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Quarter Horse (quarter + horse)

Distribution by Scientific Domains

Medical Sciences	42%

Selected Abstracts

Multisystemic eosinophilic disease in a Quarter Horse

EQUINE VETERINARY EDUCATION, Issue 5 2004
J. Carmalt
First page of article [source]

Arthroscopic reattachment of osteochondritis dissecans lesions using resorbable polydioxanone pins

EQUINE VETERINARY JOURNAL, Issue 5 2004
A. J. NIXON
Summary Reasons for performing study: Debridement of osteochondritis dissecans (OCD) cartilage lesions results in fibrocartilage and imperfect hyaline repair tissue, and forms a permanent irregularity to the subchondral bone plate. Objective: To evaluate the clinical, radiographic and outcome effects of OCD cartilage flap reattachment for select lesions as an alternative to OCD debridement. Hypothesis: Separated cartilage flaps resulting from OCD lesions may be re-incorporated into the hyaline cartilage surface by reattachment rather than debridement and removal. Methods: Resorbable polydioxanone pins were used to reattach OCD flap lesions in 16 joints of 12 horses. Criteria for attachment, rather than removal, included an unmineralised cartilage flap on preoperative radiographs and a relatively smooth surface with some residual perimeter attachment at surgery. Results: There were 12 subjects, 6 males and 6 females, 7 Thoroughbred or Standardbred weanlings, 3 Warmbloods, 1 Arabian and 1 Quarter Horse, mean age at surgery 6.8 months. All horses had effusion of the affected femoropatellar joint (n = 9), tarsocrural joint (n = 1) or fetlock (n = 2). Radiographic lesions varied in length between 1.8,6.3 cm; reattachment was used in 16 of 18 affected joints and the OCD cartilage was not satisfactory for salvage in 2 stifles. Number of pins required was 2,10. One horse was subjected to euthanasia due to a tendon laceration 8 weeks after surgery; of the remaining 11 horses, mean duration of follow-up was 3.9 years (range 4 months-8 years). Nine of these were sound and had entered work, while 2 were sound but remained unbroken 4 and 6 months post operatively, respectively. Radiographic resolution of the OCD lesion occurred in 14 of 16 pinned joints in the 9 horses with long-term follow-up. The 2 remaining joints had a 3 and a 5 mm mineralised flap in the original defect sites. Conclusions: This study indicated cartilage flap reattachment was an alternative to removal in selected OCD lesions. Potential relevance: Relatively smooth OCD cartilage flaps may be salvaged by reattachment and can result in normal radiographic subchondral contour and a high likelihood of athletic performance. Further case numbers are required to determine which lesions are too irregular or contain too much mineral for effective incorporation after reattachment. [source]

Seven novel KIT mutations in horses with white coat colour phenotypes

ANIMAL GENETICS, Issue 5 2009
B. Haase
Summary White coat colour in horses is inherited as a monogenic autosomal dominant trait showing a variable expression of coat depigmentation. Mutations in the KIT gene have previously been shown to cause white coat colour phenotypes in pigs, mice and humans. We recently also demonstrated that four independent mutations in the equine KIT gene are responsible for the dominant white coat colour phenotype in various horse breeds. We have now analysed additional horse families segregating for white coat colour phenotypes and report seven new KIT mutations in independent Thoroughbred, Icelandic Horse, German Holstein, Quarter Horse and South German Draft Horse families. In four of the seven families, only one single white horse, presumably representing the founder for each of the four respective mutations, was available for genotyping. The newly reported mutations comprise two frameshift mutations (c.1126_1129delGAAC; c.2193delG), two missense mutations (c.856G>A; c.1789G>A) and three splice site mutations (c.338-1G>C; c.2222-1G>A; c.2684+1G>A). White phenotypes in horses show a remarkable allelic heterogeneity. In fact, a higher number of alleles are molecularly characterized at the equine KIT gene than for any other known gene in livestock species. [source]

A GYS1 gene mutation is highly associated with polysaccharide storage myopathy in Cob Normand draught horses

ANIMAL GENETICS, Issue 1 2009
B. Herszberg
Summary Glycogen storage diseases or glycogenoses are inherited diseases caused by abnormalities of enzymes that regulate the synthesis or degradation of glycogen. Deleterious mutations in many genes of the glyco(geno)lytic or the glycogenesis pathways can potentially cause a glycogenosis, and currently mutations in fourteen different genes are known to cause animal or human glycogenoses, resulting in myopathies and/or hepatic disorders. The genetic bases of two forms of glycogenosis are currently known in horses. A fatal neonatal polysystemic type IV glycogenosis, inherited recessively in affected Quarter Horse foals, is due to a mutation in the glycogen branching enzyme gene (GBE1). A second type of glycogenosis, termed polysaccharide storage myopathy (PSSM), is observed in adult Quarter Horses and other breeds. A severe form of PSSM also occurs in draught horses. A mutation in the skeletal muscle glycogen synthase gene (GYS1) was recently reported to be highly associated with PSSM in Quarter Horses and Belgian draught horses. This GYS1 point mutation appears to cause a gain-of-function of the enzyme and to result in the accumulation of a glycogen-like, less-branched polysaccharide in skeletal muscle. It is inherited as a dominant trait. The aim of this work was to test for possible associations between genetic polymorphisms in four candidate genes of the glycogen pathway or the GYS1 mutation in Cob Normand draught horses diagnosed with PSSM by muscle biopsy. [source]

Equine degenerative myeloencephalopathy in five Quarter Horses: clinical and neuropathological findings

EQUINE VETERINARY JOURNAL, Issue 1 2004
G. Gandini
No abstract is available for this article. [source]