Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0262471 (ENT)
 5,307 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tonsillectomies are the most frequently performed ENT surgical procedures and are potentially beset with a number of possible complications. Post-operative secondary hemorrhage still remains the most frequent complication despite improvements in surgical techniques and preoperative diagnostic evaluations. Besides unsuitable operative techniques, disturbances of circulation and wound infections, disturbances of hemostasis may play an important part. The objective of this paper was to examine the relative frequency of platelet functional disorders as a possible cause for secondary hemorrhage after tonsillectomies. In the past, most of these have been related to medication use. Eighty-nine patients were studied and historically showed no predisposition increased hemorrhage per se or in their families or gave reasons for other factors favoring secondary hemorrhage. The diminution or lack of collagen or ADP-induced agglutination served as an indication for a platelet functional disorder. Ten percent of the 89 patients experienced secondary hemorrhage, with platelet functional disorders proved in 40% of these patients. Because of these results a correlation was attempted between secondary hemorrhage and abnormal deficits of collagen and ADP-induced agglutinations in platelet functional tests, but this was not found. Necessary preoperative studies was attempted screening for hemostasis as well as medico-legal aspects connected with the prescription of medicines inhibiting platelet agglutination, especially use of acetylsalicylic acid before tonsillectomies, are discussed.
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PMID:[Disorders of thrombocyte function as a cause of postoperative hemorrhage after tonsillectomy]. 775 99

In C6 glioma cells, adenine nucleotides, especially AMP, and adenosine inhibited cell proliferation in time- and concentration-dependent manners. alpha,beta-methylene-ADP, an ecto-5'-nucleotidase inhibitor, suppressed the hydrolysis of AMP and reversed the inhibition of cell growth induced by AMP but not by adenosine. Adenosine deaminase eliminated both AMP- and adenosine-mediated growth inhibitions. 5'-N-ethylcarboxamidoadenosine, an adenosine receptor agonist, had little effect on the cell growth. Equilibrative nucleoside transporters, ENT-1 and ENT-2, were expressed in C6 cells by determining their mRNAs. ENT inhibitors, nitrobenzylthioinosine and dipyridamole, suppressed the uptake of [(3)H]adenosine into C6 cells, and attenuated AMP- or adenosine-mediated growth inhibition. Furthermore, an adenosine kinase inhibitor 5-iodotubercidin reversed the growth inhibition induced by AMP and adenosine. When uridine was added in the extracellular space, AMP- or adenosine-induced cell growth inhibition was completely reversed, suggesting that intracellular pyrimidine starvation would be involved in their cytostatic effects. These results indicate that extracellular adenine nucleotides inhibit C6 cell growth via adenosine, which is produced by ecto-nucleotidases including CD73 at the extracellular space and then incorporated into cells by ENT2. Intracellular AMP accumulation by adenosine kinase after adenosine uptake would induce C6 cell growth inhibition through pyrimidine starvation.
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PMID:Adenosine uptake-dependent C6 cell growth inhibition. 1787 54