Consumer Preference for Food Bundles under Cognitive Load: A Grocery Shopping Experiment.

Product bundling is a common retail marketing strategy. The bundling of food items has the potential to increase profits in the grocery sector, particularly for fresh produce, which often has lower profit margins. Although prior work suggests consumers prefer bundles because they require less cognitive effort to select, no study has yet experimentally manipulated cognitive load when food bundles are included in the choice set. To test whether bundle preference differs when cognitive resources are constrained, a grocery shopping experiment was conducted with 250 consumers in the midwestern U.S., in a laboratory that featured a grocery store display. Consumers who grocery shopped under cognitive load had a higher odds of selecting a food bundle even when the bundle did not offer a price discount. Results suggest food bundles may be preferred because they require less cognitive effort to process, which could benefit consumers by simplifying the grocery shopping experience. Additional factors found to influence food bundle selection included whether the bundled items were perceived as being complementary and hunger levels. Food bundles could help lessen cognitive effort associated with grocery shopping and may especially appeal to those who do not enjoy food shopping.

Food bundling as a health nudge: Investigating consumer fruit and vegetable selection using behavioral economics.

Displaying bundles of healthy foods at the grocery store is a health nudge that simplifies shopping and may have the potential for increasing fruit and vegetable (F&V) purchasing. To evaluate the impact of food bundling, we conduct an artefactual field experiment with community participants in a laboratory set up as a grocery store. Dual-self theory suggests that food choices may differ depending on whether shoppers are under cognitive load - in our experiment, we exogenously vary whether bundles are displayed (with and without a price discount) and whether shoppers are under cognitive load. Our findings align with prior studies that suggest unhealthy options are more likely to be selected when cognitive resources are constrained. When bundles are displayed, we observe increased F&V purchasing. We also observe a significant interaction between cognitive load and price discounting. We find discounted bundles are more effective in the absence of cognitive load, but non-discounted bundles are more effective when shoppers are under cognitive load. Although more research is warranted, our findings suggest that when shopping under cognitive load, it is possible that discounts impose additional cognitive strain on the shopping experience. For retailers and policymakers, our results point to the potential power of bundling as a strategy for increasing healthy food purchasing.

Functional characterization of mutations in the promoter proximal region of the telomerase hTERC gene identified in patients with hematological disorders.

Telomerase RNA gene (hTERC) mutations have been identified in a subset of patients with bone-marrow failure syndromes (BMFS). While most of the mutations were found in the coding region of hTERC, some rare disease-associated mutations as well as polymorphic sequence changes were found in the promoter proximal region of the gene, including the -99C/G sequence change that was thought to modulate hTERC gene expression by disrupting Sp1 transcriptional factor binding [1]. We and other researchers recently identified, in addition to the -99C/G mutation, several other sequence variations (-240delCT, -714+C insertion, and -771A/G) in the hTERC promoter in other cohorts of patients with blood disorders. Using a convenient telomerase reconstitution assay coupled with the hTERC-promoter driven luciferase reporter assay, we characterized each of the hTERC's promoter sequence variants and found that these rare sequence changes did not negatively affect telomerase gene expression or function. We therefore conclude that all known mutations in the promoter proximal region of the hTERC gene to date do not necessarily contribute to the pathogenesis of hematological disorders by directly affecting telomerase transcriptional activity and/or its enzymatic function.

Transcriptional activation of TINF2, a gene encoding the telomere-associated protein TIN2, by Sp1 and NF-κB factors.

The expression of the telomere-associated protein TIN2 has been shown to be essential for early embryonic development in mice and for development of a variety of human malignancies. Recently, germ-line mutations in TINF2, which encodes for the TIN2 protein, have been identified in a number of patients with bone-marrow failure syndromes. Yet, the molecular mechanisms that regulate TINF2 expression are largely unknown. To elucidate the mechanisms involved in human TINF2 regulation, we cloned a 2.7 kb genomic DNA fragment containing the putative promoter region and, through deletion analysis, identified a 406 bp region that functions as a minimal promoter. This promoter proximal region is predicted to contain several putative Sp1 and NF-κB binding sites based on bioinformatic analysis. Direct binding of the Sp1 and NF-κB transcription factors to the TIN2 promoter sequence was demonstrated by electrophoretic mobility shift assay (EMSA) and/or chromatin immunoprecipitation (ChIP) assays. Transfection of a plasmid carrying the Sp1 transcription factor into Sp-deficient SL2 cells strongly activated TIN2 promoter-driven luciferase reporter expression. Similarly, the NF-κB molecules p50 and p65 were found to strongly activate luciferase expression in NF-κB knockout MEFs. Mutating the predicted transcription factor binding sites effectively reduced TIN2 promoter activity. Various known chemical inhibitors of Sp1 and NF-κB could also strongly inhibit TIN2 transcriptional activity. Collectively, our results demonstrate the important roles that Sp1 and NF-κB play in regulating the expression of the human telomere-binding protein TIN2, which can shed important light on its possible role in causing various forms of human diseases and cancers.

Telomere dysfunction in human diseases: the long and short of it!

It has been over one hundred years since the first reported case of dyskeratosis congenita (DC) and over twenty since the discovery of telomerase, an enzyme that adds telomeric DNA repeats to chromosome ends. Emerging evidence suggests that telomere dysfunction plays an important role in the pathogenesis of DC and other human disorders involving tissues that require rapid repair and renewal capacities. Yet we still do not fully understand how mutations in telomere maintenance genes contribute to disease development in affected individuals. In this review, we provide an up-to-date summary of the topic by discussing the results from genetic screens of patients, in vitro mutational analysis of involved molecules, and genetically engineered mouse models. While these data shed important light on the mechanisms underlying disease development, further investigation, particularly in an in vivo setting, is needed.

Identification and functional characterization of novel telomerase variant alleles in Japanese patients with bone-marrow failure syndromes.

As the incidence of bone-marrow failure syndromes (BMFS) is 2-3x higher in East Asia than in the West, we examined peripheral blood or marrow cells of 100 Japanese patients for possible pathogenic mutations in the two main components of the telomere-synthesizing enzyme telomerase (hTERC RNA and hTERT protein) that have recently been implicated in the disease pathogenesis. We analyzed samples collected from 34 patients with acquired aplastic anemia (AA), 66 patients with myelodysplastic syndromes (MDS) and 120 healthy controls. In addition to two polymorphic germ-line sequence changes (n-771A/G and n-714 C insertion) in the promoter region of hTERC and eleven hTERT polymorphisms that were identified in both patients and healthy individuals, we found a novel germ-line C323T mutation in the hTERC RNA in an MDS patient only. This heterozygous C323T mutation abolished telomerase enzymatic activity and functioned in a haploinsufficiency manner to modulate telomerase activity in cells. In summary, this study reports a novel telomerase natural variant that abolishes telomerase function, which may lead to telomere shortening and marrow hypocellularity in patients with BMFS. This study also highlights the rarity of genetic alterations in BMFS patients in Japan, which suggests that other factors may play a more prominent role in the disease pathogenesis in East Asia.