bluuebunny/crossref_metadata_2025_split huggingface dataset:
A Neurologic Syndrome in Golden Retrievers Presenting as a Sensory Ataxic Neuropathy
Authors: Jäderlund K. Hultin , Örvind E. , Johnsson E. , Matiasek K. , Hahn C.N. , Malm S. , Hedhammar Å. 
Published: March 2010

Background: A sensory ataxic neuropathy has been observed in Swedish Golden Retrievers recently.Animals: Twenty‐one affected Golden Retrievers.Methods: Clinical and neurologic status, electrophysiologic, and pathologic status as well as pedigree analyses were evaluated.Results: Clinical signs had an insidious onset between 2 and 8 months of age and a slowly progressive course. Affected dogs were ataxic and dysmetric. They had abnormal postural reactions and decreased spinal reflexes but no apparent muscle atrophy. Clinical pathology, radiography, and electrophysiology of motor systems were all within reference values. Sensory nerve conduction results of affected dogs were significantly different from those of a group of control dogs. Necropsy revealed a chronic progressive central and peripheral sensorimotor axonopathy; the proprioceptive pathways were most severely affected.Conclusions and Clinical Importance: This disease in these Golden Retrievers is distinct from other canine breed‐related neurodegenerative diseases or hereditary neurodegenerative diseases described in humans. Pedigree analyses indicated a hereditary background, but the mode of inheritance could not be established.
Procarbazine as Adjunctive Therapy for Treatment of Dogs with Presumptive Antemortem Diagnosis of Granulomatous Meningoencephalomyelitis: 21 Cases (1998–2004)
Authors: Coates Joan R. , Barone Georgina , Dewey Curtis W. , Vitale Christina L. , Holloway‐Azene Nicole M. , Sessions John K. 
Published: March 2010

Background: Granulomatous meningoencephalomyelitis (GME) is an idiopathic inflammatory disease of the central nervous system. Remission often is short‐lived in dogs treated with glucocorticoids. Procarbazine is T cell‐specific and crosses the blood‐brain barrier.Hypothesis: Dogs with presumptive antemortem diagnosis of GME given procarbazine as adjunctive therapy to prednisone will have improved long‐term outcome compared with dogs given no treatment or glucocorticoids alone.Animals: Two groups were studied: (1) Dogs with presumptive antemortem diagnosis of GME treated with procarbazine and prednisone (n = 21); (2) Dogs that had a histologic diagnosis of GME at postmortem examination and received no treatment (n = 11).Methods: Dogs with presumptive GME treated with procarbazine were identified retrospectively from medical records of 2 veterinary referral hospitals. Selection criteria required all dogs have a neurologic examination, blood work, cerebrospinal fluid analysis, and brain imaging (MRI or CT).Results: Median survival time for all dogs studied was 5.0 months. Median survival time for dogs treated with procarbazine was 14.0 months and for untreated dogs, 0.73 months. Treatment with procarbazine was significantly correlated with survival time (P< .001). Procarbazine was the only independent predictor of survival. Prednisone was reduced in dosage or discontinued in 17 dogs. Adverse reactions to procarbazine therapy included myelosuppression in 7 dogs and hemorrhagic gastroenteritis in 3 dogs.Conclusion: These data suggest that procarbazine treatment of presumptive GME may result in greater improved long‐term outcome than has been previously reported for glucocorticoid treatment alone and may complement other immunomodulatory therapies. Procarbazine‐treated dogs must be monitored for adverse reactions.
Combination Chemotherapy with L‐Asparaginase, Lomustine, and Prednisone for Relapsed or Refractory Canine Lymphoma
Authors: Saba Corey F. , Thamm Douglas H. , Vail David M. 
Published: March 2010

Background: Canine lymphoma (LSA) is responsive to initial treatment, however, it then becomes resistant to drugs in the initial protocol. New rescue protocols are needed.Hypothesis: A combination of L‐asparaginase, lomustine, and prednisone will be well tolerated and efficacious as a rescue therapy for dogs with LSA.Animals: Thirty‐one client owned dogs with cytologically confirmed multicentric LSA who were refractory or whose disease had relapsed after a CHOP (cyclophosphamide/doxorubicin/vincristine/prednisone)‐based chemotherapy protocol.Methods: Prospective clinical trial. Lomustine (target dose, 70 mg/m2) was administered orally at 3‐week intervals for a total of 5 doses or until disease progression. L‐asparaginase (400 U/kg) was administered subcutaneously concurrently with the first 2 lomustine treatments. Prednisone was administered at a tapering dose for the duration of the protocol.Results: Overall response rate for dogs treated with this protocol was 87% (27/31), with 52% (16/31) of dogs achieving a complete response. Median time to response was 21 days. Median time to progression was 63 days (111 days for dogs achieving a complete response and 42 days for dogs achieving a partial response). There were no significant differences in response rates and times to progression between dogs who had received L‐asparaginase before beginning this rescue protocol and those who had not. Toxicoses were mild and self‐limiting in 29 of 31 cases.Conclusions and Clinical Importance: This is a well‐tolerated rescue therapy for relapsing LSA in dogs. Response rates and remission durations compare favorably to other rescue protocols. Therefore, this protocol is a viable rescue option.
Expression of Receptor Activator of Nuclear Factor k‐B Ligand (RANKL) in Neoplasms of Dogs and Cats
Authors: Barger Anne M. , Fan Timothy M. , de Lorimier Louis‐Philippe , Sprandel Ian T. , O'Dell‐Anderson Kristen 
Published: March 2010

Background: Receptor activator of nuclear factor K‐B (RANK), RANK‐ligand (RANKL), and the soluble decoy receptor osteoprotegerin (OPG) form a key axis modulating osteoclastogenesis. In health, RANKL‐expressing bone stromal cells and osteoblasts activate osteoclasts through RANK ligation, resulting in homeostatic bone resorption. Skeletal tumors of dogs and cats, whether primary or metastatic, may express RANKL and directly induce malignant osteolysis. Hypothesis: Bone malignancies of dogs and cats may express RANKL, thereby contributing to pathologic bone resorption and pain. Furthermore, relative RANKL expression in bone tumors may correlate with radiographic characteristics of bone pathology. Animals: Forty‐two dogs and 6 cats with spontaneously‐occurring tumors involving bones or soft tissues were evaluated. Methods: A polyclonal anti‐human RANKL antibody was validated for use in canine and feline cells by flow cytometry and immunocytochemistry. Fifty cytologic specimens were collected from bone and soft tissue tumors of 48 tumor‐bearing animals and assessed for RANKL expression. In 15 canine osteosarcoma (OSA) samples, relative RANKL expression was correlated with radiographic characteristics of bone pathology. Results: Expression of RANKL by neoplastic cells was identified in 32/44 canine and 5/6 feline tumor samples. In 15 dogs with OSA, relative RANKL expression did not correlate with either radiographic osteolysis or bone mineral density as assessed by dual energy x‐ray absorptiometry. Conclusions and Clinical Importance: In dogs and cats, tumors classically involving bone and causing pain, often may express RANKL. Confirming RANKL expression in tumors is a necessary step toward the rational institution of novel therapies targeting malignant osteolysis via RANKL antagonism.
Tissue Doppler Imaging in Maine Coon Cats with a Mutation of Myosin Binding Protein C with or without Hypertrophy
Authors: MacDonald Kristin A. , Kittleson Mark D. , Kass Philip H. , Meurs Kathryn M. 
Published: March 2010

Background: The cardiac myosin binding protein C gene is mutated in Maine Coon (MC) cats with familial hypertrophic cardiomyopathy.Hypotheses: Early diastolic mitral annular velocity is incrementally reduced from normal cats to MC cats with only an abnormal genotype to MC cats with abnormal genotype and hypertrophy.Animals:Group 1 consisted of 6 normal domestic shorthair cats, group 2 of 6 MC cats with abnormal genotype but no hypertrophy, and group 3 of 15 MC cats with hypertrophy and abnormal genotype.Methods:The genotype and echocardiographic phenotype of cats were determined, and the cats were divided into the 3 groups. Tissue Doppler imaging (TDI) of the lateral mitral annulus from the left apical 4‐chamber view was performed. Five nonconsecutive measurements of early diastolic mitral annular velocity (EM) or summated early and late diastolic velocity (EAsum) and heart rate were averaged.Results:There was an ordered reduction in Em‐EAsum as group number increased (group 1, range 9.7–14.7 cm/s; group 2, range 7.5–13.2 cm/s; group 3, range 4.5–14.1 cm/s;P= .001). Using the lower prediction limit for normal Em‐EAsum, the proportion of cats with normal Em‐EAsum decreased as the group number increased (P= .001). However, Em‐EAsum was reduced in only 3 of 6 cats in group 2.Conclusion: The incremental reduction of Em‐EAsum as group severity increased indicates that diastolic dysfunction is an early abnormality that occurs before hypertrophy development. TDI measurement of Em or EAsum of the lateral mitral annulus is an insensitive screening test for identification of phenotypically normal, genotypically affected cats.
Synthetic Adrenocorticotropic Hormone Stimulation Tests in Healthy Neonatal Foals
Authors: Hart Kelsey A. , Ferguson Duncan C. , Heusner Gary L. , Barton Michelle Henry 
Published: March 2010

Background:Cosyntropin (adrenocorticotropic hormone [ACTH]) stimulation tests are used to evaluate adrenal function. Low‐dose ACTH stimulation tests are the most accurate method for diagnosing relative adrenal insufficiency in critically ill humans but have not been evaluated in foals.Hypothesis:Peak serum cortisol concentrations in healthy foals will not be significantly different after intravenous administration of 1, 10, 100, and 250 μg of cosyntropin.Animals:14 healthy neonatal foals, 3–4 days of age.Methods:A randomized cross‐over model was used in which cosyntropin (1, 10, 100, or 250 μg) was administered intravenously on days 3 and 4 of life. Blood samples were collected before and 30, 60, 90, 120, and 150 minutes after administration of cosyntropin for determination of serum cortisol concentration.Results:Serum cortisol concentrations did not significantly increase after administration of 1 μg of cosyntropin. Cortisol concentration peaked 30 minutes after administration of 10 μg of cosyntropin and 90 minutes after 100 and 250 μg of cosyntropin. There was no relationship between cosyntropin dose and serum cortisol concentration at 30 minutes. Compared with the 10‐μg dose, 100 and 250 μg of cosyntropin induced significantly greater cortisol concentrations at 90 minutes, at which point the 10‐μg cosyntropin‐dose cortisol values were indistinguishable from baseline. There was no significant difference in the area under the cortisol concentration curve between the 100‐and 250‐μg doses. No effect of day of testing or foal weight on peak cortisol concentration was detected.Conclusions and Clinical Importance: The results of this study suggest that 10‐and 100‐μg doses of cosyntropin would be appropriate for evaluating adrenal function in neonatal foals.
Day‐to‐Day Variation of the Urine Protein: Creatinine Ratio in Female Dogs with Stable Glomerular Proteinuria Caused by X‐Linked Hereditary Nephropathy
Authors: Nabity Mary B. , Boggess May M. , Kashtan Clifford E. , Lees George E. 
Published: March 2010

Background:Interpretation of serial urine protein: creatinine (UPC) values is confounded by a lack of data regarding random biologic variation of UPC values in dogs with stable glomerular proteinuria.Hypothesis:That there is minimal day‐to‐day variability in the UPC of dogs with unchanging proteinuria and the number of measurements needed to reliably estimate UPC varies with the magnitude of proteinuria.Animals:Forty‐eight heterozygous (carrier) female dogs with X‐linked hereditary nephropathy (XLHN) causing stable proteinuria.Methods:Urine samples were obtained daily by cystocentesis for 3 consecutive days on 183 occasions (549 samples). The UPC was measured for each sample with a single dry‐film chemistry auto‐analyzer. Data were analyzed retrospectively by a power of the mean model because the variance of UPC values within the 3‐day evaluation periods increased as the magnitude of proteinuria increased.Results:To demonstrate a significant difference (P< .05) between serial values in these proteinuric dogs, the UPC must change by at least 35% at high UPC values (near 12) and 80% at low UPC values (near 0.5). One measurement is adequate to reliably estimate the UPC when UPC < 4, but 2–5 determinations are necessary at higher UPC values.Conclusions and Clinical Importance: These guidelines for interpretation of serial UPC values in female dogs with XLHN may also be helpful for interpretation of UPC values in dogs with other glomerulopathies.
Doxorubicin and BAY 12–9566 for the Treatment of Osteosarcoma in Dogs: A Randomized, Double‐Blind, Placebo‐Controlled Study
Authors: Moore Antony S. , Dernell William S. , Ogilvie Gregory K. , Kristal Orna , Elmslie Robyn , Kitchell Barbara , Susaneck Steven , Rosenthal Robert , Klein Mary K. , Obradovoich Joyce , Legendre Alfred , Haddad Tara , Hahn Kevin , Powers Barbara E. , Warren Darren 
Published: March 2010

Background: This study was designed to assess the efficacy of a matrix metalloproteinase inhibitor in prolonging posttreatment survival for dogs with appendicular osteosarcoma after treatment with amputation and doxorubicin chemotherapy.Hypothesis: Survival will be prolonged in dogs receiving BAY 12–9566.Animals: The study included 303 dogs with appendicular osteosarcoma.Methods: Dogs were treated with doxorubicin (30 mg/m2) every 2 weeks for 5 treatments starting 2 weeks after amputation. Dogs were randomly allocated to receive a novel nonpeptidic biphenyl inhibitor of matrix metalloproteinases (MMPs, BAY 12–9566; 4‐[4–4‐(chlorophenyl)phenyl]‐4‐oxo‐2S‐(phenylthiomethyl) butanoic acid) or placebo after doxorubicin chemotherapy.Results: Median survival for all 303 dogs was 8 months; and 1‐year, 2‐year, and 3‐year survival rates were 35%, 17%, and 9%, respectively. Treatment with BAY 12–9566 did not influence survival. Multivariate analysis revealed that increasing age (P= .004), increasing weight (P= .006), high serum alkaline phosphatase (ALP) (P= .012) and high bone ALP (P< .001) were independently associated with shorter median survival times. Additional analyses on available data indicated that as the number of mitotic figures in the biopsy increased (P= .013), and as plasma active MMP‐2 concentrations increased (P= .027), the risk of dying increased.Conclusions and Clinical Importance: Doxorubicin is an effective adjuvant to amputation in prolonging survival for dogs with appendicular osteosarcoma.
Acute Effects of Carprofen and Meloxicam on Canine Gastrointestinal Permeability and Mucosal Absorptive Capacity
Authors: Craven Melanie , Chandler Marge L. , Steiner Jörg M. , Farhadi Ashkan , Welsh Elizabeth , Pratschke Kathryn , Shaw Darren J. , Williams David A. 
Published: March 2010

Background: Nonsteroidal anti‐inflammatory drugs (NSAIDs) are frequently prescribed to dogs for their analgesic, antipyretic, and anti‐inflammatory properties. Their beneficial actions can be offset by gastrointestinal (GI) toxicosis. Endoscopy has traditionally been employed to detect GI lesions, but alterations in GI permeability precede the development of mucosal damage.Hypothesis: Carprofen and meloxicam alter GI permeability and mucosal absorptive capacity of dogs.Animals: Twenty adult dogs treated with an NSAID for >.7 days were evaluated by permeability tests while receiving either carprofen (10 dogs) or meloxicam (10 dogs).Methods: Prospective, longitudinal observational study. A 6‐sugar permeability test (sucrose, lactulose, rhamnose, 3‐O‐methyl‐D‐glucose, D‐xylose, and sucralose) was performed on the day before NSAID treatment, and after 3 and 8 days of treatment.Results: There were no significant differences in the urinary recovery ratios of lactulose: rhamnose, D‐xylose:3‐O‐methyl‐D‐glucose, or sucralose recovery within either group at any time during the study. Sucrose permeability in the meloxicam group did not alter significantly over time. However, sucrose permeability in the carprofen group decreased significantly by day 3 (P= .049) and increased again by day 8 (P= .049), to a level that was not significantly different to permeability before treatment (P= .695).Conclusions and Clinical Importance: The absence of increased GI permeability and diminished mucosal absorptive capacity in this group of dogs does not support the development of acute GI toxicosis during treatment with either meloxicam or carprofen.
Hereditary Factor VII Deficiency in the Alaskan Klee Kai Dog
Authors: Kaae Jennifer A. , Callan Mary Beth , Brooks Marjory B. 
Published: March 2010

Background: Hereditary factor VII (FVII) deficiency is characterized as a mild bleeding disorder in Beagles, caused by a missense mutation in exon 5 of the FVII gene. An Alaskan Klee Kai dog with severe bleeding after trauma was diagnosed with FVII deficiency based on coagulation testing. Molecular analyses were undertaken to identify the genetic basis of the defect in this breed.Hypothesis: FVII deficiency in Alaskan Klee Kai dogs is caused by a mutation in the FVII gene.Animals: Eighteen client‐owned Alaskan Klee Kai.Methods: Coagulation screening tests and factor assays were performed to characterize the coagulopathy. All coding regions of the propositus' FVII gene were sequenced. Amplification of exon 5, sequencing, andMnlI restriction digest experiments were performed to screen for a point mutation in the remaining 17 dogs.Results: FVII deficiency was diagnosed in 6 dogs with a median FVII activity (FVII:C) of 5% (reference range, 50–150%). All FVII‐deficient Alaskan Klee Kai were homozygous for the same mutation as FVII‐deficient Beagles (ie, a G to A transition), resulting in substitution of glycine 96 by glutamic acid. An overlap in the FVII: C values obtained from heterozygote and wild‐type dogs precluded accurate detection of carriers without genetic screening.Conclusions and Clinical Importance: FVII deficiency may be associated with a bleeding tendency and should be considered in Alaskan Klee Kai dogs with prolonged prothrombin times. Plasma FVII:C accurately identifies affected dogs, but deoxyribonucleic acid testing is required for identification of carriers.
Survival, Neurologic Response, and Prognostic Factors in Dogs with Pituitary Masses Treated with Radiation Therapy and Untreated Dogs
Authors: Kent Michael S. , Bommarito David , Feldman Edward , Theon Alain P. 
Published: March 2010

Background: Pituitary masses in dogs are not uncommon tumors that can cause endocrine and neurologic signs and, if left untreated, can decrease life expectancy.Hypothesis: Dogs with pituitary masses that received radiation therapy (RT) have more favorable neurologic outcomes and longer survival times compared with untreated dogs.Animals: Nineteen dogs with a pituitary mass identified on CT or MR imaging were irradiated with 48 Gy given in 3 Gy daily‐dose fractions. Twenty‐seven untreated control dogs had pituitary masses.Methods: Medical records of dogs with pituitary masses were retrospectively reviewed for clinical signs, mass size, and outcome.Results: Median survival time was not reached in the treated group. Mean survival time in the treated group was 1,405 days (95% confidence interval [CI], 1,053–1,757 days) with 1‐, 2‐, and 3‐year estimated survival of 93, 87, and 55%, respectively. Median survival in the nonirradiated group was 359 days (95% CI, 48–916 days), with a mean of 551 days (95% CI, 271–829 days). The 1‐, 2‐, and 3‐year estimated survival was 45, 32, and 25%, respectively. Dogs that received RT for their pituitary tumors had significantly longer survival times than untreated dogs (P =.0039). Treated dogs with smaller tumors (based on maximal pituitary‐to‐brain height ratio or area of tumor to area of brain) lived longer than those with larger tumors (P <.001).Conclusions and Clinical Importance: When compared with untreated dogs, RT increased survival and controlled neurologic signs in dogs with pituitary masses.
Effect of Fentanyl on Visceral and Somatic Nociception in Conscious Horses
Authors: Sanchez L. Chris , Robertson Sheilah A. , Maxwell Lara K. , Zientek Keith , Cole Cynthia 
Published: March 2010

Background: Transdermal fentanyl is used clinically in horses based on pharmacokinetic data and antinociceptive effects documented in other species.Hypothesis: Fentanyl IV administration increases both visceral and somatic nociceptive threshold in conscious horses.Animals: Six clinically normal horses, each fitted with a permanent gastric cannula.Methods: Visceral nociception was evaluated with 2 methods of threshold detection—colorectal distention and duodenal distention. Somatic nociception was assessed by measurement of thermal threshold. Fentanyl was administered as an increasing stepwise infusion followed by a continuous‐rate infusion for a total of 2 hours. There were 4 doses of fentanyl and 1 dose each of saline and xylazine administered to each horse. Serum fentanyl concentrations were measured and the resulting data were used to determine pharmacokinetic parameters for each horse. All data were analyzed by means of a 3‐factor analysis of variance followed by either a simple t test or a Bonferroni t test for multiple comparisons.Results: Fentanyl administration did not result in significant changes in duodenal or colorectal distention threshold. Thermal threshold showed an increased trend at the 15‐minute time point for the highest fentanyl group only, with a corresponding mean serum fentanyl concentration of 7.82 ± 2.10 ng/mL. Two horses in this group became agitated and tachycardic during the first 15 minutes of the infusion.Conclusions and Clinical Importance: Fentanyl did not produce a significant antinociceptive effect at the doses used, 2 of which resulted in serum concentrations above the nociceptive threshold in other species.
Assessment of a Point‐of‐Care Lactate Monitor in Emergency Admissions of Adult Horses to a Referral Hospital
Authors: Tennent‐Brown Brett S. , Wilkins Pamela A. , Lindborg Sue , Russell Gail , Boston Raymond C. 
Published: March 2010

Background: Blood lactate concentration [LAC] is considered a useful indicator of disease severity in horses. Agreement of point‐of‐care (POC) lactate monitors with laboratory standards has not been established for clinically abnormal horses.Hypothesis: It was hypothesized that results from a POC lactate monitor would be in agreement with a laboratory‐based measurement of [LAC].Animals: The study included adult horses presented for emergency evaluation.Methods: A prospective observational study was performed. [LAC] was measured with whole blood (AWB) and plasma (APL) by means of a POC monitor (Accutrend) and compared with results from whole blood measured by a laboratory blood gas analyzer (NOVA).Results: Samples from 221 horses were used to compare the 2 lactate measurement techniques. Agreement (p ± SE) was closest between APL and NOVA (0.97 ± 0.01); an average observed difference of 0.15 ± 0.89 (mean ± SD) and 95% limits of agreement (LOA) ‐1.89, 1.59 also were found. Agreement was preserved and 95% LOA further decreased in horses with NOVA [LAC] of <5 mM and PCV <40%. Agreement was modest when testing whole blood samples on the POC monitor with increased 95% LOA.Conclusions and Clinical Importance: Results indicate close agreement between NOVA and the POC monitor when [LAC] was measured with plasma. Results were less consistent at higher [LAC] but sufficiently reliable to follow trends. Although whole blood may be used with the POC monitor to identify clinically important hyperlactatemia, results may be insufficiently reliable to monitor trends.