Publications by authors named "K Tempel"
Purpose: To evaluate bonding quality for orthodontic bracket bonding with different component combinations of self-etch primers in vitro.
Methods: Metallic brackets were bonded to bovine lower incisors and assigned to groups. Group 1: comparison of self-etch (Transbond™ Plus, 3M™ Unitek, Neuss, Germany, n = 30; BrackFix® primer SE, VOCO®, Cuxhaven, Germany, n = 20) and etch-and-rinse bonding systems (Transbond™ XT, n = 20; BrackFix®, n = 20); group 2: comparison of different self-etch primer (Transbond™ Plus; BrackFix® primer SE) and adhesive (Transbond™ XT, n = 20; BrackFix®, n = 20) product combinations; group 3: testing cyclic fatigue bond strength of self-etch bonding systems (Transbond™ Plus, n = 20; BrackFix® primer SE, n = 20).
Introduction: Bond failure during fixed orthodontic treatment is a frequently occurring problem. As bracket rebonding is associated with reduced shear bond strength, the aim of the present investigation is to analyse the effect of different innovative rebonding systems to identify optimised rebonding protocols for orthodontic patient care.
Methods: Metallic brackets were bonded to the frontal enamel surfaces of 240 bovine lower incisors embedded in resin bases.
Background: Although there is considerable support for the relationship between impulsivity and alcohol dependence, little is known about the impact of neurocognitive aspects of impulsivity on treatment outcome. The aim of this study was to prospectively investigate the impact of neurocognitive impulsivity at treatment onset on treatment completion.
Methods: Forty-three alcohol-dependent patients entering inpatient treatment for alcohol dependence completed neurocognitive measures of impulsivity at the beginning of treatment.
Aims: Since mitogen-activated protein kinases (MAPKs) were found to be implicated in the signalling of ischaemic preconditioning (IPC), we tested the hypothesis of a contribution of these protein kinases to remote preconditioning (RPC).
Methods And Results: To determine the role of p38, ERK1/2, and JNK1/2 MAPKs in mediating cardiac protection, an in vivo model of myocardial infarction was applied in male Wistar rats. RPC or IPC was induced by occlusion of the superior mesenteric artery or the left coronary artery, respectively.
Background: Angiotensin II causes hypertension not only by direct constriction of vascular smooth muscle, but also by facilitating the release of noradrenaline from sympathetic terminals and by enhancing vascular noradrenaline sensitivity. AT1 receptor antagonists attenuate all these actions, but display some evidence of substance-related selectivities.
Objective: The contribution of pre- or postsynaptic impairment of sympathetic transmission to long-term antihypertensive efficacy should be determined for four structurally different, clinically approved AT1 antagonists.