Objectives: This study was conducted to create a 3D printable snack dish model for the elderly with low food or fluid intake along with barriers towards eating. Methods: The decision was made by the hybrid-brainstorming method for creating the 3D model. Experts were assigned based on their professional areas such as clinical nutrition, food hygiene and chemical safety for the creation process. After serial feedback processes, the grape shape was suggested as the final model. After various concept sketching and making clay models, 3D-printing technology was applied to produce a prototype. Results: 3D design modeling process was conducted by SolidWorks program. After considering Dietary reference intakes for Koreans (KDRIs) and other survey data, appropriate supplementary water serving volume was decided as 285 mL which meets 30% of Adequate intake. To consider printing output conditions, this model has six grapes in one bunch with a safety lid. The FDM printer and PLA filaments were used for food hygiene and safety. To stimulate cognitive functions and interests of eating, numbers one to six was engraved on the lid of the final 3D model. Conclusions The newly-developed 3D model was designed to increase intakes of nutrients and water in the elderly with dementia during snack time. Since dementia patients often forget to eat, engraving numbers on the grapes was conducted to stimulate cognitive function related to the swallowing and chewing process. We suggest that investigations on the types of foods or fluids are needed in the developed 3D model snack dish for future studies.

We investigated the question of whether cholesterol catabolite can influence expression of inflammatory cytokines via Toll-like receptors (TLR) in monocytic cells. Treatment of THP-1 monocytic cells with 27-hydroxycholesterol (27OHChol) resulted in induction of gene transcription of TLR6 and elevated level of cell surface TLR6. Addition of FSL-1, a TLR6 agonist, to 27OHChol-treated cells resulted in transcription of the IL-1alpha gene and enhanced secretion of the corresponding gene product. However, cholesterol did not affect TLR6 expression, and addition of FSL-1 to cholesterol-treated cells did not induce expression of IL-1alpha . Using pharmacological inhibitors, we investigated molecular mechanisms underlying the expression of TLR6 and IL-1alpha. Treatment with Akt inhibitor IV or U0126 resulted in significantly attenuated expression of TLR6 and IL-1alpha induced by 27OHChol and 27OHChol plus FSL-1, respectively. In addition, treatment with LY294002, SB202190, or SP600125 resulted in significantly attenuated secretion of IL-1alpha . These results indicate that 27OHChol can induce inflammation by augmentation of TLR6-mediated production of IL-1alpha in monocytic cells via multiple signaling pathways.
Cholesterol ; Cytokines ; Inflammation ; Interleukin-1 ; Interleukin-1alpha* ; Toll-Like Receptors*