@article{gunady_ware_plumlee_devos_corcoran_prinz_misetic_ciccarelli_harrison_thorne_et al._2022, title={Exome sequencing of hepatocellular carcinoma in lemurs identifies potential cancer drivers A pilot study}, volume={10}, ISSN={["2050-6201"]}, DOI={10.1093/emph/eoac016}, abstractNote={Abstract Background and objectives Hepatocellular carcinoma occurs frequently in prosimians, but the cause of these liver cancers in this group is unknown. Characterizing the genetic changes associated with hepatocellular carcinoma in prosimians may point to possible causes, treatments and methods of prevention, aiding conservation efforts that are particularly crucial to the survival of endangered lemurs. Although genomic studies of cancer in non-human primates have been hampered by a lack of tools, recent studies have demonstrated the efficacy of using human exome capture reagents across primates. Methodology In this proof-of-principle study, we applied human exome capture reagents to tumor–normal pairs from five lemurs with hepatocellular carcinoma to characterize the mutational landscape of this disease in lemurs. Results Several genes implicated in human hepatocellular carcinoma, including ARID1A, TP53 and CTNNB1, were mutated in multiple lemurs, and analysis of cancer driver genes mutated in these samples identified enrichment of genes involved with TP53 degradation and regulation. In addition to these similarities with human hepatocellular carcinoma, we also noted unique features, including six genes that contain mutations in all five lemurs. Interestingly, these genes are infrequently mutated in human hepatocellular carcinoma, suggesting potential differences in the etiology and/or progression of this cancer in lemurs and humans. Conclusions and implications Collectively, this pilot study suggests that human exome capture reagents are a promising tool for genomic studies of cancer in lemurs and other non-human primates. Lay Summary Hepatocellular carcinoma occurs frequently in prosimians, but the cause of these liver cancers is unknown. In this proof-of-principle study, we applied human DNA sequencing tools to tumor–normal pairs from five lemurs with hepatocellular carcinoma and compared the lemur mutation profiles to those of human hepatocellular carcinomas.}, number={1}, journal={EVOLUTION MEDICINE AND PUBLIC HEALTH}, author={Gunady, Ella F. and Ware, Kathryn E. and Plumlee, Sarah Hoskinson and Devos, Nicolas and Corcoran, David and Prinz, Joseph and Misetic, Hrvoje and Ciccarelli, Francesca D. and Harrison, Tara M. and Thorne, Jeffrey L. and et al.}, year={2022}, month={Jan}, pages={221–230} }
 @article{brooks_landau_everitt_brown_grady_waskowicz_bass_d'angelo_asfaw_williams_et al._2018, title={Long-term complications of glycogen storage disease type Ia in the canine model treated with gene replacement therapy}, volume={41}, ISSN={["1573-2665"]}, DOI={10.1007/s10545-018-0223-y}, abstractNote={Abstract}, number={6}, journal={JOURNAL OF INHERITED METABOLIC DISEASE}, author={Brooks, Elizabeth D. and Landau, Dustin J. and Everitt, Jeffrey I. and Brown, Talmage T. and Grady, Kylie M. and Waskowicz, Lauren and Bass, Cameron R. and D'Angelo, John and Asfaw, Yohannes G. and Williams, Kyha and et al.}, year={2018}, month={Dec}, pages={965–976} }
 @article{gardner_mcgee_kodavanti_ledbetter_everitt_winsett_doerfler_costa_2004, title={Emission-particle-induced ventilatory abnormalities in a rat model of pulmonary hypertension}, volume={112}, ISSN={["0091-6765"]}, DOI={10.1289/ehp.6583}, abstractNote={Preexistent cardiopulmonary disease in humans appears to enhance susceptibility to the adverse effects of ambient particulate matter. Previous studies in this laboratory have demonstrated enhanced inflammation and mortality after intratracheal instillation (IT) and inhalation (INH) of residual oil fly ash (ROFA) in a rat model of pulmonary hypertension induced by monocrotaline (MCT). The present study was conducted to examine the effects of ROFA in this model on ventilatory function in unanesthetized, unrestrained animals. Sixty-day-old male CD rats were injected with MCT (60 mg/kg) or vehicle (VEH) intraperitoneally 10 days before IT of ROFA (8.3 mg/kg) or saline (SAL) (control) or nose-only INH of ROFA [15 mg/m3 for 6 hr on 3 consecutive days or air (control)]. At 24 and 72 hr after exposure, rats were studied individually in a simultaneous gas uptake/whole-body plethysmograph. Lungs were removed at 72 hr for histology. Pulmonary test results showed that tidal volume (VT) decreased 24 hr after IT of ROFA in MCT-treated rats. Breathing frequency, minute volume (VE), and the ventilatory equivalent for oxygen increased in MCT- and VEH-treated rats 24 hr after IT or INH of ROFA and remained elevated 72 hr post-IT. O2 uptake (VO2) decreased after IT of ROFA in MCT-treated rats. Carbon monoxide uptake decreased 24 hr after IT of ROFA, returning to control values in VEH-treated rats but remaining low in MCT-treated rats 72 hr post-IT. ROFA exposure induced histologic changes and abnormalities in several ventilatory parameters, many of which were enhanced by MCT treatment.}, number={8}, journal={ENVIRONMENTAL HEALTH PERSPECTIVES}, author={Gardner, SY and McGee, JK and Kodavanti, UP and Ledbetter, A and Everitt, JI and Winsett, DW and Doerfler, DL and Costa, DL}, year={2004}, month={Jun}, pages={872–878} }
 @article{newbold_diaugustine_risinger_everitt_walmer_parrott_dixon_2000, title={Advances in uterine leiomyoma research: Conference overview, summary, and future research recommendations}, volume={108}, ISSN={["0091-6765"]}, DOI={10.2307/3454304}, journal={ENVIRONMENTAL HEALTH PERSPECTIVES}, author={Newbold, RR and DiAugustine, RP and Risinger, JI and Everitt, JI and Walmer, DK and Parrott, EC and Dixon, D}, year={2000}, month={Oct}, pages={769–773} }