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Power gives people the ability to control themselves and their environment, and this control is considered a fundamental human need. We investigated whether experiencing powerlessness induces the experience of self-dehumanization using three methods: priming, role-playing, and cueing. People in a position of low power viewed themselves (Experiments 1–3) as less human relative to people in a position of high power; furthermore, people with low power believed that they were viewed as less human by others as well (Experiments 2–3). In all of the experiments, human nature traits were most negatively affected by powerlessness in self-perception judgments, and uniquely human traits were most negatively affected by powerlessness in meta-perception judgments. Furthermore, the powerless believed they were viewed as less human not only by the powerful people but also the outside observers of the power dynamic. Self-dehumanization also appears to be a consequence of powerlessness rather than an incidental result of a change in mood or a negative self-view. Our findings are an important extension of previous work on the adverse effects of powerlessness and dehumanization.

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A heteroleptic ruthenium(II) complex of [Ru(Hecip)(Hdcbpy) (NCS)2]–·[N(C4H9)4]+ (where Hecip = 2‐(9‐ethyl‐9H‐carbazol‐3‐yl)‐1H‐imidazo[4,5‐f][1,10]phenanthroline and Hdcbpy = monodeprotonated 2,2′‐bipyridyl‐4,4′‐dicarboxylic acid) has been synthesized and characterized by elementary analysis, cyclic voltammetry, MALDI‐TOF mass spectrometry, and 1H NMR, IR, UV/Vis absorption, and emission spectroscopy. The ground‐ and excited‐state acid–base properties of the complex have been studied by means of UV/Vis absorption spectrophotometric and spectrofluorimetric titrations in a Britton–Robinson/DMF (v/v, 4:1) buffer solution. The complex was found to act as pH‐induced off‐on‐off/on‐off‐on‐off‐type emission switch, when excited at 530/470 nm, with a protonation/deprotonation reaction taking place near the physiological pH range. The performance of the complex‐sensitized TiO2 nanocrystalline solar cell with 0.05 M I2 and 0.5 M LiI in 50 % acetonitrile and 50 % propylene carbonate (PC) as the electrolyte solution and a platinum film as the counter electrode has also been studied, and was compared to that of the cis‐[Ru(H2dcbpy)2(NCS)2] (N3)‐sensitized solar cell under the same experimental conditions.(© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2009)

BackgroundThe present study was designed to investigate the effects of hyperlipidemia on the cerebral lipids, vessels and neurons of rats, and to provide experimental evidence for subsequent intervention.MethodOne hundred adult SD rats, half of which were male and half of which were female, were randomly divided into five groups on the basis of serum total cholesterol (TC) levels. Four groups were fed a hypercholesterolemic diet (rat chow supplemented with 4% cholesterol, 1% cholic acid and 0.5% thiouracil – this is also called a CCT diet) for periods of 1 week, 2 weeks, 3 weeks and 4 weeks, respectively. A control group was included. The levels of serum lipids, cerebral lipids, free fatty acids (FFA), interleukin-6 (IL-6), interleukin-1 (IL-1), tumor necrosis factor alpha (TNF-α), vascular endothelial growth factor (VEGF), oxidized low density lipoprotein (ox-LDL), A-beta precursor proteins (APP), amyloid beta (Aβ), glial fibrillary acidic protein (GFAP) and tight junction protein Claudin-5 were measured after the experiment. The pathologic changes and apoptosis of the rat brains were evaluated.ResultsCompared with the control group, after 1 week of a CCT diet, the levels of serum total cholesterol (TC), triglycerides (TG), low density lipoprotein cholesterol (LDL-C) and brain triglycerides had increased by 2.40, 1.29 and 1.75 and 0.3 times, respectively. The serum high density lipoprotein cholesterol (HDL-C) had decreased by 0.74 times (P < 0.05) and the expression of IL-1, TNF-α and GFAP in the brains had increased (P < 0.05). In the second week, the expression of FFA and APP in the brains, and the amount of apoptotic neurons, had increased (P < 0.05). In the third week, the levels of VEGF, Ox-LDL and Aβ had increased, and the expression of Claudin-5 had decreased in the brains (P < 0.05). In the fourth week, the levels of TC, LDL-C and the amount of apoptotic neurons had increased (P < 0.05). The correlation analysis showed a positive correlation among FFA, TNF-α, VEGF, ox-LDL, Aβ, GFAP and neuronal apoptosis in the rat brains, and they all were negatively correlated with Claudin-5 (P < 0.05).ConclusionHyperlipidemia may activate astrocytes by means of high levels of TG that will have direct toxic effects on the cerebral vessels and neurons by causing the secretion of TNF-α and IL-1 in the brains of rats. In the metabolic procession, brain tissue was shown to generate FFA that aggravated the biosynthesis of ox-LDL. With the extension of the duration of hyperlipidemia, high levels of cerebral TC and LDL-C were shown to aggravate the deposition of Aβ, induce the secretion of VEGF, reduce the expression of tight junction protein Claudin-5 and change the permeability of blood–brain barriers to factors that could damage cerebral vessels and neurons.