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.

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.

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.

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.

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.

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.