Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.1 (aspartate aminotransferase)
21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ten children, three girls and seven boys, aged 4-10 years, were admitted with benign acute childhood myositis during spring and winter months (March 1988 to March 1990). They presented with an acute onset of symmetrical calf muscle pain and tenderness, weakness and inability to walk a few days after a flu-like illness. All had raised serum creatine kinase and a normal erythrocyte sedimentation rate, and the majority had low peripheral white blood cell counts with relative lymphocytosis. Serum aspartate aminotransferase, alanine aminotransferase and lactate dehydrogenase were found to be raised in four patients. Virological studies performed in six children gave negative results. Full clinical recovery was achieved within 1-7 days. One child developed a second episode. These ten cases of benign acute childhood myositis are the first to be reported from this region.
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PMID:Benign acute childhood myositis in Kuwait. 128 48

We have previously reported that a single meal of an arginine-free diet rapidly induces hyperammonemia in young ferrets and that aspirin administration in conjunction with influenza B infection and arginine-free diet results in clinical and biochemical alterations consistent with Reye's syndrome. The objective of the present study was to test whether ibuprofen administration, either alone or in combination with influenza infection and arginine-free diet, produces a similar effect. Two-mo-old ferrets were inoculated intranasally with influenza B virus, treated with therapeutic doses of ibuprofen, and fed a single meal of an arginine-free diet. Arginine-free diet caused a significant increase in plasma ammonia and a small increase in plasma aspartate aminotransferase activity. All ferrets fed an arginine-free diet recovered within 6 to 7 h after ingesting the diet. Ibuprofen treatment, either solely or in combination with influenza infection, did not produce significant change in the plasma levels of aspartate or ornithine aminotransferase activities. A combination of ibuprofen treatment, influenza infection, and arginine-free diet caused a significant increase in the mortality and plasma ammonia levels. Plasma aspartate aminotransferase and ornithine carbamyl transferase activities were elevated, and liver ornithine carbamyl transferase activity was decreased. However, other mitochondrial enzymes such as ornithine aminotransferase were not altered, whereas the activity of cytoplasmic enzymes such as arginase were decreased. These results suggest that ibuprofen administration resulted in generalized hepatopathy rather than specific mitochondrial injury and Reye's syndrome-like changes associated with aspirin in our previous model.
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PMID:Interactions of ibuprofen with influenza infection and hyperammonemia in an animal model of Reye's syndrome. 156 Oct 11

To develop an animal model of Reye's syndrome using a virus associated with the human disease, mice were intravenously inoculated with influenza A/PR8 virus (LD50 4000 haemagglutinin units). One to 3 days later the mice developed lethargy, seizures, coma and death. The cerebrospinal fluid cell count was normal. Serum aspartate aminotransferase levels increased 24-fold. Diffuse microvesicular fatty metamorphosis along with multiple small foci of necrosis developed in the liver. Influenza virus-like particles were seen by electron microscopy in the liver, primarily in areas of liver necrosis, but were not seen in the brain. Cerebral oedema without inflammation developed in the brain. Limited viral replication occurred within the liver. Influenza viral antigens were seen in 5-20% of hepatocytes from both necrotic and non-necrotic areas as well as in brain endothelial cells. Many of the clinical, biochemical and pathologic features of the mouse illness resemble those seen in Reye's syndrome. However, this model differs from the human disease in that focal areas of liver necrosis occurred along with limited complete viral replication in liver.
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PMID:Influenza A virus in the mouse: hepatic and cerebral lesions in a Reye's syndrome-like illness. 166 Feb 99

Comparison of large groups of patients with acute viral hepatitis A (HA), B (HB) and non-A, non-B (HNANB) revealed that the highest percentage of anicteric forms is found in HA (44.8%) followed by HNANB (27.3%) and the lowest percentage in HB (23.6%). Investigation of mean values of biochemical functional liver tests showed that 1. the highest mean values of bilirubinaemia, ALT and AST were recorded in HB. The differences are statistically significantly higher (p less than 0.01) than in the two remaining types. 2. The difference between the cholesterol serum level, GMT and ALP in HB and HNANB on the one hand and HA on the other hand was at the same level of significance. 3. The transaminase activity is only slightly higher in HA than in HNANB, the differences are not significant (p greater than 0.05). 4. The cholestatic features are more marked in HNANB than in HA. The differences are also significant (p less than 0.01). In the clinical picture in acute HNANB symptoms of influenza predominated (53.33%), followed by digestive complaints (47.5%) and the percentage of articular complaints was lowest (24.17%). Analysis of 24 cases of fulminant forms of viral hepatitis revealed that this course was most frequent in HB (50%), followed by HNANB (41.7%) and least frequent in HA (8.3%).
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PMID:[Clinical problems in non-A, non-B viral hepatitis. II. Clinical picture of non-A, non-B viral hepatitis in the acute stage]. 212 47

A total of 740 consecutive children aged between 6 months and 12 years who presented with acute encephalopathic illnesses during a three year period were assessed both clinically and by laboratory investigations. Cerebrospinal fluid was examined for the presence of cells or other abnormal substances, and any organisms were cultured. Blood examination included white cell count and estimations of haemoglobin, urea, glucose, and electrolyte concentrations and serum alanine aminotransferase and aspartate aminotransferase. A firm diagnosis was established in 278 patients (38%). Pyogenic meningitis (n = 134), measles encephalopathy (n = 38), and electrolyte imbalance (n = 23) were important causes in this group, cerebral malaria (n = 4) was uncommon and there were no cases of Reye's syndrome. The diagnoses of the remaining 462 were combined under the heading 'acute unexplained encephalopathy'. Altogether 394 of the 462 patients underwent virological investigations for arboviruses and 92 (23%) had one or more indicators of Japanese encephalitis. No other arboviruses could be isolated. Throat swabs from 187 patients with acute unexplained encephalopathy were studied on monkey kidney tissue cell lines of which 14 were positive (8%). These were identified as adenovirus, parainfluenza, influenza, poliomyelitis, Coxsackie, and echovirus; in two cases the virus was untypable. Japanese encephalitis is an important cause of acute childhood encephalopathy in this region. Clinical features of the illness may be mimicked by several disorders which require specific treatment. Thirty four of the 92 died (37%).
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PMID:Virological investigations of acute encephalopathy in India. 203 25

During the last week of December 1989, an outbreak of respiratory system infection involved 32 hospital personnel and 2 patients was detected in Gazi University Medical Faculty Hospital. White blood cells count of the patients were either normal or there were a slight leucopenia. Throat cultures of the most patients were normal. Serum ASO, CRP, bilirubin, AST and ALT were usually within normal limits. According to symptoms, signs and laboratory data we considered a viral disease, especially influenza. All patients recovered without any sequelae. Of 34 in-patients, 8 paired sera, 2 acute phase sera, and 10 convalescent phase sera were tested for the presence of Hemagglutination Inhibition (HI) antibody to three influenza virus strains recommended by WHO in the 1989-1990 season: Influenza A/Taiwan/1/86 (H1 N1), Influenza A/Shanghai/11/87 (H3 N2), Influenza B/Victoria/2/87. All of the sera were negative for Influenza B/Victoria/2/87. There were no significant rises in HT antibody titer for Influenza A/Taiwan/1/86 (H1 N1). The sera for 4 of 8 patients examined both acute and convalescent phase sera had fourfold or greater rise in HI antibody for Influenza A/Shanghai/11/87 (H3 N2). Four patients examined only convalescent sera had 1/40 or greater rises in HI antibody for this influenza subtype. It was considered that this influenza outbreak was probably caused by Influenza A/Shanghai/11/87 (H3 N2).
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PMID:[An outbreak of influenza in hospital personnel]. 228 92

Virus isolation and titration, electrocardiography, enzyme assays and light and electron microscopic studies were undertaken in male turkeys infected with influenza A/turkey/Ontario/7732/66 virus to determine its potential role in the genesis of heart disease. Virus was isolated from the heart initially before a demonstrable viremia and terminally in declining serum viral titer. Virus was isolated from the heart muscle as early as 1 day postinoculation. Highest viral titers were found in the heart at 6 days postinoculation and coincided with maximum elevations of serum glutamic-oxalacetic transaminase and lactic acid dehydrogenase, microscopic lesions in the heart and cardiac arrhythmias. Microscopic lesions in the heart were first detected at 4 days postinoculation and consisted of disseminated areas of necrosis, focal myocarditis, pericarditis and endocarditis. Alterations in myocardial ultrastructure which followed viral infection included fragmentation and dissolution of myofibrils, dilation of the sarcotubular system, increase in membrane vesicle formation in the region of the endoplasmic reticulum, discontinuity of the sarcolemma, proliferation of mitochondrial population, swelling of mitochondria with separation and disruption of the cristae, and the presence of intramitochondrial and perinuclear densities.
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PMID:Light and electron microscopic changes in the myocardium of influenza-infected turkeys. 463 35

Recent studies of Reye syndrome (RS) patients have suggested aspirin treatment as a possible factor in the etiology of this often fatal childhood disorder. the relationship of aspirin treatment to other factors that have been strongly implicated (influenza, ammonia toxicity) cannot be examined directly in patients because aspirin treatment is usually initiated by family members in the prodromal period before RS is diagnosed. In this report we describe the use of an animal model for RS in examining the interactions of these several potential etiological factors. Hyperammonemia and coma were produced in young male ferrets by a brief feeding of an arginine-deficient diet. The effects of influenza infection or aspirin treatment (or both) of control and hyperammonemic ferrets on their serum levels of ammonia, glutamic-oxaloacetic transaminase (GOT;L-aspartate:2-oxoglutarate aminotransferase, EC 2.6.1.1), ornithine carbamoyltransferase (OCT; carbamoylphosphate:L-ornithine carbamoyltransferase, EC 2.1.3.3), bilirubin, and salicylate were studied. Liver levels of lipids, proteins, and several urea-cycle enzymes were also determined in the comatose ferrets and compared with those of untreated controls and of controls treated with influenza or aspirin, or both. Synergism of these three factors (hyperammonemia, influenza infection, and aspirin treatment) in causing RS-like alterations in these parameters was observed.
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PMID:Interactions of aspirin and other potential etiologic factors in an animal model of Reye syndrome. 696 32

A formalin-inactivated aluminium hydroxide adsorbed hepatitis A vaccine was evaluated in a dose-response study on 195 healthy male adults (age range: 18-31 years) in two French hospitals (Lyon, Rouen). Four doses (20, 40, 80, 160 RIA antigen units) were administered intramuscularly (i.m.) in two injections over a 6-month period. At the time of the first vaccine injection, 32 subjects (16.4%) were found positive (> 20 mIU ml-1) for HAV antibody (total Ig RIA HAVAB assay, Abbott Laboratories) and were excluded from the analysis of immunogenicity criteria. Fourteen days after the first vaccine injection, 78.1% (95% confidence interval (CI): 62-90) of seronegative subjects who received the 160 RIA antigen unit dose seroconverted with a geometric mean titre (GMT) of 43 mIU ml-1 (95% CI: 33-56). Seroconversion was 100% (95% CI: 91-100) at 1 month with a GMT of 95 mIU ml-1 (95% CI: 79-112). Statistical analysis revealed a significant dose-related effect (p < 0.0001) on GMT by multivariate regression analysis of the results after the first injection. Biological safety was evaluated and alanine aminotransferase and aspartate aminotransferase levels were similar prior to and 14 days after the first injection in the four groups. Reactions after injection were similar in the four dosage groups: 6.2% of subjects reported immediate reactions after first vaccination (feeling sick, spontaneous pain, headache), 8.9% reported local reactions at the site of injection (spontaneous pain, haematoma, local adenopathy) and 13.5% reported general reactions ('flu-like' syndrome, gastrointestinal tract disorders, fatigue, headache).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Good immunogenicity of GBM strain inactivated hepatitis A vaccine in healthy male adults. 762 20

Fifty-one patients with histologically confirmed epithelial stage III or IV ovarian cancer were entered into a study in which gemcitabine 800 mg/m2 was given as a 30 min intravenous infusion in a cycle once a week for 3 weeks followed by a week of rest. Patients were aged 58 years (range 23-70 years) with WHO performance status 0-2, and had received up to two different chemotherapy regimens. Thirty-eight patients had received only one prior platinum-containing chemotherapy regimen whereas 9 had received a first-line regimen on more than one occasion. A further 3 patients had received two different regimens. Of 42 patients evaluable for response, 8 (19%; 95% CI: 9%-34%) were partial responders. Seven of the 8 responders were resistant to first-line platinum-based therapy. Median duration of response was 8.1 months (range 4.4-12.5 months). Median progression-free survival was 2.8 months (range 0.2-12.5 months). Haematological toxicity with gemcitabine was modest, with grade 3 leukopenia (11 patients) and grades 3 and 4 thrombocytopenia (6 patients). Grade 3 non-haematological toxicity included nausea/vomiting (6 patients) and elevated AST/ALT (1 patient), while dose-limiting non-haematologic toxicity consisted of flu-like symptoms (2 patients), peripheral oedema (1 patient) and lethargy (1 patient). The activity and modest haematological and non-haematological toxicity seen with gemcitabine suggest that this agent should be further evaluated in the treatment of patients with ovarian cancer and in combination chemotherapy regimens, primarily in combination with platinum.
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PMID:Phase II study of gemcitabine in previously platinum-treated ovarian cancer patients. 871 27


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