Institution
Animal Health Trust
Healthcare•Newmarket, Suffolk, United Kingdom•
About: Animal Health Trust is a healthcare organization based out in Newmarket, Suffolk, United Kingdom. It is known for research contribution in the topics: Population & Lameness. The organization has 1197 authors who have published 2412 publications receiving 70775 citations.
Topics: Population, Lameness, Equine influenza, Virus, Streptococcus equi
Papers published on a yearly basis
Papers
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TL;DR: A phylodynamic framework for the dissection of dynamic forces that determine the diversity of epidemiological and phylogenetic patterns observed in RNA viruses of vertebrates is introduced.
Abstract: A key priority for infectious disease research is to clarify how pathogen genetic variation, modulated by host immunity, transmission bottlenecks, and epidemic dynamics, determines the wide variety of pathogen phylogenies observed at scales that range from individual host to population. We call the melding of immunodynamics, epidemiology, and evolutionary biology required to achieve this synthesis pathogen “phylodynamics.” We introduce a phylodynamic framework for the dissection of dynamic forces that determine the diversity of epidemiological and phylogenetic patterns observed in RNA viruses of vertebrates. A central pillar of this model is the Evolutionary Infectivity Profile, which captures the relationship between immune selection and pathogen transmission.
1,248 citations
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Broad Institute1, University of Pavia2, Uppsala University3, University of Bologna4, University of Kentucky5, University of Adelaide6, University of Tampa7, University of Veterinary Medicine Vienna8, University of Bern9, University of California, Davis10, Wellcome Trust Sanger Institute11, Cornell University12, Royal Veterinary College13, Institut national de la recherche agronomique14, Japan Racing Association15, University College Dublin16, Genetic Information Research Institute17, Swedish University of Agricultural Sciences18, University of Minnesota19, University of Bari20, Texas A&M University21, Animal Health Trust22, Massachusetts Institute of Technology23
TL;DR: The analysis reveals an evolutionarily new centromere on equine chromosome 11 that displays properties of an immature but fully functioning Centromere and is devoid of centromeric satellite sequence, suggesting thatCentromeric function may arise before satellite repeat accumulation.
Abstract: We report a high-quality draft sequence of the genome of the horse (Equus caballus). The genome is relatively repetitive but has little segmental duplication. Chromosomes appear to have undergone few historical rearrangements: 53% of equine chromosomes show conserved synteny to a single human chromosome. Equine chromosome 11 is shown to have an evolutionary new centromere devoid of centromeric satellite DNA, suggesting that centromeric function may arise before satellite repeat accumulation. Linkage disequilibrium, showing the influences of early domestication of large herds of female horses, is intermediate in length between dog and human, and there is long-range haplotype sharing among breeds.
745 citations
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TL;DR: A new mutation in MSTN found in the whippet dog breed that results in a double-muscled phenotype known as the “bully” whippets is described, marking the first time a mutation in the myostatin gene has been quantitatively linked to increased athletic performance.
Abstract: Double muscling is a trait previously described in several mammalian species including cattle and sheep and is caused by mutations in the myostatin (MSTN) gene (previously referred to as GDF8). Here we describe a new mutation in MSTN found in the whippet dog breed that results in a double-muscled phenotype known as the “bully” whippet. Individuals with this phenotype carry two copies of a two-base-pair deletion in the third exon of MSTN leading to a premature stop codon at amino acid 313. Individuals carrying only one copy of the mutation are, on average, more muscular than wild-type individuals (p = 7.43 × 10−6; Kruskal-Wallis Test) and are significantly faster than individuals carrying the wild-type genotype in competitive racing events (Kendall's nonparametric measure, τ = 0.3619; p ≈ 0.00028). These results highlight the utility of performance-enhancing polymorphisms, marking the first time a mutation in MSTN has been quantitatively linked to increased athletic performance.
738 citations
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TL;DR: The results indicate that the age-associated decrease inRemyelination efficiency occurs because of an impairment of OP recruitment and the subsequent differentiation of the OPs into remyelinating oligodendrocytes, and that strategies aimed at ameliorating the age -associated decline in remyELination efficiency will therefore need to promote both components of the regenerative process.
Abstract: The age-associated decrease in the efficiency of CNS remyelination has clear implications for recovery from demyelinating diseases such as multiple sclerosis (MS) that may last for several decades. Developing strategies to reverse the age-associated decline requires the identification of how the regenerative process is impaired. We addressed whether remyelination becomes slower because of an impairment of recruitment of oligodendrocyte progenitors (OPs) or, as is the case in some MS lesions, an impairment of OP differentiation into remyelinating oligodendrocytes. The OP response during remyelination of focal, toxin-induced CNS demyelination in young and old rats was compared by in situ hybridization using probes to two OP-expressed mRNA species: platelet-derived growth factor-α receptor and the OP transcription factor myelin transcription factor 1 (MyT1). We found that the expression patterns for the two OP markers are very similar and reveal a delay in the colonization of the demyelinated focus with OPs in the old animals compared with the young animals. By comparing the mRNA expression pattern of MyT1 with that of the myelin proteins myelin basic protein and Gtx, we found that in the old animals there is also a delay in OP differentiation that increases with longer survival times. These results indicate that the age-associated decrease in remyelination efficiency occurs because of an impairment of OP recruitment and the subsequent differentiation of the OPs into remyelinating oligodendrocytes, and that strategies aimed at ameliorating the age-associated decline in remyelination efficiency will therefore need to promote both components of the regenerative process.
527 citations
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TL;DR: Investigation of the influence of oral creatine supplementation on skeletal muscle isokinetic torque and the accumulation of plasma ammonia and blood lactate during five bouts of maximal exercise found muscle peak torque production was greater and plasma ammonia accumulation was lower during and after exercise after creatine ingestion.
Abstract: 1. The present experiment was undertaken to investigate the influence of oral creatine supplementation, shown previously to increase the total creatine content of human skeletal muscle (Harris RC, Soderlund K, Hultman E. Clin Sci 1992; 83: 367–74), on skeletal muscle isokinetic torque and the accumulation of plasma ammonia and blood lactate during five bouts of maximal exercise.
2. Twelve subjects undertook five bouts of 30 maximal voluntary isokinetic contractions, interspersed with 1 min recovery periods, before and after 5 days of placebo (4 × 6 g of glucose/day, n = 6) or creatine (4 × 5 g of creatine plus 1 g of glucose/day, n = 6) oral supplementation. Muscle torque production and plasma ammonia and blood lactate accumulation were measured during and after exercise on each treatment
3. No difference was seen when comparing muscle peak torque production during exercise before and after placebo ingestion. After creatine ingestion, muscle peak torque production was greater in all subjects during the final 10 contractions of exercise bout 1 ( P <0.05), throughout the whole of exercise bouts 2 ( P <0.01), 3 ( P <0.05) and 4 ( P = 0.057) and during contractions 11–20 of the final exercise bout ( P <0.05), when compared with the corresponding measurements made before creatine ingestion. Plasma ammonia accumulation was lower during and after exercise after creatine ingestion. No differences were found when comparing blood lactate levels.
4. There is evidence to suggest that the decrease in the degree of muscle torque loss after dietary creatine supplementation may be a consequence of a creatine-induced acceleration of skeletal muscle phosphocreatine resynthesis. It is postulated that an increased availability of phosphocreatine would maintain better the required rate of ATP demand during contraction. This is supported by the observed lower accumulation of plasma ammonia during exercise after creatine ingestion.
490 citations
Authors
Showing all 1201 results
Name | H-index | Papers | Citations |
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Kyriacos A. Athanasiou | 86 | 425 | 26353 |
Paul L. Greenhaff | 72 | 270 | 16441 |
James L. N. Wood | 69 | 328 | 15748 |
Matthew Breen | 53 | 205 | 11490 |
Roger Smith | 53 | 230 | 11986 |
Matthew M. Binns | 50 | 162 | 8305 |
Padraic Dixon | 48 | 228 | 6727 |
William Henley | 46 | 178 | 10370 |
Roger C. Harris | 44 | 118 | 6620 |
Mark A. Holmes | 44 | 203 | 8248 |
Sue J. Dyson | 43 | 312 | 6987 |
Pierre Lekeux | 43 | 345 | 6480 |
Leo B. Jeffcott | 42 | 191 | 5630 |
Allen E. Goodship | 42 | 130 | 5723 |
Simon R. Platt | 40 | 209 | 5225 |