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Träfflista för sökning "WFRF:(Hultin Jäderlund Karin) srt2:(2010-2014)"

Sökning: WFRF:(Hultin Jäderlund Karin) > (2010-2014)

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2.
  • Drögemüller, Cord, et al. (författare)
  • A deletion in the N-myc downstream regulated gene 1 (NDRG1) gene in Greyhounds with polyneuropathy
  • 2010
  • Ingår i: PloS one. - : Public Library of Science (PLoS). - 1932-6203. ; 5:6, s. e11258-
  • Tidskriftsartikel (refereegranskat)abstract
    • The polyneuropathy of juvenile Greyhound show dogs shows clinical similarities to the genetically heterogeneous Charcot-Marie-Tooth (CMT) disease in humans. The pedigrees containing affected dogs suggest monogenic autosomal recessive inheritance and all affected dogs trace back to a single male. Here, we studied the neuropathology of this disease and identified a candidate causative mutation. Peripheral nerve biopsies from affected dogs were examined using semi-thin histology, nerve fibre teasing and electron microscopy. A severe chronic progressive mixed polyneuropathy was observed. Seven affected and 17 related control dogs were genotyped on the 50k canine SNP chip. This allowed us to localize the causative mutation to a 19.5 Mb interval on chromosome 13 by homozygosity mapping. The NDRG1 gene is located within this interval and NDRG1 mutations have been shown to cause hereditary motor and sensory neuropathy-Lom in humans (CMT4D). Therefore, we considered NDRG1 a positional and functional candidate gene and performed mutation analysis in affected and control Greyhounds. A 10 bp deletion in canine NDRG1 exon 15 (c.1080_1089delTCGCCTGGAC) was perfectly associated with the polyneuropathy phenotype of Greyhound show dogs. The deletion causes a frame shift (p.Arg361SerfsX60) which alters several amino acids before a stop codon is encountered. A reduced level of NDRG1 transcript could be detected by RT-PCR. Western blot analysis demonstrated an absence of NDRG1 protein in peripheral nerve biopsy of an affected Greyhound. We thus have identified a candidate causative mutation for polyneuropathy in Greyhounds and identified the first genetically characterized canine CMT model which offers an opportunity to gain further insights into the pathobiology and therapy of human NDRG1 associated CMT disease. Selection against this mutation can now be used to eliminate polyneuropathy from Greyhound show dogs.
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3.
  • Hultin Jäderlund, Karin, et al. (författare)
  • A cohort study of epilepsy among 665,000 insured dogs : Incidence, mortality and survival after diagnosis
  • 2014
  • Ingår i: Veterinary Journal. - : Elsevier BV. - 1090-0233 .- 1532-2971. ; 202, s. 471-476
  • Tidskriftsartikel (refereegranskat)abstract
    • The main objective of this study was to estimate the incidence and mortality rates of epilepsy in a large population of insured dogs and to evaluate the importance of a variety of risk factors. Survival time after a diagnosis of epilepsy was also investigated. The Swedish animal insurance database used in this study has previously been helpful in canine epidemiological investigations. More than 2,000,000 dog-years at-risk (DYAR) were available in the insurance database.In total, 5013 dogs had at least one veterinary care claim for epilepsy, and 2327 dogs were euthanased or died because of epilepsy. Based on veterinary care claims the incidence rate of epilepsy (including both idiopathic and symptomatic cases) was estimated to be 18 per 10,000 DYAR. Dogs were followed up until they were 10 (for life insurance claims) or 12 years of age (veterinary care claims). Among the 35 most common breeds in Sweden, the Boxer was at the highest risk of epilepsy with 60.3 cases per 10,000 DYAR, and also had the highest mortality rate of 46.7 per 10,000 DYAR (based on life insurance claims). Overall, males were at a higher risk than females (1.4:1). Median survival time (including euthanasia and death) after diagnosis was 1.5 years. In general, breeds kept solely for companionship lived longer after diagnosis than those kept for dual-purposes, such as hunting and shepherd and working breeds. The study demonstrates marked breed differences in incidence and mortality rates, which are assumed to reflect genetic predisposition to epilepsy.
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4.
  • Hultin Jäderlund, Karin (författare)
  • New aspects of hereditary ataxia in smooth-haired fox terriers
  • 2010
  • Ingår i: Veterinary Record. - : Wiley. - 0042-4900 .- 2042-7670. ; 166, s. 557-560
  • Tidskriftsartikel (refereegranskat)abstract
    • Hereditary ataxia was diagnosed in three smooth-haired fox terrier puppies from Sweden, 25 years after the previous known case in the breed. In addition to the characteristic spinal cord pathology, brain involvement was evident clinically, in the form of behavioural changes and bilaterally decreased menace responses, and histopathologically, with degenerative changes in the brainstem. The striking similarities to hereditary ataxia in the jack Russell terrier suggest the same disease process in both breeds. A common ancestor, a female dog born in 1951 and considered a carrier of the disease at that time, was found in both the maternal and paternal lines of the three puppies.
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5.
  • Johansson Wensman, Jonas, et al. (författare)
  • Expression of interferon gamma in the brain of cats with natural Borna disease virus infection
  • 2011
  • Ingår i: Veterinary Immunology and Immunopathology. - : Elsevier BV. - 0165-2427 .- 1873-2534. ; 141, s. 162-167
  • Tidskriftsartikel (refereegranskat)abstract
    • Borna disease virus (BDV) is a neurotropic, negative-stranded RNA virus, which causes a non-suppurative meningoencephalomyelitis in a wide range of animals. In cats, BDV infection leads to staggering disease. In spite of a vigorous immune response the virus persists in the central nervous system (CNS) in both experimentally and naturally infected animals. Since the CNS is vulnerable to cytotoxic effects mediated via NK-cells and cytotoxic T-cells, other non-cytolytic mechanisms such as the interferon (IFN) system is favourable for viral clearance. In this study, IFN-gamma expression in the brain of cats with clinical signs of staggering disease (N = 12) was compared to the expression in cats with no signs of this disease (N = 7) by quantitative RT-PCR. The IFN-gamma expression was normalised against the expression of three reference genes (HPRT, RPS7, YWHAZ). Cats with staggering disease had significantly higher expression of IFN-gamma compared to the control cats (p-value <= 0.001). There was no significant difference of the IFN-gamma expression in BDV-positive (N = 7) and negative (N = 5) cats having clinical signs of staggering disease. However, as BDV-RNA still could be detected, despite an intense IFN-gamma expression, BDV needs to have mechanisms to evade this antiviral immune response of the host, to be able to persist. (C) 2011 Elsevier B.V. All rights reserved.
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6.
  • Johansson Wensman, Jonas, et al. (författare)
  • Markers of Borna disease virus infection in cats with staggering disease
  • 2012
  • Ingår i: Journal of Feline Medicine and Surgery. - 1098-612X .- 1532-2750. ; 14, s. 573-582
  • Tidskriftsartikel (refereegranskat)abstract
    • Borna disease virus (BDV) is a RNA-virus causing neurological disorders in a wide range of mammals. In cats, BDV infection may cause staggering disease. Presently, staggering disease is a tentative clinical diagnosis, only confirmed at necropsy. In this study, cats with staggering disease were investigated to study markers of BDV infection aiming for improvement of current diagnostics. Nineteen cats fulfilled the inclusion criteria based on neurological signs and pathological findings. In 17/19 cats, BDV infection markers (BDV-specific antibodies and/or BDV-RNA) were found, and antibodies in serum (13/16, 81%) were the most common marker. BDV-RNA was found in 11/19 cats (58%). In a reference population without neurological signs, 4/25 cats were seropositive (16%). The clinical history and neurological signs in combination with presence of BDV infection markers, where serology and rRT-PCR on blood can be helpful tools, improve the diagnostic accuracy in the living cat.
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7.
  • Sundstøl Eriksen, Gunnar, et al. (författare)
  • Poisoning of dogs with tremorgenic Penicillium toxins
  • 2010
  • Ingår i: Medical Mycology. - : Oxford University Press (OUP). - 1369-3786 .- 1460-2709. ; 48, s. 188-196
  • Tidskriftsartikel (refereegranskat)abstract
    • Fungi in the genus Penicillium, particularly P. crustosum, produce tremorgenic mycotoxins, as well as suspected tremorgenic compounds. The accidental intoxication of six dogs with such toxins are reported. The clinical signs included vomiting, convulsions, tremors, ataxia, and tachycardia, all of which are indicators of intoxications affecting the nervous system. This symptomatology caused us to think that the dog poisoning was the result of tremorgenic mycotoxins. One dog was euthanized in the acute phase, while three others recovered completely within a few days. However, neurological symptoms were still observed four months after the poisoning of two of the dogs. One of these recovered completely within the next 2-3 months, while the other still suffers from ataxia three years later. Available samples of feed, stomach content and/or tissues from the intoxications were subjected to mycological and chemical analysis. Penitrem A was found in all reported poisonings and roquefortine C in all cases when this toxin was included in the analysis. The producer of these toxins, Penicillium crustosum, was detected in all cases where material suitable for mycological examinations (feed or vomit) was available. To our knowledge, this is the first report documenting the presence of penitrems and roquefortine C in organs from poisoned dogs. Furthermore, the report indicates that the recovery period after severe poisonings with P crustosum may be protracted.
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