Whilst
the proximate mechanisms of empathy, modulated in part by neuropeptides such as oxytocin, control the ways we interact with our social environment, the ultimate causes seem to have arisen along with the mechanisms involved in mammalian parental care. The conceptual boundaries of empathy, however, have been blurred by definitional check details inaccuracies of mechanisms that can be regarded as phylogenetic precursors or physiological prerequisites for empathy, including mimicry and emotion contagion. Contextual factors such as early experiences with primary care-givers (attachment), current mood states and other environmental contingencies are capable of modulating empathy. Moreover, evidence suggests that there is also a “”dark side”" of empathy, namely envy and schadenfreude (gloating) that are elicited by social comparison,
competition and ingroup-outgroup distinction. This review aims at clarifying some of the open definitional Alvespimycin cell line questions related to empathy, and emphasizing the need for considering contextual factors in the study of empathy in both normal and abnormal psychology. (C) 2013 Elsevier Ltd. All rights reserved.”
“Objective: To assess the influence of stent application on in-stent hemodynamics under standardized conditions.
Methods: Ovine common carotid arteries before and after stent (6 x 40 mm, sinus-Carotid-RXt, combined open-closed cell design; Optimed, Ettlingen, Germany) application were used. Plastic tubes, 10
mm in length, simulating stenosis were placed in the middle of the applied stent to induce different degrees of stenosis (moderate 57.8% and severe 76.4%). Flow velocity and dynamic compliance were, respectively, measured with ultrasound and laser scan; proximal, in-stent, and distal to the stented arterial segment (1 cm proximal and distal) in a pulsatile ex vivo circulation system.
Results: Stent insertion caused the in-stent peak systolic velocity to increase 22% without stenosis, 31% with moderate stenosis, and 23% with severe stenosis. Stent insertion without stenosis caused no significant increase in in-stent end-diastolic velocity (EDV) but a 17% increase with moderate stenosis. In severe stenosis, EDV was increased 56% proximal to the stenosis. Compliance buy Milciclib was reduced threefold in the middle of the stented arterial segment where flow velocity was significantly increased.
Conclusions: With or without stenosis, stent introduction caused the in-stent peak systolic velocity to become significantly elevated compared with a nonstented area. EDV was also increased by stent insertion in the case of moderate stenosis. The stent-induced compliance reduction may be causal for the increase in flow velocity since the stent-induced flow velocity elevation appeared in the stented area with low compliance.
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