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Träfflista för sökning "WFRF:(Hanson Jeanette) srt2:(2011-2014)"

Sökning: WFRF:(Hanson Jeanette) > (2011-2014)

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  • Hanson, Jeanette, et al. (författare)
  • Endokrina sjukdomar hos hund
  • 2012
  • Ingår i: Svensk Veterinärtidning. - 0346-2250. ; , s. 23-24
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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  • Hanson, Jeanette (författare)
  • Stem cells in the canine pituitary gland and in pituitary adenomas
  • 2013
  • Ingår i: Veterinary Quarterly. - : Informa UK Limited. - 0165-2176 .- 1875-5941. ; 33, s. 217-224
  • Forskningsöversikt (refereegranskat)abstract
    • Cushing's disease (CD) or pituitary-dependent hypercortisolism is a common endocrinopathy in dogs, with an estimated prevalence of 1 or 2 in 1000 dogs per year. It is caused by an adrenocorticotropic hormone secreting adenoma in the pars distalis or pars intermedia of the pituitary gland. The pituitary gland is a small endocrine gland located in the pituitary fossa. In the postnatal individual, the hypothalamus-pituitary axis plays a central role in maintaining homeostatic functions, like control of metabolism, reproduction, and growth. Stem cells are suggested to play a role in the homeostatic adaptations of the adult pituitary gland, such as the rapid specific cell-type expansion in response to pregnancy or lactation. Several cell populations have been suggested as pituitary stem cells, such as Side Population cells and cells expressing Sox2 or Nestin. These cell populations are discussed in this review. Also, stem and progenitor cells are thought to play a role in pituitary tumorigenesis, such as the development of pituitary adenomas in dogs. There are limited reports on the role of stem cells in pituitary adenomas, especially in dogs. Further studies are needed to identify and characterize this cell population and to develop specific cell targeting therapeutic strategies as a new way of treating canine CD.
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  • Olsson, Mia, 1978-, et al. (författare)
  • Thorough investigation of a canine autoinflammatory disease (AID) syndrome confirms one main risk factor and suggests a modifier locus for amyloidosis
  • 2013
  • Ingår i: PLOS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 8:10, s. e75242-
  • Tidskriftsartikel (refereegranskat)abstract
    • Autoinflammatory disease (AID) manifests from the dysregulation of the innate immune system and is characterised by systemic and persistent inflammation. Clinical heterogeneity leads to patients presenting with one or a spectrum of phenotypic signs, leading to difficult diagnoses in the absence of a clear genetic cause. We used separate genome-wide SNP analyses to investigate five signs of AID (recurrent fever, arthritis, breed specific secondary dermatitis, otitis and systemic reactive amyloidosis) in a canine comparative model, the pure bred Chinese Shar-Pei. Analysis of 255 DNA samples revealed a shared locus on chromosome 13 spanning two peaks of association. A three-marker haplotype based on the most significant SNP (p<2.6x10(-8)) from each analysis showed that one haplotypic pair (H13-11) was present in the majority of AID individuals, implicating this as a shared risk factor for all phenotypes. We also noted that a genetic signature (F-ST) distinguishing the phenotypic extremes of the breed specific Chinese Shar-Pei thick and wrinkled skin, flanked the chromosome 13 AID locus; suggesting that breed development and differentiation has played a parallel role in the genetics of breed fitness. Intriguingly, a potential modifier locus for amyloidosis was revealed on chromosome 14, and an investigation of candidate genes from both this and the chromosome 13 regions revealed significant (p<0.05) renal differential expression in four genes previously implicated in kidney or immune health (AOAH, ELMO1, HAS2 and IL6). These results illustrate that phenotypic heterogeneity need not be a reflection of genetic heterogeneity, and that genetic modifiers of disease could be masked if syndromes were not first considered as individual clinical signs and then as a sum of their component parts.
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  • Strage, Emma, et al. (författare)
  • Relationship among Insulin Resistance, Growth Hormone, and Insulin-Like Growth Factor I Concentrations in Diestrous Swedish Elkhounds
  • 2014
  • Ingår i: Journal of Veterinary Internal Medicine. - : Wiley. - 0891-6640 .- 1939-1676. ; 28:2, s. 419-428
  • Tidskriftsartikel (refereegranskat)abstract
    • Background In the dog, the normal estrous cycle includes a prolonged luteal phase. Progesterone stimulates local canine mammary growth hormone (GH) production, which may act systemically and contribute to insulin resistance. Swedish Elkhounds are predisposed to progesterone-related diabetes mellitus, and the relationship among insulin resistance, GH, and insulin-like growth factor I (IGF-I) is of particular interest. Objective To study insulin resistance in relation to GH and IGF-I in nondiabetic Swedish Elkhounds during diestrus. We also assessed whether alterations in these hormones could predict diestrus-linked diseases and all-cause mortality. Animals Eighty-four privately owned female intact Swedish Elkhounds >4years of age. Methods Blood sampling and clinical examination during luteal phase, with a follow-up questionnaire after 20months. Insulin resistance was calculated by homeostasis model assessment (HOMA-IR). Results In multivariable regression analysis, GH was positively associated with HOMA-IR (P=.009). An increase in GH of 1ng/mL was associated with a 12.7% increase in HOMA-IR. Moreover, C-peptide was positively associated with IGF-I (P=.04), and an increase in C-peptide of 0.1ng/mL was associated with a 6.9% increase in IGF-I. Structural equation modeling supported these results. Twenty-three animals were found to have previously unrecognized mammary masses and had higher GH (P<.0001) and IGF-I (P=.007) than dogs without mammary masses (n=61). There was no association between high GH and IGF-I concentrations at sampling and future mammary masses. Conclusion We showed that GH was strongly associated with insulin resistance in older Swedish Elkhounds during diestrus.
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