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

Cell transformation is associated with a dramatic collapse of a graphic fingerprint characteristic of normal cells, as measured by phase fluorimetry. This is demonstrated on adenosine deaminase (ADA, EC 3.5.4.4), an established malignancy marker. ADA activity is known to decrease markedly in chick embryo fibroblasts (CEF) transformed by Rous sarcoma virus. The high affinity between the catalytic small subunit ADA (SS-ADA) and its membranal complexing protein (ADCP) (which abounds on the plasma membrane of CEF) allowed the hybridization of fluorescent labeled SS-ADA with native ADCP on CEF. Multifrequency differential phase fluorimetry responded remarkably to the state of this hybrid membrane protein. The transformation process is shown to have led to increased membrane fluidity and rotational mobility of ADCP as well as to its reduced availability to SS-ADA binding. The hypothesis of protein vertical sinking into the lipid core of the membrane is now given support by our spectroscopic data. Additional models are considered. A regulatory role is thus suggested for the complexing protein, which may also account for (a) reduced ADA activity in transformed cells and (b) detachment, exclusive to normal cells, upon addition of SS-ADA in excess.
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PMID:Adenosine deaminase in cell transformation. Biophysical manifestation of membrane dynamics. 284 78

We report 2 cases of pseudochylothorax and review 172 published cases. Tuberculosis is by far the most frequent cause of pseudochylothorax, accounting for 54% of all caes, with a remarkable association with previous collapse therapy and long-term effusions. The remaining etiologies, including rheumatoid arthritis, are infrequent. Tuberculous pseudochylothorax is usually sterile. Successful treatment of an acute tuberculous pleurisy does not preclude the development of long-term complications such as pseudochylothorax. We do not recommend pleural biopsy initially because of its low yield for etiologic diagnosis. Currently, adenosine deaminase (ADA) values in pleural fluid are not useful to sustain diagnosis or therapeutic decisions. We advise draining only symptomatic cases and treating patients with positive Ziehl-Neelsen stain or Lowenstein culture, and those with growing effusions of suspected tuberculous origin, with antituberculous chemotherapy. Pulmonary decortication should be the last therapeutic step for recurrent and symptomatic cases.
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PMID:Pseudochylothorax. Report of 2 cases and review of the literature. 1035 51

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

Not long ago, primary tuberculosis was considered a rare disease; now with an increasing incidence worldwide, physicians should relearn many of its basic aspects and manifestations. Pericarditis is a rare finding seen with tuberculosis, but its prognosis is excellent with treatment, so early diagnosis is crucial. Pathogenesis is particularly important, and it must be taken in consideration when interpreting diagnostic tools. Herein we report on a healthy 32-year-old woman who presents with a 1-month history of febrile illness, malaise, and weakness; more recently, she also had resting dyspnea, which was progressively worsening. A positive PPD and an abnormal chest radiograph prompted hospitalization, where she was found to have pulsus paradoxus of 20 mm Hg. The echocardiogram showed diastolic right chamber collapse along with respiratory variation of the mitral inflow, consistent with pericardial tamponade. A pericardiocentesis was performed with resolution of her resting dyspnea; more than 1000 mL of serous fluid drained from the pericardial space over the following 24 hours. Although sputum and pericardial fluid cultures and smear for AFB and other organisms were negative, as well as a negative pericardial fluid PCR for Mycobacterium tuberculosis DNA; an elevated (44.4 U/L [normal, 0 to 18]) adenosine deaminase level in the pericardial fluid was consistent with the probable diagnosis of tuberculous pericardial effusion. The patient was treated with resolution of the clinical syndrome and no recurrence of the effusion thereafter. Adenosine deaminase, an enzyme marker of cell-mediated immune response activity to M tuberculosis that includes activated T-lymphocytes and macrophages, appears in pericardial fluid. The diagnosis of probable tuberculous effusion can be made without demonstration of mycobacterium.
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PMID:Adenosine deaminase in the diagnosis of tuberculous pericardial effusion. 1879 13