Traumatic losses permeate daily emotional experiences: roles of daily uplifts and subjective age.

Daily emotional experiences may vary depending on a stressor's intensity or source. The present study aimed to examine the interaction between traumatic loss, daily uplifts, and daily subjective age predicting daily negative affect. Results from a 14-day daily diary study of 440 US adults aged 50-85 showed that daily increases in uplifts were associated with decreases in negative affect, especially for those who reported a traumatic loss when they also experienced increases in subjective age. Based on our study, daily events and perceptions can have a considerable impact on daily functioning and may serve as important mechanisms after a traumatic loss. Although traumatic losses may impact individuals differently, incorporating daily uplifts, based on available resources and capacities, may foster daily emotional well-being.

Does time heal all wounds? An investigation of time, grief, and attitudes toward death.

When experiencing the loss of a loved one, individuals adapt and change how they understand death, how they interpret the meaning of the loss, and how they remember the deceased. In the present study (N = 164), we investigated whether the time since the loss - recent or distant - was associated with individuals' bereavement, attitudes toward death, and their meaning of death. We found that individuals who experienced a recent loss reported more grief and more negative death attitudes compared to individuals who experienced a loss more than 5 years ago. Moreover, the bereavement appeared to completely mediate the time since the loss and the individuals' attitudes about death. The findings suggest that time-dependent adaptations after a loss shifts individuals' death attitudes, grief symptoms, and thoughts about death.

Role of the Beta and Gamma Isoforms of the Adapter Protein SH2B1 in Regulating Energy Balance.

Human variants of the adapter protein SH2B1 are associated with severe childhood obesity, hyperphagia, and insulin resistance-phenotypes mimicked by mice lacking Sh2b1. SH2B1ß and γ isoforms are expressed ubiquitously, whereas SH2B1α and δ isoforms are expressed primarily in the brain. Restoring SH2B1ß driven by the neuron-specific enolase promoter largely reverses the metabolic phenotype of Sh2b1-null mice, suggesting crucial roles for neuronal SH2B1ß in energy balance control. Here we test this hypothesis by using CRISPR/Cas9 gene editing to delete the ß and γ isoforms from the neurons of mice (SH2B1ßγ neuron-specific knockout [NKO] mice) or throughout the body (SH2B1ßγ knockout [KO] mice). While parameters of energy balance were normal in both male and female SH2B1ßγ NKO mice, food intake, body weight, and adiposity were increased in male (but not female) SH2B1ßγ KO mice. Analysis of long-read single-cell RNA seq data from wild-type mouse brain revealed that neurons express almost exclusively the α and δ isoforms, whereas neuroglial cells express almost exclusively the ß and γ isoforms. Our work suggests that neuronal SH2B1ß and γ are not primary regulators of energy balance. Rather, non-neuronal SH2B1ß and γ in combination with neuronal SH2B1α and δ suffice for body weight maintenance. While SH2B1ß/γ and SH2B1α/δ share some functionality, SH2B1ß/γ appears to play a larger role in promoting leanness.