In 1974 an article appeared in Science magazine with the dry-sounding title “Judgment Under Uncertainty: Heuristics and Biases” by a pair of psychologists who were not well known outside their discipline of decision theory. In it Amos Tversky and Daniel Kahneman introduced the world to Prospect Theory, which mapped out how humans actually behave when faced with decisions about gains and losses, in contrast to how economists assumed that people behave. Prospect Theory turned Economics on its head by demonstrating through a series of ingenious experiments that people are much more concerned with losses than they are with gains, and that framing a choice from one perspective or the other will result in decisions that are exactly the opposite of each other, even if the outcomes are monetarily the same. Prospect Theory led cognitive psychology in a new direction that began to uncover other human biases in thinking that are probably not learned but are part of our brain’s wiring.

Thinking fast and slow.

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Statistical Parametric Mapping The Analysis Of Functional Brain Images

Scale for the Assessment of Negative Symptoms

Social scientists often estimate models from correlational data, where the independent variable has not been exogenously manipulated; they also make implicit or explicit causal claims based on these models. When can these claims be made? We answer this question by first discussing design and estimation conditions under which model estimates can be interpreted, using the randomized experiment as the gold standard. We show how endogeneity – which includes omitted variables, omitted selection, simultaneity, common-method variance, and measurement error – renders estimates causally uninterpretable. Second, we present methods that allow researchers to test causal claims in situations where randomization is not possible or when causal interpretation could be confounded; these methods include fixed-effects panel, sample selection, instrumental variable, regression discontinuity, and difference-in-differences models. Third, we take stock of the methodological rigor with which causal claims are being made in a social sciences discipline by reviewing a representative sample of 110 articles on leadership published in the previous 10 years in top-tier journals. Our key finding is that researchers fail to address at least 66% and up to 90% of design and estimation conditions that make causal claims invalid. We conclude by offering 10 suggestions on how to improve non-experimental research.

On making causal claims : A review and recommendations

http://brainmap.org/pubs/EickhoffNI12.pdf

Activation likelihood estimation meta-analysis revisited.

http://www.fil.ion.ucl.ac.uk/~karl/False%20discovery%20rate%20revisited.pdf

False discovery rate revisited: FDR and topological inference using Gaussian random fields.

Topological FDR for neuroimaging.

Negative symptoms in schizophrenia have been grouped into the 2 factors of apathy and diminished expression, which might be caused by separable pathophysiological mechanisms. Recently, it has been proposed that apathy could be due to dysfunctional integration of reward and effort during decision making. We asked whether apathy in particular is associated with stronger devaluation ("discounting") of monetary rewards that require physical effort. Thirty-one patients with schizophrenia and 20 healthy control participants performed a computerized effort discounting task in which they could choose to exert physical effort on a handgrip to obtain monetary rewards. This procedure yields an individual measure for the strength of effort discounting. The degree of effort discounting was strongly correlated with apathy, but not with diminished expression. Importantly, the association between apathy and effort discounting was not driven by cognitive ability, antipsychotic medication, or other clinical and demographic variables. This study provides the first evidence for a highly specific association of apathy with effort-based decision making in patients with schizophrenia. Within a translational framework, the present effort discounting task could provide a bridge between apathy as a psychopathological phenomenon and established behavioral tasks to address similar states in animals.

https://www.zora.uzh.ch/id/eprint/100545/1/Hartmann_SZBull_2014.pdf

Apathy But Not Diminished Expression in Schizophrenia Is Associated With Discounting of Monetary Rewards by Physical Effort

1. Block of the human two-pore domain potassium (2-PK) channel TREK-1 by fluoxetine (Prozac) and its active metabolite, norfluoxetine, was investigated using whole-cell patch-clamp recording of currents through recombinant channels in tsA 201 cells. 2. Fluoxetine produced a concentration-dependent inhibition of TREK-1 current that was reversible on wash. The IC50 for block was 19 microM. Block by fluoxetine was voltage-independent. Fluoxetine (100 microM) produced an 84% inhibition of TREK-1 currents, but only a 31% block of currents through a related 2-PK channel, TASK-3. 3. Norfluoxetine was a more potent inhibitor of TREK-1 currents with an IC50 of 9 microM. Block by norfluoxetine was also voltage-independent. 4. Truncation of the C-terminus of TREK-1 (delta89) resulted in a loss of channel function, which could be restored by intracellular acidification or the mutation E306A. The mutation E306A alone increased basal TREK-1 current and resulted in a loss of the slow phase of TREK-1 activation. 5. Progressive deletion of the C-terminus of TREK-1 had no effect on the inhibition of the channel by fluoxetine. The E306A mutation, on the other hand, reduced the magnitude of fluoxetine inhibition, with 100 microM producing only a 40% inhibition. 6. It is concluded that fluoxetine and norfluoxetine are potent inhibitors of TREK-1. Block of TREK-1 by fluoxetine may have important consequences when the drug is used clinically in the treatment of depression.

/pdf/inhibition-of-the-human-two-pore-domain-potassium-channel-3onbhvf8s6.pdf

Inhibition of the human two-pore domain potassium channel, TREK-1, by fluoxetine and its metabolite norfluoxetine.

Previous research on computer games has tended to concentrate on their more negative effects (e.g., addiction, increased aggression). This study departs from the traditional clinical and social learning explanations for these behavioral phenomena and examines the effect of personality, in-game reinforcement characteristics, gender, and skill on the emotional state of the game-player. Results demonstrated that in-game reinforcement characteristics and skill significantly effect a number of affective measures (most notably excitement and frustration). The implications of the impact of game-play on affect are discussed with reference to the concepts of "addiction" and "aggression."

/pdf/affect-and-the-computer-game-player-the-effect-of-gender-2nhtpv9h2c.pdf

Justin R. Chumbley

Papers

False discovery rate revisited: FDR and topological inference using Gaussian random fields.

Topological FDR for neuroimaging.

Apathy But Not Diminished Expression in Schizophrenia Is Associated With Discounting of Monetary Rewards by Physical Effort

Inhibition of the human two-pore domain potassium channel, TREK-1, by fluoxetine and its metabolite norfluoxetine.

Affect and the Computer Game Player: The Effect of Gender, Personality, and Game Reinforcement Structure on Affective Responses to Computer Game-Play