Invotek

Smart Predict is a novel two-tablet application developed to improve conversational efficiency for people who use augmentative and alternative communication (AAC) devices. The Smart Predict system consists of two distinct applications that were built for use with two Android tablets and/or phones with Bluetooth® capability. One application is referred to as the AAC User app and the second application is called the Partner app. Smart Predict integrates vocabulary supplementation from communication partners in real-time while persons who rely on AAC generate text and maintain full control to choose words within a word prediction line. Using single-case research designs with adapted alternating treatments under two counterbalanced treatment conditions (AAC User app alone versus AAC User app + Partner app), we examined message efficiency with persons who rely on switch scanning for on-screen keyboards. User experience questionnaires were administered to determine satisfaction and workload, and to provide feedback for future development efforts. Three adults with complex communication needs and motor impairments conversed with research staff about fourteen movie trailers. Characters per minute and switch selections per character produced by the person with complex communication needs and motor impairments were measured during 15-minute interviews to represent communication speed and effort. Results indicate that message efficiency increased with the dual-tablet Smart Predict, indicating faster message generation with the vocabulary supplementation system. User satisfaction increased and perceived effort decreased under the Smart Predict conditions. Given these results within a research and development framework, the Smart Predict concept is a viable feature that could be considered within smart AAC technologies.

Nicotinamide has been reported to induce differentiation of precursor/stem cells toward a beta-cell phenotype, increase islet regeneration, and enhance insulin biosynthesis. Exposure of INS-1 beta-cells to elevated glucose leads to reduced insulin gene transcription, and this is associated with diminished binding of pancreatic duodenal homeobox factor 1 (PDX-1) and mammalian homologue of avian MafA/l-Maf (MafA). Nicotinamide and other low-potency poly(ADP-ribose) polymerase (PARP) inhibitors were thus tested for their ability to restore insulin promoter activity. The low-potency PARP inhibitors nicotinamide, 3-aminobenzamide, or PD128763 increased expression of a human insulin reporter gene suppressed by elevated glucose. In contrast, the potent PARP-1 inhibitors PJ34 or INO-1001 had no effect on promoter activity. Antioxidants, including N-acetylcysteine, lipoic acid, or quercetin, only minimally induced the insulin promoter. Site-directed mutations of the human insulin promoter mapped the low-potency PARP inhibitor response to the C1 element, which serves as a MafA binding site. INS-1 cells exposed to elevated glucose had markedly reduced MafA protein and mRNA levels. Low-potency PARP inhibitors restored MafA mRNA and protein levels, but they had no affect on PDX-1 protein levels or binding activity. Increased MafA expression by low-potency PARP inhibitors was independent of increased MafA protein or mRNA stability. These data suggest that low-potency PARP inhibitors increase insulin biosynthesis, in part, through a mechanism involving increased MafA gene transcription.