Special section on smart grids: A hub of interdisciplinary research : IEEE ACCESS Special section editorial smart grids: A hub of interdisciplinary research

International audienceThe smart grid is an important hub of interdisciplinary research where researchers from different areas of science and technology combine their efforts to enhance the traditional electrical power grid. Due to these efforts, the traditional electrical grid is now evolving. The envisioned smart grid will bring social, environmental, ethical, legal and economic benefits. Smart grid systems increasingly involve machine-to-machine communication as well as human-to-human, or simple information retrieval. Thus, the dimensionality of the system is massive. The smart grid is the combination of different technologies, including control system theory, communication networks, pervasive computing , embedded sensing devices, electric vehicles, smart cities, renewable energy sources, Internet of Things, wireless sensor networks, cyber physical systems, and green communication. Due to these diverse activities and significant attention from researchers, education activities in the smart grid area are also growing. The smart grid is designed to replace the traditional electrical power grid. The envisioned smart grid typically consists of three networks: Home Area Networks (HANs), Neighborhood Area Networks (NANs), and Wide Area Networks (WANs). HANs connect the devices within the premises of the consumer and connect smart meters, Plug-in Electric Vehicles (PEVs), and distributed renewable energy sources. NANs connect multiple HANs and communicate the collected information to a network gateway. WANs serve as the communication backbone. Communication technologies play a vital role in the successful operation of smart grid. These communication technologies can be adopted based upon the specific features required by HANs, NANs, and WANs. Both wired and the wireless communication technologies can be used in the smart grid [1]. However, wireless communication technologies are suitable for many smart grid applications due to the continuous development in the wireless research domain. One drawback of wireless communication technologies is the limited availability of radio spectrum. The use of cognitive radio in smart grid communication will be helpful to break the spectrum gridlock through advanced radio design and operating in multiple settings, such as underlay, overlay, and interweave [2]. The smart grid is the combination of diverse sets of facilities and technologies. Thus, the monitoring and control of transmission lines, distribution facilities, energy generation plants, and as well as video monitoring of consumer premises can be conducted through the use of wireless sensor networks [3]–[6]. In remote sites and places where human intervention is not possible, wireless sensor and actuator networks can be useful for the successful smart grid operation [7], [8]. Since wireless sensor networks operate on the Industrial, Scientific, and Medical (ISM) band, the spectrum might get congested due to overlaid deployment of wireless sensor networks in the same premises. Thus, to deal with this spectrum congestion challenge, cognitive radio sensor networks can be used in smart grid environments [9], [10]. The objective of this Special Section in IEEE ACCESS is to showcase the most recent advances in the interdisciplinary research areas encompassing the smart grid. This Special Section brings together researchers from diverse fields and specializations, such as communications engineering, computer science, electrical and electronics engineering, educators, mathematicians and specialists in areas related to smart grids. In this Special Section, we invited researchers from academia, industry, and government to discuss challenging ideas, novel research contributions, demonstration results, and standardization efforts on the smart grid and related areas. This Special Section is a collection of eleven articles. These articles are grouped into the following four areas: (a) Reliability, security, and privacy for smart grid, (b), Demand response management, understanding customer behavior, and social networking applications for smart grid, (c) Smart cities, renewable energy, and green smart grid, and (d) Communication technologies, control and management for the smart grid

A critical role for suppressors of cytokine signaling 3 in regulating LPS-induced transcriptional activation of matrix metalloproteinase-13 in osteoblasts

Suppressor of cytokine signaling 3 (SOCS3) is a key regulator of cytokine signaling in macrophages and T cells. Although SOCS3 seems to contribute to the balance between the pro-inflammatory actions of IL-6 family of cytokines and anti-inflammatory signaling of IL-10 by negatively regulating gp130/Jak/Stat3 signal transduction, how and the molecular mechanisms whereby SOCS3 controls the downstream impact of TLR4 are largely unknown and current data are controversial. Furthermore, very little is known regarding SOCS3 function in cells other than myeloid cells and T cells. Our previous study demonstrates that SOCS3 is expressed in osteoblasts and functions as a critical inhibitor of LPS-induced IL-6 expression. However, the function of SOCS3 in osteoblasts remains largely unknown. In the current study, we report for the first time that LPS stimulation of osteoblasts induces the transcriptional activation of matrix metalloproteinase (MMP)-13, a central regulator of bone resorption. Importantly, we demonstrate that SOCS3 overexpression leads to a significant decrease of LPS-induced MMP-13 expression in both primary murine calvariae osteoblasts and a mouse osteoblast-like cell line, MC3T3-E1. Our findings implicate SOCS3 as an important regulatory mediator in bone inflammatory diseases by targeting MMP-13

Brain MR Spectroscopy Changes Precede Frontotemporal Lobar Degeneration Phenoconversion in Mapt Mutation Carriers.

Background and purposeThe objective of this study was to longitudinally investigate the trajectory of change in 1 H MRS measurements in asymptomatic MAPT mutation carriers who became symptomatic during follow-up, and to determine the time at which the neurochemical alterations accelerated during disease progression.MethodsWe identified eight MAPT mutations carriers who transitioned from asymptomatic to symptomatic disease during follow-up. All participants were longitudinally followed with an average of 7.75 years (range 4-11 years) and underwent two or more single voxel 1 H MRS examinations from the posterior cingulate voxel, with a total of 60 examinations. The rate of longitudinal change for each metabolite was estimated using linear mixed models. A flex point model was used to estimate the flex time point of the change in slope.ResultsThe decrease in the NAA/mI ratio accelerated 2.09 years prior to symptom onset, and continued to decline. A similar trajectory was observed in the presumed glial marker mI/Cr ratio accelerating 1.86 years prior to symptom onset.ConclusionsOur findings support the potential use of longitudinal 1 H MRS for monitoring the neurodegenerative progression in MAPT mutation carriers starting from the asymptomatic stage

Integrating renewable energy resources into the smart grid: recent developments in information and communication technologies

Rising energy costs, losses in the present-day electricity grid, risks from nuclear power generation, and global environmental changes are motivating a transformation of the conventional ways of generating electricity. Globally, there is a desire to rely more on renewable energy resources (RERs) for electricity generation. RERs reduce green house gas emissions and may have economic benefits, e.g., through applying demand side management with dynamic pricing so as to shift loads from fossil fuel-based generators to RERs. The electricity grid is presently evolving towards an intelligent grid, the so-called smart grid (SG). One of the major goals of the future SG is to move towards 100% electricity generation from RERs, i.e., towards a 100% renewable grid. However, the disparate, intermittent, and typically widely geographically distributed nature of RERs complicates the integration of RERs into the SG. Moreover, individual RERs have generally lower capacity than conventional fossil-fuel plants, and these RERs are based on a wide spectrum of different technologies. In this article, we give an overview of recent efforts that aim to integrate RERs into the SG. We outline the integration of RERs into the SG along with their supporting communication networks. We also discuss ongoing projects that seek to integrate RERs into the SG around the globe. Finally, we outline future research directions on integrating RERs into the SG

Rates of lobar atrophy in asymptomatic MAPT mutation carriers.

IntroductionThe aim of this study was to investigate the rates of lobar atrophy in the asymptomatic microtubule-associated protein tau (MAPT) mutation carriers.MethodsMAPT mutation carriers (n = 14; 10 asymptomatic, 4 converters from asymptomatic to symptomatic) and noncarriers (n = 13) underwent structural magnetic resonance imaging and were followed annually with a median of 9.2 years. Longitudinal changes in lobar atrophy were analyzed using the tensor-based morphometry with symmetric normalization algorithm.ResultsThe rate of temporal lobe atrophy in asymptomatic MAPT mutation carriers was faster than that in noncarriers. Although the greatest rate of atrophy was observed in the temporal lobe in converters, they also had increased atrophy rates in the frontal and parietal lobes compared to noncarriers.DiscussionAccelerated decline in temporal lobe volume occurs in asymptomatic MAPT mutation carriers followed by the frontal and parietal lobe in those who have become symptomatic. The findings have implications for monitoring the progression of neurodegeneration during clinical trials in asymptomatic MAPT mutation carriers

Reverse and Forward Genetics Approaches Reveal the Gene Networks That Regulate Development of Inner Ear Neurons

Stato-Acoustic Ganglion (SAG) neurons originate from the floor of the otic vesicle during a brief developmental window. They subsequently leave the otic vesicle and undergo a phase of migration and proliferation (transit-amplification). Neuroblasts finally differentiate into mature SAG neurons and extend processes to connect sensory cells of the inner ear to the information processing centers in the brain. The goal of this dissertation has been to elucidate mechanisms controlling these diverse events, which have heretofore been only poorly understood. First we showed that a threshold level of Fgf signaling initially sets the neurogenic domain in the otic epithelium. However, the level of Fgf signaling increases during development and becomes inhibitory to otic neurogenesis. Specfically, fgf5 is expressed by accumulating SAG neurons, which serves to terminate specification of new neuroblasts and delay differentiation of transit-amplifying cells. Second, we tested the role of transcription factor tfap2a, which we found is expressed in the neurogenic domain in both zebrafish and chick. Gain and loss-of-function studies revealed that Tfap2a activates expression of bmp7a, which in turn partially inhibits Fgf and Notch signaling. By modulating the inhibitory functions of Fgf and Notch, Tfap2a regulates the duration, amount and speed of SAG development. Third, we investigated the mechanism by which SAG neuroblasts leave the otic epithelium. We showed that Goosecoid (Gsc) regulates epithelial-mesenchymal transition of the otic neuroblasts. Fgf signaling regulates expression of gsc in a region iii partially overlapping with the neurogenic otic domain. The medial marker Pax2a acts in opposition to Gsc and stabilizes otic epithelia in non-neurogenic parts of the otic vesicle. Lastly, we conducted a mutagenesis screen in zebrafish to identify ENU-induced mutations that affect SAG development. We recovered a SAG deficient mutation, termed sagd1 that strongly reduces a subset of SAG neurons required for vestibular (balance) functions. Whole genome sequencing revealed that sagd1 affects the glycolytic enzyme, Phosphoglycerate kinase-1 (Pgk1). Further analysis revealed that Pgk1 acts nonautonomously to augment Fgf signaling during early stages of otic neurogenesis. Together, these studies have uncovered a number of previously unknown mechanisms for dynamic regulation of Fgf to control specification, delamination, and maturation of SAG neurons

DT-DDNN: A Physical Layer Security Attack Detector in 5G RF Domain for CAVs

The Synchronization Signal Block (SSB) is a fundamental component of the 5G New Radio (NR) air interface, crucial for the initial access procedure of Connected and Automated Vehicles (CAVs), and serves several key purposes in the network's operation. However, due to the predictable nature of SSB transmission, including the Primary and Secondary Synchronization Signals (PSS and SSS), jamming attacks are critical threats. These attacks, which can be executed without requiring high power or complex equipment, pose substantial risks to the 5G network, particularly as a result of the unencrypted transmission of control signals. Leveraging RF domain knowledge, this work presents a novel deep learning-based technique for detecting jammers in CAV networks. Unlike the existing jamming detection algorithms that mostly rely on network parameters, we introduce a double-threshold deep learning jamming detector by focusing on the SSB. The detection method is focused on RF domain features and improves the robustness of the network without requiring integration with the pre-existing network infrastructure. By integrating a preprocessing block to extract PSS correlation and energy per null resource elements (EPNRE) characteristics, our method distinguishes between normal and jammed received signals with high precision. Additionally, by incorporating of Discrete Wavelet Transform (DWT), the efficacy of training and detection are optimized. A double-threshold double Deep Neural Network (DT-DDNN) is also introduced to the architecture complemented by a deep cascade learning model to increase the sensitivity of the model to variations of signal-to-jamming noise ratio (SJNR). Results show that the proposed method achieves 96.4% detection rate in extra low jamming power, i.e., SJNR between 15 to 30 dB. Further, performance of DT-DDNN is validated by analyzing real 5G signals obtained from a practical testbed.Comment: 15 pages, 16 figure

Physical properties and functional alignment of soft-embalmed Thiel human cadaver when used as a simulator for ultrasound-guided regional anaesthesia

Background We evaluated the physical properties and functional alignment of the soft-embalmed Thiel cadaver as follows: by assessing tissue visibility; by measuring its acoustic, mechanical and elastic properties; by evaluating its durability in response to repeated injection; and by aligning images with humans. Methods In four soft-embalmed Thiel cadavers, we conducted three independent studies. We assessed the following factors: (i) soft tissue visibility in a single cadaver for 28 weeks after embalming; (ii) the displacement of tissues in response to 1 and 5 ml interscalene and femoral nerve blocks in a single cadaver; and (iii) the stiffness of nerves and perineural tissue in two cadavers. We aligned our findings with ultrasound images from three patients and one volunteer. Durability was qualified by assessing B-mode images from repetitive injections during supervised training. Results There was no difference in visibility of nerves between 2 and 28 weeks after embalming {geometric mean ratio 1.13 [95% confidence interval (CI): 0.75-1.68], P=1.0}. Mean tissue displacement was similar for cadaver femoral and interscalene blocks [geometric mean ratio 1.02 (95% CI: 0.59-1.78), P=0.86], and for 1 and 5 ml injection volumes [geometric mean ratio 0.84 (95% CI: 0.70-1.01), P=0.19]. Cadavers had higher intraneural than extraneural stiffness [Young's modulus; geometric mean ratio 3.05 (95% CI: 2.98-3.12), P</p

Connecting descent and peak polynomials

A permutation $\sigma=\sigma_1 \sigma_2 \cdots \sigma_n$ has a descent at $i$ if $\sigma_i>\sigma_{i+1}$. A descent $i$ is called a peak if $i>1$ and $i-1$ is not a descent. The size of the set of all permutations of $n$ with a given descent set is a polynomials in $n$, called the polynomial. Similarly, the size of the set of all permutations of $n$ with a given peak set, adjusted by a power of $2$ gives a polynomial in $n$, called the peak polynomial. In this work we give a unitary expansion of descent polynomials in terms of peak polynomials. Then we use this expansion to give a combinatorial interpretation of the coefficients of the peak polynomial in a binomial basis, thus giving a new proof of the peak polynomial positivity conjecture.Comment: 6 pages, 3 figures, 1 tabl

Impaired neutrophil directional chemotactic accuracy in chronic periodontitis patients

Aim: To investigate the chemotactic accuracy of peripheral blood neutrophils from patients with chronic periodontitis compared with matched healthy controls, before and after non-surgical periodontal therapy. Material &#38; Methods: Neutrophils were isolated from patients and controls (n = 18) by density centrifugation. Using the Insall chamber and video microscopy, neutrophils were analysed for directional chemotaxis towards N-formyl-methionyl-leucyl-phenylalanine [fMLP (10 nM), or CXCL8 (200 ng/ml)]. Circular statistics were utilized for the analysis of cell movement. Results: Prior to treatment, neutrophils from patients with chronic periodontitis had significantly reduced speed, velocity and chemotactic accuracy compared to healthy controls for both chemoattractants. Following periodontal treatment, patient neutrophils continued to display reduced speed in response to both chemoattractants. However, velocity and accuracy were normalized for the weak chemoattractant CXCL8 while they remained significantly reduced for fMLP. Conclusions: Chronic periodontitis is associated with reduced neutrophil chemotaxis, and this is only partially restored by successful treatment. Dysfunctional neutrophil chemotaxis may predispose patients with periodontitis to their disease by increasing tissue transit times, thus exacerbating neutrophil-mediated collateral host tissue damage