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hypoglycin a/érable sycomore

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METHODS During April and May 2014 four horses aged between 5 months and 9 years, located in the Canterbury, Marlborough and Southland regions, presented with a variety of clinical signs including recumbency, stiffness, lethargy, dehydration, depression, and myoglobinuria suggestive of acute muscle
BACKGROUND Ingestion of sycamore seeds (Acer pseudoplatanus) is the likely source of hypoglycin A in atypical myopathy (AM) but ingestion of seedlings in spring might also contribute to intoxication. OBJECTIVE To test for hypoglycin A in seeds and seedlings collected on pastures where AM cases were

Equine atypical myopathy caused by hypoglycin A intoxication associated with ingestion of sycamore maple tree seeds.

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BACKGROUND Evidence suggest there is a link between equine atypical myopathy (EAM) and ingestion of sycamore maple tree seeds. OBJECTIVE To further evaluate the hypothesis that the ingestion of hypoglycin A (HGA) containing sycamore maple tree seeds causes acquired multiple acyl-CoA dehydrogenase

Hypoglycin A concentrations in seeds of Acer pseudoplatanus trees growing on atypical myopathy-affected and control pastures.

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BACKGROUND Hypoglycin A, found in seeds of Acer negundo, appears to cause seasonal pasture myopathy (SPM) in North America and is implicated in atypical myopathy (AM) in Europe. Acer negundo is uncommon in Europe. Thus, the potential source of hypoglycin A in Europe is unknown. OBJECTIVE We

Atypical myopathy in Père David's deer (Elaphurus davidianus) associated with ingestion of hypoglycin A.

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From 2004 until 2016, 21 Père David's deer (Elaphurus davidianus) have died for unknown reason at Zoo Duisburg. These deer, also known as milu, have succumbed from a myopathy that occurred seasonally in autumn and in spring. The clinical signs shown by the animals closely resembles those of a
Hypoglycin A (HGA) toxicity, following ingestion of material from certain plants, is linked to an acquired multiple acyl-CoA dehydrogenase deficiency known as atypical myopathy, a commonly fatal form of equine rhabdomyolysis seen worldwide. Whilst some plants are known to contain this toxin, little

A validated method for quantifying hypoglycin A in whole blood by UHPLC-HRMS/MS.

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Hypoglycin A (HGA) is the toxic principle in ackee (Blighia sapida Koenig), a nutritious and readily available fruit which is a staple of the Jamaican working-class and rural population. The aril of the unripe fruit has high concentrations of HGA, the cause of Jamaican vomiting sickness, which is

Potential new sources of hypoglycin A poisoning for equids kept at pasture in spring: a field pilot study.

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Equine atypical myopathy in Europe results from hypoglycin A (HGA) exposure through the ingestion of samaras or seedlings of the sycamore maple tree. This pilot study aimed at better defining sources of HGA intoxication in spring. Samaras fallen on the ground and then seedlings were collected at

Hypoglycin A Content in Blood and Urine Discriminates Horses with Atypical Myopathy from Clinically Normal Horses Grazing on the Same Pasture.

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Hypoglycin A (HGA) in seeds of Acer spp. is suspected to cause seasonal pasture myopathy in North America and equine atypical myopathy (AM) in Europe, fatal diseases in horses on pasture. In previous studies, this suspicion was substantiated by the correlation of seed HGA content with the

Hypoglycin A Concentrations in Maple Tree Species in the Netherlands and the Occurrence of Atypical Myopathy in Horses.

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BACKGROUND Atypical myopathy (AM) in horses is caused by the plant toxin hypoglycin A, which in Europe typically is found in the sycamore maple tree (Acer pseudoplatanus). Owners are concerned about whether their horses are in danger if they graze near maple trees. OBJECTIVE To measure hypoglycin A

Clinical Research Abstracts of the British Equine Veterinary Association Congress 2015.

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BACKGROUND Hypoglycin A (HG) appears to cause atypical myopathy (AM), but to our knowledge, detection of HG in affected and unaffected horses and concurrently in plants that they were exposed to has not previously been reported. OBJECTIVE To investigate HG in samples from horses exposed to Acer

Equine atypical myopathy in the UK: Epidemiological characteristics of cases reported from 2011 to 2015 and factors associated with survival.

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BACKGROUND Equine atypical myopathy (AM) is a toxic rhabdomyolysis associated with ingestion of hypoglycin A, derived typically in Europe, from Acer pseudoplatanus tree. Despite the wide distribution of this tree species in the UK, the number of cases reported annually varies, and there has been an

Mitochondrial function is altered in horse atypical myopathy.

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Equine atypical myopathy in Europe is a fatal rhabdomyolysis syndrome that results from the ingestion of hypoglycin A contained in seeds and seedlings of Acer pseudoplatanus (sycamore maple). Acylcarnitine concentrations in serum and muscle OXPHOS capacity were determined in 15 atypical myopathy

Identification of methylenecyclopropyl acetic acid in serum of European horses with atypical myopathy.

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BACKGROUND It is hypothesised that European atypical myopathy (AM) has a similar basis as seasonal pasture myopathy in North America, which is now known to be caused by ingestion of hypoglycin A contained in seeds from the tree Acer negundo. Serum from horses with seasonal pasture myopathy contained

Detection of MCPG metabolites in horses with atypical myopathy.

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Atypical myopathy (AM) in horses is caused by ingestion of seeds of the Acer species (Sapindaceae family). Methylenecyclopropylacetyl-CoA (MCPA-CoA), derived from hypoglycin A (HGA), is currently the only active toxin in Acer pseudoplatanus or Acer negundo seeds related to AM outbreaks. However,
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