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Eating disorders are characterized by extreme emotions, beliefs, and behaviors related to weight and food. They can cause serious psychological and physical problems and have the highest mortality rate of any mental illness. Research has established the strong connection between disordered eating and emotion, namely that the disordered behaviors around eating serve as a coping response to deal with distressing and overwhelming emotion. Instead of focusing on the behaviors or outcomes of an eating disorder, effective support should include addressing the underlying emotional experience of someone with an eating disorder. Social media companies are at a unique advantage to provide support for those who post eating disorder related content by offering more supportive experiences that better match people’s needs. This paper explores ways to address the emotional needs of social media users through designing experiences that (a) make people feel seen and heard by focusing on their suffering and emotions rather than their eating behaviors; (b) help people feel they belong by focusing on activities and opportunities that enable connection with themselves and things they value; and (c) help people feel in control by focusing on resources and information to receive support or take steps toward recovery.

Figure S2. Effect of hypoxia on brain morphology and apoptosis. (PDF 8950 kb)

Figure S1. Level of brain histology sections with outline of specific brain regions. (PDF 4450 kb)

The persistence of neural precursor cells (NPCs) in distinct niches of the adult brain and spinal cord provides an important opportunity for regeneration in the affected nervous system. In the adult brain, neural precursor cells (NPCs) generate new neurons that can be integrated into the CNS circuitry to replace damaged or lost neurons, and contribute to learning and memory processes. Deregulated neurogenesis has been observed under both acute and chronic neurological conditions including stroke, Alzheimer’s disease, and Parkinson’s disease. The extent to which neurogenesis contributes to brain repair is severely limited by the neuroinflammatory processes associated with these neurodegenerative conditions. During injury, microglia, the CNS resident immune cells become activated and produce a number of anti- and pro-inflammatory factors that can modulate neurogenesis and survival of NPCs. The goal of this study was to identify mechanisms of NPC apoptosis induced by microglia-derived cytokines. Using a conditioned media model, we have identified that activation of the TNFα, IL-1β and Fas signaling pathways induces death of NPCs via the intrinsic pathway of apoptosis in vitro. TNFα activates Puma and NPC apoptosis via an NF-κB-dependent mechanism. Activation of the IL-1β pathway, by microglia-derived or rIL-1β induces cell cycle arrest and apoptosis via p53-dependent upregulation of p21 and Puma. IL-1β can also induce an increased expression of Fas via an NF-κB-dependent pathway. Fas signaling in NPCs also culminates in activation of Puma and induction of mitochondrial-dependent apoptosis of NPCs. Puma appears to be a dominant regulator of cytokine-induced NPC apoptosis in vitro, as well as in an in vivo model of spinal cord injury. This study implicates microglia-derived TNFα and IL-1β as potent inducers of the BH3-only protein Puma through activation of the NF-κB and p53 pathways, respectively. Furthermore, these findings provide novel molecular targets to improve the survival of both endogenous and transplanted NPCs in regenerative therapies for acute and chronic neurological conditions.

When behavior is directed toward activities, people, and experiences that people find most important in their lives, they are engaged in valued living. Given that valued living is associated with well-being, quality of life, and happiness, understanding ways in which value-concordant behavior can be promoted, enhanced, and maintained is of utmost importance. Two studies sought to examine the associations between mindfulness--as a dispositional trait and as developed through training--and valued living. In Study 1 dispositional mindfulness was strongly related to three aspects of valued living: the general tendency for people to understand their values and act in value-consistent ways; directing behavior toward valued activities; and clarity of, action toward, and feelings of success and satisfaction with action toward specific important values. Study 2 compared valued living scores of people participating in a Mindfulness Based Stress Reduction (MBSR) program to a control group. Mindfulness training was related to increased general valuing processes and value-relevant behavior but was not related to increased clarity of, action, or success or satisfaction with action toward specific values. The two studies also explored the mechanisms underlying the relationship between mindfulness and valued living. In Study 1, self-compassion, psychological flexibility, and self-clarity each partially mediated the relationship between dispositional mindfulness and valued living, but decentering did not. In Study 2, change in attention mediated the relationship between group (MBSR or control) and valued living, but acceptance, self-compassion, psychological flexibility, self-clarity, and decentering did not. Lastly, both studies found that valued living mediated the relationship between mindfulness and well-being. Taken together, these findings add to the growing body of literature demonstrating the benefits of mindfulness and highlight the important influence that clearly identifying and behaving in accordance with important values has on well-being.

Table S1. Primer sequences used for RT-qPCR experiments. (DOCX 13 kb)

Table S1. Primer sequences used for RT-qPCR experiments. (DOCX 13 kb)

Figure S4. The effect of hypoxia on the level of pro-inflammatory cytokines in the brain. (PDF 2120 kb)

Figure S3. Effect of hypoxia on brain cell populations. (PDF 2850 kb)

Table S2. Brain region and description. (DOCX 13 kb)

Table S2. Brain region and description. (DOCX 13 kb)

Figure S3. Effect of hypoxia on brain cell populations. (PDF 2850 kb)