PubMed Health⌕ Search

Biomedical subjects

A Brandts

Publications and source records attributed to A Brandts.

8 recordsLinked to original sources
PubMed2006

The effect of genetic variants in the thrombin activatable fibrinolysis inhibitor (TAFI) gene on TAFI-antigen levels, clot lysis time and the risk of venous thrombosis.

Thrombin activatable fibrinolysis inhibitor (TAFI) is an important inhibitor of fibrinolysis. High TAFI antigen levels are associated with an increased risk of deep venous thrombosis (DVT). Because TAFI levels are partly determined genetically, we assessed the association between three TAFI gene polymorphisms (-438 G/A, 505 A/G and 1040 C/T), TAFI antigen levels and clot lysis times and the risk of DVT. Carriers of the 505G allele, which is associated with lower TAFI antigen levels than the 505A allele, showed an increased risk of DVT. This indicates that the relationship between TAFI and venous thrombosis is more complex than previously suggested.

Adolescent↗
PubMed1998

Non-receptor-mediated activation of IK(ATP) and inhibition of IK(ACh) by diadenosine polyphosphates in guinea-pig atrial myocytes.

1. The effects of diadenosine polyphosphates (APnA, where n = 4-6) were studied on beating frequency of perfused guinea-pig hearts and on muscarinic K+ current (IK(ACh)) and ATP-regulated K+ current (IK(ATP)) in atrial myocytes from guinea-pig hearts using whole-cell voltage clamp. 2. Bradycardia induced by APnA in perfused hearts was completely inhibited by 8-cyclopentyl- 1,3-dipropylxanthine (CPX, 20 microM), a selective antagonist at A1 adenosine receptors, and was augmented by dipyridamole (Dipy), an inhibitor of cellular adenosine (Ado) uptake. 3. Whereas exposure of atrial myocytes to Ado (100 microM) within about 1 s induced a significant whole-cell IK(ACh), APnA up to 1 mM applied for some tens of seconds failed to activate IK(ACh). If present for periods > 2 min, APnA caused inhibition of agonist-evoked IK(ACh) and activation of a weakly inward rectifying K+ current, which was identified as IK(ATP) by its sensitivity to glibenclamide and its current-voltage curve. 4. The actions of extracellular APnA on IK(ACh) and IK(ATP) were mimicked by intracellular loading of compounds via the patch clamp pipette and by intracellular loading of AMP. 5. The results from isolated myocytes exclude APnA acting as A1 agonists. It is suggested that myocytes can take up APnA, which are degraded to AMP. In the presence of ATP, AMP is converted to ADP, a physiological activator of ATP-regulated K+ channels, by adenylate kinase. A similar mechanism resulting in a reduction of the [GTP]/[GDP] ratio might be responsible for inhibition of IK(ACh). 6. In the perfused heart and other multicellular cardiac preparations the actions of APnA are mediated by Ado via A1 receptors. It is suggested that APnA in multicellular cardiac tissue are hydrolysed by an ectohydrolase to yield AMP which is converted to Ado by ectonucleotidases.

Acetylcholine↗
PubMed1992

[10 years of outpatient dental surgery using endotracheal anesthesia. Research report from dental practice].

For certain groups of patients, e.g. handicapped people, children or extremely anxious adults, dental surgery with local anesthesia is not possible and hospitalisation is not desirable. In order to provide outpatient treatment using endotracheal anesthesia, a successful practice-oriented concept is presented, involving cooperation between the dental surgeon and an anesthetist in private practices. In the past 10 years, 4205 patients have received outpatient treatment according to this concept.

Adult↗