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Following the popularity of smart phones and the development of mobile Internet, the demands for accurate indoor positioning have grown rapidly in recent years. Previous indoor positioning methods focused on plane locations on a floor and did not provide accurate floor positioning. In this paper, we propose a method that uses multiple barometers as references for the floor positioning of smart phones with built-in barometric sensors. Some related studies used barometric formula to investigate the altitude of mobile devices and compared the altitude with the height of the floors in a building to obtain the floor number. These studies assume that the accurate height of each floor is known, which is not always the case. They also did not consider the difference in the barometric-pressure pattern at different floors, which may lead to errors in the altitude computation. Our method does not require knowledge of the accurate heights of buildings and stories. It is robust and less sensitive to factors such as temperature and humidity and considers the difference in the barometric-pressure change trends at different floors. We performed a series of experiments to validate the effectiveness of this method. The results are encouraging.

PI3K and STAT3 are frequently activated in cancer progression. However, little is known about the underlying mechanisms by which PI3K and STAT3 regulate head and neck squamous cell cancer (HNSCC) growth. The lncRNA HOX transcript antisense RNA () was found to modulate the progression of HNSCC. In this study, we attempted to establish the correlation of PI3K/STAT3/HOTAIR signaling with the progression of HNSCC and its sensitivity toward platinum-based and targeted anti-EGFR combination therapy. We first analyzed the STAT3/HOTAIR and PI3K/AKT level in human HNSCC samples. We then activated or suppressed STAT3/HOTAIR and determined the effects on HNSCC cell proliferation and the growth of UM1 xenograft tumor, an orthotopic model of HNSCC. The sensitivity of HNSCC cells toward cisplatin and cetuximab was determined by assays. HNSCC samples showed significantly robust expression/activation of STAT3, HOTAIR, PI3K, and AKT, compared with normal squamous epithelium. STAT3 inhibition with WP1066 decreased HOTAIR level and sensitized HNSCC to cisplatin or cetuximab. STAT3 promoted HOTAIR transcription and its interaction with pEZH2-S21, resulting in enhanced growth of HNSCC cells. In addition, overexpression of HOTAIR promoted the growth of UM1 xenograft tumors Our results suggest that STAT3 signaling promotes HNSCC progression via regulating HOTAIR and pEZH2-S21 in HNSCC with PI3K overexpression/activation. These findings provide a rationale to target the STAT3/HOTAIR/pEZH2-S21 regulatory axis for treating patients with HNSCC..