Search

We examined whether enhancing (vs. not enhancing) the emotionality of a referent public good influences the subsequent valuation of a target public good. We predicted that it would and that the directionality of its impact would depend on a fundamental cognitive process - categorisation. If the target and referent goods belong to the same domain, we expected that the effect on the target would be in the same direction as the emotional enhancement of the referent (assimilation effect). However, if the target and referent goods belong to different domains, we expected that the effect on the target would be either negligible or in the opposite direction to that of the emotional enhancement of the referent (null or contrast effect). In Experiment 1 we examined the impact of emotionally enhancing a referent public good on feelings towards a target public good, whereas in Experiment 2 on the willingness to contribute towards a target public good. The results support the predicted interaction, which was driven by an assimilation effect for same-domain goods and a null effect for different-domain goods. In doing so, the present findings highlight the interplay between cognition and emotion in the valuation of public goods. We discuss theoretical and practical implications.

Background: Increasing left ventricular assist device (LVAD) pump speed according to the patient's activity is a fascinating hypothesis. This study analyzed the short-term effects of LVAD speed increase on cardiopulmonary exercise test (CPET) performance, muscle oxygenation (near-infrared spectroscopy), diffusion capacity of the lung for carbon monoxide (Dlco) and nitric oxide (Dlno), and sleep quality., Methods: We analyzed CPET, Dlco and Dlno, and sleep in 33 patients supported with the Jarvik 2000 (Jarvik Heart Inc., New York, NY). After a maximal CPET (n = 28), patients underwent 2 maximal CPETs with LVAD speed randomly set at 3 or increased from 3 to 5 during effort (n = 15). Then, at LVAD speed randomly set at 2 or 4, we performed (1) constant workload CPETs assessing O 2 kinetics, cardiac output (CO), and muscle oxygenation (n = 15); (2) resting Dlco and Dlno (n = 18); and (3) nocturnal cardiorespiratory monitoring (n = 29)., Results: The progressive pump speed increase raised peak volume of oxygen consumption (12.5 ± 2.5 ml/min/kg vs 11.7 ± 2.8 ml/min/kg at speed 3; p = 0.001). During constant workload, from speed 2 to 4, CO increased (at rest: 3.18 ± 0.76 liters/min vs 3.69 ± 0.75 liters/min, p = 0.015; during exercise: 5.91 ± 1.31 liters/min vs 6.69 ± 0.99 liters/min, p = 0.014), and system efficiency (τ = 65.8 ± 15.1 seconds vs 49.9 ± 14.8 seconds, p = 0.002) and muscle oxygenation improved. At speed 4, Dlco decreased, and obstructive apneas increased despite a significant apnea/hypopnea index and a reduction of central apneas., Conclusions: Short-term LVAD speed increase improves exercise performance, CO, O 2 kinetics, and muscle oxygenation. However, it deteriorates lung diffusion and increases obstructive apneas, likely due to an increase of intrathoracic fluids. Self-adjusting LVAD speed is a fascinating but possibly unsafe option, probably requiring a monitoring of intrathoracic fluids., (Copyright © 2018 International Society for Heart and Lung Transplantation. Published by Elsevier Inc. All rights reserved.)

The evaluation of changes in the fatty acid composition in Lupinus species after the debittering process is crucial to determine their nutritional implications. The aim of this study was to evaluate changes in the fatty acid composition in Lupinus albus and L. mutabilis after the debittering process. Lupinus species showed different fatty acid compositions which changed depending on the debittering process applied. The debittering process changed the monounsaturated and polyunsaturated fatty acids in L. albus, whereas in L. mutabilis it changed the w-6/w-3 ratio. However, the total saturated fatty acid content remained stable in both species after the debittering process. The changes in L. albus were associated with the fatty acid desaturation and a conversion into unsaturated fatty acids, whereas in L. mutabilis with the lipid peroxidation by decreasing the linoleic acid content. Nutritional implications of these changes in the fatty acid composition are discussed., (Copyright © 2018. Published by Elsevier Ltd.)

A group of pathological gamblers and a group of problem gamblers (i.e., gamblers at risk of becoming pathological) were compared to healthy controls on their risk-taking propensity after prior losses. Each participant played both the Balloon Analogue Risk Taking task (BART) and a modified version of the same task, where individuals face five repeated predetermined early losses at the onset of the game. No significant difference in risk-taking was found between groups on the standard BART task, while significant differences emerged when comparing behaviors in the two tasks: both pathological gamblers and controls reduced their risk-taking tendency after prior losses in the modified BART compared to the standard BART, whereas problem gamblers showed no reduction in risk-taking after prior losses. We interpret these results as a sign of a reduced sensitivity to negative feedback in problem gamblers which might contribute to explain their loss-chasing tendency.

Much is known about the effect of negative arousal on decision making, but little is known about the effect of positive arousal. In this study, we manipulated positive arousal and measured individual choices under risk using an incentivized task. Participants were randomly assigned to either a low arousal or a high arousal condition and asked to choose between pairs of two-outcome monetary lotteries with the same expected value but different risk in terms of outcome variance. The probability was set at 50% for each lottery. Participants in the high arousal group selected the riskier lottery more often and took more time to make choices than participants in the low arousal group. This finding shows that introducing a pleasant arousing cue as part of the decision context shifts an individual's preferences toward the risky economic option and away from the safer one.

Putative human chemosignals have been shown to influence mood states and emotional processing, but the connection between these effects and higher-order cognitive processing is not well established. This study utilized an economic game (Dictator Game) to test whether androstadienone (AND), an odorous compound derived from testosterone, impacts on altruistic behavior. We predicted that the female participants would act more generously in the AND condition, exhibiting a significant interaction effect between gender and AND on Dictator Game contributions. We also expected that the presence of AND should increase the positive mood of the female participants, compared to a control odor condition and also compared to the mood of the male participants. The results confirm our hypotheses: for women the subliminal perception of AND led to larger monetary donations, compared to a control odor, and also increased positive mood. These effects were absent or significantly weaker in men. Our findings highlight the capacity of human putative chemosignals to influence emotions and higher cognitive processes - in particular the processes used in the context of economic decisions - in a gender-specific way.

We investigate the effect of graph scale on risky choices. By (de)compressing the scale, we manipulate the relative physical distance between options on a given attribute in a coordinate graphical context. In Experiment 1, the risky choice changes as a function of the scale in the graph. In Experiment 2, we show that the type of graph scale also affects decision times. In Experiment 3, we examine the graph scale effect by using real money among students who have taken statistics courses. Consequently, the scale effects still appear even when we control the variations in calculation ability and increase the gravity with which participants view the consequence of their decisions. This finding is inconsistent with descriptive invariance of preference. The theoretical implications and practical applications of the findings are discussed.

A way to make people save energy is by informing them that "comparable others" save more. We investigated whether, one can further improve this nudge by manipulating Who the "comparable others" are. We asked participants to imagine receiving feedback stating that their energy consumption exceeded that of "comparable others" by 10%. We varied Who the "comparable others" were in a 2 × 2 design: they were a household that was located either in the same neighborhood as themselves or in a different neighborhood, and its members were either identified (by names and a photograph) or unidentified. We also included two control conditions: one where no feedback was provided, and one where only statistical feedback was provided (feedback about an average household). We found that it matters Who the "comparable others" are. The most effective feedback was when the referent household was from the same neighborhood as the individual's and its members were not identified.

In this paper, we investigate whether cognitive reflection and numeracy skills affect the quality of the consumers' decision-making process in a purchase decision context. In a first (field) experiment, an identical product was on sale in two shops with different initial prices and discounts. One of the two deals was better than the other and the consumers were asked to choose the best one and to describe which arithmetic operations they used to solve the problem; then they were asked to complete the numeracy scale (Lipkus et al., 2001). The choice procedures used by the consumers were classified as "complete decision approach" when all the arithmetic operations needed to solve the problem were computed, and as "partial decision approach" when only some operations were computed. A mediation model shows that higher numeracy is associated with use of the complete decision approach. In turn, this approach is positively associated with the quality of the purchase decision. Given that these findings highlight the importance of the decision processes, in a second (laboratory) experiment we used a supplementary method to study the type of information search used by the participants: eye-tracking. In this experiment the participants were presented with decision problems similar to those used in Experiment 1 and they completed the Lipkus numeracy scale and the Cognitive Reflection Test (CRT; Frederick, 2005). Participants with a high CRT score chose the best deal more frequently, and showed a more profound and detailed information search pattern compared to participants with a low CRT score. Overall, results indicate that higher levels of cognitive reflection and numeracy skills predict the use of a more thorough decision process (measured with two different techniques: retrospective verbal reports and eye movements). In both experiments the decision process is a crucial factor which greatly affects the quality of the purchase decision.

We investigated whether pleasant ambient scents influence hypothetical and real money contributions toward environmental goods. We hypothesized that they would increase such contributions more when they were congruent with the target goods than when they were incongruent or when no scent was released. The results supported this congruity hypothesis. We offer a mental accessibility account: Pleasant scents that are congruent with a target good make positive information about that good more accessible and thus promote prosocial behavior., (© 2014 The Institute of Psychology, Chinese Academy of Sciences and Wiley Publishing Asia Pty Ltd.)

Research has shown that healthy people would rather avoid losses than gamble for even higher gains. On the other hand, research on pathological gamblers (PGs) demonstrates that PGs are more impaired than non-pathological gamblers in choice under risk and uncertainty. Here, we investigate loss aversion by using a rigorous and well-established paradigm from the field of economics, in conjunction with personality traits, by using self-report measures for PGs under clinical treatment. Twenty pathological gamblers, at the earlier and later stages of clinical treatment, were matched to 20 non-gamblers (NG). They played a "flip coin task" by deciding across 256 trials whether to accept or reject a 50-50 bet with a variable amount of gains and losses. They completed questionnaires aimed at assessing impulsivity. Compared to NG, pathological gamblers, specifically those in the later stages of therapy, were more loss averse and accepted a lower number of gambles with a positive expected value, whereas their impulsivity traits were significantly higher. This study shows for the first time that changes in loss aversion, but not in personality traits, are associated with the time course of pathology. These findings can be usefully employed in the fields of both gambling addiction and decision-making., (Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.)

Impulsivity is associated with several psychiatric disorders in which the loss of control of a specific behavior determines the syndrome itself. One particularly interesting population characterized by reported high impulsivity and problematic decision-making are those diagnosed with pathological gambling. However the association between impulsivity and decision making in pathological gambling has been only partially confirmed until now. We tested 23 normal controls and 23 diagnosed pathological gamblers in an intertemporal choice task, as well as other personality trait measurements. Results showed that gamblers scored higher on impulsivity questionnaires, and selected a higher percentage of impatient choices (higher percentage of smaller, sooner rewards), when compared to normal controls. Moreover, gamblers were faster in terms of reaction times at selecting the smaller, sooner options and discounted rewards more rapidly over time. Importantly, regression analyses clarified that self-reported measures of impulsivity played a significant role in biasing decisions towards small but more rapidly available rewards. In the present study we found evidence for impulsivity in personality traits and decisions in pathological gamblers relative to controls. We conclude by speculating on the need to incorporate impulsivity and decision biases in the conceptualization of pathological gambling for a better understanding and treatment of this pathology.

We present a first-principles study of the temperature- and density-dependent intrinsic electrical resistivity of graphene. We use density-functional theory and density-functional perturbation theory together with very accurate Wannier interpolations to compute all electronic and vibrational properties and electron-phonon coupling matrix elements; the phonon-limited resistivity is then calculated within a Boltzmann-transport approach. An effective tight-binding model, validated against first-principles results, is also used to study the role of electron-electron interactions at the level of many-body perturbation theory. The results found are in excellent agreement with recent experimental data on graphene samples at high carrier densities and elucidate the role of the different phonon modes in limiting electron mobility. Moreover, we find that the resistivity arising from scattering with transverse acoustic phonons is 2.5 times higher than that from longitudinal acoustic phonons. Last, high-energy, optical, and zone-boundary phonons contribute as much as acoustic phonons to the intrinsic electrical resistivity even at room temperature and become dominant at higher temperatures.

Hypoxia, the deprivation of adequate oxygen supply, constitutes a direct threat to survival by disrupting cardiovascular or respiratory homeostasis and eliciting a respiratory distress. Although hypoxia has been shown to increase brain vulnerability and impair basic cognitive functions, only one study has examined its effect on decision-making. The present study examined the effect of mild hypoxia on individual's loss aversion, that is, the tendency to be more affected by losses than equal sized gains. A sample of 26 participants were asked to either accept or reject a series of mixed gambles once in an oxygen-depleted environment (14.1% oxygen concentration) and once in a normoxic environment (20.9% oxygen concentration). Each gamble involved a 50-50 chance of winning or losing specified amounts of money. Mild hypoxia decreased loss aversion: on average in the normoxic condition participants accepted gambles if the gain was at least 2.4 times as large as the loss, whereas in the oxygen-depleted condition participants accepted gambles if the gain was at least 1.7 times as large as the loss. Mild hypoxia may push individuals to be less cautious in daily decisions that involve a trade-off between a gain and a loss.

Previous studies have reported the effect of emotion regulation (ER) strategies on both individual and social decision-making, however, the effect of regulation on socially driven emotions independent of decisions is still unclear. In the present study, we investigated the neural effects of using reappraisal to both up- and down-regulate socially driven emotions. Participants played the Dictator Game (DG) in the role of recipient while undergoing fMRI, and concurrently applied the strategies of either up-regulation (reappraising the proposer's intentions as more negative), down-regulation (reappraising the proposer's intentions as less negative), as well as a baseline "look" condition. Results showed that regions responding to the implementation of reappraisal (effect of strategy, that is, "regulating regions") were the inferior and middle frontal gyrus, temporo parietal junction and insula bilaterally. Importantly, the middle frontal gyrus activation correlated with the frequency of regulatory strategies in daily life, with the insula activation correlating with the perceived ability to reappraise the emotions elicited by the social situation. Regions regulated by reappraisal (effect of regulation, that is, "regulated regions") were the striatum, the posterior cingulate and the insula, showing increased activation for the up-regulation and reduced activation for down-regulation, both compared to the baseline condition. When analyzing the separate effects of partners' behavior, selfish behavior produced an activation of the insula, not observed when subjects were treated altruistically. Here we show for the first time that interpersonal ER strategies can strongly affect neural responses when experiencing socially driven emotions. Clinical implications of these findings are also discussed to understand how the way we interpret others' intentions may affect the way we emotionally react.

Emotion regulation strategies provide a means by which to modulate our social behavior. In this study, we investigated the effect of using reappraisal to both up- and downregulate social decision making. After being instructed on how to use reappraisal, participants played the Ultimatum Game while undergoing functional magnetic resonance imaging and applied the strategies of upregulation (reappraising the proposer's intentions as more negative), down-regulation (reappraising the proposer's intentions as less negative), as well as a baseline "look" condition. As hypothesized, when reappraising, decision acceptance rates were altered, with a greater number of unfair offers accepted while down-regulating and a greater number of unfair offers rejected while upregulating, both relative to the baseline condition. At the neural level, during reappraisal, significant activations were observed in the inferior and middle frontal gyrus (MFG), in addition to the medial prefrontal cortex and cingulate gyrus for unfair offers only. Regulated decisions involved left inferior frontal gyrus for upregulation and MFG for down-regulation strategies, respectively. Importantly, the effects of emotion modulation were evident in posterior insula, with less activation for down-regulation and more activation for upregulation in these areas. Notably, we show for the first time that top-down strategies such as reappraisal strongly affect our socioeconomic decisions.

Emotion regulation is important for psychological well-being. Although it is known that alternative regulation strategies may have different emotional consequences, the effectiveness of such strategies for socially driven emotions remains unclear. In this study we investigated the efficacy of different forms of reappraisal on responses to the selfish and altruistic behavior of others in the Dictator Game. In Experiment 1, subjects mentalized the intentions of the other player in one condition, and took distance from the situation in the other. Emotion ratings were recorded after each offer. Compared with a baseline condition, mentalizing led subjects to experience their emotions more positively when receiving both selfish and altruistic proposals, whereas distancing decreased the valence when receiving altruistic offers, but did not affect the perception of selfish behavior. In Experiment 2, subjects played with both computer and human partners while reappraising the meaning of the player's intentions (with a human partner) or the meaning of the situation (with a computer partner). Results showed that both contexts were effectively modulated by reappraisal, however a stronger effect was observed when the donor was a human partner, as compared to a computer partner. Taken together, these results demonstrate that socially driven emotions can be successfully modulated by reappraisal strategies that focus on the reinterpretation of others' intentions.

Recent fMRI studies have investigated brain activity involved in the feeling of regret and disappointment by manipulating the feedback participants saw after making a decision to play certain gambles: full-feedback (regret: participant sees the outcomes from both the chosen and unchosen gamble) vs. partial-feedback (disappointment: participant only sees the outcome from chosen gamble). However, regret and disappointment are also characterized by differential agency attribution: personal agency for regret, external agency for disappointment. In this study, we investigate the neural correlates of these two characterizations of regret and disappointment using magnetoencephalography (MEG). To do this, we experimentally induced each emotion by manipulating feedback (chosen gamble vs. unchosen gamble), agency (human vs. computer choice) and outcomes (win vs. loss) in a fully randomized design. At the behavioral level the emotional experience of regret and disappointment were indeed affected by both feedback and agency manipulations. These emotions also differentially affect subsequent choices, with regret leading to riskier behavior. At the neural level both feedback and agency affected the brain responses associated with regret and disappointment, demonstrating differential localization in the brain for each. Notably, feedback regret showed greater brain activity in the right anterior and posterior regions, with agency regret producing greater activity in the left anterior region. These findings extend the evidence for neural activity in processing both regret and disappointment by highlighting for the first time the respective importance of feedback and agency, as well as outlining the temporal dynamics of these emotions., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

Public goods (e.g., parks) and welfare services (e.g., garbage disposal and transportation policies) are extremely important for the citizens' well-being but in the complex modern societies their influence and effectiveness are affected by the citizens' support. For this reason, it is crucial to understand which are the factors that influence the citizens' perception of the benefits, costs, and risks associated to public goods and welfare services. In this chapter, we describe some psychological variables that are relevant for the evaluation process of the public goods, but that are not considered by the standard economic models. At the same time, we show that some variables of central importance for the economic models do not significantly affect the citizens' evaluations. Finally, we discuss the concept of Nudge, a policy-making approach that suggests the use of psychological mechanisms to increase the citizens' support to public provision of welfare services., (Copyright © 2013 Elsevier B.V. All rights reserved.)

Although the role of emotion in socioeconomic decision making is increasingly recognised, the impact of specific emotional disorders, such as anxiety disorders, on these decisions has been surprisingly neglected. Twenty anxious patients and twenty matched controls completed a commonly used socioeconomic task (the Ultimatum Game), in which they had to accept or reject monetary offers from other players. Anxious patients accepted significantly more unfair offers than controls. We discuss the implications of these findings in light of recent models of anxiety, in particular the importance of interpersonal factors and assertiveness in an integrated model of decision making. Finally, we were able to show that pharmacological serotonin used to treat anxious symptomatology tended to normalise decision making, further confirming and extending the role of serotonin in co-operation, prosocial behaviour, and social decision making. These results show, for the first time, a different pattern of socioeconomic behaviour in anxiety disordered patients, in addition to the known memory, attentional and emotional biases that are part of this pathological condition.

Affect can have a significant influence on decision-making processes and subsequent choice. One particularly relevant type of negative affect is anxiety, which serves to enhance responses to threatening stimuli or situations. In its exaggerated form, it can lead to psychiatric disorders, with detrimental consequences for quality of life, including the ability to make choices. This study investigated, for the first time, how pathological anxiety affects risk-taking behavior. In this study, 20 anxious participants meeting Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, criteria for either generalized anxiety disorder (n = 10) and for panic attack disorder (n = 10), as well as 20 matched nonanxious controls, performed a gambling task. To investigate the tendency toward either a risk-seeking or a risk-averse behavior, we employed a task that did not allow for learning from outcomes. Anxious participants made significantly fewer risky choices than matched nonanxious participants. Specifically, they become risk-avoidant after gains. Moreover, anxious participants not only were less happy after gains but were also less sad after losses, and they also evinced less desire to change their choices after losses than did nonanxious participants. Importantly, whereas the desire to switch choice was followed by actual choice switch for all participants, happiness directly predicted subsequent risky choices, particularly in the nonanxious participants. Further analyses revealed that the anxious participants' risk-avoidance behavior was independent of different types of anxiety disorder (panic attack disorder and generalized anxiety disorder) as well as of the effects of psychotropic drugs treatment. This study demonstrates a specific role for anxiety in individual decision making. In particular, hypersensitivity to potential threats and pessimistic evaluation of future events reduced risk-taking behavior., (PsycINFO Database Record (c) 2012 APA, all rights reserved.)

We use first-principles methods based on density functional perturbation theory to characterize the lifetimes of the acoustic phonon modes and their consequences on the thermal transport properties of graphene. We show that using a standard perturbative approach, the transverse and longitudinal acoustic phonons in free-standing graphene display finite lifetimes in the long-wavelength limit, making them ill-defined as elementary excitations in samples of dimensions larger than ∼1 μm. This behavior is entirely due to the presence of the quadratic dispersions for the out-of-plane phonon (ZA) flexural modes that appear in free-standing low-dimensional systems. Mechanical strain lifts this anomaly, and all phonons remain well-defined at any wavelength. Thermal transport is dominated by ZA modes, and the thermal conductivity is predicted to diverge with system size for any amount of strain. These findings highlight strain and sample size as key parameters in characterizing or engineering heat transport in graphene.

The thermal conductivity of ideal short-period superlattices is computed using harmonic and anharmonic force constants derived from density-functional perturbation theory and by solving the Boltzmann transport equation in the single-mode relaxation time approximation, using silicon-germanium as a paradigmatic case. We show that in the limit of small superlattice period the computed thermal conductivity of the superlattice can exceed that of both the constituent materials. This is found to be due to a dramatic reduction in the scattering of acoustic phonons by optical phonons, leading to very long phonon lifetimes. By variation of the mass mismatch between the constituent materials in the superlattice, it is found that this enhancement in thermal conductivity can be engineered, providing avenues to achieve high thermal conductivities in nanostructured materials.

We address the role of the incidental emotion of disgust in the Ultimatum Game. Participants had to choose whether or not to accept a €2 offer from a €10 pot made by another participant; 120 were in a room where a disgusting smell was released and 120 were in a room with no particular smell. Acceptance rates were higher in the room with the disgusting smell. The effect was mainly carried by the male participants who also reported more disgust with the disgusting smell and judged the offer as less unfair than females. We propose a spontaneous discounting explanation. Acceptance rates were higher in the room with the disgusting smell because participants misattributed the disgust induced by the offer to the ambient disgusting smell., (2011 APA, all rights reserved)

The thermal conductivity of disordered silicon-germanium alloys is computed from density-functional perturbation theory and with relaxation times that include both harmonic and anharmonic scattering terms. We show that this approach yields an excellent agreement at all compositions with experimental results and provides clear design rules for the engineering of nanostructured thermoelectrics. For Si(x)Ge(1-x), more than 50% of the heat is carried at room temperature by phonons of mean free path greater than 1   μm, and an addition of as little as 12% Ge is sufficient to reduce the thermal conductivity to the minimum value achievable through alloying. Intriguingly, mass disorder is found to increase the anharmonic scattering of phonons through a modification of their vibration eigenmodes, resulting in an increase of 15% in thermal resistivity.

We determine from first principles the finite-temperature properties-linewidths, line shifts, and lifetimes-of the key vibrational modes that dominate inelastic losses in graphitic materials. In graphite, the phonon linewidth of the Raman-active E(2g) mode is found to decrease with temperature; such anomalous behavior is driven entirely by electron-phonon interactions, and does not appear in the nearly degenerate infrared-active E(1u) mode. In graphene, the phonon anharmonic lifetimes and decay channels of the A(1)' mode at K dominate over E(2g) at Gamma and couple strongly with acoustic phonons, highlighting how ballistic transport in carbon-based interconnects requires careful engineering of phonon decays and thermalization.

Although expansion of trinucleotide repeats accounts for over 30 human diseases, mechanisms of repeat instability remain poorly understood. We show that a Drosophila model for the CAG/polyglutamine (polyQ) disease spinocerebellar ataxia type 3 recapitulates key features of human CAG-repeat instability, including large repeat changes and strong expansion bias. Instability is dramatically enhanced by transcription and modulated by nuclear excision repair and a regulator of DNA repair adenosine 3',5'-monophosphate (cAMP) response element-binding protein (CREB)-binding protein-a histone acetyltransferase (HAT) whose decreased activity contributes to polyQ disease. Pharmacological treatment to normalize acetylation suppressed instability. Thus, toxic consequences of pathogenic polyQ protein may include enhancing repeat instability.

The issue of tuning the relative height of the first two dehydrogenation barriers of methane (CH(4) --> CH(3) + H and CH(3) --> CH(2) + H) is addressed using density-functional theory. It is shown that the combination of a very active reaction center-such as Rh-with a more inert substrate-such as Cu(111)-may hinder the second dehydrogenation step with respect to the first, thus resulting in the reverse of the natural order of the two barriers' heights.

The occurrence of a noncollinear magnetic structure at a Mn monolayer grown epitaxially on Fe(100) is predicted theoretically, using spinor density-functional theory, and observed experimentally, using x-ray magnetic circular dichroism (XMCD) and linear dichroism (XMLD) spectroscopies. The combined use of XMCD and XMLD at the Mn-absorption edge allows us to assess the existence of ferromagnetic and antiferromagnetic order at the interface, and also to determine the moment orientations with element specificity. The experimental results thus obtained are in excellent agreement with the magnetic structure determined theoretically.

This paper studies consistency in the judged probability of a target hypothesis in lists of mutually exclusive nonexhaustive hypotheses. Specifically, it controls the role played by the support of displayed competing hypotheses and the relatedness between the target hypothesis and its alternatives. Three experiments are reported. In all experiments, groups of people were presented with a list of mutually exclusive nonexhaustive causes of a person's death. In the first two experiments, they were asked to judge the probability of each cause as that of the person's decease. In the third experiment, people were asked for a frequency estimation task. Target causes were presented in all lists. Several other alternative causes to the target ones differed across the lists. Findings show that the judged probability/frequency of a target cause changes as a function of the support of the displayed competing causes. Specifically, it is higher when its competing displayed causes have low rather than high support. Findings are consistent with the contrastive support hypothesis within the support theory.

A frequent case of irrational decision making is the tendency to escalate commitment to a chosen course of action after unsuccessful prior investments of money, effort, or time (sunk costs). In previous research it is argued that escalation does not occur when future outcomes and alternative investments are transparent. Inconsistent with this argument, in an experiment in which undergraduates were presented fictitious investment problems with sunk costs, escalation was demonstrated when full information was given about investment alternatives and estimates of future returns. Thus, it is indicated that people may escalate despite knowing that it will not make them economically better off. A more comprehensive understanding of escalation requires disentangling people's noneconomic reasons for escalation.

The first two steps of methane dissociation on Rh(111) have been investigated using density-functional theory, focusing on the dependence of the catalyst's reactivity on the atomic coordination of the active metal site. We find that, although the barrier for the dehydrogenation of methane (CH4 --> CH3 + H) decreases as expected with the coordination of the binding site, the dehydrogenation of methyl (CH3 --> CH2 + H) is hindered at an ad-atom defect, where the first reaction is instead most favored. Our findings indicate that, if it were possible to let the dissociation occur selectively at ad-atom defects, the reaction could be blocked after the first dehydrogenation step, a result of high potential interest for many dream reactions such as, for example, the direct conversion of methane to methanol.

Polycomb group (PcG) proteins function as high molecular weight complexes that maintain transcriptional repression patterns during embryogenesis. The vertebrate DNA binding protein and transcriptional repressor, YY1, shows sequence homology with the Drosophila PcG protein, pleiohomeotic (PHO). YY1 might therefore be a vertebrate PcG protein. We used Drosophila embryo and larval/imaginal disc transcriptional repression systems to determine whether YY1 repressed transcription in a manner consistent with PcG function in vivo. YY1 repressed transcription in Drosophila, and this repression was stable on a PcG-responsive promoter, but not on a PcG-non-responsive promoter. PcG mutants ablated YY1 repression, and YY1 could substitute for PHO in repressing transcription in wing imaginal discs. YY1 functionally compensated for loss of PHO in pho mutant flies and partially corrected mutant phenotypes. Taken together, these results indicate that YY1 functions as a PcG protein. Finally, we found that YY1, as well as Polycomb, required the co-repressor protein CtBP for repression in vivo. These results provide a mechanism for recruitment of vertebrate PcG complexes to DNA and demonstrate new functions for YY1.

Attributing higher "probability" to a sentence of form p-and-q, relative to p, is a reasoning fallacy only if (1) the word probability carries its modern, technical meaning and (2) the sentence p is interpreted as a conjunct of the conjunction p-and-q. Legitimate doubts arise about both conditions in classic demonstrations of the conjunction fallacy. We used betting paradigms and unambiguously conjunctive statements to reduce these sources of ambiguity about conjunctive reasoning. Despite the precautions, conjunction fallacies were as frequent under betting instructions as under standard probability instructions.

At least eight dominant human neurodegenerative diseases are due to the expansion of a polyglutamine within the disease proteins. This confers toxicity on the proteins and is associated with nuclear inclusion formation. Recent findings indicate that molecular chaperones can modulate polyglutamine pathogenesis, but the basis of polyglutamine toxicity and the mechanism by which chaperones suppress neurodegeneration remains unknown. In a Drosophila: disease model, we demonstrate that chaperones show substrate specificity for polyglutamine protein, as well as synergy in suppression of neurotoxicity. Our analysis also reveals that chaperones alter the solubility properties of the protein, indicating that chaperone modulation of neurodegeneration in vivo is associated with altered biochemical properties of the mutant polyglutamine protein. These findings have implications for these and other human neurodegenerative diseases associated with abnormal protein aggregation.

The eyes absent (eya) gene is critical to eye formation in Drosophila; upon loss of eya function, eye progenitor cells die by programmed cell death. Moreover, ectopic eya expression directs eye formation, and eya functionally synergizes in vivo and physically interacts in vitro with two other genes of eye development, sine oculis and dachshund. The Eya protein sequence, while highly conserved to vertebrates, is novel. To define amino acids critical to the function of the Eya protein, we have sequenced eya alleles. These mutations have revealed that loss of the entire Eya Domain is null for eya activity, but that alleles with truncations within the Eya Domain display partial function. We then extended the molecular genetic analysis to interactions within the Eya Domain. This analysis has revealed regions of special importance to interaction with Sine Oculis or Dachshund. Select eya missense mutations within the Eya Domain diminished the interactions with Sine Oculis or Dachshund. Taken together, these data suggest that the conserved Eya Domain is critical for eya activity and may have functional subregions within it.

Genes involved in eye development are highly conserved between vertebrates and Drosophila. Given the complex genetic network controlling early eye development, identification of regulatory sequences controlling gene expression will provide valuable insights toward understanding central events of early eye specification. We have focused on defining regulatory elements critical for Drosophila eyes absent (eya) expression. Although eya has a complex expression pattern during development, analysis of eye-specific mutations in the gene revealed a region selectively deleted in the eye-specific alleles. Here we have performed detailed analysis of the region deleted in the eye-specific eya(2) allele. This analysis shows that this region can direct early eya gene expression in a pattern consistent with that of normal eya in eye progenitor cells. Functional studies indicate that this element will restore appropriate eya transcript expression to rescue the eye-specific allele. We have examined regulation of this element during eye specification, both in normal eye development and in ectopic eye formation. These studies demonstrate that the element was activated upon ectopic expression of the eye specification genes eyeless and dachshund, but does not respond to ectopic expression of eya or sine oculis. The differential regulation of this element by genes involved during early retinal formation reveals new aspects of the genetic hierarchy of eye development., (Copyright 2000 Academic Press.)

The eyes absent (eya) gene is critical for normal eye development in Drosophila and is highly conserved to vertebrates. To define regions of the gene critical for eye function, we have defined the mutations in the four viable eya alleles. Two of these mutations are eye specific and undergo transvection with other mutations in the gene. These were found to be deletion mutations that remove regulatory sequence critical for eye cell expression of the gene. Two other viable alleles cause a reduced eye phenotype and affect the function of the gene in additional tissues, such as the ocelli. These mutations were found to be insertion mutations of different transposable elements within the 5' UTR of the transcript. Detailed analysis of one of these revealed that the transposable element has become subject to regulation by eye enhancer sequences of the eya gene, disrupting normal expression of EYA in the eye. More extended analysis of the deletion region in the eye-specific alleles indicated that the deleted region defines an enhancer that activates gene expression in eye progenitor cells. This enhancer is responsive to ectopic expression of the eyeless gene. This analysis has defined a critical regulatory region required for proper eye expression of the eya gene.

Polyglutamine (polygln) diseases are a group of inherited neurodegenerative disorders characterized by protein misfolding and aggregation. Here, we investigate the role in polygln disease of heat shock proteins (Hsps), the major class of molecular chaperones responsible for modulating protein folding in the cell. In transfected COS7 and PC12 neural cells, we show that Hsp40 and Hsp70 chaperones localize to intranuclear aggregates formed by either mutant ataxin-3, the disease protein in spinocerebellar ataxia type 3/Machado-Joseph disease (SCA3/MJD), or an unrelated green fluorescent protein fusion protein containing expanded polygln. We further demonstrate that expression of expanded polygln protein elicits a stress response in cells as manifested by marked induction of Hsp70. Studies of SCA3/MJD disease brain confirm these findings, showing localization of Hsp40 and, less commonly, Hsp70 chaperones to intranuclear ataxin-3 aggregates. In transfected cells, overexpression of either of two Hsp40 chaperones, the DNAJ protein homologs HDJ-1 and HDJ-2, suppresses aggregation of truncated or full-length mutant ataxin-3. Finally, we extend these studies to a PC12 neural model of polygln toxicity in which we demonstrate that overexpression of HDJ-1 suppresses polygln aggregation with a parallel decrease in toxicity. These results suggest that expanded polygln protein induces a stress response and that specific molecular chaperones may aid the handling of misfolded or aggregated polygln protein in neurons. This study has therapeutic implications because it suggests that efforts to increase chaperone activity may prove beneficial in this class of diseases.

Normal differentiation requires an appropriately orchestrated sequence of developmental events. Regulation of cell survival and cell death is integrated with these events to achieve proper cell number, cell type, and tissue structure. Here we review regulation of cell survival in the context of a precisely patterned neural structure: the Drosophila compound eye. Numerous mutations lead to altered differentiation and are frequently accompanied by altered patterns of cell death. We discuss various critical times of normal eye development, highlighting how inappropriate regulation of cell death contributes to different mutant phenotypes associated with genes that specify the entire eye primordia, others that pattern the retina, and those that eliminate extraneous cells to refine the precise pigment cell lattice. Finally, we address how the Drosophila eye may allow identification of additional mechanisms that contribute to the normal integration of cell survival with appropriate events of cellular differentiation., (Copyright 1999 John Wiley & Sons, Inc.)

At least eight inherited human neurodegenerative diseases are caused by expansion of a polyglutamine domain within the respective proteins. This confers dominant toxicity on the proteins, leading to dysfunction and loss of neurons. Expanded polyglutamine proteins form aggregates, including nuclear inclusions (NI), within neurons, possibly due to misfolding of the proteins. NI are ubiquitinated and sequester molecular chaperone proteins and proteasome components, suggesting that disease pathogenesis includes activation of cellular stress pathways to help refold, disaggregate or degrade the mutant disease proteins. Overexpression of specific chaperone proteins reduces polyglutamine aggregation in transfected cells, but whether this alters toxicity is unknown. Using a Drosophila melanogaster model of polyglutamine disease, we show that directed expression of the molecular chaperone HSP70 suppresses polyglutamine-induced neurodegeneration in vivo. Suppression by HSP70 occurred without a visible effect on NI formation, indicating that polyglutamine toxicity can be dissociated from formation of large aggregates. Our studies indicate that HSP70 or related molecular chaperones may provide a means of treating these and other neurodegenerative diseases associated with abnormal protein conformation and toxicity.

To apply genetics to the problem of human polyglutamine-repeat disease, we recreated polyglutamine-repeat disease in Drosophila melanogaster. To do this, we expressed forms of the human gene encoding spinocerebellar ataxia type 3, also called Machado-Joseph disease (SCA-3/MJD). This gene is responsible for the most common form of human ataxia worldwide. Expression of a normal form of the MJD protein with 27 polyglutamines (MJDtr-Q27) had no phenotype. However, expression of a form of the protein with an expanded run of 78 glutamines (MJDtr-Q78) caused late onset progressive degeneration. In addition, the MJDtr-Q78 formed abnormal protein aggregates, or nuclear inclusions (NIs), whereas the control protein was cytoplasmic. These data indicate that the mechanisms of human polyglutamine-repeat disease are conserved to Drosophila. We are currently using this model to address potential mechanisms by which the mutant disease protein causes neural degeneration, as well as to define genes that can prevent polyglutamine-induced degeneration. By applying the power of Drosophila genetics to the problem of human polyglutamine-induced neural degeneration, we hope to identify ways to prevent and treat these diseases in humans.

The inherited neurodegenerative diseases caused by an expanded glutamine repeat share the pathologic feature of intranuclear aggregates or inclusions (NI). Here in cell-based studies of the spinocerebellar ataxia type-3 disease protein, ataxin-3, we address two issues central to aggregation: the role of polyglutamine in recruiting proteins into NI and the role of nuclear localization in promoting aggregation. We demonstrate that full-length ataxin-3 is readily recruited from the cytoplasm into NI seeded either by a pathologic ataxin-3 fragment or by a second unrelated glutamine-repeat disease protein, ataxin-1. Experiments with green fluorescence protein/polyglutamine fusion proteins show that a glutamine repeat is sufficient to recruit an otherwise irrelevant protein into NI, and studies of human disease tissue and a Drosophila transgenic model provide evidence that specific glutamine-repeat-containing proteins, including TATA-binding protein and Eyes Absent protein, are recruited into NI in vivo. Finally, we show that nuclear localization promotes aggregation: an ataxin-3 fragment containing a nonpathologic repeat of 27 glutamines forms inclusions only when targeted to the nucleus. Our findings establish the importance of the polyglutamine domain in mediating recruitment and suggest that pathogenesis may be linked in part to the sequestering of glutamine-containing cellular proteins. In addition, we demonstrate that the nuclear environment may be critical for seeding polyglutamine aggregates.

Spinocerebellar ataxia type 3 (SCA3/MJD) is one of at least eight human neurodegenerative diseases caused by glutamine-repeat expansion. We have recreated glutamine-repeat disease in Drosophila using a segment of the SCA3/MJD protein. Targeted expression of the protein with an expanded polyglutamine repeat led to nuclear inclusion (NI) formation and late-onset cell degeneration. Differential sensitivity to the mutant transgene was observed among different cell types, with neurons being particularly susceptible; NI formation alone was not sufficient for degeneration. The viral antiapoptotic gene P35 mitigated polyglutamine-induced degeneration in vivo. Our results demonstrate that cellular mechanisms of human glutamine-repeat disease are conserved in invertebrates. This fly model will aid in identifying additional factors that modulate neurodegeneration.

In eyes absent (eya) mutants, eye progenitor cells undergo cell death early in development. Whereas the phenotype of eya1 is limited to the eye, other mutations are lethal. Genetic and molecular analysis reveals that mutations in one region of the gene cause embryonic lethality, whereas mutations throughout the gene cause defects in eye development. Mosaic analysis indicates that the eya requirement is cell autonomous. In eye-specific mutants, expression in the eye disc is lacking while embryonic expression is normal. Both the type I and type II transcripts are expressed in the developing eye, and expression of either can rescue the eye phenotype. These data indicate a specific requirement for eya function in eye progenitor cells that is normally fulfilled by both transcripts., (Copyright 1998 Elsevier Science Ireland Ltd. All rights reserved.)

The eyes absent (eya) gene plays an essential role in the events that lead to formation of the Drosophila eye; without expression of eya in retinal progenitor cells, they undergo programmed cell death just prior to the morphogenetic furrow, leading to an eyeless or reduced eye phenotype. The eya gene has recently been found to be highly conserved to humans, defining a new gene family. Insights into the gene's function in the fly, therefore, are likely to be relevant to the role of its homologs in vertebrates. Detailed studies at the subcellular level indicate that the Eya protein is localized to the nucleoplasm, suggesting a role in control of nuclear events. The eya gene shows expression and roles in tissues other than the eye, including subsets of cells of the adult visual system, brain, and ovary, as well as an elaborate expression pattern in the embryo. Various mutations in the eya gene cause loss of ocelli, female sterility, or lethality. Analysis of the embryonic lethal phenotype indicates that mutant alleles show defects in head morphogenesis. These data indicate that eya has critical roles in morphogenesis of a number of tissues in the animal, in addition to its role in early eye formation. Despite multiple roles at multiple stages of development of the fly, both the type I and type II forms of the protein, when expressed ectopically during larval development, can direct eye formation., (Copyright 1998 Academic Press.)

During eye development, cell death interplays dynamically with events of differentiation to achieve the remarkably patterned structure of the fly compound eye. Mutations in genes that affect the normal developmental process can lead to excessive death of progenitor cells, or, alternatively, to the differentiation of supernumerary neurons, pigment and cone cells due to survival of cells that would normally be eliminated. These data reveal that eye development contains cell selection processes: only certain cells are selected to undergo differentiation, and supernumerary cells are actively eliminated by cell death pathways to achieve the highly ordered lattice of the eye. The final number of cells that comprise the eye is controlled through a balance of cell proliferation with proper cell differentiation and removal by cell death.