OBJECTIVE To describe methods to measure the 3-D orientation of the proximal, diaphyseal, and distal segments of the canine radius by use of computer-aided design software (CADS) and to compare the repeatability and reliability of measurements derived by those methods. SAMPLE 31 canine radii with biapical deformities and 24 clinically normal (control) canine radii. PROCEDURES Select CT scans of radii were imported into a CADS program. Cartesian coordinate systems for the humerus and proximal, diaphyseal, and distal radial segments were developed. The orientation of each radial segment in the frontal, sagittal, and transverse planes was measured in triplicate by 3 methods. The repeatability and reliability of those measurements were calculated and compared among the 3 measurement methods. RESULTS The mean ± SD within-subject repeatability of radial angular measurements for all 3 methods was 1.40 ± 0.67° in the frontal plane, 3.17 ± 2.21° in the sagittal plane, and 3.01 ± 1.11° in the transverse plane for control radii and 2.56 ± 1.95° in the frontal plane, 3.59 ± 2.39° in the sagittal plane, and 3.47 ± 1.19° in the transverse plane for abnormal radii. Mean ± SD bias between radial measurement methods was 1.88 ± 2.07° in the frontal plane, 6.44 ± 6.80° in the sagittal plane, and 2.27 ± 2.81° in the transverse plane. CONCLUSIONS AND CLINICAL RELEVANCE Results indicated that use of CADS to assess the 3-D orientation of the proximal, diaphyseal, and distal segments of normal and abnormal canine radii yielded highly repeatable and reliable measurements.

The objective of this preliminary study was to identify genomic regions that may predispose Gordon setters from the United Kingdom to familial protein-losing enteropathy (PLE) at a young age. A total of 106 related Gordon setters was used, including 6 affected dogs from an affected litter, 6 case controls from the same litter, 10 related/affected dogs, and 84 related/unaffected dogs. Genomic DNA was collected from each Gordon setter and extracted from buccal mucosal swabs. Genotyping of affected and unaffected dogs was carried out using the Canine Illumina HD SNP array and data generated were analyzed with PLINK software, using fixation index (Fst) and runs of homozygosity (ROH) methods. Pairwise Fst analyses between the affected and unaffected Gordon setter dogs identified various regions of differentiation on chromosomes 10, 18, 21, and 23 that contained several important genes. These regions revealed 5 candidate genes, including RARB, TTC7A, SOCS5, PIGF, and RHOD, that are associated with human inflammatory bowel disease (IBD) and could potentially be associated with PLE in Gordon setters. Run of homozygosity (ROH) analyses revealed additional unique regions on chromosomes 15 and 17. These regions contained genes SYT1, UCN, and FNDC that could also be potential candidates for PLE in Gordon setters. The biological functions of the identified genes provided initial insights into the pathophysiology of PLE. Further large-scale studies are warranted to investigate the possible causality of these genomic regions and any possible genetic markers that could be used in predicting susceptibility to PLE syndrome.