Co-Design, Merchandising, Virtual, Store

In today’s technologically advanced, networked world, the popularity and criticality of user participation in various aspects of our lives calls for a redefinition of the boundaries between designers and users, sellers and buyers, and visual merchandisers and shoppers. Co-design is defined in the design discipline as a process that involves consumers in co-creating a product (Piller, Moeslein & Stotko, 2004), thus transforming ordinary consumers into co-designers. Traditionally, retailers primarily rely on their internal expertise for visual merchandising directives and innovations. However, exploitation of internal expertise can result in both decreased output in innovation (Katila and Ahuja, 2002) and less innovative outcomes (Kristensson, Gustafsson, & Archer, 2004)

Mitochondria-Specific Accumulation of Amyloid β Induces Mitochondrial Dysfunction Leading to Apoptotic Cell Death

Mitochondria are best known as the essential intracellular organelles that host the homeostasis required for cellular survival, but they also have relevance in diverse disease-related conditions, including Alzheimer's disease (AD). Amyloid β (Aβ) peptide is the key molecule in AD pathogenesis, and has been highlighted in the implication of mitochondrial abnormality during the disease progress. Neuronal exposure to Aβ impairs mitochondrial dynamics and function. Furthermore, mitochondrial Aβ accumulation has been detected in the AD brain. However, the underlying mechanism of how Aβ affects mitochondrial function remains uncertain, and it is questionable whether mitochondrial Aβ accumulation followed by mitochondrial dysfunction leads directly to neuronal toxicity. This study demonstrated that an exogenous Aβ1–42 treatment, when applied to the hippocampal cell line of mice (specifically HT22 cells), caused a deleterious alteration in mitochondria in both morphology and function. A clathrin-mediated endocytosis blocker rescued the exogenous Aβ1–42-mediated mitochondrial dysfunction. Furthermore, the mitochondria-targeted accumulation of Aβ1–42 in HT22 cells using Aβ1–42 with a mitochondria-targeting sequence induced the identical morphological alteration of mitochondria as that observed in the APP/PS AD mouse model and exogenous Aβ1–42-treated HT22 cells. In addition, subsequent mitochondrial dysfunctions were demonstrated in the mitochondria-specific Aβ1–42 accumulation model, which proved indistinguishable from the mitochondrial impairment induced by exogenous Aβ1–42-treated HT22 cells. Finally, cellular toxicity was directly induced by mitochondria-targeted Aβ1–42 accumulation, which mimics the apoptosis process in exogenous Aβ1–42-treated HT22 cells. Taken together, these results indicate that mitochondria-targeted Aβ1–42 accumulation is the necessary and sufficient condition for Aβ-mediated mitochondria impairments, and leads directly to cellular death rather than along with other Aβ-mediated signaling alterations

Co-Design, Merchandising, Virtual, Store

In today’s technologically advanced, networked world, the popularity and criticality of user participation in various aspects of our lives calls for a redefinition of the boundaries between designers and users, sellers and buyers, and visual merchandisers and shoppers. Co-design is defined in the design discipline as a process that involves consumers in co-creating a product (Piller, Moeslein & Stotko, 2004), thus transforming ordinary consumers into co-designers. Traditionally, retailers primarily rely on their internal expertise for visual merchandising directives and innovations. However, exploitation of internal expertise can result in both decreased output in innovation (Katila and Ahuja, 2002) and less innovative outcomes (Kristensson, Gustafsson, & Archer, 2004).</p

Keratin 13 Expression Reprograms bone and Brain Metastases of Human Prostate Cancer Cells

Lethal progression of prostate cancer metastasis can be improved by developing animal models that recapitulate the clinical conditions. We report here that cytokeratin 13 (KRT13), an intermediate filament protein, plays a directive role in prostate cancer bone, brain, and soft tissue metastases. KRT13 expression was elevated in bone, brain, and soft tissue metastatic prostate cancer cell lines and in primary and metastatic clinical prostate, lung, and breast cancer specimens. When KRT13 expression was determined at a single cell level in primary tumor tissues of 44 prostate cancer cases, KRT13 level predicted bone metastasis and the overall survival of prostate cancer patients. Genetically enforced KRT13 expression in human prostate cancer cell lines drove metastases toward mouse bone, brain and soft tissues through a RANKL-independent mechanism, as KRT13 altered the expression of genes associated with EMT, stemness, neuroendocrine/neuromimicry, osteomimicry, development, and extracellular matrices, but not receptor activator NF-κB ligand (RANKL) signaling networks in prostate cancer cells. Our results suggest new inhibitors targeting RANKL-independent pathways should be developed for the treatment of prostate cancer bone and soft tissue metastases