Behavioral Impacts of Promotion-induced Cross-buying: The Moderating Roles of Age and Gender

This study investigates the effect of cross-buying induced by price promotion on purchase amount and frequency, and how the effect varies among customers of different ages and genders. The impact of the behavior is empirically examined by using data from an online fashion retail company. The results reveal that customers who frequently cross-buy during promotion appear to spend less but purchase more frequently. However, for male customers, purchase frequency is negatively affected. Further, the negative impact on purchase amount is greater for men and younger customers. We discuss the theoretical and managerial implications of this research

Suppression of respiratory growth defect of mutant deficient in mitochondrial phospholipase A₁ by overexpression of genes involved in coenzyme Q synthesis in <i>Saccharomyces cerevisiae</i>

<p><i>DDL1</i> encodes a mitochondrial phospholipase A₁ involved in acyl chain remodeling of mitochondrial phospholipids and degradation of cardiolipin in <i>Saccharomyces cerevisiae</i>. The deletion of <i>DDL1</i> leads to respiratory growth defects. To elucidate the physiological role of <i>DDL1</i>, we screened for genes that, when overexpressed, suppress the respiratory growth defect of the <i>DDL1</i> deletion mutant. Introduction of <i>COQ8, COQ9</i>, or <i>COQ5</i>, which are involved in coenzyme Q (CoQ) synthesis, using a multicopy vector suppressed the respiratory growth defect of the <i>DDL1</i> deletion mutant. In contrast, introduction of <i>COQ8</i> using a multicopy vector did not accelerate the growth of the deletion mutants of <i>TAZ1</i> or <i>CLD1</i>, which encode an acyltransferase or phospholipase A₂, respectively, involved in the remodeling of cardiolipin. These results suggest genetic interactions between the mitochondrial phospholipase A₁ gene and the genes involved in CoQ synthesis.</p> <p><b>Abbreviations</b>: CoQ: coenzyme Q; CL: cardiolipin; ORF: open reading frame; PA: phosphatidic acid; PC: phosphatidylcholine; PE: phosphatidylethanolamine; PG: phosphatidylglycerol; PLA1: phospholipase A1; iPLA1: intracellular PLA1; PLA2: phospholipase A2</p> <p>Genetic interaction between <i>DDL1</i> encoding a mitochondrial phospholipase A₁ and genes involved in coenzyme Q synthesis.</p

Prox1 Induces Lymphatic Endothelial Differentiation via Integrin α9 and Other Signaling Cascades

During embryonic lymphatic development, a homeobox transcription factor Prox1 plays important roles in sprouting and migration of a subpopulation of blood vessel endothelial cells (BECs) toward VEGF-C–expressing cells. However, effects of Prox1 on endothelial cellular behavior remain to be elucidated. Here, we show that Prox1, via induction of integrin α9 expression, inhibits sheet formation and stimulates motility of endothelial cells. Prox1-expressing BECs preferentially migrated toward VEGF-C via up-regulation of the expression of integrin α9 and VEGF receptor 3 (VEGFR3). In mouse embryos, expression of VEGFR3 and integrin α9 is increased in Prox1-expressing lymphatic endothelial cells (LECs) compared with BECs. Knockdown of Prox1 expression in human LECs led to decrease in the expression of integrin α9 and VEGFR3, resulting in the decreased chemotaxes toward VEGF-C. These findings suggest that Prox1 plays important roles in conferring and maintaining the characteristics of LECs by modulating multiple signaling cascades and that integrin α9 may function as a key regulator of lymphangiogenesis acting downstream of Prox1