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)

Autoregulatory adjustments in the caliber of cerebral arterioles were studied in anesthetized cats equipped with cranial windows for the direct observation of the pial microcirculation. Increased venous pressure caused slight, but consistent, arteriolar dilation, at normal and at reduced arterial blood pressure and irrespective of whether or not intracranial pressure was kept constant or allowed to increase. Arterial hypotension caused arteriolar dilation which was inhibited partially by perfusion of the space under the cranial window with artificial CSF equilibrated with high concentrations of oxygen. This vasodilation was inhibited to a greater extent by perfusion of the space under the cranial window with fluorocarbon FC-80, equilibrated with high concentrations of oxygen. CSF or fluorocarbon equilibrated with nitrogen did not influence the vasodilation in response to arterial hypotension. The response to increased venous pressure was converted to vasoconstriction when fluorocarbon equilibrated with high concentrations of oxygen was flowing under the cranial window. The vasodilation in response to arterial hypotension was inhibited by topical application of adenosine deaminase. The results show that both metabolic and myogenic mechanisms play a role in cerebral arteriolar autoregulation. Under normal conditions, the metabolic mechanisms predominate. The presence of the myogenic mechanisms may be unmasked by preventing the operation of the metabolic mechanisms. The major metabolic mechanism seems to be dependent on changes in PO2 within the brain with secondary release of adenosine.
 ...
PMID:Oxygen-dependent mechanisms in cerebral autoregulation. 403 62

The purpose of this study was to investigate the possible importance of adenosine in cerebrocortical vasodilatation accompanying brain activation (epileptic seizures and direct electrical stimulation) and hypoxia (arterial hypoxia and cyanide poisoning of the brain cortex). In chloralose-anesthetized cats a circumscribed area of the brain cortex was treated with adenosine deaminase (Type III; Sigma), which potently deaminates adenosine to the nonvasoactive inosine. Cerebrocortical vascular volume and fluorescence of reduced nicotinamide adenine dinucleotide were measured in vivo by surface fluororeflectometry. The responses of small pial and intracortical vessels to brain activation and hypoxia were studied in brain cortices superfused with artificial (mock) CSF and 5 U/ml adenosine deaminase. It was found that superficially applied adenosine deaminase readily diffuses onto the brain cortex. Prolonged pretreatment of the brain cortices with 0.025 U/ml adenosine deaminase eliminated almost completely the vasodilative effect of 10(-7) mol/ml adenosine. The inhibitory effect of the enzyme on adenosine-induced cortical vasodilatation was specific, because 5 U/ml adenosine deaminase did not attenuate the vasodilative potency of 10(-8) mol/ml 2-chloroadenosine. Adenosine deaminase (5 U/ml) pretreatment of the brain cortices did not diminish the cerebrocortical vascular volume, which increased with arterial hypoxia, topical cyanide poisoning, and direct electrical stimulation. However, it slightly decreased the vasodilative effect of epileptic seizures. On the basis of these results, it seems very unlikely that adenosine is a critical factor in the control of cerebrovascular tone during arterial hypoxia and brain activation.
 ...
PMID:Effect of topical adenosine deaminase treatment on the functional hyperemic and hypoxic responses of cerebrocortical microcirculation. 647 59

Bromide partition tests were performed on 58 children with suspected tuberculous meningitis (TBM). CSF adenosine deaminase activity (ADA) was measured at the same time. Four of the 33 patients with a final diagnosis of TBM had false-negative bromide partition ratios and 5 had false-negative CSF ADA levels. One of the 25 patients in whom TBM was excluded had a false-positive ratio and 4 had false-positive CSF ADA levels. The difference between the two tests was not significant. Both provide valuable evidence for or against a diagnosis of TBM.
 ...
PMID:The bromide partition test and CSF adenosine deaminase activity in the diagnosis of tuberculosis meningitis in children. 711 20

We assayed 229 CSF samples from 180 adults with meningitis of different etiologies for adenosine deaminase activity (ADA) and evaluated the usefulness of this assay in the differential diagnosis of aseptic meningitis. Cases of meningitis were classified as tuberculous meningitis (TBM), pyogenic meningitis, viral meningitis, self-resolving aseptic meningitis without a specific diagnosis, meningitis associated with other infections, and neoplastic meningitis. We also tested 117 CSF specimens for which parameters were normal. We chose a cutoff point of 10 IU/L on the basis of our results and found elevated ADA levels in 50% of the patients with TBM (no differences between patients with AIDS and those who did not have AIDS were observed). Among samples from patients with aseptic meningitis, we observed high ADA levels in only two of five of the patients with neurobrucellosis. Therefore, we concluded that in cases of aseptic meningitis, a CSF ADA level of > or = 10 IU/L has a sensitivity of 48%, a specificity of 100%, a positive predictive value of 1, and a negative predictive value of 0.91 as a diagnostic criterion for TBM or neurobrucellosis. ADA levels were also > 10 IU/L in 30% of the patients with pyogenic meningitis, but this diagnosis was easily excluded on other grounds.
 ...
PMID:Adenosine deaminase activity in the CSF of patients with aseptic meningitis: utility in the diagnosis of tuberculous meningitis or neurobrucellosis. 775 71

Previously, it had been observed that nitric oxide (NO) contributes to hypoxia-induced pial artery dilation in the newborn pig. Additionally, it was also noted that activation of ATP-sensitive K+ channels (KATP) contribute to cGMP-mediated as well as to hypoxia-induced pial dilation. Although somewhat controversial, adenosine is also thought to contribute to hypoxic cerebrovasodilation. The present study was designed to investigate the role of NO, cyclic nucleotides, and activation of KATP channels in the elicitation of adenosine's vascular response and relate these mechanisms to the contribution of adenosine to hypoxia-induced pial artery dilation. The closed cranial window technique was used to measure pial diameter in newborn pigs. Hypoxia-induced artery dilation was attenuated during moderate (PaO2 approximately 35 mm Hg) and severe hypoxia (PaO2 approximately 25 mm Hg) by the adenosine receptor antagonist 8-phenyltheophylline (8-PT) (10(-5) M) (26 +/- 2 vs. 19 +/- 2 and 34 +/- 2 vs. 22 +/- 2% for moderate and severe hypoxia in the absence vs. presence of 8-PT, respectively). This concentration of 8-PT blocked pial dilation in response to adenosine (8 +/- 2, 16 +/- 2, and 23 +/- 2 vs. 2 +/- 2, 4 +/- 2, and 6 +/- 2% for 10(-8), 10(-6), and 10(-4) M adenosine before and after 8-PT, respectively). Similar data were also obtained using adenosine deaminase as a probe for the role of adenosine in hypoxic pial dilation. Adenosine-induced dilation was associated with increased CSF cGMP concentration (390 +/- 11 and 811 +/- 119 fmol/ml for control and 10(-4) M adenosine, respectively). The NO synthase inhibitor, L-NNA, and the cGMP antagonist, Rp 8-bromo cGMPs, blunted adenosine-induced pial dilation (8 +/- 1, 14 +/- 1, and 20 +/- 3 vs. 3 +/- 1, 5 +/- 1, and 8 +/- 3% for 10(-8), 10(-6), and 10(-4) M adenosine before and after L-NNA, respectively). Adenosine dilation was also blunted by glibenclamide, a KATP antagonist (9 +/- 2, 14 +/- 3, 21 +/- 4 vs. 4 +/- 1, 8 +/- 2, and 11 +/- 2% for 10(-8), 10(-6), and 10(-4) M adenosine before and after glibenclamide, respectively). Finally, it was also observed that adenosine-induced dilation was associated with increased CSF cAMP concentration and the cAMP antagonist, Rp 8-bromo cAMPs, blunted adenosine pial dilation. These data show that adenosine contributes to hypoxic pial dilation. These data also show that NO, cGMP, cAMP, and activation of KATP channels all contribute to adenosine induced pial dilation. Finally, these data suggest that adenosine contributes to hypoxia-induced pial artery dilation via cAMP and activation of KATP channels by NO and cGMP.
 ...
PMID:Role of nitric oxide, cyclic nucleotides, and the activation of ATP-sensitive K+ channels in the contribution of adenosine to hypoxia-induced pial artery dilation. 897 92

The aim of this work was to study the usefulness of CSF adenosine deaminase determination in the diagnosis of tuberculous meningitis and determine if the proposed cutoff value of 7.1 i.u./ml had the better sensitivity and specificity. We retrospectively studied 148 patients, 12 with tuberculous meningitis and 136 with other central nervous system diseases. Adenosine deaminase values ranged from 3.6 to 31.2 i.u./ml in patients with tuberculous meningitis and from 0.1 to 312 i.u./ml in controls. The best sensitivity/specificity ratio (83.3 and 85.3% respectively) was obtained using a cutoff value of 6.5 i.u./ml. It is concluded that CSF adenosine deaminase values are useful in the diagnosis of tuberculous meningitis and that the cutoff value should be lowered to 6.5 i.u./ml to improve its diagnostic yield.
 ...
PMID:[Usefulness of adenosine deaminase determination in cerebrospinal fluid for the diagnosis of meningeal tuberculosis: 4 years experience at a public hospital]. 933 91

Sixty patients of inflammatory brain disease were diagnosed and classified according to clinico-investigational criteria by Ahuja et al into tuberculous meningitis group (36 patients) and non-tuberculous meningitis group (24 patients). Tuberculous meningitis (TBM) patients were classified as probable (9 patients) and possible (27 patients) TBM. Non-TBM group comprised of pyogenic meningitis (8.3%), viral encephalitis (23.3%), cerebral malaria (5%) and enteric encephalopathy (3.3%). Cerebrospinal fluid-adenosine deaminase (CSF-ADA) activities were measured in both TBM and non-TBM groups. Mean CSF-ADA levels in TBM patients was 9.61 +/- 4.10 IU/L and was significantly elevated as compared to viral encephalitis and enteric encephalopathy cases; but difference was insignificant in comparison to pyogenic meningitis (7.92 +/- 0.95 IU/L) and cerebral malaria. Using 8 IU/L as cut off value for diagnosis of TBM a sensitivity of 44% and specificity of 75% was observed.
 ...
PMID:Evaluation of CSF-adenosine deaminase activity in tubercular meningitis. 1099 88

Tuberculosis (TB) has been described in kidney transplant recipients as an infection with predominantly pulmonary involvement. We report the impact of TB in kidney transplantation. Clinical records of adult kidney recipients, transplanted between 1 January 1986 and 31 December 1995 were analyzed for sex, age, graft origin, immunosuppressive therapy, TB sites, diagnostic methods and concomitant infections. Annual incidence, mean time of onset, relation to rejection treatment, tuberculin skin test (PPD) and outcome were analyzed. Patients with a history of TB or graft loss in the first month were excluded. TB was diagnosed in 14 of 384 (3.64%). Mean age at transplantation was 35 years. Twelve of these received the graft from a living donor. All had triple immunosuppression with cyclosporine. Ten had pulmonary TB, three extrapulmonary infection and one disseminated disease. In 13 cases an invasive diagnostic procedure was performed. Mycobacterium tuberculosis cultures were positive in all cases; microscopy revealed acid-fast bacilli (AFB) in 6, and adenosine deaminase was elevated in CSF and pleural effusion in 2. Annual incidence varied from 0% to 3.1%. At the time of TB presentation 8 patients had other concomitant infections (cytomegalovirus, nocardia, Pneumocystis carinii, disseminated herpes simplex virus). Median time of onset was 13 months. Diagnostic results became available post-mortem in 2 cases, and one had TB in a failing allograft. TB was treated with 4 drugs including rifampin in 10 patients. Cyclosporine was discontinued in one, lowered in one and increased in 8. During treatment 5 patients had rejection episodes. At 1 year, graft survival was 72.7% and patient survival 90.9%. TB was more prevalent when recipient and donor were both PPD positive. In summary: although TB is a growing threat in the transplant setting, early and aggressive diagnosis with meticulous monitoring of immunosuppression allows a successful outcome for both patient and graft. Optimal prophylaxis guidelines have yet to be completely defined.
 ...
PMID:Tuberculosis in renal transplant recipients. 1142 77

We report a 31-year-old man with tuberculous meningitis (TM) mimicking CNS sarcoidosis. Although Mycobacterium tuberculosis (MTB) was not detected in CSF, the level of adenosine deaminase (ADA) in CSF was significantly raised. Brain biopsy showed caseous granuloma and a diagnosis of TM was made. The diagnosis of TM is often difficult and brain biopsy should be considered if MTB is not detected in the CSF. Evaluation of CSF ADA level could also strongly contribute to distinguishing TM from other meningitis. In addition to antituberculosis drugs, corticosteroid therapy was effective in our patient but careful reduction of its dosage was required.
 ...
PMID:Biopsy-proven tuberculous meningitis mimicking CNS sarcoidosis. 1808 24

We describe the development of enterovirus meningoencephalitis associated with increased adenosine deaminase in cerebrospinal fluid of a 12-year-old boy, a known case of hypogamaglobulinemia despite monthly replacement of IVIg.The patient was referred to our center with fever, headache and vomiting for 10 days. CSF analysis was compatible with aseptic meningoencephalitis but high CSF protein (>200mg/dl) and high level of adenosine deaminase in CSF (30IU/L) were against the diagnosis of simple viral meningoencephalitis. Nested PCR of CSF for entrovirus was positive. Treatment with daily high-dose IVIg was commenced, with significant clinical improvement. For patients with increased ADA and lymphocytic pleocytosis in CSF, differential diagnoses should include enteroviral meningitis. Antibodies, although crucial, cannot on their own prevent enteroviral infection in some hypogamaglbulinemic patients.
 ...
PMID:A case of hypogammaglobulinemia with enteroviral meningoencephalitis, associated with increased adenosine deaminase in cerebrospinal fluid. 1967 42


1 2 Next >>