Living in wealthy neighborhoods increases material desires and maladaptive consumption

Despite the presumed national economic benefits that result from high levels of discretionary spending, past studies suggest that material consumption decreases individual economic and subjective well-being. However, most research on the development of materialistic values has examined how persuasive materialistic messages cause materialism. We recruited 2702 participants to test our prediction that living in wealthy neighborhoods should increase material desires and maladaptive consumption in much the same way it decreases happiness. Interestingly, our regression models revealed that individual socioeconomic status (SES) and neighborhood SES have unique, and opposite, predictive patterns of material consumption. Specifically, after controlling for age, gender, and population size, greater neighborhood SES predicted greater desires for material consumption, more impulsive buying, and fewer savings behaviors while individual SES showed the reverse pattern. Our path model suggests that greater neighborhood SES leads to increased material desires, which then predicts more frequent impulsive buying, and fewer savings behaviors. We discuss why neighborhood SES might change values and consumer behaviors

Dosimetric review of cardiac implantable electronic device patients receiving radiotherapy

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/135218/1/acm20254-sup-0002.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/135218/2/acm20254.pd

JEM_20142322 1..9

Variants in triggering receptor expressed on myeloid cells 2 (TREM2) confer high risk for Alzheimer's disease (AD) and other neurodegenerative diseases. However, the cell types and mechanisms underlying TREM2's involvement in neurodegeneration remain to be established. Here, we report that TREM2 is up-regulated on myeloid cells surrounding amyloid deposits in AD mouse models and human AD tissue. TREM2 was detected on CD45 hi Ly6C + myeloid cells, but not on P2RY2 + parenchymal microglia. In AD mice deficient for TREM2, the CD45 hi Ly6C + macrophages are virtually eliminated, resulting in reduced inflammation and ameliorated amyloid and tau pathologies. These data suggest a functionally important role for TREM2 + macrophages in AD pathogenesis and an unexpected, detrimental role of TREM2 in AD pathology. These findings have direct implications for future development of TREM2-targeted therapeutics

TREM2 deficiency eliminates TREM2+ inflammatory macrophages and ameliorates pathology in Alzheimer\u27s disease mouse models.

Variants in triggering receptor expressed on myeloid cells 2 (TREM2) confer high risk for Alzheimer\u27s disease (AD) and other neurodegenerative diseases. However, the cell types and mechanisms underlying TREM2\u27s involvement in neurodegeneration remain to be established. Here, we report that TREM2 is up-regulated on myeloid cells surrounding amyloid deposits in AD mouse models and human AD tissue. TREM2 was detected on CD45(hi)Ly6C(+) myeloid cells, but not on P2RY12(+) parenchymal microglia. In AD mice deficient for TREM2, the CD45(hi)Ly6C(+) macrophages are virtually eliminated, resulting in reduced inflammation and ameliorated amyloid and tau pathologies. These data suggest a functionally important role for TREM2(+) macrophages in AD pathogenesis and an unexpected, detrimental role of TREM2 in AD pathology. These findings have direct implications for future development of TREM2-targeted therapeutics. J Exp Med 2015 Mar 9; 212(3):287-95