The paper presents a hybrid indoor positioning solution based on a pedestrian dead reckoning (PDR) approach using built-in sensors on a smartphone. To address the challenges of flexible and complex contexts of carrying a phone while walking, a robust step detection algorithm based on motion-awareness has been proposed. Given the fact that step length is influenced by different motion states, an adaptive step length estimation algorithm based on motion recognition is developed. Heading estimation is carried out by an attitude acquisition algorithm, which contains a two-phase filter to mitigate the distortion of magnetic anomalies. In order to estimate the heading for an unconstrained smartphone, principal component analysis (PCA) of acceleration is applied to determine the offset between the orientation of smartphone and the actual heading of a pedestrian. Moreover, a particle filter with vector graph assisted particle weighting is introduced to correct the deviation in step length and heading estimation. Extensive field tests, including four contexts of carrying a phone, have been conducted in an office building to verify the performance of the proposed algorithm. Test results show that the proposed algorithm can achieve sub-meter mean error in all contexts.

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Chronic itch is a troublesome condition and often difficult to cure. Emerging evidence suggests that the periaqueductal gray-rostral ventromedial medulla (PAG-RVM) pathway may play an important role in regulation of itch, but the cellular organization and molecular mechanisms remain incompletely understood. Here, we report that a group of RVM neurons distinctively express the G protein-coupled estrogen receptor (GPER), which mediates descending inhibition of itch. We found that GPER + neurons in RVM were activated in chronic itch conditions in rats and mice. Selective ablation or chemogenetic suppression of RVM GPER + neurons resulted in mechanical alloknesis and increased scratching in response to pruritogens, whereas chemogenetic activation of GPER + neurons abrogated itch responses, indicating that GPER + neurons are antipruritic. Moreover, GPER-deficient mice and rats of either sex exhibited hypersensitivity to mechanical and chemical itch, a phenotype reversible by μ type opioid receptor (MOR) antagonism. Additionally, significant MOR phosphorylation in the RVM was detected in chronic itch models in wild-type but not in GPER -/rats. Therefore, GPER not only identifies a population of medullary antipruritic neurons but may also determine the descending antipruritic tone through regulating μ-opioid signaling.4 Significance Statement (120 words maximum) Therapeutic options for itch are limited due to as yet incomplete understanding of the mechanisms of itch processing. Our data have provided novel insights into the cellular organization and molecular mechanisms of descending regulation of itch in normal and pathological conditions: GPER + neurons (largely GABAergic) in the RVM are anti-pruritic neurons under tonic opioidergic inhibition; activation of GPER promotes phosphorylation of MOR and dis-inhibition of the anti-pruritic GPER + neurons from inhibitory opioidergic inputs; failure to mobilize GPER + neurons may result in exacerbation of itch. Our data also illuminate on some of the outstanding questions in the field, such as the mechanisms underlying sex bias in itch, pain and opioid analgesia and the paradoxical effects of morphine on pain and itch.

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