Browsing by Author "Miller D"

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    A review of dystocia in sheep
    (Elsevier B.V., 2020-11-01) Jacobson C; Bruce M; Kenyon PR; Lockwood A; Miller D; Refshauge G; Masters DG
    This review aims to describe the nutritional and non-nutritional factors that may affect parturition and dystocia in sheep. Dystocia is associated with fetopelvic disproportion, uterine inertia, failure of the cervix to fully dilate, malpresentation and disease or congenital defects in lambs. Dystocia can result in lambs that are born dead, or lambs that survive parturition but sustain birth injury including central nervous system damage. Dystocia risk is increased with high or low birthweight lambs, high (fat) or low liveweight ewes, and small first parity ewes. Other factors implicated include low muscle glycogen, pregnancy toxaemia, mineral imbalance causing hypocalcaemia, and a lack of antioxidant nutrients. Addressing these risks requires differential nutritional management for single and multiple bearing ewes. There is also evidence for stress and environmentally related dystocia. The stress related hormones cortisol, adrenaline and ACTH play a major role in the initiation and control of parturition in the sheep indicating a need for adequate supervision during lambing, provision of adequate feed and shelter at the lambing site, and small flock size to reduce physical and environmental stress. Hormonal control of parturition can be further disrupted by xenoestrogens or phytoestrogens in clovers and medics. Oestrogenic plants are still widely grown in mixed pastures but should be not be grazed by pregnant ewes. There is clearly a genetic component to dystocia. This is partly explained by incompatibility in physical size and dimensions of the ram, ewe and lamb. A rapid reduction in dystocia through direct genetic selection is problematic with low heritability of dystocia and some of its indicator traits such as lambing ease. This review provides broad interpretation of the literature, but conclusions are not definitive with widespread inconsistency in reported results. Further research is required to investigate dystocia under commercial production conditions, and this should be complemented by focussed studies under controlled conditions. Priorities include defining the fitness of the ewe to lamb, the role of stress and environment on parturition and the use of indicator traits to select for ease of birth.
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    Host genetic influence on papilloma virus-induced tumors in the Horse
    (John Wiley & Sons, 15/08/2016) Staiger EA; Tseng CT; Miller D; Cassano J; Nasir L; Garrick DJ; Brooks SA; Antczak DF
    The common equine skin tumors known as sarcoids have been causally associated with infection by bovine papillomavirus (BPV). Additionally, there is evidence for host genetic susceptibility to sarcoids. We investigated the genetic basis of susceptibility to sarcoid tumors on a cohort of 82 affected horses and 270 controls genotyped on a genome-wide platform and two custom panels. A Genome Wide Association Study (GWAS) identified candidate regions on six chromosomes. Bayesian probability analysis of the same dataset verified only the regions on equine chromosomes (ECA) 20 and 22. Fine mapping using custom-produced SNP arrays for ECA20 and ECA22 regions identified two marker loci with high levels of significance: SNP BIEC2-530826 (map position 32,787,619) on ECA20 in an intron of the DQA1 gene in the Major Histocompatibility Complex (MHC) class II region (pā€‰=ā€‰4.6e-06), and SNP BIEC2-589604 (map position 25,951,536) on ECA22 in a 200 kb region containing four candidate genes: PROCR, EDEM2, EIF6 and MMP24 (pā€‰=ā€‰2.14e-06). The marker loci yielded odds ratios of 5.05 and 4.02 for ECA20 and ECA22, respectively. Associations between genetic MHC class II variants and papillomavirus-induced tumors have been reported for human papillomavirus and cottontail rabbit papillomavirus infections. This suggests a common mechanism for susceptibility to tumor progression that may involve subversion of the host immune response. This study also identified a genomic region other than MHC that influenced papillomavirus-induced tumor development in the studied population.