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

A 65-year-old female patient was admitted to our hospital with the symptoms of chest pain, dyspnea and fatigue. She had undergone a tooth extraction three months before. She took no medication. Echocardiography revealed pericardial effusion. The serum alanine aminotransferase (ALT) at presentation was 650 IU/L and aspartate aminotransferase (AST) was 600 IU/L. Hepatitis C virus (HCV) RNA level was 150,000 IU/ml. Genotype was 1b. Acute pericarditis was considered to be caused by acute HCV infection. The patient was followed without treatment. One month later, AST and ALT were found as 65 IU/L and 82 IU/L, respectively; there were symptoms of effort dyspnea and fatigue. Echocardiography showed minimal decrease in pericardial effusion compared to one month previously. HCV RNA level was again checked and found as 155,000 IU/ml. The patient was given pegylated interferon. One month later, the pericardial effusion and related symptoms had disappeared. The pegylated interferon treatment was sustained for 24 weeks and HCV-RNA was found negative at the 3rd and 6th months of the treatment and six months after the end of treatment. We conclude that pegylated interferon may be offered to patients with symptomatic acute HCV-related pericarditis.
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PMID:Pegylated interferon treatment of acute pericarditis associated with acute hepatitis C. 1808 Sep 27

Fowl adenovirus serotype 4 (FAdV-4) is the causative agent of hydropericardium syndrome (HPS), which is characterized by the accumulation of a clear, straw-colored fluid in the pericardial sac, and high mortality rates. In order to explore the mechanism of FAdV-4-induced cardiac damage, dynamic pathology, apoptosis, and inflammatory reactions were analyzed in vivo. Moreover, we detected viral proliferation, and ultrastructure, inflammation and apoptosis of cardiomyocytes (CM) after FAdV-4 infection in vitro. The results showed that FAdV-4 impaired cardiac integrity and function by causing apoptosis and inflammation in vivo. Flow cytometry showed that CM infected with FAdV-4 did not show apoptosis in vitro. In addition, the mRNA expression of four inflammatory cytokines (interleukin (il)1B, il6, il8, and tumor necrosis factor), and activity of three myocardial enzymes were significantly different between FAdV-4 and control groups. However, in vitro, these indexes showed no significant difference between the groups. These observations collectively indicated that the heart was not the target organ of FAdV-4, and the virus may not directly lead to the occurrence of CM apoptosis and inflammation. To explore the source of pericardial effusion, we measured total protein, albumin, aspartate aminotransferase, creatine kinase isoenzyme, lactate dehydrogenase, potassium, sodium, and chloride ions in serum and pericardial effusion. Pericardial effusion was derived from vascular exudation rather than CM degeneration. Further studies are needed to investigate the exudation mechanism of vascular endothelial cells in FAdV-4 infection then weakened or eliminated pericardial effusion to minimize heart injury and/or restore damaged CM.
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PMID:Mechanism of fowl adenovirus serotype 4-induced heart damage and formation of pericardial effusion. 3032 11

Two pet rabbits were presented with an acute decrease in appetite and activity. Rabbit 1 showed severe hypothermia, bradycardia, arrhythmias, a heart murmur, dyspnea, occlusion of the nares with secretions, icterus, dehydration, and gaseous gastrointestinal dilation. The urine was dark yellow. Rabbit 2 was overweight, apathetic, and dehydrated; this animal presented with a heart murmur, gastric dilation, and intermittent nystagmus with dorsal strabismus in the right eye. Blood gas, electrolyte, hematology, plasma clinical biochemistry analysis, coagulation profile, plasma protein electrophoresis, urinalysis, and radiographic examinations were performed. The main shared findings were moderate thrombocytopenia, markedly decreased aspartate aminotransferase and alanine aminotransferase activities and fibrinogen concentrations, prolonged prothrombin and activated partial thromboplastin times, profoundly increased alkaline phosphatase and gamma-glutamyl transferase (GGT) activities, and high bile acid and bilirubin concentrations. Rabbit 1 also had respiratory acidosis, marked hypoglycemia, hyperphosphatemia, and a profoundly increased creatine kinase activity. Gastric dilation was observed on both radiographic exams. A low urinary pH of 5-6, marked bilirubinuria and proteinuria, and high urinary GGT levels were present in both patients. Marked icterus developed before death, which occurred within 22 and 30 hours post admission in rabbits 1 and 2, respectively. The necropsy of rabbit 1 showed a markedly accentuated hepatic lobular pattern, pulmonary hemorrhages, pericardial effusion with adhesions, peritoneal petechiae, and icteric and hemorrhagic abdominal fat. Histopathologic findings included hemorrhagic diathesis, severe centroacinar and midzonal hepatocellular necrosis, severe necrosuppurative bronchopneumonia, and moderate cardiomyocyte necrosis. A liver PCR assay was positive for Rabbit Hemorrhagic Disease Virus (RHDV) 2 (RHDV2) and negative for classic RHDV. This is the first description of the gross clinicopathologic abnormalities associated with naturally occurring RHDV2 infection in pet rabbits.
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PMID:Clinicopathologic findings of naturally occurring Rabbit Hemorrhagic Disease Virus 2 infection in pet rabbits. 3086 86