Ation ?genetics ?prenatal environment ?transcriptomeDennis R Grayson1 Alessandro Guidotti*,1 Department of Psychiatry, The Psychiatric Institute, University of Illinois at Chicago, 1601 W. Taylor St., Chicago, IL 60607, USA *Author for correspondence: Tel.: +1 312 413 4577 dgrayson@ psych.uic.eduThe Center for Disease Control estimates that approximately one in 88 children are diagnosed with aut
Ation ?genetics ?prenatal environment ?transcriptomeDennis R Grayson1 Alessandro Guidotti*,1 Department of Psychiatry, The Psychiatric Institute, University of Illinois at Chicago, 1601 W. Taylor St., Chicago, IL 60607, USA *Author for correspondence: Tel.: +1 312 413 4577 dgrayson@ psych.uic.eduThe Center for Disease Control estimates that approximately one in 88 children are diagnosed with aut
Impact the brain through epigenetic mechanisms. Both genetic mutations and epigenetic influences alter gene expression in different cell types of the brain. Mutations impact the expression of large numbers of genes and also have downstream consequences depending on specific pathways associated with the mutation. Environmental factors impact the expression of sets of genes by altering methylation/h
Y than acquired immunity [47], and may be especially sensitive to energetic indicators. The relationships between adipose tissue, leptin and immune function suggest that organisms increase innate immune vigilance when adipose tissue reserves are sufficient to fund acute immune responses. This framework, of considering the cost of an acute response as underlying the coupling of nonacute immune func
Y than acquired immunity [47], and may be especially sensitive to energetic indicators. The relationships between adipose tissue, leptin and immune function suggest that organisms increase innate immune vigilance when adipose tissue reserves are sufficient to fund acute immune responses. This framework, of considering the cost of an acute response as underlying the coupling of nonacute immune func
Tion (reviewed in [45]), but in human populations the relationship to immunity is often more complex. For instance, previous research in this population finds no relationship between leptin levels and acquired immune function in moderately undernourished children [46]. While the specifics of how adipose tissue influences CRP are complex, our results support a strong relationship between adiposity
Tion (reviewed in [45]), but in human populations the relationship to immunity is often more complex. For instance, previous research in this population finds no relationship between leptin levels and acquired immune function in moderately undernourished children [46]. While the specifics of how adipose tissue influences CRP are complex, our results support a strong relationship between adiposity
E both investing heavily in growth and had high adiposity, however their CRP levels (M = ?.63, SD = 0.97) did not differ significantly from girls with similar levels of adiposity who were not investing in growth (M = ?.87, SD = 1.09, t = ?.10, P = 0.28). Girls who were investing in growth and had low adiposity had the lowest CRP levels of any group (M = ?.74, SD = 1.10), significantly lower than g