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Background: Standard thoracic auscultation suffers from limitations, and no systematic analysis of breath sounds in asthmatic horses exists. Objectives: First, characterize breath sounds in horses recorded using a novel digital auscultation device (DAD). Second, use DAD to compare breath variables and occurrence of adventitious sounds in healthy and asthmatic horses. Animals: Twelve healthy control horses (ctl), 12 horses with mild to moderate asthma (mEA), 10 horses with severe asthma (sEA) (5 in remission [sEA−], and 5 in exacerbation [sEA+]). Methods: Prospective multicenter case‐control study. Horses were categorized based on the horse owner‐assessed respiratory signs index. Each horse was digitally auscultated in 11 locations simultaneously for 1 hour. One‐hundred breaths per recording were randomly selected, blindly categorized, and statistically analyzed. Results: Digital auscultation allowed breath sound characterization and scoring in horses. Wheezes, crackles, rattles, and breath intensity were significantly more frequent, higher (P <.001, P <.01, P =.01, P <.01, respectively) in sEA+ (68.6%, 66.1%, 17.7%, 97.9%, respectively), but not in sEA− (0%, 0.7%, 1.3%, 5.6%) or mEA (0%, 1.0%, 2.4%, 1.7%) horses, compared to ctl (0%, 0.6%, 1.8%, −9.4%, respectively). Regression analysis suggested breath duration and intensity as explanatory variables for groups, wheezes for tracheal mucus score, and breath intensity and wheezes for the 23‐point weighted clinical score (WCS23). Conclusions and Clinical Importance.: The DAD permitted characterization and quantification of breath variables, which demonstrated increased adventitious sounds in sEA+. Analysis of a larger sample is needed to determine differences among ctl, mEA, and sEA− horses. [ABSTRACT FROM AUTHOR]

Abstract In this paper, we present a radiation hybrid framework map of BTA13 composed of nine microsatellite loci, six genes and one EST. The map has been developed using a recently constructed 12'000 rad bovine-hamster whole-genome radiation hybrid panel. Moreover, we present a comprehensive map of BTA13 comprising 72 loci, of which 45 are microsatellites, 20 are genes and seven are ESTs. The map has an estimated length of 2694.7 cR12'000. The proposed order is in general agreement with published maps of BTA13. Our results only partially support previously published information of five blocks of conserved gene order between cattle and man. We found no evidence for the existence of an HSA20 homologous segment of coding DNA on BTA13 located centromeric of a confirmed HSA10 homologous region. The present map increases the marker density and the marker resolution on BTA13 and enables further insight into the evolutionary development of the chromosome as compared to man.

Abstract The Italian wolf is in the process of regaining the Alpine region which comes into conflict with the extensive sheep keeping practiced in Switzerland during the summer. As in Switzerland, the wolf is a protected species, the government reimburses losses caused by wolves. Therefore we wanted to know whether the Italian wolf could be distinguished from the domestic dog by microsatellite analysis if DNA samples of the predators could be secured. The evaluation of combined genotypes for the microsatellites CanBern6, CPH4, CPH7, CPH9, CPH12, CPH22 and ZuBeCa1 made it possible to identify an individual as either a domestic dog or an Italian wolf. The assignment of an individual to either one of the two populations is based on the logarithm of the likelihood ratio of an individual being an Italian wolf rather than a domestic dog, given a specific combined genotype. The distribution of the Italian wolf combined genotypes (n = 42) is clearly distinct from the distribution of the domestic dog combined genotypes (n = 90). The likelihood ratio for the "worst" Italian wolf combined genotype was 2.3 E+5 and for the "worst" domestic dog combined genotype was 3.8 E-5.

Abstract Background The high mobility group A1 proteins (HMGA1a/HMGA1b) are highly conserved between mammalian species and widely described as participating in various cellular processes. By inducing DNA conformation changes the HMGA1 proteins indirectly influence the binding of various transcription factors and therefore effect the transcription regulation. In humans chromosomal aberrations affecting the HMGA1 gene locus on HSA 6p21 were described to be the cause for various benign mesenchymal tumours while high titres of HMGA1 proteins were shown to be associated with the neoplastic potential of various types of cancer. Interestingly, the absence of HMGA1 proteins was shown to cause insulin resistance and diabetes in humans and mice. Due to the various similarities in biology and presentation of human and canine cancers the dog has joined the common rodent animal model for therapeutic and preclinical studies. Accordingly, the canine genome was sequenced completely twice but unfortunately this could not solve the structure of canine HMGA1 gene. Results Herein we report the characterisation of the genomic structure of the canine HMGA1 gene consisting of 7 exons and 6 introns spanning in total 9524 bp, the in vivo localisation of the HMGA1 protein to the nucleus, and a chromosomal assignment of the gene by FISH to CFA12q11. Additionally, we evaluated a described canine HMGA1 exon 6 SNP in 55 Dachshunds. Conclusion The performed characterisations will make comparative analyses of aberrations affecting the human and canine gene and proteins possible, thereby providing a basis for revealing mechanisms involved in HMGA1 related pathogenesis in both species.

Abstract Background Chromosomal translocations affecting the chromosome 2p21 cluster in a 450 kb breakpoint region are frequently observed in human benign thyroid adenomas. THADA (thyroid adenoma associated) was identified as the affected gene within this breakpoint region. In contrast to man tumours of the thyroid gland of dogs (Canis lupus familiaris) constitute mainly as follicular cell carcinomas, with malignant thyroid tumours being more frequent than benign thyroid adenomas. In order to elucidate if the THADA gene is also a target of chromosomal rearrangements in thyroid adenomas of the dog we have physically mapped the canine THADA gene to canine chromosome 10. A PCR was established to screen a canine genome library for a BAC clone containing the gene sequence of canine THADA. Further PCR reactions were done using the identified BAC clone as a template in order to verify the corresponding PCR product by sequencing. Canine whole blood was incubated with colcemid in order to arrest the cultured cells in metaphases. The verified BAC DNA was digoxigenin labeled and used as a probe in fluorescence in situ hybridization (FISH). Ten well spread metaphases were examined indicating a signal on canine chromosome 10 on both chromatids. A detailed fine mapping was performed indicating the canine THADA gene locus on the q-arm of chromosome 10. Results The canine THADA gene locus was mapped on chromosome 10q25. Our mapping results obtained in this study following the previously described nomenclature for the canine karyotype. Conclusion We analysed whether the THADA gene locus is a hotspot of canine chromosomal rearrangements in canine neoplastic lesions of the thyroid and in addition might play a role as a candidate gene for a possible malignant transformation of canine thyroid adenomas. Although the available cytogenetic data of canine thyroid adenomas are still insufficient the chromosomal region to which the canine THADA has been mapped seems to be no hotspot of chromosomal aberrations seen in canine thyroid adenomas.

Abstract Background Non-synonymous polymorphisms within the prion protein gene (PRNP) influence the susceptibility and incubation time for transmissible spongiform encephalopathies (TSE) in some species such as sheep and humans. In cattle, none of the known polymorphisms within the PRNP coding region has a major influence on susceptibility to bovine spongiform encephalopathy (BSE). Recently, however, we demonstrated an association between susceptibility to BSE and a 23 bp insertion/deletion (indel) polymorphism and a 12 bp indel polymorphism within the putative PRNP promoter region using 43 German BSE cases and 48 German control cattle. The objective of this study was to extend this work by including a larger number of BSE cases and control cattle of German and Swiss origin. Results Allele, genotype and haplotype frequencies of the two indel polymorphisms were determined in 449 BSE cattle and 431 unaffected cattle from Switzerland and Germany including all 43 German BSE and 16 German control animals from the original study. When breeds with similar allele and genotype distributions were compared, the 23 bp indel polymorphism again showed a significant association with susceptibility to BSE. However, some additional breed-specific allele and genotype distributions were identified, mainly related to the Brown breeds. Conclusion Our study corroborated earlier findings that polymorphisms in the PRNP promoter region have an influence on susceptibility to BSE. However, breed-specific differences exist that need to be accounted for when analyzing such data.