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- Author or Editor: Barrak M. Pressler x
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Abstract
Objective—To partially characterize the cDNA, amino acid sequence, and tertiary structure of feline myeloperoxidase, describe its cellular location in mature granulocytes, and determine whether hyperthyroid cats have anti-myeloperoxidase antibody.
Sample Population—Bone marrow RNA and whole blood from cats of various sources and feline serum samples submitted for measurement of total thyroxine concentration from September 2006 to July 2007.
Procedures—Feline myeloperoxidase cDNA was amplified from bone marrow RNA; presumptive splice sites were determined by comparison with human sequences. Intracellular localization of myeloperoxidase in granulocytes was determined by use of immunofluorescence and electron microscopy, and molecular weight and partial tertiary structure were determined by use of immunoblotting of granulocyte lysates. Anti-human myeloperoxidase (hMPO) antibody was detected via ELISA.
Results—A 2,493-bp sequence encompassing the 2,160-bp cDNA with presumably the same number and size of exons as hMPO was generated. Translation predicted 85% homology with hMPO. Feline myeloperoxidase was localized to neutrophil primary granules, and immunoblotting revealed heavy and light bands with molecular weights similar to those of hMPO. The prevalence of anti-hMPO antibody did not differ between nonhyperthyroid and hyperthyroid cats or among hyperthyroid cats subclassified by treatment modality.
Conclusions and Clinical Relevance—Moderate homology existed between feline myeloperoxidase and hMPO cDNA and protein. Although findings suggested a similar tertiary structure and function for the 2 proteins, they also suggested that inability to detect a high prevalence of anti-hMPO antibody in hyperthyroid cats may be attributable to antigenic differences between the human and feline proteins rather than a lack of autoantibody.
Abstract
Objective—To determine whether urine protein-to-creatinine (UP:C) ratio assessment provides an estimate of urine protein excretion (UPE) over a 24-hour period in horses and ponies, establish a preliminary UP:C ratio reference range, and determine UP:C ratio variation over time in healthy equids.
Animals—11 female horses and 6 female ponies.
Procedures—Urine was collected from all equids at 4-hour intervals for 24 hours. Total 24-hour UPE (mg of protein/kg of body weight) and UP:C ratio were determined; these variables were also assessed in aliquots of urine collected at 4-hour intervals. On 2 additional days, urine samples were also obtained from 6 horses (1 sample/horse/d) to determine day-to-day variation in UP:C ratio. Correlation between 4-hour or 24-hour UPE and UP:C ratio values was assessed. Reference ranges for 24-hour UPE, 24-hour UP:C ratio, and 4-hour UP:C ratios were calculated as central 95th percentiles of observed values.
Results—Mean 24-hour UPE (4.28 ± 2.99 mg/kg) and 24-hour UP:C ratio (0.0 to 0.37) had excellent correlation (R = 0.826; P < 0.001) in both horses and ponies; analysis of 4-hour data also revealed good correlation (R = 0.782; P < 0.001) with these variables. Calculated UPE and UP:C ratio reference ranges were similar to established ranges in other species. Day-to-day variability in UP:C ratio was minimal, and all results were within the reference range calculated by use of the 24-hour urine samples.
Conclusions and Clinical Relevance—Assessment of the UP:C ratio appears to be a reliable method for estimating 24-hour UPE in horses and ponies.
Abstract
Objective—To investigate the effects of heparin administration on urine protein excretion during the developmental stages of experimentally induced laminitis in horses.
Animals—13 horses.
Procedures—Horses received unfractionated heparin (80 U/kg, SC, q 8 h; n = 7) or no treatment (control group; 6) beginning 3 days prior to induction of laminitis. All horses were given 3 oligofructose loading doses (1 g/kg each) at 24-hour intervals and a laminitis induction dose (10 g of oligofructose/kg) 24 hours following the final loading dose (designated as 0 hours) via nasogastric tube. Serum glucose and insulin concentrations were measured before administration of the first loading dose (baseline) and at 0 and 24 hours; urine protein-to-creatinine (UP:C) ratio was determined at 0 hours and every 4 hours thereafter. Lameness was evaluated every 6 hours, and horses were euthanized when Obel grade 2 ameness was observed.
Results—Mean ± SD time until euthanasia did not differ significantly between the heparin-treated (28.9 ± 6.5 hours) and control (29.0 ± 6.9 hours) horses. The UP:C ratio was significantly increased from baseline at 20 to 28 hours after induction of laminitis (ie, 4 ± 4 hours before lameness was evident) in control horses but did not change significantly from baseline in heparin-treated horses. Serum glucose or insulin concentration did not change significantly from baseline in either group.
Conclusions and Clinical Relevance—Urine protein excretion increased during the developmental stages of carbohydrate-induced laminitis in horses; administration of heparin prevented that increase, but did not delay onset or decrease severity of lameness.
