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)

Ultra-marathon running is frequently associated with muscle fibre damage. However, ultra-marathon related information is scarce. The present study evaluated muscle and cartilage biomarkers, and cytokine secretion during a 200 km running event. Venous blood samples from 54 trained male ultra-marathon runners (mean +/- SD, 45.7 +/- 5.1 years). Plasma creatine phosphokinase (CPK), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate, glucose, high-sensitivity C-reactive protein (Hs-CRP), interleukin-6 (IL-6), TNF- proportional, variant and serum cartilage oligomeric matrix protein (COMP) content were determined before, midway and immediately after the race. CPK increased 90-fold (19-fold at 100 km) from pre-race value and LDH increased 3.7-fold (2.2-fold at 100 km). AST increased 15-fold (5-fold at 100 km) and ALT increased 3.9-fold (2-fold at 100 km). Blood lactate and glucose levels did not change significantly. Hs-CRP increased 23-fold (3-fold at 100 km) and IL-6 increased 121-fold at 100 km, and then remained stable up to 200 km, whereas TNF- proportional, variant did not change significantly. Serum COMP increased 3-fold (1.3-fold at 100 km). Post-run CPK was correlated with LDH (r = 0.62, P < 0.001), Hs-CRP (r = 0.45, P < 0.001), ALT (r = 0.89, P < 0.001), AST (r = 0.97, P < 0.001), and IL-6 (r = 0.61, P < 0.001). The present study demonstrated that blood biomarkers related to muscle and cartilage damage and inflammation were increased during a 200 km run and that this was particularly marked during the second half of the event. Ultra-marathon running clearly has a major impact on muscle and cartilage structures.
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PMID:Biomarkers of muscle and cartilage damage and inflammation during a 200 km run. 1720 43

The aim of this study was to characterise community-acquired pneumonia (CAP) caused by atypical pathogens by combining distinctive clinical and epidemiological features and novel biological markers. A population-based prospective study of consecutive patients with CAP included investigation of biomarkers of bacterial infection, e.g., procalcitonin, C-reactive protein and lipopolysaccharide-binding protein (LBP) levels. Clinical, radiological and laboratory data for patients with CAP caused by atypical pathogens were compared by univariate and multivariate analysis with data for patients with typical pathogens and patients from whom no organisms were identified. Two predictive scoring models were developed with the most discriminatory variables from multivariate analysis. Of 493 patients, 94 had CAP caused by atypical pathogens. According to multivariate analysis, patients with atypical pneumonia were more likely to have normal white blood cell counts, have repetitive air-conditioning exposure, be aged <65 years, have elevated aspartate aminotransferase levels, have been exposed to birds, and have lower serum levels of LBP. Two different scoring systems were developed that predicted atypical pathogens with sensitivities of 35.2% and 48.8%, and specificities of 93% and 91%, respectively. The combination of selected patient characteristics and laboratory data identified up to half of the cases of atypical pneumonia with high specificity, which should help clinicians to optimise initial empirical therapy for CAP.
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PMID:Clinical characterisation of pneumonia caused by atypical pathogens combining classic and novel predictors. 1732 27

Ischemia -modified albumin was regarded as an early marker of cardiac ischemia. On the other hand, it has been reported that increased ischemia-modified albumin levels are associated with unstable plaque processes like percutaneous coronary intervention, acute coronary syndrome or myocardial infarction. This prospective study aimed to investigate the role of ischemia-modified albumin in patients with peripheral vascular disease undergoing peripheral vascular intervention, a plaque-altering procedure without evidence of tissue ischemia. Peripheral vascular intervention was performed in 21 consecutive patients (68.2+/-13.3 years) with typical leg claudication and documented peripheral vascular disease. Additionally, 96 consecutive patients (66+/-12.0 years) undergoing routine exercise stress test for the exclusion of functionally relevant coronary artery disease were defined as controls. It was assumed that in the latter patients no unstable plaque-altering processes were present. Blood samples were drawn before, and 30 min and 3 h after, revascularization in the peripheral vascular intervention group, as well as before, and 30 min and 3 h after, maximum stress testing in the control group, respectively. Ischemia-modified albumin levels were analyzed using the albumin cobalt-binding test. In patients undergoing peripheral vascular intervention, ischemia-modified albumin increased from 116.6+/-19.1 U/ml at baseline to 132.0+/-19.3 U/ml 30 min after intervention (+14.4+/-15.7%, P<0.001) and decreased to 123.5+/-17.8 U/ml 3 h later (-5.7+/-10.5%, P<0.001 compared with postintervention, P<0.001 compared with baseline). The control group showed a slight but significant decrease in ischemia-modified albumin from 103.0+/-11.0 to 100.2+/-11.6 U/ml poststress (-2.2+/-11.5%, P<0.05) and returned close to baseline 3 h later (101.8+/-10.3 U/ml, +2.4+/-10.9%, P=NS, compared with poststress and with baseline). For both groups, ischemia-modified albumin showed no correlation with albumin (at baseline P=0.62) and total protein (P=0.67), but significant correlation with creatinine (P=0.04) and C-reactive protein (P=0.02). In addition, ischemia-modified albumin was independent of age, sex, alanine aminotransferase, aspartate aminotransferase, creatine kinase, creatine kinase-MB, cholesterol, and triglycerides. This study showed an increased basal ischemia-modified albumin level in patients with peripheral vascular disease undergoing peripheral vascular intervention. Ischemia-modified albumin levels transiently increased shortly after peripheral vascular intervention, indicating a strong correlation between serum concentration of ischemia-modified albumin and processes associated with acute plaque disruption/rupture.
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PMID:Effects of peripheral vascular intervention on ischemia-modified albumin. 1762 87

The purpose of the study was to develop a procedure for predicting a relapse of herpetic keratitis in children, by taking into account the results of tear biochemical analysis. The tears from 47 children with herpetic keratitis were examined for the levels of total protein, the concentration of acute-phase proteins, such as orosomucoid and C-reactive protein, the activities of transferases: gamma-glutamyltranspeptidase transferase, aspartate aminotransferase, and alanine aminotransferase, those of lysosomal glycosidases: alpha-mannosidase, beta-glycosidase, and beta-glucuronidase. Tear biochemical assay made it possible to evaluate the efficiency of treatment and to develop a procedure for predicting a recurrence of herpetic keratitis in children. Determination of the tear activity of the glycosidases may be used to predict recurrent herpetic keratitis in children.
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PMID:[Use of tear enzyme assay to predict recurrent herpetic keratitis in children]. 1780 56

The effects of electroconvulsive therapy (ECT) on serum levels of the acute-phase reactant C-reactive protein (CRP) and intracellular enzymes such as alkaline phosphatase (ALP), lactate dehydrogenase (LDH), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and creatine kinase (CK), have received little attention. If brain cells are damaged, CK-BB, LDH and AST levels are expected to show (minor) elevations. We measured serum levels of prolactin, AST, ALT, LDH, ALP, CK and CRP before and 5 min, 30 min, 4 h, 1 day, 2 days, and 3 days after ECT in 15 consecutive patients (eight women and seven men; mean 53.9 years old, range 3082) who did not receive ECT in the preceding 2 weeks. Prolactin levels increased (P = 0.001), but none of the other mean concentrations significantly increased over time. All concentrations remained within the normal range in every patient, except for five samples with elevated CK levels (range 333-675 IU/l). CK-MB and CK-BB fractions, however, remained low, indicating that skeletal muscle was the source of the CK elevation. Serum levels of markers of brain cell leakage and inflammation remained low following one ECT session, suggesting that ECT does not cause direct brain cell leakage, nor an inflammatory response.
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PMID:Serum markers of brain-cell damage and C-reactive protein are unaffected by electroconvulsive therapy. 1785 85

Increased hepatic abnormality has been observed in patients with systemic lupus erythematosus (SLE) and contributes to the elevated apoptosis that results in severe disease activity. Since cystamine has been demonstrated to be beneficial for NZB/W F1 mice, this study investigates the effects of cystamine on various inflammatory and stress-related proteins in liver from NZB/W F1 mice. Nephelometric analyses and immunoblots were conducted to detect aspartate aminotransferase (AST), alanine aminotransferase (ALT), C-reactive protein (CRP), p53, p21, Gadd45, heat shock protein 70 (HSP70) and cyclooxygenase-2 (COX-2). AST and ALT were reduced in NZB/W F1 mice that were given cystamine and CRP, p53, p21, Gadd45, HSP70 and COX-2 proteins in the liver were reduced in NZB/W F1 mice that were treated with cystamine. Moreover, cystamine has no obvious effect on BALB/c mice. These findings suggest that cystamine reduces the inflammation in liver of NZB/W F1 mice and provide a clue in treatment of SLE with liver abnormality.
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PMID:Transglutaminase inhibitor cystamine alleviates the abnormality in liver from NZB/W F1 mice. 1803 33

Lipocalin-2 (also known as neutrophil gelatinase-associated lipocalin [NGAL]) has been described as a promising marker of metabolic syndrome associated with inflammation. The aim of our work was to develop an assay for the determination of lipocalin-2 in human serum and to investigate its levels in healthy volunteers and donors suffering from metabolic syndrome. We also conducted a pilot study on individuals with metabolic syndrome and on healthy probands and measured lipocalin-2 in these individuals. We developed and evaluated the sandwich ELISA method for the quantitative determination of human lipocalin-2 in serum samples. We measured blood pressure, waist circumference, serum cholesterol, triglycerides, HDL cholesterol, LDL cholesterol, insulin, glucose, creatinine, hs-CRP, and adiponectin and calculated the BMI and Quicki insulin sensitivity index. In the study on 153 healthy volunteers, we showed that sex and age are not determinative for lipocalin-2 serum values. Furthermore, we tested 45 individuals with metabolic syndrome; values of lipocalin-2 did not differ (78.8 vs. 80.0 microg/l, p =0.56) from the data of healthy individuals from the first study. Neither group differed with regard to sex or age. Lipocalin-2 correlated with alanine aminotransferase (ALT) (r=-0.3, p<0.01) aspartate aminotransferase (AST) (r=-0.3, p<0.01), cholesterol (r=-0.21, p=0.047), creatinine (r=0.19, p=0.05), and high-sensitivity C-reactive protein (hs-CRP) (r=0.22, p=0.036). No significant correlation was found between serum lipocalin-2 and BMI, waist circumference, blood pressure, triglycerides, HDL, Quicki, or the number of metabolic syndrome components. When study patients with metabolic syndrome were further stratified according to the number of components of metabolic syndrome, serum concentrations of lipocalin-2 did not differ. The results presented demonstrate the analytical competence of the lipocalin-2 assay. However, we assumed that lipocalin-2 is not a routinely usable marker of metabolic syndrome or obesity. The association between serum lipocalin-2 and obesity or metabolic syndrome was not validated in our study.
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PMID:Lipocalin-2: development, analytical characterization, and clinical testing of a new ELISA. 1839 69

Enterohemorrhagic Escherichia coli (EHEC) induces hemorrhagic colitis and hemolytic uremic syndrome (HUS). Morbidity and mortality are increased in HUS patients with neurologic complications. To determine the pathogenesis of the central nervous system (CNS) involvement in HUS by EHEC, we determined the serum concentrations of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), soluble TNF receptor 1 (sTNFR1), IL-10, interferon-gamma (IFN-gamma), IL-2, IL-4, soluble E-selectin (sE-selectin), matrix metalloproteinase-9 (MMP-9), and tissue inhibitor of metalloproteinase-1 (TIMP-1) during the acute stage in children with HUS with or without CNS involvement. Serum concentrations of IL-6, IL-10, sTNFR1, sE-selectin, MMP-9, and TIMP-1, but not TNF-alpha, IFN-gamma, IL-2, or IL-4, were significantly higher in patients with HUS with encephalopathy compared with controls. Serum IL-6, sTNFR1 and TIMP-1 concentrations were significantly higher in patients with HUS with encephalopathy compared with those with HUS without encephalopathy (P=0.031, P=0.005, and P=0.007, respectively) and those with acute colitis without HUS (P=0.011, P<0.001, and P=0.005, respectively). There were no significant differences in hemoglobin, platelet counts, leukocyte counts, or serum concentrations of IL-10, sE-selectin, MMP-9, aspartate aminotransferase, lactate dehydrogenase, blood urea nitrogen, creatinine, or C-reactive protein between the HUS patients with and without encephalopathy. Our preliminary study suggests that serum IL-6, sTNFR1 and TIMP-1 levels, particularly sTNFR1 and TIMP-1, are important for predicting neurological complications in patients with HUS.
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PMID:Soluble tumor necrosis factor receptor 1 and tissue inhibitor of metalloproteinase-1 in hemolytic uremic syndrome with encephalopathy. 1841 Sep 71

Approximately 15-20% of patients with Kawasaki disease (KD) are not responsive to high-dose intravenous gammaglobulin (IVIG). We have previously reported a predictive method for identifying IVIG-non-responsive patients (high-risk KD patients). We determined the safety and effectiveness of pulse methylprednisolone with high-dose IVIG (mPSL+IVIG) as a primary treatment for high-risk KD patients. Sixty-two high-risk KD patients were treated with pulse methylprednisolone 30 mg/kg over 2 h, followed by IVIG 2 g/kg over 24 h (mPSL+IVIG group) and were compared with a historical control group of 32 high-risk patients treated with IVIG 2 g/kg alone at the participating hospitals before this study was opened (IVIG group). High-risk patients were identified with at least two of three predictors (C-reactive protein >or=7 mg/dL, total bilirubin >or=0.9 mg/dL or aspartate aminotransferase >or=200 IU/L). Sixty-six percent (95% confidence interval [CI] 54-78%) of patients had a prompt defervescence in the mPSL+IVIG group compared with 44% (95% CI 26-62%) for the IVIG group (p=0.048). Coronary artery lesions were observed in 24.2% (95% CI 13.2-35.2%) and 46.9% (95% CI 28.6-65.2%) of patients in the mPSL+IVIG and IVIG groups, respectively (p=0.025). This is the first report showing that mPSL+IVIG is effective and safe as a primary treatment for high-risk KD patients.
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PMID:Pulse methylprednisolone with gammaglobulin as an initial treatment for acute Kawasaki disease. 1844 65

It has been previously reported that serum levels of 70-kDa heat-shock protein (Hsp70) are elevated in preeclampsia. The aim of the present study was to examine whether increased serum Hsp70 levels are related to clinical characteristics and standard laboratory parameters of preeclamptic patients, as well as to markers of inflammation (C-reactive protein), endothelial activation (von Willebrand factor antigen) or endothelial injury (fibronectin), trophoblast debris (cell-free fetal DNA) and oxidative stress (malondialdehyde). Sixty-seven preeclamptic patients and 70 normotensive, healthy pregnant women were involved in this case-control study. Serum Hsp70 levels were measured with enzyme-linked immunosorbent assay (ELISA). Standard laboratory parameters (clinical chemistry) and C-reactive protein (CRP) levels were determined by an autoanalyzer using the manufacturer's kits. Plasma von Willebrand factor antigen (VWF:Ag) levels were quantified by ELISA, and plasma fibronectin concentration by nephelometry. The amount of cell-free fetal DNA in maternal plasma was determined by quantitative real-time polymerase chain reaction analysis of the sex-determining region Y gene. Plasma malondialdehyde levels were measured by the thiobarbituric acid-based colorimetric assay. Serum Hsp70 levels were increased in preeclampsia. Furthermore, serum levels of blood urea nitrogen, creatinine, bilirubin and CRP, serum alanine aminotransferase and lactate dehydrogenase (LDH) activities, as well as plasma levels of VWF:Ag, fibronectin, cell-free fetal DNA and malondialdehyde were also significantly higher in preeclamptic patients than in normotensive, healthy pregnant women. In preeclamptic patients, serum Hsp70 levels showed significant correlations with serum CRP levels (Spearman R = 0.32, p = 0.010), serum aspartate aminotransferase (R = 0.32, p = 0.008) and LDH activities (R = 0.50, p < 0.001), as well as with plasma malondialdehyde levels (R = 0.25, p = 0.043). However, there was no other relationship between serum Hsp70 levels and clinical characteristics (age, parity, body mass index, blood pressure, gestational age, fetal birth weight) and laboratory parameters of preeclamptic patients, including markers of endothelial activation or injury and trophoblast debris. In conclusion, increased serum Hsp70 levels seem to reflect systemic inflammation, oxidative stress and hepatocellular injury in preeclampsia. Nevertheless, further studies are required to determine whether circulating Hsp70 plays a causative role in the pathogenesis of the disease.
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PMID:Increased serum heat-shock protein 70 levels reflect systemic inflammation, oxidative stress and hepatocellular injury in preeclampsia. 1868 14


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