Compulsive Buying: The Impact of Attitudes Toward Body Image, Eating Disorders, and Physical Appearance Investment.

The current research examined whether eating disorder risk and the attitudinal elements related to body image predict compulsive buying. A sample of students attending two public universities located in the northeast United States were surveyed. A multiple regression indicated that attitudes related to one's physical appearance, fitness, and health as well as eating disorder risk were predictors of compulsive buying with appearance orientation being the strongest predictor of compulsive buying.

Identification of targets for rational pharmacological therapy in childhood craniopharyngioma.

Introduction: Pediatric adamantinomatous craniopharyngioma (ACP) is a histologically benign but clinically aggressive brain tumor that arises from the sellar/suprasellar region. Despite a high survival rate with current surgical and radiation therapy (75-95 % at 10 years), ACP is associated with debilitating visual, endocrine, neurocognitive and psychological morbidity, resulting in excheptionally poor quality of life for survivors. Identification of an effective pharmacological therapy could drastically decrease morbidity and improve long term outcomes for children with ACP.

RIP1 negatively regulates basal autophagic flux through TFEB to control sensitivity to apoptosis.

In a synthetic lethality/viability screen, we identified the serine-threonine kinase RIP1 (RIPK1) as a gene whose knockdown is highly selected against during growth in normal media, in which autophagy is not critical, but selected for in conditions that increase reliance on basal autophagy. RIP1 represses basal autophagy in part due to its ability to regulate the TFEB transcription factor, which controls the expression of autophagy-related and lysosomal genes. RIP1 activates ERK, which negatively regulates TFEB though phosphorylation of serine 142.

Sorting cells for basal and induced autophagic flux by quantitative ratiometric flow cytometry.

We detail here a protocol using tandem-tagged mCherry-EGFP-LC3 (C-G-LC3) to quantify autophagic flux in single cells by ratiometric flow cytometry and to isolate subpopulations of cells based on their relative levels of autophagic flux. This robust and sensitive method measures autophagic flux rather than autophagosome number and is an important addition to the autophagy researcher's array of tools for measuring autophagy. Two crucial steps in this protocol are i) generate cells constitutively expressing C-G-LC3 with low to medium fluorescence and low fluorescence variability, and ii) correctly set up gates and voltage/gain on a properly equipped flow cytometer.

Autophagy controls the kinetics and extent of mitochondrial apoptosis by regulating PUMA levels.

Macroautophagy is thought to protect against apoptosis; however, underlying mechanisms are poorly understood. We examined how autophagy affects canonical death receptor-induced mitochondrial outer membrane permeabilization (MOMP) and apoptosis. MOMP occurs at variable times in a population of cells, and this is delayed by autophagy.