster competition and had a wonderful time presenting his work alongside such amazing work in the scientific community. This award will help him to pursue research greatly by now enabling him to fund scientific and technical training courses.

His work involves modeling the kidney, in particular the segment of the kidney most prone to injury, using an "organ-on-a-chip" system that cultures kidney cells in a three dimensional orientation. Using a system that best reflects the human kidney microenvironment, he and colleagues can model toxicity of known toxic compounds and assess safety of novel compounds to advance drug discovery and development. Accurate safety assessments can be achieved in a system without the use of preclinical animal models thus reducing, refining, and eventually replacing animal use. Future goals of this work include integration of organ types to understand organ-organ interactions which may play key roles in underlying mechanisms of toxicity. He has used this system to assess a classical nephrotoxin, Polymyxin B, as well as structural analogues observed to have improved safety profiles. Using a drug discovery toxicological approach, he has generated results that parallel preclinical findings of safety for novel compounds using a novel organ-on-a-chip 3D kidney system.Mr. Weber was ecstatic when he received the award! He felt honored with the opportunity to be a selected finalist in the poster competition and had a wonderful time presenting his work alongside such amazing work in the scientific community. This award will help him to pursue research greatly by now enabling him to fund scientific and technical training courses. His work involves modeling the kidney, in particular the segment of the kidney most prone to injury, using an "organ-on-a-chip" system that cultures kidney cells in a three dimensional orientation. Using a system that best reflects the human kidney microenvironment, he and colleagues can model toxicity of known toxic compounds and assess safety of novel compounds to advance drug discovery and development. Accurate safety assessments can be achieved in a system without the use of preclinical animal models thus reducing, refining, and eventually replacing animal use. Future goals of this work include integration of organ types to understand organ-organ interactions which may play key roles in underlying mechanisms of toxicity. He has used this system to assess a classical nephrotoxin, Polymyxin B, as well as structural analogues observed to have improved safety profiles. Using a drug discovery toxicological approach, he has generated results that parallel preclinical findings of safety for novel compounds using a novel organ-on-a-chip 3D kidney system.

Emil A. Pfitzer Drug Discovery Student Award Fund

Winner: Wenyi Wang

Award Year: 2017
Current Degrees: PhD
Institution/Affiliation: Rutgers University

Dr. Wang is very excited and thankful. She feels this is an acknowledgement of her work by SOT and is encouraged to work harder through the end.

Constructed computational methods to precisely predict properties of nanoparticles, in purpose of prioritizing nanoparticle drugs with wanted properties and unwanted toxicities.Dr. Wang is very excited and thankful. She feels this is an acknowledgement of her work by SOT and is encouraged to work harder through the end. Constructed computational methods to precisely predict properties of nanoparticles, in purpose of prioritizing nanoparticle drugs with wanted properties and unwanted toxicities.

Endowment - Jean Lu Student Scholarship Award Fund

Winner: Kathy Xue

Award Year: 2017
Current Degrees: BS
Institution/Affiliation: University of Georgia

She is very happy to receive this award. This is a rare opportunity to showcase her PhD research work and will have important impact on her on-going research and future career.

Her research works, for which she won the award, focuses on studying toxic effects of naturally occurring foodborne contaminants (mycotoxins), especially for aflatoxins and fumonisins, on animal and human health, as well as their roles in contributing to cancer risks. Co-contamination of aflatoxins and fumonisins has been found world-wide, detectable in many food items, particularly in corn and corn products. Aflatoxins are known cancer causing agents in humans and can cause human liver cancer, while fumonisins are shown to be cancer promoting agents in animal models, and was associated with increased risk of human esophageal cancer. The primary objective of her research was to investigate interactions of simultaneous exposure to both aflatoxins and fumonisins in both experimental animals and highly exposed human populations. We performed sequential exposure study in F344 rat model and found a synergistic carcinogenic effect. This synergistic carcinogenic effect can be significantly reduced by the intervention with enterosorbent material which can specifically remove these toxins from the body. We also conducted a case-control study in a high-risk area for esophageal cancer and measured blood and urine levels of exposure biomarkers specific for these two mycotoxins in case and control subjects. We found a synergistic association of exposure to these two mycotoxins with riskss of human esophageal cancer. Further, a prevention trial targeting aflatoxins and fumonisins was conducted in a high risk human population for liver cancer aimed to reduce the levels of both mycotoxin biomarkers. For future works, she would further explore specific mechanisms of interaction in toxicity and carcinogenicity as well as the interaction with various genetic and environmental factors. She is very happy to receive this award. This is a rare opportunity to showcase her PhD research work and will have important impact on her on-going research and future career. Her research works, for which she won the award, focuses on studying toxic effects of naturally occurring foodborne contaminants (mycotoxins), especially for aflatoxins and fumonisins, on animal and human health, as well as their roles in contributing to cancer risks. Co-contamination of aflatoxins and fumonisins has been found world-wide, detectable in many food items, particularly in corn and corn products. Aflatoxins are known cancer causing agents in humans and can cause human liver cancer, while fumonisins are shown to be cancer promoting agents in animal models, and was associated with increased risk of human esophageal cancer.

Frank C. Lu Food Safety Students Award Fund

Winner: Blake Rushing

Award Year: 2017
Current Degrees: BS Chemistry
Institution/Affiliation: East Carolina University

When Mr. Rushing found out that he received the Frank C. Lu student award, he was absolutely ecstatic. He fels it is such a tremendous honor to be a recipient of this award and he is very grateful to be recognized for the work he put towards his dissertation research. Receiving such an award increases the attention that his lab receives which goes a long way towards improving the ability to share research with the rest of the world. His plan is to use the funds included in the award to support his travel to the SOT Annual Meeting where he can share my findings with other brilliant minds in the field and gain their feedback to bolster the quality of his work.

His research is focused on detoxifying foods that are contaminated with a particular food toxin, aflatoxin B1. This toxin occurs naturally on foods worldwide due to production of a very common fungus that grows on crops. Aflatoxin B1 is also highly linked with the development of liver cancer, making exposure to this toxin highly concerning. The research that won this award was his development of a novel treatment method that can potentially be used on contaminated foods to deactivate the toxin. He and colleagues found that after processing foods with our method, the toxin is completely transformed into a new chemical form which no longer damages DNA, preventing the initiation of cancer. This finding can be used as a basis to make aflatoxin B1-contaminated food safe to eat again and hopefully reduce the occurrence of liver cancer worldwide. Firstly, his future goals include graduating with his PhD in Pharmacology & Toxicology in approximately a year from now. Afterwards, he hopes to stay in academia where he can continue to work on issues in food safety. His home state, North Carolina, is highly involved in agriculture making food toxicology a top priority for where he lives. It is his hope to learn as much as possible about the problems faced in food safety and use his research abilities to find solutions to provide safer and cleaner foods to people around the world.When Mr. Rushing found out that he received the Frank C. Lu student award, he was absolutely ecstatic. He fels it is such a tremendous honor to be a recipient of this award and he is very grateful to be recognized for the work he put towards his dissertation research. Receiving such an award increases the attention that his lab receives which goes a long way towards improving the ability to share research with the rest of the world. His plan is to use the funds included in the award to support his travel to the SOT Annual Meeting where he can share my findings with other brilliant minds in the field and gain their feedback to bolster the quality of his work. His research is focused on detoxifying foods that are contaminated with a particular food toxin, aflatoxin B1. This toxin occurs naturally on foods worldwide due to production of a very common fungus that grows on crops. Aflatoxin B1 is also highly linked with the development of liver cancer, making exposure to this toxin highly concerning. The research that won this award was his development of a novel treatment method that can potentially be used on contaminated foods to deactivate the toxin. He and colleagues found that after processing foods with our method, the toxin is completely transformed into a new chemical form which no longer damages DNA, preventing the initiation of cancer. This finding can be used as a basis to make aflatoxin B1-contaminated food safe to eat again and hopefully reduce the occurrence of liver cancer worldwide. Firstly, his future goals include graduating with his PhD in Pharmacology & Toxicology in approximately a year from now. Afterwards, he hopes to stay in academia where he can continue to work on issues in food safety. His home state, North Carolina, is highly involved in agriculture making food toxicology a top priority for where he lives. It is his hope to learn as much as possible about the problems faced in food safety and use his research abilities to find solutions to provide safer and cleaner foods to people around the world.

Gabriel L. Plaa Education Award

Winner: Joseph Cichocki

Award Year: 2017
Current Degrees: PhD
Institution/Affiliation: Texas A&M University

Dr. Cichocki is honored to be a finalist for the Plaa award. This is one of the most highly-regarded awards that are offered to postdoc members of SOT. Being a finalist for this award has made him realize that the work that he is doing is recognized as being important for the field of Mechanistic Toxicology. He will definitely apply his knowledge in mechanistic toxicology as he pursues a career in the Pharmaceutical Industry. As he begins the next step in his career, he will be handing off some of this research to undergraduate and graduate students in the lab and will provide them guidance during their research so that they can continue to study the interaction between diet, disease, and genetics on chemical metabolism and target organ toxicity.

His research is broadly focused on investigating inter-individual variability in susceptibility to chemical-induced toxicity. The project which has lead him to being a finalist for the Plaa award is focused on the effect of nonalcoholic fatty liver disease on tetrachloroethylene disposition, metabolism, and toxicity. His future goals for this project will be to train graduate and undergraduate trainees in the lab so that they will be able to take the project over once he transitions into a career in Pharma. He feels there is always more mechanistic work to be done on a project, and while he has made considerable strides to understanding the contribution of this disease on tetrachloroethylene toxicity, the work is not completely finished. Since he had an excellent career opportunity to join a really exciting company, he had to make the decision to hand of this project to others in the lab. He anticipates that they will be able to continue to investigate molecular mechanisms and the contribution of genetics, disease, and diet to inter-individual variability in tetrachloroethylene toxicity.Dr. Cichocki is honored to be a finalist for the Plaa award. This is one of the most highly-regarded awards that are offered to postdoc members of SOT. Being a finalist for this award has made him realize that the work that he is doing is recognized as being important for the field of Mechanistic Toxicology. He will definitely apply his knowledge in mechanistic toxicology as he pursues a career in the Pharmaceutical Industry. As he begins the next step in his career, he will be handing off some of this research to undergraduate and graduate students in the lab and will provide them guidance during their research so that they can continue to study the interaction between diet, disease, and genetics on chemical metabolism and target organ toxicity. His research is broadly focused on investigating inter-individual variability in susceptibility to chemical-induced toxicity. The project which has lead him to being a finalist for the Plaa award is focused on the effect of nonalcoholic fatty liver disease on tetrachloroethylene disposition, metabolism, and toxicity. His future goals for this project will be to train graduate and undergraduate trainees in the lab so that they will be able to take the project over once he transitions into a career in Pharma. He feels there is always more mechanistic work to be done on a project, and while he has made considerable strides to understanding the contribution of this disease on tetrachloroethylene toxicity, the work is not completely finished. Since he had an excellent career opportunity to join a really exciting company, he had to make the decision to hand of this project to others in the lab. He anticipates that they will be able to continue to investigate molecular mechanisms and the contribution of genetics, disease, and diet to inter-individual variability in tetrachloroethylene toxicity.

Gabriel L. Plaa Education Award

Winner: Gregory Smith

Award Year: 2017
Current Degrees: PhD
Institution/Affiliation: University of North Carolina

Dr. Smith was beyond excited! The Gabriel L. Plaa award is the most important award that he has received thus far in his career. Additionally, it has validated a switch that he made from more descriptive to mechanism-heavy studies. It has also emphasized his desire to continue to mentor new trainees in toxicology. It will undoubtedly boost his motivation to keep on the career path that he has been clearing for himself.

His present and future work has been aimed at generating useful data that further our understanding of the mechanisms of environmentally-related disease. The research for which he won the Gabriel Plaa award investigated the role of a specific drug transport protein in the process of liver regeneration following injury using a knockout mouse model. Although the work did not rely on a specific toxicant, it has implications in our understanding of how the liver recovers from injury of all types. He is developing a research career that will continue to investigate the mechanisms of adverse health effects of chemicals, especially air pollutants. In the future he plans to investigate mechanisms of susceptibility to ozone and asthma.Dr. Smith was beyond excited! The Gabriel L. Plaa award is the most important award that he has received thus far in his career. Additionally, it has validated a switch that he made from more descriptive to mechanism-heavy studies. It has also emphasized his desire to continue to mentor new trainees in toxicology. It will undoubtedly boost his motivation to keep on the career path that he has been clearing for himself. His present and future work has been aimed at generating useful data that further our understanding of the mechanisms of environmentally-related disease. The research for which he won the Gabriel Plaa award investigated the role of a specific drug transport protein in the process of liver regeneration following injury using a knockout mouse model. Although the work did not rely on a specific toxicant, it has implications in our understanding of how the liver recovers from injury of all types. He is developing a research career that will continue to investigate the mechanisms of adverse health effects of chemicals, especially air pollutants. In the future he plans to investigate mechanisms of susceptibility to ozone and asthma.

Gabriel L. Plaa Education Award

Winner: Matthew Dodson

Award Year: 2017
Current Degrees: MS, PhD
Institution/Affiliation: University of Arizona College of Pharmacy

Dr. Dodson was very pleased to find out that he was a finalist for the Gabriel L. Plaa Education Award for this year’s annual Society of Toxicology meeting. He is a second year postdoctoral researcher new to the toxicology field, and this is his first time attending the Society of Toxicology meeting, so being nominated for this award is a great honor. His goal is to become the head of his own research laboratory at an academic institution, where he will mentor students and postdocs, receiving an award named after someone who made such significant contributions towards the education and mentoring of future toxicologists is another big step towards achieving this goal. Receiving this award, and having the opportunity to present research at the SOT conference will significantly further his training, and help ensure that he makes significant contributions to the toxicology field.

His current research project focuses on the impact of chronic exposure to inorganic arsenic on health and disease. Specifically, he is investigating the mechanisms by which arsenic inhibits the autophagy-lysosome pathway resulting in prolonged activation of the key antioxidant transcription factor NRF2. He is also interested in how arsenic and prolonged NRF2 activation affect long-term mitochondrial structure and function to contribute to the progression of metabolic syndrome. The goal of his research is to better understand specific targets affected by chronic arsenic exposure, as well as the mechanisms that contribute to the different pathologies associated with exposure to environmental toxicants. By better understanding how arsenic affects cellular function, we can begin to create more targeted therapies for the treatment of arsenic and other toxic metal-associated diseases. The research that he presented at this year’s meeting that was part of the consideration for an award focuses on the impact of arsenic on the mitochondrial network, and how NRF2 may regulate these changes.Dr. Dodson was very pleased to find out that he was a finalist for the Gabriel L. Plaa Education Award for this year’s annual Society of Toxicology meeting. He is a second year postdoctoral researcher new to the toxicology field, and this is his first time attending the Society of Toxicology meeting, so being nominated for this award is a great honor. His goal is to become the head of his own research laboratory at an academic institution, where he will mentor students and postdocs, receiving an award named after someone who made such significant contributions towards the education and mentoring of future toxicologists is another big step towards achieving this goal. Receiving this award, and having the opportunity to present research at the SOT conference will significantly further his training, and help ensure that he makes significant contributions to the toxicology field. His current research project focuses on the impact of chronic exposure to inorganic arsenic on health and disease. Specifically, he is investigating the mechanisms by which arsenic inhibits the autophagy-lysosome pathway resulting in prolonged activation of the key antioxidant transcription factor NRF2. He is also interested in how arsenic and prolonged NRF2 activation affect long-term mitochondrial structure and function to contribute to the progression of metabolic syndrome. The goal of his research is to better understand specific targets affected by chronic arsenic exposure, as well as the mechanisms that contribute to the different pathologies associated with exposure to environmental toxicants. By better understanding how arsenic affects cellular function, we can begin to create more targeted therapies for the treatment of arsenic and other toxic metal-associated diseases. The research that he presented at this year’s meeting that was part of the consideration for an award focuses on the impact of arsenic on the mitochondrial network, and how NRF2 may regulate these changes.

Harihara Mehendale Association of Scientists of Indian Origin Student Award Fund

Winner: Hanumantha Rao Madala

Award Year: 2017
Current Degrees: MS
Institution/Affiliation: Texas Tech University Health Sciences Center

It was quite a surprising announcement in the ASIO ongoing meeting. He had submitted his abstract and thought someone was awarded and had just forgotten everything but when his name was announced, he was so shocked and felt so proud of his self and the research of his lab. It gave him a lot of confidence and will help him to pursue his dream in research with same hard work and efforts in future as well.

Chemo drugs in the market kill everything non-selectively and the compound, KSS72, that we designed in our lab works with selectivity. It kills the cancer cells with around 20 times more selectivity. It's an analog of FDA approved, anti-hypertensive drug, ethacrynic acid. It permeates the brain and showed anticancer efficacy in various mouse models. It was quite a surprising announcement in the ASIO ongoing meeting. He had submitted his abstract and thought someone was awarded and had just forgotten everything but when his name was announced, he was so shocked and felt so proud of his self and the research of his lab. It gave him a lot of confidence and will help him to pursue his dream in research with same hard work and efforts in future as well. Chemo drugs in the market kill everything non-selectively and the compound, KSS72, that we designed in our lab works with selectivity. It kills the cancer cells with around 20 times more selectivity. It's an analog of FDA approved, anti-hypertensive drug, ethacrynic acid. It permeates the brain and showed anticancer efficacy in various mouse models.

HESI Young Investigator Endowment Award

Winner: Anthony Franchini

Award Year: 2017
Current Degrees: PhD
Institution/Affiliation: University of Rochester

Dr. Franchini's initial reaction to receiving the HESI Young Investigator award was glee mixed with disbelief. As a recent convert to the field of immunotoxicology, and while he has great respect for the field, he did not expect to be lauded with such an honor. Last year was his first chance to attend an SOT Annual Meeting and he was not disappointed. His greatest takeaway from that meeting was whom he met and conversations sparked during the poster sessions and the effect it had on the direction of his project. Building his professional network is a major priority at this time in his career, and the assemblage of scientists at SOT each year represents the best opportunity to do just that. It is his hope to continue to build on those relationships this year and start new ones. Receiving the award presented the greatest opportunity to better his understanding of the field of immunotoxicology and keep abreast of advancement in the field that will directly influence his work and thinking now and in the near future.

The focus of his current project is to better understand how pollutants affect the ability of our immune system and its ability to response to viral infection. Specifically, the focus is on the role of the aryl hydrocarbon receptor (AHR) within dendritic cells, a critical cell type that binds viral antigens and are required for initiating adaptive immune responses which ultimately control and clear the infection. His group had previously shown that exposure to chemicals that bind the AHR dampen the immune response, and this was traced back to the AHR's activity within the dendritic cell population. His research has built on this to investigate the exact mechanism by which this occurs. He's found that AHR activation lessens the ability of dendritic cells to attract T cells to them, via a protein called CCL17, a necessary step in presenting these immune cells with antigen and activating them to clear the infection. He also has uncovered evidence that lung dendritic cells less well equipped to pick up viral antigens because AHR activation reduces expression of a receptor called DC-SIGN. Furthermore, his work has expanded to work with human dendritic cells, where he has shown that similar changes derived from the mouse model are also seen in human dendritic cells after AHR activation. Dr. Franchini's initial reaction to receiving the HESI Young Investigator award was glee mixed with disbelief. As a recent convert to the field of immunotoxicology, and while he has great respect for the field, he did not expect to be lauded with such an honor. Last year was his first chance to attend an SOT Annual Meeting and he was not disappointed. His greatest takeaway from that meeting was whom he met and conversations sparked during the poster sessions and the effect it had on the direction of his project. Building his professional network is a major priority at this time in his career, and the assemblage of scientists at SOT each year represents the best opportunity to do just that. It is his hope to continue to build on those relationships this year and start new ones. Receiving the award presented the greatest opportunity to better his understanding of the field of immunotoxicology and keep abreast of advancement in the field that will directly influence his work and thinking now and in the near future. The focus of his current project is to better understand how pollutants affect the ability of our immune system and its ability to response to viral infection. Specifically, the focus is on the role of the aryl hydrocarbon receptor (AHR) within dendritic cells, a critical cell type that binds viral antigens and are required for initiating adaptive immune responses which ultimately control and clear the infection. His group had previously shown that exposure to chemicals that bind the AHR dampen the immune response, and this was traced back to the AHR's activity within the dendritic cell population. His research has built on this to investigate the exact mechanism by which this occurs. He's found that AHR activation lessens the ability of dendritic cells to attract T cells to them, via a protein called CCL17, a necessary step in presenting these immune cells with antigen and activating them to clear the infection. He also has uncovered evidence that lung dendritic cells less well equipped to pick up viral antigens because AHR activation reduces expression of a receptor called DC-SIGN. Furthermore, his work has expanded to work with human dendritic cells, where he has shown that similar changes derived from the mouse model are also seen in human dendritic cells after AHR activation.

John Doull Award

Winner: Tanzir Mortuza

Award Year: 2017
Current Degrees: BS
Institution/Affiliation: University of Georgia

Mr. Mortuza was really excited upon receiving this award. As a risk assessor, he always wanted to get his recognition in this field. This award provided the platform to highlight his research in risk assessment. His end goal is to construct a comprehensive PBPK model to evaluate human risk assessment that will eliminate the uncertainty factor associated with children’s exposure of pyrethroids. This award will facilitate to present research at SOT and meet with experts in risk assessment. Meeting with other experts in the field will enhance his understanding of risk assessment which will enhance his understanding of toxicology. Awards such as this will enable learning of toxicology and will help him to be an independent researcher.

Pyrethroids are widely used insecticides. There are more than 200 different kinds of pyrethroid compounds present on the commercial market. Most of these compounds are neurotoxic and highly lipophilic. The toxicity profiles of pyrethroids are compound-specific. Permethrin is one of the major pyrethroids used in pharmaceutical and household products including, lice treatment for children, shampoo, and pet spray. More than one million pounds of permethrin are used in the domestic US market every year. Children between the ages of one and three are most likely ingest these compounds by hand to mouth contact. Despite such wide use, there are limited toxicokinetic (TK) data available for permethrin. Furthermore, there are no comprehensive studies defining the age-dependent TK of pyrethroids. Permethrin is present as a mixture of its cis and trans isomer (CIS and TRANS) in commercial products. Metabolism of these two isomers is significantly different. TRANS is hydrolyzed by carboxylesterases and oxidized by cytochrome P450s (CYPs). CIS is minimally susceptible to hydrolysis and is therefore metabolized largely by CYPs. This difference impacts the overall TK of these isomers. However, there are no studies to characterize age-dependent differences in between CIS and TRANS target organ dosimetry. In many cases, animal models are used to predict human risks associated with a specific compound. Usually, a ten-fold uncertainty factor is used in risk assessment to account for inter-species and human sub-population differences. Physiologically-based pharmacokinetic (PBPK) models are widely used in human risk assessment to reduce the uncertainties associated with interspecies and intraspecies differences. Tornero-Velez et al. (2012) constructed a PBPK model for permethrin for different exposure patterns. The investigators monitored CIS and TRANS concentrations in blood and tissues of adult rats dosed with a commercial mixture of the two isomers, in order to assess the accuracy of their simulations. Additional work is necessary to extend their model to immature subjects. Time-course plasma and tissue concentration data are needed for different immature age-groups, as well as for adults. Isomer-specific TK data are required from animals dosed with the individual isomers, in order to avoid the metabolic interactions inherent with mixtures. We addressed this research gap by determining age-dependent TK in rats for CIS and TRANS at several dose levels that will facilitate construction of a comprehensive PBPK model for each isomer of permethrin. Mr. Mortuza was really excited upon receiving this award. As a risk assessor, he always wanted to get his recognition in this field. This award provided the platform to highlight his research in risk assessment. His end goal is to construct a comprehensive PBPK model to evaluate human risk assessment that will eliminate the uncertainty factor associated with children’s exposure of pyrethroids. This award will facilitate to present research at SOT and meet with experts in risk assessment. Meeting with other experts in the field will enhance his understanding of risk assessment which will enhance his understanding of toxicology. Awards such as this will enable learning of toxicology and will help him to be an independent researcher. Pyrethroids are widely used insecticides. There are more than 200 different kinds of pyrethroid compounds present on the commercial market. Most of these compounds are neurotoxic and highly lipophilic. The toxicity profiles of pyrethroids are compound-specific. Permethrin is one of the major pyrethroids used in pharmaceutical and household products including, lice treatment for children, shampoo, and pet spray. More than one million pounds of permethrin are used in the domestic US market every year. Children between the ages of one and three are most likely ingest these compounds by hand to mouth contact. Despite such wide use, there are limited toxicokinetic (TK) data available for permethrin. Furthermore, there are no comprehensive studies defining the age-dependent TK of pyrethroids. Permethrin is present as a mixture of its cis and trans isomer (CIS and TRANS) in commercial products. Metabolism of these two isomers is significantly different. TRANS is hydrolyzed by carboxylesterases and oxidized by cytochrome P450s (CYPs). CIS is minimally susceptible to hydrolysis and is therefore metabolized largely by CYPs. This difference impacts the overall TK of these isomers. However, there are no studies to characterize age-dependent differences in between CIS and TRANS target organ dosimetry. In many cases, animal models are used to predict human risks associated with a specific compound. Usually, a ten-fold uncertainty factor is used in risk assessment to account for inter-species and human sub-population differences. Physiologically-based pharmacokinetic (PBPK) models are widely used in human risk assessment to reduce the uncertainties associated with interspecies and intraspecies differences. Tornero-Velez et al. (2012) constructed a PBPK model for permethrin for different exposure patterns. The investigators monitored CIS and TRANS concentrations in blood and tissues of adult rats dosed with a commercial mixture of the two isomers, in order to assess the accuracy of their simulations. Additional work is necessary to extend their model to immature subjects. Time-course plasma and tissue concentration data are needed for different immature age-groups, as well as for adults. Isomer-specific TK data are required from animals dosed with the individual isomers, in order to avoid the metabolic interactions inherent with mixtures. We addressed this research gap by determining age-dependent TK in rats for CIS and TRANS at several dose levels that will facilitate construction of a comprehensive PBPK model for each isomer of permethrin.

Mary Amdur Student Award Fund

Winner: Sheryse Taylor

Award Year: 2017
Current Degrees: BSc
Institution/Affiliation: Rutgers University

Ms. Taylor was surprised and extremely excited to receive this award as it will help fund future studies. Using this award she will be able to purchase materials to further explore the mechanism behind the effects she has observed.

Her research focuses on understanding the role of macrophages and nitric oxide metabolism in various models lung injury. In the future she hopes to continue studying the role of the immune system in the development and treatment of cancer. The research for which she was given this award explored the effect of a nitric oxide donor in response to ozone exposure. She found that exposure to increased nitric oxide reduced ozone-induced injury by altering the pro-inflammatory response of the macrophages. Ms. Taylor was surprised and extremely excited to receive this award as it will help fund future studies. Using this award she will be able to purchase materials to further explore the mechanism behind the effects she has observed. Her research focuses on understanding the role of macrophages and nitric oxide metabolism in various models lung injury. In the future she hopes to continue studying the role of the immune system in the development and treatment of cancer. The research for which she was given this award explored the effect of a nitric oxide donor in response to ozone exposure. She found that exposure to increased nitric oxide reduced ozone-induced injury by altering the pro-inflammatory response of the macrophages.

Mary Amdur Student Award Fund

Winner: Katherine Duke

Award Year: 2017
Current Degrees: BS, MS
Institution/Affiliation: North Carolina State University

Ms. Duke is extremely honored to be selected to receive this award.

Occupational exposure to a fiber-like nanomaterial, multi-walled carbon nanotubes (MWCNTs), may pose similar human health risks as asbestos when inhaled. She and colleagues are still investigating how their physiochemical properties affect pulmonary inflammation, fibrosis, allergic lung development, and potentially pre-neoplastic lesions in mice and what this means for humans. Katherine has determined the rigidity of two markedly different MWCNTs; she utilized a full body mouse knock-out for the signal transducer and activator of transcription (STAT)-1, specifically because of its increased susceptibility to fibrogenesis in order to investigate the difference in fibrotic mechanism of each MWCNT. Her work has elucidated that the physicochemical properties of these materials result in greatly different pulmonary effects where the more rigid MWCNT cause prolonged inflammation, mucous cell metaplasia, and greater epithelial cell damage and airway fibrosis compared to the more tangled MWCNT. Furthermore, she has found that STAT1 suppresses the development of fibrosis by downregulating transforming growth factor (TGF) -β1 production and canonical downstream TGF-β1 signaling molecules. This work emphasizes the need for intelligent safe engineering of MWCNTs, considering both their applications in consumer products as well as how their physicochemical characteristics affect lung pathology and their implications in human health. Future aims of the project are to further investigate the mechanism of fibrosis resulting from these contrasting MWCNT rigidities in different cell types and to investigate the potential of these MWCNTs to cause pulmonary neoplastic lesions.Ms. Duke is extremely honored to be selected to receive this award. Occupational exposure to a fiber-like nanomaterial, multi-walled carbon nanotubes (MWCNTs), may pose similar human health risks as asbestos when inhaled. She and colleagues are still investigating how their physiochemical properties affect pulmonary inflammation, fibrosis, allergic lung development, and potentially pre-neoplastic lesions in mice and what this means for humans. Katherine has determined the rigidity of two markedly different MWCNTs; she utilized a full body mouse knock-out for the signal transducer and activator of transcription (STAT)-1, specifically because of its increased susceptibility to fibrogenesis in order to investigate the difference in fibrotic mechanism of each MWCNT. Her work has elucidated that the physicochemical properties of these materials result in greatly different pulmonary effects where the more rigid MWCNT cause prolonged inflammation, mucous cell metaplasia, and greater epithelial cell damage and airway fibrosis compared to the more tangled MWCNT. Furthermore, she has found that STAT1 suppresses the development of fibrosis by downregulating transforming growth factor (TGF) -ß1 production and canonical downstream TGF-ß1 signaling molecules. This work emphasizes the need for intelligent safe engineering of MWCNTs, considering both their applications in consumer products as well as how their physicochemical characteristics affect lung pathology and their implications in human health. Future aims of the project are to further investigate the mechanism of fibrosis resulting from these contrasting MWCNT rigidities in different cell types and to investigate the potential of these MWCNTs to cause pulmonary neoplastic lesions.

Molecular Biology Specialty Section Postdoctoral Fellow Research Award

Winner: Sarah Lacher

Award Year: 2017
Current Degrees: BS, PhD
Institution/Affiliation: University of Minnesota

Dr. Lacher was delighted and extremely honored to find out that she was the first place award winner for the MSBSS 2017 Postdoctoral Fellow Award. She chose to switch fields when starting my current Postdoctoral position, thus she is new to the field of Molecular and Systems Biology. She is honored be selected for this award as this suggests that her current research focus is meaningful to the MSBSS members. She presented a 5-minute research synopsis at the MSBSS reception which provided her with the much-needed opportunity to network with experts in the field of Molecular and Systems Biology. This extension of her network will undoubtedly lead to to future collaborations and success in her future research.

Her current research is focused upon environmental stress at the cellular level. Specifically, she is interested in how the cell responds to stress in terms of global changes in gene transcription. She and colleagues are taking a genome-wide approach to this question by characterizing the regulatory network of one of the most well known stress-responsive transcription factors, Nrf2. Historically Nrf2 activation was considered protective, however, recently evidence has been presented that in certain contexts, Nrf2 activation can be harmful. Thus it is imperative to develop more comprehensive models of Nrf2-mediated gene transcription. She predicted that full characterization of the global NRF2 gene network would provide the mechanistic information needed to understand how NRF2 binding specificity influences gene transcription. She then used this information to characterize how individual genetic variation identified in genome wide association studies (GWAS) can influence Nrf2 binding, gene transcription, and disease risk. She shifted fields when she took her current postdoctoral position, and the gained expertise in molecular genetics and biochemistry has allowed her to diversify her skill set as a toxicologist and has poised her to reach the goal of becoming an independent investigator. Dr. Lacher was delighted and extremely honored to find out that she was the first place award winner for the MSBSS 2017 Postdoctoral Fellow Award. She chose to switch fields when starting my current Postdoctoral position, thus she is new to the field of Molecular and Systems Biology. She is honored be selected for this award as this suggests that her current research focus is meaningful to the MSBSS members. She presented a 5-minute research synopsis at the MSBSS reception which provided her with the much-needed opportunity to network with experts in the field of Molecular and Systems Biology. This extension of her network will undoubtedly lead to to future collaborations and success in her future research.Her current research is focused upon environmental stress at the cellular level. Specifically, she is interested in how the cell responds to stress in terms of global changes in gene transcription. She and colleagues are taking a genome-wide approach to this question by characterizing the regulatory network of one of the most well known stress-responsive transcription factors, Nrf2. Historically Nrf2 activation was considered protective, however, recently evidence has been presented that in certain contexts, Nrf2 activation can be harmful. Thus it is imperative to develop more comprehensive models of Nrf2-mediated gene transcription. She predicted that full characterization of the global NRF2 gene network would provide the mechanistic information needed to understand how NRF2 binding specificity influences gene transcription. She then used this information to characterize how individual genetic variation identified in genome wide association studies (GWAS) can influence Nrf2 binding, gene transcription, and disease risk. She shifted fields when she took her current postdoctoral position, and the gained expertise in molecular genetics and biochemistry has allowed her to diversify her skill set as a toxicologist and has poised her to reach the goal of becoming an independent investigator.

Molecular Biology Student Award Fund

Winner: Elizabeth Mutter-Rottmayer

Award Year: 2017
Current Degrees: BS
Institution/Affiliation: University of North Carolina Chapel Hill

Ms. Mutter-Rottmayer is very excited to be the first place recipient of the Molecular and Systems Biology Specialty Section Graduate Student Award! Receiving this award is not only a great motivator, and has encouraged her to pursue future directions in understanding mechanisms of chemoresistance, but will also provide important exposure to this work that may ultimately lead to improved patient outcome.

She is currently conducting research to uncover how mechanisms of DNA repair may alter both environmental susceptibility as well as the efficacy of chemotherapeutic genotoxins, thus contributing to carcinogenesis. She was specifically acknowledged for her research investigating a cancer cell-specific regulator of the Fanconi Anemia DNA repair pathway and its contribution to resistance of type I topoisomerase poisons, a class of commonly used chemotherapeutics. Ultimately she wants to utilize the improved understanding of the molecular mechanisms of chemoresistance to develop more effective treatment options for patients.Ms. Mutter-Rottmayer is very excited to be the first place recipient of the Molecular and Systems Biology Specialty Section Graduate Student Award! Receiving this award is not only a great motivator, and has encouraged her to pursue future directions in understanding mechanisms of chemoresistance, but will also provide important exposure to this work that may ultimately lead to improved patient outcome. She is currently conducting research to uncover how mechanisms of DNA repair may alter both environmental susceptibility as well as the efficacy of chemotherapeutic genotoxins, thus contributing to carcinogenesis. She was specifically acknowledged for her research investigating a cancer cell-specific regulator of the Fanconi Anemia DNA repair pathway and its contribution to resistance of type I topoisomerase poisons, a class of commonly used chemotherapeutics. Ultimately she wants to utilize the improved understanding of the molecular mechanisms of chemoresistance to develop more effective treatment options for patients.

Molecular Biology Student Award Fund

Winner: Amin Sobh

Award Year: 2017
Current Degrees: BSc, MSc
Institution/Affiliation: University of California, Berkeley

Mr. Sobh was very delighted and grateful when he received this award. He felt proud of his accomplishments as a graduate student. Realizing that experts in the field recognize the importance of his work motivates him to work harder and be even more enthusiastic to pursue his research.

His research involves identifying cellular components and pathways that affect toxic responses to chemical exposures. The ultimate goal of his work is to better understand the toxicity mechanisms of certain chemicals and reveal the determinants of human susceptibility to such chemicals in order to advance risk assessments of corresponding exposures. In the current study, he investigated the toxicity of acetaldehyde and arsenic trioxide in human erythroleukemic cells. He used a functional genomics approach to identify genes whose disruption alters sensitivity to each of the studied chemicals. His approach identified multiple candidate genes that are potentially involved in the mechanism(s) of toxicity of each chemical. Consistent with the reported role of aldehydes in DNA damage, his work demonstrated that disruption of genes encoding DNA repair enzymes increases the toxic effect of acetaldehyde. His results also suggest a role for mitochondrial fragmentation as one of the mechanisms underlying acetaldehyde toxicity. His study on arsenic trioxide suggested a predominant role of reactive oxygen species (ROS) in the mechanism of toxicity and revealed a novel link between arsenic toxicity and selenocysteine metabolism. Mr. Sobh was very delighted and grateful when he received this award. He felt proud of his accomplishments as a graduate student. Realizing that experts in the field recognize the importance of his work motivates him to work harder and be even more enthusiastic to pursue his research. His research involves identifying cellular components and pathways that affect toxic responses to chemical exposures. The ultimate goal of his work is to better understand the toxicity mechanisms of certain chemicals and reveal the determinants of human susceptibility to such chemicals in order to advance risk assessments of corresponding exposures. In the current study, he investigated the toxicity of acetaldehyde and arsenic trioxide in human erythroleukemic cells. He used a functional genomics approach to identify genes whose disruption alters sensitivity to each of the studied chemicals. His approach identified multiple candidate genes that are potentially involved in the mechanism(s) of toxicity of each chemical. Consistent with the reported role of aldehydes in DNA damage, his work demonstrated that disruption of genes encoding DNA repair enzymes increases the toxic effect of acetaldehyde. His results also suggest a role for mitochondrial fragmentation as one of the mechanisms underlying acetaldehyde toxicity. His study on arsenic trioxide suggested a predominant role of reactive oxygen species (ROS) in the mechanism of toxicity and revealed a novel link between arsenic toxicity and selenocysteine metabolism.

Molecular Biology Student Award Fund

Winner: Gloria Garcia

Award Year: 2017
Current Degrees: BS in Biology
Institution/Affiliation: Oregon State University

Ms. Garcia was pleased to win the award. She is not sure how winning this award will help me pursue my research. Preparing the submission did help me with my science communication skills.

The foundation of her research is based on the pursuit of understanding the relationship between the genotype-environment-phenotype. Her dream is to stay in academia and eventually run her own lab. Using the zebrafish model and a combination of techniques including anti-sense knockdown, qPCR, in situ hybridization, larval behavioral assays, and RNA-seq we are interested in testing the hypothesize that a conserved non-coding RNA (slincR) is a direct Ahr target gene that represses Sox9b upon induction by strong Ahr ligands to produce target organ toxicity. Ms. Garcia was pleased to win the award. She is not sure how winning this award will help me pursue my research. Preparing the submission did help me with my science communication skills. The foundation of her research is based on the pursuit of understanding the relationship between the genotype-environment-phenotype. Her dream is to stay in academia and eventually run her own lab. Using the zebrafish model and a combination of techniques including anti-sense knockdown, qPCR, in situ hybridization, larval behavioral assays, and RNA-seq we are interested in testing the hypothesize that a conserved non-coding RNA (slincR) is a direct Ahr target gene that represses Sox9b upon induction by strong Ahr ligands to produce target organ toxicity.

Perry J. Gehring Biological Modeling Endowment Award

Winner: Marie-Emilie Willemin

Award Year: 2017
Current Degrees: PhD, PharmD
Institution/Affiliation: US FDA/NCTR

Dr. Willemin was very excited and honored to receive this award, especially because her work was rewarded by the Biological Modeling Specialty section in relation to my field of expertise (computational modeling). As a young researcher, receiving such a prestigious award by her peers is very rewarding in light of all her efforts and commitment towards the research project as a postdoctoral fellow. For the team, the award recognizes the interest among members in the field in the methodology and the outcomes of our research topic. The award will definitely highlight the ongoing and future research of the lab. And it has already helped her to pursue her career goals in research as she takes her next career step from a postdoctoral researcher to a research scientist.

The objective of the project is the evaluation of the effects of a mixture of environmental chemicals (e.g., perchlorate, thiocyanate), on the thyroid system of pregnant women and her fetuses. Pregnant women are sensitive to thyroid perturbations which could lead to thyroid hormone insufficiency. This is a health concern due to the key role thyroid hormones play in the neurodevelopment of the fetus. She and her team chose to model mechanistically the various modes of action of the global mixture of these thyroid-active chemicals, found in food, drinking water, or cigarette smoke, as the scenario of co-exposure is a more realistic one. Specifically, in this work, we modelled the different mechanisms of action of thiocyanate on the thyroid system in rats, in addition to the development of a PBPK model for thiocyanate in rats and its extrapolation to humans. In the future, the thiocyanate mode of action model will be extrapolated to pregnant women and integrated with perchlorate dose-response model in pregnant women developed earlier in our lab.Dr. Willemin was very excited and honored to receive this award, especially because her work was rewarded by the Biological Modeling Specialty section in relation to my field of expertise (computational modeling). As a young researcher, receiving such a prestigious award by her peers is very rewarding in light of all her efforts and commitment towards the research project as a postdoctoral fellow. For the team, the award recognizes the interest among members in the field in the methodology and the outcomes of our research topic. The award will definitely highlight the ongoing and future research of the lab. And it has already helped her to pursue her career goals in research as she takes her next career step from a postdoctoral researcher to a research scientist. The objective of the project is the evaluation of the effects of a mixture of environmental chemicals (e.g., perchlorate, thiocyanate), on the thyroid system of pregnant women and her fetuses. Pregnant women are sensitive to thyroid perturbations which could lead to thyroid hormone insufficiency. This is a health concern due to the key role thyroid hormones play in the neurodevelopment of the fetus. She and her team chose to model mechanistically the various modes of action of the global mixture of these thyroid-active chemicals, found in food, drinking water, or cigarette smoke, as the scenario of co-exposure is a more realistic one. Specifically, in this work, we modelled the different mechanisms of action of thiocyanate on the thyroid system in rats, in addition to the development of a PBPK model for thiocyanate in rats and its extrapolation to humans. In the future, the thiocyanate mode of action model will be extrapolated to pregnant women and integrated with perchlorate dose-response model in pregnant women developed earlier in our lab.

Perry J. Gehring Risk Assessment Best Postdoctoral Fellow Abstract Award

Winner: Fabian Grimm

Award Year: 2017
Current Degrees: PhD
Institution/Affiliation: Texas A&M University

Dr. Grimm felt honored having been selected as the recipient of the 2017 Perry J. Gehring Risk Assessment Best Postdoctoral Abstract Award. Selection for this award by the Risk Assessment Specialty Section is strongly motivating, as it is not only reflective of the quality of his research, but it is an affirmation that he can make a meaningful impact in the field.

His research focuses on advancing chemical safety evaluations through biological read-across and inter-individual variability assessments using high-content screening of organotypic in vitro models. Currently, the implementation of such models is impeded by the lack of testing strategies that are amenable for (1) inter-individual susceptibility assessments and (2) extrapolation of in vitro data to physiologically-relevant exposure levels. His SOT abstract summarizes one of his team's projects that addresses these two key challenges using a population-based cardiotoxicity model. After completing his postdoctoral training, he is interested in pursuing a career either in industry or academia. Dr. Grimm felt honored having been selected as the recipient of the 2017 Perry J. Gehring Risk Assessment Best Postdoctoral Abstract Award. Selection for this award by the Risk Assessment Specialty Section is strongly motivating, as it is not only reflective of the quality of his research, but it is an affirmation that he can make a meaningful impact in the field. His research focuses on advancing chemical safety evaluations through biological read-across and inter-individual variability assessments using high-content screening of organotypic in vitro models. Currently, the implementation of such models is impeded by the lack of testing strategies that are amenable for (1) inter-individual susceptibility assessments and (2) extrapolation of in vitro data to physiologically-relevant exposure levels. His SOT abstract summarizes one of his team's projects that addresses these two key challenges using a population-based cardiotoxicity model. After completing his postdoctoral training, he is interested in pursuing a career either in industry or academia.

Perry J. Gehring Risk Assessment Student Award Fund

Winner: Abhishek Venkatratnam

Award Year: 2017
Current Degrees: BTech, MS
Institution/Affiliation: University of North Carolina

Mr. Venkatratnam is deeply honored to be the recipient of this award. His doctoral research focuses on evaluating and characterizing population-variability in responses to trichloroethylene (TCE), a ubiquitous environmental contaminant and a known human carcinogen. In addition, provide mechanistic underpinnings on the molecular events driving differences in TCE toxicity. The award recognizes the current findings of this study and its relevance to risk assessment for which he is very grateful.

One of the many challenges in toxicology is addressing human variability in adverse effects with exposure to agents. Traditional toxicity testing of chemicals is routinely performed in a single strain of rodent for dose-response assessment and to derive toxicity values, a key aspect in the risk assessment framework that aids in the regulatory decision making processes. The goal of this study is to provide experimental data by evaluating the quantitative extent of variability in toxic responses in a genetically-diverse mouse population and also characterize the mechanistic underpinnings driving such responses by incorporating genetic data. The findings from this study provide mechanistic evidence on variability in TCE toxicokinetics and also demonstrates a novel feedback loop between PPAR signaling, an adverse outcome pathway in rodents, and oxidative metabolism of TCE. My long-term goal is to become a toxicologist and conduct research relevant to risk assessment either in academia or industry. Mr. Venkatratnam is deeply honored to be the recipient of this award. His doctoral research focuses on evaluating and characterizing population-variability in responses to trichloroethylene (TCE), a ubiquitous environmental contaminant and a known human carcinogen. In addition, provide mechanistic underpinnings on the molecular events driving differences in TCE toxicity. The award recognizes the current findings of this study and its relevance to risk assessment for which he is very grateful. One of the many challenges in toxicology is addressing human variability in adverse effects with exposure to agents. Traditional toxicity testing of chemicals is routinely performed in a single strain of rodent for dose-response assessment and to derive toxicity values, a key aspect in the risk assessment framework that aids in the regulatory decision making processes. The goal of this study is to provide experimental data by evaluating the quantitative extent of variability in toxic responses in a genetically-diverse mouse population and also characterize the mechanistic underpinnings driving such responses by incorporating genetic data. The findings from this study provide mechanistic evidence on variability in TCE toxicokinetics and also demonstrates a novel feedback loop between PPAR signaling, an adverse outcome pathway in rodents, and oxidative metabolism of TCE. My long-term goal is to become a toxicologist and conduct research relevant to risk assessment either in academia or industry.

Renal Toxicology Fellowship Award Fund

Winner: Priyanka Trivedi

Award Year: 2017
Current Degrees: PhD
Institution/Affiliation: Harvard Medical School

Dr. Trivedi was really excited and pleased when she received this award. She immediately shared the good news with her advisor and also thanked him for all his support and encouragement. This award will provide recognition to her work and complement her research in the field of renal toxicology. She will use this award as a springboard for her career in which she plans to make important contributions to advancing our understanding of toxicology research.

Her research focuses on discovering therapeutic targets for acute and chronic kidney diseases. In order to identify druggable targets, she and her team performed RNA sequencing in mouse model of toxic kidney fibrosis and identified Phospholipase D4 (PLD4), a single pass transmembrane glycoprotein, as one of the highly up-regulated genes. Up-regulation of PLD4 was confirmed in three mechanistically distinct mouse models as well as in patients with biopsy-proven kidney fibrosis. Mechanistically, they show that PLD4 facilitates fibrogenesis by modulating innate and adaptive immune responses thereby promoting a TGF-β signaling pathway. Moreover, PLD4 induced the expression of α1-antitrypsin protein (a serine protease inhibitor) that resulted in subsequent down-regulation of a protease neutrophil elastase (NE) expression, thereby leading to the accumulation of extracellular matrix proteins. Interestingly, therapeutic targeting of PLD4 using specific siRNA also protected the mice from kidney fibrosis by inhibiting TGF-β signaling and inducing NE expression. In conclusion, their findings identified PLD4 as a novel therapeutic target for kidney fibrosis - an unmet medical need. Her future goal is to continue contributing to the toxicological science, which can be directly applied clinically to benefit the society.Dr. Trivedi was really excited and pleased when she received this award. She immediately shared the good news with her advisor and also thanked him for all his support and encouragement. This award will provide recognition to her work and complement her research in the field of renal toxicology. She will use this award as a springboard for her career in which she plans to make important contributions to advancing our understanding of toxicology research. Her research focuses on discovering therapeutic targets for acute and chronic kidney diseases. In order to identify druggable targets, she and her team performed RNA sequencing in mouse model of toxic kidney fibrosis and identified Phospholipase D4 (PLD4), a single pass transmembrane glycoprotein, as one of the highly up-regulated genes. Up-regulation of PLD4 was confirmed in three mechanistically distinct mouse models as well as in patients with biopsy-proven kidney fibrosis. Mechanistically, they show that PLD4 facilitates fibrogenesis by modulating innate and adaptive immune responses thereby promoting a TGF-ß signaling pathway. Moreover, PLD4 induced the expression of a1-antitrypsin protein (a serine protease inhibitor) that resulted in subsequent down-regulation of a protease neutrophil elastase (NE) expression, thereby leading to the accumulation of extracellular matrix proteins. Interestingly, therapeutic targeting of PLD4 using specific siRNA also protected the mice from kidney fibrosis by inhibiting TGF-ß signaling and inducing NE expression. In conclusion, their findings identified PLD4 as a novel therapeutic target for kidney fibrosis - an unmet medical need. Her future goal is to continue contributing to the toxicological science, which can be directly applied clinically to benefit the society.

Renal Toxicology Fellowship Award Fund

Winner: Qian Lin

Award Year: 2017
Current Degrees: PhD
Institution/Affiliation: University of Louisville

Dr. Lin was very surprised when she received the award. She felt really appreciative of her mentor. She was so happy to get this award and feels confidence in her project. She felt that only a very interesting project would gain the attentions from other scientists. It makes her feel motivated to do more to further studies in her field.

She is a PhD student in UofL, and is working on diabetes. She is interested in doing research in diabetes. To explore promising drugs and to discover the deep mechanisms of how drugs work on diabetes is meaningful to our society. Her goal is to join a group which is working on drug discovery in diabetes. After the graduation, she would like to find a Postdoc position to learn more about diabetes. To her present project on diabetic nephropathy, which part of kidney is really affected by the FGF1 and which targets of FGF1 is working on should be further studied. She would like to continue exploring this field in the future. Dr. Lin was very surprised when she received the award. She felt really appreciative of her mentor. She was so happy to get this award and feels confidence in her project. She felt that only a very interesting project would gain the attentions from other scientists. It makes her feel motivated to do more to further studies in her field. She is a PhD student in UofL, and is working on diabetes. She is interested in doing research in diabetes. To explore promising drugs and to discover the deep mechanisms of how drugs work on diabetes is meaningful to our society. Her goal is to join a group which is working on drug discovery in diabetes. After the graduation, she would like to find a Postdoc position to learn more about diabetes. To her present project on diabetic nephropathy, which part of kidney is really affected by the FGF1 and which targets of FGF1 is working on should be further studied. She would like to continue exploring this field in the future.

Robert J. Rubin Student Award Fund

Winner: Yvonne Chang

Award Year: 2017
Current Degrees: BS
Institution/Affiliation: Oregon State University

Ms. Chang is very excited to be able to present her research at the 56th SOT Annual Meeting, and looks forward to attending platform presentations and learning more about carcinogenesis and systems biology.

Her dissertation research in Dr. Susan Tilton’s lab focuses on studying mechanisms of carcinogenesis of polycyclic aromatic hydrocarbons (PAHs) and PAH mixtures in a human bronchial epithelial cell (HBEC) model. The goal is to use in vitro data to predict in vivo tumor outcomes and to classify PAHs as carcinogenic or non-carcinogenic. Currently, she has analyzed global gene expression and pathway enrichment between two carcinogenic PAH treatments to our human bronchial epithelial model, benzo[a]pyrene (BAP) and dibenzo-[def,p]chrysene (DBC). She and her colleagues found that short-term 48-hour exposures to BAP and DBC treatment results in a markedly unique transcriptional signature through qRT-PCR and global gene expression analysis. They have identified subsets of shared and uniquely significant pathways, as well as genes that are oppositely regulated by these two PAHs. By using computational and bioinformatics approaches, they were able to extensively profile the mechanisms of toxicity. She has also analyzed global gene expression data for additional treatments of carcinogenic and non-carcinogenic PAHs, as well as one synthetic mixture and one complex environmental mixture. Ms. Chang is very excited to be able to present her research at the 56th SOT Annual Meeting, and looks forward to attending platform presentations and learning more about carcinogenesis and systems biology. Her dissertation research in Dr. Susan Tilton’s lab focuses on studying mechanisms of carcinogenesis of polycyclic aromatic hydrocarbons (PAHs) and PAH mixtures in a human bronchial epithelial cell (HBEC) model. The goal is to use in vitro data to predict in vivo tumor outcomes and to classify PAHs as carcinogenic or non-carcinogenic. Currently, she has analyzed global gene expression and pathway enrichment between two carcinogenic PAH treatments to our human bronchial epithelial model, benzo[a]pyrene (BAP) and dibenzo-[def,p]chrysene (DBC). She and her colleagues found that short-term 48-hour exposures to BAP and DBC treatment results in a markedly unique transcriptional signature through qRT-PCR and global gene expression analysis. They have identified subsets of shared and uniquely significant pathways, as well as genes that are oppositely regulated by these two PAHs. By using computational and bioinformatics approaches, they were able to extensively profile the mechanisms of toxicity. She has also analyzed global gene expression data for additional treatments of carcinogenic and non-carcinogenic PAHs, as well as one synthetic mixture and one complex environmental mixture.

Robert J. Rubin Student Award Fund

Winner: Gopi Gadupudi

Award Year: 2017
Current Degrees: PhD
Institution/Affiliation: University of Iowa

Dr. Gadupudi feels that this award is a very nice recognition from the Risk Assessment and Mechanisms Specialty Section! He appreciates the efforts of both of these specialty sections in making this "Robert J. Rubin Student Travel Award – Honorable Mention" award possible. It clearly speaks, how dedicated the SOT Specialty Sections work in order to recognize and encourage early career toxicologists.

He has been trying to understand the role of environmental contaminants such as PCBs, in causing metabolic diseases, especially fatty liver. Non-alcoholic fatty liver, a disease condition caused by undue accumulation of fat in the liver, compromises the function of the liver in maintaining metabolic and energy balance. Despite being one of the most prevalent metabolic disease, the underlying mechanisms that cause this is largely unknown. Going forward, he would like to understand the mechanistic role of toxicants in causing this fatty liver disease. The specific research that helped me win this award, was to identify and characterize a molecular event that leads to decreased phosphorylation of protein called CREB, during PCB126-induced Fatty liver. Dr. Gadupudi feels that this award is a very nice recognition from the Risk Assessment and Mechanisms Specialty Section! He appreciates the efforts of both of these specialty sections in making this "Robert J. Rubin Student Travel Award – Honorable Mention" award possible. It clearly speaks, how dedicated the SOT Specialty Sections work in order to recognize and encourage early career toxicologists. He has been trying to understand the role of environmental contaminants such as PCBs, in causing metabolic diseases, especially fatty liver. Non-alcoholic fatty liver, a disease condition caused by undue accumulation of fat in the liver, compromises the function of the liver in maintaining metabolic and energy balance. Despite being one of the most prevalent metabolic disease, the underlying mechanisms that cause this is largely unknown. Going forward, he would like to understand the mechanistic role of toxicants in causing this fatty liver disease. The specific research that helped me win this award, was to identify and characterize a molecular event that leads to decreased phosphorylation of protein called CREB, during PCB126-induced Fatty liver.

Ronald G. Thurman Student Travel Award

Winner: Yu Syuan  Luo

Award Year: 2017
Current Degrees: PhD
Institution/Affiliation: Texas A&M University

Dr. Luo feels it is a great honor to receive this award. This travel award not only provides him with financial support to cover the traveling expenses, but also recognizes his work on the metabolism and toxicities of trichloroethylene. It also offers an great opportunity to present his work in the 2017 SOT Annual Meeting, and to receive very valuable feedback from the audience. He believes that these intellectual inputs can further improve his research, and increase scientific impacts of his efforts.

His work is to understand the role of an important enzyme, cytochrome P450 2E1 (CYP2E1), on the metabolism and toxicities of trichloroethylene(TCE). Metabolism of TCE is associated with its organ-specific toxicities. His research will clarify how CYP2E1 gets involved in the metabolism of TCE, and how the altered levels of TCE metabolites further modified the exerted TCE toxicities. In addition, he also advances our understanding of the inter-individual and inter-species differences in metabolism and toxicities of TCE by using CYP2E1 knockout and humanized transgenic mice, which could be critical to conducting health risk assessment of TCE. His future work will further investigate the metabolism and toxicities of a structural-similar chemical of TCE, perchloroethylene (PERC), and then conduct a parallel comparison of TCE and PERC. Collectively, their study is expected to advance our knowledge in metabolism and toxicities of these chlorinated solvents, which are of critical concerns in their health risk assessments. Dr. Luo feels it is a great honor to receive this award. This travel award not only provides him with financial support to cover the traveling expenses, but also recognizes his work on the metabolism and toxicities of trichloroethylene. It also offers an great opportunity to present his work in the 2017 SOT Annual Meeting, and to receive very valuable feedback from the audience. He believes that these intellectual inputs can further improve his research, and increase scientific impacts of his efforts.His work is to understand the role of an important enzyme, cytochrome P450 2E1 (CYP2E1), on the metabolism and toxicities of trichloroethylene(TCE). Metabolism of TCE is associated with its organ-specific toxicities. His research will clarify how CYP2E1 gets involved in the metabolism of TCE, and how the altered levels of TCE metabolites further modified the exerted TCE toxicities. In addition, he also advances our understanding of the inter-individual and inter-species differences in metabolism and toxicities of TCE by using CYP2E1 knockout and humanized transgenic mice, which could be critical to conducting health risk assessment of TCE. His future work will further investigate the metabolism and toxicities of a structural-similar chemical of TCE, perchloroethylene (PERC), and then conduct a parallel comparison of TCE and PERC. Collectively, their study is expected to advance our knowledge in metabolism and toxicities of these chlorinated solvents, which are of critical concerns in their health risk assessments.

Ronald G. Thurman Student Travel Award

Winner: Ramiya Kumar

Award Year: 2017
Current Degrees: PhD
Institution/Affiliation: Clemson University

Dr. Kumar would like to thank Mechanisms Specialty section officers and Ronald G. Thurman Travel award's committee for presenting me this travel award. She is very happy and excited to have received this award, which is given for research focused on mechanistic studies on liver and getting recognized by mechanisms SS will help me to meet new collaborators and progress her research. The travel award will help her to attend SOT 2017 at Baltimore, MD and present her research at the poster session, network with Toxicology experts through chat with the expert and poster tour events and also meet fellow aspiring toxicologists from around the world. This meeting will give her the opportunity to meet with experts at different career stages and from different domains such as industry, academia and government who are willing to share their career and research experiences. Overall, she feels this meeting will enlighten her about career choices and prospective employers, brief idea about job responsibilities, current trends in toxicology research, meet future collaborators and make new friends. As a doctoral candidate closer to graduation this meeting will give her a broad perspective about toxicology research in general while she plans her next steps to achieve her career goal of joining industrial research career with a focus on development of personalized medicine.

World health organization has declared that over 600 million adults are obese around the world. There is a dire need to develop new strategies to tackle the increasing obesity numbers because the current treatment regimes of healthier food choices and active lifestyle changes are not successful. We are exposed to growing number of chemicals, which are metabolized and cleared from our body by specific liver enzymes- “Cytochrome P450 (CYP)”. And earlier studies in obese patients have shown significant changes in CYP genes. Consequently, they used a mouse model missing CYP3A genes and developed a mouse model missing CYP2B and compared their responses to mice that have all genes (wild type mice) to demonstrate if the absence of CYP genes would increase the progression of obesity. They also treat them with diet rich in 60% fat, which resemble western diet to determine role-played by CYP3A and CYP2B in lipid metabolism. In future, they plan to identify chemicals that can inhibit CYP2B and determine if they perturb lipid metabolism. Her current SOT poster is on "Cyp2b9/10/13-null male mice are susceptible to diet-induced obesity". They developed the mouse model missing Cyp2b9, 10 and 13 and treated them with high fat (60% fat) and other group with chow diet to demonstrate if lack of three cyp2b genes exacerbate lipid metabolism when coupled with high fat diet. Their data indicate that male Cyp2b-null but not female mice gain 15% more body weight and 1x more white adipose tissue weight than wild type mice when they were fed a high fat diet. Male cyp2b-null mice on high fat diet show significant metabolic changes such as higher blood cholesterol and increased levels hormones such as adiponectin and leptin. Male cyp2b-null mice accumulate significantly more triglyceride in liver and lower serum triglyceride compared to the wild type mice. They are yet to determine changes in gene and protein expression and also changes in lipid profile. Overall, her results show that lack of cyp2b9, 10 and 13 perturbs lipid metabolism and increase progression to diet-induced obesity. Also, gender based differences are observed in the Cyp2b-null mice while responding to the diet treatment. Dr. Kumar would like to thank Mechanisms Specialty section officers and Ronald G. Thurman Travel award's committee for presenting me this travel award. She is very happy and excited to have received this award, which is given for research focused on mechanistic studies on liver and getting recognized by mechanisms SS will help me to meet new collaborators and progress her research. The travel award will help her to attend SOT 2017 at Baltimore, MD and present her research at the poster session, network with Toxicology experts through chat with the expert and poster tour events and also meet fellow aspiring toxicologists from around the world. This meeting will give her the opportunity to meet with experts at different career stages and from different domains such as industry, academia and government who are willing to share their career and research experiences. Overall, she feels this meeting will enlighten her about career choices and prospective employers, brief idea about job responsibilities, current trends in toxicology research, meet future collaborators and make new friends. As a doctoral candidate closer to graduation this meeting will give her a broad perspective about toxicology research in general while she plans her next steps to achieve her career goal of joining industrial research career with a focus on development of personalized medicine. World health organization has declared that over 600 million adults are obese around the world. There is a dire need to develop new strategies to tackle the increasing obesity numbers because the current treatment regimes of healthier food choices and active lifestyle changes are not successful. We are exposed to growing number of chemicals, which are metabolized and cleared from our body by specific liver enzymes- “Cytochrome P450 (CYP)”. And earlier studies in obese patients have shown significant changes in CYP genes. Consequently, they used a mouse model missing CYP3A genes and developed a mouse model missing CYP2B and compared their responses to mice that have all genes (wild type mice) to demonstrate if the absence of CYP genes would increase the progression of obesity. They also treat them with diet rich in 60% fat, which resemble western diet to determine role-played by CYP3A and CYP2B in lipid metabolism. In future, they plan to identify chemicals that can inhibit CYP2B and determine if they perturb lipid metabolism. Her current SOT poster is on "Cyp2b9/10/13-null male mice are susceptible to diet-induced obesity". They developed the mouse model missing Cyp2b9, 10 and 13 and treated them with high fat (60% fat) and other group with chow diet to demonstrate if lack of three cyp2b genes exacerbate lipid metabolism when coupled with high fat diet. Their data indicate that male Cyp2b-null but not female mice gain 15% more body weight and 1x more white adipose tissue weight than wild type mice when they were fed a high fat diet. Male cyp2b-null mice on high fat diet show significant metabolic changes such as higher blood cholesterol and increased levels hormones such as adiponectin and leptin. Male cyp2b-null mice accumulate significantly more triglyceride in liver and lower serum triglyceride compared to the wild type mice. They are yet to determine changes in gene and protein expression and also changes in lipid profile. Overall, her results show that lack of cyp2b9, 10 and 13 perturbs lipid metabolism and increase progression to diet-induced obesity. Also, gender based differences are observed in the Cyp2b-null mice while responding to the diet treatment.

Ronald G. Thurman Student Travel Award

Winner: Diptadip Dattaroy

Award Year: 2017
Current Degrees: MS
Institution/Affiliation: University of South Carolina

Mr. Dattaroy was very excited and happy about receiving the award. This award is very encouraging and it has definitely improved his CV.

His research here describes the therapeutic role of a plant derived anti-inflammatory compound which can be a possible drug to treat liver inflammation and fibrosis in a disease called nonalcoholic steatohepatitis. He would like to pursue a postdoctoral position after my PhD and would like to venture into industry/academic position after that.Mr. Dattaroy was very excited and happy about receiving the award. This award is very encouraging and it has definitely improved his CV. His research here describes the therapeutic role of a plant derived anti-inflammatory compound which can be a possible drug to treat liver inflammation and fibrosis in a disease called nonalcoholic steatohepatitis. He would like to pursue a postdoctoral position after my PhD and would like to venture into industry/academic position after that.

Sheldon D. Murphy Award Fund

Winner: Gopi Gadupudi

Award Year: 2017
Current Degrees: PhD
Institution/Affiliation: University of Iowa

Dr. Gadupudi is very thankful to the mechanisms specialty section and the SOT for providing this award, especially for encouraging early career scientists to pursue further research.

He has been working towards understanding the role of pollutants such as PCBs on liver metabolism. The current work identifies the disruption of a critical event called "REBECA-phosphorylation" that is necessary to produce glucose in the liver during a process called gluconeogenesis. Moving forward, he and colleagues would like to understand the implications of the Persistent organic pollutant accumulation in the liver and their effects on metabolic and energy homeostasis.Dr. Gadupudi is very thankful to the mechanisms specialty section and the SOT for providing this award, especially for encouraging early career scientists to pursue further research. He has been working towards understanding the role of pollutants such as PCBs on liver metabolism. The current work identifies the disruption of a critical event called "REBECA-phosphorylation" that is necessary to produce glucose in the liver during a process called gluconeogenesis. Moving forward, he and colleagues would like to understand the implications of the Persistent organic pollutant accumulation in the liver and their effects on metabolic and energy homeostasis.

Sheldon D. Murphy Award Fund

Winner: Kelly Fader

Award Year: 2017
Current Degrees: BSc
Institution/Affiliation: Michigan State University

Ms. Fader felt it was an honor to learn that she had been selected to receive the 2017 Sheldon D. Murphy Student Travel Award. She immediately shared the news with my principal investigator, Dr. Timothy Zacharewski, as well as the postdoctoral researchers in the lab, who shared in her excitement. This award allowed her to present her research at the 2017 Society of Toxicology Annual Meeting, providing the opportunity to receive valuable feedback and develop collaborations with other researchers in the field of biomedical toxicology.

Metabolic syndrome, a disease which consists of obesity, elevated blood lipids, high blood pressure and high blood sugar, is approaching epidemic levels in the United States. In the liver, MetS is first observed as fat accumulation which can develop into non-alcoholic fatty liver disease (NAFLD), a risk factor for diabetes, cardiovascular disease, and liver cancer. Recently, several environmental contaminants including dioxin have been implicated in MetS development. In mice, dioxin causes accumulation of fat in the liver (fatty liver), primarily originating from the diet, which progresses to inflammation and fibrosis over time. Her research investigates dioxin-induced changes along the intestinal tract that promote the development of NAFLD and other complex metabolic disorders. Specifically, her application for the Sheldon D. Murphy Student Travel Award discussed the role of dioxin-elicited iron overloading in the progression of NAFLD. Upon completing her PhD at Michigan State University, she plans to obtain further postdoctoral training before pursuing an independent research career at either an academic institution or the Environmental Protection Agency (EPA). She would like to remain in the field of biomedical toxicology, investigating the effects of environmental contaminants, food ingredients, and drugs on human health and disease. In particular, She is interested in investigating the role of gene-environment interactions in the development and progression of complex multifactorial diseases such as metabolic syndrome and cancer. Ms. Fader felt it was an honor to learn that she had been selected to receive the 2017 Sheldon D. Murphy Student Travel Award. She immediately shared the news with my principal investigator, Dr. Timothy Zacharewski, as well as the postdoctoral researchers in the lab, who shared in her excitement. This award allowed her to present her research at the 2017 Society of Toxicology Annual Meeting, providing the opportunity to receive valuable feedback and develop collaborations with other researchers in the field of biomedical toxicology. Metabolic syndrome, a disease which consists of obesity, elevated blood lipids, high blood pressure and high blood sugar, is approaching epidemic levels in the United States. In the liver, MetS is first observed as fat accumulation which can develop into non-alcoholic fatty liver disease (NAFLD), a risk factor for diabetes, cardiovascular disease, and liver cancer. Recently, several environmental contaminants including dioxin have been implicated in MetS development. In mice, dioxin causes accumulation of fat in the liver (fatty liver), primarily originating from the diet, which progresses to inflammation and fibrosis over time. Her research investigates dioxin-induced changes along the intestinal tract that promote the development of NAFLD and other complex metabolic disorders. Specifically, her application for the Sheldon D. Murphy Student Travel Award discussed the role of dioxin-elicited iron overloading in the progression of NAFLD. Upon completing her PhD at Michigan State University, she plans to obtain further postdoctoral training before pursuing an independent research career at either an academic institution or the Environmental Protection Agency (EPA). She would like to remain in the field of biomedical toxicology, investigating the effects of environmental contaminants, food ingredients, and drugs on human health and disease. In particular, She is interested in investigating the role of gene-environment interactions in the development and progression of complex multifactorial diseases such as metabolic syndrome and cancer.

Sheldon D. Murphy Award Fund

Winner: Cory Gerlach

Award Year: 2017
Current Degrees: BS
Institution/Affiliation: Harvard Medical School

When Mr. Gerlach learned that he won this award, he yelled out loud in his lab with excitement. Not only will the money help pay for his expenses incurred by coming to the SOT Annual Meeting, but it was also an enormous honor to be recognized for his work. This award gives him the confidence that what he is researching is important to the field of toxicology. Also, it will be great to get feedback on his project at the meeting.

Acute kidney injury (AKI) is increasing worldwide and if severe or repeated could lead to chronic kidney disease (CKD) or end-stage renal failure. Currently, there are no treatments that prevent the progression of AKI to CKD, and if kidney function deteriorates only dialysis or kidney transplantation are available. Therefore, our goal is to identify the mechanisms of kidney disease progression so that we can intervene and improve outcomes for patients. To this end, we have identified microRNA (miR)-132 as potentially mediating kidney injury. MicroRNAs have gained immense interest over the years as researchers have identified their importance in disease pathogenesis and have developed methods to modulate their expression. Specifically, miR-132 is highly expressed in response to injury in various kidney disease models in mice. When overexpressed in primary human kidney cells, important protective pathways are downregulated. Importantly, overexpression of miR-132 makes these cell more sensitive to the nephrotoxin cisplatin. He is interested in investigating these pathways more carefully in mice to see if inhibition will lead to protection from acute injury and therefore improve kidney function in the long-term.When Mr. Gerlach learned that he won this award, he yelled out loud in his lab with excitement. Not only will the money help pay for his expenses incurred by coming to the SOT Annual Meeting, but it was also an enormous honor to be recognized for his work. This award gives him the confidence that what he is researching is important to the field of toxicology. Also, it will be great to get feedback on his project at the meeting. Acute kidney injury (AKI) is increasing worldwide and if severe or repeated could lead to chronic kidney disease (CKD) or end-stage renal failure. Currently, there are no treatments that prevent the progression of AKI to CKD, and if kidney function deteriorates only dialysis or kidney transplantation are available. Therefore, our goal is to identify the mechanisms of kidney disease progression so that we can intervene and improve outcomes for patients. To this end, we have identified microRNA (miR)-132 as potentially mediating kidney injury. MicroRNAs have gained immense interest over the years as researchers have identified their importance in disease pathogenesis and have developed methods to modulate their expression. Specifically, miR-132 is highly expressed in response to injury in various kidney disease models in mice. When overexpressed in primary human kidney cells, important protective pathways are downregulated. Importantly, overexpression of miR-132 makes these cell more sensitive to the nephrotoxin cisplatin. He is interested in investigating these pathways more carefully in mice to see if inhibition will lead to protection from acute injury and therefore improve kidney function in the long-term.

Sheldon D. Murphy Award Fund

Winner: Nehal Gupta

Award Year: 2017
Current Degrees: MPharm, BPharm,
Institution/Affiliation: Texas Tech University Health Sciences Center

Ms. Gupta was very excited after receiving Sheldon D. Murphy travel Award. She would like to thank Mechanisms Specialty Section for selecting her for this award. This award would offer a tremendous financial support to attend the 2017 SOT Annual Meeting. It will be an excellent opportunity to meet scientists across the globe and share her work with them, which will provide novel insights to her work. Also, recognition by awards committee has boosted her morale to do better work.

She started her project on breast cancer, which is one of the most malignant carcinoma in women worldwide. Despite of current available treatment options, breast cancer kills approximately 40,000 women every year, making it the second-leading cause of cancer related deaths. Resistance to current chemotherapeutics is the major obstacle in treating breast cancer patients. She and colleagues developed resistance towards paclitaxel in various breast cancer cell lines (MCF-7, 4T1, HCC1806). With extensive research, they are able to unravel the mechanism behind the resistance and based on previous publication (Ranjan et al. “Penfluridol: An antipsychotic agent suppresses metastatic tumor growth in triple negative breast cancer by inhibiting integrin signaling axis” Cancer Research 2015), they are able to develop penfluridol as a treatment option to overcome resistance. Their results showed that penfluridol treatment synergistically enhanced the growth suppressive effects of paclitaxel in vitro as well as in vivo. They also observed that chronic treatment of mice with penfluridol was not associated with any toxicity or behavioral side effect. Therefore, combining penfluridol with paclitaxel will reduce the dose as well as toxic side effects of current chemotherapy. Since penfluridol is an FDA approved drug, the pharmacology, formulation and potential toxicities are already known. Their 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 breast tumors. For her long term goal, she would like to develop her professional career as an academic scientist in the field of Oncology. She has been mentored by one student that gave her motivation to train new researchers in cancer field. Ms. Gupta was very excited after receiving Sheldon D. Murphy travel Award. She would like to thank Mechanisms Specialty Section for selecting her for this award. This award would offer a tremendous financial support to attend the 2017 SOT Annual Meeting. It will be an excellent opportunity to meet scientists across the globe and share her work with them, which will provide novel insights to her work. Also, recognition by awards committee has boosted her morale to do better work. She started her project on breast cancer, which is one of the most malignant carcinoma in women worldwide. Despite of current available treatment options, breast cancer kills approximately 40,000 women every year, making it the second-leading cause of cancer related deaths. Resistance to current chemotherapeutics is the major obstacle in treating breast cancer patients. She and colleagues developed resistance towards paclitaxel in various breast cancer cell lines (MCF-7, 4T1, HCC1806). With extensive research, they are able to unravel the mechanism behind the resistance and based on previous publication (Ranjan et al. “Penfluridol: An antipsychotic agent suppresses metastatic tumor growth in triple negative breast cancer by inhibiting integrin signaling axis” Cancer Research 2015), they are able to develop penfluridol as a treatment option to overcome resistance. Their results showed that penfluridol treatment synergistically enhanced the growth suppressive effects of paclitaxel in vitro as well as in vivo. They also observed that chronic treatment of mice with penfluridol was not associated with any toxicity or behavioral side effect. Therefore, combining penfluridol with paclitaxel will reduce the dose as well as toxic side effects of current chemotherapy. Since penfluridol is an FDA approved drug, the pharmacology, formulation and potential toxicities are already known. Their 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 breast tumors. For her long term goal, she would like to develop her professional career as an academic scientist in the field of Oncology. She has been mentored by one student that gave her motivation to train new researchers in cancer field.

Sheldon D. Murphy Award Fund

Winner: Madelyn Huang

Award Year: 2017
Current Degrees: BS
Institution/Affiliation: University of North Carolina Chapel Hill

Ms. Huang was very honored to receive this award from the Mechanisms Specialty Section. She feels that it is encouraging to see that scientists from different fields of research value the work that she has done. With the award, she will be able to fund her attendance at the SOT Annual Meeting, to present her research and build her network. She anticipates graduating at the end of 2017 so attendance at the SOT Annual Meeting this year is most advantageous in finding the next step in her career.

Numerous epidemiological studies have found a significant association between exposure to arsenic and increased incidence or prevalence of type 2 diabetes. However, the mechanisms underlying this association is unclear. The team at her lab seeks to understand mechanisms of arsenic-associated diabetes, through cell and animal studies. Previously, they have shown that arsenic exposure inhibits insulin secretion in pancreatic beta-cells. Her research shows that this inhibition in insulin secretion may be due, at least in part, to inhibition of calcium signaling in the beta-cell. In the future, she would like to continue research in the field of environmental endocrine disruptors, and also investigate how nutritional status can modify an individual's susceptibility to toxicants. Ms. Huang was very honored to receive this award from the Mechanisms Specialty Section. She feels that it is encouraging to see that scientists from different fields of research value the work that she has done. With the award, she will be able to fund her attendance at the SOT Annual Meeting, to present her research and build her network. She anticipates graduating at the end of 2017 so attendance at the SOT Annual Meeting this year is most advantageous in finding the next step in her career. Numerous epidemiological studies have found a significant association between exposure to arsenic and increased incidence or prevalence of type 2 diabetes. However, the mechanisms underlying this association is unclear. The team at her lab seeks to understand mechanisms of arsenic-associated diabetes, through cell and animal studies. Previously, they have shown that arsenic exposure inhibits insulin secretion in pancreatic beta-cells. Her research shows that this inhibition in insulin secretion may be due, at least in part, to inhibition of calcium signaling in the beta-cell. In the future, she would like to continue research in the field of environmental endocrine disruptors, and also investigate how nutritional status can modify an individual's susceptibility to toxicants.

Toshio Narahashi Neurotoxicology Fellowship Award Fund

Winner: Shelbie Burchfield

Award Year: 2017
Current Degrees: BS
Institution/Affiliation: Northeast Ohio Medical University

Ms. Burchfield was very excited and grateful when she found out that she had received this award. The award greatly helped her to pay for travel to and from the Society of Toxicology meeting, where she had the opportunity to present her data, learn about current progress in the field, and network with great scientists.

She is currently working on research that is looking at the role of neuroinflammation in neurodegenerative diseases such as Parkinson's disease. The research she did for this award involves the investigation of a bile acid receptor most commonly found in the liver and intestine as a potential therapeutic target for inflammation in the brain. It is her hope to continue investigating the role of inflammation in neurodegenerative disease and finding other potential therapeutic targets for neuroinflammation.Ms. Burchfield was very excited and grateful when she found out that she had received this award. The award greatly helped her to pay for travel to and from the Society of Toxicology meeting, where she had the opportunity to present her data, learn about current progress in the field, and network with great scientists. She is currently working on research that is looking at the role of neuroinflammation in neurodegenerative diseases such as Parkinson's disease. The research she did for this award involves the investigation of a bile acid receptor most commonly found in the liver and intestine as a potential therapeutic target for inflammation in the brain. It is her hope to continue investigating the role of inflammation in neurodegenerative disease and finding other potential therapeutic targets for neuroinflammation.

Toshio Narahashi Neurotoxicology Fellowship Award Fund

Winner: Gelareh  Alam

Award Year: 2017
Current Degrees: Pharm D, PhD
Institution/Affiliation: Northeast Ohio Medical University

Dr. Alam was really honored and grateful to receive this award. She has been working really hard in the field of neurotoxicology for the past couple of years, and has tried her best to be an active member of the scientific field and society. However, due to financial limitations attending the relevant meetings can be challenging sometimes. Receiving this award has provided motivation to work harder as a researcher and also has provided her with the opportunity to attend the SOT Annual Meeting. Presenting her research in the meeting and interacting with other great researchers will give her an exceptional opportunity to learn the progressive science in the field and also inspire her to come up with great ideas and projects that might be of significance in the field.

She has been working on neurodegenerative disease with a focus on Parkinson's disease. Investigating the role of gene environment interactions in the progression of the disease is where her true interest lies. Additionally, detecting the genetic and protein profile of the distinct dopaminergic neuronal populations susceptible to toxicant-induced neruodegeneration is the focus of her current research for which she has received the award. Her long term goal is to become a successful independent researcher, making significant contributions to the field of neurotoxicology and neurodegenerative diseases. Also she would like to be a great teacher to the student who are passionate about science and the beauty it has to offer. Dr. Alam was really honored and grateful to receive this award. She has been working really hard in the field of neurotoxicology for the past couple of years, and has tried her best to be an active member of the scientific field and society. However, due to financial limitations attending the relevant meetings can be challenging sometimes. Receiving this award has provided motivation to work harder as a researcher and also has provided her with the opportunity to attend the SOT Annual Meeting. Presenting her research in the meeting and interacting with other great researchers will give her an exceptional opportunity to learn the progressive science in the field and also inspire her to come up with great ideas and projects that might be of significance in the field. She has been working on neurodegenerative disease with a focus on Parkinson's disease. Investigating the role of gene environment interactions in the progression of the disease is where her true interest lies. Additionally, detecting the genetic and protein profile of the distinct dopaminergic neuronal populations susceptible to toxicant-induced neruodegeneration is the focus of her current research for which she has received the award. Her long term goal is to become a successful independent researcher, making significant contributions to the field of neurotoxicology and neurodegenerative diseases. Also she would like to be a great teacher to the student who are passionate about science and the beauty it has to offer.

Toshio Narahashi Neurotoxicology Fellowship Award Fund

Winner: Pallavi Pilaka

Award Year: 2017
Current Degrees: Undergraduate
Institution/Affiliation: Virginia Commonwealth University

When Ms. Pilaka received the Toshio Narahashi Award she was honored and excited. This award will help her pursue her research interests by allowing her to cover the costs of travel to the 2017 SOT Annual Meeting. It is a particularly important opportunity, given her upcoming transition from undergraduate to graduate studies. This meeting will allow her to interface with faculty and students from laboratories that she is considering for graduate studies. The exposure and networking opportunities that this meeting affords are critical to an informed decision this spring. Attending SOT 2017 and interfacing with the Neurotoxicology Specialty Section will also give her a greater appreciation of the field, ongoing research and career opportunities available beyond her training.

Secondhand smoke exposure during the juvenile developmental period continues to be a problem in the United States. Previous studies have shown that secondhand smoke exposure increases mitochondrial densities in the brain. Behavioral studies have revealed deficits in attention and impulsivity in juvenile animals exposed to secondhand smoke. The goal of my research project is to understand the causal relationship between mitochondrial densities caused by secondhand smoke exposure and behavioral problems in attention and impulsivity. Her future goals are to attend a graduate program to further understand the brain and the pathways involved in different neurological and toxicological disorders.When Ms. Pilaka received the Toshio Narahashi Award she was honored and excited. This award will help her pursue her research interests by allowing her to cover the costs of travel to the 2017 SOT Annual Meeting. It is a particularly important opportunity, given her upcoming transition from undergraduate to graduate studies. This meeting will allow her to interface with faculty and students from laboratories that she is considering for graduate studies. The exposure and networking opportunities that this meeting affords are critical to an informed decision this spring. Attending SOT 2017 and interfacing with the Neurotoxicology Specialty Section will also give her a greater appreciation of the field, ongoing research and career opportunities available beyond her training. Secondhand smoke exposure during the juvenile developmental period continues to be a problem in the United States. Previous studies have shown that secondhand smoke exposure increases mitochondrial densities in the brain. Behavioral studies have revealed deficits in attention and impulsivity in juvenile animals exposed to secondhand smoke. The goal of my research project is to understand the causal relationship between mitochondrial densities caused by secondhand smoke exposure and behavioral problems in attention and impulsivity. Her future goals are to attend a graduate program to further understand the brain and the pathways involved in different neurological and toxicological disorders.

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

Winner: Krishnaprahlad Maremanda

Award Year: 2017
Current Degrees: MS Pharm
Institution/Affiliation: Niper

He feels that receiving this award is really encouraging as it will definitely leave a positive imprint on his mind to further apply and do these kinds of research. He highly appreciates and thanks the team for giving him this opportunity. He looks forward to serving the society when ever and which ever way it is possible in future.

His research involves elucidating the mechanism of the germ cell toxicity in rat induced by anti-cancer drugs. Especially involving the role of zinc in counteracting these toxicity. we found that zinc homeostasis is disturbed by anticancer drugs in testes, which might contribute to the toxicity. So in a nut shell zinc supplementation studies deserve further attention in patients undergoing chemotherapy and their levels need to be monitored.He feels that receiving this award is really encouraging as it will definitely leave a positive imprint on his mind to further apply and do these kinds of research. He highly appreciates and thanks the team for giving him this opportunity. He looks forward to serving the society when ever and which ever way it is possible in future. His research involves elucidating the mechanism of the germ cell toxicity in rat induced by anti-cancer drugs. Especially involving the role of zinc in counteracting these toxicity. we found that zinc homeostasis is disturbed by anticancer drugs in testes, which might contribute to the toxicity. So in a nut shell zinc supplementation studies deserve further attention in patients undergoing chemotherapy and their levels need to be monitored.

Vera W. Hudson and Elizabeth K. Weisburger Scholarship Fund

Winner: Lisa Weatherly

Award Year: 2017
Current Degrees: BA
Institution/Affiliation: University of Maine

She was very excited and honored to receive this award. This award will enable her to attend the SOT Annual Meeting where she will participate in many networking activities and forums for learning about postdoctoral job opportunities.

Triclosan (TCS) is an antimicrobial that has recently been banned from soap products following the FDA’s 2016 risk assessment. However, TCS still remains in other consumer products such as toothpaste and surgical soaps. TCS is readily absorbed into human skin and oral mucosa and has been found in various human tissues and fluids. Mast cells are ubiquitous immune effector cells that are involved in allergies and asthma. Mast cells release chemical mediators (such as histamine) through a signaling cascade, termed degranulation, after stimulation. Our previous studies show that TCS inhibits mast cell degranulation. We also show that non-cytotoxic, µM levels of TCS inhibit the cells energy production via disruption of ATP and oxygen consumption rate in multiple cell types. These results indicate that TCS is a mitochondrial uncoupler. Known mitochondrial uncouplers have been shown to disrupt mitochondrial morphology. Using fluorescence photoactivation localization microscopy (FPALM) with the outer mitochondrial membrane marker Dendra2-TOM20, we show that TCS disrupts mitochondrial ultrastructure. TCS decreases mitochondrial perimeter, major axis, and elongation: evidence that TCS causes mitochondrial fission. TCS can also cause mitochondria to undergo a recently described morphology termed toroid or “donut” morphology. Also, TCS increases reactive oxygen species production and inhibits calcium signaling, processes which have been linked to fission. In antigen-stimulated RBL-2H3 mast cells, TCS inhibits mitochondrial translocation, which is critical for degranulation. Our findings provide a mechanism for TCS disruption of both mast cell degranulation and universal dysfunction of mitochondria. She hopes to continue working on toxicant effects on mitochondrial function in her postdoc.She was very excited and honored to receive this award. This award will enable her to attend the SOT Annual Meeting where she will participate in many networking activities and forums for learning about postdoctoral job opportunities. Triclosan (TCS) is an antimicrobial that has recently been banned from soap products following the FDA’s 2016 risk assessment. However, TCS still remains in other consumer products such as toothpaste and surgical soaps. TCS is readily absorbed into human skin and oral mucosa and has been found in various human tissues and fluids. Mast cells are ubiquitous immune effector cells that are involved in allergies and asthma. Mast cells release chemical mediators (such as histamine) through a signaling cascade, termed degranulation, after stimulation. Our previous studies show that TCS inhibits mast cell degranulation. We also show that non-cytotoxic, µM levels of TCS inhibit the cells energy production via disruption of ATP and oxygen consumption rate in multiple cell types. These results indicate that TCS is a mitochondrial uncoupler. Known mitochondrial uncouplers have been shown to disrupt mitochondrial morphology. Using fluorescence photoactivation localization microscopy (FPALM) with the outer mitochondrial membrane marker Dendra2-TOM20, we show that TCS disrupts mitochondrial ultrastructure. TCS decreases mitochondrial perimeter, major axis, and elongation: evidence that TCS causes mitochondrial fission. TCS can also cause mitochondria to undergo a recently described morphology termed toroid or “donut” morphology. Also, TCS increases reactive oxygen species production and inhibits calcium signaling, processes which have been linked to fission. In antigen-stimulated RBL-2H3 mast cells, TCS inhibits mitochondrial translocation, which is critical for degranulation. Our findings provide a mechanism for TCS disruption of both mast cell degranulation and universal dysfunction of mitochondria.

Vera W. Hudson and Elizabeth K. Weisburger Scholarship Fund

Winner: Katelyn Lavrich

Award Year: 2017
Current Degrees: BS
Institution/Affiliation: University of North Carolina Chapel Hill

She is extremely grateful for this generous award. This award will allow jer to travel to the 2017 SOT Annual Meeting, where she hopes to discuss her research with other scientists from around the world and brainstorm new insights. She also hopes to network with fellow toxicologists to foster new collaborations and explore career opportunities for the next step.

She is currently researching how air pollution causes human health effects. While the diseases associated with air pollution exposure have been well-described, the mechanisms that initiate adverse health effects have not been characterized. One frequently cited mechanism involved in the development of adverse health effects after air pollution exposure is oxidative stress, or the imbalance of harmful oxidants and antioxidants. Mitochondria are potent sources of oxidants in the cell. She is investigating how air pollution components increase oxidants in the cell through inhibiting mitochondria. For this award, she optimized new techniques to measure mitochondrial function in primary macrophages collected from human subjects via two different techniques. Using these techniques, she showed that macrophages from different physical locations within human airways respond differently to an air pollution component. Ultimately, we hope to use this information to better understand and prevent air pollution health effects. Her long term goals are to improve human health by better understanding how different pollutants cause toxic effects and translate that research into effective policy.She is extremely grateful for this generous award. This award will allow jer to travel to the 2017 SOT Annual Meeting, where she hopes to discuss her research with other scientists from around the world and brainstorm new insights. She also hopes to network with fellow toxicologists to foster new collaborations and explore career opportunities for the next step. She is currently researching how air pollution causes human health effects. While the diseases associated with air pollution exposure have been well-described, the mechanisms that initiate adverse health effects have not been characterized. One frequently cited mechanism involved in the development of adverse health effects after air pollution exposure is oxidative stress, or the imbalance of harmful oxidants and antioxidants. Mitochondria are potent sources of oxidants in the cell. She is investigating how air pollution components increase oxidants in the cell through inhibiting mitochondria. For this award, she optimized new techniques to measure mitochondrial function in primary macrophages collected from human subjects via two different techniques. Using these techniques, she showed that macrophages from different physical locations within human airways respond differently to an air pollution component. Ultimately, we hope to use this information to better understand and prevent air pollution health effects. Her long term goals are to improve human health by better understanding how different pollutants cause toxic effects and translate that research into effective policy.

Vera W. Hudson and Elizabeth K. Weisburger Scholarship Fund

Winner: Kristal Rychlik

Award Year: 2017
Current Degrees: BS
Institution/Affiliation: Texas A&M University

She was happily surprised when she opened the email stating that she had received the award. In past years, when she has seen the scholarship awardees’ credentials, she always thought that those women seemed so accomplished. Is that her now? She is honored to be awarded the Vera W. Hudson and Elizabeth K. Weisburger Scholarship Fund Student Award. It validates the work that she has done in the past and motivates her to continue to give the same level of commitment to her research, mentoring, and leadership roles as she finishes up her PhD work this year. Being awarded this scholarship puts her mind at ease and allows her to focus on her research goals and not worry about the financial burdens that graduate school can place on a family.

Her dissertation research has been dedicated to better understanding the interaction between environmental exposures during pregnancy, genetic differences, and asthma development in children. She has been investigating these interactions in a mouse model of exposure to particulate air pollution during pregnancy and allergic airway disease induction during early life. Specifically, the work included in her abstract for SOT involves two strains of mice, C57Bl/6 and BALB/c, time-mated and exposed throughout pregnancy to a representative mixture of air pollutants similar in makeup to measured pollutant levels in Beijing, China. Following birth, the pups were chronically exposed to house dust mite allergen to induce an asthma-like state. After four weeks of exposure, the mice were sacrificed and multiple assessments were performed to evaluate airway hyperresponsiveness, inflammation, and remodeling. Interestingly, preliminary findings indicate an immunosuppressive effect of exposure to pollutants during pregnancy. This may reveal a window of susceptibility to respiratory infection following exposure to relevant levels of air pollutants during pregnancy. Importantly, pregnant mice were exposed to 101.94 µg/m3 of PM2.5 (particulate matter 2.5 µm in diameter or less) for 6 hours per day during pregnancy which averages over 24 hours to a level of 25.49 µg/m3 PM2.5. This level is lower than the current NAAQS standard of 35 µg/m3 over a 24 hour period. Since the exposure levels are so low, this work outlines the need for more research into susceptible populations, such as pregnant women and young children, when assessing inhaled pollutants and determining safe standard levels. Future work in her current lab includes assessing these samples for epigenetic alterations in multiple tissue types and moving on to characterize methylation patterns in cord blood samples from a small cohort of pregnant women in Nanjing, China. Her future career goals include finding a postdoctoral position in a lab involved with prenatal exposure assessment and childhood health outcomes. She hopes to add to her expertise in animal models and biomarker assessments by learning more about statistical modelling methods in larger data sets during my postdoctoral training.She was happily surprised when she opened the email stating that she had received the award. In past years, when she has seen the scholarship awardees’ credentials, she always thought that those women seemed so accomplished. Is that her now? She is honored to be awarded the Vera W. Hudson and Elizabeth K. Weisburger Scholarship Fund Student Award. It validates the work that she has done in the past and motivates her to continue to give the same level of commitment to her research, mentoring, and leadership roles as she finishes up her PhD work this year. Being awarded this scholarship puts her mind at ease and allows her to focus on her research goals and not worry about the financial burdens that graduate school can place on a family. Her dissertation research has been dedicated to better understanding the interaction between environmental exposures during pregnancy, genetic differences, and asthma development in children. She has been investigating these interactions in a mouse model of exposure to particulate air pollution during pregnancy and allergic airway disease induction during early life. Specifically, the work included in her abstract for SOT involves two strains of mice, C57Bl/6 and BALB/c, time-mated and exposed throughout pregnancy to a representative mixture of air pollutants similar in makeup to measured pollutant levels in Beijing, China. Following birth, the pups were chronically exposed to house dust mite allergen to induce an asthma-like state. After four weeks of exposure, the mice were sacrificed and multiple assessments were performed to evaluate airway hyperresponsiveness, inflammation, and remodeling. Interestingly, preliminary findings indicate an immunosuppressive effect of exposure to pollutants during pregnancy. This may reveal a window of susceptibility to respiratory infection following exposure to relevant levels of air pollutants during pregnancy. Importantly, pregnant mice were exposed to 101.94 µg/m3 of PM2.5 (particulate matter 2.5 µm in diameter or less) for 6 hours per day during pregnancy which averages over 24 hours to a level of 25.49 µg/m3 PM2.5. This level is lower than the current NAAQS standard of 35 µg/m3 over a 24 hour period. Since the exposure levels are so low, this work outlines the need for more research into susceptible populations, such as pregnant women and young children, when assessing inhaled pollutants and determining safe standard levels. Future work in her current lab includes assessing these samples for epigenetic alterations in multiple tissue types and moving on to characterize methylation patterns in cord blood samples from a small cohort of pregnant women in Nanjing, China. Her future career goals include finding a postdoctoral position in a lab involved with prenatal exposure assessment and childhood health outcomes. She hopes to add to her expertise in animal models and biomarker assessments by learning more about statistical modelling methods in larger data sets during my postdoctoral training.

Women in Toxicology SIG Celebrating Women in Toxicology Award

Winner: Alison Sanders

Award Year: 2017
Current Degrees: PhD, MS
Institution/Affiliation: Icahn School of Medicine at Mount Sinai

She is honored to receive the 2017 postdoctoral CWIT award. For the last decade, she has dedicated her career to the field of toxicology and to developing the research, teaching and leadership skills that will carry her through her future academic career. SOT's recognition of her efforts through the CWIT award will undoubtedly help her to achieve her overarching career goal of becoming an independent investigator environmental perinatal health, and conducting research that will protect vulnerable populations from toxic insults.

Her research focuses on how toxic metal exposure (e.g. lead, mercury, cadmium) during pregnancy alters epigenetic marks and molecular pathways of pediatric and later life hypertension. She has acquired interdisciplinary training ranging from geospatial statistics, computational and molecular biology, and epigenetic epidemiology to in vitro toxicology. During her pre- and postdoctoral training in environmental health, she applied these approaches to the study of birth defects and preterm birth, two leading causes of infant mortality in the US. She has published 16 peer-reviewed manuscripts (10 as first or last author). In a series of recent studies, she analyzed levels of 800 microRNAs in cervical samples collected from 80 pregnant women. She identified several candidate microRNAs and signaling pathways associated with lead exposure and shorter gestations. In parallel, she conducted analyses of 400 children in the same cohort with prenatal lead exposure and blood pressure measured at 4 years of age; she identified a significant positive relationship among children born preterm. It is this work that has inspired her current research, which investigates how prenatal metal exposure mediates childhood hypertension through epigenetic mechanisms, and the unique susceptibility of babies that are born prematurely. The knowledge gained will ultimately lead to a better understanding of epigenetic pathways in chronic disease and new avenues for therapeutic development. She has been a member of SOT for 5 years, and holds the position of Postdoctoral Representative with both the Women in Toxicology (WIT) Special Interest Group (elected), and the Education Committee (appointed). In her role with WIT, she contributes to the mission of promoting recruitment, retention, leadership and career development for women in the toxicological sciences. She contributes to their quarterly newsletter, serves as a resource for career development by planning/hosting webinars, and actively works to increase the visibility and recognition of women in SOT. From 2015-2016 she served as co-chair of the ISMMS Postdoc Executive Committee (PEC), a group charged with improving the postdoctoral training environment. As co-chair of the ISMMS PEC, she oversaw a committee of 35 postdocs representing 600 postdoc constituents, interfaced directly with Graduate School Deans, and drafted policy for postdoctoral issues. She authored guidelines that defined institutional policies, and crafted the 2017 Strategic Plan, which outlined my vision and recommendations for fostering a successful and productive postdoc training culture. At her current and former institutions, she has organized symposia (some up to 300 attendees), and established successful teaching, mentoring, communication, and project management training programs. For example, she developed and now directs a science communication and teaching course for postdoctoral fellows, and successfully secured extramural funding from the Burroughs Wellcome Fund. Over 25 postdoctoral fellows have trained in her program, and in the first year alone 20% have received promotions or attained new positions. Overall, her scientific and extracurricular activities encompass many of the same values: promoting science literacy, advocacy, and career development while maintaining scientific excellence. She is honored to receive the 2017 postdoctoral CWIT award. For the last decade, she has dedicated her career to the field of toxicology and to developing the research, teaching and leadership skills that will carry her through her future academic career. SOT's recognition of her efforts through the CWIT award will undoubtedly help her to achieve her overarching career goal of becoming an independent investigator environmental perinatal health, and conducting research that will protect vulnerable populations from toxic insults. Her research focuses on how toxic metal exposure (e.g. lead, mercury, cadmium) during pregnancy alters epigenetic marks and molecular pathways of pediatric and later life hypertension. She has acquired interdisciplinary training ranging from geospatial statistics, computational and molecular biology, and epigenetic epidemiology to in vitro toxicology. During her pre- and postdoctoral training in environmental health, she applied these approaches to the study of birth defects and preterm birth, two leading causes of infant mortality in the US. She has published 16 peer-reviewed manuscripts (10 as first or last author). In a series of recent studies, she analyzed levels of 800 microRNAs in cervical samples collected from 80 pregnant women. She identified several candidate microRNAs and signaling pathways associated with lead exposure and shorter gestations. In parallel, she conducted analyses of 400 children in the same cohort with prenatal lead exposure and blood pressure measured at 4 years of age; she identified a significant positive relationship among children born preterm. It is this work that has inspired her current research, which investigates how prenatal metal exposure mediates childhood hypertension through epigenetic mechanisms, and the unique susceptibility of babies that are born prematurely. The knowledge gained will ultimately lead to a better understanding of epigenetic pathways in chronic disease and new avenues for therapeutic development.

Women in Toxicology SIG Celebrating Women in Toxicology Award

Winner: Priyanka Trivedi

Award Year: 2017
Current Degrees: PhD
Institution/Affiliation: Harvard Medical School

She was really excited and pleased when she received this award. She immediately shared the good news with her advisor and also thanked him for all his support and encouragement. This award will provide recognition to her work and complement her research in the field of renal toxicology. She will use this award as a springboard for her career in which she will make important contributions to advancing our understanding of toxicology research.

Her research focuses on discovering therapeutic targets for acute and chronic kidney diseases. In order to identify druggable targets, we performed RNA sequencing in mouse model of toxic kidney fibrosis and identified Phospholipase D4 (PLD4), a single pass transmembrane glycoprotein, as one of the highly up-regulated genes. Up-regulation of PLD4 was confirmed in three mechanistically distinct mouse models as well as in patients with biopsy-proven kidney fibrosis. Mechanistically, we show that PLD4 facilitates fibrogenesis by modulating innate and adaptive immune responses thereby promoting a TGF-β signaling pathway. Moreover, PLD4 induced the expression of α1-antitrypsin protein (a serine protease inhibitor) that resulted in subsequent down-regulation of a protease neutrophil elastase (NE) expression, thereby leading to the accumulation of extracellular matrix proteins. Interestingly, therapeutic targeting of PLD4 using specific siRNA also protected the mice from kidney fibrosis by inhibiting TGF-β signaling and inducing NE expression. In conclusion, our findings identified PLD4 as a novel therapeutic target for kidney fibrosis - an unmet medical need. Her future goal is to continue contributing to the toxicological science, which can be directly applied clinically to benefit the society.She was really excited and pleased when she received this award. She immediately shared the good news with her advisor and also thanked him for all his support and encouragement. This award will provide recognition to her work and complement her research in the field of renal toxicology. She will use this award as a springboard for her career in which she will make important contributions to advancing our understanding of toxicology research. Her research focuses on discovering therapeutic targets for acute and chronic kidney diseases. In order to identify druggable targets, we performed RNA sequencing in mouse model of toxic kidney fibrosis and identified Phospholipase D4 (PLD4), a single pass transmembrane glycoprotein, as one of the highly up-regulated genes. Up-regulation of PLD4 was confirmed in three mechanistically distinct mouse models as well as in patients with biopsy-proven kidney fibrosis. Mechanistically, we show that PLD4 facilitates fibrogenesis by modulating innate and adaptive immune responses thereby promoting a TGF-ß signaling pathway. Moreover, PLD4 induced the expression of a1-antitrypsin protein (a serine protease inhibitor) that resulted in subsequent down-regulation of a protease neutrophil elastase (NE) expression, thereby leading to the accumulation of extracellular matrix proteins. Interestingly, therapeutic targeting of PLD4 using specific siRNA also protected the mice from kidney fibrosis by inhibiting TGF-ß signaling and inducing NE expression. In conclusion, our findings identified PLD4 as a novel therapeutic target for kidney fibrosis - an unmet medical need. Her future goal is to continue contributing to the toxicological science, which can be directly applied clinically to benefit the society.

Women in Toxicology SIG Celebrating Women in Toxicology Award

Winner: Jessica Sapiro

Award Year: 2017
Current Degrees: MS
Institution/Affiliation: University of Arizona/Wayne State University

Upon notification, she was quite pleased and honored that my research and leadership was found noteworthy and significant by colleagues in the Women in Toxicology Special Interest Group to be an award recipient. As a young and rising scientist and leader, it is important to see herself advancing in the field. SOT awards are quite competitive so being recognized as a strong researcher and leader to compete against her peers is quite rewarding.

Acute renal injury is increasing in occurrence resulting from various compound exposure to the body and the formation of breakdown products in the body. It can present itself as a co-morbidity with other medical conditions in patients yielding a substantial concern. My dissertation work explores how a vitamin A metabolite, all-trans-retinoic acid (ATRA), can protect against kidney injury. This work demonstrates that ATRA can induce several cellular stress proteins in its mechanism of protection. Specifically, the cellular stress kinase, ERK, plays a key role in the protection process. Based on our findings, we hope that ATRA and/or analogs thereof may serve as an effective therapeutic intervention in acute renal injury. Currently, we have established a cell culture model to assess ATRA cytoprotection and have generated mechanistic findings. This award will allow for more extensive mechanistic investigation exploring ERK activation and the continued development of a rodent model to assess ATRA protection. Following graduate school, she wishes to continue exploring the discovery and investigative toxicology space. The development of agents that have therapeutic potential against injuries and diseases is prominent in our goal of creating a safer and healthier world. In addition to kidney toxicity, it would be interesting to explore the development of a therapeutic agent that has clinical application to multiple organs. She also plans to continue in her future endeavors mentoring and training younger scientists to keep our field growing with fresh talent and innovation.Upon notification, she was quite pleased and honored that my research and leadership was found noteworthy and significant by colleagues in the Women in Toxicology Special Interest Group to be an award recipient. As a young and rising scientist and leader, it is important to see herself advancing in the field. SOT awards are quite competitive so being recognized as a strong researcher and leader to compete against her peers is quite rewarding. Acute renal injury is increasing in occurrence resulting from various compound exposure to the body and the formation of breakdown products in the body. It can present itself as a co-morbidity with other medical conditions in patients yielding a substantial concern. My dissertation work explores how a vitamin A metabolite, all-trans-retinoic acid (ATRA), can protect against kidney injury. This work demonstrates that ATRA can induce several cellular stress proteins in its mechanism of protection. Specifically, the cellular stress kinase, ERK, plays a key role in the protection process. Based on our findings, we hope that ATRA and/or analogs thereof may serve as an effective therapeutic intervention in acute renal injury. Currently, we have established a cell culture model to assess ATRA cytoprotection and have generated mechanistic findings. This award will allow for more extensive mechanistic investigation exploring ERK activation and the continued development of a rodent model to assess ATRA protection. Following graduate school, she wishes to continue exploring the discovery and investigative toxicology space. The development of agents that have therapeutic potential against injuries and diseases is prominent in our goal of creating a safer and healthier world. In addition to kidney toxicity, it would be interesting to explore the development of a therapeutic agent that has clinical application to multiple organs. She also plans to continue in her future endeavors mentoring and training younger scientists to keep our field growing with fresh talent and innovation.

Go to: Historical Archive of Endowment Fund Award Recipients