Intrinsic dimensionality of human behavioral activity data.

Patterns of spatial behavior dictate how we use our infrastructure, encounter other people, or are exposed to services and opportunities. Understanding these patterns through the analysis of data commonly available through commodity smartphones has become an important arena for innovation in both academia and industry. The resulting datasets can quickly become massive, indicating the need for concise understanding of the scope of the data collected. Some data is obviously correlated (for example GPS location and which WiFi routers are seen). Codifying the extent of these correlations could identify potential new models, provide guidance on the amount of data to collect, and even provide actionable features. However, identifying correlations, or even the extent of correlation, is difficult because the form of the correlation must be specified. Fractal-based intrinsic dimensionality directly calculates the minimum number of dimensions required to represent a dataset. We provide an intrinsic dimensionality analysis of four smartphone datasets over seven input dimensions, and empirically demonstrate an intrinsic dimension of approximately two.

Metformin induces the AP-1 transcription factor network in normal dermal fibroblasts.

Metformin is a widely-used treatment for type 2 diabetes and is reported to extend health and lifespan as a caloric restriction (CR) mimetic. Although the benefits of metformin are well documented, the impact of this compound on the function and organization of the genome in normal tissues is unclear. To explore this impact, primary human fibroblasts were treated in culture with metformin resulting in a significant decrease in cell proliferation without evidence of cell death. Furthermore, metformin induced repositioning of chromosomes 10 and 18 within the nuclear volume indicating altered genome organization. Transcriptome analyses from RNA sequencing datasets revealed that alteration in growth profiles and chromosome positioning occurred concomitantly with changes in gene expression profiles. We further identified that different concentrations of metformin induced different transcript profiles; however, significant enrichment in the activator protein 1 (AP-1) transcription factor network was common between the different treatments. Comparative analyses revealed that metformin induced divergent changes in the transcriptome than that of rapamycin, another proposed mimetic of CR. Promoter analysis and chromatin immunoprecipitation assays of genes that changed expression in response to metformin revealed enrichment of the transcriptional regulator forkhead box O3a (FOXO3a) in normal human fibroblasts, but not of the predicted serum response factor (SRF). Therefore, we have demonstrated that metformin has significant impacts on genome organization and function in normal human fibroblasts, different from those of rapamycin, with FOXO3a likely playing a role in this response.