Human congestive heart failure is characterized by complex neurohumoral activation associated with the up-regulation of vasoconstricting and salt-retaining mediators and the compensatory rise of counter-regulatory hormones. In the present study, we provide the first evidence that relaxin (RLX), known as a pregnancy hormone, represents a potential compensatory mediator in human heart failure: plasma concentrations of RLX and myocardial expression of the two RLX genes (H1 and H2) correlate with the severity of disease and RLX responds to therapy. The failing human heart is a relevant source of circulating RLX peptides, and myocytes as well as interstitial cells produce RLX. Elevation of ventricular filling pressure up-regulates RLX expression and the hormone acts as a potent inhibitor of endothelin 1, the most powerful vasoconstrictor in heart failure. Furthermore, RLX modulates effects of angiotensin II, another crucial mediator. Our data identify RLX as a new player in human heart failure with potential diagnostic and therapeutic relevance.

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Abstract. In this paper, we present three different ways of interrupting people to posture guidance. We developed an ergonomically adjustable office chair equipped with four sensors measuring the office worker's posture. It is important that users do some training after bad posture and be alerted of this; therefore, we implemented three different alert modalities (Graphical Feedback, Physical Feedback, and Vibrotactile Feedback), with the goal to find out which of the techniques is the most effective interruption modality without causing a huge disruption effect. To measure the task-performance, we conducted a formal user study. Our user study results show there are different effects on performance and disruptiveness caused by the three interruption techniques. While the vibrotactile feedback might have higher information awareness benefits at the beginning, it causes a huge intrusion side-effect. Thus, the physical feedback was rated less disruptive to the workflow as the other two feedback modalities.

Abstract-We have recently demonstrated that relaxin (RLX) acts as compensatory mediator in human heart failure. RLX inhibits the stimulation of endothelin-1, the most potent vasoconstrictor in heart failure. Key Words: endothelin Ⅲ receptors Ⅲ signal transduction Ⅲ vasoconstriction Ⅲ vasodilation T he insulin-related peptide relaxin (RLX) has long been regarded as a central hormone of human pregnancy that contributes to changes in connective tissue composition and to the regulation of implantation, myometrial activity, and labor. 1 On the other hand, we have recently found that RLX is constitutively expressed in human cardiovascular tissues and that myocardial gene expression of RLX is remarkably upregulated in human congestive heart failure. 2 What renders RLX particularly intriguing as a neurohumoral player and as a potential new therapeutic tool is its antagonism vis-à-vis endothelin-1 (ET-1), one of the most potent vasoconstrictors and a powerful mediator of salt retention, fibroproliferation, and myocardial remodeling. 3 We have shown that RLX induces upregulation of the endothelial endothelin type-B receptor (ET B ). 2 This receptor subtype stimulates endothelium-dependent vasodilation via NO and prostacyclin as well as clearance of ET-1. 3 Moreover, RLX, via this ET B mechanism, inhibits stimulated ET-1 release in endothelial cells and may cause the inverse correlation between circulating RLX and ET-1 in patients with end-stage heart failure. 2 Given the obvious importance of the RLX-induced ET B upregulation, it is crucial to know whether this phenomenon is restricted to endothelial cells only, because ET B is also found on epithelial and vascular smooth muscle cells (VSMCs). 3 Additionally, it would be of particular interest to investigate the ensuing signaling cascades. Because other members of the insulin family represent strong activators of extracellular signal-regulated kinases-1/2 (ERK-1/2) 4,5 and of nu-