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- Baranowska, Izabella, et al.
(författare)
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Sensory ataxic neuropathy in golden retriever dogs is caused by a deletion in the mitochondrial tRNATyr gene
- 2009
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Ingår i: PLoS Genetics. - : Public Library of Science (PLoS). - 1553-7390 .- 1553-7404. ; 5:5, s. e1000499-
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Tidskriftsartikel (refereegranskat)abstract
- Sensory ataxic neuropathy (SAN) is a recently identified neurological disorder in golden retrievers. Pedigree analysis revealed that all affected dogs belong to one maternal lineage, and a statistical analysis showed that the disorder has a mitochondrial origin. A one base pair deletion in the mitochondrial tRNA(Tyr) gene was identified at position 5304 in affected dogs after re-sequencing the complete mitochondrial genome of seven individuals. The deletion was not found among dogs representing 18 different breeds or in six wolves, ruling out this as a common polymorphism. The mutation could be traced back to a common ancestor of all affected dogs that lived in the 1970s. We used a quantitative oligonucleotide ligation assay to establish the degree of heteroplasmy in blood and tissue samples from affected dogs and controls. Affected dogs and their first to fourth degree relatives had 0-11% wild-type (wt) sequence, while more distant relatives ranged between 5% and 60% wt sequence and all unrelated golden retrievers had 100% wt sequence. Northern blot analysis showed that tRNA(Tyr) had a 10-fold lower steady-state level in affected dogs compared with controls. Four out of five affected dogs showed decreases in mitochondrial ATP production rates and respiratory chain enzyme activities together with morphological alterations in muscle tissue, resembling the changes reported in human mitochondrial pathology. Altogether, these results provide conclusive evidence that the deletion in the mitochondrial tRNA(Tyr) gene is the causative mutation for SAN.
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| 3. |
- Fall, Tove, 1979-, et al.
(författare)
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Diabetes mellitus in a population of 180,000 insured dogs : incidence, survival, and breed distribution
- 2007
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Ingår i: Journal of Veterinary Internal Medicine. - : Wiley. - 0891-6640 .- 1939-1676. ; 21:6, s. 1209-1216
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Tidskriftsartikel (refereegranskat)abstract
- Background: Canine diabetes mellitus (DM) is a common endocrinopathy with an unclear etiology. For a better understanding of the underlying mechanisms, there is a need for comprehensive epidermiologic studies. Earlier studies have shown that the risk of disease is higher in certain dog breeds. Hypothesis: Incidence, age of onset, survival and sex proportion of DM vary by breed. Animals: Data from a cohort of 182,087 insured dogs aged 5-12 years accounting for 652,898 dog-years at risk were studied retrospectively. Methods: Incidence rates by sex, breed, and geography were calculated with exact denominators. Age-specific incidence and survival after 1st DM claim were computed with Cox's regression and Kaplan-Meier survival function. Multivariable survival analysis was performed for the outcome diagnosis of DM with age, sex, and geography tested as fixed effects, previous endocrine or pancreatic diseases tested as time-dependent covariates, and breed tested as a random effect. Results: The mean age at 1st insurance claim for the 860 DM dogs (72% females) was 8.6 years. The incidence of DM was 13 cases per 10,000 dog-years at risk. Australian Terriers, Samoyeds, Swedish Elkhounds, and Swedish Lapphunds were found to have the highest incidence. The proportion of females with DM varied significantly among breeds. Swedish Elkhounds, Beagles, Norwegian Elkhounds, and Border Collies that developed DM were almost exclusively females. The multivariable model showed that breed, previous hyperadrenocorticism, and female sex were risk factors for developing DM. Median survival time was 57 days after 1st claim. Excluding the 223 dogs that died within I day, the median survival time was 2 years after 1st claim of DM. Conclusion: The significant breed-specific sex and age differences shown in this study indicate that genetic variation could make breeds more or less susceptible to different types of DM.
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| 5. |
- Hultin Jäderlund, Karin, et al.
(författare)
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Cerebrospinal Fluid PCR and Antibody Concentrations against Anaplasma phagocytophilum and Borrelia burgdorferi sensu lato in Dogs with Neurological Signs
- 2009
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Ingår i: Journal of Veterinary Internal Medicine. - : Wiley. - 0891-6640 .- 1939-1676. ; 23, s. 669-672
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Tidskriftsartikel (refereegranskat)abstract
- The tick-borne bacteria Borrelia burgdorferi sensu lato (sl) and Anaplasma phagocytophilum have been suspected to cause neurological signs in dogs. Diagnosis often has been made based on positive antibody titers in serum of dogs with neurological signs, but a high seroprevalence in dogs in at-risk populations makes diagnosis difficult.To determine if the neurological signs in dogs examined were caused by any of these bacteria.Fifty-four dogs presented to a board-certified neurologist.Prospective study. We divided dogs into 2 groups: those with inflammatory diseases of the central nervous system (CNS) and those with neurological signs from other diseases. Blood and cerebrospinal fluid (CSF) from all dogs were analyzed.Dogs with inflammatory CNS diseases showed no serum antibodies against any of the agents. Among dogs with neurological signs from other diseases, 10.3% had serum antibodies for B. burgdorferi sl and 20.5% for A. phagocytophilum. All blood samples analyzed for bacterial deoxyribonucleic acid (DNA) and all CSF analyzed for antibodies and bacterial DNA for the 2 agents were negative.Based on this study, these bacteria are unlikely causes of neurologic disease in dogs and the presence of serum antibodies alone does not document or establish a definitive diagnosis of CNS disease caused by these organisms. Dogs that have neurologic disease and corresponding serum antibodies against these agents should have additional tests performed to assess for other potential etiologies of the signs.
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| 6. |
- Karlsson, Elinor K., et al.
(författare)
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Efficient mapping of mendelian traits in dogs through genome-wide association
- 2007
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Ingår i: Nature Genetics. - : Springer Science and Business Media LLC. - 1061-4036 .- 1546-1718. ; 39:11, s. 1321-1328
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Tidskriftsartikel (refereegranskat)abstract
- With several hundred genetic diseases and an advantageous genome structure, dogs are ideal for mapping genes that cause disease. Here we report the development of a genotyping array with |[sim]|27,000 SNPs and show that genome-wide association mapping of mendelian traits in dog breeds can be achieved with only |[sim]|20 dogs. Specifically, we map two traits with mendelian inheritance: the major white spotting (S) locus and the hair ridge in Rhodesian ridgebacks. For both traits, we map the loci to discrete regions of <1 Mb. Fine-mapping of the S locus in two breeds refines the localization to a region of |[sim]|100 kb contained within the pigmentation-related gene MITF. Complete sequencing of the white and solid haplotypes identifies candidate regulatory mutations in the melanocyte-specific promoter of MITF. Our results show that genome-wide association mapping within dog breeds, followed by fine-mapping across multiple breeds, will be highly efficient and generally applicable to trait mapping, providing insights into canine and human health.
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| 7. |
- Sallander, Marie, et al.
(författare)
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The Effect of Early Diet on Canine Atopic Dermatitis (CAD) in Three High-Risk Breeds
- 2009
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Ingår i: Open Dermatology Journal. - : Bentham Science Publishers Ltd.. - 1874-3722. ; 3, s. 73-80
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Tidskriftsartikel (refereegranskat)abstract
- Abstract: The effect of diet on the occurrence of canine atopic dermatitis (CAD) in the high-risk breeds boxer, English bull terrier and West Highland white terrier was investigated as part of an extensive case-control study. In that study, a sparing association was seen for feeding the bitch a diet containing non-commercial ingredients during lactation and the subsequent development of CAD in the offspring. The purpose of this study was to further explore the role of diet of the bitch during lactation as well as early dietary exposure of puppies (up to six months of age) on the occurrence of CAD. Two factors were significant in a final logistic regression model: “not feeding non-commercial animal products (meat, egg or milk-products) to the bitch during lactation” (OR = 3.39, 95% CI 1.46-7.92) and “feeding non-commercial meat to the puppy between the age of 2-6 months” (OR = 2.97, 95% CI 1.27-6.93), and further analysis revealed that there was an interaction between these two factors. If a bitch didn't receive non-commercial animal products during lactation, and the puppy was fed non-commercial meat any time until 6 months of age, the puppy had an increased risk of developing CAD (OR = 5.1, 95% CI 1.2-21.9). If the bitch received at least some non-commercial animal products during lactation there was no difference in risk of CAD for the offspring, regardless of whether the puppy was fed non-commercial meat or not until the age of 6 months (OR = 1.6, 95% CI 0.5-5.6). It seems prudent to feed bitches some non-commercial animal products during lactation
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