Hybrid Weighted Least Square Multi-Verse Optimizer (WLS–MVO) Framework for Real-Time Estimation of Harmonics in Non-Linear Loads

Data Availability Statement: Not applicable.Copyright © 2023 by the authors. The electric power quality has become a serious concern for electric utilities and end users owing to its undesirable effects on system capabilities and performance. Harmonic levels on power systems have been pronounced to a greater extent with the continuous growth in the application of solid-state and reactive power compensatory devices. Harmonics are the key constituents that are mainly responsible for power quality deterioration. Power system harmonics need to be correctly estimated and filtered to increase power quality. This research work focuses on accurate estimation of power system harmonics with the proposed hybrid weighted least-square multi-verse optimizer (WLS–MVO) based framework. Multi-verse optimizer replicates the phenomenon of the formation of new universes as described by multi-verse theory to solve complex real-world optimization problems. The proposed WLS–MVO framework is tested and validated by estimating the harmonics present in multiple test signals with different noise levels. Amplitudes and phases of harmonics present in the polluted signal were estimated, and the framework computational time was compared with the previously developed technique’s results which are reported in the literature. There was 80% reduction in computational time and 82% improvement in terms of accuracy in estimating harmonics using WLS–MVO as compared to previously developed techniques. The performance of the developed framework is further validated by estimating the harmonics present in the real-time voltage and current waveforms obtained from axial flux permanent magnet generator (AFPMSG), uninterruptible power supply (UPS), and light-emitting diode (LED). The purposed technique technique outperforms the already-developed techniques, in terms of accuracy and computational time.This research received no external funding

A Multiobjective Artificial-Hummingbird-Algorithm-Based Framework for Optimal Reactive Power Dispatch Considering Renewable Energy Sources

Data Availability Statement: Not applicable.Copyright © 2022 by the authors. This paper proposes a new artificial hummingbird algorithm (AHA)-based framework to investigate the optimal reactive power dispatch (ORPD) problem which is a critical problem in the capacity of power systems. This paper aims to improve the performance of power systems by minimizing two distinct objective functions namely active power loss in the transmission network and total voltage deviation at the load buses subjected to various constraints within multiobjective framework. The proposed AHA-based framework maps the inherent flight and foraging capabilities exhibited by hummingbirds in nature to determine the best settings for the control variables (i.e., voltages at generation buses, the tap positions of on-load tap-changing transformers (OLTCs) and the size of switchable shunt VAR compensators) to minimize the overall objective functions. A multiobjective optimal reactive power dispatch framework (MO-ORPD) considering renewable energy sources (RES) and load uncertainties is also proposed to minimize the individual objectives simultaneously. The competency and robustness of the proposed AHA-based framework is validated and tested on IEEE 14 bus and IEEE 39 bus test systems to solve the ORPD problem. Eventually, the results are compared with other well-known optimization techniques in the literature. Box plots and statistical tests using SPSS are performed and validated to justify the effectiveness of the proposed framework.This research received no external funding

Genetic risk variants associated with in situ breast cancer

INTRODUCTION: Breast cancer in situ (BCIS) diagnoses, a precursor lesion for invasive breast cancer, comprise about 20 % of all breast cancers (BC) in countries with screening programs. Family history of BC is considered one of the strongest risk factors for BCIS. METHODS: To evaluate the association of BC susceptibility loci with BCIS risk, we genotyped 39 single nucleotide polymorphisms (SNPs), associated with risk of invasive BC, in 1317 BCIS cases, 10,645 invasive BC cases, and 14,006 healthy controls in the National Cancer Institute's Breast and Prostate Cancer Cohort Consortium (BPC3). Using unconditional logistic regression models adjusted for age and study, we estimated the association of SNPs with BCIS using two different comparison groups: healthy controls and invasive BC subjects to investigate whether BCIS and BC share a common genetic profile. RESULTS: We found that five SNPs (CDKN2BAS-rs1011970, FGFR2-rs3750817, FGFR2-rs2981582, TNRC9-rs3803662, 5p12-rs10941679) were significantly associated with BCIS risk (P value adjusted for multiple comparisons <0.0016). Comparing invasive BC and BCIS, the largest difference was for CDKN2BAS-rs1011970, which showed a positive association with BCIS (OR = 1.24, 95 % CI: 1.11-1.38, P = 1.27 x 10(-4)) and no association with invasive BC (OR = 1.03, 95 % CI: 0.99-1.07, P = 0.06), with a P value for case-case comparison of 0.006. Subgroup analyses investigating associations with ductal carcinoma in situ (DCIS) found similar associations, albeit less significant (OR = 1.25, 95 % CI: 1.09-1.42, P = 1.07 x 10(-3)). Additional risk analyses showed significant associations with invasive disease at the 0.05 level for 28 of the alleles and the OR estimates were consistent with those reported by other studies. CONCLUSIONS: Our study adds to the knowledge that several of the known BC susceptibility loci are risk factors for both BCIS and invasive BC, with the possible exception of rs1011970, a putatively functional SNP situated in the CDKN2BAS gene that may be a specific BCIS susceptibility locus

Radiative and magnetohydrodynamics flow of third grade viscoelastic fluid past an isothermal inverted cone in the presence of heat generation/absorption

A mathematical analysis is presented to investigate the nonlinear, isothermal, steady-state, free convection boundary layer flow of an incompressible third grade viscoelastic fluid past an isothermal inverted cone in the presence of magnetohydrodynamic, thermal radiation and heat generation/absorption. The transformed conservation equations for linear momentum, heat and mass are solved numerically subject to the realistic boundary conditions using the second-order accurate implicit finite-difference Keller Box Method. The numerical code is validated with previous studies. Detailed interpretation of the computations is included. The present simulations are of interest in chemical engineering systems and solvent and low-density polymer materials processing

Harnessing hypoxic adaptation to prevent, treat, and repair stroke

The brain demands oxygen and glucose to fulfill its roles as the master regulator of body functions as diverse as bladder control and creative thinking. Chemical and electrical transmission in the nervous system is rapidly disrupted in stroke as a result of hypoxia and hypoglycemia. Despite being highly evolved in its architecture, the human brain appears to utilize phylogenetically conserved homeostatic strategies to combat hypoxia and ischemia. Specifically, several converging lines of inquiry have demonstrated that the transcription factor hypoxia-inducible factor-1 (HIF1-1) mediates the activation of a large cassette of genes involved in adaptation to hypoxia in surviving neurons after stroke. Accordingly, pharmacological or molecular approaches that engage hypoxic adaptation at the point of one of its sensors (e.g., inhibition of HIF prolyl 4 hydroxylases) leads to profound sparing of brain tissue and enhanced recovery of function. In this review, we discuss the potential mechanisms that could subserve protective and restorative effects of augmenting hypoxic adaptation in the brain. The strategy appears to involve HIF-dependent and HIF-independent pathways and more than 70 genes and proteins activated transcriptionally and post-transcriptionally that can act at cellular, local, and system levels to compensate for oxygen insufficiency. The breadth and depth of this homeostatic program offers a hopeful alternative to the current pessimism towards stroke therapeutics

Tuftsin Promotes an Anti-Inflammatory Switch and Attenuates Symptoms in Experimental Autoimmune Encephalomyelitis

Multiple sclerosis (MS) is a demyelinating autoimmune disease mediated by infiltration of T cells into the central nervous system after compromise of the blood-brain barrier. We have previously shown that administration of tuftsin, a macrophage/microglial activator, dramatically improves the clinical course of experimental autoimmune encephalomyelitis (EAE), a well-established animal model for MS. Tuftsin administration correlates with upregulation of the immunosuppressive Helper-2 Tcell (Th2) cytokine transcription factor GATA-3. We now show that tuftsin-mediated microglial activation results in shifting microglia to an anti-inflammatory phenotype. Moreover, the T cell phenotype is shifted towards immunoprotection after exposure to tuftsin-treated activated microglia; specifically, downregulation of pro-inflammatory Th1 responses is triggered in conjunction with upregulation of Th2-specific responses and expansion of immunosuppressive regulatory T cells (Tregs). Finally, tuftsin-shifted T cells, delivered into animals via adoptive transfer, reverse the pathology observed in mice with established EAE. Taken together, our findings demonstrate that tuftsin decreases the proinflammatory environment of EAE and may represent a therapeutic opportunity for treatment of MS

An ancestral 10-bp repeat expansion in VWA1 causes recessive hereditary motor neuropathy.

The extracellular matrix comprises a network of macromolecules such as collagens, proteoglycans and glycoproteins. VWA1 (von Willebrand factor A domain containing 1) encodes a component of the extracellular matrix that interacts with perlecan/collagen VI, appears to be involved in stabilizing extracellular matrix structures, and demonstrates high expression levels in tibial nerve. Vwa1-deficient mice manifest with abnormal peripheral nerve structure/function; however, VWA1 variants have not previously been associated with human disease. By interrogating the genome sequences of 74 180 individuals from the 100K Genomes Project in combination with international gene-matching efforts and targeted sequencing, we identified 17 individuals from 15 families with an autosomal-recessive, non-length dependent, hereditary motor neuropathy and rare biallelic variants in VWA1. A single disease-associated allele p.(G25Rfs*74), a 10-bp repeat expansion, was observed in 14/15 families and was homozygous in 10/15. Given an allele frequency in European populations approaching 1/1000, the seven unrelated homozygote individuals ascertained from the 100K Genomes Project represents a substantial enrichment above expected. Haplotype analysis identified a shared 220 kb region suggesting that this founder mutation arose >7000 years ago. A wide age-range of patients (6-83 years) helped delineate the clinical phenotype over time. The commonest disease presentation in the cohort was an early-onset (mean 2.0 ± 1.4 years) non-length-dependent axonal hereditary motor neuropathy, confirmed on electrophysiology, which will have to be differentiated from other predominantly or pure motor neuropathies and neuronopathies. Because of slow disease progression, ambulation was largely preserved. Neurophysiology, muscle histopathology, and muscle MRI findings typically revealed clear neurogenic changes with single isolated cases displaying additional myopathic process. We speculate that a few findings of myopathic changes might be secondary to chronic denervation rather than indicating an additional myopathic disease process. Duplex reverse transcription polymerase chain reaction and immunoblotting using patient fibroblasts revealed that the founder allele results in partial nonsense mediated decay and an absence of detectable protein. CRISPR and morpholino vwa1 modelling in zebrafish demonstrated reductions in motor neuron axonal growth, synaptic formation in the skeletal muscles and locomotive behaviour. In summary, we estimate that biallelic variants in VWA1 may be responsible for up to 1% of unexplained hereditary motor neuropathy cases in Europeans. The detailed clinical characterization provided here will facilitate targeted testing on suitable patient cohorts. This novel disease gene may have previously evaded detection because of high GC content, consequential low coverage and computational difficulties associated with robustly detecting repeat-expansions. Reviewing previously unsolved exomes using lower QC filters may generate further diagnoses

A novel fetal movement simulator for the performance evaluation of vibration Sensors for wearable fetal movement monitors

Fetal movements (FM) are an important factor in the assessment of fetal health. However, there is currently no reliable way to monitor FM outside clinical environs. While extensive research has been carried out using accelerometer-based systems to monitor FM, the desired accuracy of detection is yet to be achieved. A major challenge has been the difficulty of testing and calibrating sensors at the pre-clinical stage. Little is known about fetal movement features, and clinical trials involving pregnant women can be expensive and ethically stringent. To address these issues, we introduce a novel FM simulator, which can be used to test responses of sensor arrays in a laboratory environment. The design uses a silicon-based membrane with material properties similar to that of a gravid abdomen to mimic the vibrations due to fetal kicks. The simulator incorporates mechanisms to pre-stretch the membrane and to produce kicks similar to that of a fetus. As a case study, we present results from a comparative study of an acoustic sensor, an accelerometer, and a piezoelectric diaphragm as candidate vibration sensors for a wearable FM monitor. We find that the acoustic sensor and the piezoelectric diaphragm are better equipped than the accelerometer to determine durations, intensities, and locations of kicks, as they have a significantly greater response to changes in these conditions than the accelerometer. Additionally, we demonstrate that the acoustic sensor and the piezoelectric diaphragm can detect weaker fetal movements (threshold wall displacements are less than 0.5 mm) compared to the accelerometer (threshold wall displacement is 1.5 mm) with a trade-off of higher power signal artefacts. Finally, we find that the piezoelectric diaphragm produces better signal-to-noise ratios compared to the other two sensors in most of the cases, making it a promising new candidate sensor for wearable FM monitors. We believe that the FM simulator represents a key development towards enabling the eventual translation of wearable FM monitoring garments