Malignant ovine theileriosis: serum concentrations of some inflammatory components and adenosine deaminase activity

2014 ◽  
Vol 24 (3) ◽  
pp. 639-643 ◽  
Author(s):  
S. M. Razavi ◽  
A. Espandarnia ◽  
E. Rakhshandehroo ◽  
M. Ghane ◽  
S. Nazifi
1988 ◽  
Vol 47 (5) ◽  
pp. 394-397 ◽  
Author(s):  
I Ocana ◽  
E Ribera ◽  
J M Martinez-Vazquez ◽  
I Ruiz ◽  
E Bejarano ◽  
...  

2004 ◽  
Vol 341 (1-2) ◽  
pp. 101-107 ◽  
Author(s):  
Mo-Lung Chen ◽  
Wai-Cho Yu ◽  
Ching-Wan Lam ◽  
Kam-Ming Au ◽  
Fuk-Yip Kong ◽  
...  

2007 ◽  
Vol 22 (4) ◽  
pp. 718 ◽  
Author(s):  
Soo Jin Lee ◽  
Han Sung Hwang ◽  
Bit Na Rae Kim ◽  
Min A Kim ◽  
Jae Wook Lee ◽  
...  

Thorax ◽  
1986 ◽  
Vol 41 (11) ◽  
pp. 888-889 ◽  
Author(s):  
J M Martinez-Vazquez ◽  
E Ribera ◽  
I Ocana ◽  
R M Segura ◽  
R Serrat ◽  
...  

1983 ◽  
Vol 244 (3) ◽  
pp. H454-H457
Author(s):  
M. T. Knabb ◽  
R. Rubio ◽  
R. M. Berne

The effects of endogenous adenosine on rat atrial and ventricular slow action potentials (AP) were studied using theophylline, an adenosine receptor antagonist, or "micro" adenosine deaminase (mADA), small polypeptides having adenosine deaminase activity. Exogenous adenosine (10(-6) M) depressed slow APs at low and high isoproterenol concentrations and shifted the isoproterenol dose-response curve to the right in the atrium. In the ventricle, exogenous adenosine inhibited slow APs at low isoproterenol doses and only shifted the bottom of the dose-response relationship to the right. mADA (0.84 U) or theophylline (5 X 10(-5) M) potentiated the response to threshold concentrations of isoproterenol and caused a parallel shift of the curve to the left in the atrium but only shifted the bottom portion of the curve in the ventricle. This potentiation of slow APs in the presence of mADA or theophylline suggests that endogenous adenosine attenuates the response to isoproterenol in cardiac muscle.


2012 ◽  
Vol 64 (2) ◽  
pp. 489-495 ◽  
Author(s):  
G. Stevanovic ◽  
M. Pelemis ◽  
S. Pelemis ◽  
M. Pavlovic

Serum concentrations of adenosine deaminase were determined in 223 febrile patients. In 62, we discovered extrapulmonary tuberculosis. Serum levels of immunoglobulin G were monitored in 287 febrile patients, and 68 had extra-pulmonary tuberculosis. Serum concentrations of adenosine deaminase were significantly higher in patients with tuberculosis compared to other patients with fever of unknown origin. Serum concentrations declined during antituberculosis therapy. A correlation with the localization of infection was not found. Levels of immunoglobulin G were higher in patients with tuberculosis. Both tests had high sensitivity and specificity and could therefore be used for screening extrapulmonary tuberculosis; however, they can only be interpreted adequately following a full clinical investigation.


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