Distributed Target Tracking with Fading Channels over Underwater Wireless Sensor Networks

This paper investigates the problem of distributed target tracking via underwater wireless sensor networks (UWSNs) with fading channels. The degradation of signal quality due to wireless channel fading can significantly impact network reliability and subsequently reduce the tracking accuracy. To address this issue, we propose a modified distributed unscented Kalman filter (DUKF) named DUKF-Fc, which takes into account the effects of measurement fluctuation and transmission failure induced by channel fading. The channel estimation error is also considered when designing the estimator and a sufficient condition is established to ensure the stochastic boundedness of the estimation error. The proposed filtering scheme is versatile and possesses wide applicability to numerous real-world scenarios, e.g., tracking a maneuvering underwater target with acoustic sensors. Simulation results demonstrate the effectiveness of the proposed filtering algorithm. In addition, considering the constraints of network energy resources, the issue of investigating a trade-off between tracking performance and energy consumption is discussed accordingly.Comment: 12 pages, 6 figures, 6 table

Durative sleep fragmentation with or without hypertension suppress rapid eye movement sleep and generate cerebrovascular dysfunction

Either hypertension or chronic insomnia is the risk factor of developing vascular dementia. Durative hypertension can induce vascular remodeling and is used for modeling small vessel disease in rodents. It remains undetermined if the combination of hypertension and sleep disturbance exacerbates vascular dysfunction or pathologies. Previously, we found chronic sleep fragmentation (SF) dampened cognition in young mice without disease predispositions. In the current study, we superimposed SF with hypertension modeling in young mice. Angiotensin II (AngII)-releasing osmotic mini pumps were subcutaneously implanted to generate persistent hypertension, while sham surgeries were performed as controls. Sleep fragmentation with repetitive arousals (10 s every 2 min) during light-on 12 h for consecutive 30 days, while mice undergoing normal sleep (NS) processes were set as controls. Sleep architectures, whisker-stimulated cerebral blood flow (CBF) changes, vascular responsiveness as well as vascular pathologies were compared among normal sleep plus sham (NS + sham), SF plus sham (SF + sham), normal sleep plus AngII (NS + AngII), and SF plus AngII (SF + AngII) groups. SF and hypertension both alter sleep structures, particularly suppressing REM sleep. SF no matter if combined with hypertension strongly suppressed whisker-stimulated CBF increase, suggesting the tight association with cognitive decline. Hypertension modeling sensitizes vascular responsiveness toward a vasoactive agent, Acetylcholine (ACh, 5 mg/ml, 10 μl) delivered via cisterna magna infusion, while SF exhibits a similar but much milder effect. None of the modeling above was sufficient to induce arterial or arteriole vascular remodeling, but SF or SF plus hypertension increased vascular network density constructed by all categories of cerebral vessels. The current study would potentially help understand the pathogenesis of vascular dementia, and the interconnection between sleep and vascular health