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:3.5.4.4 (adenosine deaminase)
5,136 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The adenosine deaminase (ADA), lysozyme (LZM) and lactate dehydrogenase (LDH) of serum and cerebrospinal fluid (CSF) were determined in 36 patients with tuberculous meningitis (TBM), 47 patients with non-tuberculous meningitis (N-T-BM) and 20 patients with non-central nervous system diseases(control group). The results showed that the assessment of serum and CSF ADA and LZM activity may be helpful to the differential diagnosis between TBM and N-TBM.
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PMID:[The activities of 3 enzymes in serum and cerebrospinal fluid for diagnosis of tuberculous meningitis]. 840 61

We selected the common shrew (Sorex araneus) to generate the first insectivore gene map. Shrew-Chinese hamster and shrew- mouse somatic cell hybrid cells were constructed. When the 119 shrew-rodent clones were characterized, only shrew chromosomes were found to have segregated. A panel of hybrid clones was selected for gene assignment. The genes for hypoxanthine phosphoribosyl transferase (HPRT), glucose-6- phosphate dehydrogenase (G6PD), and malate dehydrogenase 1 (MDH1) were assigned to shrew Chromosome (Chr) de [which is the product of a tandem fusion between the 'original' mammalian X Chromosome (Chr) and an autosome], the gene for adenosine deaminase (ADA) and 6-phosphogluconate dehydrogenase se (PGD) to Chromosome jl, the gene for thymidine kinase (TK) to Chromosome hn, and the gene for lactate dehydrogenase (LDHA) to chromosome ik. Further studies in progress.
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PMID:Gene mapping in the common shrew (Sorex araneus; Insectivora) by shrew-rodent cell hybrids: chromosome localization of the loci for HPRT, TK, LDHA, MDH1, G6PD, PGD, and ADA. 859 34

When a patient with an undiagnosed pleural effusion is evaluated, the first question to answer is whether the patient has a transudate or an exudate. This is best done using Light's criteria, but these criteria occasionally misidentify a transudate as an exudate. If the patient's pleural fluid meets exudative criteria, but the patient appears clinically to have a transudative effusion, then the serum-pleural fluid albumin gradient should be measured. If this is greater than 1.2 g-dL-1, the patient probably does have a transudative effusion. If the patient has an exudative pleural effusion, additional tests are indicated to determine the aetiology of the effusion. The gross appearance and the odour of the pleural fluid should be noted and samples of all exudates should be sent for bacterial cultures. Laboratory tests that are useful in the differential diagnosis of exudative pleural effusions include: differential white cell count of the pleural fluid; cytology of the pleural fluid; and levels of adenosine deaminase, glucose, amylase and lactate dehydrogenase in the pleural fluid. If pleural tuberculosis is suspected, a needle biopsy of the pleura is indicated. Thoracoscopy is very efficient at diagnosing malignant pleural effusion and tuberculosis pleuritis, but rarely establishes any other diagnosis.
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PMID:Diagnostic principles in pleural disease. 904 52

Diagnosis of pleural effusion is difficult in children. The etiologies are numerous; however, infectious agents are more frequent. Thoracocentesis proves to be the first-line diagnostic tool. Light's criteria are the best for distinguishing whether the effusion is a transudate or an exudate. If the patient has an exudative pleural effusion, other tests are indicated to determine the etiology and in some cases the treatment: macroscopic appearance, cytology and differential white cell count (level of glucose, lactate dehydrogenase, adenosine deaminase, pH, bacterial cultures). Others investigations--biopsy of pleura by thoracoscopy or video-assisted thoracoscopy, bronchofibroscopy, CT scan--are sometimes useful. Intrapleural instillation of urokinase appears to be useful and safe. Evaluation is necessary for video-assisted thoracoscopy used early.
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PMID:[Pleurisy: diagnostic and therapeutic management]. 1079 45

This review summarizes current strategies in the treatment of patients with pleural effusion. To determine whether a patient has a transudative or exudative pleural effusion, Light's criteria should be applied to measure the concentrations of protein and lactate dehydrogenase (LDH) in the pleural fluid and serum. If the effusion is transudative, therapy should be directed toward the underlying congestive heart failure, cirrhosis, or nephrosis. Consideration should be given to pleurodesis with a sclerosant if patients with recurrent transudative effusion have severe dyspnea due to their effusion. If the effusion is exudative, attempts should be made to define the etiology. The diagnosis of pleural malignancy is most easily established via pleural fluid cytology. If this is negative and the patient is suspected of having pleural malignancy, thoracoscopy is indicated. The concentrations of adenosine deaminase and gamma-interferon in pleural fluid are useful in the diagnosis of pleural tuberculosis. Patients with pneumonia and pleural effusion should undergo therapeutic thoracentesis; the pleural fluid should be Gram-stained and cultured, and the differential cell count, glucose and LDH concentration, and pH should be determined. Indicators of a poor prognosis include the presence of frank pus, a positive Gram-stain, a pleural glucose concentration of less than 2.2 mmol/L, a pH less than 7.00, the presence of pleural loculations, and an LDH concentration greater than three times the upper limit of normal in serum. If the pleural fluid cannot be completely evacuated because of loculations, intrapleural thrombolytic therapy should be considered. If thrombolytics are ineffective, thoracoscopy or thoracotomy with decortication should be performed. Dyspneic patients with malignant pleural effusions whose dyspnea is relieved with therapeutic thoracentesis should be considered for pleurodesis using a tetracycline derivative. Talc is not recommended because it induces acute respiratory distress syndrome in about 5% of patients, with an overall mortality of 1%.
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PMID:Management of pleural effusions. 1092 61

Adenosine (ADO) is a well-known regulator of a variety of physiological functions in the heart. In stress conditions, like hypoxia or ischemia, the concentration of adenosine in the extracellular fluid rises dramatically, mainly through the breakdown of ATP. The degradation of adenosine in the ischemic myocytes induced damage in these cells, but it may simultaneously exert protective effects in the heart by activation of the adenosine receptors. The contribution of ADO to stimulation of protective effects was reported in human and animal hearts, but not in rat hearts. The aim of this study was to evaluate the role of adenosine A1 and A3 receptors (A1R and A3R), in protection of isolated cardiac myocytes of newborn rats from ischemic injury. The hypoxic conditions were simulated by exposure of cultured rat cardiomyocytes (4-5 days in vitro), to an atmosphere of a N2 (95%) and CO2 (5%) mixture, in glucose-free medium for 90 min. The cardiotoxic and cardioprotective effects of ADO ligands were measured by the release of lactate dehydrogenase (LDH) into the medium. Morphological investigation includes immunohistochemistry, image analysis of living and fixed cells and electron microscopy were executed. Pretreatment with the adenosine deaminase considerably increased the hypoxic damage in the cardiomyocytes indicating the importance of extracellular adenosine. Blocking adenosine receptors with selective A1 and A3 receptor antagonists abolished the protective effects of adenosine. A1R and A3R activation during the hypoxic insult delays onset of irreversible cell injury and collapse of mitochondrial membrane potential as assessed using DASPMI fluorochrom. Cardioprotection induced by the A1R agonist, CCPA, was abolished by an A1R antagonist, DPCPX, and was not affected by an A3R antagonist, MRS 1523. Cardioprotection caused by the A3R agonist, Cl-IB-MECA, was antagonized completely by MRS 1523 and only partially by DPCPX. Activation of both A1R and A3R together was more efficient in protection against hypoxia than by each one alone. Our study indicates that activation of either A1 or A3 adenosine receptors in the rat can attenuate myocyte injury during hypoxia. Highly selective A1R and A3R agonists may have potential as cardioprotective agents against ischemia or heart surgery.
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PMID:Cardioprotective effects of adenosine A1 and A3 receptor activation during hypoxia in isolated rat cardiac myocytes. 1126 59

Biochemical examination of pleural fluid is usually done to try to identify the cause of a pleural effusion. The various analytes that have been suggested for this are reviewed and evaluated. Distinguishing whether the effusion is an exudate or transudate is a pragmatic first step. with further investigations dictated by the clinical features and these results. Total protein and lactate dehydrogenase were used first; Light's criteria were published in 1972 and since then additional markers including cholesterol, bilirubin and albumin gradient plus combinations of these have been proposed. Although combination testing does improve the sensitivity for diagnosis of an exudate. this is at the expense of specificity. Measurement of fluid to serum ratios appears to confer no advantage, and if a single test is required total protein performs as well as any. Additional tests may be useful in specific circumstances: pleural fluid pH may aid decisions over drainage of a parapneumonic effusion; glucose may indicate an effusion associated with rheumatoid arthritis; and adenosine deaminase may help with the diagnosis of tuberculous effusions.
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PMID:Biochemical analysis of pleural fluid: what should we measure? 1147 71

The aim of this study was to define the number of pleural biopsy samples necessary for optimum diagnostic performance and determine to what extent they are complementary. Eighty-four closed pleural biopsies were performed in our department between June 1996 and January 1998 on 55 males and 29 females with an average age of 64.4 +/- 16.7 years. The study of the pleural fluid included: pH, biochemical testing of pleura/serum (proteins, lactate dehydrogenase, glucose, cholesterol, triglycerides, albumin and adenosine deaminase), haemogram, cytology and microbiological testing (Gram-staining, aerobes, anaerobes and mycobacteriae cultures). The biopsies were performed using a Cope needle, with a total of five biopsies for each patient: four for pathological examination (taken numerically in the order in which they were performed: D1, D2, D3 and D4) and one for microbiological testing. In those cases in which the diagnosis was uncertain or effusion persisted, a thoracoscopy or thoracotomy was performed. There were no significant differences in the diagnostic yield of each individual sample (D1, D2, D3 and D4), but there were differences in the sum of the samples, depending on the number of biopsies performed.This was true for total group and the group with carcinomas, but not for the group with tuberculosis. The increase in diagnostic yield with the number of biopsies was more remarkable in the carcinoma cases, where it increased by 35% when four biopsies were performed (54% with one biopsy versus 89% with four biopsies, P < 0.002). In conclusion, the diagnostic yield increased with the number of biopsy samples in the total group and the group with malignancy but not in the group with tuberculous effusions. The best diagnostic performance for malignant pathology was obtained with four samples. In pleural tuberculosis, the diagnostic yield did not increase with more biopsy samples. One high quality sample should be enough to obtain a diagnosis.
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PMID:Determining the optimal number of specimens to obtain with needle biopsy of the pleura. 1186 4

The level of adenosine deaminase (ADA; EC 3.5.4.4) was estimated at different passages in six confluent fibroblast cultures established from forearm skin biopsies of healthy adult normal volunteers. After determination of the zinc concentration in standard growth medium, ADA activity was estimated at different passages of subculture in media with different zinc concentrations. The results indicated that the specific activity of ADA in control confluent skin fibroblast cultures (passage 2) cultivated in standard growth medium containing 15.4 microM zinc (similar to that present in normal human plasma) was equal to 226.6+/-19.64 micromol min(-1) mg(-1) protein. The results showed that there were no significant changes in ADA specific activity in any of the control cultures as the zinc concentration of the medium was increased. To characterize the passage of subculture at which fibroblasts enter the ageing phase, three marker enzymes were assayed namely, phosphofructokinase, lactate dehydrogenase and glycogen phosphorylase. The result showed that the cells enter the ageing phase at passage 20 and beyond. Further investigation showed that ADA activity of serially subcultured confluent cultures cultivated in standard growth medium significantly dropped at passages 20, 25 and 30. ADA activity however was not significantly altered in cells at passage 2, 10 and 15 cultivated in standard growth medium and in the presence of higher zinc levels (23.1, 34.6, 53.8 and 73.1 microM). Furthermore there was significant lowering of ADA activities in cells at passages 20, 25 and 30 when cells were cultured in the presence of 15.4, 23.1 and 34.6 microM zinc. Such lowered activities of ADA were restored to normal when the cells were cultured in the presence of higher zinc concentration equal to 53.8 and 73.1 microM. From the results we concluded that it is possible to restore ADA activity in aged skin fibroblasts to normal levels by raising the zinc concentration in the culture medium to four or five times the control normal plasma zinc level.
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PMID:Changes in adenosine deaminase activity in ageing cultured human cells and the role of zinc. 1291 Apr 82

Among the extrapulmonary presentations of tuberculosis, pleural tuberculosis is the second most frequent. Failure to diagnose and treat pleural tuberculosis can result in progressive disease with involvement of other organs in as many as 65% of patients. Conventional methods such as direct examination of pleural fluid, pleural fluid culture and pleural biopsy have proven to be insufficient for diagnoses of pleural tuberculosis. In this study, we examined a statistical method by combining the diagnostic efficiency of adenosine deaminase activity, pleural fluid protein, lactate dehydrogenase and cellular components in patients with tuberculous pleural effusions. Eighty eight patients over 12 years of age presenting with pleural effusions were included. A positive result by either three of the methods was considered to be indicative of a positive diagnosis of pleural tuberculosis. The determination of adenosine deaminase activity, lactate dehydrogenase levels, and lymphocyte to neutrophil ratio in the pleural fluid yielded a sensitivity of 100% for pleural tuberculosis. A patient was considered positive if any of the three tests was positive, with a specificity of 100%. A positive diagnosis was made when all three tests were positive. Similarly, these different approaches to the combination of pleural adenosine deaminase and lactate dehydrogenase result in sensitivity and specificity of 91.4% and 100% respectively.
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PMID:Simple method for rapid diagnosis of tuberculosis pleuritis: a statistical approach. 1497 37


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