Purpose -The purpose of this paper is to explore relationships between consumer innovativeness, market mavenism, shopping enjoyment, and beliefs, attitude, and patronage intentions toward pop-up retail. Design/methodology/approach -A survey technique using a national sample of consumers resulted in 869 usable responses. Structural equation modeling is used to test the hypothesized relationships among variables. Findings -Findings show that consumer innovativeness and shopping enjoyment influence beliefs about the importance of hedonic elements of pop-up retail (novelty/uniqueness factor) and attitude toward pop-up retail, which affects patronage intentions. Practical implications -Findings provide support for the effectiveness of pop-up retail, an experiential marketing strategy, at enhancing the appeal of a retail venue to consumers exhibiting higher tendencies in innovativeness and shopping. Originality/value -This paper provides an investigation of consumer psychographic characteristics and their effect on attitude and behavioral intentions towards a new experiential marketing format, pop-up retail. This paper demonstrates empirically how consumer innovativeness and shopping enjoyment, noted as growing tendencies among consumers, affect beliefs, attitude, and behavioral intentions towards pop-up retail.

Mitochondria and lysosomes are functionally linked, and their interdependent decline is a hallmark of aging and disease. Despite the long-standing connection between these organelles, the function(s) of lysosomes required to sustain mitochondrial health remains unclear. Here, working in yeast, we show that the lysosome-like vacuole maintains mitochondrial respiration by spatially compartmentalizing amino acids. Defects in vacuole function result in a breakdown in intracellular amino acid homeostasis, which drives age-related mitochondrial decline. Among amino acids, we find that cysteine is most toxic for mitochondria and show that elevated nonvacuolar cysteine impairs mitochondrial respiration by limiting intracellular iron availability through an oxidant-based mechanism. Cysteine depletion or iron supplementation restores mitochondrial health in vacuole-impaired cells and prevents mitochondrial decline during aging. These results demonstrate that cysteine toxicity is a major driver of age-related mitochondrial deterioration and identify vacuolar amino acid compartmentation as a cellular strategy to minimize amino acid toxicity.Iron Starvation Underlies Mitochondrial Dysfunction in V-ATPase-Deficient Cells Based on our above findings that iron supplementation restores mitochondrial function in V-ATPase-depleted cells and previous

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In order to elucidate the role of the mitogen-activated protein kinases, including JNK, p38 MAPK and ERK, as well as the survival-associated PI3K/Akt signaling pathway, in the response to chemotherapy, we have conducted a comparative study regarding the effects of doxorubicin on these pathways. Doxorubicin was determined to elicit the apoptosis of NIH3T3 cells in a dose-dependent manner. Prior to cell death, both Akt and p38 MAPK were transiently activated, and subsequently inactivated almost wholly, whereas ERK and JNK evidenced sustained activations in response to the drug treatment. The inhibition of PI3K/Akt and p38 MAPK both accelerated and enhanced doxorubicin-induced apoptosis and ERK inhibition apparently exerted negative effect on apoptosis. The modulation of PI3K/Akt activation by treatment of LY294002 or expression of Akt mutants such as Akt-DN or Myr-Akt exerted a significant effect on the activation of ERK1/2. We also observed that PI3K/Akt and sustained ERK activation were associated intimately with the etoposide-induced apoptosis. Taken together, our results clearly suggest that the differential regulation of the PI3K/Akt, ERK1/2, and p38 MAPK signaling pathways are crucial in the context of DNA-damaging drug-induced apoptosis, and this has compelled us to propose that the sustained activation of ERK1/2 pathway may be generally involved in the apoptosis induced by anticancer DNA-damaging drugs, including doxorubicin and etoposide.