@article{reuter_defrancesco_robertson_meurs_2024, title={Clinical outcome of idiopathic juvenile ventricular arrhythmias in 25 dogs}, volume={51}, ISSN={["1875-0834"]}, url={https://doi.org/10.1016/j.jvc.2023.12.001}, DOI={10.1016/j.jvc.2023.12.001}, abstractNote={Juvenile ventricular arrhythmias in the absence of structural heart disease have been characterized in a small number of canine breeds with limited long-term follow up. The objective of this study was to describe the clinical outcome of dogs with JVA presenting to a university teaching hospital.Twenty five dogs, less than two years old with idiopathic ventricular arrhythmias were retrospectively identified via a medical record search. Young dogs with ventricular arrhythmias were excluded if they had structural heart disease, systemic illness, or an abnormal troponin (if performed). Electrocardiographic and Holter monitor data was evaluated for arrhythmia frequency and complexity at the time of diagnosis and over time. Long-term follow up was achieved through client and primary veterinarian contact.Breeds included German Shepherd (eight), Boxer (four), Great Dane (three), mixed breed (two) and one each of the following: Anatolian Shepherd, French Bulldog, golden retriever, Great Pyrenees, Labrador retriever, Shiloh Shepherd, miniature Poodle and Siberian Husky. The average age at diagnosis was 7.9 months (range, 2-22 months). The overall median survival was 10.96 years (range, 1.75-15.66 years). There was an average reduction in the number of ventricular beats by 86.7 % per year (P value -0.0257) based on Holter data.In most cases, idiopathic juvenile ventricular arrhythmias had a favorable long-term prognosis with reduced ectopy over time in this case series. Juvenile ventricular arrhythmias remains a diagnosis of exclusion but can be considered in a broader range of dog breeds than previously described.}, journal={JOURNAL OF VETERINARY CARDIOLOGY}, author={Reuter, A. and DeFrancesco, T. C. and Robertson, J. B. and Meurs, K. M.}, year={2024}, month={Feb}, pages={188–194} }
 @article{kaplan_rivas_walker_grubb_farrell_fitzgerald_kennedy_pjauregui_crofton_pmclaughlin_et al._2023, title={Delayed-release rapamycin halts progression of left ventricular hypertrophy in subclinical feline hypertrophic results of the RAPACAT trial}, volume={261}, ISSN={["1943-569X"]}, url={https://publons.com/wos-op/publon/65523912/}, DOI={10.2460/javma.23.04.0187}, abstractNote={Abstract}, number={11}, journal={JAVMA-JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Kaplan, Joanna L. and Rivas, Victor N. and Walker, Ashley L. and Grubb, Louise and Farrell, Aisling and Fitzgerald, Stuart and Kennedy, Susan and Pjauregui, Carina E. and Crofton, Amanda E. and Pmclaughlin, Chris and et al.}, year={2023}, month={Nov}, pages={1628–1637} }
 @article{adin_atkins_domenig_glahn_defrancesco_meurs_2023, title={Evaluation of Renin-Angiotensin-Aldosterone System Components and Enzymes in Systemically Hypertensive Cats Receiving Amlodipine}, volume={13}, ISSN={["2076-2615"]}, url={https://www.mdpi.com/2076-2615/13/22/3479}, DOI={10.3390/ani13223479}, abstractNote={Background: Chronic renin–angiotensin–aldosterone system (RAAS) activation is harmful. Amlodipine activates RAAS in humans and dogs, but contradictory data exist for systemically hypertensive (SHT) cats. Hypothesis: Cats with SHT and chronic kidney disease treated with amlodipine (SHT/CKD-A) are RAAS activated. Animals: Client-owned cats: unmedicated normotensive (NT) cats (n = 9); SHT/CKD-A cats (n = 5) with median systolic blood pressure of 170 mmHg (vs. 195 mmHg, pre-treatment), chronic kidney disease, and receiving no RAAS-suppressive therapy. Methods: Serum was frozen (−80 °C) until RAAS analysis via equilibrium analysis. The RAAS variables (reported as median (minimum–maximum)) were compared between groups, using Mann–Whitney U test. Results: Angiotensin 1, angiotensin 1,7, angiotensin III, and angiotensin 1,5, and angiotensin-converting enzyme (ACE)-2 activity were higher in SHT/CKD-A cats compared to NT cats, while ACE activity was lower in SHT/CKD-A cats compared to NT cats (p < 0.05 all). A marker for alternative RAAS influence (ALT-S) was significantly higher (69; 58–73 pmol/pmol) in SHT/CKD-A cats compared to NT cats (35; 14–63 pmol/pmol; p = 0.001). Aldosterone concentrations were significantly higher (393; 137–564 pmol/L) in SHT/CKD-A cats compared to NT cats (129; 28–206 pmol/L; p = 0.007). Conclusion and Clinical Importance: Circulating RAAS is activated in systemically hypertensive cats receiving amlodipine. Although this study did not parse out the individual contributions of SHT, chronic kidney disease, and amlodipine, the findings suggest that the use of concurrent RAAS-suppressant therapy, specifically aldosterone antagonism, in amlodipine-treated SHT cats with chronic kidney disease might be indicated.}, number={22}, journal={ANIMALS}, author={Adin, Darcy and Atkins, Clarke and Domenig, Oliver and Glahn, Catherine and Defrancesco, Teresa and Meurs, Kathryn}, year={2023}, month={Nov} }
 @article{walker_li_nguyen_jauregui_meurs_gagnon_stern_2023, title={Evaluation of autoantibodies to desmoglein-2 in dogs with and without cardiac disease}, volume={13}, ISSN={2045-2322}, url={http://dx.doi.org/10.1038/s41598-023-32081-x}, DOI={10.1038/s41598-023-32081-x}, abstractNote={Abstract}, number={1}, journal={Scientific Reports}, publisher={Springer Science and Business Media LLC}, author={Walker, Ashley L. and Li, Ronald H. L. and Nguyen, Nghi and Jauregui, Carina E. and Meurs, Kathryn M. and Gagnon, Allison L. and Stern, Joshua A.}, year={2023}, month={Mar} }
 @article{agarwal_cote_o'sullivan_meurs_steiner_2023, title={Investigation of the cardiac effects of exercise testing on apparently healthy Boxer dogs}, volume={8}, ISSN={["1939-1676"]}, DOI={10.1111/jvim.16830}, abstractNote={Abstract}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Agarwal, Deepmala and Cote, Etienne and O'Sullivan, Lynne and Meurs, Kathryn M. and Steiner, Jorg}, year={2023}, month={Aug} }
 @article{reimann_faisst_knold_meurs_stern_cremer_moller_ljungvall_haggstrom_olsen_2023, title={No impact of polymorphism in the phosphodiesterase 5A gene in Cavalier King Charles Spaniels on pimobendan-induced inhibition of platelet aggregation response}, volume={9}, ISSN={["1939-1676"]}, url={https://onlinelibrary.wiley.com/doi/pdfdirect/10.1111/jvim.16871}, DOI={10.1111/jvim.16871}, abstractNote={Abstract}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Reimann, Maria J. and Faisst, Daniel N. and Knold, Mads and Meurs, Kathryn M. and Stern, Joshua A. and Cremer, Signe E. and Moller, Jacob E. and Ljungvall, Ingrid and Haggstrom, Jens and Olsen, Lisbeth H.}, year={2023}, month={Sep} }
 @article{mcmanamey_defrancesco_meurs_papich_2023, title={Pharmacokinetics of pimobendan after oral administration to dogs with myxomatous mitral valve disease}, volume={9}, ISSN={["1939-1676"]}, url={https://doi.org/10.1111/jvim.16891}, DOI={10.1111/jvim.16891}, abstractNote={Abstract}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={McManamey, Anna K. and DeFrancesco, Teresa C. and Meurs, Kathryn M. and Papich, Mark G.}, year={2023}, month={Sep} }
 @article{brethel_locker_girens_rivera_meurs_adin_2023, title={The effect of taurine supplementation on the renin-angiotensin-aldosterone system of dogs with congestive heart failure}, volume={13}, ISSN={["2045-2322"]}, DOI={10.1038/s41598-023-37978-1}, abstractNote={Abstract}, number={1}, journal={SCIENTIFIC REPORTS}, author={Brethel, Sara and Locker, Seth and Girens, Renee and Rivera, Paulo and Meurs, Kathryn and Adin, Darcy}, year={2023}, month={Jul} }
 @article{woelfel_meurs_friedenberg_debruyne_olby_2022, title={A novel mutation of the CLCN1 gene in a cat with myotonia congenita: Diagnosis and treatment}, volume={7}, ISSN={["1939-1676"]}, url={https://doi.org/10.1111/jvim.16471}, DOI={10.1111/jvim.16471}, abstractNote={Abstract}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Woelfel, Christian and Meurs, Kathryn and Friedenberg, Steven and DeBruyne, Nicole and Olby, Natasha J.}, year={2022}, month={Jul} }
 @misc{shen_estrada_meurs_sleeper_vulpe_martyniuk_pacak_2022, title={A review of the underlying genetics and emerging therapies for canine cardiomyopathies}, volume={40}, ISSN={["1875-0834"]}, DOI={10.1016/j.jvc.2021.05.003}, abstractNote={Cardiomyopathies such as dilated cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy are common in large breed dogs and carry an overall poor prognosis. Research shows that these diseases have strong breed predilections, and selective breeding has historically been recommended to reduce the disease prevalence in affected breeds. Treatment of these diseases is typically palliative and aimed at slowing disease progression and managing clinical signs of heart failure as they develop. The discovery of specific genetic mutations underlying cardiomyopathies, such as the striatin mutation in Boxer arrhythmogenic right ventricular cardiomyopathy and the pyruvate dehydrogenase kinase 4 and titin mutations in Doberman Pinschers, has strengthened our ability to screen and selectively breed individuals in an attempt to produce unaffected offspring. The discovery of these disease-linked mutations has also opened avenues for the development of gene therapies, including gene transfer and genome-editing approaches. This review article discusses the known genetics of cardiomyopathies in dogs, reviews existing gene therapy strategies and the status of their development in canines, and discusses ongoing challenges in the clinical translation of these technologies for treating heart disease. While challenges remain in using these emerging technologies, the exponential growth of the gene therapy field holds great promise for future clinical applications.}, journal={JOURNAL OF VETERINARY CARDIOLOGY}, author={Shen, L. and Estrada, A. H. and Meurs, K. M. and Sleeper, M. and Vulpe, C. and Martyniuk, C. J. and Pacak, C. A.}, year={2022}, month={Apr}, pages={2–14} }
 @article{walker_defrancesco_bonagura_keene_meurs_tou_kurtz_aona_barron_mcmanamey_et al._2022, title={Association of diet with clinical outcomes in dogs with dilated cardiomyopathy and congestive heart failure*}, volume={40}, ISSN={["1875-0834"]}, DOI={10.1016/j.jvc.2021.02.001}, abstractNote={Dilated cardiomyopathy (DCM) in dogs has been associated with feeding of grain-free (GF), legume-rich diets. Some dogs with presumed diet-associated DCM have shown improved myocardial function and clinical outcomes following a change in diet and standard medical therapy. Prior GF (pGF) diet influences reverse cardiac remodeling and clinical outcomes in dogs with DCM and congestive heart failure (CHF). A retrospective study was performed with 67 dogs with DCM and CHF for which diet history was known. Dogs were grouped by diet into pGF and grain-inclusive (GI) groups. Dogs in the pGF group were included if diet change was a component of therapy. Survival was analyzed using Kaplan–Meier curves and the Cox proportional-hazards model. The median survival time was 344 days for pGF dogs vs. 253 days for GI dogs (P = 0.074). Statistically significant differences in median survival were identified when the analysis was limited to dogs surviving longer than one week (P = 0.033). Prior GF dogs had a significantly worse outcome the longer a GF diet was fed prior to diagnosis (P = 0.004) or if they were diagnosed at a younger age (P = 0.017). Prior GF dogs showed significantly greater improvement in normalized left ventricular internal diastolic diameter (P = 0.038) and E-point septal separation (P = 0.031) measurements and significant decreases in their furosemide (P = 0.009) and pimobendan (P < 0.005) dosages over time compared to GI dogs. Prior GF dogs that survived at least one week after diagnosis of DCM, treatment of CHF, and diet change had better clinical outcomes and showed reverse ventricular remodeling compared to GI dogs.}, journal={JOURNAL OF VETERINARY CARDIOLOGY}, author={Walker, A. L. and DeFrancesco, T. C. and Bonagura, J. D. and Keene, B. W. and Meurs, K. M. and Tou, S. P. and Kurtz, K. and Aona, B. and Barron, L. and McManamey, A. and et al.}, year={2022}, month={Apr}, pages={99–109} }
 @article{meurs_2022, title={Hands-on learning: from at-risk wolves to teeming Galapagos}, volume={260}, ISSN={["1943-569X"]}, DOI={10.2460/javma.22.05.0216}, abstractNote={N C State is unsurpassed in the variety of ways we offer rare hands-on experiences for our veterinary students}, number={10}, journal={JAVMA-JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Meurs, Kathryn}, year={2022}, month={Jul}, pages={1140–1140} }
 @article{meurs_montgomery_friedenberg_williams_gilger_2021, title={A defect in the NOG gene increases susceptibility to spontaneous superficial chronic corneal epithelial defects (SCCED) in boxer dogs}, volume={17}, ISSN={1746-6148}, url={http://dx.doi.org/10.1186/s12917-021-02955-1}, DOI={10.1186/s12917-021-02955-1}, abstractNote={Abstract}, number={1}, journal={BMC Veterinary Research}, publisher={Springer Science and Business Media LLC}, author={Meurs, Kathryn M. and Montgomery, Keith and Friedenberg, Steven G. and Williams, Brian and Gilger, Brian C.}, year={2021}, month={Jul} }
 @article{meurs_williams_deprospero_friedenberg_malarkey_ezzell_keene_adin_defrancesco_tou_2021, title={A deleterious mutation in the ALMS1 gene in a naturally occurring model of hypertrophic cardiomyopathy in the Sphynx cat}, volume={16}, ISSN={["1750-1172"]}, DOI={10.1186/s13023-021-01740-5}, abstractNote={Abstract}, number={1}, journal={ORPHANET JOURNAL OF RARE DISEASES}, author={Meurs, Kathryn M. and Williams, Brian G. and DeProspero, Dylan and Friedenberg, Steven G. and Malarkey, David E. and Ezzell, J. Ashley and Keene, Bruce W. and Adin, Darcy B. and DeFrancesco, Teresa C. and Tou, Sandra}, year={2021}, month={Feb} }
 @article{hedgespeth_birkenheuer_friedenberg_olby_meurs_2021, title={A novel missense mutation of the NAT10 gene in a juvenile Schnauzer dog with chronic respiratory tract infections}, volume={35}, ISSN={["1939-1676"]}, url={https://doi.org/10.1111/jvim.16100}, DOI={10.1111/jvim.16100}, abstractNote={Abstract}, number={3}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Hedgespeth, Barry A. and Birkenheuer, Adam J. and Friedenberg, Steven G. and Olby, Natasha J. and Meurs, Kathryn M.}, year={2021}, month={May}, pages={1542–1546} }
 @article{k. o'donnell_adin_atkins_defrancesco_keene_tou_meurs_2021, title={Absence of known feline MYH7 and MYBPC3 variants in a diverse cohort of cats with hypertrophic cardiomyopathy}, volume={52}, ISSN={["1365-2052"]}, DOI={10.1111/age.13074}, abstractNote={Summary}, number={4}, journal={ANIMAL GENETICS}, author={K. O'Donnell and Adin, D. and Atkins, C. E. and DeFrancesco, T. and Keene, B. W. and Tou, S. and Meurs, K. M.}, year={2021}, month={Aug}, pages={542–544} }
 @article{herrmann_linder_meurs_friedenberg_cullen_olby_bizikova_2021, title={Canine junctional epidermolysis bullosa due to a novel mutation in LAMA3 with severe upper respiratory involvement}, volume={32}, ISSN={["1365-3164"]}, url={https://doi.org/10.1111/vde.12972}, DOI={10.1111/vde.12972}, abstractNote={BackgroundJunctional epidermolysis bullosa (JEB) is a group of congenital blistering skin diseases characterized by clefting through the lamina lucida of the basement membrane zone.}, number={4}, journal={VETERINARY DERMATOLOGY}, author={Herrmann, Ina and Linder, Keith E. and Meurs, Kathryn M. and Friedenberg, Steven G. and Cullen, Jonah and Olby, Natasha and Bizikova, Petra}, year={2021}, month={Aug}, pages={379-+} }
 @article{deprospero_kerry a. o'donnell_defrancesco_keene_tou_adin_atkins_meurs_2021, title={Myxomatous mitral valve disease in Miniature Schnauzers and Yorkshire Terriers: 134 cases (2007-2016)}, volume={259}, ISSN={["1943-569X"]}, DOI={10.2460/javma.20.05.0291}, abstractNote={Abstract}, number={12}, journal={JAVMA-JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={DeProspero, Dylan J. and Kerry A. O'Donnell and DeFrancesco, Teresa C. and Keene, Bruce W. and Tou, Sandra P. and Adin, Darcy B. and Atkins, Clarke E. and Meurs, Kathryn M.}, year={2021}, month={Dec}, pages={1428–1432} }
 @article{reimann_fredholm_cremer_christiansen_meurs_moller_haggstrom_lykkesfeldt_olsen_2021, title={Polymorphisms in the serotonin transporter gene and circulating concentrations of neurotransmitters in Cavalier King Charles Spaniels with myxomatous mitral valve disease}, volume={10}, ISSN={["1939-1676"]}, DOI={10.1111/jvim.16277}, abstractNote={Abstract}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Reimann, Maria J. and Fredholm, Merete and Cremer, Signe E. and Christiansen, Liselotte B. and Meurs, Kathryn M. and Moller, Jacob E. and Haggstrom, Jens and Lykkesfeldt, Jens and Olsen, Lisbeth H.}, year={2021}, month={Oct} }
 @article{williams_friedenberg_keene_tou_defrancesco_meurs_2021, title={Use of whole genome analysis to identify shared genomic variants across breeds in canine mitral valve disease}, volume={6}, ISSN={["1432-1203"]}, DOI={10.1007/s00439-021-02297-w}, abstractNote={Familial mitral valve prolapse in human beings has been associated with several genetic variants; however, in most cases, a known variant has not been identified. Dogs also have a naturally occurring form of familial mitral valve disease (MMVD) with similarities to the human disease. A shared genetic background and clinical phenotype of this disease in some dog breeds has indicated that the disease may share a common genetic cause. We evaluated DNA from 50 affected dogs from five different dog breeds in a whole genome sequencing approach to identify shared variants across and within breeds that could be associated with MMVD. No single causative genetic mutation was found from the 50 dogs with MMVD. Ten variants were identified in 37/50 dogs around and within the MED13L gene. These variants were no longer associated with MMVD when evaluated with a larger cohort including both affected and unaffected dogs. No high/moderate impact variants were identified in 10/10 miniature poodles, one was identified in 10/10 Yorkshire Terriers and 10/10 dachshunds, respectively, 14 were identified in 10/10 Miniature schnauzers, and 19 in 10/10 CKCS. Only one of these could be associated with the cardiac valve (Chr12:36801705, COL12A1; CKCS) but when evaluated in an additional 100 affected CKCS the variant was only identified in 84/100 affected dogs, perhaps indicating genetic heterogeneity in this disease. Our findings indicate that development of MMVD in the dog may be related to a combination of genetic and environmental factors that impact specific molecular pathways rather than a single shared genetic variant across or within breeds.}, journal={HUMAN GENETICS}, author={Williams, Brian and Friedenberg, Steven G. and Keene, Bruce W. and Tou, Sandy P. and DeFrancesco, Teresa C. and Meurs, Kathryn M.}, year={2021}, month={Jun} }
 @article{olby_friedenberg_meurs_deprospero_guevar_lau_yost_guo_shelton_2020, title={A mutation in MTM1 causes X-Linked myotubular myopathy in Boykin spaniels}, volume={30}, ISSN={0960-8966}, url={http://dx.doi.org/10.1016/j.nmd.2020.02.021}, DOI={10.1016/j.nmd.2020.02.021}, abstractNote={The purpose of this study was to report the findings of clinical and genetic evaluation of a 3-month old male Boykin spaniel (the proband) that presented with progressive weakness. The puppy underwent a physical and neurological examination, serum biochemistry and complete blood cell count, electrophysiological testing, muscle biopsy and whole genome sequencing. Clinical evaluation revealed generalized neuromuscular weakness with tetraparesis and difficulty holding the head up and a dropped jaw. There was diffuse spontaneous activity on electromyography, most severe in the cervical musculature. Nerve conduction studies were normal, the findings were interpreted as consistent with a myopathy. Skeletal muscle was grossly abnormal on biopsy and there were necklace fibers and abnormal triad structure localization on histopathology, consistent with myotubular myopathy. Whole genome sequencing revealed a premature stop codon in exon 13 of MTM1 (ChrX: 118,903,496 C > T, c.1467C>T, p.Arg512X). The puppy was humanely euthanized at 5 months of age. The puppy's dam was heterozygous for the variant, and 3 male puppies from a subsequent litter all of which died by 2 weeks of age were hemizygous for the variant. This naturally occurring mutation in Boykin spaniels causes a severe form of X-linked myotubular myopathy, comparable to the human counterpart.}, number={5}, journal={Neuromuscular Disorders}, publisher={Elsevier BV}, author={Olby, Natasha J. and Friedenberg, Steven and Meurs, Kathryn and DeProspero, Dylan and Guevar, Julien and Lau, Jeanie and Yost, Oriana and Guo, Ling T. and Shelton, G. Diane}, year={2020}, month={Mar}, pages={353–359} }
 @article{adin_atkins_domenig_defrancesco_keene_tou_stern_meurs_2020, title={Renin-angiotensin aldosterone profile before and after angiotensin-converting enzyme-inhibitor administration in dogs with angiotensin-converting enzyme gene polymorphism}, volume={34}, ISSN={["1939-1676"]}, url={https://doi.org/10.1111/jvim.15746}, DOI={10.1111/jvim.15746}, abstractNote={Abstract}, number={2}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Adin, Darcy and Atkins, Clarke and Domenig, Oliver and DeFrancesco, Teresa and Keene, Bruce and Tou, Sandra and Stern, Joshua A. and Meurs, Kathryn M.}, year={2020}, month={Mar}, pages={600–606} }
 @article{meurs_friedenberg_olby_condit_weidman_rosenthal_shelton_2019, title={A QIL1 Variant Associated with Ventricular Arrhythmias and Sudden Cardiac Death in the Juvenile Rhodesian Ridgeback Dog}, volume={10}, ISSN={2073-4425}, url={http://dx.doi.org/10.3390/genes10020168}, DOI={10.3390/genes10020168}, abstractNote={The QIl1 gene produces a component of the Mitochondrial Contact Site and Cristae Organizing System that forms and stabilizes mitochondrial cristae junctions and is important in cellular energy production. We previously reported a family of Rhodesian Ridgebacks with cardiac arrhythmias and sudden cardiac death. Here, we performed whole genome sequencing on a trio from the family. Variant calling was performed using a standardized bioinformatics approach. Variants were filtered against variants from 247 dogs of 43 different breeds. High impact variants were validated against additional affected and unaffected dogs. A single missense G/A variant in the QIL1 gene was associated with the cardiac arrhythmia (p < 0.0001). The variant was predicted to change the amino acid from conserved Glycine to Serine and to be deleterious. Ultrastructural analysis of the biceps femoris muscle from an affected dog revealed hyperplastic mitochondria, cristae rearrangement, electron dense inclusions and lipid bodies. We identified a variant in the Q1l1 gene resulting in a mitochondrial cardiomyopathy characterized by cristae abnormalities and cardiac arrhythmias in a canine model. This natural animal model of mitochondrial cardiomyopathy provides a large animal model with which to study the development and progression of disease as well as genotypic phenotypic relationships.}, number={2}, journal={Genes}, publisher={MDPI AG}, author={Meurs, Kathryn and Friedenberg, Steven and Olby, Natasha and Condit, Julia and Weidman, Jess and Rosenthal, Steve and Shelton, G.}, year={2019}, month={Feb}, pages={168} }
 @article{meurs_friedenberg_kolb_saripalli_tonino_woodruff_olby_keene_adin_yost_et al._2019, title={A missense variant in the titin gene in Doberman pinscher dogs with familial dilated cardiomyopathy and sudden cardiac death}, volume={138}, ISSN={0340-6717 1432-1203}, url={http://dx.doi.org/10.1007/s00439-019-01973-2}, DOI={10.1007/s00439-019-01973-2}, abstractNote={The dog provides a large animal model of familial dilated cardiomyopathy for the study of important aspects of this common familial cardiovascular disease. We have previously demonstrated a form of canine dilated cardiomyopathy in the Doberman pinscher breed that is inherited as an autosomal dominant trait and is associated with a splice site variant in the pyruvate dehydrogenase kinase 4 (PDK4) gene, however, genetic heterogeneity exists in this species as well and not all affected dogs have the PDK4 variant. Whole genome sequencing of a family of Doberman pinchers with dilated cardiomyopathy and sudden cardiac death without the PDK4 variant was performed. A pathologic missense variant in the titin gene located in an immunoglobulin-like domain in the I-band spanning region of the molecule was identified and was highly associated with the disease (p < 0.0001). We demonstrate here the identification of a variant in the titin gene highly associated with the disease in this spontaneous canine model of dilated cardiomyopathy. This large animal model of familial dilated cardiomyopathy shares many similarities with the human disease including mode of inheritance, clinical presentation, genetic heterogeneity and a pathologic variant in the titin gene. The dog is an excellent model to improve our understanding of the genotypic phenotypic relationships, penetrance, expression and the pathophysiology of variants in the titin gene.}, number={5}, journal={Human Genetics}, publisher={Springer Science and Business Media LLC}, author={Meurs, Kathryn M. and Friedenberg, Steven G. and Kolb, Justin and Saripalli, Chandra and Tonino, Paola and Woodruff, Kathleen and Olby, Natasha J. and Keene, Bruce W. and Adin, Darcy B. and Yost, Oriana L. and et al.}, year={2019}, month={Feb}, pages={515–524} }
 @article{gandolfi_alhaddad_abdi_bach_creighton_davis_decker_dodman_ginns_grahn_et al._2019, title={Applications and efficiencies of the first cat 63 K DNA array (vol 8, 7024, 2018)}, volume={9}, ISSN={["2045-2322"]}, DOI={10.1038/s41598-018-38073-6}, abstractNote={A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has been fixed in the paper.}, journal={SCIENTIFIC REPORTS}, author={Gandolfi, Barbara and Alhaddad, Hasan and Abdi, Mona and Bach, Leslie H. and Creighton, Erica K. and Davis, Brian W. and Decker, Jared E. and Dodman, Nicholas H. and Ginns, Edward I. and Grahn, Jennifer C. and et al.}, year={2019}, month={Mar} }
 @article{adin_defrancesco_keene_tou_meurs_atkins_aona_kurtz_barron_saker_et al._2019, title={Echocardiographic phenotype of canine dilated cardiomyopathy differs based on diet type}, volume={21}, ISSN={["1875-0834"]}, DOI={10.1016/j.jvc.2018.11.002}, abstractNote={Canine dilated cardiomyopathy (DCM) can result from numerous etiologies including genetic mutations, infections, toxins, and nutritional imbalances. This study sought to characterize differences in echocardiographic findings between dogs with DCM fed grain-free (GF) diets and grain-based (GB) diets.Forty-eight dogs with DCM and known diet history.This was a retrospective analysis of dogs with DCM from January 1, 2015 to May 1, 2018 with a known diet history. Dogs were grouped by diet (GF and GB), and the GF group was further divided into dogs eating the most common grain-free diet (GF-1) and other grain-free diets (GF-o). Demographics, diet history, echocardiographic parameters, taurine concentrations, and vertebral heart scale were compared between GB, all GF, GF-1, and GF-o groups at diagnosis and recheck.Dogs eating GF-1 weighed less than GB and GF-o dogs, but age and sex were not different between groups. Left ventricular size in diastole and systole was greater, and sphericity index was less for GF-1 compared with GB dogs. Diastolic left ventricular size was greater for all GF compared with that of GB dogs. Fractional shortening, left atrial size, and vertebral heart scale were not different between groups. Taurine deficiency was not identified in GF dogs, and presence of congestive heart failure was not different between groups. Seven dogs that were reevaluated after diet change (6 received taurine supplementation) had clinical and echocardiographic improvement.Dietary-associated DCM occurs with some GF diets and can improve with nutritional management, including diet change. The role of taurine supplementation, even without deficiency, is uncertain.}, journal={JOURNAL OF VETERINARY CARDIOLOGY}, author={Adin, Darcy and DeFrancesco, Teresa and Keene, Bruce and Tou, Sandra and Meurs, Kathryn and Atkins, Clarke and Aona, Brent and Kurtz, Kari and Barron, Lara and Saker, Korinn and et al.}, year={2019}, month={Feb}, pages={1–9} }
 @article{agler_friedenberg_olivry_meurs_olby_2019, title={Genome-wide association analysis in West Highland White Terriers with atopic dermatitis}, volume={209}, ISSN={0165-2427}, url={http://dx.doi.org/10.1016/j.vetimm.2019.01.004}, DOI={10.1016/j.vetimm.2019.01.004}, abstractNote={Atopic dermatitis (AD) is a common disease of dogs and humans. In both species, the interplay of genetic and environmental factors affect disease expression. In dogs with AD, differences in the breed studied and in their geographical origin have led to heterogeneity in genetic association and while different loci have been identified, a causative genetic mutation has not. We hypothesized that AD could be mapped in a large cohort of rigorously phenotyped, geographically restricted West Highland White Terriers (WHWT), a breed with a high prevalence of the disease. A) Collect phenotypes and DNA from a large cohort of WHWT born in the USA. B) Perform a genome-wide association study (GWAS) for AD in these dogs to identify associated regions and genes of interest. C) Sequence genes of interest to identify pathologic variants. We collected DNA from 96 WHWT with AD and 87 controls from the same breed. DNA was isolated and dogs were genotyped using the Illumina CanineHD BeadChip. A GWAS was performed using EMMAX and associated regions were examined for genes of interest. Genes with possible relevance to AD were examined more closely in two affected and two normal WHWT using next-generation sequencing. Variants in these genes that were unique to the two affected WHWT were compared to a database of variants derived from whole genome sequencing of 200 non-WHWT dogs across 33 additional breeds. The GWAS identified a 2.7 Mb genomic region on CFA3 that included 37 genes. There was a missense variant in the F2R gene in both affected dogs but this variant was also found in 35 dogs in 9 breeds in the database of whole genome sequences for whom the phenotype regarding atopic dermatitis was unknown. Atopic dermatitis in WHWT is associated with a region on CFA3 that contains several candidate genes. Of these, a homozygous variant in the F2R gene present in multiple breeds that also suffer from AD warrants further evaluation.}, journal={Veterinary Immunology and Immunopathology}, publisher={Elsevier BV}, author={Agler, Cary S. and Friedenberg, Steven and Olivry, Thierry and Meurs, Kate M. and Olby, Natasha J.}, year={2019}, month={Mar}, pages={1–6} }
 @article{williams_friedenberg_meurs_2019, title={INVOLVEMENT OF SEROTONIN IN A CANINE MODEL OF MITRAL VALVE PROLAPSE: A COMPLEX GENETIC APPROACH}, volume={73}, ISSN={0735-1097}, url={http://dx.doi.org/10.1016/S0735-1097(19)31564-5}, DOI={10.1016/S0735-1097(19)31564-5}, abstractNote={In humans, mitral valve prolapse (MVP) is a common heritable condition. Dogs serve as a spontaneous animal model of familial MVP, with several breeds genetically predisposed. As in humans, previous studies have suggested that canine MVP may be polygenic and may be associated with alterations in the}, number={9}, journal={Journal of the American College of Cardiology}, publisher={Elsevier BV}, author={Williams, Brian and Friedenberg, Steven G. and Meurs, Kathryn M.}, year={2019}, month={Mar}, pages={957} }
 @article{meurs_adin_k. o'donnell_keene_atkins_defrancesco_tou_2019, title={Myxomatous mitral valve disease in the miniature poodle: A retrospective study}, volume={244}, ISSN={["1532-2971"]}, DOI={10.1016/j.tvjl.2018.12.019}, abstractNote={Myxomatous mitral valve disease (MMVD) is the most common cardiovascular disease in the dog. The natural history of the disease is wide ranging and includes patients without clinical signs as well as those with significant clinical consequences from cardiac arrhythmias, pulmonary hypertension and/or congestive heart failure. The factors that determine which dogs remain asymptomatic and which develop clinical disease are not known. Disease characteristics could be breed or family related; some breeds of dogs, particularly the Cavalier King Charles spaniels, develop MMVD at an early age. The purpose of this study was to retrospectively characterize MMVD in the miniature poodle, a commonly affected breed in which MMVD has not been well characterized. Thirty-two miniature poodles met the inclusion criteria. Mean age was 11±three years. Clinical signs included exercise intolerance, syncope and coughing. Eighteen dogs were classified as ACVIM Stage B1, 12 as stage B2, and two as stage C. Mean vertebral heart scale (VHS) was 10.2 (±standard deviation of 0.9); 15 of 28 dogs had a VHS <10.3. One dog had radiographic evidence of congestive heart failure. Mean diastolic left ventricle dimension normalized to body weight was 1.6 (±0.4) and mean systolic was 0.8 (±0.3). Mitral valve prolapse was subjectively classified as mild or moderate in 19 dogs and severe in two. In the miniature poodles reported here, MMVD appears to be a fairly late onset disease and often is a mild phenotype.}, journal={VETERINARY JOURNAL}, author={Meurs, K. M. and Adin, D. and K. O'Donnell and Keene, B. W. and Atkins, C. E. and DeFrancesco, T. and Tou, S.}, year={2019}, month={Feb}, pages={94–97} }
 @article{yost_friedenberg_jesty_olby_meurs_2019, title={The R9H phospholamban mutation is associated with highly penetrant dilated cardiomyopathy and sudden death in a spontaneous canine model}, volume={697}, ISSN={0378-1119}, url={http://dx.doi.org/10.1016/j.gene.2019.02.022}, DOI={10.1016/j.gene.2019.02.022}, abstractNote={Causative mutations for familial dilated cardiomyopathy (DCM) have been identified in the phospholamban gene. There are many poorly understood aspects about familial DCM (variable penetrance, expression) which may be studied in natural animal models. We characterized genetic aspects of familial DCM in a canine model with a high incidence of sudden death. A missense G > A mutation in exon 1 of the phospholamban gene that changed an amino acid from arginine to histidine was identified in affected dogs. This variant was predicted to be deleterious. We describe a spontaneous canine model of familial DCM and sudden death with the R9H mutation. In comparison to a reported human family, the variant was highly penetrant and resulted in sudden death. Genetic penetrance of this mutation may be influenced by genetic or environmental modifiers. The dog provides an excellent model in which to study complex aspects of familial DCM.}, journal={Gene}, publisher={Elsevier BV}, author={Yost, Oriana and Friedenberg, Steven G. and Jesty, Sophy A. and Olby, Natasha J. and Meurs, Kathryn M.}, year={2019}, month={May}, pages={118–122} }
 @article{friedenberg_vansteenkiste_yost_treeful_meurs_tokarz_olby_2018, title={A de novo mutation in the EXT2 gene associated with osteochondromatosis in a litter of American Staffordshire Terriers}, volume={32}, ISSN={0891-6640}, url={http://dx.doi.org/10.1111/jvim.15073}, DOI={10.1111/jvim.15073}, abstractNote={BackgroundWe aimed to identify mutations associated with osteochondromatosis in a litter of American Staffordshire Terrier puppies.}, number={3}, journal={Journal of Veterinary Internal Medicine}, publisher={Wiley}, author={Friedenberg, Steven G. and Vansteenkiste, Daniella and Yost, Oriana and Treeful, Amy E. and Meurs, Kathryn M. and Tokarz, Debra A. and Olby, Natasha J.}, year={2018}, month={Feb}, pages={986–992} }
 @article{meurs_olsen_reimann_keene_atkins_adin_aona_condit_defrancesco_reina-doreste_et al._2018, title={Angiotensin-converting enzyme activity in Cavalier King Charles Spaniels with an ACE gene polymorphism and myxomatous mitral valve disease}, volume={28}, url={https://doi.org/10.1097/FPC.0000000000000322}, DOI={10.1097/FPC.0000000000000322}, abstractNote={Objectives Myxomatous mitral valve disease (MMVD) is the most common heart disease in the dog. It is particularly common in the Cavalier King Charles Spaniel (CKCS) breed and affected dogs are frequently managed with angiotensin-converting enzyme inhibitors (ACE-I). We have previously identified a canine ACE gene polymorphism associated with a decrease in angiotensin-converting enzyme (ACE) activity. The aim of this study was to evaluate for the prevalence of the ACE polymorphism in CKCS with mitral valve disease and to determine whether the presence of the polymorphism is associated with alterations in ACE activity at different stages of cardiac disease. Methods Seventy-three dogs with a diagnosis of mitral valve disease were evaluated and a blood sample was drawn for ACE polymorphism genotyping and ACE activity measurement. Results Forty-three dogs were homozygous for the ACE polymorphism; five were heterozygous and 25 were homozygous wild type. The mean age and the median severity of disease were not different for dogs with the polymorphism and dogs with the wild-type sequence. The median baseline ACE activity was significantly lower for the ACE polymorphism (27.0 U/l) than the wild-type sequence dogs (31.0 U/l) (P=0.02). Dogs with more severe disease and the ACE polymorphism had significantly lower levels of ACE activity than dogs with the wild-type sequence (P=0.03). Conclusion The CKCS appears to have a high prevalence of the ACE variant. Dogs with the ACE variant had lower levels of ACE activity even in more advanced mitral valve disease than dogs without the variant. The clinical significance of this finding and its impact on the need for ACE-I in dogs with the polymorphism and heart disease deserves further study.}, number={2}, journal={Pharmacogenetics and Genomics}, author={Meurs, K.M. and Olsen, L.H. and Reimann, M.J. and Keene, B.W. and Atkins, C.E. and Adin, D. and Aona, B. and Condit, J. and DeFrancesco, T. and Reina-Doreste, Y. and et al.}, year={2018}, month={Feb}, pages={37–40} }
 @article{gandolfi_alhaddad_abdi_bach_creighton_davis_decker_dodman_ginns_grahn_et al._2018, title={Applications and efficiencies of the first cat 63K DNA array}, volume={8}, ISSN={2045-2322}, url={http://dx.doi.org/10.1038/S41598-018-25438-0}, DOI={10.1038/S41598-018-25438-0}, abstractNote={Abstract}, number={1}, journal={Scientific Reports}, publisher={Springer Science and Business Media LLC}, author={Gandolfi, Barbara and Alhaddad, Hasan and Abdi, Mona and Bach, Leslie H. and Creighton, Erica K. and Davis, Brian W. and Decker, Jared E. and Dodman, Nicholas H. and Ginns, Edward I. and Grahn, Jennifer C. and et al.}, year={2018}, month={May} }
 @article{gandolfi_alhaddad_abdi_bach_creighton_davis_decker_dodman_grahn_grahn_et al._2018, title={Applications and efficiencies of the first cat 63K DNA array}, volume={8}, journal={Scientific Reports}, author={Gandolfi, B. and Alhaddad, H. and Abdi, M. and Bach, L. H. and Creighton, E. K. and Davis, B. W. and Decker, J. E. and Dodman, N. H. and Grahn, J. C. and Grahn, R. A. and et al.}, year={2018} }
 @article{gandolfi_alhaddad_abdi_bach_creighton_davis_decker_dodman_grahn_grahn_et al._2018, title={Applications and efficiencies of the first cat 63K DNA array (vol 8, 7024, 2018)}, volume={8}, journal={Scientific Reports}, author={Gandolfi, B. and Alhaddad, H. and Abdi, M. and Bach, L. H. and Creighton, E. K. and Davis, B. W. and Decker, J. E. and Dodman, N. H. and Grahn, J. C. and Grahn, R. A. and et al.}, year={2018} }
 @article{gandolfi_alhaddad_abdi_bach_creighton_davis_decker_dodman_ginns_grahn_et al._2018, title={Author Correction: Applications and efficiencies of the first cat 63K DNA array}, volume={8}, ISSN={2045-2322}, url={http://dx.doi.org/10.1038/S41598-018-26885-5}, DOI={10.1038/S41598-018-26885-5}, abstractNote={A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has been fixed in the paper.}, number={1}, journal={Scientific Reports}, publisher={Springer Science and Business Media LLC}, author={Gandolfi, Barbara and Alhaddad, Hasan and Abdi, Mona and Bach, Leslie H. and Creighton, Erica K. and Davis, Brian W. and Decker, Jared E. and Dodman, Nicholas H. and Ginns, Edward I. and Grahn, Jennifer C. and et al.}, year={2018}, month={Jun} }
 @inbook{meurs_2018, place={Philadelphia}, edition={XVI}, title={Cardiomyopathy in the boxer dog}, booktitle={Current Veterinary Therapy (Small Animal Practice)}, publisher={WB Saunders}, author={Meurs, K. M.}, editor={Scansen, B. and Bonagura, J.Editors}, year={2018} }
 @article{guevar_olby_meurs_yost_friedenberg_2018, title={Deafness and vestibular dysfunction in a Doberman Pinscher puppy associated with a mutation in the PTPRQ
 gene}, volume={32}, ISSN={0891-6640}, url={http://dx.doi.org/10.1111/jvim.15060}, DOI={10.1111/jvim.15060}, abstractNote={BackgroundA congenital syndrome of hearing loss and vestibular dysfunction affects Doberman Pinschers. Its inheritance pattern is suspected to be autosomal recessive and it potentially represents a spontaneous animal model of an autosomal recessive syndromic hearing loss.}, number={2}, journal={Journal of Veterinary Internal Medicine}, publisher={Wiley}, author={Guevar, Julien and Olby, Natasha J. and Meurs, Kathryn M. and Yost, Oriana and Friedenberg, Steven G.}, year={2018}, month={Feb}, pages={665–669} }
 @article{meurs_friedenberg_williams_keene_atkins_adin_aona_defrancesco_tou_mackay_et al._2018, title={Evaluation of genes associated with human myxomatous mitral valve disease in dogs with familial myxomatous mitral valve degeneration}, volume={232}, ISSN={["1532-2971"]}, DOI={10.1016/j.tvjl.2017.12.002}, abstractNote={Myxomatous mitral valve disease (MMVD) is the most common heart disease in the dog. It is believed to be heritable in Cavalier King Charles spaniels (CKCS) and Dachshunds. Myxomatous mitral valve disease is a familial disease in human beings as well and genetic mutations have been associated with its development. We hypothesized that a genetic mutation associated with the development of the human form of MMVD was associated with the development of canine MMVD. DNA was isolated from blood samples from 10 CKCS and 10 Dachshunds diagnosed with MMVD, and whole genome sequences from each animal were obtained. Variant calling from whole genome sequencing data was performed using a standardized bioinformatics pipeline for all samples. After filtering, the canine genes orthologous to the human genes known to be associated with MMVD were identified and variants were assessed for likely pathogenic implications. No variant was found in any of the genes evaluated that was present in least eight of 10 affected CKCS or Dachshunds. Although mitral valve disease in the CKCS and Dachshund is a familial disease, we did not identify genetic cause in the genes responsible for the human disease in the dogs studied here.}, journal={VETERINARY JOURNAL}, author={Meurs, Kathryn and Friedenberg, S. G. and Williams, B. and Keene, B. W. and Atkins, C. E. and Adin, D. and Aona, B. and DeFrancesco, Teresa and Tou, S. and Mackay, T. and et al.}, year={2018}, month={Feb}, pages={16–19} }
 @inbook{meurs_2018, place={Philadelphia}, title={Genetic cardiac disease in the dog and cat}, booktitle={Current Veterinary Therapy (Small Animal Practice) XVI}, publisher={WB Saunders}, author={Meurs, K.M.}, year={2018} }
 @article{friedenberg_brown_meurs_law_2018, title={Lymphocyte Subsets in the Adrenal Glands of Dogs With Primary Hypoadrenocorticism}, volume={55}, ISSN={["1544-2217"]}, DOI={10.1177/0300985816684914}, abstractNote={ Primary hypoadrenocorticism, or Addison’s disease, is an autoimmune condition common in certain dog breeds that leads to the destruction of the adrenal cortex and a clinical syndrome involving anorexia, gastrointestinal upset, and electrolyte imbalances. Previous studies have demonstrated that this destruction is strongly associated with lymphocytic-plasmacytic inflammation and that the lymphocytes are primarily T cells. In this study, we used both immunohistochemistry and in situ hybridization to characterize the T-cell subtypes involved. We collected postmortem specimens of 5 dogs with primary hypoadrenocorticism and 2 control dogs and, using the aforementioned techniques, showed that the lymphocytes are primarily CD4+ rather than CD8+. These findings have important implications for improving our understanding of the pathogenesis and in searching for the underlying causative genetic polymorphisms. }, number={1}, journal={VETERINARY PATHOLOGY}, author={Friedenberg, S. G. and Brown, D. L. and Meurs, K. M. and Law, J. McHugh}, year={2018}, month={Jan}, pages={177–181} }
 @article{lichtenberger_meurs_cote_2018, title={Preliminary Assessment of a Novel 14-Day Electrocardiographic Adhesive Patch Monitor in Dogs}, volume={54}, ISSN={["1547-3317"]}, DOI={10.5326/jaaha-ms-6626}, abstractNote={ABSTRACT}, number={3}, journal={JOURNAL OF THE AMERICAN ANIMAL HOSPITAL ASSOCIATION}, author={Lichtenberger, Jonathan and Meurs, Kathryn M. and Cote, Etienne}, year={2018}, pages={138–143} }
 @article{meurs_stern_atkins_adin_aona_condit_defrancesco_reina-doreste_keene_tou_et al._2017, title={Angiotensin-converting enzyme activity and inhibition in dogs with cardiac disease and an angiotensin-converting enzyme polymorphism}, volume={18}, ISSN={["1752-8976"]}, url={https://europepmc.org/articles/PMC5843865}, DOI={10.1177/1470320317737184}, abstractNote={Objective: The objective of this study was to evaluate angiotensin-converting enzyme (ACE) activity in dogs and with and without an ACE polymorphism in the canine ACE gene, before and after treatment with an ACE inhibitor. Methods: Thirty-one dogs (20 wild-type, 11 ACE polymorphism) with heart disease were evaluated with ACE activity measurement and systolic blood pressure before and after administration of an ACE inhibitor (enalapril). Results: Median pre-treatment ACE activity was significantly lower for ACE polymorphism dogs than for dogs with the wild-type sequence (P=0.007). After two weeks of an ACE inhibitor, ACE activity was significantly reduced for both genotypes (wild-type, P<0.0001; ACE polymorphism P=0.03); mean post-therapy ACE activity was no different between the groups. Conclusion: An ACE polymorphism is associated with lower levels of ACE activity. Dogs with the polymorphism still experience suppression of ACE activity in response to an ACE inhibitor. It is possible that the genetic status and ACE activity of dogs may impact the response of dogs with this variant to an ACE inhibitor.}, number={4}, journal={JOURNAL OF THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM}, author={Meurs, Kathryn M. and Stern, Joshua A. and Atkins, Clarke E. and Adin, Darcy and Aona, Brent and Condit, Julia and DeFrancesco, Teresa and Reina-Doreste, Yamir and Keene, Bruce W. and Tou, Sandy and et al.}, year={2017}, month={Oct} }
 @article{meurs_2017, title={Arrhythmogenic Right Ventricular Cardiomyopathy in the Boxer Dog: An Update}, volume={47}, ISSN={["1878-1306"]}, DOI={10.1016/j.cvsm.2017.04.007}, abstractNote={Arrhythmogenic right ventricular cardiomyopathy is an inheritable form of myocardial disease characterized most commonly by ventricular tachycardias, syncope, and sometimes systolic dysfunction and heart failure. A genetic mutation in the striatin gene has been identified in many affected dogs. Dogs with only one copy of the mutation (heterozygous) have a variable prognosis, with many dogs remaining asymptomatic or being successfully managed on antiarrhythmic drugs for years. Dogs that are homozygous for the mutation seem to have a worse prognosis.}, number={5}, journal={VETERINARY CLINICS OF NORTH AMERICA-SMALL ANIMAL PRACTICE}, author={Meurs, Kathryn M.}, year={2017}, month={Sep}, pages={1103-+} }
 @article{hensley_tang_woodruff_defrancesco_tou_williams_breen_meurs_keene_cheng_et al._2017, title={Intracoronary allogeneic cardiosphere-derived stem cells are safe for use in dogs with dilated cardiomyopathy}, volume={21}, ISSN={1582-1838}, url={http://dx.doi.org/10.1111/jcmm.13077}, DOI={10.1111/jcmm.13077}, abstractNote={Abstract}, number={8}, journal={Journal of Cellular and Molecular Medicine}, publisher={Wiley}, author={Hensley, Michael Taylor and Tang, Junnan and Woodruff, Kathleen and Defrancesco, Teresa and Tou, Sandra and Williams, Christina M. and Breen, Mathew and Meurs, Kathryn and Keene, Bruce and Cheng, Ke and et al.}, year={2017}, month={Mar}, pages={1503–1512} }
 @inproceedings{talley_zimmer_bolotnov_2016, title={Coalescence prevention algorithm for level set method}, DOI={10.1115/fedsm2016-7608}, abstractNote={The application of interface tracking methods to bubbly flow modeling has grown in recent years due to improvements in computing performance and development of more efficient solvers. However, the standard formulation of most interface tracking methods is not designed to physically handle the interface interactions at reasonable grid sizes. Regardless of the method used, a high grid resolution is required in the liquid film region in order to properly model drainage process during bubble interaction, which in certain conditions prevents the coalescence. This makes large scale (many bubbles) simulations unaffordable. One of the popular interface tracking approached is the level-set (LS) method. To simulate realistic bubble coalescence behavior in the LS method an algorithm with the capability of delaying or preventing the process of multiple simultaneous coalescence events has been developed.}, booktitle={Proceedings of the asme fluids engineering division summer meeting, 2016, vol 1b}, author={Talley, M. L. and Zimmer, M. D. and Bolotnov, I. A.}, year={2016} }
 @article{friedenberg_meurs_mackay_2016, title={Evaluation of artificial selection in Standard Poodles using whole-genome sequencing}, volume={27}, ISSN={0938-8990 1432-1777}, url={http://dx.doi.org/10.1007/S00335-016-9660-9}, DOI={10.1007/S00335-016-9660-9}, abstractNote={Identifying regions of artificial selection within dog breeds may provide insights into genetic variation that underlies breed-specific traits or diseases-particularly if these traits or disease predispositions are fixed within a breed. In this study, we searched for runs of homozygosity (ROH) and calculated the d i statistic (which is based upon F ST) to identify regions of artificial selection in Standard Poodles using high-coverage, whole-genome sequencing data of 15 Standard Poodles and 49 dogs across seven other breeds. We identified consensus ROH regions ≥1 Mb in length and common to at least ten Standard Poodles covering 0.6 % of the genome, and d i regions that most distinguish Standard Poodles from other breeds covering 3.7 % of the genome. Within these regions, we identified enriched gene pathways related to olfaction, digestion, and taste, as well as pathways related to adrenal hormone biosynthesis, T cell function, and protein ubiquitination that could contribute to the pathogenesis of some Poodle-prevalent autoimmune diseases. We also validated variants related to hair coat and skull morphology that have previously been identified as being under selective pressure in Poodles, and flagged additional polymorphisms in genes such as ITGA2B, CBX4, and TNXB that may represent strong candidates for other common Poodle disorders.}, number={11-12}, journal={Mammalian Genome}, publisher={Springer Nature}, author={Friedenberg, Steven G. and Meurs, Kathryn M. and Mackay, Trudy F. C.}, year={2016}, month={Aug}, pages={599–609} }
 @article{friedenberg_lunn_meurs_2016, title={Evaluation of the genetic basis of primary hypoadrenocorticism in Standard Poodles using SNP array genotyping and whole-genome sequencing}, volume={28}, ISSN={0938-8990 1432-1777}, url={http://dx.doi.org/10.1007/s00335-016-9671-6}, DOI={10.1007/s00335-016-9671-6}, abstractNote={Primary hypoadrenocorticism, also known as Addison's disease, is an autoimmune disorder leading to the destruction of the adrenal cortex and subsequent loss of glucocorticoid and mineralocorticoid hormones. The disease is prevalent in Standard Poodles and is believed to be highly heritable in the breed. Using genotypes derived from the Illumina Canine HD SNP array, we performed a genome-wide association study of 133 carefully phenotyped Standard Poodles (61 affected, 72 unaffected) and found no markers significantly associated with the disease. We also sequenced the entire genomes of 20 Standard Poodles (13 affected, 7 unaffected) and analyzed the data to identify common variants (including SNPs, indels, structural variants, and copy number variants) across affected dogs and variants segregating within a single pedigree of highly affected dogs. We identified several candidate genes that may be fixed in both Standard Poodles and a small population of dogs of related breeds. Further studies are required to confirm these findings more broadly, as well as additional gene-mapping efforts aimed at fully understanding the genetic basis of what is likely a complex inherited disorder.}, number={1-2}, journal={Mammalian Genome}, publisher={Springer Nature}, author={Friedenberg, Steven G. and Lunn, Katharine F. and Meurs, Kathryn M.}, year={2016}, month={Nov}, pages={56–65} }
 @inbook{meurs_2016, title={Genetics of Feline Heart Disease}, volume={7}, ISBN={9780323226523}, url={http://dx.doi.org/10.1016/b978-0-323-22652-3.00040-2}, DOI={10.1016/b978-0-323-22652-3.00040-2}, booktitle={August's Consultations in Feline Internal Medicine}, publisher={Elsevier}, author={Meurs, Kathryn M.}, year={2016}, pages={412–416} }
 @article{friedenberg_meurs_2016, title={Genotype imputation in the domestic dog}, volume={27}, ISSN={["1432-1777"]}, DOI={10.1007/s00335-016-9636-9}, abstractNote={Application of imputation methods to accurately predict a dense array of SNP genotypes in the dog could provide an important supplement to current analyses of array-based genotyping data. Here, we developed a reference panel of 4,885,283 SNPs in 83 dogs across 15 breeds using whole genome sequencing. We used this panel to predict the genotypes of 268 dogs across three breeds with 84,193 SNP array-derived genotypes as inputs. We then (1) performed breed clustering of the actual and imputed data; (2) evaluated several reference panel breed combinations to determine an optimal reference panel composition; and (3) compared the accuracy of two commonly used software algorithms (Beagle and IMPUTE2). Breed clustering was well preserved in the imputation process across eigenvalues representing 75 % of the variation in the imputed data. Using Beagle with a target panel from a single breed, genotype concordance was highest using a multi-breed reference panel (92.4 %) compared to a breed-specific reference panel (87.0 %) or a reference panel containing no breeds overlapping with the target panel (74.9 %). This finding was confirmed using target panels derived from two other breeds. Additionally, using the multi-breed reference panel, genotype concordance was slightly higher with IMPUTE2 (94.1 %) compared to Beagle; Pearson correlation coefficients were slightly higher for both software packages (0.946 for Beagle, 0.961 for IMPUTE2). Our findings demonstrate that genotype imputation from SNP array-derived data to whole genome-level genotypes is both feasible and accurate in the dog with appropriate breed overlap between the target and reference panels.}, number={9-10}, journal={MAMMALIAN GENOME}, author={Friedenberg, S. G. and Meurs, K. M.}, year={2016}, month={Oct}, pages={485–494} }
 @article{friedenberg_chdid_keene_sherry_motsinger-reif_meurs_2016, title={Use of RNA-seq to identify cardiac genes and gene pathways differentially expressed between dogs with and without dilated cardiomyopathy}, volume={77}, ISSN={["1943-5681"]}, DOI={10.2460/ajvr.77.7.693}, abstractNote={Abstract}, number={7}, journal={AMERICAN JOURNAL OF VETERINARY RESEARCH}, author={Friedenberg, Steven G. and Chdid, Lhoucine and Keene, Bruce and Sherry, Barbara and Motsinger-Reif, Alison and Meurs, Kathryn M.}, year={2016}, month={Jul}, pages={693–699} }
 @article{meurs_weidman_rosenthal_lahmers_friedenberg_2016, title={Ventricular arrhythmias in Rhodesian Ridgebacks with a family history of sudden death and results of a pedigree analysis for potential inheritance patterns}, volume={248}, ISSN={["1943-569X"]}, DOI={10.2460/javma.248.10.1135}, abstractNote={Abstract}, number={10}, journal={JAVMA-JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Meurs, Kathryn M. and Weidman, Jess A. and Rosenthal, Steven L. and Lahmers, Kevin K. and Friedenberg, Steven G.}, year={2016}, month={May}, pages={1135–1138} }
 @inbook{meurs_2015, place={Philadelphia}, edition={10th}, title={Antiarrhythmic Agents}, booktitle={Veterinary Pharmacology and Therapeutics}, publisher={Wiley-Blackwell}, author={Meurs, K.M.}, year={2015} }
 @inbook{meurs_stern_2015, edition={8th}, title={Basic veterinary genetics}, booktitle={Ettinger’s Textbook of Veterinary Internal Medicine}, publisher={Elsevier, St Louis}, author={Meurs, K.M. and Stern, J.A.}, year={2015} }
 @article{hensley_andrade_keene_meurs_tang_wang_caranasos_piedrahita_li_cheng_et al._2015, title={Cardiac regenerative potential of cardiosphere-derived cells from adult dog hearts}, volume={19}, ISSN={1582-1838}, url={http://dx.doi.org/10.1111/jcmm.12585}, DOI={10.1111/jcmm.12585}, abstractNote={Abstract}, number={8}, journal={Journal of Cellular and Molecular Medicine}, publisher={Wiley}, author={Hensley, M. T. and Andrade, J. and Keene, B. and Meurs, Kathryn and Tang, J. N. and Wang, Z. G. and Caranasos, T. G. and Piedrahita, J. and Li, T. S. and Cheng, K. and et al.}, year={2015}, month={Apr}, pages={1805–1813} }
 @inbook{meurs_stern_2015, edition={8th}, title={Clinical veterinary genetics}, booktitle={Ettinger’s Textbook of Veterinary Internal Medicine}, publisher={Elsevier, St Louis}, author={Meurs, K.M. and Stern, J.A.}, year={2015} }
 @article{friedenberg_buhrman_chdid_olby_olivry_guillaumin_o’toole_goggs_kennedy_rose_et al._2015, title={Evaluation of a DLA-79 allele associated with multiple immune-mediated diseases in dogs}, volume={68}, ISSN={0093-7711 1432-1211}, url={http://dx.doi.org/10.1007/s00251-015-0894-6}, DOI={10.1007/s00251-015-0894-6}, abstractNote={Immune-mediated diseases are common and life-threatening disorders in dogs. Many canine immune-mediated diseases have strong breed predispositions and are believed to be inherited. However, the genetic mutations that cause these diseases are mostly unknown. As many immune-mediated diseases in humans share polymorphisms among a common set of genes, we conducted a candidate gene study of 15 of these genes across four immune-mediated diseases (immune-mediated hemolytic anemia, immune-mediated thrombocytopenia, immune-mediated polyarthritis (IMPA), and atopic dermatitis) in 195 affected and 206 unaffected dogs to assess whether causative or predictive polymorphisms might exist in similar genes in dogs. We demonstrate a strong association (Fisher’s exact p = 0.0004 for allelic association, p = 0.0035 for genotypic association) between two polymorphic positions (10 bp apart) in exon 2 of one allele in DLA-79, DLA-79*001:02, and multiple immune-mediated diseases. The frequency of this allele was significantly higher in dogs with immune-mediated disease than in control dogs (0.21 vs. 0.12) and ranged from 0.28 in dogs with IMPA to 0.15 in dogs with atopic dermatitis. This allele has two non-synonymous substitutions (compared with the reference allele, DLA-79*001:01), resulting in F33L and N37D amino acid changes. These mutations occur in the peptide-binding pocket of the protein, and based upon our computational modeling studies, are likely to affect critical interactions with the peptide N-terminus. Further studies are warranted to confirm these findings more broadly and to determine the specific mechanism by which the identified variants alter canine immune system function.}, number={3}, journal={Immunogenetics}, publisher={Springer Science and Business Media LLC}, author={Friedenberg, Steven G. and Buhrman, Greg and Chdid, Lhoucine and Olby, Natasha J. and Olivry, Thierry and Guillaumin, Julien and O’Toole, Theresa and Goggs, Robert and Kennedy, Lorna J. and Rose, Robert B. and et al.}, year={2015}, month={Dec}, pages={205–217} }
 @article{stern_lahmers_meurs_2015, title={Identification of striatin, a desmosomal protein, in the canine corneal epithelium}, volume={102}, ISSN={["1532-2661"]}, url={https://doi.org/10.1016/j.rvsc.2015.08.009}, DOI={10.1016/j.rvsc.2015.08.009}, abstractNote={Striatin is a scaffolding protein expressed in brain and cardiac tissues. In the heart, striatin has been localized to the region of the cardiac desmosome. A causal mutation within the gene encoding for this scaffolding protein has been described as the etiology for arrhythmogenic right ventricular cardiomyopathy, a disease of the cardiac desmosome, in a canine model. Hemidesmosomes are cell adhesion complexes located within the cornea where they anchor the corneal epithelium to the stroma at the basement membrane and participate in cell-signaling processes. Traditional cell adhesion desmosomes are also known to link the corneal epithelial cells together. We hypothesized that striatin may be found in the cornea localized to regions of either hemidesmosomes and/or desmosomes. Immunohistochemical evaluation was performed to evaluate for striatin labeling in normal canine cornea. Striatin was localized to the cytoplasmic region of corneal epithelial cells. The role of striatin in corneal disease warrants investigation.}, journal={RESEARCH IN VETERINARY SCIENCE}, author={Stern, Joshua A. and Lahmers, Sunshine and Meurs, Kathryn M.}, year={2015}, month={Oct}, pages={182–183} }
 @article{meurs_stern_reina-doreste_maran_chdid_lahmers_keene_mealey_2015, title={Impact of the canine double-deletion beta 1 adrenoreceptor polymorphisms on protein structure and heart rate response to atenolol, a beta 1-selective beta-blocker}, volume={25}, ISSN={["1744-6880"]}, url={https://doi.org/10.1097/FPC.0000000000000152}, DOI={10.1097/fpc.0000000000000152}, abstractNote={Objective &bgr;-Adrenergic receptor antagonists are widely utilized for the management of cardiac diseases in dogs. We have recently identified two deletion polymorphisms in the canine adrenoreceptor 1 (ADRB1) gene. We hypothesized that canine ADRB1 deletions would alter the structure of the protein, as well as the heart rate response to the &bgr;-adrenergic receptor antagonist, atenolol. The objectives of this study were to predict the impact of these deletions on the predicted structure of the protein and on the heart rate response to atenolol in a population of healthy adult dogs. Methods Eighteen apparently healthy, mature dogs with (11) and without (seven) ADRB1 deletions were evaluated. The heart rate of the dogs was evaluated with a baseline ambulatory ECG before and 14–21 days after atenolol therapy (1 mg/kg orally q12 h). Minimum, average, and maximum heart rates were compared between groups of dogs (deletions, controls) using an unpaired t-test and within each group of dogs using a paired t-test. The protein structure of ADRB1 was predicted by computer modeling. Results Deletions were predicted to alter the structure of the ADRB1 protein. The heart rates of the dogs with deletions were lower than those of the control dogs (the average heart rates were significantly lower). Conclusion ADRB1 deletions appear to have structural and functional consequences. Individual genome-based treatment recommendations could impact the management of dogs with heart disease.}, number={9}, journal={PHARMACOGENETICS AND GENOMICS}, author={Meurs, Kathryn M. and Stern, Josh A. and Reina-Doreste, Yamir and Maran, Brian A. and Chdid, Lhoucine and Lahmers, Sunshine and Keene, Bruce W. and Mealey, Katrina L.}, year={2015}, month={Sep}, pages={427–431} }
 @article{meurs_chdid_reina-doreste_stern_2015, title={Polymorphisms in the canine and feline renin-angiotensin-aldosterone system genes}, volume={46}, ISSN={["1365-2052"]}, url={https://doi.org/10.1111/age.12260}, DOI={10.1111/age.12260}, abstractNote={Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.}, number={2}, journal={ANIMAL GENETICS}, author={Meurs, Kathryn M. and Chdid, Lhoucine and Reina-Doreste, Yamir and Stern, Joshua A.}, year={2015}, month={Apr}, pages={226–226} }
 @inbook{stern_meurs_2015, place={Philadelphia}, edition={7th}, title={Primary myocardial disease in the dog}, booktitle={Textbook of Veterinary Internal Medicine}, publisher={WB Saunders}, author={Stern, J.A. and Meurs, K.M.}, year={2015}, pages={1320–1328} }
 @article{ware_reina-doreste_stern_meurs_2015, title={Sudden Death Associated with QT Interval Prolongation and KCNQ1 Gene Mutation in a Family of English Springer Spaniels}, volume={29}, ISSN={["1939-1676"]}, url={https://europepmc.org/articles/PMC4895492}, DOI={10.1111/jvim.12550}, abstractNote={BackgroundA 5‐year‐old, healthy English Springer Spaniel died suddenly 4 months after delivering a litter of 7 puppies. Within 4 months of the dam's death, 3 offspring also died suddenly.}, number={2}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Ware, W. A. and Reina-Doreste, Y. and Stern, J. A. and Meurs, K. M.}, year={2015}, pages={561–568} }
 @article{kittleson_meurs_harris_2015, title={The genetic basis of hypertrophic cardiomyopathy in cats and humans}, volume={17}, ISSN={1760-2734}, url={http://dx.doi.org/10.1016/j.jvc.2015.03.001}, DOI={10.1016/j.jvc.2015.03.001}, abstractNote={Mutations in genes that encode for muscle sarcomeric proteins have been identified in humans and two breeds of domestic cats with hypertrophic cardiomyopathy (HCM). This article reviews the history, genetics, and pathogenesis of HCM in the two species in order to give veterinarians a perspective on the genetics of HCM. Hypertrophic cardiomyopathy in people is a genetic disease that has been called a disease of the sarcomere because the preponderance of mutations identified that cause HCM are in genes that encode for sarcomeric proteins (Maron and Maron, 2013). Sarcomeres are the basic contractile units of muscle and thus sarcomeric proteins are responsible for the strength, speed, and extent of muscle contraction. In people with HCM, the two most common genes affected by HCM mutations are the myosin heavy chain gene (MYH7), the gene that encodes for the motor protein β-myosin heavy chain (the sarcomeric protein that splits ATP to generate force), and the cardiac myosin binding protein-C gene (MYBPC3), a gene that encodes for the closely related structural and regulatory protein, cardiac myosin binding protein-C (cMyBP-C). To date, the two mutations linked to HCM in domestic cats (one each in Maine Coon and Ragdoll breeds) also occur in MYBPC3 (Meurs et al., 2005, 2007). This is a review of the genetics of HCM in both humans and domestic cats that focuses on the aspects of human genetics that are germane to veterinarians and on all aspects of feline HCM genetics.}, journal={Journal of Veterinary Cardiology}, publisher={Elsevier BV}, author={Kittleson, Mark D. and Meurs, Kathryn M. and Harris, Samantha P.}, year={2015}, month={Dec}, pages={S53–S73} }
 @article{borgeat_stern_meurs_fuentes_connolly_2015, title={The influence of clinical and genetic factors on left ventricular wall thickness in Ragdoll cats}, volume={17}, ISSN={1760-2734}, url={http://dx.doi.org/10.1016/j.jvc.2015.06.005}, DOI={10.1016/j.jvc.2015.06.005}, abstractNote={To investigate the effect of various genetic and environmental modifiers on left ventricular (LV) wall thickness in a cohort of cats genotyped for the myosin binding protein C3 mutation (MYBPC3).Sixty-four Ragdoll cats.All cats were screened for HCM with echocardiography and genotyping for the HCM-associated MYBPC3:R820W mutation. Cats were also genotyped for previously identified variant polymorphisms of the angiotensin-converting enzyme (ACE) and cardiac beta-adrenergic receptor (ADRB1) genes. Plasma N-terminal pro-B-type natriuretic peptide and cardiac troponin I were also measured. Associations were evaluated between genotype (MYBPC3 negative/positive, and ACE and ADRB1 negative/heterozygous/homozygous), patient factors (body weight, age and sex) and echocardiographic measurements of LV wall thickness.Male cats had greater maximum wall thickness (LVmax; 5.8 mm, IQR 5.1-6.4 mm) than females (4.7 mm, IQR 4.4-5.3 mm, p = 0.002). Body weight positively correlated with LVmax (ρ = 0.604, p < 0.001). The MYBPC3:R820W-positive cats had a greater LVmax (5.44 mm, IQR 4.83-6.28 mm) than the negative cats (4.76 mm, IQR 4.36-5.32 mm, p = 0.001). Also, the ACE polymorphism genotype was associated with LVmax: the homozygous cats (5.37 mm, IQR 5.14-6.4 mm) had greater LVmax than the heterozygous cats (4.73 mm, IQR 4.41-5.55 mm, p = 0.014). Only the MYBPC3 genotype and body weight were independently associated with wall thickness in multivariable analysis.This study provides evidence that the MYBPC3:R820W mutation is independently associated with LV wall thickness in Ragdoll cats. Body weight is also independently associated with maximum LV wall thickness, but is not currently accounted for in HCM screening. In addition, other genetic modifiers may be associated with variation in LV wall thickness in Ragdolls.}, journal={Journal of Veterinary Cardiology}, publisher={Elsevier BV}, author={Borgeat, Kieran and Stern, Joshua and Meurs, Kathryn M. and Fuentes, Virginia Luis and Connolly, David J.}, year={2015}, month={Dec}, pages={S258–S267} }
 @article{stern_white_lehmkuhl_reina-doreste_ferguson_nascone-yoder_meurs_2014, title={A single codon insertion in PICALM is associated with development of familial subvalvular aortic stenosis in Newfoundland dogs}, volume={133}, ISSN={0340-6717 1432-1203}, url={http://dx.doi.org/10.1007/s00439-014-1454-0}, DOI={10.1007/s00439-014-1454-0}, abstractNote={Familial subvalvular aortic stenosis (SAS) is one of the most common congenital heart defects in dogs and is an inherited defect of Newfoundlands, golden retrievers and human children. Although SAS is known to be inherited, specific genes involved in Newfoundlands with SAS have not been defined. We hypothesized that SAS in Newfoundlands is inherited in an autosomal dominant pattern and caused by a single genetic variant. We studied 93 prospectively recruited Newfoundland dogs, and 180 control dogs of 30 breeds. By providing cardiac screening evaluations for Newfoundlands we conducted a pedigree evaluation, genome-wide association study and RNA sequence analysis to identify a proposed pattern of inheritance and genetic loci associated with the development of SAS. We identified a three-nucleotide exonic insertion in phosphatidylinositol-binding clathrin assembly protein (PICALM) that is associated with the development of SAS in Newfoundlands. Pedigree evaluation best supported an autosomal dominant pattern of inheritance and provided evidence that equivocally affected individuals may pass on SAS in their progeny. Immunohistochemistry demonstrated the presence of PICALM in the canine myocardium and area of the subvalvular ridge. Additionally, small molecule inhibition of clathrin-mediated endocytosis resulted in developmental abnormalities within the outflow tract (OFT) of Xenopus laevis embryos. The ability to test for presence of this PICALM insertion may impact dog-breeding decisions and facilitate reduction of SAS disease prevalence in Newfoundland dogs. Understanding the role of PICALM in OFT development may aid in future molecular and genetic investigations into other congenital heart defects of various species.}, number={9}, journal={Human Genetics}, publisher={Springer Nature}, author={Stern, Joshua A. and White, Stephen N. and Lehmkuhl, Linda B. and Reina-Doreste, Yamir and Ferguson, Jordan L. and Nascone-Yoder, Nanette M. and Meurs, Kathryn M.}, year={2014}, month={Jun}, pages={1139–1148} }
 @article{reina-doreste_stern_keene_tou_atkins_defrancesco_ames_hodge_meurs_2014, title={Case-control study of the effects of pimobendan on survival time in cats with hypertrophic cardiomyopathy and congestive heart failure}, volume={245}, ISSN={["1943-569X"]}, url={https://doi.org/10.2460/javma.245.5.534}, DOI={10.2460/javma.245.5.534}, abstractNote={Abstract}, number={5}, journal={JAVMA-JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Reina-Doreste, Yamir and Stern, Joshua A. and Keene, Bruce W. and Tou, Sandra P. and Atkins, Clarke E. and DeFrancesco, Teresa C. and Ames, Marisa K. and Hodge, Timothy E. and Meurs, Kathryn M.}, year={2014}, month={Sep}, pages={534–539} }
 @article{stern_reina-doreste_chdid_meurs_2014, title={Identification of PDE5A:E90K: A Polymorphism in the Canine Phosphodiesterase 5A Gene Affecting Basal cGMP Concentrations of Healthy Dogs}, volume={28}, ISSN={["1939-1676"]}, url={https://europepmc.org/articles/PMC4895552}, DOI={10.1111/jvim.12256}, abstractNote={BackgroundCyclic guanosine monophosphate (cGMP)‐specific phosphodiesterase (PDE5A) is the target of phosphodiesterase inhibitors such as sildenafil. Polymorphisms in the PDE5A gene that may predict response to therapy with sildenafil and nitric oxide, be linked to disease progression, and aid in risk assessment have been identified in human beings. Identification of polymorphisms in PDE5A could affect the physiologic actions of PDE5A and the effects of phosphodiestrase type 5 inhibitor drugs.}, number={1}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Stern, J. A. and Reina-Doreste, Y. and Chdid, L. and Meurs, K. M.}, year={2014}, month={Jan}, pages={78–83} }
 @article{meurs_stern_reina-doreste_spier_koplitz_baumwart_2014, title={Natural History of Arrhythmogenic Right Ventricular Cardiomyopathy in the Boxer Dog: A Prospective Study}, volume={28}, ISSN={["1939-1676"]}, url={https://europepmc.org/articles/PMC4857953}, DOI={10.1111/jvim.12385}, abstractNote={BackgroundBoxer arrhythmogenic right ventricular cardiomyopathy (ARVC) is a disease that may result in sudden death or heart failure.}, number={4}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Meurs, K. M. and Stern, J. A. and Reina-Doreste, Y. and Spier, A. W. and Koplitz, S. L. and Baumwart, R. D.}, year={2014}, pages={1214–1220} }
 @article{meurs_stern_sisson_kittleson_cunningham_ames_atkins_defrancesco_hodge_keene_et al._2013, title={Association of Dilated Cardiomyopathy with the Striatin Mutation Genotype in Boxer Dogs}, volume={27}, ISSN={["1939-1676"]}, url={https://onlinelibrary.wiley.com/doi/pdfdirect/10.1111/jvim.12163}, DOI={10.1111/jvim.12163}, abstractNote={BackgroundMyocardial disease in the Boxer dog is characterized by 1 of 2 clinical presentations, dilated cardiomyopathy (DCM) characterized by ventricular systolic dysfunction, dilatation and tachyarrhythmias, and arrhythmogenic right ventricular cardiomyopathy (ARVC) characterized by ventricular tachyarrhythmias, syncope, and sudden death. Boxer ARVC has been associated with a deletion in the striatin gene in some families.}, number={6}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Meurs, K. M. and Stern, J. A. and Sisson, D. D. and Kittleson, M. D. and Cunningham, S. M. and Ames, M. K. and Atkins, C. E. and DeFrancesco, T. and Hodge, T. E. and Keene, B. W. and et al.}, year={2013}, month={Nov}, pages={1437–1440} }
 @inbook{meurs_2013, place={Philadelphia}, title={Cardiomyopathy in the boxer dog}, booktitle={Current Veterinary Therapy (Small Animal Practice) XV}, publisher={WB Saunders}, author={Meurs, K.M.}, year={2013} }
 @article{stern_white_meurs_2013, title={Extent of linkage disequilibrium in large-breed dogs: chromosomal and breed variation}, volume={24}, ISSN={["1432-1777"]}, url={https://doi.org/10.1007/s00335-013-9474-y}, DOI={10.1007/s00335-013-9474-y}, abstractNote={The aim of this study was to better define the extent of linkage disequilibrium (LD) in populations of large-breed dogs and its variation by breed and chromosomal region. Understanding the extent of LD is a crucial component for successful utilization of genome-wide association studies and allows researchers to better define regions of interest and target candidate genes. Twenty-four Golden Retriever dogs, 28 Rottweiler dogs, and 24 Newfoundland dogs were genotyped for single-nucleotide polymorphism (SNP) data using a high-density SNP array. LD was calculated for all autosomes using Haploview. Decay of the squared correlation coefficient (r (2)) was plotted on a per-breed and per-chromosome basis as well as in a genome-wide fashion. The point of 50 % decay of r (2) was used to estimate the difference in extent of LD between breeds. Extent of LD was significantly shorter for Newfoundland dogs based upon 50 % decay of r (2) data at a mean of 344 kb compared to Golden Retriever and Rottweiler dogs at 715 and 834 kb, respectively (P < 0.0001). Notable differences in LD by chromosome were present within each breed and not strictly related to the length of the corresponding chromosome. Extent of LD is breed and chromosome dependent. To our knowledge, this is the first report of SNP-based LD for Newfoundland dogs, the first report based on genome-wide SNPs for Rottweilers, and an almost tenfold improvement in marker density over previous genome-wide studies of LD in Golden Retrievers.}, number={9-10}, journal={MAMMALIAN GENOME}, author={Stern, Joshua A. and White, Stephen N. and Meurs, Kathryn M.}, year={2013}, month={Oct}, pages={409–415} }
 @article{maran_mealey_lahmers_nelson_meurs_2013, title={Identification of DNA variants in the canine beta-1 adrenergic receptor gene}, volume={95}, ISSN={0034-5288}, url={http://dx.doi.org/10.1016/j.rvsc.2013.02.021}, DOI={10.1016/j.rvsc.2013.02.021}, abstractNote={Beta-adrenergic receptor antagonists are utilized for the management of several cardiac diseases in the dog. In humans the beneficial effects of beta-adrenergic receptor antagonists are variable and are associated with a genetic variability in the beta one adrenergic receptor gene (ADRB1). To determine if DNA variants were present in the canine ADRB1 gene, DNA from five breeds of dogs was evaluated. Two deletions were identified within the region of the gene that encodes the cytoplasmic tail of ADRB1. The functions of this region are not well understood although it is important in differentiating subtypes of adrenergic receptors and may be associated with control of receptor downregulation. The functional consequences of these identified variants deserve further study.}, number={1}, journal={Research in Veterinary Science}, publisher={Elsevier BV}, author={Maran, B.A. and Mealey, K.L. and Lahmers, S.M. and Nelson, O.L. and Meurs, K.M.}, year={2013}, month={Aug}, pages={238–240} }
 @article{meurs_lahmers_keene_white_oyama_mauceli_lindblad-toh_2012, title={A splice site mutation in a gene encoding for PDK4, a mitochondrial protein, is associated with the development of dilated cardiomyopathy in the Doberman pinscher}, volume={131}, ISSN={["1432-1203"]}, DOI={10.1007/s00439-012-1158-2}, abstractNote={Familial dilated cardiomyopathy is a primary myocardial disease that can result in the development of congestive heart failure and sudden cardiac death. Spontaneous animal models of familial dilated cardiomyopathy exist and the Doberman pinscher dog is one of the most commonly reported canine breeds. The objective of this study was to evaluate familial dilated cardiomyopathy in the Doberman pinscher dog using a genome-wide association study for a genetic alteration(s) associated with the development of this disease in this canine model. Genome-wide association analysis identified an area of statistical significance on canine chromosome 14 (p(raw) = 9.999e-05 corrected for genome-wide significance), fine-mapping of additional SNPs flanking this region localized a signal to 23,774,190-23,781,919 (p = 0.001) and DNA sequencing identified a 16-base pair deletion in the 5' donor splice site of intron 10 of the pyruvate dehydrogenase kinase 4 gene in affected dogs (p < 0.0001). Electron microscopy of myocardium from affected dogs demonstrated disorganization of the Z line, mild to moderate T tubule and sarcoplasmic reticulum dilation, marked pleomorphic mitochondrial alterations with megamitochondria, scattered mitochondria with whorling and vacuolization and mild aggregates of lipofuscin granules. In conclusion, we report the identification of a splice site deletion in the PDK4 gene that is associated with the development of familial dilated cardiomyopathy in the Doberman pinscher dog.}, number={8}, journal={HUMAN GENETICS}, author={Meurs, Kathryn M. and Lahmers, Sunshine and Keene, Bruce W. and White, Stephen N. and Oyama, Mark A. and Mauceli, Evan and Lindblad-Toh, Kerstin}, year={2012}, month={Aug}, pages={1319–1325} }
 @article{trafny_freeman_bulmer_macgregor_rush_meurs_oyama_2012, title={Auscultatory, echocardiographic, biochemical, nutritional, and environmental characteristics of mitral valve disease in Norfolk terriers}, volume={14}, ISSN={1760-2734}, url={http://dx.doi.org/10.1016/j.jvc.2011.10.002}, DOI={10.1016/j.jvc.2011.10.002}, abstractNote={In order to more fully understand degenerative mitral valve disease (DMVD) in the Norfolk terrier, we sought to characterize findings from the physical and echocardiographic examination; biochemical, biomarker, and nutritional profiles; and select environmental variables from a cohort of apparently healthy Norfolk terriers.Overtly healthy Norfolk terriers ≥ 6 yrs old were recruited by 3 different veterinary hospitals and underwent historical, physical, electrocardiographic (ECG), and 2D/color-flow Doppler echocardiographic examinations. Anterior mitral valve leaflet length, maximal thickness, area, and degree of prolapse were measured or calculated from two-dimensional images. Blood samples were obtained for serum biochemistry, serum serotonin, plasma NT-proBNP, amino acid profile, C-reactive protein, and cardiac troponin I.Of the 48 dogs entered into the study, 23 (48%) had murmurs, 2 (4%) had mid-systolic clicks, 11 (23%) had ECG P pulmonale, and 41 (85%) were deemed to have echocardiographic evidence of DMVD, including 18 Norfolk terriers without a murmur. Seven (15%), 28 (58%), and 13 (27%) dogs were classified as normal (stage 0), International Small Animal Cardiac Health Council (ISACHC) stage 1a, and 1b, respectively. Mean indexed echocardiographic mitral leaflet thickness (P = 0.017), area (P = 0.0002), prolapse (P = 0.0004), and left atrial to aortic diameter (P = 0.01) were significantly different between ISACHC 0, 1a, and 1b.DMVD is relatively common in Norfolk terriers and echocardiographic changes consistent with mild DMVD can be seen in dogs without a heart murmur.}, number={1}, journal={Journal of Veterinary Cardiology}, publisher={Elsevier BV}, author={Trafny, Dennis J. and Freeman, Lisa M. and Bulmer, Barret J. and MacGregor, John M. and Rush, John E. and Meurs, Kathryn M. and Oyama, Mark A.}, year={2012}, month={Mar}, pages={261–267} }
 @article{freeman_rush_meurs_bulmer_cunningham_2012, title={Body size and metabolic differences in Maine Coon cats with and without hypertrophic cardiomyopathy}, volume={15}, ISSN={1098-612X 1532-2750}, url={http://dx.doi.org/10.1177/1098612x12460847}, DOI={10.1177/1098612x12460847}, abstractNote={ An interplay between growth, glucose regulation and hypertrophic cardiomyopathy (HCM) may exist, but has not been studied in detail. The purpose of this study was to characterize morphometric features, insulin-like growth factor-1 (IGF-1) and glucose metabolism in Maine Coon cats with HCM. Body weight, body condition score (BCS), head length and width, and abdominal circumference were measured in Maine Coon cats >2 years of age. Echocardiography and thoracic radiography (for measurement of humerus length, and fourth and twelfth vertebrae length) were also performed. Blood was collected for biochemistry profile, DNA testing, insulin and IGF-1. Sixteen of 63 cats had HCM [myosin binding protein C (MYBPC)+, n = 3 and MYBPC−, n = 13] and 47/63 were echocardiographically normal (MYBPC+, n = 17 and MYBPC−, n = 30). There were no significant differences in any measured parameter between MYBPC+ and MYBPC− cats. Cats with HCM were significantly older ( P <0.001), heavier ( P = 0.006), more obese ( P = 0.008), and had longer humeri ( P = 0.02) compared with the HCM− group. Cats with HCM also had higher serum glucose ( P = 0.01), homeostasis model assessment (HOMA) and IGF-1 ( P = 0.01) concentrations, were from smaller litters ( P = 0.04), and were larger at 6 months ( P = 0.02) and at 1 year of age ( P = 0.03). Multivariate analysis revealed that age ( P <0.001), BCS ( P = 0.03) and HOMA ( P = 0.047) remained significantly associated with HCM. These results support the hypothesis that early growth and nutrition, larger body size and obesity may be environmental modifiers of genetic predisposition to HCM. Further studies are warranted to evaluate the effects of early nutrition on the phenotypic expression of HCM. }, number={2}, journal={Journal of Feline Medicine and Surgery}, publisher={SAGE Publications}, author={Freeman, Lisa M and Rush, John E and Meurs, Kathryn M and Bulmer, Barret J and Cunningham, Suzanne M}, year={2012}, month={Sep}, pages={74–80} }
 @article{stern_meurs_nelson_lahmers_lehmkuhl_2012, title={Familial subvalvular aortic stenosis in golden retrievers: inheritance and echocardiographic findings}, volume={53}, ISSN={0022-4510}, url={http://dx.doi.org/10.1111/j.1748-5827.2011.01187.x}, DOI={10.1111/j.1748-5827.2011.01187.x}, abstractNote={Objectives: To describe the echocardiographic findings and pedigree analysis of golden retrievers with subvalvular aortic stenosis.}, number={4}, journal={Journal of Small Animal Practice}, publisher={Wiley}, author={Stern, J. A. and Meurs, K. M. and Nelson, O. L. and Lahmers, S. M. and Lehmkuhl, L. B.}, year={2012}, month={Mar}, pages={213–216} }
 @article{silverman_stern_meurs_2012, title={Hypertrophic cardiomyopathy in the Sphynx cat: A retrospective evaluation of clinical presentation and heritable etiology}, volume={14}, ISSN={["1532-2750"]}, url={https://doi.org/10.1177/1098612X11435040}, DOI={10.1177/1098612x11435040}, abstractNote={Hypertrophic cardiomyopathy is an inherited disease in some feline breeds including the Maine Coon and Ragdoll. In these breeds, distinct causative genetic mutations have been identified. The two breeds appear to have slightly different clinical presentations, including age of diagnosis. The observation that these two breeds may have different clinical presentations, as well as different genetic mutations, suggests that hypertrophic cardiomyopathy is a diverse disease in the cat. Hypertrophic cardiomyopathy is poorly described in the Sphynx. The objective of this study was to phenotypically characterize Sphynx hypertrophic cardiomyopathy and to evaluate for a familial etiology. Records of 18 affected cats (11 female, seven male) were evaluated. Age of affected cats ranged from 0.5 to 7 years (median, 2 years). Four affected cats were from a single family and included an affected cat in each of four generations (three females, one male). Further studies are warranted to evaluate for a causative mutation and better classify the phenotypic expression.}, number={4}, journal={JOURNAL OF FELINE MEDICINE AND SURGERY}, author={Silverman, Sarah J. and Stern, Joshua A. and Meurs, Kathryn M.}, year={2012}, month={Apr}, pages={246–249} }
 @article{maran_meurs_lahmers_nelson_2012, title={Identification of beta-1 adrenergic receptor polymorphisms in cats}, volume={93}, ISSN={0034-5288}, url={http://dx.doi.org/10.1016/j.rvsc.2011.05.007}, DOI={10.1016/j.rvsc.2011.05.007}, abstractNote={In human beings, genetic polymorphisms within the beta-1 adrenergic receptor (ADRB1) gene have been associated with variable pharmacologic responses to beta blocker therapy. Beta-blockers are commonly given to cats with heart disease, particularly hypertrophic cardiomyopathy, a common cause of feline heart disease. We hypothesized that polymorphisms are present in the feline ADRB1 gene, which could result in an altered pharmacologic response to beta-blocker therapy. We sequenced the feline ADRB1 gene in 42 cats of five breeds. We identified three polymorphisms within the ADRB1 gene. Two polymorphisms did not change the amino acid produced and are unlikely to be clinically significant. A third polymorphism identified was an AA/CC substitution at the 830-831 base pair sites. This alteration changed the amino acid produced from proline to glutamine at position 277 and computer modeling predicts an altered protein structure. Further study is warranted to determine if this polymorphism alters response to beta blocker therapy.}, number={1}, journal={Research in Veterinary Science}, publisher={Elsevier BV}, author={Maran, B.A. and Meurs, K.M. and Lahmers, S.M. and Nelson, O.L.}, year={2012}, month={Aug}, pages={210–212} }
 @article{meurs_heaney_atkins_defrancesco_fox_keene_kellihan_miller_oyama_oaks_et al._2011, title={Comparison of Polymerase Chain Reaction with Bacterial 16s Primers to Blood Culture to Identify Bacteremia in Dogs with Suspected Bacterial Endocarditis}, volume={25}, ISSN={0891-6640}, url={http://dx.doi.org/10.1111/j.1939-1676.2011.0742.x}, DOI={10.1111/j.1939-1676.2011.0742.x}, abstractNote={Background:  Identification of the bacterial organism in dogs with endocarditis is challenging. Human studies have reported the utility of the polymerase chain reaction (PCR) to amplify and identify bacterial nucleic acid from infected valvular tissue and blood.}, number={4}, journal={Journal of Veterinary Internal Medicine}, publisher={Wiley}, author={Meurs, K.M. and Heaney, A.M. and Atkins, C.E. and DeFrancesco, T.C. and Fox, P.R. and Keene, B.W. and Kellihan, H.B. and Miller, M.W. and Oyama, M.A. and Oaks, J.L. and et al.}, year={2011}, month={Jun}, pages={959–962} }
 @article{stern_meurs_spier_koplitz_baumwart_2010, title={Ambulatory electrocardiographic evaluation of clinically normal adult Boxers}, volume={236}, ISSN={0003-1488}, url={http://dx.doi.org/10.2460/javma.236.4.430}, DOI={10.2460/javma.236.4.430}, abstractNote={Abstract}, number={4}, journal={Journal of the American Veterinary Medical Association}, publisher={American Veterinary Medical Association (AVMA)}, author={Stern, Joshua A. and Meurs, Kathryn M. and Spier, Alan W. and Koplitz, Shianne L. and Baumwart, Ryan D.}, year={2010}, month={Feb}, pages={430–433} }
 @article{lamb_meurs_hamlin_2010, title={Correlation of heart rate to body weight in apparently normal dogs}, volume={12}, ISSN={1760-2734}, url={http://dx.doi.org/10.1016/j.jvc.2010.04.001}, DOI={10.1016/j.jvc.2010.04.001}, abstractNote={To evaluate the correlation between heart rate and body weight in the apparently healthy dog. Sixty dogs weighing between 2 and 80 kg. Heart rate was evaluated with a 24-h ambulatory electrocardiogram. Minimum, average, maximum heart rate, ventricular premature complex (VPC) number and supraventricular premature complex (SVC) number were tabulated for each dog. Minimum, maximum and average heart rate did not correlate to body weight. For all dogs, the median minimum heart rate was 42 bpm (beats per minute), median average heart rate was 73 bpm, and median maximum heart rate was 190. The median number of VPCs and SVC was zero. The present study does not support a correlation between heart rate and body weight in apparently healthy dogs.}, number={2}, journal={Journal of Veterinary Cardiology}, publisher={Elsevier BV}, author={Lamb, Allison P. and Meurs, Kathryn M. and Hamlin, Robert L.}, year={2010}, month={Aug}, pages={107–110} }
 @article{meurs_kuan_2010, title={Differential methylation of CpG sites in two isoforms of myosin binding protein C, an important hypertrophic cardiomyopathy gene}, volume={52}, ISSN={0893-6692}, url={http://dx.doi.org/10.1002/em.20596}, DOI={10.1002/em.20596}, abstractNote={Abstract}, number={2}, journal={Environmental and Molecular Mutagenesis}, publisher={Wiley}, author={Meurs, Kathryn M. and Kuan, Mani}, year={2010}, month={Aug}, pages={161–164} }
 @inbook{meurs_2010, place={Philadelphia}, title={Genetic screening of familial hypertrophic cardiomyopathy}, booktitle={Consultations in Feline Internal Medicine}, publisher={WB Saunders}, author={Meurs, K.M.}, year={2010}, pages={406–408} }
 @article{meurs_2010, title={Genetics of Cardiac Disease in the Small Animal Patient}, volume={40}, ISSN={0195-5616}, url={http://dx.doi.org/10.1016/j.cvsm.2010.03.006}, DOI={10.1016/j.cvsm.2010.03.006}, abstractNote={There is increasing evidence that many forms of congenital and acquired cardiovascular disease in small animal patients are of familial origin. The large number of familial diseases in domestic purebred animals is thought to be associated with the desire to breed related animals to maintain a specific appearance and the selection of animals from a small group of popular founders (founder effect). Clinicians can use knowledge that a particular trait or disease may be inherited to provide guidance to owners and animal breeders to reduce the frequency of the trait. Even if the molecular cause is not known, identification of a pattern of inheritance and information on clinical screening can be useful for a breeder trying to make breeding decisions. Common forms of inheritance for veterinary diseases include autosomal recessive, autosomal dominant, X-linked recessive, and polygenic. These genetic traits and their possible involvement in cardiac disease in small animals are discussed in this article.}, number={4}, journal={Veterinary Clinics of North America: Small Animal Practice}, publisher={Elsevier BV}, author={Meurs, Kathryn M.}, year={2010}, month={Jul}, pages={701–715} }
 @article{meurs_mauceli_lahmers_acland_white_lindblad-toh_2010, title={Genome-wide association identifies a deletion in the 3′ untranslated region of Striatin in a canine model of arrhythmogenic right ventricular cardiomyopathy}, volume={128}, ISSN={0340-6717 1432-1203}, url={http://dx.doi.org/10.1007/s00439-010-0855-y}, DOI={10.1007/s00439-010-0855-y}, abstractNote={Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a familial cardiac disease characterized by ventricular arrhythmias and sudden cardiac death. It is most frequently inherited as an autosomal dominant trait with incomplete and age-related penetrance and variable clinical expression. The human disease is most commonly associated with a causative mutation in one of several genes encoding desmosomal proteins. We have previously described a spontaneous canine model of ARVC in the boxer dog. We phenotyped adult boxer dogs for ARVC by performing physical examination, echocardiogram and ambulatory electrocardiogram. Genome-wide association using the canine 50k SNP array identified several regions of association, of which the strongest resided on chromosome 17. Fine mapping and direct DNA sequencing identified an 8-bp deletion in the 3′ untranslated region (UTR) of the Striatin gene on chromosome 17 in association with ARVC in the boxer dog. Evaluation of the secondary structure of the 3′ UTR demonstrated that the deletion affects a stem loop structure of the mRNA and expression analysis identified a reduction in Striatin mRNA. Dogs that were homozygous for the deletion had a more severe form of disease based on a significantly higher number of ventricular premature complexes. Immunofluorescence studies localized Striatin to the intercalated disc region of the cardiac myocyte and co-localized it to three desmosomal proteins, Plakophilin-2, Plakoglobin and Desmoplakin, all involved in the pathogenesis of ARVC in human beings. We suggest that Striatin may serve as a novel candidate gene for human ARVC.}, number={3}, journal={Human Genetics}, publisher={Springer Science and Business Media LLC}, author={Meurs, Kathryn M. and Mauceli, Evan and Lahmers, Sunshine and Acland, Gregory M. and White, Stephen N. and Lindblad-Toh, Kerstin}, year={2010}, month={Jul}, pages={315–324} }
 @inbook{meurs_2010, place={Philadelphia}, edition={7th}, title={Primary myocardial disease in the dog}, booktitle={Textbook of Veterinary Internal Medicine}, publisher={WB Saunders}, author={Meurs, K.M.}, year={2010}, pages={1320–1328} }
 @article{craven_acland_mezey_boyko_wang_meurs_mcdonough_simpson_2010, title={W1250 Genome-Wide Association Scan Reveals Polymorphisms in the P67phox Subunit (Ncf2) of the NADPH Oxidase Complex in Boxer Dogs With Adherent and Invasive E.Coli-Associated Granulomatous Colitis: A Potential Model of Chronic Granulomatous Disease}, volume={138}, ISSN={0016-5085}, url={http://dx.doi.org/10.1016/S0016-5085(10)63141-1}, DOI={10.1016/S0016-5085(10)63141-1}, abstractNote={within the same year.Six of ten CD pairs shared similar smoking history (4 smokers, 2 exsmokers), and 6 of nine pairs were concordant for severity of disease.Of the five dizygotic twins with CD, disease location and behaviour were also identical in all twin pairs.In nine monozygotic twins with UC (4 females; 5 males), there was good agreement for the use of thiopurine (kappa 0.73; 95%CI 0.10, 1.00) and disease extent (5 total colitis; 1 distal colitis; 1 proctitis) (κappa 0.60; 95% CI 0.13, 1.00).Agreement was poor for disease severity, smoking status, need for steroids and extraintestinal symptoms in UC twins.UC twins were diagnosed at (mean±SEM) 5±1 years of each other.There was no concordance for colectomy in UC twins (2 patients out of 9 UC twin pairs).The majority of concordant IBD twins shared same bedrooms and attended the same school up to a median age of 17 years (range 9-24).CONCLUSION: Our findings suggest that age of disease onset, disease location and disease behaviour in CD, and disease extent in UC, but not extraintestinal manifestations, appeared to be strongly genetically-influenced.}, number={5}, journal={Gastroenterology}, publisher={Elsevier BV}, author={Craven, Melanie and Acland, Gregory M. and Mezey, Jason and Boyko, Adam and Wang, Wei and Meurs, Kathryn and McDonough, Sean and Simpson, Kenneth W.}, year={2010}, month={May}, pages={S-683} }
 @inbook{meurs_2009, title={Acquired Heart Diseases in Cattle}, ISBN={9781416035916}, url={http://dx.doi.org/10.1016/b978-141603591-6.10050-8}, DOI={10.1016/b978-141603591-6.10050-8}, booktitle={Food Animal Practice}, publisher={Elsevier}, author={Meurs, Kathryn M.}, year={2009}, pages={216–219} }
 @article{meurs_norgard_kuan_haggstrom_kittleson_2009, title={Analysis of 8 Sarcomeric Candidate Genes for Feline Hypertrophic Cardiomyopathy Mutations in Cats with Hypertrophic Cardiomyopathy}, volume={23}, ISSN={0891-6640 1939-1676}, url={http://dx.doi.org/10.1111/j.1939-1676.2009.0341.x}, DOI={10.1111/j.1939-1676.2009.0341.x}, abstractNote={Background:  Hypertrophic cardiomyopathy (HCM) is the most common heart disease in cats. Causative mutations have been identified in the Maine Coon (MC) and Ragdoll breed in the cardiac myosin binding protein C gene (MYBPC3). HCM is thought to be inherited in other breeds.}, number={4}, journal={Journal of Veterinary Internal Medicine}, publisher={Wiley}, author={Meurs, K.M. and Norgard, M.M. and Kuan, M. and Haggstrom, J. and Kittleson, M.}, year={2009}, month={Jul}, pages={840–843} }
 @inbook{meurs_spier_2009, place={Philadelphia}, title={Cardiomyopathy in the boxer dog}, booktitle={Current Veterinary Therapy (Small Animal Practice) XIV}, publisher={WB Saunders}, author={Meurs, K.M. and Spier, A.W.}, year={2009}, pages={797–799} }
 @inbook{meurs_2009, title={Congenital Heart Disease in Cattle}, ISBN={9781416035916}, url={http://dx.doi.org/10.1016/b978-141603591-6.10049-1}, DOI={10.1016/b978-141603591-6.10049-1}, booktitle={Food Animal Practice}, publisher={Elsevier}, author={Meurs, Kathryn M.}, year={2009}, pages={215–216} }
 @inbook{meurs_2009, title={Examination of the Bovine Patient with Heart Disease}, ISBN={9781416035916}, url={http://dx.doi.org/10.1016/b978-141603591-6.10048-x}, DOI={10.1016/b978-141603591-6.10048-x}, booktitle={Food Animal Practice}, publisher={Elsevier}, author={Meurs, Kathryn M.}, year={2009}, pages={214–215} }
 @article{baumwart_meurs_raman_2009, title={Magnetic Resonance Imaging of Right Ventricular Morphology and Function in Boxer Dogs with Arrhythmogenic Right Ventricular Cardiomyopathy}, volume={23}, ISSN={0891-6640 1939-1676}, url={http://dx.doi.org/10.1111/j.1939-1676.2008.0266.x}, DOI={10.1111/j.1939-1676.2008.0266.x}, abstractNote={Background:  Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a myocardial disease characterized by fibrofatty replacement of the right ventricle and ventricular tachyarrhythmias, reported most commonly in the Boxer dog. Although ARVC is characterized as a myocardial disease, the impact of the disease on the function of the right ventricle has not been well studied.}, number={2}, journal={Journal of Veterinary Internal Medicine}, publisher={Wiley}, author={Baumwart, R.D. and Meurs, K.M. and Raman, S.V.}, year={2009}, month={Mar}, pages={271–274} }
 @article{scansen_meurs_spier_koplitz_baumwart_2009, title={Temporal Variability of Ventricular Arrhythmias in Boxer Dogs with Arrhythmogenic Right Ventricular Cardiomyopathy}, volume={23}, ISSN={0891-6640 1939-1676}, url={http://dx.doi.org/10.1111/j.1939-1676.2009.0366.x}, DOI={10.1111/j.1939-1676.2009.0366.x}, abstractNote={Background:  Arrhythmogenic right ventricular cardiomyopathy (ARVC) is prevalent in the Boxer. There is little information on the temporal variability of ventricular arrhythmias within affected dogs.}, number={5}, journal={Journal of Veterinary Internal Medicine}, publisher={Wiley}, author={Scansen, B.A. and Meurs, K.M. and Spier, A.W. and Koplitz, S. and Baumwart, R.D.}, year={2009}, month={Sep}, pages={1020–1024} }
 @inbook{calvert_meurs_2009, place={Philadelphia}, title={Update on Doberman pinscher cardiomyopathy}, booktitle={Current Veterinary Therapy (Small Animal Practice) XIV}, publisher={WB Saunders}, author={Calvert, C. and Meurs, K.M.}, year={2009}, pages={800–803} }
 @article{baumwart_meurs_2008, title={An index of myocardial performance applied to the right ventricle of Boxers with arrhythmogenic right ventricular cardiomyopathy}, volume={69}, ISSN={0002-9645}, url={http://dx.doi.org/10.2460/ajvr.69.8.1029}, DOI={10.2460/ajvr.69.8.1029}, abstractNote={Abstract}, number={8}, journal={American Journal of Veterinary Research}, publisher={American Veterinary Medical Association (AVMA)}, author={Baumwart, Ryan D. and Meurs, Kathryn M.}, year={2008}, month={Aug}, pages={1029–1033} }
 @article{oyama_reiken_lehnart_chittur_meurs_stern_marks_2008, title={Arrhythmogenic right ventricular cardiomyopathy in Boxer dogs is associated with calstabin2 deficiency}, volume={10}, ISSN={1760-2734}, url={http://dx.doi.org/10.1016/j.jvc.2008.04.003}, DOI={10.1016/j.jvc.2008.04.003}, abstractNote={To examine the presence and effect of calstabin2-deficiency in Boxer dogs with arrhythmogenic right ventricular cardiomyopathy (ARVC).Thirteen Boxer dogs with ARVC.Tissue samples were collected for histopathology, oligonucleotide microarray, PCR, immunoelectrophoresis, ryanodine channel immunoprecipitation and single-channel recordings, and calstabin2 DNA sequencing.In cardiomyopathic Boxer dogs, myocardial calstabin2 mRNA and protein were significantly decreased as compared to healthy control dogs (calstabin2 protein normalized to tetrameric cardiac ryanodine receptor (RyR2) complex: affected, 0.51+/-0.04; control, 3.81+/-0.22; P<0.0001). Calstabin2 deficiency in diseased dog hearts was associated with a significantly increased open probability of single RyR2 channels indicating intracellular Ca(2+) leak. PCR-based sequencing of the promoter, exonic and splice site regions of the canine calstabin2 gene did not identify any causative mutations.Calstabin2 deficiency is a potential mechanism of Ca(2+) leak-induced ventricular arrhythmias and heart disease in Boxer dogs with ARVC.}, number={1}, journal={Journal of Veterinary Cardiology}, publisher={Elsevier BV}, author={Oyama, Mark A. and Reiken, Steve and Lehnart, Stephan E. and Chittur, Sridar V. and Meurs, Kathryn M. and Stern, Joshua and Marks, Andrew R.}, year={2008}, month={Jun}, pages={1–10} }
 @article{mealey_meurs_2008, title={Breed distribution of the ABCB1-1Δ (multidrug sensitivity) polymorphism among dogs undergoing ABCB1 genotyping}, volume={233}, ISSN={0003-1488}, url={http://dx.doi.org/10.2460/javma.233.6.921}, DOI={10.2460/javma.233.6.921}, abstractNote={Abstract}, number={6}, journal={Journal of the American Veterinary Medical Association}, publisher={American Veterinary Medical Association (AVMA)}, author={Mealey, Katrina L. and Meurs, Kathryn M.}, year={2008}, month={Sep}, pages={921–924} }
 @article{meurs_mealey_2008, title={Evaluation of the flanking nucleotide sequences of sarcomeric hypertrophic cardiomyopathy substitution mutations}, volume={642}, ISSN={0027-5107}, url={http://dx.doi.org/10.1016/j.mrfmmm.2008.04.005}, DOI={10.1016/j.mrfmmm.2008.04.005}, abstractNote={Hypertrophic cardiomyopathy (HCM) is a familial myocardial disease with a prevalence of 1 in 500. More than 400 causative mutations have been identified in 13 sarcomeric and myofilament related genes, 350 of these are substitution mutations within eight sarcomeric genes. Within a population, examples of recurring identical disease causing mutations that appear to have arisen independently have been noted as well as those that appear to have been inherited from a common ancestor. The large number of novel HCM mutations could suggest a mechanism of increased mutability within the sarcomeric genes. The objective of this study was to evaluate the most commonly reported HCM genes, beta myosin heavy chain (MYH7), myosin binding protein C, troponin I, troponin T, cardiac regulatory myosin light chain, cardiac essential myosin light chain, alpha tropomyosin and cardiac alpha-actin for sequence patterns surrounding the substitution mutations that may suggest a mechanism of increased mutability. The mutations as well as the 10 flanking nucleotides were evaluated for frequency of di-, tri- and tetranucleotides containing the mutation as well as for the presence of certain tri- and tetranculeotide motifs. The most common substitutions were guanine (G) to adenine (A) and cytosine (C) to thymidine (T). The CG dinucleotide had a significantly higher relative mutability than any other dinucleotide (p < 0.05). The relative mutability of each possible trinucleotide and tetranucleotide sequence containing the mutation was calculated; none were at a statistically higher frequency than the others. The large number of G to A and C to T mutations as well as the relative mutability of CG may suggest that deamination of methylated CpG is an important mechanism for mutation development in at least some of these cardiac genes.}, number={1-2}, journal={Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis}, publisher={Elsevier BV}, author={Meurs, Kathryn M. and Mealey, Katrina L.}, year={2008}, month={Jul}, pages={86–89} }
 @article{meurs_hendrix_norgard_2008, title={Molecular evaluation of five cardiac genes in Doberman Pinschers with dilated cardiomyopathy}, volume={69}, ISSN={0002-9645}, url={http://dx.doi.org/10.2460/ajvr.69.8.1050}, DOI={10.2460/ajvr.69.8.1050}, abstractNote={Abstract}, number={8}, journal={American Journal of Veterinary Research}, publisher={American Veterinary Medical Association (AVMA)}, author={Meurs, Kathryn M. and Hendrix, Kristina P. and Norgard, Michelle M.}, year={2008}, month={Aug}, pages={1050–1053} }
 @article{smith_freeman_meurs_rush_lamb_2008, title={Plasma fatty acid concentrations in Boxers and Doberman Pinschers}, volume={69}, DOI={10.2460/ajvr.69.2.195}, abstractNote={Abstract}, number={2}, journal={American Journal of Veterinary Research}, author={Smith, C.E. and Freeman, L.M. and Meurs, K.M. and Rush, J.E. and Lamb, A.}, year={2008}, pages={195–198} }
 @article{fries_heaney_meurs_2008, title={Prevalence of the Myosin-Binding Protein C Mutation in Maine Coon Cats}, volume={22}, ISSN={0891-6640 1939-1676}, url={http://dx.doi.org/10.1111/j.1939-1676.2008.0113.x}, DOI={10.1111/j.1939-1676.2008.0113.x}, abstractNote={Background:  An autosomal dominant mutation has been identified in the myosin‐binding protein C (MYBPC3) gene of Maine Coon cats. This mutation changes a conserved amino acid and computationally alters the protein conformation of this gene in Maine Coon cats with hypertrophic cardiomyopathy. The prevalence of this mutation is unknown.}, number={4}, journal={Journal of Veterinary Internal Medicine}, publisher={Wiley}, author={Fries, R. and Heaney, A.M. and Meurs, K.M.}, year={2008}, month={Jul}, pages={893–896} }
 @article{meurs_fox_norgard_spier_lamb_koplitz_baumwart_2007, title={A Prospective Genetic Evaluation of Familial Dilated Cardiomyopathy in the Doberman Pinscher}, volume={21}, ISSN={0891-6640 1939-1676}, url={http://dx.doi.org/10.1111/j.1939-1676.2007.tb03058.x}, DOI={10.1111/j.1939-1676.2007.tb03058.x}, abstractNote={ Background: The Doberman Pinscher is one of the most common breeds of dogs to develop dilated cardiomyopathy (DCM), a primary heart muscle disorder characterized by myocardial dysfunction, cardiac arrhythmias, and congestive heart failure. In the Doberman Pinscher, the disease is typically adult onset, and a familial etiology has been suggested.}, number={5}, journal={Journal of Veterinary Internal Medicine}, publisher={Wiley}, author={Meurs, Kathryn M. and Fox, Philip R. and Norgard, Michelle and Spier, Alan W. and Lamb, Allison and Koplitz, Shianne L. and Baumwart, Ryan D.}, year={2007}, month={Sep}, pages={1016–1020} }
 @article{meurs_norgard_ederer_hendrix_kittleson_2007, title={A substitution mutation in the myosin binding protein C gene in ragdoll hypertrophic cardiomyopathy}, volume={90}, ISSN={0888-7543}, url={http://dx.doi.org/10.1016/j.ygeno.2007.04.007}, DOI={10.1016/j.ygeno.2007.04.007}, abstractNote={Familial hypertrophic cardiomyopathy (HCM) is a primary myocardial disease with a prevalence of 1 in 500 in human beings. Causative mutations have been identified in several sarcomeric genes, including the cardiac myosin binding protein C (MYBPC3) gene. Heritable HCM also exists in a large-animal model, the cat, and we have previously reported a mutation in the MYBPC3 gene in the Maine coon breed. We now report a separate mutation in the MYBPC3 gene in ragdoll cats with HCM. The mutation changes a conserved arginine to tryptophan and appears to alter the protein structure. The ragdoll is not related to the Maine coon and the mutation identified is in a domain different from that of the previously identified feline mutation. The identification of two separate mutations within this gene in unrelated breeds suggests that these mutations occurred independently rather than being passed on from a common founder.}, number={2}, journal={Genomics}, publisher={Elsevier BV}, author={Meurs, Kathryn M. and Norgard, Michelle M. and Ederer, Martina M. and Hendrix, Kristina P. and Kittleson, Mark D.}, year={2007}, month={Aug}, pages={261–264} }
 @inbook{meurs_2007, place={Ames}, title={Boxer Cardiomyopathy}, booktitle={Five Minute Veterinary Consult}, publisher={Blackwell Publishing}, author={Meurs, K.M.}, year={2007}, pages={206–208} }
 @article{meurs_ederer_stern_2007, title={Desmosomal gene evaluation in Boxers with arrhythmogenic right ventricular cardiomyopathy}, volume={68}, ISSN={0002-9645}, url={http://dx.doi.org/10.2460/ajvr.68.12.1338}, DOI={10.2460/ajvr.68.12.1338}, abstractNote={Abstract}, number={12}, journal={American Journal of Veterinary Research}, publisher={American Veterinary Medical Association (AVMA)}, author={Meurs, Kathryn M. and Ederer, Martina M. and Stern, Joshua A.}, year={2007}, month={Dec}, pages={1338–1341} }
 @article{koffas_fuentes_boswood_connolly_brockman_bonagura_meurs_koplitz_baumwart_2007, title={Double Chambered Right Ventricle in 9 Cats}, volume={21}, ISSN={0891-6640 1939-1676}, url={http://dx.doi.org/10.1111/j.1939-1676.2007.tb02931.x}, DOI={10.1111/j.1939-1676.2007.tb02931.x}, abstractNote={ Background: Double‐chambered right ventricle (DCRV) is a frequently recognized cardiac congenital abnormality in humans. It has been described in dogs and in 1 cat. However systemic description of clinical and echocardiographic features of the disease in cats is currently lacking from the veterinary literature.}, number={1}, journal={Journal of Veterinary Internal Medicine}, publisher={Wiley}, author={Koffas, H. and Fuentes, V. Luis and Boswood, A. and Connolly, D.J. and Brockman, D.J. and Bonagura, J.D. and Meurs, K.M. and Koplitz, S. and Baumwart, R.}, year={2007}, month={Jan}, pages={76–80} }
 @article{baumwart_orvalho_meurs_2007, title={Evaluation of serum cardiac troponin I concentration in Boxers with arrhythmogenic right ventricular cardiomyopathy}, volume={68}, ISSN={0002-9645}, url={http://dx.doi.org/10.2460/ajvr.68.5.524}, DOI={10.2460/ajvr.68.5.524}, abstractNote={Abstract}, number={5}, journal={American Journal of Veterinary Research}, publisher={American Veterinary Medical Association (AVMA)}, author={Baumwart, Ryan D. and Orvalho, João and Meurs, Kathryn M.}, year={2007}, month={May}, pages={524–528} }
 @inbook{meurs_2007, place={Ames}, title={Lamb A Ambulatory electrocardiography}, booktitle={Five-Minute Veterinary Consult}, publisher={Diagnostic Procedures and Laboratory Tests Blackwell Publishing}, author={Meurs, K.M.}, year={2007}, pages={312–314} }
 @article{atkins_keene_brown_coats_crawford_defrancesco_edwards_fox_lehmkuhl_luethy_et al._2007, title={Results of the veterinary enalapril trial to prove reduction in onset of heart failure in dogs chronically treated with enalapril alone for compensated, naturally occurring mitral valve insufficiency}, volume={231}, ISSN={0003-1488}, url={http://dx.doi.org/10.2460/javma.231.7.1061}, DOI={10.2460/javma.231.7.1061}, abstractNote={Abstract}, number={7}, journal={Journal of the American Veterinary Medical Association}, publisher={American Veterinary Medical Association (AVMA)}, author={Atkins, Clarke E. and Keene, Bruce W. and Brown, William A. and Coats, Julie R. and Crawford, Mary Ann and DeFrancesco, Teresa C. and Edwards, N. Joel and Fox, Phillip R. and Lehmkuhl, Linda B. and Luethy, Michael W. and et al.}, year={2007}, month={Oct}, pages={1061–1069} }
 @article{macdonald_kittleson_kass_meurs_2007, title={Tissue Doppler Imaging in Maine Coon Cats with a Mutation of Myosin Binding Protein C with or without Hypertrophy}, volume={21}, DOI={10.1111/j.1939-1676.2007.tb02954.x}, abstractNote={Background: The cardiac myosin binding protein C gene is mutated in Maine Coon (MC) cats with familial hypertrophic cardiomyopathy.}, number={2}, journal={Journal of Veterinary Internal Medicine}, author={MacDonald, K.M. and Kittleson, M.D. and Kass, P.H. and Meurs, K.M.}, year={2007}, month={Mar}, pages={232–237} }
 @article{miller_gordon_saunders_arsenault_meurs_lehmkuhl_bonagura_fox_2006, title={Angiographic classification of patent ductus arteriosus morphology in the dog}, volume={8}, ISSN={1760-2734}, url={http://dx.doi.org/10.1016/j.jvc.2006.07.001}, DOI={10.1016/j.jvc.2006.07.001}, abstractNote={To characterize angiographic morphology and minimum internal transverse diameter of left-to-right shunting patent ductus arteriosus (PDA) in a large series of dogs. PDA is the most common congenital cardiac malformation in the dog. Transarterial ductal occlusion is increasingly performed to close this defect. While accurate assessment of ductal morphology and luminal diameter is important to assure optimal occlusion using catheter-delivered devices, such information is currently limited. In 246 dogs representing 31 breeds with left-to-right shunting PDA, right lateral selective aortic angiograms were recorded and reviewed. PDA morphology conformed to four general phenotypes (types I, IIA, IIB, and III) which varied according to degree of ductal tapering, and the presence, absence, or location of abrupt ductal narrowing. Minimum internal ductal diameter for all dogs averaged 2.9 mm (median, 2.5 mm; range, 1.0–9.5 mm) and was not correlated to age or body weight. There was no significant difference in minimum internal diameters between types I, IIA or IIB PDA, whereas, type III PDA was significantly wider (p = 0.024) than other phenotypes. The most frequently-encountered variant (type IIA) was identified in 54.4% of cases (average minimum internal diameter, 2.3 mm [median, 2.2 mm; range, 1.0–5.5 mm]). PDA angiographic morphology was categorized based upon the degree, presence, or absence of ductal narrowing, and the location of ductal attenuation. When planning PDA repair, this information should assist planning, selection and deployment of transcatheter occluding devices.}, number={2}, journal={Journal of Veterinary Cardiology}, publisher={Elsevier BV}, author={Miller, Matthew W. and Gordon, Sonya G. and Saunders, Ashley B. and Arsenault, Wendy G. and Meurs, Kathryn M. and Lehmkuhl, Linda B. and Bonagura, John D. and Fox, Philip R.}, year={2006}, month={Nov}, pages={109–114} }
 @article{meurs_lacombe_dryburgh_fox_reiser_kittleson_2006, title={Differential expression of the cardiac ryanodine receptor in normal and arrhythmogenic right ventricular cardiomyopathy canine hearts}, volume={120}, ISSN={0340-6717 1432-1203}, url={http://dx.doi.org/10.1007/s00439-006-0193-2}, DOI={10.1007/s00439-006-0193-2}, abstractNote={Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a form of cardiomyopathy characterized by ventricular tachyarrhythmias and a fibrofatty infiltrate that is believed to preferentially affect the right ventricle. Mutations in the cardiac ryanodine receptor (RyR2) gene have been identified in some human families with a unique form of ARVC, ARVC2. Although the RyR2 has significant importance in excitation-contraction coupling across the ventricles, mutations in the gene encoding for it appear to have the greatest impact on the right ventricle in ARVC2. Using a canine model (boxer), the RyR2 protein and message RNA in the right ventricle, left ventricle and interventricular septum from normal dogs and dogs with ARVC were investigated by immunoblotting and real time PCR. The cardiac RyR2 message and protein expression were differentially expressed across the cardiac walls in the normal heart, with the lowest concentration expressed in the right ventricle (P < 0.05). The message and protein expression of the RyR2 were reduced in all chambers in the canine model of ARVC. We propose that the increased susceptibility of the right ventricle to ARVC may be associated with the lower baseline protein concentration of RyR2 in the normal right ventricle compared to the left ventricle and interventricular septum and that all three areas are equally affected in this canine model of ARVC. Using this naturally occurring model of canine ARVC, we may have provided new insights into the pathogenesis of this cardiomyopathy.}, number={1}, journal={Human Genetics}, publisher={Springer Science and Business Media LLC}, author={Meurs, Kathryn M. and Lacombe, Veronique A. and Dryburgh, Keith and Fox, Philip R. and Reiser, Peter R. and Kittleson, Mark D.}, year={2006}, month={May}, pages={111–118} }
 @article{koplitz_meurs_bonagura_2006, title={Echocardiographic Assessment of the Left Ventricular Outflow Tract in the Boxer}, volume={20}, ISSN={0891-6640 1939-1676}, url={http://dx.doi.org/10.1111/j.1939-1676.2006.tb01804.x}, DOI={10.1111/j.1939-1676.2006.tb01804.x}, abstractNote={Background: Soft, variable ejection murmurs are common in Boxers and are associated with increased left ventricular outflow tract (LVOT) ejection velocities. Whether these murmurs are physiologic or indicate mild aortic stenosis is controversial. Ejection velocity is impacted by LVOT area and ventricular stroke volume (SV), suggesting that these variables are pertinent to murmur development.}, number={4}, journal={Journal of Veterinary Internal Medicine}, publisher={Wiley}, author={Koplitz, S.L. and Meurs, K.M. and Bonagura, J.D.}, year={2006}, month={Jul}, pages={904–911} }
 @article{parker_meurs_ostrander_2006, title={Finding cardiovascular disease genes in the dog}, volume={8}, ISSN={1760-2734}, url={http://dx.doi.org/10.1016/j.jvc.2006.04.002}, DOI={10.1016/j.jvc.2006.04.002}, abstractNote={Recent advances in canine genomics are changing the landscape of veterinary biology, and by default, veterinary medicine. No longer are clinicians locked into traditional methods of diagnoses and therapy. Rather, major advances in canine genetics and genomics from the past five years are now changing the way the veterinarian of the 21st century practices medicine. First, the availability of a dense genome map gives canine genetics a much-needed foothold in comparative medicine, allowing advances made in human and mouse genetics to be applied to companion animals. Second, the recently released 7.5x whole genome sequence of the dog is facilitating the identification of hereditary disease genes. Finally, development of genetic tools for rapid screening of families and populations at risk for inherited disease means that the cost of identifying and testing for disease loci will significantly decrease in coming years. Out of these advances will come major changes in companion animal diagnostics and therapy. Clinicians will be able to offer their clients genetic testing and counseling for a myriad of disorders. In this review we summarize recent findings in canine genomics and discuss their application to the study of canine cardiac health.}, number={2}, journal={Journal of Veterinary Cardiology}, publisher={Elsevier BV}, author={Parker, Heidi G. and Meurs, Kathryn M. and Ostrander, Elaine A.}, year={2006}, month={Nov}, pages={115–127} }
 @article{meurs_sanchez_david_bowles_towbin_reiser_kittleson_munro_dryburgh_macdonald_et al._2005, title={A cardiac myosin binding protein C mutation in the Maine Coon cat with familial hypertrophic cardiomyopathy}, volume={14}, DOI={10.1093/hmg/ddi386}, abstractNote={Hypertrophic cardiomyopathy (HCM) is one of the most common causes of sudden cardiac death in young adults and is a familial disease in at least 60% of cases. Causative mutations have been identified in several sarcomeric genes, including the myosin binding protein C (MYBPC3) gene. Although numerous causative mutations have been identified, the pathogenetic process is still poorly understood. A large animal model of familial HCM in the cat has been identified and may be used for additional study. As the first spontaneous large animal model of this familial disease, feline familial HCM provides a valuable model for investigators to evaluate pathophysiologic processes and therapeutic (pharmacologic or genetic) manipulations. The MYBPC3 gene was chosen as a candidate gene in this model after identifying a reduction in the protein in myocardium from affected cats in comparison to control cats (P<0.001). DNA sequencing was performed and sequence alterations were evaluated for evidence that they changed the amino acid produced, that the amino acid was conserved and that the protein structure was altered. We identified a single base pair change (G to C) in the feline MYBPC3 gene in affected cats that computationally alters the protein conformation of this gene and results in sarcomeric disorganization. We have identified a causative mutation in the feline MYBPC3 gene that results in the development of familial HCM. This is the first report of a spontaneous mutation causing HCM in a non-human species. It should provide a valuable model for evaluating pathophysiologic processes and therapeutic manipulations.}, number={23}, journal={Human Molecular Genetics}, author={Meurs, K.M. and Sanchez, X. and David, R.M. and Bowles, N.E. and Towbin, J.A. and Reiser, P.J. and Kittleson, J.A. and Munro, M.J. and Dryburgh, K. and MacDonald, K.A. and et al.}, year={2005}, month={Dec}, pages={3587–3593} }
 @article{baumwart_meurs_2005, title={Assessment of plasma brain natriuretic peptide concentration in Boxers with arrhythmogenic right ventricular cardiomyopathy}, volume={66}, ISSN={0002-9645}, url={http://dx.doi.org/10.2460/ajvr.2005.66.2086}, DOI={10.2460/ajvr.2005.66.2086}, abstractNote={Abstract}, number={12}, journal={American Journal of Veterinary Research}, publisher={American Veterinary Medical Association (AVMA)}, author={Baumwart, Ryan D. and Meurs, Kathryn M.}, year={2005}, month={Dec}, pages={2086–2089} }
 @inbook{meurs_2005, place={Philadelphia}, edition={6th}, title={Canine Myocardial Disease}, booktitle={Textbook of Veterinary Internal Medicine}, publisher={WB Saunders}, author={Meurs, K.M.}, year={2005}, pages={1077–1081} }
 @article{baumwart_meurs_atkins_bonagura_defrancesco_keene_koplitz_fuentes_miller_rausch_et al._2005, title={Clinical, echocardiographic, and electrocardiographic abnormalities in Boxers with cardiomyopathy and left ventricular systolic dysfunction: 48 cases (1985-2003)}, volume={226}, ISSN={0003-1488}, url={http://dx.doi.org/10.2460/javma.2005.226.1102}, DOI={10.2460/javma.2005.226.1102}, abstractNote={Abstract}, number={7}, journal={Journal of the American Veterinary Medical Association}, publisher={American Veterinary Medical Association (AVMA)}, author={Baumwart, R.B. and Meurs, K.M. and Atkins, C.E. and Bonagura, J.D. and DeFrancesco, T.C. and Keene, B.W. and Koplitz, S. and Fuentes, V. L. and Miller, M.W. and Rausch, W. and et al.}, year={2005}, pages={1102–1104} }
 @inbook{stabej_meurs_van oost_2005, title={Molecular genetics of dilated cardiomyaopthy in the dog}, booktitle={Canine Genetics}, publisher={Cold Spring Harbor}, author={Stabej, P. and Meurs, K.M. and van Oost, B.A.}, year={2005}, pages={365–382} }
 @article{meurs_lehmkuhl_bonagura_2005, title={Survival times in dogs with severe subvalvular aortic stenosis treated with balloon valvuloplasty or atenolol}, volume={227}, ISSN={0003-1488}, url={http://dx.doi.org/10.2460/javma.2005.227.420}, DOI={10.2460/javma.2005.227.420}, abstractNote={Abstract}, number={3}, journal={Journal of the American Veterinary Medical Association}, publisher={American Veterinary Medical Association (AVMA)}, author={Meurs, Kathryn M. and Lehmkuhl, Linda B. and Bonagura, John D.}, year={2005}, month={Aug}, pages={420–424} }
 @article{baumwart_meurs_bonagura_2005, title={Tei Index of Myocardial Performance Applied to the Right Ventricle in Normal Dogs}, volume={19}, ISSN={0891-6640 1939-1676}, url={http://dx.doi.org/10.1111/j.1939-1676.2005.tb02772.x}, DOI={10.1111/j.1939-1676.2005.tb02772.x}, abstractNote={Right ventricular (RV) dysfunction is a cause of exercise intolerance, hypotension, syncope, and heart failure in dogs with cardiac and respiratory disorders. The study objective was to determine Doppler-derived reference values that reflect global RV function in healthy dogs. We measured systolic time intervals and an RV index of myocardial performance (IMP) in 45 healthy dogs between 8 months and 8 years of age. Pulsed-wave Doppler recordings of mitral, tricuspid, aortic, and pulmonic were acquired. Pre-ejection period (PEP), ejection time (ET), PEP/ET, and IMP were determined for both ventricles by separate cardiac cycles. Compared to the mean left ventricular (LV) IMP (0.410; 95% confidence intervals [CI] 0.378-0.442), mean RV IMP (0.250; 95% CI 0.222-0.278) was significantly smaller, and mean ET for the RV (187 millisecond [ms]; 95% CI 182-192) was significantly longer than the LV (173 ms; 95% CI 168-179). A clinically relevant correlation was not found among RV IMP and body weight, heart rate, RV ET, RV PEP, or RV PEP/ET. Calculation of LV IMP with 2 separate sample volumes yielded smaller values than from a single sample volume, with a difference in means of 0.040. We conclude that the RV IMP is relatively independent of body weight and heart rate within the ranges studied and is consistently lower than values derived from the LV in healthy dogs. This study provides additional reference values for RV function in dogs and may be useful for identification of RV dysfunction in dogs.}, number={6}, journal={Journal of Veterinary Internal Medicine}, publisher={Wiley}, author={Baumwart, Ryan D. and Meurs, Kathryn M. and Bonagura, John D.}, year={2005}, month={Nov}, pages={828–832} }
 @article{basso_fox_meurs_towbin_spier_calabrese_maron_thiene_2004, title={Arrhythmogenic Right Ventricular Cardiomyopathy Causing Sudden Cardiac Death in Boxer Dogs}, volume={109}, ISSN={0009-7322 1524-4539}, url={http://dx.doi.org/10.1161/01.cir.0000118494.07530.65}, DOI={10.1161/01.cir.0000118494.07530.65}, abstractNote={Background—Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a primary familial heart muscle disease associated with substantial cardiovascular morbidity and risk of sudden death. Efforts to discern relevant pathophysiological mechanisms have been impaired by lack of a suitable animal model.}, number={9}, journal={Circulation}, publisher={Ovid Technologies (Wolters Kluwer Health)}, author={Basso, Cristina and Fox, Philip R. and Meurs, Kathryn M. and Towbin, Jeffrey A. and Spier, Alan W. and Calabrese, Fiorella and Maron, Barry J. and Thiene, Gaetano}, year={2004}, month={Mar}, pages={1180–1185} }
 @article{spier_meurs_2004, title={Assessment of heart rate variability in Boxers with arrhythmogenic right ventricular cardiomyopathy}, volume={224}, ISSN={0003-1488}, url={http://dx.doi.org/10.2460/javma.2004.224.534}, DOI={10.2460/javma.2004.224.534}, abstractNote={Abstract}, number={4}, journal={Journal of the American Veterinary Medical Association}, publisher={American Veterinary Medical Association (AVMA)}, author={Spier, Alan W. and Meurs, Kathryn M.}, year={2004}, month={Feb}, pages={534–537} }
 @article{meurs_2004, title={Boxer dog cardiomyopathy: an update}, volume={34}, ISSN={0195-5616}, url={http://dx.doi.org/10.1016/j.cvsm.2004.05.003}, DOI={10.1016/j.cvsm.2004.05.003}, abstractNote={Dilated cardiomyopathy (DCM) is the most common cardiac disease in large breed dogs. The disease can start with arrhythmias or with systolic dysfunction of the myocardium.To describe screening methods for DCM in various breeds and provide a new, modified staging system.Screening for occult DCM should start at three years of age and use Holter monitoring in Boxers and Dobermans and might be useful also in other breeds. Single ventricular premature complexes (VPCs) can be detected in many healthy dogs, but healthy animals typically have <50 VPCs in 24 h and demonstrate minimal complexity most often occurring only as single ectopic beats. In general, >100 VPCs in 24 h was recommended as the cut-off value for establishing a diagnosis of DCM. However, there are breed-specific recommendations related to Holter recording diagnosis of DCM in Dobermans and Boxers. Yearly screening over the life of a dog is recommended, as a one-time screening is not sufficient to rule out the future development of DCM. Several echocardiographic methods such as M-mode derived measurements, the measurement of the left ventricular (LV) volume by Simpson's method of discs (SMOD), and E-point to septal separation (EPSS) are recommended for screening purposes. The value of additional tests such as cardiac biomarkers (troponin I and N-terminal pro-B-type natriuretic peptide) as well as a 5-min resting electrocardiogram (ECG) or newer echocardiographic methods such as strain measurements is discussed.This review suggests some guidelines for screening for DCM in various breeds.}, number={5}, journal={Veterinary Clinics of North America: Small Animal Practice}, publisher={Elsevier BV}, author={Meurs, Kathryn M.}, year={2004}, month={Sep}, pages={1235–1244} }
 @article{kraus_calvert_spier_meurs_anderson_2004, title={Determination of electrocardiographic parameters in healthy llamas and alpacas}, volume={65}, ISSN={0002-9645}, url={http://dx.doi.org/10.2460/ajvr.2004.65.1719}, DOI={10.2460/ajvr.2004.65.1719}, abstractNote={Abstract}, number={12}, journal={American Journal of Veterinary Research}, publisher={American Veterinary Medical Association (AVMA)}, author={Kraus, Marc S. and Calvert, Clay A. and Spier, Alan W. and Meurs, Kathryn M. and Anderson, David E.}, year={2004}, month={Dec}, pages={1719–1723} }
 @article{spier_meurs_2004, title={Evaluation of spontaneous variability in the frequency of ventricular arrhythmias in Boxers with arrhythmogenic right ventricular cardiomyopathy}, volume={224}, ISSN={0003-1488}, url={http://dx.doi.org/10.2460/javma.2004.224.538}, DOI={10.2460/javma.2004.224.538}, abstractNote={Abstract}, number={4}, journal={Journal of the American Veterinary Medical Association}, publisher={American Veterinary Medical Association (AVMA)}, author={Spier, Alan W. and Meurs, Kathryn M.}, year={2004}, month={Feb}, pages={538–541} }
 @article{davainis_meurs_wright_2004, title={The Relationship of Resting S-T Segment Depression to the Severity of Subvalvular Aortic Stenosis and the Presence of Ventricular Premature Complexes in the Dog}, volume={40}, ISSN={0587-2871 1547-3317}, url={http://dx.doi.org/10.5326/0400020}, DOI={10.5326/0400020}, abstractNote={Electrocardiograms (ECG) from 35 dogs with subvalvular aortic stenosis (SAS) with a left ventricular outflow tract pressure gradient (PG) of ≥50 mm Hg were retrospectively evaluated for S-T segment depression (STD, ≥0.2 mV in lead II). Pressure gradient, age, heart rate (HR), and number of ventricular premature complexes (VPCs) on a 24-hour ambulatory ECG for dogs with STD were not significantly different from those for dogs without STD. The S-T segment deviation did not correlate significantly with PG, age, HR, or VPCs. The significance of STD in the dog with SAS remains uncertain. Long-term prospective studies are needed to fully understand this observation.}, number={1}, journal={Journal of the American Animal Hospital Association}, publisher={American Animal Hospital Association}, author={Davainis, Grace M. and Meurs, Kathryn M. and Wright, Nicola A.}, year={2004}, month={Jan}, pages={20–23} }
 @article{spier_meurs_2004, title={Use of signal-averaged electrocardiography in the evaluation of arrhythmogenic right ventricular cardiomyopathy in Boxers}, volume={225}, ISSN={0003-1488}, url={http://dx.doi.org/10.2460/javma.2004.225.1050}, DOI={10.2460/javma.2004.225.1050}, abstractNote={Abstract}, number={7}, journal={Journal of the American Veterinary Medical Association}, publisher={American Veterinary Medical Association (AVMA)}, author={Spier, Alan W. and Meurs, Kathryn M.}, year={2004}, month={Oct}, pages={1050–1055} }
 @article{koplitz_meurs_spier_bonagura_fuentes_wright_2003, title={Aortic ejection velocity in healthy Boxers with soft cardiac murmurs and Boxers without cardiac murmurs: 201 cases (1997–2001)}, volume={222}, ISSN={0003-1488}, url={http://dx.doi.org/10.2460/javma.2003.222.770}, DOI={10.2460/javma.2003.222.770}, abstractNote={Abstract}, number={6}, journal={Journal of the American Veterinary Medical Association}, publisher={American Veterinary Medical Association (AVMA)}, author={Koplitz, Shianne L. and Meurs, Kathryn M. and Spier, Alan W. and Bonagura, John D. and Fuentes, Virginia Luis and Wright, Nicola A.}, year={2003}, month={Mar}, pages={770–774} }
 @article{nout_hinchcliff_bonagura_meurs_papenfuss_2003, title={Cardiac Amyloidosis in a Horse}, volume={17}, ISSN={0891-6640 1939-1676}, url={http://dx.doi.org/10.1111/j.1939-1676.2003.tb02484.x}, DOI={10.1111/j.1939-1676.2003.tb02484.x}, abstractNote={Journal of Veterinary Internal MedicineVolume 17, Issue 4 p. 588-592 Open Access Cardiac Amyloidosis in a Horse Yvette S. Nout, Yvette S. Nout Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus, OH DVM, Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, 601 Vernon L Tharp Street, Columbus, OH 43210-4007; E-mail: nout.1@osu.eduSearch for more papers by this authorKenneth W. Hinchcliff, Kenneth W. Hinchcliff Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus, OHSearch for more papers by this authorJohn D. Bonagura, John D. Bonagura Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus, OHSearch for more papers by this authorKathryn M. Meurs, Kathryn M. Meurs Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus, OHSearch for more papers by this authorTracey L. Papenfuss, Tracey L. Papenfuss Department of Veterinary Biosciences, College of Veterinary Medicine, The Ohio State University, Columbus, OHSearch for more papers by this author Yvette S. Nout, Yvette S. Nout Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus, OH DVM, Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, 601 Vernon L Tharp Street, Columbus, OH 43210-4007; E-mail: nout.1@osu.eduSearch for more papers by this authorKenneth W. Hinchcliff, Kenneth W. Hinchcliff Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus, OHSearch for more papers by this authorJohn D. Bonagura, John D. Bonagura Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus, OHSearch for more papers by this authorKathryn M. Meurs, Kathryn M. Meurs Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus, OHSearch for more papers by this authorTracey L. Papenfuss, Tracey L. Papenfuss Department of Veterinary Biosciences, College of Veterinary Medicine, The Ohio State University, Columbus, OHSearch for more papers by this author First published: 28 June 2008 https://doi.org/10.1111/j.1939-1676.2003.tb02484.xCitations: 9 AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat References 1 Marr CM. Cardiology of the Horse. London : WB Saunders; 1999: 10, 102, 298– 311. 2 Davis JL, Gardner SY, Schwabenton B., Breuhaus BA. Congestive heart failure in horses: 14 cases (1984–2001). J Am Vet Med Assoc 2002; 220: 1512– 1515. 3 Hoffman A., Levi O., Orgad U., Nyska A. Myocarditis following envenoming with Vipera palaestinae in two horses. Toxicon 1993; 31: 1623– 1628. 4 Peet RL, McDermott J., Williams JM, Maclean AA. Fungal myocarditis and nephritis in a horse. Aust Vet J 1981; 57: 439– 440. 5 Cranley JJ, McCullagh KG. Ischaemic myocardial fibrosis and aortic strongylosis in the horse. Equine Vet J 1981; 13: 35– 42. 6 Bonagura JD, Reef VB. Cardiovascular diseases. In: SM Reed, WM Bayly, eds. Equine Internal Medicine. Philadelphia , PA : WB Saunders; 1998; 290– 370. 7 Reef VB. Equine diagnostic ultrasound. Philadelphia , PA : WB Saunders; 1998: 222, 249– 254. 8 Keren A., Popp RL. Assignment of patients into the classification of cardiomyopathies. Circulation 1992; 86: 1622– 1633. 9 Ammash NM, Seward JB, Bailey KR, et al. Clinical profile and outcome of idiopathic restrictive cardiomyopathy. Circulation 2000; 101: 2490– 2496. 10 Artz G., Wynne J. Restrictive cardiomyopathy. Curr Treat Options Cardiovasc Med 2000; 2: 431– 438. 11 Felker GM, Thompson RE, Hare JM, et al. Underlying causes and long-term survival in patients with initially unexplained cardio-myopathy. N Engl J Med 2000; 342: 1077– 1084. 12 Brummer DG, Moise NS. Infiltrative cardiomyopathy responsive to combination chemotherapy in a cat with lymphoma. J Am Vet Med Assoc 1989; 195: 1116– 1119. 13 Stalis IH, Bossbaly MJ, Van Winkle TJ. Feline endomyocarditis and left ventricular endocardial fibrosis. Vet Pathol 1995; 32: 122– 126. 14 Fox PR. Feline cardiomyopathies. In: PR Fox, DD Sisson, NS Mo-ise, eds. Textbook of canine and feline cardiology, 2nd ed. Philadelphia , PA : WB Saunders; 1999: 641– 645. 15 La Vecchia L., Mezzena G., Zanolla L., et al. Cardiac troponin I as diagnostic and prognostic marker in severe heart failure. J Heart Lung Transplant 2000; 19: 644– 652. 16 Sleeper MM, Clifford CA, Laster LL. Cardiac troponin I in the normal dog and cat. J Vet Intern Med 2001; 15: 501– 503. 17 Reef VB, Levitan CW, Spencer PA. Factors affecting prognosis and conversion in equine atrial fibrillation. J Vet Intern Med 1988; 2: 1– 6. 18 Husby G. Equine amyloidosis. Equine Vet J 1988; 20: 235– 238. 19 DiBartola SP, Benson MD. The pathogenesis of reactive systemic amyloidosis. J Vet Intern Med 1989; 3: 31– 41. 20 Jubb KVF, Kennedy PC, Palmer N. Pathology of Domestic Animals, 4th ed. San Diego , CA : Academic Press; 1993: 484– 486. 21 Stunzi H., Ehrensperger F., Wild P., Leemann W. Systemic cutaneous and subcutaneous amyloidosis in the horse. Vet Pathol 1975; 12: 405– 414. 22 Shaw DP, Gunson DE, Evans LH. Nasal amyloidosis in four horses. Vet Pathol 1987; 24: 183– 185. 23 Van Andel AC, Gruys E., Kroneman J., Veerkamp J. Amyloid in the horse: A report of nine cases. Equine Vet J 1988; 20: 277– 285. 24 Mould JR, Munroe GA, Eckersall PD, et al. Conjunctival and nasal amyloidosis in a horse. Equine Vet J Suppl 1990; 10: 8– 11. 25 Hayden DW, Johnson KH, Wolf CB, Westermark P. AA amyloid-associated gastroenteropathy in a horse. J Comp Pathol 1988; 98: 195– 204. 26 Hawthorne TB, Bolon B., Meyer DJ. Systemic amyloidosis in a mare. J Am Vet Med Assoc 1990; 196: 323– 325. 27 Glenner GG. Amyloid deposits and amyloidosis. The beta-fi-brilloses (first of two parts). N Engl J Med 1980; 302: 1283– 1292. 28 Khan MF, Falk RH. Amyloidosis. Postgrad Med J 2001; 77: 686– 693. 29 Buxbaum JN, Genega EM, Lazowski P., et al. Infiltrative non-amyloidotic monoclonal immunoglobulin light chain cardiomyopathy: An underappreciated manifestation of plasma cell dyscrasias. Cardiology 2000; 93: 220– 228. 30 Braunwald E. Heart disease: A textbook of cardiovascular medicine, 4th ed. Philadelphia , PA : WB Saunders; 1992: 1416– 1419. 31 Willerson JT, Cohn JN. Cardiovascular medicine, 2nd ed. Philadelphia , PA : Harcourt; 2000: 1082– 1086. Citing Literature Volume17, Issue4July 2003Pages 588-592 ReferencesRelatedInformation}, number={4}, journal={Journal of Veterinary Internal Medicine}, publisher={Wiley}, author={Nout, Yvette S. and Hinchcliff, Kenneth W. and Bonagura, John D. and Meurs, Kathryn M. and Papenfuss, Tracey L.}, year={2003}, month={Jul}, pages={588–592} }
 @inbook{meurs_2003, place={Philadelphia}, edition={4th}, title={Myocardial Disease}, booktitle={Handbook of Small Animal Practice}, publisher={WB Saunders}, author={Meurs, K.M.}, editor={Morgan, Rhea V. and Bright, Ronald and Swartout, MargaretEditors}, year={2003}, pages={101–111} }
 @article{meurs_spier_wright_atkins_defrancesco_gordon_hamlin_keene_miller_moise_et al._2002, title={Comparison of the effects of four antiarrhythmic treatments for familial ventricular arrhythmias in Boxers}, volume={221}, ISSN={0003-1488}, url={http://dx.doi.org/10.2460/javma.2002.221.522}, DOI={10.2460/javma.2002.221.522}, abstractNote={Abstract}, number={4}, journal={Journal of the American Veterinary Medical Association}, publisher={American Veterinary Medical Association (AVMA)}, author={Meurs, K. M. and Spier, A. W. and Wright, N. A. and Atkins, C. E. and DeFrancesco, Teresa and Gordon, S. G. and Hamlin, R. L. and Keene, B. W. and Miller, M. W. and Moise, N. S. and et al.}, year={2002}, month={Aug}, pages={522–527} }
 @article{atkins_brown_coats_crawford_defrancesco_edwards_fox_keene_lehmkuhl_luethy_et al._2002, title={Effects of long-term administration of enalapril on clinical indicators of renal function in dogs with compensated mitral regurgitation}, volume={221}, ISSN={0003-1488}, url={http://dx.doi.org/10.2460/javma.2002.221.654}, DOI={10.2460/javma.2002.221.654}, abstractNote={Abstract}, number={5}, journal={Journal of the American Veterinary Medical Association}, publisher={American Veterinary Medical Association (AVMA)}, author={Atkins, Clarke E. and Brown, William A. and Coats, Julie R. and Crawford, Mary Ann and DeFrancesco, Teresa C. and Edwards, Joel and Fox, Philip R. and Keene, Bruce W. and Lehmkuhl, Linda and Luethy, Michael and et al.}, year={2002}, month={Sep}, pages={654–658} }
 @article{meurs_fox_miller_kapadia_mann_2002, title={Plasma concentrations of tumor necrosis factor-α in cats with congestive heart failure}, volume={63}, ISSN={0002-9645}, url={http://dx.doi.org/10.2460/ajvr.2002.63.640}, DOI={10.2460/ajvr.2002.63.640}, abstractNote={Abstract}, number={5}, journal={American Journal of Veterinary Research}, publisher={American Veterinary Medical Association (AVMA)}, author={Meurs, Kathryn M. and Fox, Philip R. and Miller, Matthew W. and Kapadia, Samir and Mann, Douglas L.}, year={2002}, month={May}, pages={640–642} }
 @article{meurs_miller_wright_2001, title={Clinical features of dilated cardiomyopathy in Great Danes and results of a pedigree analysis: 17 cases (1990-2000)}, volume={218}, ISSN={0003-1488}, url={http://dx.doi.org/10.2460/javma.2001.218.729}, DOI={10.2460/javma.2001.218.729}, abstractNote={Abstract}, number={5}, journal={Journal of the American Veterinary Medical Association}, publisher={American Veterinary Medical Association (AVMA)}, author={Meurs, Kathryn M. and Miller, Matthew W. and Wright, Nicola A.}, year={2001}, month={Mar}, pages={729–732} }
 @article{meurs_spier_wright_hamlin_2001, title={Comparison of in-hospital versus 24-hour ambulatory electrocardiography for detection of ventricular premature complexes in mature Boxers}, volume={218}, ISSN={0003-1488}, url={http://dx.doi.org/10.2460/javma.2001.218.222}, DOI={10.2460/javma.2001.218.222}, abstractNote={Abstract}, number={2}, journal={Journal of the American Veterinary Medical Association}, publisher={American Veterinary Medical Association (AVMA)}, author={Meurs, Kathryn M. and Spier, Alan W. and Wright, Nicola A. and Hamlin, Robert L.}, year={2001}, month={Jan}, pages={222–224} }
 @article{spier_meurs_muir_lehmkuhl_hamlin_2001, title={Correlation of QT dispersion with indices used to evaluate the severity of familial ventricular arrhythmias in Boxers}, volume={62}, ISSN={0002-9645}, url={http://dx.doi.org/10.2460/ajvr.2001.62.1481}, DOI={10.2460/ajvr.2001.62.1481}, abstractNote={Abstract}, number={9}, journal={American Journal of Veterinary Research}, publisher={American Veterinary Medical Association (AVMA)}, author={Spier, Alan W. and Meurs, Kathryn M. and Muir, William W. and Lehmkuhl, Linda B. and Hamlin, Robert L.}, year={2001}, month={Sep}, pages={1481–1485} }
 @article{meurs_magnon_spier_miller_lehmkuhl_towbin_2001, title={Evaluation of the cardiac actin gene in Doberman Pinschers with dilated cardiomyopathy}, volume={62}, ISSN={0002-9645}, url={http://dx.doi.org/10.2460/ajvr.2001.62.33}, DOI={10.2460/ajvr.2001.62.33}, abstractNote={Abstract}, number={1}, journal={American Journal of Veterinary Research}, publisher={American Veterinary Medical Association (AVMA)}, author={Meurs, Kathryn M. and Magnon, Alex L. and Spier, Alan W. and Miller, Mathew W. and Lehmkuhl, Linda B. and Towbin, Jeffrey A.}, year={2001}, month={Jan}, pages={33–36} }
 @inbook{meurs_spier_2001, title={Hypertrophic Cardiomyopathy}, volume={IV}, booktitle={Consultations in Feline Internal Medicine}, publisher={WB Saunders}, author={Meurs, K.M. and Spier, A.W.}, year={2001}, pages={56–78} }
 @article{maxson_meurs_lehmkuhl_magnon_weisbrode_atkins_2001, title={Polymerase chain reaction analysis for viruses in paraffin-embedded myocardium from dogs with dilated cardiomyopathy or myocarditis}, volume={62}, ISSN={0002-9645}, url={http://dx.doi.org/10.2460/ajvr.2001.62.130}, DOI={10.2460/ajvr.2001.62.130}, abstractNote={Abstract}, number={1}, journal={American Journal of Veterinary Research}, publisher={American Veterinary Medical Association (AVMA)}, author={Maxson, Tracy R. and Meurs, Kathryn M. and Lehmkuhl, Linda B. and Magnon, Alex L. and Weisbrode, Steven E. and Atkins, Clarke E.}, year={2001}, month={Jan}, pages={130–135} }
 @article{meurs_spier_wright_hamlin_2001, title={Use of ambulatory electrocardiography for detection of ventricular premature complexes in healthy dogs}, volume={218}, DOI={10.2460/javma.2001.218.1291}, abstractNote={Abstract}, number={8}, journal={Journal of the American Veterinary Medical Association}, author={Meurs, K.M. and Spier, A.W. and Wright, N.A. and Hamlin, R.A.}, year={2001}, month={Apr}, pages={1291–1295} }
 @article{defrancesco_atkins_miller_meurs_keene_2001, title={Use of echocardiography for the diagnosis of heartworm disease in cats: 43 cases (1985-1997)}, volume={218}, ISSN={0003-1488}, url={http://dx.doi.org/10.2460/javma.2001.218.66}, DOI={10.2460/javma.2001.218.66}, abstractNote={Abstract}, number={1}, journal={Journal of the American Veterinary Medical Association}, publisher={American Veterinary Medical Association (AVMA)}, author={DeFrancesco, Teresa C. and Atkins, Clarke E. and Miller, Matthew W. and Meurs, Kathryn M. and Keene, Bruce W.}, year={2001}, month={Jan}, pages={66–69} }
 @article{spier_meurs_coovert_lehmkuhl_o'grady_freeman_burghes_towbin_2001, title={Use of western immunoblot for evaluation of myocardial dystrophin, -sarcoglycan, and -dystroglycan in dogs with idiopathic dilated cardiomyopathy}, volume={62}, ISSN={0002-9645}, url={http://dx.doi.org/10.2460/ajvr.2001.62.67}, DOI={10.2460/ajvr.2001.62.67}, abstractNote={Abstract}, number={1}, journal={American Journal of Veterinary Research}, publisher={American Veterinary Medical Association (AVMA)}, author={Spier, Alan W and Meurs, Kathryn M. and Coovert, Daniel D and Lehmkuhl, Linda B. and O'Grady, Michael R. and Freeman, Lisa M. and Burghes, Arthur H. and Towbin, Jeffrey A.}, year={2001}, month={Jan}, pages={67–71} }
 @article{magnon_meurs_kittleson_ware_2000, title={A highly polymorphic marker identified in intron 15 of the feline cardiac troponin T gene by SSCP analysis}, volume={31}, journal={Animal Genetics}, author={Magnon, A.L. and Meurs, K.M. and Kittleson, M.D. and Ware, W.A.}, year={2000}, pages={236–237} }
 @article{meurs_miller_slater_glaze_2000, title={Arterial blood pressure measurement in a population of healthy geriatric dogs}, volume={36}, ISSN={0587-2871 1547-3317}, url={http://dx.doi.org/10.5326/15473317-36-6-497}, DOI={10.5326/15473317-36-6-497}, abstractNote={The purpose of this study was to evaluate healthy geriatric dogs for the presence of systemic hypertension. Thirty-three geriatric dogs (i.e., dogs exceeding the geriatric age range for their weight group) and 22 control dogs (i.e., dogs less than six years of age) were evaluated by measuring blood pressure with an oscillometric monitor. Five consecutive blood pressure measurements were taken in each dog, averaged, and compared. Diastolic and mean blood pressure measurements were significantly lower in the geriatric group as compared to the control group. Systolic blood pressure measurements were not significantly different between the two groups. Systemic hypertension does not appear to be a common clinical problem in the healthy geriatric dog.}, number={6}, journal={Journal of the American Animal Hospital Association}, publisher={American Animal Hospital Association}, author={Meurs, KM and Miller, MW and Slater, MR and Glaze, K}, year={2000}, month={Nov}, pages={497–500} }
 @article{meurs_fox_magnon_liu_towbin_2000, title={Molecular Screening by Polymerase Chain Reaction Detects Panleukopenia Virus DNA in Formalin-Fixed Hearts from Cats with Idiopathic Cardiomyopathy and Myocarditis}, volume={9}, ISSN={1054-8807}, url={http://dx.doi.org/10.1016/s1054-8807(00)00031-4}, DOI={10.1016/s1054-8807(00)00031-4}, abstractNote={Viral myocarditis has been suggested as an etiology for cardiomyopathy in several mammalian species. Myocarditis and idiopathic cardiomyopathy have been reported in the domestic cat, although a viral etiology has not been demonstrated. Because of the continuing interest in the potential relationship between viral myocarditis and cardiomyopathy, we evaluated hearts from cats with spontaneous, idiopathic cardiomyopathy for viral genomic material within myocytes by polymerase chain reaction, and for the presence of myocarditis by light microscopy. Thirty-one (31) formalin-fixed hearts from domestic cats who died of idiopathic cardiomyopathy were randomly selected from pathology archives. Seventeen (17) formalin-fixed hearts from healthy cats were similarly selected as normal controls. The polymerase chain reaction (PCR) was used to evaluate myocardial tissue for the presence of viral genome from feline panleukopenia virus, herpes virus, calici virus, and corona virus. Hearts were examined using light microscopy for histologic evidence of myocarditis according to the Dallas criteria. Panleukopenia virus was identified by PCR in 10 of 31 cats with cardiomyopathy but in none of the controls. Neither cardiomyopathic or control cats tested positive by PCR for herpes virus, calici virus, and corona virus. Myocarditis was detected by histologic examination in 18 of 31 cardiomyopathic cats and in none of 17 control cats. Myocarditis and or feline panleukopenia virus genome was detected in felines with idiopathic hypertrophic, dilated, and restrictive cardiomyopathy, suggesting a possible role of viral infection and inflammation in the pathogenesis of cardiomyopathy in this species.}, number={2}, journal={Cardiovascular Pathology}, publisher={Elsevier BV}, author={Meurs, Kathryn M and Fox, Philip R and Magnon, Alexander L and Liu, Si-Kwang and Towbin, Jeffrey A}, year={2000}, month={Mar}, pages={119–126} }
 @article{magnon_meurs_kittleson_ware_2000, title={Single nucleotide polymorphisms in intron 5 of the feline myosin regulatory light chain gene detected by SSCP analysis}, volume={31}, ISSN={0268-9146 1365-2052}, url={http://dx.doi.org/10.1046/j.1365-2052.2000.00620.x}, DOI={10.1046/j.1365-2052.2000.00620.x}, abstractNote={Recently, we published the mapping of the chicken leptin gene to a microchromosome. This work was done through PCR-SSCP analysis, using primers designed from a published sequence (, EMBL accession number AF012727), presenting 97% similarity to the mouse and 83% to the human leptin genes. This sequence was also published by another group and the primers were therefore supposed to be homologous ones. We have now sequenced our PCR product: although it was amplified with primers chosen from a chicken sequence, it is neither homologous to the published leptin sequence, nor to any other sequence in Genebank/EMBL databases. Therefore, the amplimer we have localised can not be considered as a part of the chicken leptin gene.}, number={4}, journal={Animal Genetics}, publisher={Wiley}, author={Magnon, A L and Meurs, K M and Kittleson, M D and Ware, W A}, year={2000}, month={Aug}, pages={281–282} }
 @article{meurs_kittleson_ware_miller_2000, title={The identification of nine polymorphisms identified within the head region of feline Beta Myosin heavy chain gene}, volume={31}, journal={Animal Genetics}, author={Meurs, K.M. and Kittleson, M.D. and Ware, W.A. and Miller, M.W.}, year={2000}, pages={231} }
 @inbook{calvert_meurs_2000, place={Philadelphia}, title={Update on Doberman pinscher cardiomyopathy}, booktitle={Current Veterinary Therapy (Small Animal Practice) XIII}, publisher={WB Saunders}, author={Calvert, C. and Meurs, K.M.}, year={2000}, pages={756–760} }
 @article{schatzberg_olby_steingold_keene_atkins_meurs_solomon_goedegebuure_wilton_sharp_1999, title={A polymerase chain reaction screening strategy for the promoter of the canine dystrophin gene}, volume={60}, number={9}, journal={American Journal of Veterinary Research}, author={Schatzberg, S. and Olby, N. and Steingold, S. and Keene, B. and Atkins, C. and Meurs, K.M. and Solomon, G. and Goedegebuure, S.A. and Wilton, S. and Sharp, N.}, year={1999}, month={Aug}, pages={1040–1046} }
 @article{kittleson_meurs_munro_kittleson_liu_pion_towbin_1999, title={Familial Hypertrophic Cardiomyopathy in Maine Coon Cats}, volume={99}, DOI={10.1161/01.cir.99.24.3172}, abstractNote={
            Background
            —A naturally occurring animal model of familial hypertrophic cardiomyopathy (FHCM) is lacking. We identified a family of Maine coon cats with HCM and developed a colony to determine mode of inheritance, phenotypic expression, and natural history of the disease.
          }, number={24}, journal={Circulation}, author={Kittleson, M.D. and Meurs, K.M. and Munro, M. and Kittleson, J.A. and Liu, Si-Kwang and Pion, P.D. and Towbin, J.A.}, year={1999}, month={Jun}, pages={3172–3180} }
 @article{meurs_spier_miller_lehmkuhl_towbin_1999, title={Familial Ventricular Arrhythmias in Boxers}, volume={13}, ISSN={0891-6640 1939-1676}, url={http://dx.doi.org/10.1111/j.1939-1676.1999.tb01460.x}, DOI={10.1111/j.1939-1676.1999.tb01460.x}, abstractNote={The purposes of this study were to evaluate families of Boxers with ventricular arrhythmias to determine whether this disorder is a familial trait and, if so, to determine the mode of inheritance. Eighty‐two Boxers were evaluated by physical examination, electrocardiogram, echocardiogram, and 24‐hour ambulatory electrocardiogram. Dogs were considered affected if at least 50 premature ventricular complexes (PVCs) were observed during a 24‐hour period. All dogs were at least 6 years of age at evaluation. Complete cardiovascular examinations were performed on dogs from 6 extended families. The 2 most complete pedigrees were used to determine the pattern of inheritance. The number of PVCs observed during a 24‐hour period in affected dogs ranged from 112 to 4,894 (mean ± SD, median; 1,309 ± 2,609, 1,017). The number of PVCs observed during a 24‐hour period in the unaffected dogs ranged from 0 to 16 (7 ± 10, 12). Pedigree evaluation was performed to determine pattern of inheritance. An autosomal dominant pattern was determined to be most likely because a sex predisposition was not observed, affected individuals were observed in every generation, and 2 affected individuals produced unaffected offspring. We conclude that familial ventricular arrhythmias is inherited as an autosomal dominant trait in some Boxers.}, number={5}, journal={Journal of Veterinary Internal Medicine}, publisher={Wiley}, author={Meurs, Kathryn M. and Spier, Alan W. and Miller, Matthew W. and Lehmkuhl, Linda and Towbin, Jeffrey A.}, year={1999}, month={Sep}, pages={437–439} }
 @article{meurs_anthony_slater_miller_1998, title={Chronic Trypanosoma cruzi infection in dogs: 11 cases (1987–1996)}, volume={213}, number={4}, journal={Journal of the American Veterinary Medical Association}, author={Meurs, K.M. and Anthony, M.A. and Slater, M. and Miller, M.W.}, year={1998}, pages={497–500} }
 @article{meurs_1998, title={Insights into the Hereditability of Canine Cardiomyopathy}, volume={28}, ISSN={0195-5616}, url={http://dx.doi.org/10.1016/s0195-5616(98)50131-3}, DOI={10.1016/s0195-5616(98)50131-3}, abstractNote={There is evidence for a genetic etiology of dilated cardiomyopathy in at least two breeds, the Doberman pinscher and the Boxer dog. Significant effort toward determining a genetic etiology in these breeds will depend on careful characterization of the disease, determination of criteria for diagnosing asymptomatic affected individuals, determination of a pattern of inheritance, and, eventually, molecular evaluation of the specific gene.}, number={6}, journal={Veterinary Clinics of North America: Small Animal Practice}, publisher={Elsevier BV}, author={Meurs, Kathryn M.}, year={1998}, month={Nov}, pages={1449–1457} }
 @article{atkins_defrancesco_miller_meurs_keene_1998, title={Prevalence of heartworm infection in cats with signs of cardiorespiratory abnormalities}, volume={212}, number={4}, journal={Journal of the American Veterinary Medical Association}, author={Atkins, C.E. and DeFrancesco, T. and Miller, M.W. and Meurs, K.M. and Keene, B.}, year={1998}, month={Feb}, pages={517–520} }
 @article{meurs_miller_hanson_honnas_1997, title={Tricuspid valve atresia with main pulmonary artery atresia in an Arabian foal}, volume={29}, DOI={10.1111/j.2042-3306.1997.tb01661.x}, abstractNote={Equine Veterinary JournalVolume 29, Issue 2 p. 160-162 Tricuspid valve atresia with main pulmonary artery atresia in an Arabian foal K. M. MEURS, K. M. MEURS Departments of Small Animal Medicine and Surgery, University College of Veterinary Medicine College Station, Texas 77843-4474, USA.Search for more papers by this authorM. W. MILLER, M. W. MILLER Departments of Small Animal Medicine and Surgery, University College of Veterinary Medicine College Station, Texas 77843-4474, USA.Search for more papers by this authorC. HANSON, C. HANSON Large Animal Medicine and Surgery, Texas A & M University College of Veterinary Medicine College Station, Texas 77843-4474, USA.Search for more papers by this authorC. HONNAS, C. HONNAS Large Animal Medicine and Surgery, Texas A & M University College of Veterinary Medicine College Station, Texas 77843-4474, USA.Search for more papers by this author K. M. MEURS, K. M. MEURS Departments of Small Animal Medicine and Surgery, University College of Veterinary Medicine College Station, Texas 77843-4474, USA.Search for more papers by this authorM. W. MILLER, M. W. MILLER Departments of Small Animal Medicine and Surgery, University College of Veterinary Medicine College Station, Texas 77843-4474, USA.Search for more papers by this authorC. HANSON, C. HANSON Large Animal Medicine and Surgery, Texas A & M University College of Veterinary Medicine College Station, Texas 77843-4474, USA.Search for more papers by this authorC. HONNAS, C. HONNAS Large Animal Medicine and Surgery, Texas A & M University College of Veterinary Medicine College Station, Texas 77843-4474, USA.Search for more papers by this author First published: 23 April 2010 https://doi.org/10.1111/j.2042-3306.1997.tb01661.xCitations: 9AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat References Bayly, W., Reed, S., Leathers, C., Brown, C., Traub, J., Paradis, M. and Palmer, G. (1982) Multiple congenital heart anomalies in five Arabian foals. J. Am. vet. med. Ass. 181, 684–689. CASPubMedWeb of Science®Google Scholar Button, C., Gross, D., Allert, J. and Kitzman, J. (1978) Tricuspid atresia in a foal. J. Am. vet. med. Ass. 172, 825–830. CASPubMedWeb of Science®Google Scholar Fink, B. (1991) Differential diagnosis of cyanotic heart disease. In: Congenital Heart Disease, 3rd edn. Mosby Year Book, St. Louis . pp 103–106. Web of Science®Google Scholar Hadlow, W. and Ward J. (1980) Atresia of the right atrioventricular orifice in an Arabian foal. Vet. Path. 17, 622–637. 10.1177/030098588001700511 CASPubMedWeb of Science®Google Scholar Lombard, C., Scarratt, W. and Buergelt, W. C. (1983) Ventricular septal defects in the horse. J. Am. vet. med. Ass. 183, 562–565. CASPubMedWeb of Science®Google Scholar Nugent, E., Plauth, W., Edwards, J. and Williams, W. (1990) The pathology, abnormal physiology, clinical recognition, and medical and surgical treatment of congenital heart disease. In: The Heart, 7th edn. Ed: J. W. Hurst McGraw-Hill, New York , pp 744–746. Google Scholar Reef, V. (1985) Cardiovascular disease in the equine neonate. Vet. Clin. N. Am.: Equine Pract. 1, 117–129. 10.1016/S0749-0739(17)30772-1 CASPubMedWeb of Science®Google Scholar Reef, V. (1991) Echocardiographic findings in horses with congenital cardiac diseases. Comp. cont. Educ. pract. Vet. 13, 109–117. Web of Science®Google Scholar Reef, V.B., Mann, P.C. and Orsini, P.G. (1987) Echocardiographic detection of tricuspid atresia in two foals. J. Am. vet. med. Ass. 191, 225–228. CASPubMedWeb of Science®Google Scholar Thoele, D., Ursell, P.C., Ho, S.Y., Smith, A., Bowman, F.O., Gersony, W.M. and Anderson, R.H. (1991) Atrial morphologic features in tricuspid atresia. J. thorac. cardiovasc. Surg. 102, 606–610. 10.1016/S0022-5223(20)31434-3 CASPubMedWeb of Science®Google Scholar Vitums, A. and Bayly, W. (1982) Pulmonary atresia with dextroposition of the aorta and ventricular septal defect in three arabian foals. Vet. Path. 19, 160–168. 10.1177/030098588201900207 CASPubMedWeb of Science®Google Scholar Citing Literature Volume29, Issue2March 1997Pages 160-162 ReferencesRelatedInformation}, number={2}, journal={Equine Veterinary Journal}, author={Meurs, K.M. and Miller, M.W. and Hanson, C. and Honnas, C.}, year={1997}, month={Mar}, pages={160–162} }
 @article{meurs_miller_slater_1996, title={Comparison of the indirect oscillometric and direct arterial methods for blood pressure measurements in anesthetized dogs}, volume={32}, DOI={10.5326/15473317-32-6-471}, abstractNote={The indirect oscillometric method of blood pressure measurement was compared to the direct arterial puncture method in 15 anesthetized dogs, divided into three weight groups, undergoing a variety of surgical procedures. The objectives of this study were to determine the accuracy of the indirect oscillometric method at a single point in time and when sequential values were averaged. Additionally, the ability to detect systemic hypotension (i.e., mean systemic arterial pressure less than 60 mmHg) was evaluated. The method had the highest correlation coefficient (r of 0.8) when five sequential values were averaged and compared, and it appeared to be sensitive (100%) and specific (91%) for detecting hypotension.}, number={6}, journal={Journal of the American Animal Hospital Association}, author={Meurs, K.M. and Miller, M.W. and Slater, M.}, year={1996}, pages={471–475} }
 @inbook{meurs_1996, place={Philadelphia}, edition={3rd}, title={Myocardial Disease}, booktitle={Handbook of Small Animal Practice}, publisher={WB Saunders}, author={Meurs, K.M.}, year={1996}, pages={560–568} }
 @inbook{meurs_miller_helman_1995, place={Philadelphia}, title={Canine Chagas' Myocarditis}, booktitle={Current Veterinary Therapy (Small Animal Practice) XII}, publisher={WB Saunders}, author={Meurs, K.M. and Miller, M.W. and Helman, R.G.}, year={1995}, pages={850–853} }
 @article{glaze_meurs_1995, title={Cardiovascular consequences of feline hyperthyroidism}, volume={16}, journal={Veterinary Technician}, author={Glaze, K. and Meurs, K.M.}, year={1995}, pages={23–26} }
 @article{meurs_miller_1995, title={ECG of the Month}, volume={206}, journal={Journal of the American Veterinary Medical Association}, author={Meurs, K.M. and Miller, M.W.}, year={1995}, pages={957–959} }
 @inbook{meurs_breitschwerdt_1995, place={Philadelphia}, title={Zinc Toxicosis}, booktitle={Current Veterinary Therapy (Small Animal Practice) XII}, publisher={WB Saunders}, author={Meurs, K.M. and Breitschwerdt, E.B.}, year={1995}, pages={238–240} }
 @inbook{meurs_1995, place={Baltimore}, title={Zinc toxicity}, booktitle={Five Minute Veterinary Consult}, publisher={Williams & Wilkens}, author={Meurs, K.M.}, year={1995}, pages={1164} }
 @article{meurs_atkins_khoo_keene_1994, title={Aberrant migration of toxocara larva as a cause of myocarditis in the dog}, volume={30}, number={6}, journal={Journal of the American Animal Hospital Association}, author={Meurs, K.M. and Atkins, C.E. and Khoo, L. and Keene, B.}, year={1994}, pages={580–582} }
 @article{meurs_miller_mackie_mathison_1994, title={Syncope associated with cardiac lymphoma in a cat}, volume={30}, journal={Journal of the American Animal Hospital Association}, author={Meurs, K.M. and Miller, M.W. and Mackie, J. and Mathison, P.}, year={1994}, pages={583–585} }
 @article{fossum_miller_rogers_bonagura_meurs_1993, title={Chylothorax associated with right-sided heart failure in five cats}, volume={204}, number={1}, journal={Journal of the American Veterinary Medical Association}, author={Fossum, T.W. and Miller, M.W. and Rogers, K.S. and Bonagura, J.D. and Meurs, K.M.}, year={1993}, month={Dec}, pages={84–89} }
 @article{meurs_miller_1993, title={ECG of the Month}, volume={203}, journal={Journal of the American Veterinary Medical Association}, author={Meurs, K.M. and Miller, M.W.}, year={1993}, pages={649–650} }
 @article{sinclair_meurs_1992, title={Challenging cases in internal medicine - Beagle polyarteritis}, volume={87}, journal={Veterinary Medicine}, author={Sinclair, L. and Meurs, K.M.}, year={1992}, pages={986–990} }
 @article{meurs_breitschwerdt_baty_1991, title={Postsurgical mortality secondary to zinc toxicity in dogs}, volume={33}, number={6}, journal={Veterinary and Human Toxicology}, author={Meurs, K. M. and Breitschwerdt, E. B. and Baty, C. J.}, year={1991}, pages={579} }
 @article{meurs_breitschwerdt_baty_young_1991, title={Postsurgical mortality secondary to zinc toxicity in dogs}, volume={33}, number={6}, journal={Veterinary and Human Toxicology}, author={Meurs, K.M. and Breitschwerdt, E.B. and Baty, C.J. and Young, M.E.}, year={1991}, month={Dec}, pages={579–583} }
 @article{friedenberg_meurs_mackay, title={Evaluation of artificial selection in Standard Poodles using whole-genome sequencing}, volume={27}, number={11-12}, journal={Mammalian Genome}, author={Friedenberg, S. G. and Meurs, K. M. and Mackay, T. F. C.}, pages={599–609} }