Young children's choices and thoughts about pro-social behaviour towards others with overweight.

OBJECTIVES: This study aimed to investigate weight bias within young children's pro-social choices between characters who differed in body size. METHODS: Seventy-six children aged 4-6 years read stories asking them to choose who they would first help, share with, comfort, and steal from, between a healthy weight and child with overweight. They also selected the one character they would most like to play with. Children's reasoning for these choices was recorded and analysed. RESULTS: The character with overweight was helped first in only a third of the choices made. Children chose the characters with overweight more often as the target for anti-social action. In friendship selections, children overwhelmingly rejected the characters with overweight. However, weight bias was not prominent in the reasons children gave for the choices. Most children were not negative about body shape, weight or appearance. Similarly, in friendship choices, these were mostly expressed positively to the character chosen. Only a small minority of children were explicitly negative about the character with overweight. CONCLUSIONS: A better understanding of weight bias acquisition and variation between children will benefit those working in health care and educational settings. Future research should link with developmental theory, such as on social categorization and theory of mind.

Multiplex single-cell chemical genomics reveals the kinase dependence of the response to targeted therapy.

Chemical genetic screens are a powerful tool for exploring how cancer cells' response to drugs is shaped by their mutations, yet they lack a molecular view of the contribution of individual genes to the response to exposure. Here, we present sci-Plex-Gene-by-Environment (sci-Plex-GxE), a platform for combined single-cell genetic and chemical screening at scale. We highlight the advantages of large-scale, unbiased screening by defining the contribution of each of 522 human kinases to the response of glioblastoma to different drugs designed to abrogate signaling from the receptor tyrosine kinase pathway. In total, we probed 14,121 gene-by-environment combinations across 1,052,205 single-cell transcriptomes. We identify an expression signature characteristic of compensatory adaptive signaling regulated in a MEK/MAPK-dependent manner. Further analyses aimed at preventing adaptation revealed promising combination therapies, including dual MEK and CDC7/CDK9 or nuclear factor κB (NF-κB) inhibitors, as potent means of preventing transcriptional adaptation of glioblastoma to targeted therapy.