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To create a context-aware environment, human locations and movement paths must be considered. In this paper, we propose an algorithm that tracks human movement paths using only binary sensed data obtained by infrared (IR) sensors attached to the ceiling of a room. Our algorithm can estimate multiple human movement paths without a priori knowledge of the number of humans in the room. By repeating predictions and estimations of human positions and links from the previous human positions to the estimated ones at each time period, human movement paths can be estimated. Simulation-based evaluation results show that our algorithm can dynamically trace human movement paths.

Cultured tubule cells from TGF-β1 null mice exhibit impaired hypertrophy and fibronectin expression in high glucose. Background To firmly establish the role of the transforming growth factor-β1 (TGF-β1) isoform in the pathophysiology of diabetic tubulointerstitial hypertrophy and fibrosis, we examined how the total absence of TGF-β1 would alter the effect of high glucose on cellular hypertrophy and matrix expression in tubuloepithelial cells cultured from TGF-β1 null mice. Methods Primary tubule cell cultures, obtained from kidneys of TGF-β1 knockout mice and their wild-type littermates, were treated with exogenous TGF-β1 or high glucose. The TGF-β system was characterized at the ligand and receptor levels using Northern and Western blotting. Cellular hypertrophy and growth were assessed by thymidine incorporation, cell counting, leucine incorporation, and protein content. Fibronectin expression was assessed by Northern analysis and enzyme-linked immunosorbent assay (ELISA). Results Knockout cells did not express TGF-β1 but did express TGF-β2, TGF-β3, and TGF-β type I and type II receptors. Exogenous TGF-β1 down-regulated the ligand-binding type II receptor but up-regulated type I receptor expression. Knockout cells proliferated more rapidly than wild-type cells, but restoring TGF-β1 to knockout cells slowed their proliferation. In wild-type cells, high glucose caused cellular hypertrophy, evidenced by greater leucine incorporation and protein content along with decreased thymidine incorporation. High glucose also increased fibronectin message and protein. However, in knockout cells, high glucose failed to induce hypertrophy and was severely limited in its capacity to stimulate fibronectin. Conclusion In tubular epithelial cells, TGF-β1 mediates the hypertrophic and fibronectin-stimulatory effects of high glucose, confirming the role of the TGF-β1 isoform in the pathogenesis of diabetic tubular hypertrophy and fibronectin overexpression.

Podocyte-derived vascular endothelial growth factor (VEGF) is upregulated in diabetes and may contribute to albuminuria. Although believed to act upon the glomerular endothelium, VEGF may have pronounced effects on the podocyte itself. The functionality of this VEGF autocrine loop was investigated in conditionally immortalized mouse podocytes. Exogenous VEGF(164) increased the production of alpha3(IV) collagen, an integral component of the glomerular basement membrane (GBM); this effect was completely prevented by SU5416, a pan-VEGF receptor inhibitor. The VEGF inhibitor also partially prevented the stimulation of alpha3(IV) collagen by transforming growth factor (TGF)-beta1, establishing a novel role for endogenous VEGF. However, VEGF did not influence the production of another novel chain of collagen IV, alpha5(IV) collagen, and SU5416 failed to reverse the known inhibitory effect of TGF-beta1 on alpha5(IV) collagen production. Cultured mouse podocytes possess at least the VEGFR-1 receptor, confirmed by RT-PCR, immunoblotting, and immunocytochemistry. By these techniques, however, VEGFR-2 is absent. VEGF signaling proceeds via autophosphorylation of VEGFR-1 and activation of the phosphatidylinositol 3-kinase (PI3K) pathway. Thus, podocyte-derived VEGF operates in an autocrine loop, likely through VEGFR-1 and PI3K, to stimulate alpha3(IV) collagen production. The TGF-beta1-stimulated endogenous VEGF may have significant implications for podocyte dysfunction in diabetic glomerulopathy, manifesting as GBM thickening and altered macromolecular permeability.