@article{arguedas_hines_papich_farnsworth_sellon_2008, title={Pharmacokinetics of Butorphanol and Evaluation of Physiologic and Behavioral Effects after Intravenous and Intramuscular Administration to Neonatal Foals}, volume={22}, ISSN={["1939-1676"]}, DOI={10.1111/j.1939-1676.2008.0200.x}, abstractNote={Background:Despite frequent clinical use, information about the pharmacokinetics (PK), clinical effects, and safety of butorphanol in foals is not available.}, number={6}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Arguedas, M. G. and Hines, M. T. and Papich, M. G. and Farnsworth, K. D. and Sellon, D. C.}, year={2008}, pages={1417–1426} }
 @article{alward_corriher_barton_sellon_blikslager_jones_2006, title={Red maple (Acer rubrum) leaf toxicosis in horses: A retrospective study of 32 cases}, volume={20}, ISSN={["0891-6640"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-33750326132&partnerID=MN8TOARS}, DOI={10.1892/0891-6640(2006)20[1197:RMARLT]2.0.CO;2}, abstractNote={Ingestion of wilted red maple leaves by horses can result in severe hemolytic anemia and methemoglobinemia. Little is known about what factors influence the outcome of red maple leaf toxicosis in horses.Our hypothesis was that physical examination findings, clinicopathologic variables or therapeutic modalities may predict outcome in horses with red maple leaf toxicity.Horses with red maple leaf toxicosis presented to referral hospitals in the southeast region of the United States.A multi-institutional retrospective study was designed to identify factors that predict mortality in horses with red maple toxicosis.Thirty-two horses with red maple toxicosis were identified, 19 of which died. Twenty-nine horses presented with anemia and 24 had clinicopathologic evidence of systemic inflammation. Renal insufficiency was identified in 12/30 (41%) horses. Laminitis (9/28) and colic (13/30) also were identified in horses with red maple toxicosis, but development of these 2 conditions did not have a negative effect on short-term survival. Horses with red maple toxicosis that survived to discharge were likely to have developed pyrexia during hospitalization (P = .030). Horses that were treated with a corticosteroid had a significantly increased likelihood of death (P = .045). There was no significant relationship between initial serum hemoglobin concentration, methemoglobin concentration, or percentage methemoglobin and mortality in this horse series.This study suggests that information obtained on initial examination cannot be used to accurately predict survival in horses with red maple toxicosis, but horses that receive corticosteroids are unlikely to survive.}, number={5}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Alward, Ashley and Corriher, Candice A. and Barton, Michelle H. and Sellon, Debra C. and Blikslager, Anthony T. and Jones, Samuel L.}, year={2006}, pages={1197–1201} }
 @article{sellon_roberts_blikslager_ulibarri_papich_2004, title={Effects of continuous rate intravenous infusion of butorphanol on physiologic and outcome variables in horses after celiotomy}, volume={18}, ISSN={["0891-6640"]}, DOI={10.1892/0891-6640(2004)18<555:EOCRII>2.0.CO;2}, abstractNote={A randomized, controlled, blinded clinical trial was performed to determine whether butorphanol administered by continuous rate infusion (CRI) for 24 hours after abdominal surgery would decrease pain and surgical stress responses and improve recovery in horses. Thirty-one horses undergoing exploratory celiotomy for abdominal pain were randomly assigned to receive butorphanol CRI (13 microg/kg/h for 24 hours after surgery; treatment) or isotonic saline (control). All horses received flunixin meglumine (1.1 mg/kg IV q12h). There were no significant differences between treatment and control horses in preoperative or operative variables. Treatment horses had significantly lower plasma cortisol concentration compared with control horses at 2, 8, 12, 24, 36, and 48 hours after surgery. Mean weight loss while hospitalized was significantly less for treatment horses than control horses, whether expressed as total decrease in body weight (13.9+/-3.4 and 27.9+/-4.5 kg, respectively) or as a percentage decrease in body weight (2.6+/-0.7 and 6.3+/-1.1%, respectively). Treatment horses were significantly delayed in time to first passage of feces (median times of 15 and 4 hours, respectively). Treatment horses had significantly improved behavior scores during the first 24 hours after surgery, consistent with the conclusion that they experienced less pain during that time. Butorphanol CRI during the immediate postoperative period significantly decreased plasma cortisol concentrations and improved recovery characteristics in horses undergoing abdominal surgery.}, number={4}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Sellon, DC and Roberts, MC and Blikslager, AT and Ulibarri, C and Papich, MG}, year={2004}, pages={555–563} }
 @article{rothschild_hines_breuhaus_gay_sellon_2004, title={Effects of trimethoprim-sulfadiazine on thyroid function of horses}, volume={18}, ISSN={["1939-1676"]}, DOI={10.1892/0891-6640(2004)18<370:EOTOTF>2.0.CO;2}, abstractNote={Trimethoprim-sulfadiazine was administered to horses in a randomized, placebo controlled study to determine the effects of potentiated sulfonamides on thyroid function in normal horses. The treatment group included eight horses that received trimethoprim-sulfadiazine mixed with molasses orally at 30 mg/kg once daily for eight weeks. The control group included 8 horses that received an oral placebo (flour mixed with molasses) once daily for the same period. Thyroid function was evaluated prior to initiation of treatment and after 8 weeks of treatment. Serum concentrations of total and free triiodothyronine (T3), total and free thyroxine (T4), and thyroid stimulating hormone (TSH) were determined at rest and after a thyrotropin-releasing hormone (TRH) stimulation test. There was no detectable difference between treatment and control groups.}, number={3}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Rothschild, CM and Hines, MT and Breuhaus, B and Gay, J and Sellon, DC}, year={2004}, pages={370–373} }
 @article{sellon_spaulding_breuhaus_katz_mealey_2000, title={Hepatic abscesses in three horses}, volume={216}, ISSN={["0003-1488"]}, DOI={10.2460/javma.2000.216.882}, abstractNote={Hepatic abscesses were diagnosed in 3 adult horses. Two were < 4 years old and had evidence of concurrent immune-mediated conditions, including aseptic arthritis, immune-mediated thrombocytopenia, and immune-mediated anemia. Predisposing factors for hepatic abscess formation in these horses included prior abdominal surgery, proximal duodenitis/jejunitis, inflammatory bowel disease, and a penetrating foreign body in the large colon. Serum hepatic enzyme activities were within or slightly greater then reference limits in all 3 horses. The most pronounced and consistent abnormalities on CBC and serum biochemical analyses were hyperproteinemia, hyperglobulinemia, and a decreased albumin-to-globulin concentration ratio. Hepatic ultrasonography identified hepatic abscesses in all 3 horses. A variety of bacteria were isolated from these abscesses, including Staphylococus aureus and Bacteroides fragilis. One horse developed septic tibiotarsal arthritis, presumably as a result of intermittent bacteremia. Despite aggressive medical treatment, all horses were euthanatized because of a worsening condition and poor prognosis.}, number={6}, journal={JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Sellon, DC and Spaulding, K and Breuhaus, BA and Katz, L and Mealey, R}, year={2000}, month={Mar}, pages={882-+} }
 @article{sellon_russell_monroe_walker_1999, title={Increased interleukin-6 activity in the serum of ponies acutely infected with equine infectious anaemia virus}, volume={66}, ISSN={["0034-5288"]}, DOI={10.1053/rvsc.1998.0245}, abstractNote={Seven ponies were infected with the virulent wild-type Wyoming strain of equine infectious anaemia virus (EIAV). Infection status was monitored by serum reverse transcriptase activity, rectal temperature, and complete blood count. Preinfection serum and serum obtained during the initial febrile episode following infection were assayed for interleukin 6 (IL-6) activity. Postinfection IL-6 activity was significantly increased as compared to preinfection values. The magnitude of increase in IL-6 was positively correlated with reverse transcriptase activity (an indirect measure of viraemia) but was not correlated with rectal temperature. IL-6 production in response to EIAV infection may play a role in pathogenesis of disease, especially the hyperglobulinaemia and apparent polyclonal B cell activation in these horses.}, number={1}, journal={RESEARCH IN VETERINARY SCIENCE}, author={Sellon, DC and Russell, KE and Monroe, VL and Walker, KM}, year={1999}, month={Feb}, pages={77–80} }
 @article{russell_perkins_hoffman_miller_walker_fuller_sellon_1999, title={Platelets from thrombocytopenic ponies acutely infected with equine infectious anemia virus are activated in vivo and hypofunctional}, volume={259}, ISSN={["0042-6822"]}, DOI={10.1006/viro.1999.9737}, abstractNote={Thrombocytopenia is a consistent finding and one of the earliest hematological abnormalities in horses acutely infected with equine infectious anemia virus (EIAV), a lentivirus closely related to human immunodeficiency virus. Multifactorial mechanisms, including immune-mediated platelet destruction and impaired platelet production, are implicated in the pathogenesis of EIAV-associated thrombocytopenia. This study was undertaken to investigate whether regenerative thrombopoiesis and platelet destruction occurred in ponies acutely infected with EIAV. Circulating large, immature platelets were increased in ponies acutely infected with EIAV late in the infection when platelet count was at a nadir. Morphometric analysis of bone marrow from acutely infected ponies revealed significant increased in megakaryocyte area and megakaryocyte nuclear area. A trend toward increased numbers of megakaryocytes was also observed. Platelets from acutely infected ponies had increased surface-bound fibrinogen and ultrastructural changes consistent with in vivo platelet activation. Platelets also had hypofunctional aggregation responses to three agonists in vitro. We conclude that thrombocytopenia in ponies acutely infected with EIAV is regenerative and suggest that bone marrow platelet production is not severely compromised in these ponies. Our findings reveal that in vivo platelet activation occurs in ponies acutely infected with EIAV, and as a result platelets are hypofunctional in vitro. Activation of platelets in vivo may cause platelet degranulation or formation of platelet aggregates, which would result in removal of these damages platelets from circulation. This may represent a form of nonimmune-mediated platelet destruction in ponies acutely infected with EIAV.}, number={1}, journal={VIROLOGY}, author={Russell, KE and Perkins, PC and Hoffman, MR and Miller, RT and Walker, KM and Fuller, FJ and Sellon, DC}, year={1999}, month={Jun}, pages={7–19} }
 @article{mcfarlane_sellon_gaffney_hedgpeth_papich_gibbs_1998, title={Hematologic and serum biochemical variables and plasma corticotropin concentration in healthy aged horses}, volume={59}, number={10}, journal={American Journal of Veterinary Research}, author={McFarlane, D. and Sellon, D. C. and Gaffney, D. and Hedgpeth, V. and Papich, M. and Gibbs, S.}, year={1998}, pages={1247–1251} }
 @article{russell_walker_miller_sellon_1998, title={Hyperglobulinemia and lymphocyte subset changes in naturally infected, in apparent carriers of equine infectious anemia virus}, volume={59}, number={8}, journal={American Journal of Veterinary Research}, author={Russell, K. E. and Walker, K. M. and Miller, R. T. and Sellon, D. C.}, year={1998}, pages={1009–1015} }
 @article{mcfarlane_sellon_parker_1998, title={Primary erythrocytosis in a 2-year-old Arabian gelding}, volume={12}, ISSN={["0891-6640"]}, DOI={10.1111/j.1939-1676.1998.tb02139.x}, abstractNote={Journal of Veterinary Internal MedicineVolume 12, Issue 5 p. 384-388 Open Access Primary Erythrocytosis in a 2-Year-Old Arabian Gelding Dianne McFarlane, Corresponding Author Dianne McFarlane Department of Food Animal and Equine Medicine, College of Veterinary Medicine, North Carolina State University, Raleigh, NC Department of Food Animal and Equine Medicine, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, NC 27606; e-mail: [email protected]Search for more papers by this authorDebra C. Sellon, Debra C. Sellon Department of Food Animal and Equine Medicine, College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this authorBert Parker, Bert Parker South Ridge Veterinary HospitalSearch for more papers by this author Dianne McFarlane, Corresponding Author Dianne McFarlane Department of Food Animal and Equine Medicine, College of Veterinary Medicine, North Carolina State University, Raleigh, NC Department of Food Animal and Equine Medicine, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, NC 27606; e-mail: [email protected]Search for more papers by this authorDebra C. Sellon, Debra C. Sellon Department of Food Animal and Equine Medicine, College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this authorBert Parker, Bert Parker South Ridge Veterinary HospitalSearch for more papers by this author First published: 05 February 2008 https://doi.org/10.1111/j.1939-1676.1998.tb02139.xCitations: 16 Dr Sellon is presently affiliated with the Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Washington State University, Pullman, WA 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 Russell KE, Sellon DC, Grindem CB. Bone marrow handling in horses: Indications, sample handling, and complications. Compend Cont Educ Pract Vet 1994; 16: 1359– 1365. 2 Murphy S. Polycythemia vera. In: WJ Williams, E. Beutler, AJ Erslev, MA Lichtman, eds. Hematology, 4th ed. New York , NY : McGraw-Hill, Inc; 1990: 193– 202. 3 Murray JE. Classification of polycythemic disorders. With comments on the diagnostic value of arterial blood oxygen analysis. Ann Intern Med 1969; 64: 892– 903. 4 Berlin NI. Diagnosis and classification of the polycythemias. Semin Hematol 1975; 12: 339– 351. 5 Berk PD. Erythrocytosis and polycythemia. In: JB Wyngaarden, LH Smith, eds. Cecil Textbook of Medicine, 17th ed. Philadelphia , PA : WB Saunders; 1988: 975– 982. 6 Koeffler HP, Goldwasser E. Erythropoietin radioimmunoassay in evaluating patients with polycythemia. Ann Intern Med 1981; 94: 44– 47. 7 Cotes PM, Dore CJ, LiuYin JA, et al. Determination of serum immunoreactive erythropoietin in the investigation of erythrocytosis. N Engl J Med 1986; 315: 283– 287. 8 Campbell KL. Diagnosis and management of polycythemia in dogs. Compend Cont Educ Pract Vet 1990; 12: 543– 550. 9 Cook SM, Lothrop CD. Serum erythropoietin concentrations measured by radioimmunoassay in normal, polycythemic and anemic dogs and cats. J Vet Intern Med 1994; 8: 18– 25. 10 Hasler AH, Giger U. Serum erythropoietin values in polycythemic cats. J Am Anim Hosp Assoc 1996; 32: 294– 301. 11 Birgegard G., Miller O., Caro J., et al. Serum erythropoietin levels by radioimmunoassay in polycythaemia. Scand J Haematol 1982; 29: 161– 167. 12 Napier JA, Janowska-Wieczorek A. Erythropoietin measurements in the differential diagnosis of polycythaemia. Br J Haematol 1981; 48: 393– 401. 13 Woods PR, Campbell G., Cowell RL. Nondegenerative anaemia associated with administration of recombinant human erythropoietin to a Thoroughbred racehorse. Equine Vet J 1997; 29: 326– 328. 14 Gilbert HS. Definition, clinical features and diagnosis of polycythaemia vera. Clin Haematol 1975; 4: 263– 290. 15 Roby KA, Beech J., Bloom JC, et al. Hepatocellular carcinoma associated with erythrocytosis and hypoglycemia in a yearling filly. J Am Vet Med Assoc 1990: 1106– 1108. 16 Cook G., Divers TJ, Rowland PH. Hypercalcaemia and erythrocytosis in a mare associated with a metastatic carcinoma. Equine Vet J 1995; 27: 316– 318. 17 Berk PD, Goldberg JD, Donovan PB, et al. Therapeutic recommendations in polycythemia vera based on polycythemia vera study group protocols. Semin Hematol 1986; 23: 132– 143. 18 Kralovics R., Indrak K., Stopka T., et al. Two new EPO receptor mutations: Truncated EPO receptors are most frequently associated with primary familial and congenital polycythemias. Blood 1997; 90: 2057– 2061. 19 Prchal JT, Sokol L. Benign erythrocytosis” and other familial and congenital polycythemias. Eur J Haematol 1996; 57: 263– 268. 20 Distelhorst CW, Wagner DS, Goldwasser E., et al. Autosomal dominant familial erythrocytosis due to autonomous erythropoietin production. Blood 1981; 58: 1155– 1158. 21 de la Chapelle A., Traskelin AI, Juvonen E. Truncated erythropoietin receptor causes dominantly inherited benign human erythrocytosis. Proc Natl Acad Sci USA 1993; 90: 4495– 4499. 22 Beech J., Bloom JC, Hodge TG. Erythrocytosis in a horse. J Am Vet Med Assoc 1984; 184: 986– 989. 23 Morris DD. Erythrocytosis (polycythemia). In: BR Smith ed. Large Animal Internal Medicine, 2nd ed. St Louis , MO : CV Mosby; 1996: 1235– 1237. 24 Perman V., Schall WD. Diseases of the red blood cells. In: SJ Ettinger, ed. Textbook of Veterinary Internal Medicine. Diseases of the Dog and Cat, 2nd ed. Philadelphia , PA : WB Saunders; 1983: 1938– 2000. 25 Salmon SE, Sartorelli AC. Cancer chemotherapy. In: BG Katzung, ed. Basic and Clinical Pharmacology, 4th ed. Norwalk , CT : Appleton & Lange; 1989: 700– 701. 26 Hillyer MH, Mair TS. Multisystemic eosinophilic epitheliotropic disease in a horse: Attempted treatment with hydroxyurea and dexamethasone. Vet Rec 1992; 130: 392– 395. 27 Eyre P., Elmes PJ, Strickland S. Corticosteroid-potentiated vascular response of the equine digit: A possible pharmacological basis for laminitis. Am J Vet Res 1979; 40: 135– 138. Citing Literature Volume12, Issue5September 1998Pages 384-388 ReferencesRelatedInformation}, number={5}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={McFarlane, D and Sellon, DC and Parker, P}, year={1998}, pages={384–388} }
 @article{russell_perkins_grindem_walker_sellon_1997, title={Flow cytometric method for detecting thiazole orange positive (reticulated) platelets in thrombocytopenic horses}, volume={58}, number={10}, journal={American Journal of Veterinary Research}, author={Russell, K. E. and Perkins, P. C. and Grindem, C. B. and Walker, K. M. and Sellon, D. C.}, year={1997}, pages={1092–1096} }
 @article{sellon_walker_suyemoto_altier_1997, title={Nucleic acid amplification for rapid detection of Rhodococcus equi in equine blood and tracheal wash fluids}, volume={58}, number={11}, journal={American Journal of Veterinary Research}, author={Sellon, D. C. and Walker, K. and Suyemoto, M. M. and Altier, C.}, year={1997}, pages={1232–1237} }
 @article{sellon_levine_palmer_millikin_grindem_covington_1997, title={Thrombocytosis in 24 Horses (1989-1994)}, volume={11}, ISSN={0891-6640 1939-1676}, url={http://dx.doi.org/10.1111/j.1939-1676.1997.tb00069.x}, DOI={10.1111/j.1939-1676.1997.tb00069.x}, abstractNote={The records of horses presented to the Veterinary Teaching Hospital of North Carolina State University College of Veterinary Medicine between January 1, 1989 and April 30, 1994 were evaluated to determine risk factors associated with thrombocytosis. Of the 2,346 horses for which a CBC was performed, 24 (1.0%) had a platelet count > 400,000/μL. Demographic, diagnostic, physical examination, and clinicopathologic variables from these cases were compared with a reference population consisting of 189 horses with a normal platelet count presenting during the same period. Infectious/inflammatory disorders were observed more commonly in horses with high platelet counts than in horses with normal platelet counts. Initial independent evaluation of demographic variables revealed that horses more than 3 years of age, females, and geldings were less likely to have thrombocytosis than were younger horses or stallions. Independent analysis of clinicopathologic variables revealed that horses with thrombocytosis were more likely to have hyper‐fibrinogenemia, leukocytosis, hypoproteinemia, and anemia than were horses with normal platelet counts. Physical examination parameters associated with thrombocytosis included tachycardia and pyrexia. In the final multivariable model, the variables with the strongest association with thrombocytosis included leukocytosis, anemia, and hyper‐fibrinogenemia. Thrombocytosis rarely causes clinical problems in horses and is not likely to require specific antiplatelet therapy. The strong association of thrombocytosis with infectious/inflammatory disorders, however, should lead clinicians to suspect these types of conditions in horses with high platelet counts.}, number={1}, journal={Journal of Veterinary Internal Medicine}, publisher={Wiley}, author={Sellon, Debra C. and Levine, Jay F. and Palmer, Kate and Millikin, Everett and Grindem, Carol and Covington, Patrice}, year={1997}, month={Jan}, pages={24–29} }
 @article{sellon_walker_russell_perry_covington_fuller_1996, title={Equine infectious anemia virus replication is upregulated during differentiation of blood monocytes from acutely infected horses}, volume={70}, number={1}, journal={Journal of Virology}, author={Sellon, D. C. and Walker, K. M. and Russell, K. E. and Perry, S. T. and Covington, P. and Fuller, F. J.}, year={1996}, pages={590} }
 @article{sellon_walker_russell_perry_fuller_1996, title={Phorbol ester stimulation of equine macrophage cultures alters expression of equine infectious anemia virus}, volume={52}, ISSN={0378-1135}, url={http://dx.doi.org/10.1016/s0378-1135(96)00071-5}, DOI={10.1016/S0378-1135(96)00071-5}, abstractNote={Equine infectious anemia virus (EIAV) is a lentivirus that replicates predominantly in mature tissue macrophages. Viral expression is strongly influenced by the state of differentiation of the host cell. While blood monocytes can be infected, viral transcription is limited until the cell differentiates into a mature macrophage. Activation of mature macrophages infected with EIAV might also alter viral expression, presumably through binding of cellular transcription factors to viral nucleic acid sequences within the long terminal repeat (LTR). Using DNA amplification techniques, we compared LTR sequences of U.S. field strains of EIAV to sequences of a laboratory adapted strain of the virus. All field strain sequences were more closely related to Wyoming strain than to the Malmquist laboratory adapted strain or a previously sequenced infectious molecular clone of EIAV. Primary equine monocyte-derived macrophage cultures were infected with virulent and avirulent strains of EIAV and the effects of macrophage stimulation on EIAV expression were determined. Stimulation of macrophages with phorbol ester activated the cells to secrete tumor necrosis factor α (TNFα). This activation signal also resulted in a significant downregulation of viral expression as determined by supernatant reverse transcriptase activity. This effect occurred independent of the virulence of the virus strain used or the nucleic acid sequence of the viral LTR. This may represent an adaptive response of EIAV to evade the host immune response and establish a persistent infection.}, number={3-4}, journal={Veterinary Microbiology}, publisher={Elsevier BV}, author={Sellon, Debra C. and Walker, Kathy M. and Russell, Karen E. and Perry, Stephanie T. and Fuller, Frederick J.}, year={1996}, month={Oct}, pages={209–221} }
 @article{sellon_levine_millikin_palmer_covington_grindem_1996, title={Risk factors associated with thrombocytopenia in horses}, volume={10}, journal={Journal of Veterinary Internal Medicine}, author={Sellon, D. C. and Levine, J. F. and Millikin, E. and Palmer, K. and Covington, P. and Grindem, C.}, year={1996}, pages={127–132} }
 @article{sellon_levine_millikin_palmer_grindem_covington_1996, title={Thrombocytopenia in Horses: 35 Cases (1989-1994)}, volume={10}, ISSN={0891-6640 1939-1676}, url={http://dx.doi.org/10.1111/j.1939-1676.1996.tb02044.x}, DOI={10.1111/j.1939-1676.1996.tb02044.x}, abstractNote={The records of 3,952 equine patients presenting to the Veterinary Teaching Hospital at North Carolina State University College of Veterinary Medicine were evaluated to determine risk factors associated with thrombocytopenia. Of 2,346 horses from which a CBC was obtained, 35 (1.49%) were thrombocytopenic (platelet count < 75,000/μL). A reference population of 189 horses with normal platelet counts (75,000 to 300,000/μL) was also studied. Standardbred horses were at increased risk for thrombocytopenia. but age and gender were not identified as significant risk factors. Horses with infectious or inflammatory diseases were at increased risk for thrombocytopenia. The potential association of clinical and clinicopathologic factors with thrombocytopenia were assessed by reviewing a series of multiple logistic regression models. Clinical and clinicopathologic variables significantly associated with thrombocytopenia in the final model included increased PCV, increased band neutrophil count, increased total WBC, and decreased plasma protein concentration. Increased mature neutrophil count was associated with normal platelet counts. Thrombocytopenic horses were significantly more likely to die or be euthanized than were horses with normal platelet counts.J Vet Intern Med 1996;10:127–132. Copyright © 1996 by the American College of Veterinary Internal Medicine.}, number={3}, journal={Journal of Veterinary Internal Medicine}, publisher={Wiley}, author={Sellon, Debra C. and Levine, Jay and Millikin, Everett and Palmer, Kate and Grindem, Carol and Covington, Patrice}, year={1996}, month={May}, pages={127–132} }
 @article{sellon_cullen_whetter_gebhard_coggins_fuller_1993, title={Production and characterization of a monoclonal antibody recognizing a cytoplasmic antigen of equine mononuclear phagocytes}, volume={36}, ISSN={0165-2427}, url={http://dx.doi.org/10.1016/0165-2427(93)90027-2}, DOI={10.1016/0165-2427(93)90027-2}, abstractNote={An IgG1 mouse monoclonal antibody, designated 1.646, is described which recognizes a cytoplasmic antigen of equine mononuclear phagocytes. Indirect fluorescent antibody staining of peripheral blood leukocytes reveals a granular cytoplasmic staining, predominantly in adherent blood mononuclear cells. Indirect fluorescent antibody staining is positive for alveolar and peritoneal macrophages. In some horses, a few neutrophils are also stained. In equine tissue samples stained by immunohistochemistry, the distribution of positive cells is consistent with the distribution of tissue macrophages. The most intense and reliable staining occurs with splenic and lymph node macrophages. Hepatic Kupffer cells also stain with antibody 1.646, although the intensity of that staining is somewhat variable between horses. A granular pattern of staining typical of lipofuscin deposition is also seen in liver sections. There is also pale staining of some biliary and renal tubular epithelium. Equine erythrocytes, platelets and lymphocytes are not recognized by this antibody, and neither are monocyte/macrophages of human, canine or feline origin. Antibody 1.646 recognizes two proteins (150 and 30 kDa) of equine monocyte-derived macrophages when assayed by Western immunoblot. Because of the distribution of staining (tissue mononuclear phagocytes, lipofuscin-containing storage granules, biliary and renal tubular epithelium, and some neutrophils) we hypothesize that antibody 1.646 recognizes a cytoplasmic antigen that is closely associated with lysosomal membranes.}, number={4}, journal={Veterinary Immunology and Immunopathology}, publisher={Elsevier BV}, author={Sellon, Debra C. and Cullen, John M. and Whetter, Linda E. and Gebhard, Douglas H. and Coggins, Leroy and Fuller, Frederick J.}, year={1993}, month={May}, pages={303–318} }