Publications by authors named "Thomas Nordt"

Aims: Restenosis in bare-metal stents is in part related to stent design and material. Optimized strut design of cobalt-chrome (CoCr) stents may yield nearly comparable results to drug-eluting stents (DES) in selected lesions. The prospective multicenter DaVinci registry investigates the clinical outcome of a CoCr coronary stent (MULTI-LINK VISION), particularly in terms of patients with diabetes and complex lesions (B1, B2, C).

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  • PAI-1 is a key biomarker linked to cardiovascular risk, mainly produced in fat tissue, and its levels can be influenced by fibrates, which are medications that also help lower lipid levels.
  • Fibrates like gemfibrozil and fenofibrate significantly reduce PAI-1 protein levels in fat cells, indicating their potential role in heart disease prevention through this mechanism.
  • The study suggests that the reduction in PAI-1 expression by fibrates works at the transcriptional level and may help explain their anti-atherosclerotic effects observed in clinical settings.
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Background And Purpose: Computer-assisted teaching and learning tools offer new opportunities for improving education and training of medical professionals. CAMPUS represents a software for computer-based, problem-oriented learning. It is a case-based training system which provides the patient's history within a highly realistic, multimedia format.

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  • Adipose tissue produces plasminogen activator inhibitor type-1 (PAI-1), which is linked to increased cardiovascular risk.
  • Thiazolidinediones, drugs that sensitize insulin, were found to significantly reduce PAI-1 expression in human preadipocytes and adipocytes, except for pioglitazone, which had no effect.
  • The reduction of PAI-1 was mediated through PPAR-gamma signaling and may help patients with insulin resistance lower their cardiovascular risk.
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Background: Due to considerably high rates of reocclusion under standard thrombolytic therapy GP IIb/IIIa inhibitors have been combined with thrombolytics to improve therapeutic outcomes. Potential reasons for arterial reocclusion may be increased platelet activation, interaction of platelets with other cell types such as leukocytes and inadequate drug dosing due to lack of ideal platelet monitoring. We compared combination therapy regimens consisting of GP IIb/IIIa inhibitors and thrombolytics with respect to platelet inhibition and platelet-leukocyte interactions.

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Fibrin targeting of the thrombin inhibitor hirudin via chemical coupling is effective in vitro and in vivo. However, since chemical coupling has limitations, a recombinant approach was taken to improve the fibrin-targeting ability of hirudin. Additionally, to activate hirudin selectively at the target area and thereby limit side effects in an in vivo setting, the authors aimed to construct an inactive precursor molecule that is converted into an active thrombin inhibitor only upon cleavage by factor Xa.

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Implantation of stents into stenosed arteries helps to restore normal blood flow in ischemic organs. However, limited biocompatibility of the applied medical steel can cause acute thrombosis and long-term restenosis. Adhesion of monocytes to stent metal may participate in those acute and long-term complications of stent placement.

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Increased PAI-1 expression has been implicated in accelerating atherogenesis. Increases under some conditions are modulated by growth factors. Genetic factors such as the 4G/5G polymorphism in the promoter of the PAI-1 gene play a role under certain circumstances.

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Cross-reactivity with integrins other than glycoprotein IIb/IIIa (GP IIb/IIIa) is discussed as a potential reason for the overall clinical benefits of the GP IIb/IIIa-blocking antibody-fragment abciximab. We evaluated whether abciximab binds to the leukocyte integrin Mac-1, whether it inhibits binding of the distinct ligands and thereby may modulate inflammation, cell proliferation and coagulation. Binding of fluorescence-labelled abciximab to phorbolmyristate acetate-stimulated monocytes and to a monocytic cell line (THP-1) could be detected in flow cytometry.

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