Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.5.4.4 (adenosine deaminase)
 5,136 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Biochemical and cellular characteristics of pleural fluid from two patients with pleuropulmonary tularemia and 39 patients with tuberculous pleurisy were compared. High pleural fluid concentrations of adenosine deaminase, lysozyme, and beta 2-microglobulin occurred in both diseases. As is the case with tuberculous pleural effusions, pleural fluid in tularemia showed an abundance of lymphocytes, predominantly CD4-positive T lymphocytes. The similar pleural fluid findings suggest analogous local pathogenetic mechanisms in tularemia and tuberculosis. In the diagnostic evaluation of a lymphocyte-rich exudative pleural effusion with a high adenosine deaminase concentration, a possible cause to consider is tularemia.
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PMID:Similar pleural fluid findings in pleuropulmonary tularemia and tuberculous pleurisy. 862 Jul 43

A microparticle-enhanced nephelometric immunoassay, based on polystyrene beads coated with antihuman lysozyme antibody, has been developed for lysozyme quantification in sera and pleural effusions. The standard curve extends from 0.58 mg/l to 18.75 mg/l and no antigen effect was observed. The results showed a good serial precision. The intra-assay precision (n = 20) expressed as CV was between 2.2 and 4.2 in three different concentrations. The inter-assay precision, with different calibration curves (n = 12) was between 6.4 and 7.1. The analytical assay showed a sufficient linearity (r > 0.999). There were no interferences either with haemoglobin (up to 4 g/l), lipids (up to 0.5%, expressed as 1% Lipofundina content), or bilirubin (up to 5 mg/dl). The analytical sensitivity was lower than 0.6 mg/l. The correlation with a Micrococcus lysodeikticus turbidimetric assay showed a correlation coefficient of 0.915. We have studied 92 patients with pleural effusion. In each case, pleural fluid adenosine deaminase activity and pleural fluid to plasma lysozyme ratio were determined. The lysozyme ratio showed similar clinical sensitivity and specificity as to adenosine deaminase.
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PMID:Development of a microparticle-enhanced nephelometric immunoassay for quantitation of human lysozyme in pleural effusion and plasma. 1063 99

Serum adenosine deaminase (ADA) activity and lysozyme levels were measured in 51 patients with tuberculosis (21 pulmonary, 15 miliary, 11 neurotuberculoma and four abdominal plus osteoarticular) and 20 healthy controls. The mean serum ADA activity and lysozyme levels were significantly raised in children with different forms of tuberculosis in comparison with controls (p < 0.001). The neurotuberculoma cases had the lowest mean enzyme levels and the differences were significant when compared with other forms of tuberculosis. The cut-off serum ADA activity of > or = 42 IU/l and lysozyme level of > or = 20 U/l were diagnostic of tuberculosis with 100 per cent sensitivity. A significant correlation was observed between the two parameters (r = 0.66; p < 0.001). Thus, with compatible clinical presentation, the raised serum level of either ADA or lysozyme can be used as a supportive diagnostic test.
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PMID:Adenosine deaminase activity and lysozyme levels in children with tuberculosis. 1089 21

To describe the set of mRNA and protein expressed in the salivary glands (sialome) of Aedes aegypti mosquitoes, we randomly sequenced a full-length cDNA library of this insect and performed Edman degradation of PVDF-transferred protein bands from salivary homogenates. We found 238 cDNA clusters which contained those coding for 10 of the 11 proteins found by aminoterminal degradation. All six previously described salivary proteins were found in this library. Full-length sequences of 32 novel cDNA sequences are reported, one of which is the product of a transposable element. Among the 31 novel protein sequences are 4 additional members of the D7 protein family; 4 novel members of the antigen 5 family (a protein family not reported in Aedes); a novel serpin; a novel member of the 30-kDa allergen of Ae. Aegypti; a secreted calreticulin; 2 proteins similar to mammalian angiopoietins; adenosine deaminase; purine hydrolase; lysozyme; a C-type lectin; 3 serine proteases, including one with high similarity to Bombyx prophenoloxidase activating enzyme; 2 proteins related to invertebrate immunity; and several sequences that have no significant matches to known proteins. The possible role of these proteins in blood and sugar feeding by the mosquito is discussed.
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PMID:Toward a description of the sialome of the adult female mosquito Aedes aegypti. 1221 46

Management of patients with tuberculous pleuritis can be improved by establishing early diagnosis accurately, administering effective chemotherapy, and close monitoring of progress for early detection and prompt management of severe pleural inflammation in the hope of preventing or reducing subsequent residual pleural fibrosis. In addition to the conventional diagnostic tools, chemical markers, especially pleural fluid adenosine deaminase and interferon-gamma levels and new microbiological tests such as polymerase chain reaction and BACTEC culture of pleural biopsy specimens for Mycobacterium tuberculosis, can increase the diagnostic yield for tuberculous pleuritis. Indicators of the severity of pleural inflammation, including high pleural fluid tumour necrosis factor-alpha and lysozyme levels, and low pleural fluid glucose and pH, can help to predict residual pleural fibrosis. It is likely that patients will require surgery: (i) complete drainage of pleural fluid for prevention; and (ii) pleurectomy for the treatment of residual pleural fibrosis.
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PMID:Management of tuberculous pleuritis: can we do better? 1582 77

Disorders of the pericardium are commonly associated with pericardial effusion. Its etiology comprises a broad spectrum of diseases including also malignancies. Pericardiocentesis, pericardioscopy and targeted epicardial biopsy with consecutive pericardial fluid and epicardial biopsy analysis by cytology, molecular biology and immunology establish the underlying etiology in the majority of cases. Of particular therapeutic and prognostic importance is the definite differentiation of malignant pericardial effusion from benign pericardial effusion. Biomarkers for cardiovascular diseases can be divided into biochemical, histological, immunologic, serologic and molecular markers as well as imaging biomarkers. Biomarkers have proven to be useful in the diagnosis, differential diagnosis and prognosis of ischemic heart disease and heart failure. With respect to pericardial disorders, a comprehensive approach combining clinical information, imaging biomarkers, biomarkers of pericardial effusion and analysis of epicardial biopsies often leads to the definite etiologic diagnosis of pericardial effusion. Computed tomography and magnetic resonance imaging allow further characterization of the effusion and, of note, also of the surrounding tissue, which is of particular interest in case of malignancies. Biomarkers of pericardial effusion include biochemical markers, autoantibodies, tumor markers, and cytokines. Analysis of pericardial fluid specific gravity, protein level and lactate dehydrogenase (LDH) separates transudates from exsudates. High adenosine deaminase levels (ADA) and low levels of carcinoembryonic antigen (CEA) in the pericardial effusion are observed in tuberculous pericarditis allowing the differentiation from malignant pericardial effusion. Additional markers, such as interferon and lysozyme, have also been suggested for the diagnosis of tuberculous pericarditis. Tumor markers in pericardial fluid have been used to diagnose malignant pericarditis. CEA levels are significantly higher in malignant than benign effusion. By a cutoff level of CEA > 5 ng/ml the diagnostic sensitivity and specificity are 75% and 100%, respectively, in the diagnosis of malignant pericardial effusion. Further analysis of cytokines and mediators, serologic, immunologic and inflammatory markers may help to understand the pathophysiology of the pericardial disease and provide useful diagnostic information.
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PMID:[Differentiation of malignant from nonmalignant, inflammatory pericardial effusions with biomarkers]. 2002 42

Free radicals play an important role in the pathogenesis of tissue damage in many clinical disorders, including atherosclerosis. Antioxidants protect the body from damage caused by free radicals. In this study we investigated oxidative stress, antioxidants and inflammatory molecules in patients with acute myocardial infarction. This study has been carried out on 106 patients with acute myocardial infarction, (89 men and 17 females). The control group consisted of 50 healthy, age-matched subjects (40 men and 10 females). Levels of Glucose, lipid profile, glutathione reduced, glutathione peroxidase, Superoxide dismutase, Glycosylated hemoglobin, fibrinogen, vitamin C, vitamin E, malondialdehyde, ceruloplasmin, adenosine deaminase, lysozyme and sialic acid were measured. Malondialdehyde and ceruloplasmin levels were significantly high and antioxidants such as vitamin C, vitamin E, glutathione reduced, glutathione peroxidase and superoxide dismutase were significantly decreased in diabetic and non-diabetic AMI patients as compared with control (p<0.001). Inflammatory markers showed significant rise in diabetic patients as compared with controls. Our results clearly show increased inflammation and oxidative stress in patients with acute myocardial infarction. Depression of antioxidant system in these patients confirms this conclusion.
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PMID:Antioxidant status in patients with acute myocardial infarction. 2310 51


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