When job performance is all relative: how family motivation energizes effort and compensates for intrinsic motivation

Supporting one's family is a major reason why many people work, yet surprisingly little research has examined the implications of family motivation. Drawing on theories of prosocial motivation and action identification, we propose that family motivation increases job performance by enhancing energy and reducing stress, and it is especially important when intrinsic motivation is lacking. Survey and diary data collected across multiple time points in a Mexican maquiladora generally support our model. Specifically, we find that family motivation enhances job performance when intrinsic motivation is low—in part by providing energy, but not by reducing stress. We conclude that supporting a family provides a powerful source of motivation that can boost performance in the workplace, offering meaningful implications for research on motivation and the dynamics of work and family engagement

The X-chromosome and susceptibility to ankylosing spondylitis

OBJECTIVE: Ankylosing spondylitis (AS) affects 0.25-1.0% of the population, and its etiology is incompletely understood. Susceptibility to this highly familial disease (lambda(s) = 58) is primarily genetically determined. There is a significant sex bias in AS, and there are differences in recurrence risk to the offspring of affected mothers and fathers, suggesting that there may be an X-linked recessive effect. We undertook an X-chromosome linkage study to determine any contribution of the X-chromosome to AS susceptibility. METHODS: A linkage study of the X-chromosome using 234 affected sibling pairs was performed to investigate this hypothesis. RESULTS: No linkage of the X-chromosome with susceptibility to AS was found. Model-free multipoint linkage analysis strongly excluded any significant genetic contribution (lambda > or = 1.5) to AS susceptibility encoded on the X-chromosome (logarithm of odds [LOD] <-2.0). Smaller genetic effects (lambda > or = 1.3) were also found to be unlikely (LOD <-1.0). CONCLUSION: The sex bias in AS is not explained by X-chromosome-encoded genetic effects. The disease model best explaining the sex bias in occurrence and transmission of AS is a polygenic model with a higher susceptibility threshold in females