Accurate Indoor Localization Based on CSI and Visibility Graph

Passive indoor localization techniques can have many important applications. They are nonintrusive and do not require users carrying measuring devices. Therefore, indoor localization techniques are widely used in many critical areas, such as security, logistics, healthcare, etc. However, because of the unpredictable indoor environment dynamics, the existing nonintrusive indoor localization techniques can be quite inaccurate, which greatly limits their real-world applications. To address those problems, in this work, we develop a channel state information (CSI) based indoor localization technique. Unlike the existing methods, we employ both the intra-subcarrier statistics features and the inter-subcarrier network features. Specifically, we make the following contributions: (1) we design a novel passive indoor localization algorithm which combines the statistics and network features; (2) we modify the visibility graph (VG) technique to build complex networks for the indoor localization applications; and (3) we demonstrate the effectiveness of our technique using real-world deployments. The experimental results show that our technique can achieve about 96% accuracy on average and is more than 9% better than the state-of-the-art techniques

Multiple Access for Heterogeneous Wireless Networks with Imperfect Channels Based on Deep Reinforcement Learning

In heterogeneous wireless networks, when multiple nodes need to share the same wireless channel, they face the issue of multiple access, which necessitates a Medium Access Control (MAC) protocol to coordinate the data transmission of multiple nodes on the shared communication channel. This paper presents Proximal Policy Optimization-based Multiple Access (PPOMA), a novel multiple access protocol for heterogeneous wireless networks based on the Proximal Policy Optimization (PPO) algorithm from deep reinforcement learning (DRL). Specifically, we explore a network scenario where multiple nodes employ different MAC protocols to access an Access Point (AP). The novel PPOMA approach, leveraging deep reinforcement learning, adapts dynamically to coexist with other nodes. Without prior knowledge, it learns an optimal channel access strategy, aiming to maximize overall network throughput. We conduct simulation analyses using PPOMA in two scenarios: perfect channel and imperfect channel. Experimental results demonstrate that our proposed PPOMA continuously learns and refines its channel access strategy, achieving an optimal performance level in both perfect and imperfect channel scenarios. Even when faced with suboptimal channel conditions, PPOMA outperforms alternative methods by achieving higher overall network throughput and faster convergence rates. In a perfect channel scenario, PPOMA’s advantage over other algorithms is primarily evident in its convergence speed, reaching convergence on average 500 iterations faster. In an imperfect channel scenario, PPOMA’s advantage is mainly reflected in its higher overall network throughput, with an approximate increase of 0.04

OSMR deficiency aggravates pressure overload-induced cardiac hypertrophy by modulating macrophages and OSM/LIFR/STAT3 signalling

Abstract Background Oncostatin M (OSM) is a secreted cytokine of the interleukin (IL)-6 family that induces biological effects by activating functional receptor complexes of the common signal transducing component glycoprotein 130 (gp130) and OSM receptor β (OSMR) or leukaemia inhibitory factor receptor (LIFR), which are mainly involved in chronic inflammatory and cardiovascular diseases. The effect and underlying mechanism of OSM/OSMR/LIFR on the development of cardiac hypertrophy remains unclear. Methods and results OSMR-knockout (OSMR-KO) mice were subjected to aortic banding (AB) surgery to establish a model of pressure overload-induced cardiac hypertrophy. Echocardiographic, histological, biochemical and immunological analyses of the myocardium and the adoptive transfer of bone marrow-derived macrophages (BMDMs) were conducted for in vivo studies. BMDMs were isolated and stimulated with lipopolysaccharide (LPS) for the in vitro study. OSMR deficiency aggravated cardiac hypertrophy, fibrotic remodelling and cardiac dysfunction after AB surgery in mice. Mechanistically, the loss of OSMR activated OSM/LIFR/STAT3 signalling and promoted a proresolving macrophage phenotype that exacerbated inflammation and impaired cardiac repair during remodelling. In addition, adoptive transfer of OSMR-KO BMDMs to WT mice after AB surgery resulted in a consistent hypertrophic phenotype. Moreover, knockdown of LIFR in myocardial tissue with Ad-shLIFR ameliorated the effects of OSMR deletion on the phenotype and STAT3 activation. Conclusions OSMR deficiency aggravated pressure overload-induced cardiac hypertrophy by modulating macrophages and OSM/LIFR/STAT3 signalling, which provided evidence that OSMR might be an attractive target for treating pathological cardiac hypertrophy and heart failure

NAD+ exhaustion by CD38 upregulation contributes to blood pressure elevation and vascular damage in hypertension

Abstract Hypertension is characterized by endothelial dysfunction and arterial stiffness, which contribute to the pathogenesis of atherosclerotic cardiovascular diseases. Nicotinamide adenine dinucleotide (NAD+) is an indispensable cofactor in all living cells that is involved in fundamental biological processes. However, in hypertensive patients, alterations in NAD+ levels and their relation with blood pressure (BP) elevation and vascular damage have not yet been studied. Here we reported that hypertensive patients exhibited lower NAD+ levels, as detected by high-performance liquid chromatography-mass spectrometry (HPLC-MS), in both peripheral blood mononuclear cells (PBMCs) and aortas, which was parallel to vascular dysfunction. NAD+ boosting therapy with nicotinamide mononucleotide (NMN) supplement reduced BP and ameliorated vascular dysfunction in hypertensive patients (NCT04903210) and AngII-induced hypertensive mice. Upregulation of CD38 in endothelial cells led to endothelial NAD+ exhaustion by reducing NMN bioavailability. Pro-inflammatory macrophages infiltration and increase in IL-1β generation derived from pro-inflammatory macrophages resulted in higher CD38 expression by activating JAK1-STAT1 signaling pathway. CD38 KO, CD38 inhibitors treatment, or adeno-associated virus (AAV)-mediated endothelial CD38 knockdown lowered BP and improved vascular dysfunction in AngII-induced hypertensive mice. The present study demonstrated for the first time that endothelial CD38 activation and subsequently accelerated NAD+ degradation due to enhanced macrophage-derived IL-1β production was responsible for BP elevation and vascular damage in hypertension. NAD+ boosting therapy can be used as a novel therapeutic strategy for the management of hypertensive patients

Generation and basic characterization of a gene-trap knockout mouse model of Scn2a with a substantial reduction of voltage-gated sodium channel Na

Large-scale genetic studies revealed SCN2A as one of the most frequently mutated genes in patients with neurodevelopmental disorders. SCN2A encodes for the voltage-gated sodium channel isoform 1.2 (Nav 1.2) expressed in the neurons of the central nervous system. Homozygous knockout (null) of Scn2a in mice is perinatal lethal, whereas heterozygous knockout of Scn2a (Scn2a+/- ) results in mild behavior abnormalities. The Nav 1.2 expression level in Scn2a+/- mice is reported to be around 50-60% of the wild-type (WT) level, which indicates that a close to 50% reduction of Nav 1.2 expression may not be sufficient to lead to major behavioral phenotypes in mice. To overcome this barrier, we characterized a novel mouse model of severe Scn2a deficiency using a targeted gene-trap knockout (gtKO) strategy. This approach produces viable homozygous mice (Scn2agtKO/gtKO ) that can survive to adulthood, with about a quarter of Nav 1.2 expression compared to WT mice. Innate behaviors like nesting and mating were profoundly disrupted in Scn2agtKO/gtKO mice. Notably, Scn2agtKO/gtKO mice have a significantly decreased center duration compared to WT in the open field test, suggesting anxiety-like behaviors in a novel, open space. These mice also have decreased thermal and cold tolerance. Additionally, Scn2agtKO/gtKO mice have increased fix-pattern exploration in the novel object exploration test and a slight increase in grooming, indicating a detectable level of repetitive behaviors. They bury little to no marbles and have decreased interaction with novel objects. These Scn2a gene-trap knockout mice thus provide a unique model to study pathophysiology associated with severe Scn2a deficiency