@article{conley_till_berglund_jones_sheats_2023, title={A myristoylated alanine-rich C-kinase substrate (MARCKS) inhibitor peptide attenuates neutrophil outside-in & beta;(2)-integrin activation and signaling}, volume={17}, ISSN={["1933-6926"]}, url={https://doi.org/10.1080/19336918.2023.2233204}, DOI={10.1080/19336918.2023.2233204}, abstractNote={MARCKS is an actin and PIP2-binding protein that plays an essential role in neutrophil migration and adhesion; however, the molecular details regarding MARCKS function in these processes remains unclear. Neutrophil adhesion and migration also require the cell surface receptors β2-integrins. We hypothesized that MARCKS inhibition would alter neutrophil β2-integrin activation and signaling. We utilized a MARCKS-targeting peptide to inhibit MARCKS in inside-out and outside-in β2-integrin activation in neutrophils. MANS-mediated MARCKS inhibition had no significant effect on inside-out β2-integrin activation. MANS treatment significantly attenuated ICAM-1/Mn2+-stimulated static adhesion, cell spreading and β2-integrin clustering, suggesting a role for MARCKS function in outside-in β2-integrin activation. Additional work is needed to better understand the molecular mechanisms of MARCKS role in outside-in β2-integrin activation and signaling.}, number={1}, journal={CELL ADHESION & MIGRATION}, author={Conley, Haleigh and Till, Rebecca L. and Berglund, Alix K. and Jones, Samuel L. and Sheats, M. Katie}, year={2023}, month={Dec}, pages={1–16} }
 @article{bayless_bayless_sheats_jones_2022, title={Withaferin A Inhibits Neutrophil Adhesion, Migration, and Respiratory Burst and Promotes Timely Neutrophil Apoptosis}, volume={9}, ISSN={["2297-1769"]}, url={https://europepmc.org/articles/PMC9247543}, DOI={10.3389/fvets.2022.900453}, abstractNote={Neutrophils play a major role in many equine conditions, including equine asthma, laminitis, and intestinal ischemia and reperfusion injury, and therefore represent an attractive target for innovative therapeutic approaches. Novel strategies for reducing neutrophilic inflammation include modulation of neutrophil functions and lifespan. Withaferin A (WFA) is a phytochemical with well-established in vitro and in vivo anti-inflammatory properties, but its direct effects on neutrophils are largely unknown. We hypothesized that WFA would inhibit adhesion, migration, and respiratory burst by equine neutrophils and promote timely apoptosis of primed equine neutrophils. Consistent with this hypothesis, our data show that WFA causes a significant, concentration-dependent inhibition of equine neutrophil adhesion, migration, and respiratory burst in response to diverse stimuli. Further, WFA treatment increased apoptosis of equine neutrophils exposed to GM-CSF for 24 h. This pro-apoptotic effect of WFA was not observed in unprimed neutrophils, nor at the 2-h time point relevant to our functional neutrophil experiments. Our data demonstrate that WFA may reduce neutrophil-mediated inflammation through multiple mechanisms, including suppression of inflammatory responses and promotion of apoptosis. Additional research is needed to elucidate the molecular mechanisms for these effects and evaluate the potential clinical use of WFA in veterinary and human patients.}, journal={FRONTIERS IN VETERINARY SCIENCE}, author={Bayless, Rosemary and Bayless, RL and Sheats, M. Katie and Jones, Sam}, editor={Bayless, RosemaryEditor}, year={2022}, month={Jun} }
 @article{martin_schirmer_jones_davis_2018, title={Pharmacokinetics and ex vivo anti‐inflammatory effects of oral misoprostol in horses}, volume={51}, ISSN={0425-1644 2042-3306}, url={http://dx.doi.org/10.1111/evj.13024}, DOI={10.1111/evj.13024}, abstractNote={Misoprostol is an E prostanoid (EP) 2, 3 and 4 receptor agonist that is anecdotally used to treat and prevent NSAID-induced GI injury in horses. Misoprostol elicits anti-inflammatory effects in vivo in men and rodents, and inhibits TNFα production in equine leucocytes in vitro.Define the pharmacokinetic parameters of oral misoprostol in horses, and determine the inhibitory effect of oral misoprostol administration on equine leucocyte TNFα production in an ex vivo inflammation model.Pharmacokinetic study, ex vivo experimental study.Six healthy adult horses of mixed breeds were used. In phase one, horses were given 5 μg/kg misoprostol orally, and blood was collected at predetermined times for determination of misoprostol free acid (MFA) by UHPLC-MS/MS. Pharmacokinetic parameters were calculated. In phase two, horses were dosed as in phase one, and blood was collected at T0, 0.5, 1 and 4 h following misoprostol administration for leucocyte isolation. Leucocytes were stimulated with 100 ng/mL LPS, and TNFα mRNA concentrations were determined via quantitative real-time PCR.About 5 μg/kg oral misoprostol produced a rapid time to maximum concentration (Tmax ) of 23.4 ± 2.4 min, with a maximum concentration (Cmax ) of 0.29 ± 0.07 ng/mL and area under the curve (AUC0-∞ ) of 0.4 ± 0.12 h ng/mL. LPS stimulation of equine leucocytes ex vivo significantly increased TNFα mRNA concentrations, and there was no significant effect of misoprostol even at the Tmax .Only a single dose was used, and sample size was small.Misoprostol is rapidly absorbed following oral administration in horses, and a single 5 μg/kg dose had no significant inhibitory effect on ex vivo LPS-stimulated TNFα mRNA production in leucocytes. Further studies analysing different dosing strategies, including repeat administration or combination with other anti-inflammatory drugs, are warranted.}, number={3}, journal={Equine Veterinary Journal}, publisher={Wiley}, author={Martin, E. M. and Schirmer, J. M. and Jones, S. L. and Davis, J. L.}, year={2018}, month={Oct}, pages={415–421} }
 @article{levine_cianciolo_linder_bizikova_birkenheuer_brooks_salous_nordone_bellinger_marr_et al._2017, title={Endothelial alterations in a canine model of immune thrombocytopenia}, volume={30}, ISSN={0953-7104 1369-1635}, url={http://dx.doi.org/10.1080/09537104.2017.1378807}, DOI={10.1080/09537104.2017.1378807}, abstractNote={Bleeding heterogeneity amongst patients with immune thrombocytopenia (ITP) is poorly understood. Platelets play a role in maintaining endothelial integrity, and variable thrombocytopenia-induced endothelial changes may influence bleeding severity. Platelet-derived endothelial stabilizers and markers of endothelial integrity in ITP are largely underexplored. We hypothesized that, in a canine ITP model, thrombocytopenia would lead to alterations in the endothelial ultrastructure and that the Von Willebrand factor (vWF) would serve as a marker of endothelial injury associated with thrombocytopenia. Thrombocytopenia was induced in healthy dogs with an antiplatelet antibody infusion; control dogs received an isotype control antibody. Cutaneous biopsies were obtained prior to thrombocytopenia induction, at platelet nadir, 24 hours after nadir, and on platelet recovery. Cutaneous capillaries were assessed by electron microscopy for vessel thickness, the number of pinocytotic vesicles, the number of large vacuoles, and the number of gaps between cells. Pinocytotic vesicles are thought to represent an endothelial membrane reserve that can be used for repair of damaged endothelial cells. Plasma samples were assessed for vWF. ITP dogs had significantly decreased pinocytotic vesicle numbers compared to control dogs (P = 0.0357) and the increase in plasma vWF from baseline to 24 hours correlated directly with the endothelial large vacuole score (R = 0.99103; P < 0.0001). This direct correlation between plasma vWF and the number of large vacuoles, representing the vesiculo-vacuolar organelle (VVO), a permeability structure, suggests that circulating vWF could serve as a biomarker for endothelial alterations and potentially a predictor of thrombocytopenic bleeding. Overall, our results indicate that endothelial damage occurs in the canine ITP model and variability in the degree of endothelial damage may account for differences in the bleeding phenotype among patients with ITP.}, number={1}, journal={Platelets}, publisher={Informa UK Limited}, author={LeVine, Dana N. and Cianciolo, Rachel E. and Linder, Keith E. and Bizikova, Petra and Birkenheuer, Adam J. and Brooks, Marjory B. and Salous, Abdelghaffar K. and Nordone, Shila K. and Bellinger, Dwight A. and Marr, Henry and et al.}, year={2017}, month={Nov}, pages={88–97} }
 @article{martin_jones_2017, title={Inhibition of microsomal prostaglandin E-synthase-1 (mPGES-1) selectively suppresses PGE 2 in an in vitro equine inflammation model}, volume={192}, ISSN={0165-2427}, url={http://dx.doi.org/10.1016/j.vetimm.2017.09.008}, DOI={10.1016/j.vetimm.2017.09.008}, abstractNote={Inhibition of prostaglandin E2 (PGE2) production effectively limits inflammation in horses, however nonspecific prostaglandin blockade via cyclooxygenase (COX) inhibition elicits deleterious gastrointestinal side effects in equine patients. Thus, more selective PGE2 targeting therapeutics are needed to treat inflammatory disease in horses. One potential target is microsomal prostaglandin E-synthase-1 (mPGES-1), which is the terminal enzyme downstream of COX-2 in the inducible PGE2 synthesis cascade. This enzyme has yet to be studied in equine leukocytes, which play a pivotal role in equine inflammatory disease. The objective of this study was to determine if mPGES-1 is a PGE2-selective anti-inflammatory target in equine leukocytes. To evaluate this objective, leukocyte-rich plasma (LRP) was isolated from equine whole blood collected via jugular venipuncture of six healthy adult horses of mixed breeds and genders. LRP was primed with granulocyte-monocyte colony-stimulating factor (GM-CSF) and stimulated with lipopolysaccharide (LPS) in the presence or absence of an mPGES-1 inhibitor (MF63), a COX-2 inhibitor (NS-398), or a nonselective COX inhibitor (indomethacin). Following treatment, mPGES-1 and COX-2 mRNA and protein levels were measured via qPCR and western blot, respectively, and PGE2, thromboxane (TXA2) and prostacyclin (PGI2) levels were measured in cellular supernatants via ELISA. This study revealed that LPS significantly increased mPGES-1 mRNA, but not protein levels in equine LRP as measured by qPCR and western blot, respectively. In contrast, COX-2 mRNA and protein were coordinately induced by LPS. Importantly, treatment of LPS-stimulated leukocytes with indomethacin and NS-398 significantly reduced extracellular concentrations of multiple prostanoids (PGE2, TXA2 and PGI2), while the mPGES-1 inhibitor MF63 selectively inhibited PGE2 production only. mPGES-1 inhibition also preserved higher basal levels of PGE2 production when compared to either COX inhibitor, which might be beneficial in a clinical setting. In conclusion, this work identifies mPGES-1 as a key regulator of PGE2 production and a PGE2-selective target in equine leukocytes. This study demonstrates that mPGES-1 is a potentially safer and effective therapeutic target for treatment of equine inflammatory disease when compared to traditional non-steroidal anti-inflammatory drugs.}, journal={Veterinary Immunology and Immunopathology}, publisher={Elsevier BV}, author={Martin, Emily M. and Jones, Samuel L.}, year={2017}, month={Oct}, pages={33–40} }
 @article{martin_till_sheats_jones_2017, title={Misoprostol Inhibits Equine Neutrophil Adhesion, Migration, and Respiratory Burst in an In Vitro Model of Inflammation}, volume={4}, ISSN={2297-1769}, url={http://dx.doi.org/10.3389/fvets.2017.00159}, DOI={10.3389/fvets.2017.00159}, abstractNote={In many equine inflammatory disease states, neutrophil activities, such as adhesion, migration, and reactive oxygen species (ROS) production become dysregulated. Dysregulated neutrophil activation causes tissue damage in horses with asthma, colitis, laminitis, and gastric glandular disease. Non-steroidal anti-inflammatory drugs do not adequately inhibit neutrophil inflammatory functions and can lead to dangerous adverse effects. Therefore, novel therapies that target mechanisms of neutrophil-mediated tissue damage are needed. One potential neutrophil-targeting therapeutic is the PGE1 analog, misoprostol. Misoprostol is a gastroprotectant that induces intracellular formation of the secondary messenger molecule cyclic AMP (cAMP), which has been shown to have anti-inflammatory effects on neutrophils. Misoprostol is currently used in horses to treat NSAID-induced gastrointestinal injury; however, its effects on equine neutrophils have not been determined. We hypothesized that treatment of equine neutrophils with misoprostol would inhibit equine neutrophil adhesion, migration, and ROS production, in vitro. We tested this hypothesis using isolated equine peripheral blood neutrophils collected from 12 healthy adult teaching/research horses of mixed breed and gender. The effect of misoprostol treatment on adhesion, migration, and respiratory burst of equine neutrophils was evaluated via fluorescence-based adhesion and chemotaxis assays, and luminol-enhanced chemiluminescence, respectively. Neutrophils were pretreated with varying concentrations of misoprostol, vehicle, or appropriate functional inhibitory controls prior to stimulation with LTB4, CXCL8, PAF, lipopolysaccharide (LPS) or immune complex (IC). This study revealed that misoprostol pretreatment significantly inhibited LTB4-induced adhesion, LTB4-, CXCL8-, and PAF-induced chemotaxis, and LPS-, IC-, and PMA-induced ROS production in a concentration-dependent manner. This data indicate that misoprostol-targeting of E-prostanoid (EP) receptors potently inhibits equine neutrophil effector functions in vitro. Additional studies are indicated to further elucidate the role of EP receptors in regulating neutrophil function. Overall, our results suggest misoprostol may hold promise as a novel anti-inflammatory therapeutic in the horse.}, journal={Frontiers in Veterinary Science}, publisher={Frontiers Media SA}, author={Martin, Emily Medlin and Till, Rebecca Louise and Sheats, Mary Katherine and Jones, Samuel L.}, year={2017}, month={Sep} }
 @article{martin_messenger_sheats_jones_2017, title={Misoprostol Inhibits Lipopolysaccharide-Induced Pro-inflammatory Cytokine Production by Equine Leukocytes}, volume={4}, ISSN={2297-1769}, url={http://dx.doi.org/10.3389/fvets.2017.00160}, DOI={10.3389/fvets.2017.00160}, abstractNote={Pro-inflammatory cytokines including tumor necrosis factor α (TNFα), IL-1β, IL-6, and IL-8 are potent immune mediators that exacerbate multiple equine diseases such as sepsis and laminitis. Unfortunately, safe and effective cytokine-targeting therapies are lacking in horses; therefore, novel mechanisms of inhibiting cytokine production are critically needed. One potential mechanism for inhibiting cytokine synthesis is elevation of intracellular cyclic AMP (cAMP). In human leukocytes, intracellular cAMP production is induced by activation of E-prostanoid (EP) receptors 2 and 4. These receptors can be targeted by the EP2/4 agonist and prostaglandin E}, journal={Frontiers in Veterinary Science}, publisher={Frontiers Media SA}, author={Martin, Emily Medlin and Messenger, Kristen M. and Sheats, Mary Katherine and Jones, Samuel L.}, year={2017}, month={Sep} }
 @inbook{jones_barton_2015, place={St Louis, MO}, edition={5th}, title={Diagnostic procedures in the examination of the equine alimentary system}, booktitle={Large Animal Internal Medicine}, publisher={Elsevier}, author={Jones, S.L. and Barton, M.H.}, editor={Smith, B.P.Editor}, year={2015}, pages={638–653} }
 @inbook{jones_2015, place={St Louis, MO}, edition={5th}, title={Disorders of the esophagus}, booktitle={Large Animal Internal Medicine}, publisher={Elsevier}, author={Jones, S.L.}, editor={Smith, B.P.Editor}, year={2015}, pages={663–668} }
 @inbook{jones_2015, place={St Louis, MO}, edition={5th}, title={Non-steroidal anti-inflammatory drug toxicity}, booktitle={Large Animal Internal Medicine}, publisher={Elsevier}, author={Jones, S.L.}, editor={Smith, B.P.Editor}, year={2015}, pages={732–734} }
 @article{levine_birkenheuer_brooks_nordone_bellinger_jones_fischer_oglesbee_frey_brinson_et al._2014, title={A novel canine model of immune thrombocytopenia: has immune thrombocytopenia (ITP) gone to the dogs?}, volume={167}, ISSN={0007-1048}, url={http://dx.doi.org/10.1111/bjh.13005}, DOI={10.1111/bjh.13005}, abstractNote={Summary Canine immune thrombocytopenia ( ITP ) is analogous to human ITP , with similar platelet counts and heterogeneity in bleeding phenotype among affected individuals. With a goal of ultimately investigating this bleeding heterogeneity, a canine model of antibody‐mediated ITP was developed. Infusion of healthy dogs with 2 F 9, a murine I g G 2a monoclonal antibody to the canine platelet glycoprotein GPII b (a common target of autoantibodies in ITP ) resulted in profound, dose‐dependent thrombocytopenia. Model dogs developed variable bleeding phenotypes, e.g. petechiae and haematuria, despite similar degrees of thrombocytopenia. 2 F 9 infusion was not associated with systemic inflammation, consumptive coagulopathy, or impairment of platelet function. Unexpectedly however, evaluation of cytokine profiles led to the identification of platelets as a potential source of serum interleukin‐8 ( IL 8) in dogs. This finding was confirmed in humans with ITP , suggesting that platelet IL 8 may be a previously unrecognized modulator of platelet‐neutrophil crosstalk. The utility of this model will allow future study of bleeding phenotypic heterogeneity including the role of neutrophils and endothelial cells in ITP .}, number={1}, journal={British Journal of Haematology}, publisher={Wiley}, author={LeVine, Dana N. and Birkenheuer, Adam J. and Brooks, Marjory B. and Nordone, Shila K. and Bellinger, Dwight A. and Jones, Sam L. and Fischer, Thomas H. and Oglesbee, Stephen E. and Frey, Kahlina and Brinson, Nicole S. and et al.}, year={2014}, month={Jul}, pages={110–120} }
 @article{sheats_sung_adler_jones_inflammation_2014, title={In Vitro Neutrophil Migration Requires Protein Kinase C-Delta (δ-PKC)-Mediated Myristoylated Alanine-Rich C-Kinase Substrate (MARCKS) Phosphorylation}, volume={38}, ISSN={0360-3997 1573-2576}, url={http://dx.doi.org/10.1007/s10753-014-0078-9}, DOI={10.1007/s10753-014-0078-9}, abstractNote={Dysregulated release of neutrophil reactive oxygen species and proteolytic enzymes contributes to both acute and chronic inflammatory diseases. Therefore, molecular regulators of these processes are potential targets for new anti-inflammatory therapies. We have shown previously that myristoylated alanine-rich C-kinase substrate (MARCKS), a well-known actin binding protein and protein kinase C (PKC) substrate, is a key regulator of neutrophil functions. In the current study, we investigate the role of PKC-mediated MARCKS phosphorylation in neutrophil migration and adhesion in vitro. We report that treatment of human neutrophils with the δ-PKC inhibitor rottlerin significantly attenuates f-Met-Leu-Phe (fMLF)-induced MARCKS phosphorylation (IC50 = 5.709 μM), adhesion (IC50 = 8.4 μM), and migration (IC50 = 6.7 μM), while α-, β-, and ζ-PKC inhibitors had no significant effect. We conclude that δ-PKC-mediated MARCKS phosphorylation is essential for human neutrophil migration and adhesion in vitro. These results implicate δ-PKC-mediated MARCKS phosphorylation as a key step in the inflammatory response of neutrophils.}, number={3}, journal={Inflammation}, publisher={Springer Science and Business Media LLC}, author={Sheats, M.K. and Sung, E.J. and Adler, K.B. and Jones, S.L. and Inflammation}, year={2014}, month={Dec}, pages={1126–1141} }
 @article{sheats_pescosolido_hefner_sung_adler_jones_2014, title={Myristoylated Alanine Rich C Kinase Substrate (MARCKS) is essential to β2-integrin dependent responses of equine neutrophils}, volume={160}, ISSN={0165-2427}, url={http://dx.doi.org/10.1016/j.vetimm.2014.04.009}, DOI={10.1016/j.vetimm.2014.04.009}, abstractNote={Neutrophil infiltration is a prominent feature in a number of pathologic conditions affecting horses including recurrent airway obstruction, ischemia-reperfusion injury, and laminitis. Cell signaling components involved in neutrophil migration represent targets for novel anti-inflammatory therapies. In order to migrate into tissue, neutrophils must respond to chemoattractant signals in their external environment through activation of adhesion receptors (i.e. integrins) and reorganization of the actin cytoskeleton. Myristoylated Alanine-Rich C-Kinase Substrate (MARCKS), a highly conserved actin-binding protein, has a well demonstrated role in cytoskeletal dependent cellular functions (i.e. adhesion, spreading, and migration), but the details of MARCKS involvement in these processes remain vague. We hypothesized that MARCKS serves as a link between the actin cytoskeleton and integrin function in neutrophils. Using a MARCKS-specific inhibitor peptide known as MANS on equine neutrophils in vitro, we demonstrate that inhibition of MARCKS function significantly attenuates β2-integrin-dependent neutrophil functions including migration, adhesion, and immune complex-mediated respiratory burst. The MANS peptide did not, however, inhibit the β2-integrin-independent PMA mediated respiratory burst. These results attest to the essential role of MARCKS function in regulating neutrophil responses, and strongly implicate MARCKS as a potential regulator of β2-integrins in neutrophils.}, number={3-4}, journal={Veterinary Immunology and Immunopathology}, publisher={Elsevier BV}, author={Sheats, Mary K. and Pescosolido, Kimberly C. and Hefner, Ethan M. and Sung, Eui Jae and Adler, Kenneth B. and Jones, Samuel L.}, year={2014}, month={Aug}, pages={167–176} }
 @article{li_d’annibale-tolhurst_adler_fang_yin_birkenheuer_levy_jones_sung_hawkins_et al._2013, title={A Myristoylated Alanine-Rich C Kinase Substrate–Related Peptide Suppresses Cytokine mRNA and Protein Expression in LPS-Activated Canine Neutrophils}, volume={48}, ISSN={1044-1549 1535-4989}, url={http://dx.doi.org/10.1165/rcmb.2012-0278OC}, DOI={10.1165/rcmb.2012-0278oc}, abstractNote={Section:ChooseTop of pageAbstract <<Materials and MethodsResultsDiscussionReferencesCITING ARTICLES}, number={3}, journal={American Journal of Respiratory Cell and Molecular Biology}, publisher={American Thoracic Society}, author={Li, Jingjing and D’Annibale-Tolhurst, Melissa A. and Adler, Kenneth B. and Fang, Shijing and Yin, Qui and Birkenheuer, Adam J. and Levy, Michael G. and Jones, Samuel L. and Sung, Eui Jae and Hawkins, Eleanor C. and et al.}, year={2013}, month={Mar}, pages={314–321} }
 @article{ott_sung_melvin_sheats_haugh_adler_jones_2013, title={Fibroblast Migration Is Regulated by Myristoylated Alanine-Rich C-Kinase Substrate (MARCKS) Protein}, volume={8}, ISSN={["1932-6203"]}, url={http://europepmc.org/abstract/med/23840497}, DOI={10.1371/journal.pone.0066512}, abstractNote={Myristoylated alanine-rich C-kinase substrate (MARCKS) is a ubiquitously expressed substrate of protein kinase C (PKC) that is involved in reorganization of the actin cytoskeleton. We hypothesized that MARCKS is involved in regulation of fibroblast migration and addressed this hypothesis by utilizing a unique reagent developed in this laboratory, the MANS peptide. The MANS peptide is a myristoylated cell permeable peptide corresponding to the first 24-amino acids of MARCKS that inhibits MARCKS function. Treatment of NIH-3T3 fibroblasts with the MANS peptide attenuated cell migration in scratch wounding assays, while a myristoylated, missense control peptide (RNS) had no effect. Neither MANS nor RNS peptide treatment altered NIH-3T3 cell proliferation within the parameters of the scratch assay. MANS peptide treatment also resulted in inhibited NIH-3T3 chemotaxis towards the chemoattractant platelet-derived growth factor-BB (PDGF-BB), with no effect observed with RNS treatment. Live cell imaging of PDGF-BB induced chemotaxis demonstrated that MANS peptide treatment resulted in weak chemotactic fidelity compared to RNS treated cells. MANS and RNS peptides did not affect PDGF-BB induced phosphorylation of MARCKS or phosphoinositide 3-kinase (PI3K) signaling, as measured by Akt phosphorylation. Further, no difference in cell migration was observed in NIH-3T3 fibroblasts that were transfected with MARCKS siRNAs with or without MANS peptide treatment. Genetic structure-function analysis revealed that MANS peptide-mediated attenuation of NIH-3T3 cell migration does not require the presence of the myristic acid moiety on the amino-terminus. Expression of either MANS or unmyristoylated MANS (UMANS) C-terminal EGFP fusion proteins resulted in similar levels of attenuated cell migration as observed with MANS peptide treatment. These data demonstrate that MARCKS regulates cell migration and suggests that MARCKS-mediated regulation of fibroblast migration involves the MARCKS amino-terminus. Further, this data demonstrates that MANS peptide treatment inhibits MARCKS function during fibroblast migration and that MANS mediated inhibition occurs independent of myristoylation.}, number={6}, journal={PLOS ONE}, publisher={Public Library of Science (PLoS)}, author={Ott, Laura E. and Sung, Eui Jae and Melvin, Adam T. and Sheats, Mary K. and Haugh, Jason M. and Adler, Kenneth B. and Jones, Samuel L.}, editor={Aspenstrom, PontusEditor}, year={2013}, month={Jun} }
 @article{cherry_jones_maggi_davis_breitschwerdt_2012, title={Bartonellaspp. Infection in Healthy and Sick Horses and Foals from the Southeastern United States}, volume={26}, ISSN={0891-6640}, url={http://dx.doi.org/10.1111/j.1939-1676.2012.00998.x}, DOI={10.1111/j.1939-1676.2012.00998.x}, abstractNote={Background B artonella species bacteremia has been identified in numerous animal species. These bacteria cause, or have been associated with, a spectrum of clinical manifestations in dogs and human patients. The frequency of exposure to or infection with B artonella spp. among healthy and sick horses has not been reported. Objective To test healthy and sick horses and sick foals from the southeastern U nited S tates for serological, microbiological, and molecular evidence of B artonella infection. Animals Forty‐seven healthy horses, 15 sick foals, 22 horses with musculoskeletal manifestations, and 8 horses with colic were tested for B artonella . Methods IFA serology and PCR before and after BAPGM ( B artonella alpha‐Proteobacteria Growth Medium) enrichment blood culture. Results B artonella antibodies were not detected in foals or horses. Three B artonella species, B . henselae , B . vinsonii subsp. berkhoffii (genotypes I and III ), and a B artonella species with closest homology to C andidatus Bartonella volans, were PCR ‐amplified and sequenced from blood or BAPGM enrichment blood culture samples from 1/47 healthy horses, 3/15 sick foals, 5/22 horses with musculoskeletal disease, and 0/8 horses with colic. Conclusions and Clinical Importance Horses in the southeastern United States are naturally infected with B . henselae , B . vinsonii subsp. berkhofii genotypes I and III , and a bacteria most similar to C andidatus Bartonella volans. Antibodies were not detectable by indirect fluorescent antibody assay ( IFA ) testing in bacteremic foals or horses, and prolonged enrichment culture for periods up to 21 days were necessary to document bacteremia in most horses. Further investigation into the pathogenic potential of B artonella spp. infection in horses is warranted.}, number={6}, journal={Journal of Veterinary Internal Medicine}, publisher={Wiley}, author={Cherry, N.A. and Jones, S.L. and Maggi, R.G. and Davis, J.L. and Breitschwerdt, E.B.}, year={2012}, month={Sep}, pages={1408–1412} }
 @article{green_park_yin_fang_crews_jones_adler_2012, title={Directed migration of mouse macrophages in vitro involves myristoylated alanine-rich C-kinase substrate (MARCKS) protein}, volume={92}, ISSN={0741-5400}, url={http://dx.doi.org/10.1189/jlb.1211604}, DOI={10.1189/jlb.1211604}, abstractNote={Abstract MARCKS is involved in directed migration of macrophages via a process involving its phosphorylation, cytoplasmic translocation, and interaction with actin. A role for MARCKS protein in directed migration of macrophages toward a chemoattractant was investigated. A peptide identical to the N-terminus of MARCKS (the MANS peptide), shown previously to inhibit the function of MARCKS in various cell types, was used. We investigated whether this MARCKS-related peptide could affect migration of macrophages, using the mouse macrophage-like J774A.1 cell line and primary murine macrophages. Both of these cell types migrated in response to the chemoattractants macrophage/MCPs, MCP-1 (25–100 ng/ml) or C5a (5–20 ng/ml). Cells were preincubated (15 min) with MANS or a mis-sense control peptide (RNS), both at 50 μM, and effects on migration determined 3 h after addition of chemoattractants. The movement and interactions of MARCKS and actin also were followed visually via confocal microscopy using a fluorescently labeled antibody to MARCKS and fluorescently tagged phalloidin to identify actin. MANS, but not RNS, attenuated migration of J774A.1 cells and primary macrophages in response to MCP-1 or C5a, implicating MARCKS in the cellular mechanism of directed migration. Exposure of cells to MCP-1 resulted in rapid phosphorylation and translocation of MARCKS from plasma membrane to cytosol, whereas actin appeared to spread through the cell and into cell protrusions; there was visual and biochemical evidence of a transient interaction between MARCKS and actin during the process of migration. These results suggest that MARCKS is involved in directed migration of macrophages via a process involving its phosphorylation, cytoplasmic translocation, and interaction with actin.}, number={3}, journal={Journal of Leukocyte Biology}, publisher={Wiley}, author={Green, T. D. and Park, J. and Yin, Q. and Fang, S. and Crews, A. L. and Jones, S. L. and Adler, K. B.}, year={2012}, month={May}, pages={633–639} }
 @article{royal_lascelles_lewbart_correa_jones_2012, title={EVALUATION OF CYCLOOXYGENASE PROTEIN EXPRESSION IN TRAUMATIZED VERSUS NORMAL TISSUES FROM EASTERN BOX TURTLES (TERRAPENE CAROLINA CAROLINA)}, volume={43}, ISSN={1042-7260 1937-2825}, url={http://dx.doi.org/10.1638/2011-0154.1}, DOI={10.1638/2011-0154.1}, abstractNote={This pilot study was designed to determine whether cyclooxygenase (COX)-1, COX-2, or both are expressed in normal turtle tissues and whether level of expression changes when tissue becomes inflamed. Five eastern box turtles, Terrapene carolina carolina, that either died or were euthanatized due to disease or injuries were used for this work. Tissues were obtained from the five turtles. Western blot analysis was used to evaluate tissues for COX-1 and COX-2 proteins. Densiometric analysis was used to compare Western blot bands within each turtle. COX-1 and COX-2 were found in the liver, kidney, grossly normal muscle, and grossly traumatized (inflamed) muscle of all study turtles. In all cases, COX-1 and COX-2 proteins were increased in traumatized muscle over grossly normal nontraumatized muscle. The highest levels of COX-1 and COX-2 proteins were found in kidney and liver. There was no statistical difference between the amount of COX-1 protein in liver and kidney, but traumatized muscle compared with grossly normal muscle had significantly greater COX-1 but not COX 2 protein concentrations. There was no statistical difference between the amount of COX-2 protein in liver and kidney. Traumatized muscle expressed nonstatistically significant greater amounts of COX-2 compared with grossly normal muscle. COX-1 and COX-2 proteins are expressed in turtle tissues, and both isoforms are up-regulated during inflammation of muscle tissue. Traditional nonsteroidal anti-inflammatory drugs (NSAIDs) that block both COX isoforms might be more efficacious than COX-2–selective drugs. This work suggests that NSAIDs should be evaluated for potential liver and kidney toxicity in turtles.}, number={2}, journal={Journal of Zoo and Wildlife Medicine}, publisher={American Association of Zoo Veterinarians}, author={Royal, Lillian W and Lascelles, B. Duncan X and Lewbart, Gregory A and Correa, Maria T and Jones, Samuel L}, year={2012}, month={Jun}, pages={289–295} }
 @article{cherry_liebisch_liebisch_breitschwerdt_jones_ulrich_allmers_wolf_hewicker-trautwein_2011, title={Identification of Bartonella henselae in a horse from Germany}, volume={150}, ISSN={0378-1135}, url={http://dx.doi.org/10.1016/j.vetmic.2011.02.010}, DOI={10.1016/j.vetmic.2011.02.010}, abstractNote={To investigate the occurrence of Bartonella sp. infection in asymptomatic horses and donkeys living in Tuscany, Central Italy.Blood samples were collected from 77 horses and 15 donkeys and tested by indirect immunofluorescent test to detect antibodies against Bartonella sp. and by PCR to detect the pathogen.Fifty-four (58.69%; 95% CI: 47.95%–68.87%) animals, 9 donkeys and 45 horses, were seropositive with antibody titers ranging from 1:64 to 1:512. PCR assays detected 9 horses positive for Bartonella sp. and 3 donkeys for Bartonella henselae genotype I.The detected sero-prevalence suggests a common and frequent exposure of equids living in Central Italy to bartonellae and PCR results show that Bartonella sp. infection is possible both in horses and donkeys. At the best of our knowledge, this is the first report of Bartonella henselae infection in donkeys.}, number={3-4}, journal={Veterinary Microbiology}, publisher={Elsevier BV}, author={Cherry, N.A. and Liebisch, G. and Liebisch, A. and Breitschwerdt, E.B. and Jones, S.L. and Ulrich, R. and Allmers, E. and Wolf, P. and Hewicker-Trautwein, M.}, year={2011}, month={Jun}, pages={414–415} }
 @article{ott_mcdowell_turner_law_adler_yoder_jones_2011, place={Hoboken, N.J}, title={Two Myristoylated Alanine-Rich C-Kinase Substrate (MARCKS) Paralogs are Required for Normal Development in Zebrafish}, volume={294}, ISSN={1932-8486}, url={http://dx.doi.org/10.1002/ar.21453}, DOI={10.1002/ar.21453}, abstractNote={Myristoylated alanine-rich C-kinase substrate (MARCKS) is an actin binding protein substrate of protein kinase C (PKC) and critical for mouse and Xenopus development. Herein two MARCKS paralogs, marcksa and marcksb, are identified in zebrafish and the role of these genes in zebrafish development is evaluated. Morpholino-based targeting of either MARCKS protein resulted in increased mortality and a range of gross phenotypic abnormalities. Phenotypic abnormalities were classified as mild, moderate or severe, which is characterized by a slight curve of a full-length tail, a severe curve or twist of a full-length tail and a truncated tail, respectively. All three phenotypes displayed abnormal neural architecture. Histopathology of Marcks targeted embryos revealed abnormalities in retinal layering, gill formation and skeletal muscle morphology. These results demonstrate that Marcksa and Marcksb are required for normal zebrafish development and suggest that zebrafish are a suitable model to further study MARCKS function.}, note={: 2007),}, number={9}, journal={The Anatomical Record: Advances in Integrative Anatomy and Evolutionary Biology}, publisher={Wiley}, author={Ott, Laura E. and Mcdowell, Zachary T. and Turner, Poem M. and Law, J. Mchugh and Adler, Kenneth B. and Yoder, Jeffrey A. and Jones, Samuel L.}, year={2011}, month={Aug}, pages={1511–1524} }
 @article{eckert_neuder_park_adler_jones_2010, title={Myristoylated Alanine-Rich C-Kinase Substrate (MARCKS) Protein Regulation of Human Neutrophil Migration}, volume={42}, ISSN={["1535-4989"]}, url={http://europepmc.org/abstract/med/19574534}, DOI={10.1165/rcmb.2008-0394oc}, abstractNote={Section:ChooseTop of pageAbstract <<MATERIALS AND METHODSRESULTSDISCUSSIONReferencesCITING ARTICLES}, number={5}, journal={AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY}, author={Eckert, Rachael E. and Neuder, Laura E. and Park, Joungjoa and Adler, Kenneth B. and Jones, Samuel L.}, year={2010}, month={May}, pages={586–594} }
 @inbook{jones_2009, place={St. Louis, MO}, edition={6th}, title={Antibiotic associated diarrhea}, ISBN={9781416054757}, booktitle={Current Therapy in Equine Medicine}, publisher={Saunders}, author={Jones, S.L.}, editor={Robinson, N.E.Editor}, year={2009}, pages={433–435} }
 @inbook{blikslager_jones_2009, place={St Louis, MO}, edition={4th}, title={Disorders of the esophagus}, booktitle={Large Animal Internal Medicine}, publisher={Mosby-Elsevier}, author={Blikslager, A.T. and Jones, S.L.}, editor={Smith, B.P.Editor}, year={2009}, pages={688–695} }
 @article{lascelles_king_roe_marcellin-little_jones_2009, title={Expression and activity of COX-1 and 2 and 5-LOX in joint tissues from dogs with naturally occurring coxofemoral joint osteoarthritis}, volume={27}, ISSN={0736-0266 1554-527X}, url={http://dx.doi.org/10.1002/jor.20864}, DOI={10.1002/jor.20864}, abstractNote={Abstract Understanding the neurobiology of pain in naturally occurring models of osteoarthritis (OA) may improve the understanding of human OA pain. Both COX and LOX have been associated with joint pain. This study evaluated COX‐1, COX‐2, and 5‐LOX expression and activity in a naturally occurring canine model of secondary OA. Hip joint capsule with synovial tissue (HJC) and femoral head subchondral bone (FH) was collected from normal dogs and dogs undergoing total hip replacement for coxofemoral joint OA. Tissues were analyzed for COX‐1, COX‐2, and LOX protein, and PGE 2 and LTB 4 . Significantly more COX‐2 protein was present in OA HJC than normal joints ( p = 0.0009). There was no significant difference in COX‐1 or LOX protein, although LOX protein was increased ( p = 0.069). PGE 2 concentration in normal and OA HJC was similar ( p = 1.0). LTB 4 concentration in OA HJC was significantly greater than normal HJC ( p = 0.028). Significantly more COX‐1 ( p = 0.0098), COX‐2 ( p = 0.0028), and LOX ( p = 0.0095) protein was present in OA FH tissue compared to normal FH tissue. There were no differences in PGE 2 or LTB 4 concentration in normal and OA FH tissue ( p = 0.77 and p = 0.11). Together, these data suggest both COX‐2 and 5‐LOX are appropriate targets for the management of pain associated with naturally occurring OA. © 2009 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res}, number={9}, journal={Journal of Orthopaedic Research}, publisher={Wiley}, author={Lascelles, B. Duncan X. and King, Stephanie and Roe, Simon and Marcellin-Little, Denis J. and Jones, Samuel}, year={2009}, month={Sep}, pages={1204–1208} }
 @inbook{jones_2009, place={Philadelphia, Pa}, edition={3rd}, title={Inflammatory diseases of the gastrointestinal tract causing diarrhea}, booktitle={Equine Internal Medicine}, publisher={WB Saunders}, author={Jones, S.L.}, editor={Reed, S.M. and Bayly, W.M. and Sellon, D.C.Editors}, year={2009}, pages={857–876} }
 @inbook{jones_2009, place={St Louis, MO}, edition={4th}, title={Medical disorders of the large intestine}, booktitle={Large Animal Internal Medicine}, publisher={Mosby-Elsevier}, author={Jones, S.L.}, editor={Smith, B.P.Editor}, year={2009}, pages={742–750} }
 @inbook{jones_2009, place={St Louis, MO}, edition={4th}, title={Non-steroidal anti-inflammatory drug toxicity}, booktitle={Large Animal Internal Medicine}, publisher={Mosby-Elsevier}, author={Jones, S.L.}, editor={Smith, B.P.Editor}, year={2009}, pages={754–757} }
 @inbook{jones_2009, place={Philadelphia, PA}, edition={3rd}, title={Pathophysiology of gastrointestinal inflammation}, booktitle={Equine Internal Medicine}, publisher={WB Saunders}, author={Jones, S.L.}, editor={Reed, S.M. and Bayly, W.M. and Sellon, D.C.Editors}, year={2009}, pages={785–790} }
 @inbook{jones_2009, place={St. Louis, MO}, edition={6th}, title={Right dorsal ulcerative colitis}, ISBN={9781416054757}, booktitle={Current Therapy in Equine Medicine}, publisher={Saunders}, author={Jones, S.L.}, editor={Robinson, N.E. and Sprayberry, K.A.Editors}, year={2009}, pages={430–432} }
 @article{neuder_keener_eckert_trujillo_jones_2009, title={Role of p38 MAPK in LPS induced pro-inflammatory cytokine and chemokine gene expression in equine leukocytes}, volume={129}, ISSN={["1873-2534"]}, url={http://europepmc.org/abstract/med/19070370}, DOI={10.1016/j.vetimm.2008.11.006}, abstractNote={Endotoxemia occurs when bacterial lipopolysaccharide (LPS) in the blood induces a dysregulated inflammatory response, resulting in circulatory shock and multi-organ failure. Laminitis is a common complication in endotoxemic horses and is frequently the reason for humane euthanasia of these cases. Blood leukocytes are a principal target of LPS in endotoxemia leading to activation of multiple signal transduction pathways involved in the induction of a number of pro-inflammatory genes. In other animal models, the p38 mitogen activated protein kinase (MAPK) pathway has been associated with induced expression of tumor necrosis factor-α (TNFα), interleukin (IL)-1β, IL-6 and IL-8. The goal of this study was to determine the role of the p38 MAPK pathway in the induction of these pro-inflammatory cytokine and chemokine genes in LPS-stimulated equine leukocytes. Stimulation of equine peripheral blood leukocytes resulted in an increase in TNFα, IL-1β, IL-6 and IL-8 mRNA levels. Pharmacological inhibition of p38 MAPK activity with SB203580 or SB202190 reduced the ability of LPS stimulation to increase mRNA concentrations for all four genes. However, only SB203580 pretreatment significantly reduced LPS-stimulated IL-1β and IL-8 mRNA expression and only pretreatment with SB202190 significantly reduced LPS-stimulated TNFα and IL-6 mRNA expression. From this study we conclude TNFα, IL-1β, IL-6 and IL-8 are induced upon LPS stimulation of equine leukocytes and that this induction of gene expression is dependent on the p38 MAPK pathway. However, there are differences in the efficacy of the p38 inhibitors tested here that may be explained by differences in specificity or potency. This study provides evidence for the use of selective p38 MAPK inhibitors as potential therapeutics for the treatment of equine endotoxemia.}, number={3-4}, journal={VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY}, author={Neuder, Laura E. and Keener, Jamie M. and Eckert, Rachael E. and Trujillo, Jennifer C. and Jones, Samuel L.}, year={2009}, month={Jun}, pages={192–199} }
 @article{cook_neuder_blikslager_jones_2009, title={The effect of lidocaine on in vitro adhesion and migration of equine neutrophils}, volume={129}, ISSN={0165-2427}, url={http://dx.doi.org/10.1016/j.vetimm.2008.12.017}, DOI={10.1016/j.vetimm.2008.12.017}, abstractNote={The effect of lidocaine on in vitro migration and adhesion of equine neutrophils was evaluated. Neutrophils were isolated from equine whole blood using a Percoll-gradient centrifugation protocol. Purified neutrophils were incubated with lidocaine at concentrations from 0.1 to 1000 microg/ml for 30 min at 37 degrees C, after calcein loading. Neutrophil integrin-mediated adhesion in response to stimulation with 100 nM LTB(4), 100 nM PAF, or 100 ng/ml IL-8, or integrin-mediated migration in response to stimulation with 100 nM LTB(4), 150 nM PAF, or 100 ng/ml IL-8 was assessed. Statistical significance was set at P<0.05. Neutrophil adhesion was significantly increased in response to all three stimulants. IL-8-stimulated adhesion was significantly increased when neutrophils were incubated with 1mg/ml lidocaine, compared to lower lidocaine concentrations. LTB(4)-stimulated adhesion was significantly increased when neutrophils were incubated with 1mg/ml lidocaine compared to that at 5 microg/ml lidocaine. Migration was significantly increased in response to IL-8. IL-8 and LTB(4) stimulated migration was significantly increased when neutrophils were incubated with 1mg/ml lidocaine, compared to lower lidocaine concentrations. In conclusion, lidocaine did not inhibit neutrophil migration or adhesion in vitro at therapeutic concentrations, and increased migration and adhesion at higher concentrations.}, number={1-2}, journal={Veterinary Immunology and Immunopathology}, publisher={Elsevier BV}, author={Cook, Vanessa L. and Neuder, Laura E. and Blikslager, Anthony T. and Jones, Samuel L.}, year={2009}, month={May}, pages={137–142} }
 @article{sheats_cook_jones_blikslager_pease_2009, title={Use of ultrasound to evaluate outcome following colic surgery for equine large colon volvulus}, volume={42}, ISSN={0425-1644 2042-3306}, url={http://dx.doi.org/10.2746/042516409X456040}, DOI={10.2746/042516409X456040}, abstractNote={The post operative response of the large colon wall after a surgically corrected large colon volvulus (LCV) has not been investigated.To use transabdominal ultrasound to monitor the post operative change in large colon wall thickness following surgical correction of LCV.A prolonged period to colon wall involution is correlated with an increased rate of post operative morbidity and mortality.A prospective clinical study including horses that presented to the North Carolina State University Veterinary Teaching Hospital for colic between September 2006 and March, 2008, had surgically diagnosed and corrected LCV (at least 360 degrees ) without resection and recovered from anaesthesia. Ultrasound of the ventral large colon was performed at the time of anaesthetic recovery and every 6-8 h until the colon wall returned to normal thickness (< or = 5 mm). Outcome was evaluated using a one-way ANOVA to compare average time to colon wall involution between: 1) survivors and nonsurvivors; and 2) horses that developed multiple organ dysfunction syndrome (MODS) during the post operative period and those that recovered without evidence of MODS.Sixteen horses that recovered without evidence of MODS had a significantly shorter period to colon wall involution (< or = 5 mm) compared to those diagnosed with MODS (mean +/- s.e. 19.6 h +/- 2.5 and 39.7 h +/- 6.7 respectively, P = 0.006). There was no significant difference in mean period to colon wall involution between survivors and nonsurvivors (26.2 +/- 4.9 and 33.2 +/- 7.8 h, respectively).A shorter time to colon wall involution was associated with decreased post operative morbidity in horses presented for surgical correction of large colon volvulus without resection.Ultrasonographic monitoring of colon wall involution after surgical correction of LCV may aid in identifying those cases at risk of MODS. Further investigation of colon wall involution time using a larger number of horses is warranted.}, number={1}, journal={Equine Veterinary Journal}, publisher={Wiley}, author={Sheats, M. K. and Cook, V. L. and Jones, S. L. and Blikslager, A. T. and Pease, A. P.}, year={2009}, month={Dec}, pages={47–52} }
 @article{eckert_sharief_jones_2009, title={p38 mitogen-activated kinase (MAPK) is essential for equine neutrophil migration}, volume={129}, ISSN={["1873-2534"]}, url={http://europepmc.org/abstract/med/19095309}, DOI={10.1016/j.vetimm.2008.11.007}, abstractNote={Equine laminar tissues do not contain resident neutrophils and have less superoxide dismutase (SOD) activity than other equine tissues, which makes them inherently more vulnerable to damage induced by reactive oxygen species (ROS) produced by neutrophils that enter the tissues. In the advanced clinical stages of acute laminitis, pathologic events in affected feet include a breakdown in the basement membrane, neutrophil infiltration, and platelet-neutrophil aggregates in laminar dermal veins, highlighting the contribution of neutrophils to the pathophysiology of the disease. The aim of this study was to determine the role of p38 MAPK in the mechanism underlying equine neutrophil migration to potentially reveal therapeutic targets that may limit lamellar damage from the neutrophil influx that occurs in acute laminitis. We determined that the endogenous chemoattractant LTB(4) transiently activated p38 MAPK and induced chemotaxis of equine primary neutrophils. Inhibition with the p38 MAPK specific inhibitor SB203580 reduced LTB(4)-induced migration in a dose-dependent manner with an IC(50) of 2.8 microM. We then examined the potential mechanisms underlying the ability of SB203580 to abolish migration. We determined that inhibition of p38 MAPK with 10 microM SB203580 disrupted the ability of neutrophils to polarize in response to LTB(4) and PAF. In contrast, p38 MAPK did not appear to be required for chemoattractant- or PKC-induced beta2 integrin-dependent adhesion or chemoattractant-induced upregulation of surface beta2 integrins, but was required for TNFalpha-induced adhesion. These findings support a function for p38 MAPK in equine neutrophil migration and suggest the potential for the ability of p38 MAPK inhibition to limit neutrophilic inflammation in the laminae during acute laminitis.}, number={3-4}, journal={VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY}, author={Eckert, Rachael E. and Sharief, Yousuf and Jones, Samuel L.}, year={2009}, month={Jun}, pages={181–191} }
 @article{jones_maggi_shuler_alward_breitschwerdt_2008, title={Detection ofBartonella henselaein the Blood of 2 Adult Horses}, volume={22}, ISSN={0891-6640 1939-1676}, url={http://dx.doi.org/10.1111/j.1939-1676.2008.0043.x}, DOI={10.1111/j.1939-1676.2008.0043.x}, abstractNote={Bartonella spp. are emerging zoonotic agents that have been found in a wide variety of domestic animals and wildlife and cause a number of clinical syndromes. Bartonella sp. infection has been identified in a growing number of animal species, including cats, rodents, porpoises, and canids, but has not been reported in horses.To document the presence of Bartonella sp. in the blood of horses.One horse with chronic arthropathy and 1 horse with presumptive vasculitis.Blood samples were tested for the presence of Bartonella sp. by a combination of multiplex real-time polymerase chain reaction and enrichment culture technique.Bartonella henselae was isolated or detected in the blood of both horses.Bartonella henselae infection should be investigated as the cause of disease in horses.}, number={2}, journal={Journal of Veterinary Internal Medicine}, publisher={Wiley}, author={Jones, S.L. and Maggi, R. and Shuler, J. and Alward, A. and Breitschwerdt, E.B.}, year={2008}, month={Mar}, pages={495–498} }
 @inbook{jones_pease_2008, place={St Louis, MO}, edition={4th edition.}, title={Diagnostic procedures in the examination of the equine alimentary system}, booktitle={Large Animal Internal Medicine}, publisher={Mosby-Elsevier}, author={Jones, S.L. and Pease, A.P.}, editor={Smith, B.P.Editor}, year={2008}, pages={667–676} }
 @article{sheats_wetter_snyder_jones_2008, title={Disseminated large granular lymphoma in a horse}, volume={20}, ISSN={["2042-3292"]}, DOI={10.2746/095777308X343860}, abstractNote={Summary A 21‐year‐old pony gelding presented for a 5 week history of diarrhoea, inappetance, progressive weight loss and lethargy. Differential diagnoses for chronic diarrhoea and weight loss in horses include: chronic salmonellosis, sand enteropathy, enterolith, parasitism (strongylosis, cyathostomiasis), NSAID induced ulcerative colitis, inflammatory bowel disease (granulomatous, lymphocytic‐plasmacytic or eosinophilic enterocolitis), gastrointestinal neoplasia (lymphosarcoma, squamous cell carcinoma), antibiotic associated clostridial overgrowth, altered diet or bacterial fermentation, peritonitis, Strongylus vulgaris induced arteriopathy (now quite rare) and abdominal mass or abscess. In this gelding, ante mortem diagnosis of CD3 + intestinal large granular lymphoma was made via cytology of abdominal fluid and immunohistochemistry of a rectal muscle biopsy. This report details the clinical, cytological and immunophenotypic findings of a case of large granular lymphoma in a horse.}, number={9}, journal={EQUINE VETERINARY EDUCATION}, author={Sheats, M. K. and Wetter, A. J. N. J. and Snyder, L. A. and Jones, S. L.}, year={2008}, month={Sep}, pages={459–463} }
 @article{chilcoat_sharief_jones_2008, title={Tonic protein kinase A activity maintains inactive beta 2 integrins in unstimulated neutrophils by reducing myosin light-chain phosphorylation: role of myosin light-chain kinase and Rho kinase}, volume={83}, ISSN={["0741-5400"]}, url={http://europepmc.org/abstract/med/18218860}, DOI={10.1189/jlb.0405192}, abstractNote={Activation of beta2 integrins is necessary for neutrophil adhesion and full activation of neutrophil effector functions. We demonstrated previously that inhibition of protein kinase A (PKA) activity in quiescent neutrophils is sufficient to increase beta2-integrin cell surface expression, affinity, and adhesion. Thus, a tonic level of PKA activity prevents inappropriate activation of beta2 integrins in unstimulated neutrophils. Myosin light-chain (MLC) phosphorylation is an important regulator of leukocyte integrin function and adhesion. Moreover, PKA regulates MLC phosphorylation via inhibiting MLC kinase (MLCK) and MLC dephosphorylation via effects on the Rho kinase (ROCK)/MLC phosphatase pathway. We hypothesize that the tonic inhibitory effect of PKA on beta2-integrin activation neutrophils operates via its inhibition of MLC phosphorylation. We demonstrate here that inhibition of PKA activity with KT5720 activated beta2 integrins and adhesion coincident with an increase in MLC serine 19 (Ser 19) phosphorylation. KT5720-induced activation of beta2 integrins, adhesion, and MLC Ser 19 phosphorylation was abolished by pretreatment with the MLCK inhibitor ML-7 and specific MLCK inhibitory peptides but not the ROCK inhibitor Y-27632. These findings demonstrate that tonic PKA activity prevents activation of beta2 integrins and adhesion by inhibiting MLC phosphorylation via a MLCK-dependent but ROCK-independent pathway.}, number={4}, journal={JOURNAL OF LEUKOCYTE BIOLOGY}, author={Chilcoat, Clayton D. and Sharief, Yousuf and Jones, Samuel L.}, year={2008}, month={Apr}, pages={964–971} }
 @article{green_eckert_sharief_crews_adler_jones_2007, title={A peptide against the N-terminus of MARCKS protein attenuates leukocyte migration.}, volume={175}, journal={404nOtfound}, author={Green, T. D. and Eckert, B. S. and Sharief, Y. and Crews, A. L. and Adler, K. B. and Jones, S. L.}, year={2007}, pages={A915} }
 @article{little_jones_blikslager_2007, title={Cyclooxygenase (COX) Inhibitors and the Intestine}, volume={21}, ISSN={0891-6640 1939-1676}, url={http://dx.doi.org/10.1111/j.1939-1676.2007.tb02978.x}, DOI={10.1111/j.1939-1676.2007.tb02978.x}, abstractNote={Nonsteroidal anti‐inflammatory drugs (NSAIDs) have long been used for the treatment of pain and inflammation because of their inhibitory effects on cyclooxygenase (COX). For almost as long as NSAIDs have been in use, multiple adverse effects have been noted. Assessment of many of these adverse effects have been complicated because of the discovery of multiple splice variants of the cox gene, and a greater array of COX inhibitors, especially the COX‐2 selective inhibitors have become available. Some of these adverse effects cannot be readily explained by the effect of these drugs on COX. This has sparked a new field of investigation into the COX‐independent effects of the COX inhibitors. The major noncyclooxygenase targets of the COX inhibitors of particular relevance to inflammation and the gastrointestinal tract are phosphatidylinositol 3'‐kinase Akt signaling, uncoupling of oxidative phosphorylation, PPARγ, nuclear factor kB, mitogen activated protein kinases, and heat shock proteins.}, number={3}, journal={Journal of Veterinary Internal Medicine}, publisher={Wiley}, author={Little, Dianne and Jones, Samuel L. and Blikslager, Anthony T.}, year={2007}, month={May}, pages={367–377} }
 @article{morton_davis_redding_jones_2007, title={Nonsecretory multiple myeloma in a horse}, volume={19}, ISSN={["0957-7734"]}, DOI={10.2746/095777307X217852}, abstractNote={Equine Veterinary EducationVolume 19, Issue 11 p. 564-568 Nonsecretory multiple myeloma in a horse A. J. Morton, Corresponding Author A. J. Morton University of Florida Veterinary Medical Center, Department of Large Animal Clinical Sciences, Box 100136 Gainesville, Florida 32610, USA*University of Florida Veterinary Medical Center, Department of Large Animal Clinical Sciences, Box 100136 Gainesville, Florida 32610, USASearch for more papers by this authorJ. L. Davi, J. L. Davi North Carolina State University Veterinary Medical Teaching Hospital, Department of Clinical Sciences, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USASearch for more papers by this authorW. R. Redding, W. R. Redding North Carolina State University Veterinary Medical Teaching Hospital, Department of Clinical Sciences, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USASearch for more papers by this authorS. L. Jones, S. L. Jones North Carolina State University Veterinary Medical Teaching Hospital, Department of Clinical Sciences, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USASearch for more papers by this author A. J. Morton, Corresponding Author A. J. Morton University of Florida Veterinary Medical Center, Department of Large Animal Clinical Sciences, Box 100136 Gainesville, Florida 32610, USA*University of Florida Veterinary Medical Center, Department of Large Animal Clinical Sciences, Box 100136 Gainesville, Florida 32610, USASearch for more papers by this authorJ. L. Davi, J. L. Davi North Carolina State University Veterinary Medical Teaching Hospital, Department of Clinical Sciences, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USASearch for more papers by this authorW. R. Redding, W. R. Redding North Carolina State University Veterinary Medical Teaching Hospital, Department of Clinical Sciences, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USASearch for more papers by this authorS. L. Jones, S. L. Jones North Carolina State University Veterinary Medical Teaching Hospital, Department of Clinical Sciences, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USASearch for more papers by this author First published: 05 January 2010 https://doi.org/10.2746/095777307X217852Citations: 5AboutPDF ToolsExport 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 Citing Literature Volume19, Issue11December 2007Pages 564-568 RelatedInformation}, number={11}, journal={EQUINE VETERINARY EDUCATION}, author={Morton, A. J. and Davis, J. L. and Redding, W. R. and Jones, S. L.}, year={2007}, month={Dec}, pages={564–568} }
 @article{eckert_jones_2007, title={Regulation of VASP serine 157 phosphorylation in human neutrophils after stimulation by a chemoattractant}, volume={82}, ISSN={["1938-3673"]}, url={http://europepmc.org/abstract/med/17684042}, DOI={10.1189/jlb.0206107}, abstractNote={Abstract Vasodilator-stimulated phosphoprotein (VASP) is a cAMP-dependent protein kinase A (PKA) substrate, which links cellular signaling to cytoskeletal organization and cellular movement. VASP is phosphorylated by PKA on serine 157 (Ser 157), which is required for VASP function in platelet adhesion and fibroblast motility. Our hypothesis is that PKA regulates neutrophil migration through VASP Ser 157 phosphorylation. The objective of this study was to characterize VASP Ser 157 phosphorylation in chemoattractant-stimulated neutrophils. fMLF, IL-8, leukotriene B4, or platelet-activating factor stimulation resulted in an initial increase in VASP Ser 157 phosphorylation, which was maximal by 30 s and was followed by a return to baseline Ser 157 phosphorylation by 10 min. In contrast, stimulation with the nonchemoattractant, proinflammatory cytokine TNF-α did not affect Ser 157 phosphorylation. The kinetics of fMLF-induced VASP Ser 157 phosphorylation levels closely matched the kinetics of the fold-change in F-actin levels in fMLF-stimulated neutrophils. fMLF-induced Ser 157 phosphorylation was abolished by pretreatment with the PKA inhibitor H89 and the adenylyl cyclase inhibitor SQ22536. In contrast, fMLF-induced Ser 157 phosphorylation was unaffected by the PKC inhibitors calphostin and staurosporine, the PKG inhibitors Rp-8-pCPT-cGMP and KT5823, and the calmodulin-dependent protein kinase II inhibitor KN-62. Inhibition of adhesion with EDTA or the anti-β2-integrin antibody IB4 did not alter fMLF-induced VASP phosphorylation or dephosphorylation. These data show that chemoattractant stimulation of human neutrophils induces a rapid and transient PKA-dependent VASP Ser 157 phosphorylation. Adhesion does not appear to be an important regulator of the state of VASP Ser 157 phosphorylation in chemoattractant-stimulated neutrophils.}, number={5}, journal={JOURNAL OF LEUKOCYTE BIOLOGY}, author={Eckert, Rachael E. and Jones, Samuel L.}, year={2007}, month={Nov}, pages={1311–1321} }
 @article{blikslager_moeser_gookin_jones_odle_2007, title={Restoration of Barrier Function in Injured Intestinal Mucosa}, volume={87}, ISSN={0031-9333 1522-1210}, url={http://dx.doi.org/10.1152/physrev.00012.2006}, DOI={10.1152/physrev.00012.2006}, abstractNote={Mucosal repair is a complex event that immediately follows acute injury induced by ischemia and noxious luminal contents such as bile. In the small intestine, villous contraction is the initial phase of repair and is initiated by myofibroblasts that reside immediately beneath the epithelial basement membrane. Subsequent events include crawling of healthy epithelium adjacent to the wound, referred to as restitution. This is a highly regulated event involving signaling via basement membrane integrins by molecules such as focal adhesion kinase and growth factors. Interestingly, however, ex vivo studies of mammalian small intestine have revealed the importance of closure of the interepithelial tight junctions and the paracellular space. The critical role of tight junction closure is underscored by the prominent contribution of the paracellular space to measures of barrier function such as transepithelial electrical resistance. Additional roles are played by subepithelial cell populations, including neutrophils, related to their role in innate immunity. The net result of reparative mechanisms is remarkably rapid closure of mucosal wounds in mammalian tissues to prevent the onset of sepsis.}, number={2}, journal={Physiological Reviews}, publisher={American Physiological Society}, author={Blikslager, Anthony T. and Moeser, Adam J. and Gookin, Jody L. and Jones, Samuel L. and Odle, Jack}, year={2007}, month={Apr}, pages={545–564} }
 @article{fogle_gerard_johansson_breuhaus_blikslager_jones_2007, title={Spontaneous rupture of the guttural pouch as a complication of treatment for guttural pouch empyema}, volume={19}, ISSN={["0957-7734"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-34547981740&partnerID=MN8TOARS}, DOI={10.2746/095777307X196900}, abstractNote={Equine Veterinary EducationVolume 19, Issue 7 p. 351-355 Spontaneous rupture of the guttural pouch as a complication of treatment for guttural pouch empyema C. A. Fogle, Corresponding Author C. A. Fogle Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.*Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorM. P. Gerard, M. P. Gerard Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorA. M. Johansson, A. M. Johansson Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorB. A. Breuhaus, B. A. Breuhaus Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorA. T. Blikslager, A. T. Blikslager Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorS. L. Jones, S. L. Jones Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this author C. A. Fogle, Corresponding Author C. A. Fogle Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.*Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorM. P. Gerard, M. P. Gerard Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorA. M. Johansson, A. M. Johansson Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorB. A. Breuhaus, B. A. Breuhaus Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorA. T. Blikslager, A. T. Blikslager Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorS. L. Jones, S. L. Jones Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this author First published: 05 January 2010 https://doi.org/10.2746/095777307X196900Citations: 14AboutPDF ToolsExport 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 Adkins, A.R., Yovich, J.V. and Colbourne, C.M. (1997) Nonsurgical treatment of chondroids of the guttural pouch in a horse. Aust. vet. J. 75, 332–333. 10.1111/j.1751-0813.1997.tb15703.x CASPubMedWeb of Science®Google Scholar Bentz, B.G., Dowd, A.L. and Freeman, D.E. (1996) Treatment of guttural pouch empyema with acetylcysteine irrigation. Equine Pract. 18, 33–35. Web of Science®Google Scholar Freeman, D.E. (1991) Guttural pouches. In: Equine Respiratory Disorders, Ed: J. Beech, Lea and Febiger, Philadelphia. pp 305–328. Web of Science®Google Scholar Freeman, D.E. (1999) Guttural pouch. In: Equine Surgery, Eds: J.A. Auer and J.A. Stick, W.B. Saunders, Philadelphia. pp 368–375. Google Scholar Hawkins, J.F., Frank, N., Sojka, J.E. and Levy, M. (2001) Fistulation of the auditory tube diverticulum (guttural pouch) with a neodymiumyttrium-aluminum-garnet laser for treatment of chronic empyema in two horses. J. Am. vet. med. Ass. 218, 405–407. 10.2460/javma.2001.218.405 CASPubMedWeb of Science®Google Scholar Judy, C.E., Chaffin, M.K. and Cohen, N.D. (1999) Empyema of the guttural pouch (auditory tube diverticulum) in horses: 91 cases (1977–1997). J. Am. vet. med. Ass. 215, 1666–1670. CASPubMedWeb of Science®Google Scholar McAllister, E.S. (1978) Guttural pouch disease. Proc. Am. Ass. equine Practnrs. 23, 251–256. Web of Science®Google Scholar Perkins, G.A., Pease, A., Crotty, E. and Fubini, S.L. (2003) Diagnosing guttural pouch disorders and managing guttural pouch empyema in adult horses. Comp. cont. Educ. pract. Vet. 25, 966–973. Web of Science®Google Scholar Citing Literature Volume19, Issue7August 2007Pages 351-355 ReferencesRelatedInformation}, number={7}, journal={EQUINE VETERINARY EDUCATION}, author={Fogle, C. A. and Gerard, M. P. and Johansson, A. M. and Breuhaus, B. A. and Blikslager, A. T. and Jones, S. L.}, year={2007}, month={Aug}, pages={351–355} }
 @article{eckert_neuder_bell_trujillo_jones_2007, title={The role of p38 mitogen-activated kinase (MAPK) in the mechanism regulating cyclooxygenase gene expression in equine leukocytes}, volume={118}, ISSN={["1873-2534"]}, url={http://europepmc.org/abstract/med/17614138}, DOI={10.1016/j.vetimm.2007.06.001}, abstractNote={The goal of this study was to define the role for p38 mitogen-activated kinase (MAPK) in the signaling mechanism regulating pro-inflammatory cyclooxygenase (COX) gene expression in lipopolysaccharide (LPS)-activated equine leukocytes for the purposes of identifying novel targets for anti-inflammatory therapy in endotoxemic horses. The p38 MAPK has been shown to positively regulate inflammatory gene expression in human leukocytes and can be activated by a variety of stimuli including LPS, TNF-α, and IL-1. Activation-associated phosphorylated p38 MAPK has been implicated in the up-regulation of several inflammatory genes, including COX-2 which ultimately results in the production of prostanoids that are responsible for the pathophysiology associated with endotoxemia. Our hypothesis is that activation of p38 MAPK is essential for LPS-induced COX-2 expression in equine peripheral blood leukocytes. We tested our hypothesis by investigating the effects of the specific p38 MAPK inhibitors SB203580 and SB202190 on LPS-induced COX-2 protein expression and PGE2 production in equine leukocytes. LPS stimulation activated p38 MAPK and increased COX-2 expression in a dose-dependent manner with maximal activation observed after 30 min and 4 h, respectively, at a concentration of 10 ng/ml LPS. In contrast, LPS stimulation did not affect COX-1 protein expression. Pretreatment with SB203580 or SB202190 significantly inhibited LPS-induced activation-associated p38 MAPK phosphorylation, COX-2 mRNA and protein levels, and PGE2 production in equine leukocytes. Maximal inhibition of LPS-induced COX-2 protein expression was achieved at a concentration of 10 μM SB203580. We concluded that p38 MAPK is essential for LPS-induced COX-2 expression suggesting that p38 MAPK is a potential target for anti-inflammatory therapy during equine endotoxemia.}, number={3-4}, journal={VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY}, author={Eckert, Rachael E. and Neuder, Laura E. and Bell, Jennifer L. and Trujillo, Jennifer C. and Jones, Samuel L.}, year={2007}, month={Aug}, pages={294–303} }
 @article{alward_pease_jones_2007, title={Thoracic discospondylitis with associated epaxial muscle atrophy in a Quarter Horse gelding}, volume={19}, ISSN={["0957-7734"]}, DOI={10.2746/095777307X180268}, abstractNote={Equine Veterinary EducationVolume 19, Issue 2 p. 67-71 Thoracic discospondylitis with associated epaxial muscle atrophy in a Quarter Horse gelding A. L. Alward, A. L. Alward Southwest Equine Medical and Surgical Center, Scottsdale, Arizona 85254, USASearch for more papers by this authorA. P. Pease, A. P. Pease North Carolina State University College of Veterinary Medicine, Raleigh, North Carolina 27606Search for more papers by this authorS. L. Jones, Corresponding Author S. L. Jones North Carolina State University College of Veterinary Medicine, Raleigh, North Carolina 27606*North Carolina State University College of Veterinary Medicine, Raleigh, North Carolina 27606Search for more papers by this author A. L. Alward, A. L. Alward Southwest Equine Medical and Surgical Center, Scottsdale, Arizona 85254, USASearch for more papers by this authorA. P. Pease, A. P. Pease North Carolina State University College of Veterinary Medicine, Raleigh, North Carolina 27606Search for more papers by this authorS. L. Jones, Corresponding Author S. L. Jones North Carolina State University College of Veterinary Medicine, Raleigh, North Carolina 27606*North Carolina State University College of Veterinary Medicine, Raleigh, North Carolina 27606Search for more papers by this author First published: 05 January 2010 https://doi.org/10.2746/095777307X180268Citations: 9AboutPDF ToolsExport 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 onFacebookTwitterLinked InRedditWechat Citing Literature Volume19, Issue2March 2007Pages 67-71 RelatedInformation}, number={2}, journal={EQUINE VETERINARY EDUCATION}, author={Alward, A. L. and Pease, A. F. and Jones, S. L.}, year={2007}, month={Mar}, pages={67–71} }
 @article{jones_valenzisi_sontakke_sprayberry_maggi_hegarty_breitschwerdt_2007, title={Use of an insect cell culture growth medium to isolate bacteria from horses with effusive, fibrinous pericarditis: A preliminary study}, volume={121}, ISSN={0378-1135}, url={http://dx.doi.org/10.1016/j.vetmic.2006.11.024}, DOI={10.1016/j.vetmic.2006.11.024}, abstractNote={Effusive, fibrinous pericarditis is an uncommon disease entity in horses. In 2001, pericarditis occurred in conjunction with an epizootic in central Kentucky that was associated with exposure to eastern tent caterpillars (ETCs). Bacterial isolation from equine pericardial fluid samples was attempted using an insect cell culture growth medium (ICCGM). Using previously cultured, stored frozen samples from four horses with fibrinous pericarditis, inoculation of 10% blood agar plates yielded no growth, whereas simultaneous inoculation of ICCGM resulted in the isolation of Proprionibacterium acnes, Staphylococcus equorum, a Streptococcus sp. and Pseudomonas rhodesiae from pericardial fluid samples. A similar or novel caterpillar-associated bacteria was not identified; however, use of an ICCGM might enhance isolation of bacteria from equine pericardial fluid.}, number={1-2}, journal={Veterinary Microbiology}, publisher={Elsevier BV}, author={Jones, Samuel L. and Valenzisi, Amy and Sontakke, Sushama and Sprayberry, Kimberly A. and Maggi, Ricardo and Hegarty, Barbara and Breitschwerdt, Edward}, year={2007}, month={Mar}, pages={177–181} }
 @article{jones_2006, title={Cholangiohepatitis, suppurative cholangitis, and cholelithiasis}, volume={1}, journal={Compendium on Continuing Education for the Practicing Veterinarian Equine Edition}, author={Jones, S.L.}, year={2006}, pages={222–225} }
 @article{zadrozny_stauffer_armstrong_jones_gookin_2006, title={Neutrophils do not mediate the pathophysiological sequelae of Cryptosporidium parvum infection in neonatal piglets}, volume={74}, ISSN={["1098-5522"]}, url={http://europepmc.org/abstract/med/16988224}, DOI={10.1128/IAI.00153-06}, abstractNote={Cryptosporidium parvum is a minimally invasive protozoal pathogen of intestinal epithelium that results in villus atrophy, mucosal lipid peroxidation, diarrhea, and diminished barrier function. Influx of neutrophils is a consistent feature of human and animal cryptosporidiosis, and yet their contribution to the pathological sequelae of infection has not been investigated. Accordingly, we used an established neonatal piglet model of C. parvum infection to examine the role of neutrophils in disease pathogenesis by inhibiting their recruitment and activation in vivo using a monoclonal anti-CD18 antibody. Infected piglets were treated daily with anti-CD18 or isotype control immunoglobulin G and euthanized at peak infection, at which time neutrophil infiltrates, lipid peroxidation, severity of infection, and intestinal barrier function were quantified. C. parvum infection resulted in a significant increase in mucosal neutrophil myeloperoxidase activity that was prevented by treatment of piglets with anti-CD18 antibody. Neutrophil recruitment was dependent on mucosal superoxide formation (prevented by treatment of infected piglets with superoxide dismutase). Neutrophils did not contribute to peroxynitrite formation or peroxidative injury of C. parvum-infected mucosa and had no impact on the severity of epithelial infection, villus atrophy, or diarrhea. The presence of neutrophils in C. parvum-infected mucosa was associated with enhanced barrier function that could not be attributed to mucosal elaboration of prostaglandins or stimulation of their synthesis. These studies are the first to demonstrate that neutrophilic inflammation arising in response to infection by a noninvasive epithelial pathogen results in physiologic rather than pathological effects in vivo.}, number={10}, journal={INFECTION AND IMMUNITY}, author={Zadrozny, Leah M. and Stauffer, Stephen H. and Armstrong, Martha U. and Jones, Samuel L. and Gookin, Jody L.}, year={2006}, month={Oct}, pages={5497–5505} }
 @article{frederico_jones_blikslager_2006, title={Predisposing factors for small colon impaction in horses and outcome of medical and surgical treatment: 44 cases (1999–2004)}, volume={229}, ISSN={0003-1488}, url={http://dx.doi.org/10.2460/javma.229.10.1612}, DOI={10.2460/javma.229.10.1612}, abstractNote={Abstract Objective —To identify factors associated with development of small colon impaction in horses and with selection of medical versus surgical treatment and to determine the prognosis for affected horses following medical or surgical management. Design —Retrospective case series. Animals —44 horses with primary impaction of the small colon. Procedures —Medical records were reviewed for signalment, history, clinical findings, treatment (medical vs surgical), hospitalization time, and outcome. For comparison purposes, the same information was collected for 83 horses with primary impaction of the large colon. Results —Diarrhea was the only factor found to be associated with development of small colon impaction. Horses with small colon impaction were 10.8 times as likely to have diarrhea at the time of initial examination as were horses with large colon impaction. Abdominal distension was the only factor associated with use of surgical versus medical treatment. Horses with small colon impaction that were treated surgically were 5.2 times as likely to have had abdominal distension at the time of admission as were horses with small colon impaction that were treated medically. Overall, 21 of 23 (91%) horses treated medically and 20 of 21 (95%) horses treated surgically survived to discharge. Conclusions and Clinical Relevance —Results suggest that diarrhea may be a risk factor for development of small colon impaction and that horses with small colon impaction that have abdominal distension at the time of initial examination are more likely to require surgical than medical treatment.}, number={10}, journal={Journal of the American Veterinary Medical Association}, publisher={American Veterinary Medical Association (AVMA)}, author={Frederico, Lisa M. and Jones, Samuel L. and Blikslager, Anthony T.}, year={2006}, month={Nov}, pages={1612–1616} }
 @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{alward_corriher_barton_sellon_blikslager_jones_2006, title={Red maple (Acer rubrum) leaf toxicosis in horses: a retrospective study of 32 cases.}, volume={20}, url={http://europepmc.org/abstract/med/17063716}, DOI={10.1111/j.1939-1676.2006.tb00722.x}, abstractNote={Background: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. Hypothesis:Our hypothesis was that physical examination findings, clinicopathologic variables or therapeutic modalities may predict outcome in horses with red maple leaf toxicity. Animals:Horses with red maple leaf toxicosis presented to referral hospitals in the southeast region of the United States. Methods:A multi‐institutional retrospective study was designed to identify factors that predict mortality in horses with red maple toxicosis. Results: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. Conclusions and Clinical Importance: 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, A and Corriher, CA and Barton, MH and Sellon, DC and Blikslager, AT and Jones, SL}, year={2006}, pages={1197–1201,} }
 @article{barton_hurley_norton_heusner_costa_jones_byars_watanabe_2006, title={Serum lactoferrin and immunoglobulin G concentrations in healthy or ill neonatal foals and healthy adult horses}, volume={20}, ISSN={["0891-6640"]}, url={http://europepmc.org/abstract/med/17186865}, DOI={10.1111/j.1939-1676.2006.tb00766.x}, abstractNote={Background:Lactoferrin is a colostral glycoprotein with antimicrobial properties. Hypotheses: (1) Serum lactoferrin and immunoglobulin G (IgG) concentrations are correlated and increase in healthy foals after ingestion of colostrum; (2) compared to healthy foals, ill foals will have lower lactoferrin concentrations that correlate with their IgG concentration, neutrophil count, the diagnosis of sepsis, and survival; and (3) plasma concentrations of lactoferrin will be less than serum concentrations. Animals:Healthy foals (n = 16), mature horses (n = 10), and ill foals 1–4 days old (n = 111) that were examined for suspected sepsis were used for blood collection. Colostrum was obtained from 10 healthy mares unrelated to the foals. Methods:Blood was obtained from the healthy foals at birth and 1–3 days of age and from the ill foals at admission. Serum IgG was quantified by single radial immunodiffusion (SRID). Lactoferrin concentrations in colostrum and blood were determined by an enzyme‐linked immunosorbant assay. The sepsis score, blood culture results, neutrophil counts, and survival were obtained on ill foals. Results:The mean colostral lactoferrin concentration was 21.7 μg/mL. Compared to values at birth, serum IgG (18 ± 2 versus 2,921 ± 245 mg/dL, SEM) and lactoferrin (249 ± 39 versus 445 ± 63 ng/mL, SEM) concentrations were significantly greater in healthy foals 1–3 days old. Serum lactoferrin concentration in 1–3‐day‐old healthy foals was not different from mature horses or ill foals. IgG and lactoferrin concentrations were significantly correlated only in healthy foals. Serum lactoferrin concentrations were significantly lower in ill neutropenic foals. The serum IgG concentration was significantly lower in ill foals as compared to healthy foals. Only serum IgG was significantly less in ill foals with a positive sepsis score and in nonsurvivors. Plasma lactoferrin concentrations were lower than serum concentrations, although values were significantly correlated. Clinical Importance: Although both serum IgG and lactoferrin concentrations increase in healthy foals after ingestion of colostrum, only serum IgG is significantly correlated with the sepsis score and outcome.}, number={6}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Barton, Michelle Henry and Hurley, David and Norton, Natalie and Heusner, Gary and Costa, Lais and Jones, Samuel and Byars, Doug and Watanabe, Kiyotaka}, year={2006}, pages={1457–1462} }
 @article{jones_sharief_2005, title={Asymmetrical protein kinase A activity establishes neutrophil cytoskeletal polarity and enables chemotaxis}, volume={78}, ISSN={["1938-3673"]}, url={http://europepmc.org/abstract/med/15817703}, DOI={10.1189/jlb.0804459}, abstractNote={Neutrophil chemotaxis requires precise spatial organization of the actin cytoskeleton and integrin activation to polarize the cell and enable migration. Protein kinase A (PKA) activity regulates integrin activation and actin cytoskeletal organization, suggesting that PKA is a key element in the mechanism regulating neutrophil chemotaxis. Our hypothesis is that asymmetrical PKA activity is critical for establishing neutrophil adhesive and cytoskeletal polarity required for migration during chemotaxis. To test this hypothesis, we first determined that global treatment with the PKA inhibitor KT5720 decreased formylated Met-Leu-Phe (fMLF)-induced migration. The ability of PKA inhibitors to reduce migration correlated with increased overall beta2 integrin cell-surface expression, affinity activation, and cellular adhesion. We next determined whether asymmetrical PKA activity was sufficient to induce migration. Exposure to gradient of the PKA inhibitors KT5720 or H-89 or a stearated, cell-permeant peptide (St-Ht31), which inhibits PKA binding to anchorage proteins, stimulated neutrophil migration in a chemotaxis chamber. Global treatment with KT5720 abolished the ability of fMLF to polarize the neutrophil actin cytoskeleton. In contrast to global treatment with KT5720, a point source of KT5720 was sufficient to polarize the actin cytoskeleton. The ability of KT5720 and St-Ht31 to stimulate migration was abolished by pretreatment with the phosphatidylinositol-3 kinase (PI-3K) inhibitors wortmannin and LY294002. These data suggest that asymmetrical PKA activity is necessary and sufficient for actin cytoskeletal polarization and migration during neutrophil chemotaxis. In addition, our data suggest PI-3K is an effector of PKA during chemotaxis.}, number={1}, journal={JOURNAL OF LEUKOCYTE BIOLOGY}, author={Jones, SL and Sharief, Y}, year={2005}, month={Jul}, pages={248–258} }
 @article{blikslager_jones_2005, title={NSAIDs}, volume={25}, ISSN={["0737-0806"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-14944341260&partnerID=MN8TOARS}, DOI={10.1016/j.jevs.2005.02.004}, abstractNote={Objective pain assessment is important to guide and tailor therapy in clinical practice. This study describes the clinical applicability and validity of two pain scales, the Composite Pain Scale (CPS) and the Equine Utrecht University Scale for Facial Assessment of Pain (EQUUS-FAP) in horses with orthopaedic trauma or after orthopaedic surgery. A cohort follow-up study was performed using 77 adult horses (n = 43 with orthopaedic trauma or injury; n = 34 controls). Composite and facial expression-based pain scores were assessed by direct observations of pairs of two independent observers. All horses were assessed at arrival, and on the first and second day after arrival or after surgery.Both CPS and EQUUS-FAP scores demonstrated high inter-observer reliability (Crohnbach’s alpha = 0.97 for CPS; Crohnbach’s alpha = 0.93 for EQUUS-FAP; P < 0.001), with low bias (0.07 and −0.08 respectively) and limits of agreement of −1.9 to 1.9 for CPS and −1.9 to 1.9 for EQUUS-FAP. Both CPS and EQUUS-FAP scores showed significant differences between control horses and orthopaedic cases (P < 0.001). Trauma cases had significantly higher pain scores compared to postoperative cases for both CPS (P < 0.05) and for EQUUS-FAP (P < 0.01) and both pain scores significantly decreased after nonsteroidal anti-inflammatory drug (NSAID) administration. In accordance with the findings in other types of equine pain, the CPS and FAP proved useful and valid for objective and repeatable assessment of pain in horses with orthopaedic trauma or after orthopaedic surgery. This can further aid treatment of horses in clinical practice and might improve equine welfare.}, number={3}, journal={JOURNAL OF EQUINE VETERINARY SCIENCE}, author={Blikslager, A and Jones, S}, year={2005}, month={Mar}, pages={98–102} }
 @article{martens_cohen_jones_moore_edwards_2005, title={Protective role of neutrophils in mice experimentally infected with Rhodococcus equi}, volume={73}, ISSN={["0019-9567"]}, url={http://europepmc.org/abstract/med/16177388}, DOI={10.1128/IAI.73.10.7040-7042.2005}, abstractNote={ABSTRACT Neutrophils are important in controlling early infections with the intracellular bacterium Rhodococcus equi . Antineutrophil monoclonal antibody (RB6-8C5)-induced neutrophil deficiency during the first week after experimental infection of mice with R. equi resulted in more severe disease and significantly increased tissue concentrations of R. equi.}, number={10}, journal={INFECTION AND IMMUNITY}, author={Martens, RJ and Cohen, ND and Jones, SL and Moore, TA and Edwards, JF}, year={2005}, month={Oct}, pages={7040–7042} }
 @article{zimmerman_jones_rotstein_2004, title={Large granular lymphoma in a mule}, volume={155}, ISSN={["0042-4900"]}, DOI={10.1136/vr.155.15.462}, abstractNote={Veterinary RecordVolume 155, Issue 15 p. 462-463 Short Communications Large granular lymphoma in a mule B. Zimmerman DVM, B. Zimmerman DVM Department of Veterinary Biosciences, College of Veterinary Medicine, Ohio State University, Columbus, OH, 43210 USASearch for more papers by this authorS. Jones DVM, PhD, DACVIM,, S. Jones DVM, PhD, DACVIM, Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, 27606 USASearch for more papers by this authorD. S. Rotstein DVM, MPVM, DACVP, D. S. Rotstein DVM, MPVM, DACVP Department of Population Health and Pathobiology, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, 27606 USASearch for more papers by this author B. Zimmerman DVM, B. Zimmerman DVM Department of Veterinary Biosciences, College of Veterinary Medicine, Ohio State University, Columbus, OH, 43210 USASearch for more papers by this authorS. Jones DVM, PhD, DACVIM,, S. Jones DVM, PhD, DACVIM, Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, 27606 USASearch for more papers by this authorD. S. Rotstein DVM, MPVM, DACVP, D. S. Rotstein DVM, MPVM, DACVP Department of Population Health and Pathobiology, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, 27606 USASearch for more papers by this author First published: 09 October 2004 https://doi.org/10.1136/vr.155.15.462Citations: 3Read the full textAboutPDF 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 onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume155, Issue15October 2004Pages 462-463 RelatedInformation}, number={15}, journal={VETERINARY RECORD}, author={Zimmerman, B and Jones, S and Rotstein, DS}, year={2004}, month={Oct}, pages={462–463} }
 @article{shifflett_jones_moeser_blikslager_2004, title={Mitogen-activated protein kinases regulate COX-2 and mucosal recovery in ischemic-injured porcine ileum}, volume={286}, ISSN={0193-1857 1522-1547}, url={http://dx.doi.org/10.1152/ajpgi.00478.2003}, DOI={10.1152/ajpgi.00478.2003}, abstractNote={Mitogen-activated protein kinase (MAPK) pathways transduce signals from a diverse array of extracellular stimuli. The three primary MAPK-signaling pathways are the extracellular regulated kinases (ERK1/2), p38 MAPK, and c-Jun NH(2)-terminal kinase (JNK). Previous research in our laboratory has shown that COX-2-elaborated prostanoids participate in recovery of mucosal barrier function in ischemic-injured porcine ileum. Because COX-2 expression is regulated in part by MAPKs, we postulated that MAPK pathways would play an integral role in recovery of injured mucosa. Porcine mucosa was subjected to 45 min of ischemia, after which tissues were mounted in Ussing chambers, and transepithelial electrical resistance (TER) was monitored as an index of recovery of barrier function. Treatment of tissues with the p38 MAPK inhibitor SB-203580 (0.1 mM) or the ERK1/2 inhibitor PD-98059 (0.1 mM) abolished recovery. Western blot analysis revealed that SB-203580 inhibited upregulation of COX-2 that was observed in untreated ischemic-injured mucosa, whereas PD-98059 had no effect on COX-2 expression. Inhibition of TER recovery by SB-203580 or PD-98059 was overcome by administration of exogenous prostaglandin E(2) (1 microM). The JNK inhibitor SP-600125 (0.1 mM) significantly increased TER and resulted in COX-2 upregulation. COX-2 expression appears to be positively and negatively regulated by the p38 MAPK and the JNK pathways, respectively. Alternatively, ERK1/2 appear to be involved in COX-2-independent reparative events that remain to be defined.}, number={6}, journal={American Journal of Physiology-Gastrointestinal and Liver Physiology}, publisher={American Physiological Society}, author={Shifflett, Donnie E. and Jones, Samuel L. and Moeser, Adam J. and Blikslager, Anthony T.}, year={2004}, month={Jun}, pages={G906–G913} }
 @article{gardner_davis_jones_lafevers_hoskins_mcarver_papich_2004, title={Moxifloxacin pharmacokinetics in horses and disposition into phagocytes after oral dosing}, volume={27}, ISSN={["1365-2885"]}, url={http://europepmc.org/abstract/med/14995968}, DOI={10.1046/j.0140-7783.2003.00529.x}, abstractNote={Journal of Veterinary Pharmacology and TherapeuticsVolume 27, Issue 1 p. 57-60 Moxifloxacin pharmacokinetics in horses and disposition into phagocytes after oral dosing S. Y. Gardner, S. Y. Gardner Department of Clinical SciencesSearch for more papers by this authorJ. L. Davis, J. L. Davis Department of Clinical SciencesSearch for more papers by this authorS. L. Jones, S. L. Jones Department of Clinical SciencesSearch for more papers by this authorD. H. LaFevers, D. H. LaFevers Department of Clinical SciencesSearch for more papers by this authorM. S. Hoskins, M. S. Hoskins Department of Clinical SciencesSearch for more papers by this authorE. M. Mcarver, E. M. Mcarver Department of Clinical SciencesSearch for more papers by this authorM. G. Papich, M. G. Papich Department of Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USASearch for more papers by this author S. Y. Gardner, S. Y. Gardner Department of Clinical SciencesSearch for more papers by this authorJ. L. Davis, J. L. Davis Department of Clinical SciencesSearch for more papers by this authorS. L. Jones, S. L. Jones Department of Clinical SciencesSearch for more papers by this authorD. H. LaFevers, D. H. LaFevers Department of Clinical SciencesSearch for more papers by this authorM. S. Hoskins, M. S. Hoskins Department of Clinical SciencesSearch for more papers by this authorE. M. Mcarver, E. M. Mcarver Department of Clinical SciencesSearch for more papers by this authorM. G. Papich, M. G. Papich Department of Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USASearch for more papers by this author First published: 18 February 2004 https://doi.org/10.1046/j.0140-7783.2003.00529.xCitations: 28 Sarah Y. Gardner, Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, NC 27606, USA. E-mail: [email protected] Read the full textAboutPDF 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 Citing Literature Volume27, Issue1February 2004Pages 57-60 RelatedInformation}, number={1}, journal={JOURNAL OF VETERINARY PHARMACOLOGY AND THERAPEUTICS}, author={Gardner, SY and Davis, JL and Jones, SL and Lafevers, DH and Hoskins, MS and Mcarver, M and Papich, MG}, year={2004}, month={Feb}, pages={57–60} }
 @article{shifflett_bottone_young_moeser_jones_blikslager_2004, title={Neutrophils augment recovery of porcine ischemia-injured ileal mucosa by an IL-1β- and COX-2-dependent mechanism}, volume={287}, ISSN={0193-1857 1522-1547}, url={http://dx.doi.org/10.1152/ajpgi.00076.2003}, DOI={10.1152/ajpgi.00076.2003}, abstractNote={Polymorphonuclear neutrophils (PMNs) play a critical role in intestinal mucosal injury and repair. To study effects of PMNs on acutely injured mucosa, we applied PMNs isolated from circulation or peritoneal fluid from animals with chemically induced peritonitis to ischemia-injured porcine ileal mucosa. In preliminary experiments, PMNs enhanced recovery of transepithelial electrical resistance (TER), and this action was inhibited by pretreatment with the nonselective cyclooxygenase (COX) inhibitor indomethacin. Because COX-2 is upregulated by inflammatory mediators such as IL-1beta, which is released by PMNs, we postulated that PMNs enhance recovery of ischemia-injured mucosa by a pathway involving IL-1beta and COX-2. Application of 5 x 10(6) PMNs to the serosal surface of ischemia-injured mucosa significantly enhanced recovery of TER (P < 0.05), an effect that was inhibited by the selective COX-2 inhibitor NS-398 (5 microM) and by an IL-1beta receptor antagonist (0.1 mg/ml). Addition of 10 ng/ml IL-1beta to the serosal surface of injured tissues caused a significant increase in TER (P < 0.05) that was inhibited by pretreatment with NS-398. Western blot analysis of mucosal homogenates revealed dramatic upregulation of COX-2 in response to IL-1beta or peritoneal PMNs, and the latter was inhibited by an IL-1beta receptor antagonist. Real-time PCR revealed that increased mRNA COX-2 expression preceded increased COX-2 protein expression in response to IL-1beta. We concluded that PMNs augment recovery of TER in ischemia-injured ileal mucosa via IL-1beta-dependent upregulation of COX-2.}, number={1}, journal={American Journal of Physiology-Gastrointestinal and Liver Physiology}, publisher={American Physiological Society}, author={Shifflett, Donnie E. and Bottone, Frank G., Jr. and Young, Karen M. and Moeser, Adam J. and Jones, Samuel L. and Blikslager, Anthony T.}, year={2004}, month={Jul}, pages={G50–G57} }
 @article{davis_blikslager_catto_jones_2003, title={A Retrospective Analysis of Hepatic Injury in Horses with Proximal Enteritis (1984-2002)}, volume={17}, ISSN={0891-6640 1939-1676}, url={http://dx.doi.org/10.1111/j.1939-1676.2003.tb02530.x}, DOI={10.1111/j.1939-1676.2003.tb02530.x}, abstractNote={The purpose of this study was to test the hypothesis that horses with proximal enteritis (PE) are predisposed to hepatic injury. We also determined whether the presence of liver injury in horses with PE was associated with other clinicopathologic abnormalities or affected outcome. The medical records of all horses admitted for evaluation of colic and gastric reflux between 1984 and 2002 were reviewed. Horses were considered to have PE if the diagnosis was made at surgery or postmortem examination or if they had clinical findings consistent with PE. Horses with a small intestinal strangulating obstruction (SISO) were used as the control group. Historic and clinicopathologic data were collected for each horse. The data were analyzed by descriptive statistics, parametric and nonparametric analyses, and logistic regression. Horses with PE had significantly higher serum gamma‐glutamyltransferase (GGT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) activities than horses with SISO (P < .05). Horses with PE were 12.1 times more likely to have high GGT activities than were horses with SISO. Horses with PE had an increased risk of at least 1 hepatic enzyme being increased if a high anion gap or large volume of reflux was present. Our conclusion is that horses with PE are more likely to have hepatic injury than horses with SISO. The mechanism of hepatic injury may involve ascending infection from the common bile duct, absorption of endotoxin or inflammatory mediators from the portal circulation, or hepatic hypoxia resulting from systemic inflammation and endotoxemic shock.}, number={6}, journal={Journal of Veterinary Internal Medicine}, publisher={Wiley}, author={Davis, Jennifer L. and Blikslager, Anthony T. and Catto, Katrina and Jones, Samuel L.}, year={2003}, month={Nov}, pages={896–901} }
 @article{davis_blikslager_catto_jones_2003, title={A retrospective analysis of hepatic injury in horses with proximal enteritis (1984-2002)}, volume={17}, ISSN={["0891-6640"]}, DOI={10.1892/0891-6640(2003)017<0896:ARAOHI>2.3.CO;2}, number={6}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Davis, JL and Blikslager, AT and Catto, K and Jones, SL}, year={2003}, pages={896–901} }
 @article{davis_jones_2003, title={Equine primary immunodeficiencies}, volume={25}, number={7}, journal={Compendium on Continuing Education for the Practicing Veterinarian}, author={Davis, J. L. and Jones, S. L.}, year={2003}, pages={548–556} }
 @inbook{davis_jones_2003, place={Philadelphia, Pa}, edition={2nd}, title={Examination for disorders of the gastrointestinal tract}, booktitle={Equine Internal Medicine}, publisher={WB Saunders}, author={Davis, J.L. and Jones, S.L.}, editor={Reed, S.M. and Bayly, W. M. and Sellon, D.C.Editors}, year={2003}, pages={769–780} }
 @article{johansson_gardner_jones_fuquay_reagan_levine_2003, title={Hypomagnesemia in Hospitalized Horses}, volume={17}, ISSN={0891-6640 1939-1676}, url={http://dx.doi.org/10.1111/j.1939-1676.2003.tb02526.x}, DOI={10.1111/j.1939-1676.2003.tb02526.x}, abstractNote={This study was initiated to identify the signalment and clinical variables potentially associated with hypomagnesemia in horses evaluated at the North Carolina State University, College of Veterinary Medicine (NCSU-CVM) veterinary teaching hospital between January 1999 and May 2001. A nested case reference study (nested case-control study) was conducted to examine the potential relationship between hypomagnesemia and signalment, serum chemistry panel analyses, number of hospitalization days, discharge status, and diagnosis. A series of independent and multivariable logistic regression models were used to assess the potential association of each variable with low total serum magnesium concentrations. Four hundred one of 823 (48.7%) horses had serum total magnesium concentrations below the normal reference range. Hypomagnesemia was more likely to occur in horses older than I month of age. Colic (odds ratio [OR]: 2.96, 95% confidence intervals [CI]: 2.14-4.08), acute diarrhea (OR: 5.91, 95% CI: 2.32-15.06), other gastrointestinal disease (OR: 2.07, 95% CI: 1.15-3.71), infectious respiratory disease (OR: 5.07, 95% CI: 2.09-12.28), and multiorgan system disease (OR: 2.31, 95% CI: 1.24-4.28) were associated with hypomagnesemia in adult horses, whereas foals with diarrhea (excluding septic foals) (OR: 0.11, 95% CI: 0.01-0.84) were less likely to have hypomagnesemia. Overall, there was no relationship between hypomagnesemia and mortality (OR: 1.00, 95% CI: 0.72-1.41), but horses with colic and hypomagnesemia were less likely to die than horses with colic and normal or high total magnesium (OR: 0.53, 95% CI: 0.30-0.95). Among horses that survived, hypomagnesemia at admission was associated with a longer hospitalization period (OR: 1.45, 95% CI: 1.00-2.11).}, number={6}, journal={Journal of Veterinary Internal Medicine}, publisher={Wiley}, author={Johansson, AM and Gardner, SY and Jones, SL and Fuquay, LR and Reagan, VH and Levine, JF}, year={2003}, month={Nov}, pages={860–867} }
 @article{johansson_gardner_jones_fuquay_reagan_levine_2003, title={Hypomagnesemia in hospitalized horses}, volume={17}, ISSN={["1939-1676"]}, DOI={10.1892/0891-6640(2003)017<0860:HIHH>2.3.CO;2}, abstractNote={This study was initiated to identify the signalment and clinical variables potentially associated with hypomagnesemia in horses evaluated at the North Carolina State University, College of Veterinary Medicine (NCSU-CVM) veterinary teaching hospital between January 1999 and May 2001. A nested case reference study (nested case-control study) was conducted to examine the potential relationship between hypomagnesemia and signalment, serum chemistry panel analyses, number of hospitalization days, discharge status, and diagnosis. A series of independent and multivariable logistic regression models were used to assess the potential association of each variable with low total serum magnesium concentrations. Four hundred one of 823 (48.7%) horses had serum total magnesium concentrations below the normal reference range. Hypomagnesemia was more likely to occur in horses older than 1 month of age. Colic (odds ratio [OR]: 2.96, 95% confidence intervals [CI]: 2.14–4.08), acute diarrhea (OR: 5.91, 95% CI: 2.32–15.06), other gastrointestinal disease (OR: 2.07, 95% CI: 1.15–3.71), infectious respiratory disease (OR: 5.07, 95% CI: 2.09–12.28), and multiorgan system disease (OR: 2.31, 95% CI: 1.24–4.28) were associated with hypomagnesemia in adult horses, whereas foals with diarrhea (excluding septic foals) (OR: 0.11, 95% CI: 0.01–0.84) were less likely to have hypomagne-semia. Overall, there was no relationship between hypomagnesemia and mortality (OR: 1.00, 95% CI: 0.72–1.41), but horses with colic and hypomagnesemia were less likely to die than horses with colic and normal or high total magnesium (OR: 0.53, 95% CI: 0.30–0.95). Among horses that survived, hypomagnesemia at admission was associated with a longer hospitalization period (OR: 1.45, 95% CI: 1.00–2.11).}, number={6}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Johansson, AM and Gardner, SY and Jones, SL and Fuquay, LR and Reagan, VH and Levine, JF}, year={2003}, pages={860–867} }
 @inbook{jones_2003, place={Philadelphia, Pa}, edition={2nd}, title={Inflammatory diseases of the gastrointestinal tract causing diarrhea}, booktitle={Equine Internal Medicine}, publisher={WB Saunders}, author={Jones, S.L.}, editor={Reed, S.M. and Bayly, W.M. and Sellon, D.C.Editors}, year={2003}, pages={884–913} }
 @inbook{jones_2003, place={Philadelphia, PA}, edition={2nd}, title={Oral diseases}, booktitle={Equine Internal Medicine}, publisher={WB Saunders}, author={Jones, S.L.}, editor={Reed, S.M. and Bayly, W.M. and Sellon, D.C.Editors}, year={2003}, pages={846–855} }
 @article{little_dean_young_mckane_martin_jones_blikslager_2003, title={PI3K signaling is required for prostaglandin-induced  mucosal recovery in ischemia-injured porcine ileum}, volume={284}, ISSN={0193-1857 1522-1547}, url={http://dx.doi.org/10.1152/ajpgi.00121.2002}, DOI={10.1152/ajpgi.00121.2002}, abstractNote={We have previously shown that PGE(2) and PGI(2) induce recovery of transepithelial resistance (TER) in ischemia-injured porcine ileal mucosa, associated with initial increases in Cl(-) secretion. We believe that the latter generates an osmotic gradient that stimulates resealing of tight junctions. Because of evidence implicating phosphatidylinositol 3-kinase (PI3K) in regulating tight junction assembly, we postulated that this signaling pathway is involved in PG-induced mucosal recovery. Porcine ileum was subjected to 45 min of ischemia, after which TER was monitored for a 180-min recovery period. Endogenous PG production was inhibited with indomethacin (5 microM). PGE(2) (1 microM) and PGI(2) (1 microM) stimulated recovery of TER, which was inhibited by serosal application of the osmotic agent urea (300 mosmol/kgH(2)O). The PI3K inhibitor wortmannin (10 nM) blocked recovery of TER in response to PGs or mucosal urea. Immunofluorescence imaging of recovering epithelium revealed that PGs restored occludin and zonula occludens-1 distribution to interepithelial junctions, and this pattern was disrupted by pretreatment with wortmannin. These experiments suggest that PGs stimulate recovery of paracellular resistance via a mechanism involving transepithelial osmotic gradients and PI3K-dependent restoration of tight junction protein distribution.}, number={1}, journal={American Journal of Physiology-Gastrointestinal and Liver Physiology}, publisher={American Physiological Society}, author={Little, Dianne and Dean, Rebecca A. and Young, Karen M. and McKane, Shaun A. and Martin, Linda D. and Jones, Samuel L. and Blikslager, Anthony T.}, year={2003}, month={Jan}, pages={G46–G56} }
 @inbook{jones_2003, place={Philadelphia, Pa}, edition={2nd}, title={Pathophysiology of gastrointestinal inflammation}, booktitle={Equine Internal Medicine}, publisher={WB Saunders}, author={Jones, S.L.}, editor={Reed, S.M. and Bayly, W.M. and Sellon, D.C.Editors}, year={2003}, pages={780–789} }
 @inbook{jones_2003, title={Right Dorsal Colitis}, ISBN={9780721695402}, url={http://dx.doi.org/10.1016/b978-0-7216-9540-2.50044-x}, DOI={10.1016/b978-0-7216-9540-2.50044-x}, booktitle={Current Therapy in Equine Medicine}, publisher={Elsevier}, author={Jones, S}, year={2003}, pages={141–143} }
 @article{davis_jones_2003, title={Suppurative cholangiohepatitis and enteritis in adult horses}, volume={17}, ISSN={["0891-6640"]}, DOI={10.1892/0891-6640(2003)017<0583:SCAEIA>2.3.CO;2}, abstractNote={Journal of Veterinary Internal MedicineVolume 17, Issue 4 p. 583-587 Open Access Suppurative Cholangiohepatitis and Enteritis in Adult Horses Jennifer L. Davis, Jennifer L. Davis Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this authorSamuel L. Jones, Samuel L. Jones Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC DVM, PhD, DACVIM, College of Veterinary Medicine, North Carolina State University, 4700Hillsborough Street, Raleigh, NC 27606; E-mail: [email protected]Search for more papers by this author Jennifer L. Davis, Jennifer L. Davis Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this authorSamuel L. Jones, Samuel L. Jones Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC DVM, PhD, DACVIM, College of Veterinary Medicine, North Carolina State University, 4700Hillsborough Street, Raleigh, NC 27606; E-mail: [email protected]Search for more papers by this author First published: 28 June 2008 https://doi.org/10.1111/j.1939-1676.2003.tb02483.xCitations: 13 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 References 1 Thornburg LP, Kintner LD. Cholangiohepatitis in a horse. Vet Med Small Anim Clin 1980; 75: 1895– 1896. 2 Johnston JK, Divers TJ, Reef VB, et al. Cholelithiasis in horses: Ten cases (1982–1986). J Am Vet Med Assoc 1989; 194: 405– 409. 3 Peek SF, Divers TJ. Medical treatment of cholangiohepatitis and cholelithiasis in mature horses: 9 cases (1991–1998). Equine Vet J 2000; 32: 301– 306. 4 Pearson EG. Liver disease in the mature horse. Equine Vet Educ 1999; 11: 87– 96. 5 Gerros TC. Gallbladder and biliary tract disease. In: BP Smith, ed. Large Animal Internal Medicine, 2nd ed. St Louis , MO : Mosby; 1996: 946– 948. 6 Acland HM, Gunson DE, Gillette DM. Ulcerative duodenitis in foals. Vet Pathol 1983; 20: 653– 661. 7 Ettlinger JJ, Ford T., Palmer JE. Ulcerative duodenitis with lu-minal constriction in two horses. J Am Vet Med Assoc 1990; 196: 1628– 1630. 8 Zeuzem S.. Gut-liver axis. Int J Colorectal Dis 2000; 15: 59– 82. 9 Schulz KS, Simmons TR, Johnson R.. Primary cholangiohepatitis in a horse. Cornell Vet 1990; 80: 35– 40. 10 Crawford JM. Biliary system. In: SL Robbins, ed. Pathologic Basis of Disease, 5th ed. Philadelphia , PA : WB Saunders; 1994: 883– 896. 11 Hanau LH, Steigbigel NH. Acute (ascending) cholangitis. Infect Dis Clin North Am 2000; 14: 521– 546. 12 Madara JL. Pathobiology of the intestinal epithelial barrier. Am J Pathol 1990; 137: 1273– 1281. 13 Losser M., Payen D.. Mechanisms of liver damage. Semin Liver Dis 1996; 16: 357– 367. 14 Tennant B.. Acute hepatitis in horses: Problems of differentiating toxic and infectious causes in the adult. Proceedings of the 24th Annual Convention of the American Association of Equine Practitioners, St. Louis, MO, 1978. 15 Al-Mashat RR, Taylor DJ. Bacteria in enteric lesions of horses. Vet Rec 1986; 118: 453– 458. 16 Matthews S., Dart AJ, Dowling BA, et al. Peritonitis associated with Actinobacillus equuli in horses: 51 cases. Aust Vet J 2001; 79: 536– 539. 17 Seahorn TL, Cornick JL, Cohen ND. Prognostic indicators for horses with duodenitis-proximal jejunitis. J Vet Int Med 1992; 6: 307– 311. 18 Johnston JK, Morris DD. Comparison of duodenitis/proximal jejunitis and small intestinal obstruction in horses: 68 cases (1977-- 1985). J Am Vet Med Assoc 1987; 191: 849– 854. Citing Literature Volume17, Issue4July 2003Pages 583-587 ReferencesRelatedInformation}, number={4}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Davis, JL and Jones, SL}, year={2003}, pages={583–587} }
 @article{davis_jones_2003, title={Suppurative cholangiohepatitis and enteritis in adult horses.}, volume={17}, url={http://europepmc.org/abstract/med/12892313}, DOI={10.1111/j.1939-1676.2003.tb02483.x}, abstractNote={Journal of Veterinary Internal MedicineVolume 17, Issue 4 p. 583-587 Open Access Suppurative Cholangiohepatitis and Enteritis in Adult Horses Jennifer L. Davis, Jennifer L. Davis Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this authorSamuel L. Jones, Samuel L. Jones Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC DVM, PhD, DACVIM, College of Veterinary Medicine, North Carolina State University, 4700Hillsborough Street, Raleigh, NC 27606; E-mail: sam-jones@ncsu.eduSearch for more papers by this author Jennifer L. Davis, Jennifer L. Davis Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this authorSamuel L. Jones, Samuel L. Jones Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC DVM, PhD, DACVIM, College of Veterinary Medicine, North Carolina State University, 4700Hillsborough Street, Raleigh, NC 27606; E-mail: sam-jones@ncsu.eduSearch for more papers by this author First published: 28 June 2008 https://doi.org/10.1111/j.1939-1676.2003.tb02483.xCitations: 13 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 Thornburg LP, Kintner LD. Cholangiohepatitis in a horse. Vet Med Small Anim Clin 1980; 75: 1895– 1896. 2 Johnston JK, Divers TJ, Reef VB, et al. Cholelithiasis in horses: Ten cases (1982–1986). J Am Vet Med Assoc 1989; 194: 405– 409. 3 Peek SF, Divers TJ. Medical treatment of cholangiohepatitis and cholelithiasis in mature horses: 9 cases (1991–1998). Equine Vet J 2000; 32: 301– 306. 4 Pearson EG. Liver disease in the mature horse. Equine Vet Educ 1999; 11: 87– 96. 5 Gerros TC. Gallbladder and biliary tract disease. In: BP Smith, ed. Large Animal Internal Medicine, 2nd ed. St Louis , MO : Mosby; 1996: 946– 948. 6 Acland HM, Gunson DE, Gillette DM. Ulcerative duodenitis in foals. Vet Pathol 1983; 20: 653– 661. 7 Ettlinger JJ, Ford T., Palmer JE. Ulcerative duodenitis with lu-minal constriction in two horses. J Am Vet Med Assoc 1990; 196: 1628– 1630. 8 Zeuzem S.. Gut-liver axis. Int J Colorectal Dis 2000; 15: 59– 82. 9 Schulz KS, Simmons TR, Johnson R.. Primary cholangiohepatitis in a horse. Cornell Vet 1990; 80: 35– 40. 10 Crawford JM. Biliary system. In: SL Robbins, ed. Pathologic Basis of Disease, 5th ed. Philadelphia , PA : WB Saunders; 1994: 883– 896. 11 Hanau LH, Steigbigel NH. Acute (ascending) cholangitis. Infect Dis Clin North Am 2000; 14: 521– 546. 12 Madara JL. Pathobiology of the intestinal epithelial barrier. Am J Pathol 1990; 137: 1273– 1281. 13 Losser M., Payen D.. Mechanisms of liver damage. Semin Liver Dis 1996; 16: 357– 367. 14 Tennant B.. Acute hepatitis in horses: Problems of differentiating toxic and infectious causes in the adult. Proceedings of the 24th Annual Convention of the American Association of Equine Practitioners, St. Louis, MO, 1978. 15 Al-Mashat RR, Taylor DJ. Bacteria in enteric lesions of horses. Vet Rec 1986; 118: 453– 458. 16 Matthews S., Dart AJ, Dowling BA, et al. Peritonitis associated with Actinobacillus equuli in horses: 51 cases. Aust Vet J 2001; 79: 536– 539. 17 Seahorn TL, Cornick JL, Cohen ND. Prognostic indicators for horses with duodenitis-proximal jejunitis. J Vet Int Med 1992; 6: 307– 311. 18 Johnston JK, Morris DD. Comparison of duodenitis/proximal jejunitis and small intestinal obstruction in horses: 68 cases (1977-- 1985). J Am Vet Med Assoc 1987; 191: 849– 854. Citing Literature Volume17, Issue4July 2003Pages 583-587 ReferencesRelatedInformation}, number={4}, journal={Journal of veterinary internal medicine}, author={Davis, JL and Jones, SL}, year={2003}, pages={583–587,} }
 @article{jones_2003, title={Therapeutics for gastrointestinal diseases}, volume={19}, DOI={10.1016/j.cveq.2003.08.013}, number={3}, journal={Veterinary Clinics of North America. Equine Practice}, author={jones}, year={2003}, pages={XI-} }
 @article{jones_2003, title={Treatment of acute and chronic gastrointestinal inflammation.}, volume={19}, url={http://europepmc.org/abstract/med/14740764}, DOI={10.1016/j.cveq.2003.08.010}, abstractNote={Treating inflammation in the equine gastrointestinal tract remains a challenge. Our most potent anti-inflammatory drugs, COX inhibitors and glucocorticoids, have unwanted effects on the gastrointestinal tract and host defense that often limit their use. Newer strategies targeting specific cells and molecules that regulate a subset of the events occurring during inflammation are rapidly becoming available and should allow clinicians to reduce the detrimental effects of inflammation without inhibiting the beneficial aspects.}, number={3}, journal={Veterinary Clinics of North America. Equine Practice}, author={Jones, SL}, year={2003}, month={Dec}, pages={697-} }
 @article{jones_davis_rowlingson_2003, title={Ultrasonographic findings in horses with right dorsal colitis: five cases (2000-2001)}, volume={222}, ISSN={["0003-1488"]}, url={http://europepmc.org/abstract/med/12725314}, DOI={10.2460/javma.2003.222.1248}, abstractNote={Abstract Objective —To determine whether ultrasonography would be useful in the diagnosis of right dorsal colitis in horses. Design —Retrospective study. Animals —5 horses with right dorsal colitis and 15 healthy adult horses. Procedure —Mural thickness and appearance of the right dorsal colon were determined from ultrasonographic images obtained at right intercostal spaces 10, 11, 12, 13, and 14. Results —The right dorsal colon could be imaged most consistently at the right 11th, 12th, and 13th intercostal spaces, below the margin of the lung and axial to the liver. Mural thickness measured from ultrasonographic images was significantly greater in horses with right dorsal colitis than in healthy horses. The right dorsal colon in affected horses had a prominent hypoechoic layer associated with submucosal edema and inflammatory infiltrates. Successful treatment of 1 horse with right dorsal colitis was associated with a decrease in mural thickness coincident with an increase in serum albumin and total protein concentrations and weight gain. A decrease in mural thickness was also observed in a second horse treated for right dorsal colitis that was not associated with healing of the right dorsal colon or an increase in serum albumin concentration but rather thinning of a segment of the right dorsal colon that eventually ruptured. Conclusions and Clinical Relevance —Results suggest that ultrasonographic measurement of mural thickness and evaluation of the appearance of the right dorsal colon may be useful in the diagnosis of right dorsal colitis in horses. ( J Am Vet Med Assoc 2003;222:1248–1251)}, number={9}, journal={JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Jones, SL and Davis, J and Rowlingson, K}, year={2003}, month={May}, pages={1248–1251} }
 @article{stanar_little_redding_jones_2002, title={Equine rounds-Case presentation: Idiopathic eosinophilic enteritis in a 10-week-old colt}, volume={24}, number={4}, journal={Compendium on Continuing Education for the Practicing Veterinarian}, author={Stanar, L.S. and Little, D. and Redding, W.R. and Jones, S.L.}, year={2002}, pages={342–344} }
 @article{davis_gilger_spaulding_robertson_jones_2002, title={Nasal adenocarcinoma with diffuse metastases involving the orbit, cerebrum, and multiple cranial nerves in a horse}, volume={221}, ISSN={["0003-1488"]}, url={http://europepmc.org/abstract/med/12458617}, DOI={10.2460/javma.2002.221.1460}, abstractNote={A 9-year-old Trakehner gelding was examined because of right exophthalmus. Clinical findings included a lack of menace response in the right eye, reduced direct and consensual right pupillary light reflexes, ventrolateral strabismus of the right eye, mild right-sided facial asymmetry, a head tilt to the left, and increased extensor tone in the right limbs. Findings were suggestive of a multifocal lesion affecting the right forebrain; right optic, oculomotor, and facial nerves; and left vestibulocochlear nerve. Ultrasonographic examination of the right eye revealed a vascular retrobulbar mass. Computed tomographic imaging revealed a mass that filled the nasal cavity and invaded the forebrain. Necropsy revealed an undifferentiated nasal adenocarcinoma affecting the orbit with metastases to the right parotid gland, cranial cervical lymph nodes, fascial planes of the neck, and lungs. No evidence of direct involvement of the right facial and left vestibulocochlear nerves was found, suggesting the possibility of paraneoplastic peripheral neuropathy.}, number={10}, journal={JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Davis, JL and Gilger, BC and Spaulding, K and Robertson, ID and Jones, SL}, year={2002}, month={Nov}, pages={1460–1463} }
 @article{gayle_jones_argenzio_blikslager_surgery_2002, title={Neutrophils increase paracellular permeability of restituted ischemic-injured porcine ileum}, volume={132}, ISSN={["0039-6060"]}, url={http://europepmc.org/abstract/med/12324760}, DOI={10.1067/msy.2002.125320}, abstractNote={Background. We have previously shown minimal evidence of neutrophil infiltration during early reperfusion of porcine ischemic ileum. However, we noted marked neutrophil infiltration 6 to 18 hours after ischemia during mucosal repair. We postulated such neutrophil infiltration would disrupt restituting epithelium. Methods. Pigs were pretreated with anti-CD11/CD18 monoclonal antibody, superoxide dismutase-polyethylene glycol, or saline solution before inducing 1 hour of ischemia. Pigs recovered for up to 18 hours, after which mucosal repair was assessed. Results. One hour of ischemia induced loss of 19 ± 7% of the villous epithelial surface area. Epithelial restitution covered the mucosal defect within 2 hours, although full recovery of mucosal barrier function required 6 hours. By 18 hours, a significant decrease in transepithelial electrical resistance and increase in transmucosal mannitol flux was noted despite the continued presence of complete epithelial coverage. Accumulation of neutrophils within restituting epithelium was noted on histologic examination, associated with electron-microscopic evidence of widened paracellular spaces. Pretreatment with anti-CD11/CD18 monoclonal antibody and superoxide dismutase-polyethylene glycol significantly reduced neutrophil infiltration and normalized transepithelial electrical resistance and mannitol fluxes. Conclusions. Mucosal inflammation during epithelial repair resulted in increased paracellular permeability as neutrophils traversed restituted epithelium. Blocking neutrophil adhesion or scavenging superoxide prevented mucosal dysfunction in recovering tissue. (Surgery 2002;132:461-70.)}, number={3}, journal={SURGERY}, author={Gayle, J. and Jones, S.L. and Argenzio, R.A. and Blikslager, A.T. and Surgery}, year={2002}, month={Sep}, pages={461–470} }
 @article{little_keene_bruton_smith_powell_jones_2002, title={Percutaneous retrieval of a jugular catheter fragment from the pulmonary artery of a foal}, volume={220}, ISSN={["0003-1488"]}, url={http://europepmc.org/abstract/med/12126133}, DOI={10.2460/javma.2002.220.212}, abstractNote={A 49-kg (107.8-lb) sexually intact male Arabian foal was evaluated at 3 days of age because of profuse watery diarrhea, anorexia, and signs of abdominal pain. Physical examination findings were unremarkable except for evidence of diarrhea. A catheter was placed in the right jugular vein for administration of antimicrobials and lactated Ringer's solution. The foal was discharged with instructions to the owner to continue antimicrobial administration and fluid therapy; at home, the owner inadvertently cut the catheter at the level of the hub during attempted removal, and the catheter fragment migrated distally in the jugular vein and subsequently lodged in the pulmonary artery. The foal was readmitted to the hospital for retrieval of the fragment, using a percutaneous retrieval technique. Catheter fragmentation is a well-recognized risk of catheterization in horses. Catheter fragments can be retrieved somewhat easily from the jugular vein; however, if the fragment migrates to the heart or pulmonary artery, imaging the fragment to locate and retrieve it can be difficult. Complications associated with catheter fragmentation include septicemia, endocarditis, lung abscesses, pulmonary embolism, dysrhythmias, cardiac perforation, pulmonary or caval thrombosis, and death. To our knowledge, this is the first report of successful retrieval of a catheter fragment from the pulmonary artery in a horse.}, number={2}, journal={JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Little, D and Keene, BW and Bruton, C and Smith, LJ and Powell, S and Jones, SL}, year={2002}, month={Jan}, pages={212–214} }
 @article{davis_gardner_jones_schwabenton_papich_2002, title={Pharmacokinetics of azithromycin in foals after i.v. and oral dose and disposition into phagocytes}, volume={25}, ISSN={["1365-2885"]}, url={http://europepmc.org/abstract/med/12000529}, DOI={10.1046/j.1365-2885.2002.00387.x}, abstractNote={The properties of azithromycin suggest that it may be an alternative to erythromycin for treatment of Rhodococcus equi pneumonia in foals. To investigate this possibility, the disposition of azithromycin in plasma, polymorphonuclear leukocytes (PMN), and alveolar cells was examined after a single administration in foals. Azithromycin suspension was administered orally (p.o.) at a dose of 10 mg/kg to five healthy 2-3-month-old foals. Two weeks later, azithromycin for injection was administered by intravenous (i.v.) infusion at a dose of 5 mg/kg to the same foals. Plasma samples were collected after p.o. and i.v. administration. Peripheral blood PMN and bronchoalveolar lavage fluid and alveolar cells were collected after p.o. administration. Azithromycin concentrations were determined by reverse-phase high-performance liquid chromatography (HPLC) with coulometric electrochemical detection. Azithromycin p.o. absorption was variable with a mean systemic availability of 39% (+/-20%). The plasma half-life was 16 and 18.3 h after i.v. and p.o. administration, respectively. Azithromycin had a very large volume of distribution (V(d)) of 11.6 L/kg [V(d(ss))] and 12.4 L/kg [V(d(area))]. The large V(d) can be attributed to high tissue and intracellular concentrations, exhibited by the high concentration of azithromycin in PMN and alveolar cells. The PMN half-life was 49.2 h. Dosage of 10 mg/kg of azithromycin p.o. once daily for foals with R. equi pneumonia is recommended for further study.}, number={2}, journal={JOURNAL OF VETERINARY PHARMACOLOGY AND THERAPEUTICS}, author={Davis, JL and Gardner, SY and Jones, SL and Schwabenton, BA and Papich, MG}, year={2002}, month={Apr}, pages={99–104} }
 @article{jones_2002, title={Protein kinase A regulates beta 2 integrin avidity in neutrophils}, volume={71}, number={6}, journal={Journal of Leukocyte Biology}, author={Jones, S. L.}, year={2002}, pages={1042–1048} }
 @article{jones_2002, title={Protein kinase A regulates beta2 integrin avidity in neutrophils.}, volume={71}, url={http://europepmc.org/abstract/med/12050191}, number={6}, journal={Journal of leukocyte biology}, author={Jones, SL}, year={2002}, month={Jun}, pages={1042–1048,} }
 @misc{jones_blikslager_2002, title={Role of the enteric nervous system in the pathophysiology of secretory diarrhea}, volume={16}, ISSN={["0891-6640"]}, DOI={10.1892/0891-6640(2002)016<0222:ROTENS>2.3.CO;2}, abstractNote={Details of the physiology and pathophysiology of epithelial secretion in the gastrointestinal tract are becoming clear, leading to new models of the mechanisms underlying diarrhea. The enteric nervous system is a critical component of the mechanism regulating fluid secretion in the normal gut and a key element in the pathophysiology of diarrhea. Neural reflex pathways increase epithelial fluid secretion in response to several enteric pathogens of veterinary importance such as Salmonella spp., Cryptosporidium parvum, rotavirus, and Clostridium difficile. Moreover, the enteric nervous system has an important role in epithelial secretion triggered by products of activated leukocytes during inflammation. New approaches targeting the enteric nervous system show promise for the treatment of secretory diarrhea.}, number={3}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Jones, SL and Blikslager, AT}, year={2002}, pages={222–228} }
 @article{jones_blikslager_2002, title={Role of the enteric nervous system in the pathophysiology of secretory diarrhea.}, volume={16}, url={http://europepmc.org/abstract/med/12041649}, DOI={10.1111/j.1939-1676.2002.tb02361.x}, abstractNote={Details of the physiology and pathophysiology of epithelial secretion in the gastrointestinal tract are becoming clear, leading to new models of the mechanisms underlying diarrhea. The enteric nervous system is a critical component of the mechanism regulating fluid secretion in the normal gut and a key element in the pathophysiology of diarrhea. Neural reflex pathways increase epithelial fluid secretion in response to several enteric pathogens of veterinary importance such as Salmonella spp., Cryptosporidium parvum , rotavirus, and Clostridium difficile . Moreover, the enteric nervous system has an important role in epithelial secretion triggered by products of activated leukocytes during inflammation. New approaches targeting the enteric nervous system show promise for the treatment of secretory diarrhea.}, number={3}, journal={Journal of veterinary internal medicine}, author={Jones, SL and Blikslager, AT}, year={2002}, pages={222–228,} }
 @article{chilcoat_rowlingson_jones_2002, title={The effects of cAMP modulation upon the adhesion and respiratory burst activity of immune complex-stimulated equine neutrophils}, volume={88}, ISSN={["0165-2427"]}, url={http://europepmc.org/abstract/med/12088646}, DOI={10.1016/S0165-2427(02)00137-X}, abstractNote={Toxic products such as reactive oxygen intermediates released by activated polymorphonuclear neutrophil (PMN) have an important role in the pathophysiology of diseases associated with the deposition of immune complexes (IC) in tissues. IC-induced activation of PMN requires adhesion mediated by integrin adhesion receptors. Of the integrins expressed on PMN, the beta(2) family has been found to be of particular importance for activation of PMN by IC. beta(2) Integrin ligand binding must be activated to enable adhesion to IC. Both activating and inhibitory signals regulate beta(2) integrin ligand avidity and adhesion. The second messenger cyclic adenosine monophosphate (cAMP) has been demonstrated to inhibit the activation of PMN in response to a variety of stimuli. The purpose of this study is to test the hypothesis that cAMP-dependent signals inhibit beta(2) integrin-dependent adhesion of equine PMN to immobilized IC and subsequent adhesion-dependent activation of respiratory burst activity. Treatment of equine PMN with beta(2) adrenergic agonists isoproterenol or clenbuterol, which trigger an increase in intracellular cAMP concentration, inhibited adhesion of equine PMN to IC in a dose dependent manner. Similarly, inhibition of cAMP hydrolysis by the non-specific phosphodiesterase (PDE) inhibitor pentoxifylline and the PDE 4-specific inhibitor rolipram inhibited adhesion of equine PMN to IC. Elevation of intracellular cAMP levels with pentoxifylline, clenbuterol and rolipram also inhibited IC-induced activation of respiratory burst activity in equine PMN. Importantly, co-treatment of equine PMN with rolipram and either beta(2) adrenergic agonist synergistically inhibited both the adhesion of equine PMN to IC as well as the subsequent respiratory burst activity.}, number={1-2}, journal={VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY}, author={Chilcoat, CD and Rowlingson, KA and Jones, SL}, year={2002}, month={Sep}, pages={65–77} }
 @article{campbell_jones_blikslager_2002, title={The effects of cyclo-oxygenase inhibitors on bile-injured and normal equine colon}, volume={34}, ISSN={["0425-1644"]}, DOI={10.2746/042516402776117737}, abstractNote={A potential adverse effect of cyclo-oxygenase (COX) inhibitors (nonsteroidal anti-inflammatory drugs [NSAIDs]) in horses is colitis. In addition, we have previously shown an important role for COX-produced prostanoids in recovery of ischaemic-injured equine jejunum. It was hypothesised that the nonselective COX inhibitor flunixin would retard repair of bile-injured colon by preventing production of reparative prostaglandins, whereas the selective COX-2 inhibitor, etodolac would not inhibit repair as a result of continued COX-1 activity. Segments of the pelvic flexure were exposed to 1.5 mmol/l deoxycholate for 30 min, after which they were recovered for 4 h in Ussing chambers. Contrary to the proposed hypothesis, recovery of bile-injured colonic mucosa was not affected by flunixin or etodolac, despite significantly depressed prostanoid production. However, treatment of control tissue with flunixin led to increases in mucosal permeability, whereas treatment with etodolac had no significant effect. Therefore, although recovery from bile-induced colonic injury maybe independent of COX-elaborated prostanoids, treatment of control tissues with nonselective COX inhibitors may lead to marked increases in permeability. Alternatively, selective inhibition of COX-2 may reduce the incidence of adverse effects in horses requiring NSAID therapy.}, number={5}, journal={EQUINE VETERINARY JOURNAL}, author={Campbell, NB and Jones, SL and Blikslager, AT}, year={2002}, month={Jul}, pages={493–498} }
 @article{campbell_jones_blikslager_2002, title={The effects of cyclo-oxygenase inhibitors on bile-injured and normal equine colon.}, volume={34}, url={http://europepmc.org/abstract/med/12358053}, number={5}, journal={Equine veterinary journal}, author={Campbell, NB and Jones, SL and Blikslager, AT}, year={2002}, month={Jul}, pages={493–498,} }
 @article{davis_ramirez_campbell_jones_2001, title={Acute and chronic mineral oil pneumonitis in two horses}, volume={13}, DOI={10.1111/j.2042-3292.2001.tb00099.x}, abstractNote={Equine Veterinary EducationVolume 13, Issue 5 p. 230-234 Acute and chronic mineral oil pneumonitis in two horses J. L. Davis, J. L. Davis Departments of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina 27606, USA.Search for more papers by this authorS. Ramirez, S. Ramirez Anatomy, Physiology and Radiology, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina 27606, USA.Search for more papers by this authorN. Campbell, N. Campbell Departments of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina 27606, USA.Search for more papers by this authorS. L. Jones, Corresponding Author S. L. Jones Departments of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina 27606, USA.†Departments of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina 27606, USA.Search for more papers by this author J. L. Davis, J. L. Davis Departments of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina 27606, USA.Search for more papers by this authorS. Ramirez, S. Ramirez Anatomy, Physiology and Radiology, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina 27606, USA.Search for more papers by this authorN. Campbell, N. Campbell Departments of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina 27606, USA.Search for more papers by this authorS. L. Jones, Corresponding Author S. L. Jones Departments of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina 27606, USA.†Departments of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina 27606, USA.Search for more papers by this author First published: 05 January 2010 https://doi.org/10.1111/j.2042-3292.2001.tb00099.xCitations: 6AboutPDF ToolsExport 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 Blinkhorn, R.J. (1998) Embolic infections of the lung and lipoid pneumonia. In: Textbook of Pulmonary Diseases, Vol. I, 6th edn., Eds: G.L. Baum, J.D. Crapo, B.R. Celli and J.B. Karlinsky, Lippincott-Raven, Philadelphia. pp 639–644. Google Scholar Cassiere, H.A. and Niederman, M.S. (1998) Aspiration pneumonia, lipoid pneumonia and lung abscesses. In: Textbook of Pulmonary Diseases, Vol. I, 6th edn., Eds: G.L. Baum, J.D. Crapo, B.R. Celli and J.B. Karlinsky, Lippincott-Raven, Philadelphia. pp 645–654. Google Scholar Corcoran, B.M., Martin, M., Danke, P.G.G., Anderson, A., Head, K.W., Clutton, R.E., Else, R.W. and Fuentes, V.L. (1992) Lipoid pneumonia in a rough collie dog. J. small Anim. Pract. 33, 544–548. 10.1111/j.1748-5827.1992.tb01050.x Web of Science®Google Scholar Scarratt, W.K., Moon, M.L., Sponenberg, D.P. and Feldman, B. (1998) Inappropriate administration of mineral oil resulting in lipoid pneumonia in three horses. Equine vet. J. 30, 85–88. 10.1111/j.2042-3306.1998.tb04094.x CASPubMedWeb of Science®Google Scholar Stauffer, B.D. (1982) Stomach intubation accidents. J. Am. vet. med. Ass. 181, 448. CASPubMedWeb of Science®Google Scholar Sweeney, C.R. and Baker, J.C. (1996) Diseases of the respiratory system. In: Large Animal Internal Medicine, 2nd edn., Ed: B.P. Smith, Mosby, St. Louis. pp 650–651. Google Scholar Wright, J.L. (1995) Consequences of aspiration and bronchial obstruction. In: Pathology of the Lung, 2nd edn., Ed: W.M. Thurlbeck and A.M. Churg, Thieme Medical Publishing, New York. pp 1111–1129. Google Scholar Citing Literature Volume13, Issue5October 2001Pages 230-234 ReferencesRelatedInformation}, number={5}, journal={Equine Veterinary Education}, author={Davis, J. L. and Ramirez, S. and Campbell, N. and jones}, year={2001}, pages={230–234} }
 @article{jones_zimmel_tate_campbell_redding_carlson_2001, title={Case presentation - Dysphagia caused by squamous cell carcinoma in two horses}, volume={23}, number={11}, journal={Compendium on Continuing Education for the Practicing Veterinarian}, author={Jones, S. L. and Zimmel, D. and Tate, L. P. and Campbell, N. and Redding, W. R. and Carlson, G. P.}, year={2001}, pages={1020–1024} }
 @article{blikslager_tate_jones_2001, title={Neodymium:yttrium-aluminum-garnet laser ablation of a urethral web to relieve urinary outflow obstruction in a horse}, volume={218}, ISSN={0003-1488}, url={http://dx.doi.org/10.2460/javma.2001.218.1970}, DOI={10.2460/javma.2001.218.1970}, abstractNote={In horses, intraurethral obstructive lesions may be amenable to transendoscopic laser ablation by use of a neodymium:yttrium-aluminum-garnet laser.}, number={12}, journal={Journal of the American Veterinary Medical Association}, publisher={American Veterinary Medical Association (AVMA)}, author={Blikslager, Anthony T. and Tate, Lloyd P. and Jones, Samuel L.}, year={2001}, month={Jun}, pages={1970–1972} }
 @article{jones_sharief_chilcoat_2001, title={Signaling mechanism for equine neutrophil activation by immune complexes}, volume={82}, ISSN={["0165-2427"]}, url={http://europepmc.org/abstract/med/11557296}, DOI={10.1016/S0165-2427(01)00350-6}, abstractNote={Neutrophils (PMN) are critical host defense cells that have a role in the pathophysiology of a variety of inflammatory diseases, particularly those diseases associated with antigen-antibody immune complexes (IC) deposited in tissues. Activation of PMN by IC is most efficient if the IC are presented immobilized on a surface. Adhesion to the immobilized IC is important for subsequent activation of PMN effector functions, such as generation of reactive oxygen metabolites. Adhesion of human PMN to immobilized IC requires the expression and activation of adhesion receptors called integrins. Of the integrins expressed on PMN, the beta 2 family has been found to be of particular importance for PMN function. The mechanism of beta 2 integrin activation during adhesion to IC has been studied in human PMN, but not in equine PMN. We show here that adhesion of equine PMN to immobilized IC requires beta 2 integrins. Like adhesion, IC-induced respiratory burst activity is dependent on beta 2 integrins. Furthermore, the signaling pathway triggering beta 2 integrin-dependent adhesion of equine PMN to IC and subsequent generation of respiratory burst activity is inhibited by the specific phosphatidylinositol 3-kinase (PI3K) antagonists wortmannin and LY294002 with IC(50) (concentration at which 50% inhibition is achieved) similar to the published values for inhibition of PI3K enzymatic activity. In contrast, PMA-induced activation of beta 2 integrin-dependent adhesion and respiratory burst activity are wortmannin and LY294002 insensitive. These data demonstrate that like in human PMN, IC-induced activation of beta 2 integrins and beta 2 integrin-dependent functions in equine PMN is dependent on PI3K activity.}, number={1-2}, journal={VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY}, author={Jones, SL and Sharief, Y and Chilcoat, CD}, year={2001}, month={Sep}, pages={87–100} }
 @article{jones_blikslager_2001, title={The future of antiinflammatory therapy}, volume={17}, ISSN={["0749-0739"]}, DOI={10.1016/S0749-0739(17)30060-3}, abstractNote={The cells and mediators that make up the inflammatory response have the potential to injure tissues and contribute to the pathophysiology of many inflammatory diseases. Strategies to reduce neutrophil migration into sites of inflammation and subsequent activation by inhibiting integrin-mediated adhesion hold promise for successful treatment of a variety of inflammatory diseases. New pharmacologic agents that specifically target prostanoid mediators of inflammation by specifically inhibiting the activity of cyclooxygenase 2 are potent antiinflammatory agents with fewer gastrointestinal side effects than nonspecific cyclooxygenase inhibitors. These areas of antiinflammatory research are rapidly yielding drugs with diverse future applications in equine medicine.}, number={2}, journal={VETERINARY CLINICS OF NORTH AMERICA-EQUINE PRACTICE}, author={Jones, SL and Blikslager, A}, year={2001}, month={Aug}, pages={245-+} }
 @article{jones_blikslager_2001, title={The future of antiinflammatory therapy.}, volume={17}, url={http://europepmc.org/abstract/med/15658174}, number={2}, journal={Equine practice}, author={Jones, SL and Blikslager, A}, year={2001}, month={Aug}, pages={245–62,} }
 @article{byrne_cohen_jones_zimmel_valberg_2000, title={Rhabdomyolysis in two foals with polysaccharide storage myopathy}, volume={22}, number={5}, journal={Compendium on Continuing Education for the Practicing Veterinarian}, author={Byrne, E. and Cohen, N. and Jones, S. L. and Zimmel, D. N. and Valberg, S.}, year={2000}, pages={503} }
 @article{gayle_blikslager_jones_2000, title={Role of neutrophils in intestinal mucosal injury}, volume={217}, ISSN={["0003-1488"]}, url={http://europepmc.org/abstract/med/10953711}, DOI={10.2460/javma.2000.217.498}, number={4}, journal={JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Gayle, JM and Blikslager, AT and Jones, SL}, year={2000}, month={Aug}, pages={498–500} }
 @article{little_redding_spaulding_dupree_jones_2000, title={Unusual presentation of nutritional secondary hyperparathyroidism in a Paint colt}, volume={2}, DOI={10.1111/j.2042-3292.2000.tb00064.x}, abstractNote={Equine Veterinary EducationVolume 12, Issue 6 p. 297-302 Unusual presentation of nutritional secondary hyperparathyroidism in a Paint colt D. Little, Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorW. R. Redding, Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorK. A. Spaulding, Anatomy, Physiology and Radiology, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorS. H. Dupree, Veterinary Teaching Hospital, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorS. L. Jones, Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this author D. Little, Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorW. R. Redding, Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorK. A. Spaulding, Anatomy, Physiology and Radiology, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorS. H. Dupree, Veterinary Teaching Hospital, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorS. L. Jones, Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this author First published: 05 January 2010 https://doi.org/10.1111/j.2042-3292.2000.tb00064.xCitations: 3AboutPDF ToolsExport 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 onEmailFacebookTwitterLinked InRedditWechat Citing Literature Volume12, Issue6December 2000Pages 297-302 RelatedInformation}, number={6}, journal={Equine Veterinary Education}, author={Little, D. and Redding, W.R. and Spaulding, K.A. and Dupree, S.H. and Jones, S.L.}, year={2000}, pages={388–394} }
 @article{zimmel_blikslager_jones_mcfarlane_young_2000, title={Vaccine-associated anaphylactic-like reaction in a horse}, volume={22}, number={1}, journal={Compendium on Continuing Education for the Practicing Veterinarian}, author={Zimmel, D. N. and Blikslager, A. T. and Jones, S. L. and McFarlane, D. and Young, K.}, year={2000}, month={Jan}, pages={81–84} }
 @article{betsuyaku_liu_senior_haug_brown_jones_matsushima_link_1999, title={A functional granulocyte colony-stimulating factor receptor is required for normal chemoattractant-induced neutrophil activation}, volume={103}, ISSN={["1558-8238"]}, url={http://europepmc.org/abstract/med/10079103}, DOI={10.1172/JCI5191}, abstractNote={Granulocyte colony-stimulating factor (G-CSF) is a hematopoietic growth factor that is widely used to treat neutropenia. In addition to stimulating polymorphonuclear neutrophil (PMN) production, G-CSF may have significant effects on PMN function. Because G-CSF receptor (G-CSFR)–deficient mice do not have the expected neutrophilia after administration of human interleukin-8 (IL-8), we examined the effect of the loss of G-CSFR on IL-8–stimulated PMN function. Compared with wild-type PMNs, PMNs isolated from G-CSFR–deficient mice demonstrated markedly decreased chemotaxis to IL-8. PMN emigration into the skin of G-CSFR–deficient mice in response to IL-8 was also impaired. Significant chemotaxis defects were also seen in response to N-formyl-methionyl-leucyl-phenylalanine, zymosan-activated serum, or macrophage inflammatory protein-2. The defective chemotactic response to IL-8 does not appear to be due to impaired chemoattractant receptor function, as the number of IL-8 receptors and chemoattractant-induced calcium influx, actin polymerization, and release of gelatinase B were comparable to those of wild-type PMNs. Chemoattractant-induced adhesion of G-CSFR–deficient PMNs was significantly impaired, suggesting a defect in β2-integrin activation. Collectively, these data demonstrate that selective defects in PMN activation are present in G-CSFR–deficient mice and indicate that G-CSF plays an important role in regulating PMN chemokine responsiveness.}, number={6}, journal={JOURNAL OF CLINICAL INVESTIGATION}, author={Betsuyaku, T and Liu, F and Senior, RM and Haug, JS and Brown, EJ and Jones, SL and Matsushima, K and Link, DC}, year={1999}, month={Mar}, pages={825–832} }
 @inbook{jones_lindberg_brown_1999, title={Phagocytosis}, booktitle={Fundamental Immunology}, publisher={New York: Raven Press}, author={Jones, S. L. and Lindberg, F. L. and Brown, E. J.}, year={1999}, pages={997–1020} }
 @article{jones_wang_turck_brown_1998, title={A role for the actin-bundling protein L-plastin in the regulation of leukocyte integrin function}, volume={95}, ISSN={["0027-8424"]}, url={http://europepmc.org/abstract/med/9689080}, DOI={10.1073/pnas.95.16.9331}, abstractNote={Regulation of leukocyte integrin avidity is a crucial aspect of inflammation and immunity. The actin cytoskeleton has an important role in the regulation of integrin function, but the cytoskeletal proteins involved are largely unknown. Because inflammatory stimuli that activate integrin-mediated adhesion in human polymorphonuclear neutrophils (PMN) and monocytes cause phosphorylation of the actin-bundling protein l -plastin, we tested whether l -plastin phosphorylation was involved in integrin activation. l -plastin-derived peptides that included the phosphorylation site (Ser-5) rapidly induced leukocyte integrin-mediated adhesion when introduced into the cytosol of freshly isolated primary human PMN and monocytes. Substitution of Ala for Ser-5 abolished the ability of the peptide to induce adhesion. Peptide-induced adhesion was sensitive to pharmacologic inhibition of phosphoinositol 3-kinase and protein kinase C, but adhesion induced by a peptide containing a phosphoserine at position 5 was insensitive to inhibition. These data establish a novel role for l -plastin in the regulation of leukocyte adhesion and suggest that many signaling events implicated in integrin regulation act via induction of l -plastin phosphorylation.}, number={16}, journal={PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA}, author={Jones, SL and Wang, J and Turck, CW and Brown, EJ}, year={1998}, month={Aug}, pages={9331–9336} }
 @inbook{jones_spear_snyder_1998, title={Disorders of the large intestine}, booktitle={Equine internal medicine}, publisher={Philadelphia, PA: W.B. Saunders}, author={Jones, S. L. and Spear, S. and Snyder, J. R.}, editor={W. Bailey, S. ReedEditor}, year={1998}, pages={636–694} }
 @article{perkins_valberg_madigan_carlson_jones_1998, title={Electrolyte disturbances in foals with severe rhabdomyolysis}, volume={12}, ISSN={["0891-6640"]}, DOI={10.1111/j.1939-1676.1998.tb02114.x}, abstractNote={Marked electrolyte abnormalities characterized by profound hyperkalemia, hyponatremia, hypocalcemia, and hyperphosphatemia were noted in 4 neonatal foals with acute rhabdomyolysis and pigmenturia. In 2 foals, rhabdomyolysis developed 4–6 days after admission for dysmaturity, and in 2 foals, rhabdomyolysis was evident on presentation. Rhabdomyolysis was a consequence of selenium deficiency with or without vitamin E deficiency, possibly combined with increased oxidant stress due to sepsis or hypoxia and reperfusion injury after parturition. Foals gained from 7 to 15% of their initial body weight within 48 hours of developing rhabdomyolysis. Three of the foals developed cardiac arrhythmias characterized by spiked T waves and decreased‐amplitude P waves. Postmortem examination of 2 foals revealed extensive myodegeneration and renal tubular nephrosis; renal cortical necrosis with myocardial necrosis was noted in 1 foal. Destruction of the major intracellular compartment (intracellular fluid [ICF]) through extensive myonecrosis combined, in some cases, with myoglobinuric renal insufficiency produced major fluid shifts and life‐threatening electrolyte derangements. With the major ICF compartment disrupted, hyperkalemia was most effectively treated using mineralocorticoids, loop diuretics, and ion exchange resins to enhance elimination. In addition, IV calcium, glucose, insulin, and sodium bicarbonate were administered, which helped redistribute potassium to the ICE Severe rhabdomyolysis should be included in the differential diagnoses of hyperkalemia, hyponatremia, hypocalcemia, and hyperphosphatemia in neonatal foals.}, number={3}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Perkins, G and Valberg, SJ and Madigan, JM and Carlson, GP and Jones, SL}, year={1998}, pages={173–177} }
 @article{perkins_valberg_madigan_carlson_jones_1998, title={Electrolyte disturbances in foals with severe rhabdomyolysis.}, volume={12}, url={http://europepmc.org/abstract/med/9595379}, number={3}, journal={Journal of veterinary internal medicine}, author={Perkins, G and Valberg, SJ and Madigan, JM and Carlson, GP and Jones, SL}, year={1998}, pages={173–177,} }
 @inbook{jones_snyder_spier_1998, place={Philadelphia, Pa}, title={Examination for disorders of the large intestine}, ISBN={9780721635248}, booktitle={Equine Internal Medicine}, publisher={WB Saunders}, author={Jones, S.L. and Snyder, J.R. and Spier, S.}, editor={Bayly, W. and Reed, S.Editors}, year={1998}, pages={655–660} }
 @inbook{jones_spier_1998, place={Philadelphia, Pa}, title={Inflammatory diseases of the large intestine causing diarrhea}, ISBN={9780721635248}, booktitle={Equine Internal Medicine}, publisher={WB Saunders}, author={Jones, S.L. and Spier, S.}, editor={Bayly, W. and Reed, S.Editors}, year={1998}, pages={663–682} }
 @inbook{jones_snyder_spier_1998, place={Philadelphia, Pa}, title={Obstructive conditions of the large intestine}, ISBN={9780721635248}, booktitle={Equine Internal Medicine}, publisher={WB Saunders}, author={Jones, S.L. and Snyder, J.R. and Spier, S.}, editor={Bayly, W. and Reed, S.Editors}, year={1998}, pages={682–694} }
 @inbook{jones_spier_1998, place={Philadelphia, Pa}, title={Pathophysiology of colonic inflammation and diarrhea}, ISBN={9780721635248}, publisher={WB Saunders}, author={Jones, S.L. and Spier, S.}, editor={Bayly, W. and Reed, S.Editors}, year={1998}, pages={660–663} }
 @inbook{jones_snyder_spier_1998, place={Philadelphia, Pa}, title={Pathophysiology of intestinal injury}, ISBN={9780721635248}, booktitle={Equine Internal Medicine}, publisher={WB Saunders}, author={Jones, S.L. and Snyder, J.R. and Spier, S.}, editor={Bayly, W. and Reed, S.Editors}, year={1998}, pages={636–639} }
 @article{jones_wilson_milhalyi_1998, title={Pharmacokinetics of gentamicin in healthy adult horses during intravenous fluid administration}, volume={21}, ISSN={["0140-7783"]}, url={http://europepmc.org/abstract/med/9673967}, DOI={10.1046/j.1365-2885.1998.00123.x}, abstractNote={Journal of Veterinary Pharmacology and TherapeuticsVolume 21, Issue 3 p. 247-249 Pharmacokinetics of gentamicin in healthy adult horses during intravenous fluid administration S.L. Jones, S.L. Jones Present address: Division of Infectious Diseases, Washington University School of Medicine, Box 8051, 660 S. Euclid Ave, St Louis, MO 66110,Search for more papers by this authorW.D. Wilson, W.D. Wilson CorrespondenceSearch for more papers by this authorJ.E. Milhalyi, J.E. Milhalyi Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California, Davis, CA 95616,Search for more papers by this author S.L. Jones, S.L. Jones Present address: Division of Infectious Diseases, Washington University School of Medicine, Box 8051, 660 S. Euclid Ave, St Louis, MO 66110,Search for more papers by this authorW.D. Wilson, W.D. Wilson CorrespondenceSearch for more papers by this authorJ.E. Milhalyi, J.E. Milhalyi Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California, Davis, CA 95616,Search for more papers by this author First published: 05 January 2002 https://doi.org/10.1046/j.1365-2885.1998.00123.xCitations: 10Read the full textAboutPDF 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 onFacebookTwitterLinked InRedditWechat Citing Literature Volume21, Issue3June 1998Pages 247-249 RelatedInformation}, number={3}, journal={JOURNAL OF VETERINARY PHARMACOLOGY AND THERAPEUTICS}, author={Jones, SL and Wilson, WD and Milhalyi, JE}, year={1998}, month={Jun}, pages={247–249} }
 @inbook{jones_snyder_spier_1998, place={Philadelphia, Pa}, title={Physiology of the large intestine}, ISBN={9780721635248}, booktitle={Equine internal medicine}, publisher={WB Saunders}, author={Jones, S.L. and Snyder, J.R. and Spier, S.}, editor={Bayly, W. and Reed, S.Editors}, year={1998}, pages={651–655} }
 @article{jones_knaus_bokoch_brown_1998, title={Two signaling mechanisms for activation of alpha(M)beta(2) avidity in polymorphonuclear neutrophils}, volume={273}, ISSN={["0021-9258"]}, url={http://europepmc.org/abstract/med/9553116}, DOI={10.1074/jbc.273.17.10556}, abstractNote={Circulating polymorphonuclear neutrophils (PMN) are quiescent, nonadherent cells that rapidly activate at sites of inflammation, where they develop the capacity to perform a repertoire of functions that are essential for host defense. Induction of integrin-mediated adhesion, which requires an increase in integrin avidity, is critical for the development of these effector functions. Although a variety of stimuli can activate integrins in PMN, the signaling cascades involved are unclear. Phosphatidylinositol (PI) 3-kinase has been implicated in integrin activation in a variety of cells, including PMN. In this work, we have examined activation of the PMN integrin α<sub>M</sub>β<sub>2</sub>, assessing both adhesion and generation of the epitope recognized by the activation-specific antibody CBRM1/5. We have found that PI 3-kinase has a role in activation of α<sub>M</sub>β<sub>2</sub> by immune complexes, but we have found no role for it in α<sub>M</sub>β<sub>2</sub> activation by ligands for trimeric G protein-coupled receptors, including formylmethionylleucylphenylalanine (fMLP), interleukin-8, and C5a. Cytochalasin D inhibition suggests a role for the actin cytoskeleton in immune complex activation of α<sub>M</sub>β<sub>2</sub>, but cytochalasin has no effect on fMLP-induced activation. Similarly, immune complex activation of the Rac/Cdc42-dependent serine/threonine kinase Pak1 is blocked by PI 3-kinase inhibitors, but fMLP-induced activation is not. These results demonstrate that two signaling pathways exist in PMN for activation of α<sub>M</sub>β<sub>2</sub>. One, induced by FcγR ligation, is PI 3-kinase-dependent and requires the actin cytoskeleton. The second, initiated by G protein-linked receptors, is PI 3-kinase-independent and cytochalasin-insensitive. Pak1 may be in a final common pathway leading to activation of α<sub>M</sub>β<sub>2</sub>.}, number={17}, journal={JOURNAL OF BIOLOGICAL CHEMISTRY}, author={Jones, SL and Knaus, UG and Bokoch, GM and Brown, EJ}, year={1998}, month={Apr}, pages={10556–10566} }
 @article{jones_brown_1996, title={FcγRII-mediated Adhesion and Phagocytosis Induce L-Plastin Phosphorylation in Human Neutrophils}, volume={271}, ISSN={0021-9258 1083-351X}, url={http://dx.doi.org/10.1074/jbc.271.24.14623}, DOI={10.1074/jbc.271.24.14623}, abstractNote={L-Plastin is a calcium-regulated actin bundling protein expressed in leukocytes and some transformed cells, which is phosphorylated on serine in response to several different leukocyte-activating stimuli. Adhesion to immune complexes induced L-plastin phosphorylation in neutrophils, as did phagocytosis of IgG-opsonized particles, but insoluble immune complexes in suspension were very inefficient activators of L-plastin phosphorylation. Neutrophils express two IgG Fc receptors, the transmembrane FcγRII and the glycan phosphoinositol-linked FcγRIIIB. Use of monoclonal antibodies that distinguished the two Fc receptors demonstrated that FcγRII ligation was 100-fold more potent at signaling L-plastin phosphorylation than occupancy of FcγRIIIB. Depletion of intracellular calcium did not affect FcγRII-activated L-plastin phosphorylation, demonstrating that any potential regulation of plastin function by calcium did not affect its phosphorylation. Adhesion to immune complexes caused L-plastin to localize to podosomes, since it colocalized with actin to discrete, punctate Triton X-100-insoluble sites on the adherent neutrophil surface in a pattern indistinguishable from vinculin and α-actinin. Nonetheless, localization to podosomes was not required for L-plastin phosphorylation, since both neutrophils from a patient with leukocyte adhesion deficiency (CD18 deficiency) and neutrophils treated with anti-CD18 F(ab′)2, which do not form podosomes upon adhesion to immune complexes, phosphorylated L-plastin normally. Indeed, L-plastin was normally phosphorylated in response to adhesion to immune complexes even when the actin cytoskeleton was disrupted with cytochalasin D. We conclude that efficient FcγRII-mediated phosphorylation of L-plastin requires cell adhesion but does not require IgG-induced rearrangements of the actin cytoskeleton. These data suggest a model in which plastin phosphorylation and localization to the actin cytoskeleton can act as two distinct mechanisms regulating L-plastin functions in neutrophils adherent to immune complexes. L-Plastin is a calcium-regulated actin bundling protein expressed in leukocytes and some transformed cells, which is phosphorylated on serine in response to several different leukocyte-activating stimuli. Adhesion to immune complexes induced L-plastin phosphorylation in neutrophils, as did phagocytosis of IgG-opsonized particles, but insoluble immune complexes in suspension were very inefficient activators of L-plastin phosphorylation. Neutrophils express two IgG Fc receptors, the transmembrane FcγRII and the glycan phosphoinositol-linked FcγRIIIB. Use of monoclonal antibodies that distinguished the two Fc receptors demonstrated that FcγRII ligation was 100-fold more potent at signaling L-plastin phosphorylation than occupancy of FcγRIIIB. Depletion of intracellular calcium did not affect FcγRII-activated L-plastin phosphorylation, demonstrating that any potential regulation of plastin function by calcium did not affect its phosphorylation. Adhesion to immune complexes caused L-plastin to localize to podosomes, since it colocalized with actin to discrete, punctate Triton X-100-insoluble sites on the adherent neutrophil surface in a pattern indistinguishable from vinculin and α-actinin. Nonetheless, localization to podosomes was not required for L-plastin phosphorylation, since both neutrophils from a patient with leukocyte adhesion deficiency (CD18 deficiency) and neutrophils treated with anti-CD18 F(ab′)2, which do not form podosomes upon adhesion to immune complexes, phosphorylated L-plastin normally. Indeed, L-plastin was normally phosphorylated in response to adhesion to immune complexes even when the actin cytoskeleton was disrupted with cytochalasin D. We conclude that efficient FcγRII-mediated phosphorylation of L-plastin requires cell adhesion but does not require IgG-induced rearrangements of the actin cytoskeleton. These data suggest a model in which plastin phosphorylation and localization to the actin cytoskeleton can act as two distinct mechanisms regulating L-plastin functions in neutrophils adherent to immune complexes.}, number={24}, journal={Journal of Biological Chemistry}, publisher={American Society for Biochemistry & Molecular Biology (ASBMB)}, author={Jones, Samuel L. and Brown, Eric J.}, year={1996}, month={Jun}, pages={14623–14630} }
 @inbook{jones_brown_1996, place={Georgetown, Texas}, series={Molecular biology intelligence unit}, title={Functional cooperation between Fc receptors and complement receptors in phagocytes}, ISBN={9781570593291 9780412100710}, booktitle={Human IgG Fc Receptors}, publisher={RG Landes Co}, author={Jones, S.L. and Brown, E.J.}, editor={van de Winkel, J.G.J. and Capel, P.J.A.Editors}, year={1996}, pages={149–163}, collection={Molecular biology intelligence unit} }
 @article{jones_fecteau_1995, title={Hydrops uteri in a caprine doe pregnant with goat-sheep hybrid fetuses.}, volume={206}, url={http://europepmc.org/abstract/med/7790309}, number={12}, journal={Journal of the American Veterinary Medical Association}, author={Jones, SL and Fecteau, G}, year={1995}, month={Jun}, pages={1920–1922,} }
 @article{jones_fecteau_1995, title={Hydrops uteri in a goat pregnant with goat-sheep hybrid fetuses}, volume={206}, number={12}, journal={Journal of the American Veterinary Medical Association}, author={Jones, S.L. and Fecteau, G.}, year={1995}, pages={1920–1922} }
 @article{rosales_jones_mccourt_brown_1994, title={Bromophenacyl bromide binding to the actin-bundling protein l-plastin inhibits inositol trisphosphate-independent increase in Ca2+ in human neutrophils.}, volume={91}, ISSN={0027-8424 1091-6490}, url={http://dx.doi.org/10.1073/pnas.91.9.3534}, DOI={10.1073/pnas.91.9.3534}, abstractNote={Ligation of IgG Fc receptors on polymorphonuclear leukocytes causes an increase in the concentration of free intracytoplasmic Ca2+ ([Ca2+]i) which arises from release of intracellular stores but is independent of inositol 1,4,5-trisphosphate. We found that bromophenacyl bromide (BPB), an alkylating agent which inhibits leukocyte degranulation, adherence, and phagocytosis, inhibited IgG-stimulated increases in [Ca2+]i with an IC50 of 0.2 microM. In contrast, BPB had no effect on inositol 1,4,5-trisphosphate-dependent [Ca2+]i increases induced by fMet-Leu-Phe, complement fragment C5a, ATP, or platelet-activating factor. Using a monoclonal antibody specific for BPB, we identified in polymorphonuclear leukocytes a single cytosolic protein of 66 kDa and isoelectric point pH 5.6 which bound BPB when intact cells were treated with the alkylating agent. This BPB-binding protein was identified as l-plastin, a Ca(2+)-regulated actin-bundling protein. l-Plastin was found associated with the Triton X-100-insoluble cytoskeleton in polymorphonuclear leukocytes adherent to immune complexes, suggesting that BPB affects Fc receptor-mediated signal transduction by altering the actin cytoskeleton. Consistent with this hypothesis, both cytochalasin B and cytochalasin D inhibited the IgG-dependent increase in [Ca2+]i, without any effect on fMet-Leu-Phe-induced Ca2+ release. These data suggest that the actin cytoskeleton is essential for signal transduction from plasma membrane Fc receptors and that l-plastin has a critical role in activation of this pathway.}, number={9}, journal={Proceedings of the National Academy of Sciences}, publisher={Proceedings of the National Academy of Sciences}, author={Rosales, C. and Jones, S. L. and McCourt, D. and Brown, E. J.}, year={1994}, month={Apr}, pages={3534–3538} }
 @article{jones_langer_sterner-kock_snyder_carlson_1994, title={Renal dysplasia and benign ureteropelvic polyps associated with hydronephrosis in a foal}, volume={204}, number={8}, journal={Journal of the American Veterinary Medical Association}, author={Jones, S.L. and Langer, D.L. and Sterner-Kock, A. and Snyder, J.R. and Carlson, G.P.}, year={1994}, pages={1230–1234} }
 @article{jones_langer_sterner-kock_snyder_g.p._1994, title={Renal dysplasia and benign ureteropelvic polyps associated with hydronephrosis in a foal.}, volume={204}, url={http://europepmc.org/abstract/med/8014095}, number={8}, journal={Journal of the American Veterinary Medical Association}, author={Jones, S.L. and Langer, D.L. and Sterner-Kock, A. and Snyder, Carlson, JR and G.P.}, year={1994}, month={Apr}, pages={1230–1234,} }
 @article{jones_wilson_1993, title={Clostridium septicum septicemia in a neonatal foal with hemorrhagic enteritis}, volume={83}, url={http://europepmc.org/abstract/med/8467700}, number={2}, journal={The Cornell Veterinarian}, author={Jones, S.L. and Wilson, W.D.}, year={1993}, month={Apr}, pages={143–151} }
 @article{mattoon_andrews_jones_linford_1991, title={Subepiglottic cyst causing upper airway obstruction in a neonatal calf}, volume={199}, number={6}, journal={Journal of the American Veterinary Medical Association}, author={Mattoon, J.S. and Andrews, D. and Jones, S.L. and Linford, R.L.}, year={1991}, pages={747–749} }
 @article{jones_brumbaugh_1991, title={What is your diagnosis: Mandibular ameloblastoma in a horse}, volume={199}, journal={Journal of the American Veterinary Medical Association}, author={Jones, S.L. and Brumbaugh, G.W.}, year={1991}, pages={630–631} }
 @article{jones_schumacher_1990, title={What is your diagnosis: Retropharyngeal caseous lymphadenitis in a goat}, volume={197}, journal={Journal of the American Veterinary Medical Association}, author={Jones, S.L. and Schumacher, J.}, year={1990}, pages={395–396} }
 @inbook{blikslager_jones, title={Disorders of the esophagus}, booktitle={Large animal internal medicine  (3rd Ed.)}, publisher={St. Louis: Mosby}, author={Blikslager, A. T. and Jones, S. L.}, pages={607–617} }
 @inbook{jones_blikslager, title={Esophageal diseases}, ISBN={0721697771}, booktitle={Equine internal medicine}, publisher={Philadelphia: W. B. Saunders}, author={Jones, S. L. and Blikslager, A. T.}, editor={S. M. Reed, W. M. Bayly and Sellon, D. C.Editors}, pages={855–863} }
 @inbook{blikslager_jones, title={Ischemic disorders of the intestinal tract}, ISBN={0721697771}, booktitle={Equine internal medicine}, publisher={Philadelphia: W. B. Saunders}, author={Blikslager, A. T. and Jones, S. L.}, editor={S. M. Reed, W. M. Bayly and Sellon, D. C.Editors}, pages={913–922} }
 @inbook{blikslager_jones, title={Obstructive disorders of the intestinal tract}, ISBN={0721697771}, booktitle={Equine internal medicine}, publisher={Philadelphia: W. B. Saunders}, author={Blikslager, A. T. and Jones, S. L.}, editor={S. M. Reed, W. M. Bayly and Sellon, D. C.Editors}, pages={922–936} }
 @inbook{blikslager_jones_grondhal_merritt_malbert, title={Pathophysiology of the gastronintestinal tract}, ISBN={0813828260}, booktitle={Veterinary pathophysiology}, publisher={Ames, IA: Blackwell Pub.}, author={Blikslager, A. T. and Jones, S. L. and Grondhal, M. L. and Merritt, A. M. and Malbert, C. H.}, editor={R. H. Dunlop and Malbert, C. H.Editors}, pages={111–142} }