Effect of signs and signals of need on prosocial pulling.

<p>Percentage of trials in which prosocial pulling occurred following different kinds of signaling (dark bars) or without signaling (light bars). Figures inside the bars represent numbers of trials. For instance, prosocial pulling occurred in 85% of 121 trials in which no signaling of any kind occurred (total). Looking = recipient looks at reward; reaching = recipient tries to access reward with arm, request = recipient verbally asks for reward.</p

Experimental setting.

<p>Two playpens serve as compartment for the donor (D) and the recipient child (R). The handles (H) of the apparatus can be manipulated from the donor compartment only, and allow to pull the boards (U: upper board; L: lower board) with the dishes within reach. Between trials, the curtains are drawn.</p

Pulling latencies.

<p>Latency to pull the prosocial tray during test trials in the costly version, the cost-free version, and to pull the board baited for oneself during motivation trials. The presence of a reward for the partner in addition to a reward to the subject herself does not increase the latency to pull.</p

Prosocial games played with nonhuman primates.

<p>Studies differ with regard to <b>payoff distribution,</b> and whether help is <b>costly</b>. Included are studies only in which subjects have to choose between physically presented payoff distributions by pulling an apparatus within reach.</p><p>Ref.: ¹Silk et al. 2005, ²Jensen et al. 2006, ³Vonk et al. 2008, ⁴Burkart et al. 2007, ⁵Lakshminarayanan and Santos 2008, ⁶Takimoto et al. 2010, ⁷Cronin et al. 2009, ⁸Stevens 2010, ⁹Massen et al. 2010.</p>a<p>reward written in „()“ goes to an empty compartment and is therefore out of reach for both subjects.</p>b<p>donor is allowed to choose both distributions during one trial.</p>c<p><b>1</b> = favored reward; 1 = less favored reward; 1 = non-favored reward.</p>d<p>tested one-tailed t-test; but not statistically significant if tested two-tailed like other studies did.</p>e<p>yes for subdominant recipient, no for dominant recipient; no for subdominant if invisible, neg. for dominant if invisible.</p>f<p>yes for kin partner; no for non-kin partner; under both conditions prosocial tendency declined with increasing rank number.</p

Rasch analyses.

<p>The higher the “item difficulty” - score, the higher the difficulty level of the item. Fit statistics (standardized infit and outfit values) have an expected value of 0. Values >2.0 indicate a misfit <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0068440#pone.0068440-Wright1" target="_blank">[77]</a>.</p

Prosocial effect.

<p>Donors’ (n = 31) pulling of the prosocial distribution ([0,1], or [1,1], respectively) in the presence (test condition, dark bar) or absence (control condition, light bar) of a recipient, for both versions of the dictator game. A prosocial effect was present only in the costly version of the game. ***: p<0.001.</p

Reactions of the donor children to recipients taking the provisioned reward.

<p>The children could either not attend to the recipient at all, attend with a neutral emotional expression, or attend with a positive emotional expression.</p

Attention of donors to the partner’s plate before pulling.

<p>Percentage of trials when donors looked at the partner’s plate in test sessions of the costly version (reward on partner’s side), the cost-free version (reward on both sides) and during motivation trials (one reward on donor’s side). The presence of a reward for the partner in addition to a reward to the subject herself does not increase attention to the partner’s plate.</p

Preschool children fail primate prosocial game because of attentional task demands

Various nonhuman primate species have been tested with prosocial games (i.e. derivates from dictator games) in order to better understand the evolutionary origin of proactive prosociality in humans. Results of these efforts are mixed, and it is difficult to disentangle true species differences from methodological artifacts. We tested 2- to 5-year-old children with a costly and a cost-free version of a prosocial game that differ with regard to the payoff distribution and are widely used with nonhuman primates. Simultaneously, we assessed the subjects' level of Theory of Mind understanding. Prosocial behavior was demonstrated with the prosocial game, and did not increase with more advanced Theory of Mind understanding. However, prosocial behavior could only be detected with the costly version of the game, whereas the children failed the cost-free version that is most commonly used with nonhuman primates. A detailed comparison of the children's behavior in the two versions of the game indicates that the failure was due to higher attentional demands of the cost-free version, rather than to a lack of prosociality per se. Our results thus show (i) that subtle differences in prosociality tasks can substantially bias the outcome and thus prevent meaningful species comparisons, and (ii) that like in nonhuman primates, prosocial behavior in human children does not require advanced Theory of Mind understanding in the present context. However, both developmental and comparative psychology accumulate increasing evidence for the multidimensionality of prosocial behaviors, suggesting that different forms of prosociality are also regulated differentially. For future efforts to understand the evolutionary origin of prosociality it is thus crucial to take this heterogeneity into account

Mutations in MMP9 and MMP13 Determine the Mode of Inheritance and the Clinical Spectrum of Metaphyseal Anadysplasia

The matrix metalloproteinases MMP9 and MMP13 catalyze the degradation of extracellular matrix (ECM) components in the growth plate and at the same time cleave and release biologically active molecules stored in the ECM, such as VEGFA. In mice, ablation of Mmp9, Mmp13, or both Mmp9 and Mmp13 causes severe distortion of the metaphyseal growth plate. We report that mutations in either MMP9 or MMP13 are responsible for the human disease metaphyseal anadysplasia (MAD), a heterogeneous group of disorders for which a milder recessive variant and a more severe dominant variant are known. We found that recessive MAD is caused by homozygous loss of function of either MMP9 or MMP13, whereas dominant MAD is associated with missense mutations in the prodomain of MMP13 that determine autoactivation of MMP13 and intracellular degradation of both MMP13 and MMP9, resulting in a double enzymatic deficiency