Acoustic signalling reflects personality in a social mammal

Social interactions among individuals are often mediated through acoustic signals. If acoustic signals are consistent and related to an individual's personality, these consistent individual differences in signalling may be an important driver in social interactions. However, few studies in non-human mammals have investigated the relationship between acoustic signalling and personality. Here we show that acoustic signalling rate is repeatable and strongly related to personality in a highly social mammal, the domestic pig (Sus scrofa domestica). Furthermore, acoustic signalling varied between environments of differing quality, with males from a poor-quality environment having a reduced vocalization rate compared with females and males from an enriched environment. Such differences may be mediated by personality with pigs from a poor-quality environment having more reactive and more extreme personality scores compared with pigs from an enriched environment. Our results add to the evidence that acoustic signalling reflects personality in a non-human mammal. Signals reflecting personalities may have far reaching consequences in shaping the evolution of social behaviours as acoustic communication forms an integral part of animal societies.

Tyrosine kinase inhibitor insensitivity of non-cycling CD34+ human acute myeloid leukaemia cells with FMS-like tyrosine kinase 3 mutations.

The efficacy of tyrosine kinase (TK) inhibitors on non-cycling acute myeloid leukaemia (AML) cells, previously shown to have potent tumourigenic potential, is unknown. This pilot study describes the first attempt to characterize non-cycling cells from a small series of human FMS-like tyrosine kinase 3 (FLT3) mutation positive samples. CD34+ AML cells from patients with FLT3 mutation positive AML were cultured on murine stroma. In expansion cultures, non-cycling cells were found to retain CD34+ expression in contrast to dividing cells. Leukaemic gene rearrangements could be detected in non-cycling cells, indicating their leukaemic origin. Significantly, the FLT3-internal tandem duplication (ITD) mutation was found in the non-cycling fraction of four out of five cases. Exposure to the FLT3-directed inhibitor TKI258 clearly inhibited the growth of AML CD34+ cells in short-term cultures and colony-forming unit assays. Crucially, non-cycling cells were not eradicated, with the exception of one case, which exhibited exquisite sensitivity to the compound. Moreover, in longer-term cultures, TKI258-treated non-cycling cells showed no growth impairment compared to treatment-naive non-cycling cells. These findings suggest that non-cycling cells in AML may constitute a disease reservoir that is resistant to TK inhibition. Further studies with a larger sample size and other inhibitors are warranted.