Who Influences Whom? Examining Self-Control and Delinquent Peer Dynamics among Justice-Involved Youth.

Myeloid cell plasticity maintains organ health. As we age, myelopoiesis is biased and the functional landscape of monocytes, macrophages and their precursors narrows as they adopt inflammatory phenotypes. Ageing also commonly leads to haematopoietic stem cells (HSCs) spontaneously acquiring somatic genetic variants, which accelerate inflammatory phenotypic switching, erode myeloid diversity and promote disease. Yet, how lifestyle behaviours facilitate or oppose mutation-driven myeloid cell homogenization is not well defined. CH is the accrual of somatic mutations in bone marrow (BM) HSCs that confer proliferative and survival advantages causing their clonal outgrowth. CH is commonly diagnosed when blood variant allele frequency attains 2%, but as CH clones expand, variant allele frequency can reach 50% or higher. Whether the speed and extent of clonal expansion is strictly inscribed by mutation-directed intracellular signalling or if external cues have a role remains unclear. CH mutant macrophages display increased inflammation, elevating the risk of atherosclerosis. It is unsettled whether exposomic factors modify CH or the programming of mutant cells. In silico modelling has suggested that changes in HSC proliferation modulate CH clone evolution through neutral drift. In agreement, cross-sectional analyses have shown that an unhealthy diet, inflammation or infection increase the prevalence of CH. However, atherosclerosis per se and biochemical cardiovascular risk factors do not associate with incident CH or changes in variant allele frequency. Disentanglement of the relationships between CH and atherogenic factors is needed and biological synergies between mutation-governed processes and lifestyle modulators have yet to be considered.