@article{green_wall_weeks_mattingly_marsden_planchart_2023, title={Developmental cadmium exposure disrupts zebrafish vestibular calcium channels interfering with otolith formation and inner ear function}, volume={96}, ISSN={["1872-9711"]}, DOI={10.1016/j.neuro.2023.04.006}, abstractNote={Dizziness or balance problems are estimated to affect approximately 3.3 million children aged three to 17 years. These disorders develop from a breakdown in the balance control system and can be caused by anything that affects the inner ear or the brain, including exposure to environmental toxicants. One potential environmental toxicant linked to balance disorders is cadmium, an extremely toxic metal that occurs naturally in the earth’s crust and is released as a byproduct of industrial processes. Cadmium is associated with balance and vestibular dysfunction in adults exposed occupationally, but little is known about the developmental effects of low-concentration cadmium exposure. Our findings indicate that zebrafish exposed to 10–60 parts per billion (ppb) cadmium from four hours post-fertilization (hpf) to seven days post-fertilization (dpf) exhibit abnormal behaviors, including pronounced increases in auditory sensitivity and circling behavior, both of which are linked to reductions in otolith growth and are rescued by the addition of calcium to the media. Pharmacological intervention shows that agonist-induced activation of the P2X calcium ion channel in the presence of cadmium restores otolith size. In conclusion, cadmium-induced ototoxicity is linked to vestibular-based behavioral abnormalities and auditory sensitivity following developmental exposure, and calcium ion channel function is associated with these defects.}, journal={NEUROTOXICOLOGY}, author={Green, Adrian J. and Wall, Alex R. and Weeks, Ryan D. and Mattingly, Carolyn J. and Marsden, Kurt C. and Planchart, Antonio}, year={2023}, month={May}, pages={129–139} }
 @article{weeks_banack_howell_thunga_green_cox_planchart_metcalf_2023, title={The Effects of Long-term, Low-dose & beta;-N-methylamino-l-alanine (BMAA) Exposures in Adult SODG93R Transgenic Zebrafish}, volume={8}, ISSN={["1476-3524"]}, DOI={10.1007/s12640-023-00658-z}, journal={NEUROTOXICITY RESEARCH}, author={Weeks, Ryan D. and Banack, Sandra A. and Howell, Shaunacee and Thunga, Preethi and Green, Adrian J. and Cox, Paul A. and Planchart, Antonio and Metcalf, James S.}, year={2023}, month={Aug} }
 @article{weeks_banack_howell_thunga_metcalf_green_cox_planchart_2023, title={The Effects of Long-term, Low-dose beta-N-methylamino-L-alanine (BMAA) Exposures in Adult SODG93R (Aug, 10.1007/s12640-023-00658-z, 2023)}, volume={8}, ISSN={["1476-3524"]}, DOI={10.1007/s12640-023-00664-1}, journal={NEUROTOXICITY RESEARCH}, author={Weeks, Ryan D. and Banack, Sandra A. and Howell, Shaunacee and Thunga, Preethi and Metcalf, James S. and Green, Adrian J. and Cox, Paul A. and Planchart, Antonio}, year={2023}, month={Aug} }
 @article{quinlan_may_weeks_yuan_luff_2021, title={Canine Papillomavirus 2 E6 Does Not Interfere With UVB-Induced Upregulation of p53 and p53-Regulated Genes}, volume={8}, ISSN={["2297-1769"]}, DOI={10.3389/fvets.2021.570982}, abstractNote={Cutaneous papillomaviruses are oncogenic viruses that cause severe, persistent infections that can develop into skin cancers within ultraviolet (UV)-exposed skin of immunodeficient individuals, such as those with X-linked severe combined immunodeficiency (XSCID). A canine research model of XSCID exhibits a similar phenotype; these dogs develop severe canine papillomavirus 2 (CPV2) infections that often progress to cancer. Thus, the dog is a natural, spontaneous model to investigate cutaneous papillomavirus infections in immunodeficient patients. The human papillomavirus oncogene E6 contributes to cancer development, in part, by initiating degradation of the tumor suppressor protein p53, or by inhibiting upregulation of p53-dependent genes required within the cell growth arrest and apoptotic pathways, thereby leading to an accumulation of DNA damage required for oncogenesis. Currently, little is known about CPV2, and how it promotes cancer development. The aim of this study was to determine if CPV2 oncogene E6 similarly affects p53 upon activation by UV radiation, as well as the downstream p53-regulated genes necessary to control growth arrest and apoptosis. We determined that cutaneous CPV2 E6 does not degrade p53, or interfere with the upregulation of p53-regulated genes p21, Bax, Bak, or lncRNA-p21, suggesting that CPV2 may use a p53-independent mechanism to contribute to oncogenesis.}, journal={FRONTIERS IN VETERINARY SCIENCE}, author={Quinlan, Sarah and May, Susan and Weeks, Ryan and Yuan, Hang and Luff, Jennifer}, year={2021}, month={Mar} }
 @article{quinlan_may_weeks_yuan_luff_2020, title={Abrogation of Constitutive and Induced Type I and Type III Interferons and Interferon-Stimulated Genes in Keratinocytes by Canine Papillomavirus 2 E6 and E7}, volume={12}, ISSN={["1999-4915"]}, DOI={10.3390/v12060677}, abstractNote={Cutaneous papillomaviruses can cause severe, persistent infections and skin cancer in immunodeficient patients, including people with X-linked severe combined immunodeficiency (XSCID). A similar phenotype is observed in a canine model of XSCID; these dogs acquire severe cutaneous papillomavirus infections that can progress to cancer in association with canine papillomavirus type 2 (CPV2). This canine model system provides a natural spontaneous animal model for investigation of papillomavirus infections in immunodeficient patients. Currently, it is unknown if CPV2 can subvert the innate immune system and interfere with its ability to express antiviral cytokines, which are critical in the host defense against viral pathogens. The aim of the current study was to determine if the oncogenes E6 and E7 from CPV2 interfere with expression of antiviral cytokines in keratinocytes, the target cells of papillomavirus infections. We determined that E6 but not E7 interferes with the constitutive expression of some antiviral cytokines, including interferon (IFN)-β and the IFN-stimulated gene IFIT1. Both E6 and E7 interfere with the transcriptional upregulation of the antiviral cytokines in response to stimulation with the dsDNA Poly(dA:dT). In contrast, while E6 also interferes with the transcriptional upregulation of antiviral cytokines in response to stimulation with the dsRNA Poly(I:C), E7 interferes with only a subset of these antiviral cytokines. Finally, we demonstrated that E7 but not E6 abrogates signaling through the type I IFN receptor. Taken together, CPV2 E6 and E7 both impact expression of antiviral cytokines in canine keratinocytes, albeit likely through different mechanisms.}, number={6}, journal={VIRUSES-BASEL}, author={Quinlan, Sarah and May, Susan and Weeks, Ryan and Yuan, Hang and Luff, Jennifer A.}, year={2020}, month={Jun} }