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)

To determine the frequency and significance of alpha-fetoprotein elevation in severe hepatitis B surface antigen-negative chronic active hepatitis, 558 serum samples obtained from 83 patients were tested by an immunoenzymometric assay. All patients received corticosteroids and sampling occurred at 6-12-mo intervals during 96 +/- 6 mo of follow-up. Twenty-nine patients (35%) had an abnormal level. In 26 patients, the abnormality was at presentation. In 3 patients, the abnormality developed 11-127 mo later. Two of these patients had primary hepatocellular carcinoma. Serum aspartate aminotransferase levels were higher in patients with an alpha-fetoprotein elevation at presentation (p less than 0.02). After therapy, the alpha-fetoprotein level normalized and patients entering remission had lower levels than at entry (p less than 0.001). alpha-Fetoprotein levels, however, did not correlate closely with serum aspartate aminotransferase levels at entry nor did they distinguish patients with different patterns of histologic activity. Outcomes after therapy were similar in patients with and without alpha-fetoprotein elevation. Three patients (4%) developed primary hepatocellular carcinoma after 113 +/- 26 mo but only 2 had elevated alpha-fetoprotein levels. We conclude that elevation of the alpha-fetoprotein level occurs commonly at presentation. The abnormality frequently resolves after corticosteroid therapy and it does not have prognostic significance. An elevation that occurs after treatment suggests primary hepatocellular carcinoma.
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PMID:Frequency and significance of serum alpha-fetoprotein elevation in severe hepatitis B surface antigen-negative chronic active hepatitis. 244 60

Oral bropirimine (an immunomodulator shown to induce interferon) was administered to timed-pregnant Sprague-Dawley rats in five experiments utilizing several different dosing schedules. Concentrations of 100, 200, and 400 mg/kg of bropirimine were used. Interferon levels were determined in maternal serum, spleen, and whole embryo extracts and uterine contents were evaluated for survival of the embryos. Maternal toxicity occurred in all experiments as evidenced by dose-related decreases in body weight during the first 24 hr postdosing. Hematoxicology analyses of maternal serum revealed significant decreases in urea nitrogen, potassium, and albumin, along with increases in aspartate transaminase, alanine transaminase, and total bilirubin, in bropirimine-treated dams as compared to the vehicle controls. In addition, the means for maternal thymus weight decreased while the means for spleen weight increased with increasing concentration of bropirimine. As compared to the vehicle controls, interferon titers were high in maternal serum, maternal spleen, and, to a lesser extent, whole embryos, 2 hr postdosing, but had decreased or were below detectable levels 24 hr postdosing. Embryolethality was pronounced (increases in pre- and postimplantational loss) after a single dose (Gestation Day 3, 4, 5, 8, 9, or 10) of bropirimine, as well as after 7 or 8 consecutive days (Gestation Days 6-12 or 6-13) of treatment. Although embryotoxicity never occurred in these experiments in the absence of pronounced maternal toxicity, the pregnant dams never died as the result of bropirimine treatment, whereas the embryos frequently failed to survive.
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PMID:Bropirimine-induced embryolethality after oral administration to the pregnant rat. 247 83

This paper describes a longitudinal study in which clinical parameters and aspartate aminotransferase (AST) in gingival crevicular fluid (GCF) were monitored bimonthly over a 6-12 months period in 970 sites from 7 treated periodontitis patients. In this study, 21 out of 970 sites exhibited new attachment loss (AL) of at least 2mm between two consecutive visits. The GCF-AST levels and clinical parameters at sites with active tissue destruction (> or = 2mm AL within two months) were significantly higher than those at control sites on the same tooth. The GCF-AST levels and clinical parameters at sites with active tissue destruction decreased significantly after re-treatment. The measurement of GCF-AST could be an useful adjunctive criterion for detection of disease activity. However, it seems to be unsatisfactory in predicting disease activity.
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PMID:[Relationship between levels of aspartate aminotransferase in gingival crevicular fluid and periodontal disease activity]. 778 35

Changes in the serum concentrations of aspartic aminotransferase (AST), alanine aminotransferase (ALT), rhodanese and arginase were measured in dogs, sheep and cattle with hepatic necrosis induced by the oral administration of carbon tetrachloride. A new method for arginase assay was based on the determination of remaining arginine (after its conversion to urea and ornithine) by its reaction with p-nitrophenyl glyoxal (PNPG). In all species studied the serum arginase increased 6-12 h after liver damage, reached a peak value in 48 h and returned to normal thereafter. Rhodanese activity did not change in dogs but rose significantly in sheep and, to a lesser extent, in cattle. AST increased strikingly in sheep as compared with dogs and cattle and remained high for > 5 days. In dogs ALT rose sharply and remained elevated for > 10 days. No change in ALT was seen in sheep or cattle. The determination of arginase by a simple procedure such as the PNPG method, in conjunction with AST or ALT assay, may be of value in assessing the stage of liver necrosis.
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PMID:Changes in arginase, aminotransferases and rhodanese in sera of domestic animals with experimentally induced liver necrosis. 804 Mar 68

Tissue iron loading in hypotransferrinaemic (hpx/hpx) mice was investigated as a model for genetic (primary) haemochromatosis. Iron loading of liver preceded that in the pancreas and heart. One-year-old hpx/hpx mice showed iron staining in exocrine pancreas, liver parenchymal cells, and cardiac and intestinal smooth muscle cells. Iron-loaded macrophages were observed in all these tissues. Islets of Langerhans, biliary epithelial cells, and spleen were iron-free. The pancreas was fibrotic with massive macrophage infiltration and loss of secretory epithelium. Liver showed evidence of chronic inflammatory infiltration with increased collagen fibres in the parenchymal region but no cirrhosis. Serum aspartate aminotransferase activity and plasma glucose were increased in hpx/hpx compared with wild-type mice. Heavy iron loading with haemosiderin deposition in the liver could be demonstrated in hpx/hpx mice from 6 weeks of age. Heterozygous hypotransferrinaemic mice showed minor increases in liver iron stores at 6-12 weeks, but not at 1 year of age. Serum ferritin levels in heterozygous mice were also increased at 6-8 weeks of age. It was concluded that 1-year-old hpx/hpx mice showed evidence of liver and pancreatic damage secondary to tissue iron overload. The iron loading pattern and tissue damage showed some features which were distinct from those observed in haemochromatosis.
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PMID:Tissue iron loading and histopathological changes in hypotransferrinaemic mice. 827 72

We applied a multivariate analysis to a large series of serum biochemical tests in an attempt to identify a function that could efficiently discriminate cirrhosis from hepatocellular carcinoma (HC). We analyzed two successive temporal cohorts (1987-90; 1991-94) of HC and cirrhotic patients, all histologically classified (first cohort: 69 cirrhosis and 39 HC; second cohort: 66 cirrhosis and 38 HC). Using data from the first temporal cohort of patients, we obtained a discriminant function based on seven serum analytes: alpha-fetoprotein, the hepatic isoenzyme of alkaline phosphatase, lactate dehydrogenase isoenzyme 5, total gamma-glutamyltransferase (GGT), GGT isoforms complexed with low-density lipoprotein, aspartate aminotransferase, and copper. The same panel of analytes emerged when the second cohort was tested and also when both cohorts were tested together. In the two successive cohorts (total, 212 patients) with a prevalence of cirrhosis vs HC of approximately 2:1, the discriminant function correctly classified 93% of cases, the highest percentage of correct classification of the two diseases obtained so far by laboratory approaches. Validation with the jackknife reallocation statistical algorithm confirmed these results. In addition, of six patients with liver cirrhosis for whom we had the opportunity of following up and observing the evolution to HC, five were classified as HC at diagnosis by the multivariate discriminant analysis; i.e., discriminant analysis provided a diagnostic lead time of 6-12 months over histology. This discriminant function, based on easy-to-perform serum biochemical tests, may help solve a fundamental problem of differential diagnosis in the evolution of chronic liver diseases from cirrhosis to HC.
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PMID:Differential diagnosis between hepatocellular carcinoma and cirrhosis through a discriminant function based on results for serum analytes. 869 87

Previous studies have implied a relationship between Se-deficiency and oxidative stress. In the present study, the occurrence of oxidative stress due to Se-deficiency was investigated by evaluating the age dependence of growth and indices of oxidative damage for the liver of Se-deficient (SeD) rats. The ratios of liver weight to body weight of the SeD rats were greater than those of the normal rats. The values of AST and ALT (clinical indices of liver damage) were higher in the SeD rats than the normal ones especially in the young (6-12 weeks of age). The TBARS level of the 4-week-old SeD group were higher than the normal group while the level decreased with age. Conversely, the TBARS level of the normal group gradually increased and became higher than SeD group in older rats (12-20 weeks of age). Vitamin E rather than vitamin C may be consumed during oxidative stress due to Se-deficiency. Damage induced by Se-deficiency may be related to growth and the mechanisms of this damage may alter with age.
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PMID:Evaluation of oxidative damage in the liver of selenium-deficient rats. 1268 28

Keeping patients on mechanical ventilation after orthotopic liver transplantation (OLT) has been a standard anesthetic approach since the first utilization of liver transplantation. Advances in anesthetic management, surgical techniques and patient preparation, in addition to improved postoperative care and the reported advantages of early postoperative tracheal extubation of liver recipients. encouraged us to extubate most recipients at the end of the operation. The aim of the present study is to evaluate the pediatric liver recipients who were extubated immediately at the end of transplantation, in terms of respiratory complications and allograft function during their stay in the ICU. We retrospectively reviewed the records of 40 pediatric recipients who had undergone OLT at the Ege University Organ Transplantation Center between December 1997 and July 2002. Twelve out of 40 patients who had consecutively undergone OLT were extubated immediately at the end of the operation and were included this study. Mean Child Pugh scores of the patients were 9 +/- 2.3 (range 6-12) and the mean PELD score was 23.1 +/- 12.3 (range 7-41). The mean age of the patients was 8.4 +/- 5.2 (range 0.8-16.8 yr). Five of the 12 extubated patients received a cadaveric and seven a living donor liver graft. The mean ICU stay of the patients was 49.1 +/- 24.2 h (6-120 h). No patients required reintubation or mechanical ventilation in the ICU. Respiratory complications diagnosed in the 12 extubated patients were hypercapnia without hypoxemia in three, atelectasis in one and pleural effusion in two. No primary non-function or delayed graft function was detected. The aspartate transaminase (AST), alanine transaminase (ALT) and protrombin time (PT) were normalized within a week. We believe that immediate tracheal extubation in the operating room is a safe procedure for selected cadaveric and living-related liver transplant recipients and will facilitate the patients' recovery and mobilization leading to reduction in complications and a reduced ICU stay.
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PMID:Immediate tracheal extubation of pediatric liver transplant recipients in the operating room. 1473 99

Pyrazinamide (PZA) combined with either ethambutol (EMB) or a fluoroquinolone for 6-12 months is one of the treatments recommended for latent tuberculosis infection (LTBI) in contacts exposed to multidrug-resistant tuberculosis (MDR-TB). The aim of the present study was to describe the side effects related to combined PZA and EMB treatment given for LTBI, in contacts previously exposed to MDR-TB. In total, 12 consecutive contacts, all of African origin and aged 38+/-5 yrs, were treated with daily PZA (23+/-4 mg.kg(-1)) and EMB (17+/-4 mg.kg(-1)) at Geneva University Hospital outpatient clinic (Switzerland), as a result of contact-tracing procedures for two patients with contagious MDR-TB. Clinical status and liver function tests (aspartate aminotransferase (ALAT) and alanine aminotransferase (ASAT)) were monitored monthly. In seven cases (58%) treatment was discontinued after a median of 119 days, due to hepatic toxicity in six cases (ALAT or ASAT elevation more than four times the upper normal limit), and gastrointestinal symptoms in one case. In conclusion, combined pyrazinamide and ethambutol for latent tuberculosis infection may be associated with a high risk of hepatic toxicity, and warrants close monitoring. There is clearly a need for alternative preventive treatments for contacts exposed to multidrug-resistant tuberculosis.
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PMID:High hepatotoxicity of pyrazinamide and ethambutol for treatment of latent tuberculosis. 1613 29

Recent evidence indicates that inhibition of the Na+/H+ exchanger improves heart and brain injuries induced by I/R. Studies were performed to investigate whether FR183998, a Na/H exchanger inhibitor, has protective effects on hepatic I/R injury in rats. Male Sprague-Dawley rats were subjected to 70% hepatic ischemia by occluding the hepatic artery, portal vein, and bile duct associated with the left and median liver lobes with a microvascular clip for 2 h. FR183998 (1 mg/kg) was administered i.v. 10 min before the hepatic ischemia. Hepatic I/R increased the serum levels of aspartate transaminase, alanine transaminase, and lactate dehydrogenase, which peaked at 9 h after reperfusion. FR183998 reduced these injury markers and recovered liver functions. Histopathologic analysis revealed that FR183998 prevented the incidences of hepatic necrosis, apoptosis, and neutrophil infiltration at 6 and 9 h (P < 0.05). FR183998 reduced the increases in proinflammatory cytokines such as TNF-alpha (1-6 h), IL-6 (1-12 h), interferon-gamma (6-12 h), IL-1beta (1-3 h), and cytokine-induced neutrophil chemoattractant 1 (1-3 h), but enhanced the anti-inflammatory cytokine IL-10 (1 h). FR183998 inhibited the hepatic I/R-induced activation of the transcription factor nuclear factor-kappaB at 1 to 6 h and reduced the induction of iNOS at 6 to 12 h, followed by inhibition of nitric oxide production. Furthermore, FR183998 decreased the expression of the iNOS gene antisense transcript, which is involved in the stability of iNOS messenger RNA, at 9 to 12 h in the liver of hepatic I/R rats. These results demonstrate that FR183998 reduces the induction of proinflammatory cytokines and iNOS at least in part through inhibition of nuclear factor-kappaB activation and iNOS antisense transcript expression, thereby preventing hepatic I/R injury.
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PMID:Protective effect of FR183998, a Na+/H+ exchanger inhibitor, and its inhibition of iNOS induction in hepatic ischemia-reperfusion injury in rats. 1827 53


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