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A meta-analytic review was conducted to explain divergent findings on the relation between children's aggressive behavior and hostile attribution of intent to peers. Forty-one studies with 6,017 participants were included in the analysis. Ten studies concerned representative samples from the general population, 24 studies compared nonaggressive to extremely aggressive nonreferred samples, and 7 studies compared nonreferred samples with children referred for aggressive behavior problems. A robust significant association between hostile attribution of intent and aggressive behavior was found. Effect sizes differed considerably between studies. Larger effects were associated with more severe aggressive behavior, rejection by peers as one of the selection criteria, inclusion of 8- to-12-year-old participants, and absence of control for intelligence. Video and picture presentation of stimuli were associated with smaller effect sizes than was audio presentation. Staging of actual social interactions was associated with the largest effects. The importance of understanding moderators of effect size for theory development is stressed.

Boys with aggressive behavior problems are frequently taught to \"stop and think\" before they act. In provocative situations, pausing to monitor their own feelings, to consider the feelings of others, or to delay their response is believed to reduce aggressive behavior. This study aimed to test these assumptions. Thirty-two highly aggressive boys in special education and 31 normal comparison boys were presented vignettes concerning provocation by a peer and given specific cognitive assignments. Participants were either asked to (1) monitor and regulate their own emotions, (2) consider the provocateur's emotions and intentions, (3) wait 10 s, or (4) answer a factual question. The cognitive assignments differentially affected response aggressiveness. Monitoring and regulation of own emotions reduced aggressiveness in the aggressive group. Considering the peer's emotions and intentions tended to decrease aggressiveness in the normal comparison group and increase aggressiveness in the aggressive group. Delay increased response aggressiveness in the aggressive group as well. Answering factual questions had no effect on response aggressiveness. Implications for cognitive-behavioral interventions for aggressive boys are discussed.

Myelodysplastic syndrome (MDS) is characterized by bone marrow failure, clonal evolution and leukemic progression, but the pathophysiologic processes driving these events remain incompletely understood. Here, by establishing a comprehensive single-cell transcriptional taxonomy of human MDS, we reveal that inflammatory remodeling of bone marrow stromal niches is a common early feature, irrespective of the genetic driver landscape. We identify an activated CD8-T-cell subset as a source of stromal inflammation via TNF-receptor signaling, which prompts the inflammatory rewiring and loss of repopulating ability of residual normal hematopoietic stem/progenitor cells (HSPC). Mutant HSPCs display relative resistance to this inflammatory stress and reside predominantly in a transcriptional ‘high output’ state, providing a biological framework to their competitive advantage in an inflammatory microenvironment. Consistent with this, stromal inflammation associates with leukemic progression and reduced survival. Our data thus support a model of immune-stromal inflammatory signaling driving tissue failure and clonal evolution in the hematopoietic system. Mechanisms of clonal evolution in myeloid neoplasms remain incompletely understood. Darwinian theory predicts that the (micro)environment of clone-propagating stem cells may contribute to clonal selection. Here, we provide data fitting this model, establishing a relationship between stromal niche inflammation, inflammatory stress in HSPCs, clonal resistance and leukemic evolution in human MDS. Mechanisms of clonal evolution in myeloid neoplasms remain incompletely understood. Darwinian theory predicts that the (micro)environment of clone-propagating stem cells may contribute to clonal selection. Here, authors provide data fitting this model, establishing a relationship between stromal niche inflammation, inflammatory stress in HSPCs, clonal resistance and leukemic evolution in human myelodysplastic syndrome.