Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An epidemic of chronic rhinitis in a population of 50 captive spur-thighed tortoises (Testudo graeca graeca) from Palafrugell (Girona, Spain) is described, in which eight animals died and 12 were euthanatized to perform necropsies and post-mortem studies. The main clinical sign was a bilateral, seromucous rhinitis often accompanied by stomatitis and glossitis. Hematology and serum biochemistry were performed in 33 of the 50 ill animals and in 29 healthy tortoises from three disease-free populations. Lymphocyte count, aspartate aminotransferase (AST) activity, and alpha-globulin levels were significantly higher in the animals from the sick population. The heterophil count was significantly lower in the sick animals. Some of the diseased tortoises also showed a normocytic-normochromic anemia. Lesions were restricted to the respiratory system and oral cavity. Marked epithelial hyperplasia and presence of a severe mixed inflammatory infiltrate in the epithelium of the oral, nasal, and tracheal mucosae were observed. Electron microscopy demonstrated the presence of intracytoplasmic and intranuclear viral particles of the size, shape, and distribution pattern typical of a herpesvirus.
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PMID:Chronic rhinitis associated with herpesviral infection in captive spur-thighed tortoises from Spain. 970 58

Juvenile cobalamin deficiency is a rare disease in border collies and its diagnosis requires a high level of clinical suspicion. The goal of this study was to increase awareness of this disease by describing the clinical and laboratory findings in four young border collies with inherited cobalamin deficiency. The median age of the dogs was 11.5 mo (range, 8-42 mo), and two of the four dogs were full siblings. Clinical signs included intermittent lethargy (n = 4), poor body condition (n = 4), odynophagia (n = 2), glossitis (n = 1), and bradyarrhythmia (n = 1). Pertinent laboratory abnormalities were mild to moderate normocytic nonregenerative anemia (n = 3), increased aspartate aminotransferase (AST) activity (n = 3), and mild proteinuria (n = 3). All of the dogs had serum cobalamin levels below the detection limit of the assay, marked methylmalonic aciduria, and hyperhomocysteinemia. Full clinical recovery was achieved in all dogs with regular parenteral cobalamin supplementation, and laboratory abnormalities resolved, except the proteinuria and elevated AST activity persisted. This case series demonstrates the diverse clinical picture of primary cobalamin deficiency in border collies. Young border collies presenting with ambiguous clinical signs should be screened for cobalamin deficiency.
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PMID:Clinical and laboratory findings in border collies with presumed hereditary juvenile cobalamin deficiency. 2353 54