消费者对犯错品牌评价的时间打折效应及其影响因素

通过研究品牌犯错的时间打折效应,本文试图探讨潜在消费者（未购买者）对犯错品牌评价的心理倾向。实验1研究发现,随着品牌犯错事件时间距离的延伸,消费者对身体性危害-品牌犯错的评价不会改善,即没有出现时间打折效应,而对功能性危害-品牌犯错的评价则逐渐提高,从而表现出时间打折效应。但实验2研究进一步发现,随着品牌犯错事件相关性的增强,功能性危害-品牌犯错的时间打折效应也消失。结论：潜在消费者对犯错品牌评价的心理倾向表现为“消费者防御”,并且身体性危害-品牌犯错启动的消费者防御要强于功能性危害。     

趋近和回避动机的区分及其对心理病理学的影响

趋近和回避是动机的两种最基本形式, 反映着个体与环境的相互作用方式, 是个体适应环境的核心机能。回避动机保证了个体的生存, 趋近动机则促进个体的成长。两类动机系统在前额叶皮层呈不对称偏侧化分布, 趋近动机与左侧额叶皮层激活相连, 回避动机与右侧额叶皮层激活相连。Youngstorm 和Izard等认为两类动机系统失调可能与一系列的情绪和行为问题有关, 如躁狂、抑郁、焦虑和儿童多动症等。这一观点已得到一些相关研究和临床研究证实。建议未来研究关注趋近-回避动机区分与情绪和认知功能研究的融合, 进一步检验趋近-回避动机系统失调模型, 并加强趋近和回避动机系统的可塑性研究。     

Burnout predictors among prison officers: The moderating effect of temperamental endurance

The study investigates whether work stressors, coping styles, and work-related social support predict burnout among prison officers (N = 476). It was hypothesized that coping and social support would mediate the effects of work stressors on burnout and that these effects would be moderated by temperamental endurance. Results of structural equation modeling showed that emotion-oriented coping was positively related to emotional exhaustion, and negatively to personal accomplishment. Task-oriented coping was positively related to personal accomplishment. Social support from work was negatively related to emotional exhaustion. The effects of work stressors on burnout were mediated by work-related social support and by emotion-oriented coping. Additionally, some of these mediating effects were moderated by endurance. Work-related social support was negatively related to depersonalization only among participants with strong endurance. High level of work stressors predicted high emotion-oriented coping only among individuals with weak endurance.     

Coping self-efficacy mediates the effects of negative cognitions on posttraumatic distress

Although cognitive distortions have predicted posttraumatic distress after various types of traumatic events, the mechanisms through which cognitive distortions influence posttraumatic distress remain unclear. We hypothesized that coping self-efficacy, the belief in one's own ability to manage posttraumatic recovery demands, would operate as a mediator between negative cognitions (about self, about the world, and self-blame beliefs) and posttraumatic distress. In the cross-sectional Study 1, data collected among 66 adult female victims of child sexual abuse indicated that coping self-efficacy mediated the effects of negative cognitions about self and about the world on posttraumatic distress. The same pattern of results was found in a longitudinal Study 2, conducted among 70 survivors of motor vehicle accidents. Coping self-efficacy measured at 1 month after the trauma mediated the effects of 7-day negative cognitions about self and about the world on 3-month posttraumatic distress. In both studies self-blame was not related to posttraumatic distress and the effect of self-blame on posttraumatic distress was not mediated by coping self-efficacy. The results provide insight into a mechanism through which negative cognitions may affect posttraumatic distress and highlight the potential importance of interventions aimed at enhancing coping self-efficacy beliefs.     

Negative Affectivity and Drinking in Adolescents: An Examination of Moderators Predicted by Affect Regulation Theory

This investigation examined potential moderators of the longitudinal relation between negative affectivity and drinking. Specifically tested was the degree to which alcohol expectancies and coping styles moderate the relation between negative affectivity in early adolescence and drinking in middle and late adolescence. Four hundred ninety nine early adolescents completed inventories of negative affectivity, coping style, and tension reduction expectancies, and were followed up with inventories of drinking in middle and late adolescence. Constructive coping moderated the relation between negative affectivity and drinking in middle adolescence, such that only those with poor coping skills exhibited this positive relation. Although early negative affectivity was directly related to drinking in late adolescence, no interactions between negative affectivity and expectancies or coping were detected for drinking at that age. This absence of consistent moderating effects indicates significant limitations in the ability of the traditionally-conceived affect regulation model to reliably predict adolescent drinking. This research was conducted at the Center for Education and Drug Abuse Research (CEDAR) which is located in the School of Pharmaceutical Sciences at the University of Pittsburgh and is supported by grant P50-DA-05605 from the National Institute on Drug Abuse.     

Temporomandibular Disorder in Brazilian Patients: A Preliminary Study

The objective of the current study was to evaluate disease-related beliefs, adherence to treatment, quality of life, coping strategies and cognitive status in a group of Brazilian patients with Temporomandibular Disorder (TMD). Thirty patients were evaluated with a semi-directed interview, the Coping Strategies Inventory, and a Mini-Mental State Examination. Although half (50%) of the patients had known their diagnosis long term, 40% of the sample were not correctly following proposed treatment. All patients had a similar pattern of pain behavior related to TMD, while disease-related beliefs, quality of life and coping strategies were variable. Expectations about treatment also had significant association with treatment adherence. The findings of this study suggest that a more thorough understanding of individual differences in TMD is warranted.     

Ethanol state-dependent memory: involvement of dorsal hippocampal muscarinic and nicotinic receptors

In the present study, the effects of bilateral injections of cholinergic agents into the hippocampal CA1 regions (intra-CA1) on ethanol state-dependent memory were examined in mice. A single-trial step-down passive avoidance task was used for the assessment of memory retention in adult male NMRI mice. Pre-training intraperitoneal injection (i.p.) of ethanol (0.25, 0.5 and 1 g/kg) dose dependently induced impairment of memory retention. Pre-test administration of ethanol (0.5 and 1 g/kg, i.p.) induced state-dependent retrieval of the memory acquired under pre-training ethanol (1 g/kg, i.p.) influence. Pre-test intra-CA1 injection of physostigmine (2.5 and 5 μg/mouse, intra-CA1) or nicotine (0.3 and 0.5 μg/mouse, intra-CA1) improved pre-training ethanol (1 g/kg)-induced retrieval impairment. Moreover, pre-test administration of physostigmine (2.5 and 5 μg/mouse, intra-CA1) or nicotine (0.3 and 0.5 μg/mouse, intra-CA1) with an ineffective dose of ethanol (0.25 g/kg) significantly restored the retrieval and induced ethanol state-dependent memory. Pre-test intra-CA1 injection of the muscarinic receptor antagonist, atropine (4 and 8 μg/mouse, intra-CA1) or the nicotinic receptor antagonist, mecamylamine (2 and 4 μg/mouse, intra-CA1) 5 min before the administration of ethanol (1 g/kg, i.p.) dose dependently inhibited ethanol state-dependent memory. Pre-test intra-CA1 administration of physostigmine (0.5, 2.5 and 5 μg/mouse), atropine (2, 4 and 8 μg/mouse), nicotine (0.1, 0.3 and 0.5 μg/mouse) or mecamylamine (1, 2 and 4 μg/mouse) alone cannot affect memory retention. These findings implicate the involvement of a dorsal hippocampal cholinergic mechanism in ethanol state-dependent memory and also it can be concluded that there may be a cross-state dependency between ethanol and acetylcholine.     

Rigidity in social and emotional memory in the R6/2 mouse model of Huntington's disease

Four experiments were conducted to examine social and emotional memory in the R6/2 transgenic mouse model of Huntington’s disease. First, R6/2 mice were tested in a social transmission of food preference task where they had to acquire a preference for a flavoured food (acquisition) and subsequently to learn a preference for a different flavour (shifted reinforcement). R6/2 mice performed well in the acquisition trial. However, they were impaired in the shifted reinforcement trial and perseverated on the first preference learned. Second, mice were trained in an inhibitory avoidance paradigm, with either one or two footshocks delivered during the training. WT mice given one footshock showed retention levels lower than those of mice trained with two footshocks. By contrast, there was no difference in retention levels of R6/2 mice given either one or two footshocks. Third, mice were tested in an active avoidance task that paired a mild footshock with a warning light. R6/2 mice had a strong age-dependent deficit in this task. Finally, mice were tested in a conditioned taste aversion task that paired a saccharine solution with a nausea-inducing agent (LiCl). R6/2 mice displayed normal aversion, however this was not extinguished following repeated exposure to saccharine solution alone. Our data show that while R6/2 mice have functional hippocampus-based memory, they have deficits in striatum-based memory skills. Further, social and emotional memories appear to be encoded in a rigid way that is not influenced by subsequent learning or by arousal levels.     

Upregulation of hippocampal TrkB and synaptotagmin is involved in treadmill exercise-enhanced aversive memory in mice

Cognitive functions usually involve various synaptic proteins and neurotrophic factors in the hippocampus. However, whether treadmill exercise can improve learning and memory by upregulating some of these molecules remain unraveled. To address this question, male BALB/c mice were divided into control and exercise groups, the latter group went through 4 weeks of treadmill exercise training. At the end of exercise training period, they were either tested for passive avoidance (PA) performance or sacrificed for quantifying the hippocampal levels of brain-derived neurotrophic factor (BDNF), tropomyosin-related kinase B (TrkB, the BDNF receptor), synaptotagmin (a Ca²⁺-dependent synaptic vesicle protein), and SNAP-25 (a presynaptic vesicular fusion protein). Our results showed that treadmill exercise training (1) increased the retention latency without affecting the fear acquisition in the PA test, (2) transiently increased the hippocampal BDNF level at 1, 2, and 4 h after the completion of exercise training, and (3) persistently increased the hippocampal protein levels of full-length TrkB, phosphorylated TrkB and synaptotagmin, but not truncated TrkB or SNAP-25. Moreover, the protein expression level of full-length TrkB or synaptotagmin was positively correlated with PA performance in mice. Finally, inhibition of TrkB signaling by K252a abolished the exercise-facilitated PA performance and upregulation of TrkB and synaptotagmin. Taken together, these data suggest that the upregulation of TrkB and synaptotagmin in the hippocampus contributes to the exercise-facilitated aversive memory.     

Avoidance of timeout from response-independent food: effects of delivery rate and quality

In three experiments, a rat's lever presses could postpone timeouts from food pellets delivered on response-independent schedules. In Experiment 1, the pellets were delivered at variable-time (VT) rates ranging from VT 0.5 to VT 8 min. Experiment 2 replicated the VT 1 min and VT 8 min conditions of Experiment 1 with new subjects. Finally, subjects in Experiment 3 could postpone timeouts from delivery of pellets that differed in quality rather than quantity (unsweetened versus sweetened pellets). In general, response rates and success in avoiding increased as a function of the rate and quality of the pellets. Also, performance efficiency increased as the experiments progressed, that is, the avoidance response occurred later and later in the response-timeout interval. The results support the conclusion that timeout from reinforcement has functional properties similar to those of more commonly studied aversive stimuli (e.g., shock).