Energy Efficient Power Allocation for OFDM-Based Cognitive Radio Systems with Partial Intersystem CSI

This paper investigates energy efficient power allocation for orthogonal frequency division multiplexing- (OFDM-) based cognitive radio (CR) systems with partial intersystem channel state information (CSI) available. The goal is to maximize energy efficiency (EE) while ensuring the minimum rate of secondary user (SU) and keeping the average interference power (AIP) introduced to primary user (PU) within a target probability level. We propose a suboptimal algorithm to solve this optimization problem based on classic water-filling (WF) technique. Moreover, we first address the relation between EE and water level. In order to reduce complexity, a simplified algorithm with closed-form solution is also proposed. Numerical results are provided to corroborate our theoretical analysis and to demonstrate the effectiveness of the proposed schemes

Tensioned flexible riser vibrations under wave excitation, an investigation on the scale effect

In order to study the scale effect in wave-structure interactions and the role that structure-related parameters (tension T or bending stiffness EI) plays, riser model tests under regular waves were conducted using the model with multiple geometric scales (1:15, 1:12 and 1:9) in a wave basin. The riser model used is a novel structural design combing the outer polyvinyl chloride pipe with the core steel rod which could be simplified as a cantilever beam. Different initial tension T acting on the riser are tested by adjusting the slotted weight. The results show that the amplitude varies in a cubic fashion with the distance from the fixed end. In addition, the influence of the wave period and top tension T on the amplitude are investigated, which ultimately leads to a dimensionless number π1 = KCd·TL2/EI where KC is the classical Keulegan–Carpenter number (KC), EI shows the bending stiffness of the riser model and L gives the pipe length. With the KC number revised to take the distance from the fixed end into the calculation, this parameter provides a good measure in estimating the amplitudes of the riser vibrations induced by the waves

Predictions for combined in-line and cross-flow VIV responses with a novel model for estimation of tension

The dynamic responses of slender cylinders with high aspect ratios undergoing vortex-induced vibrations (VIV) are studied. In detail, a three-dimensional model predicting the VIV responses in both the In-Line and Cross-Flow directions of slender cylinders is proposed based on the nonlinear equation governing the dynamic deformation and a wake oscillator. The tension in the cylinder is estimated according to the incoming stream velocities. To predict the VIV responses, the cylinder is discretized into finite segments, and the vibrations of each segment are estimated from solving the governing equation when the excitation forces are modelled using the Van Der Pol's wake oscillator. Considering that the wake oscillator model estimates the excitation forces according to the dynamics of the cylinder, it reveals the interactions between the flow and the dynamics of the cylinder. In order to verify the model calculating the mean tension, the VIV responses, which has been experimentally tested, is numerically studied. The comparison between the numerically predicted and experimentally measured responses shows that, the approach, especially the novel tension model, proposed herein is reliable as the frequency of vibrations, dominant mode number and vibration amplitude are all in good agreement with the experimental measurements and results from peer-reviewed publications

Case report: Two cases of Poirier-Bienvenu neurodevelopmental syndrome and review of literature

The Poirier-Bienvenu neurodevelopmental syndrome (POBINDS) is a rare disease caused by mutations in the CSNK2B gene, which is characterized by intellectual disability and early-onset epilepsy. Mosaicism has not been previously reported in CSNK2B gene. POBINDS is autosomal dominant and almost all reported cases were de novo variants. Here, we report two patients were diagnosed with POBINDS. Using Whole Exome Sequencing (WES), we detected two novel CSNK2B variants in the two unrelated individuals: c.634_635del (p.Lys212AspfsTer33) and c.142C > T (p.Gln48Ter) respectively. Both of them showed mild developmental delay with early-onset and clustered seizures. The patient with c.634_635del(p.Lys212AspfsTer33) variant was mutant mosaicism, and the proportion of alleles in peripheral blood DNA was 28%. Further, the literature of patients with a de novo mutation of the CSNK2B gene was reviewed, particularly seizure semiology and genotype-phenotype correlations

PCB169 exposure aggravated the development of non-alcoholic fatty liver in high-fat diet-induced male C57BL/6 mice

Polychlorinated biphenyls (PCBs) are lipophilic environmental toxicants. Epidemiological studies have established a link between PCBs and both metabolic syndrome and nonalcoholic fatty liver disease (NAFLD). Multiple studies have reported that exposure to both PCB156 and PCB126 among the 12 dioxin-like PCBs leads to the development of NAFLD. However, studies to elucidate whether PCB169 induces the development of NAFLD by constructing in vivo models have not been reported. Therefore, we evaluated the effects of exposure to PCB169 (5 mg/kg-bw) on hepatic lipid metabolism in C57BL/6 mice from control diet and high-fat diet cohorts. The results showed that PCB169 exposure reduced body weight and intraperitoneal fat mass in mice on the control diet, but the liver lipid levels were significantly increased, exacerbating NAFLD in mice on a high-fat diet. Through transcriptomics studies, it was found that PCB169 exposure induced significant up-regulation of Pparγ, Fasn, and Aacs genes involved in hepatic lipogenesis, as well as remarkable up-regulation of Hmgcr, Lss, and Sqle genes involved in cholesterol synthesis. Additionally, there was notable down-regulation of Pparα and Cpt1 genes involved in lipid β-oxidation, leading to abnormal lipid accumulation in the liver. In addition, we found that PCB169 exposure significantly activated the Arachidonic acid metabolism, PPAR signaling pathway, Metabolism of xenobiotics by cytochrome P450, and Retinol metabolism pathways, and so on. Our study suggests that PCB169 can modify gene expression related to lipid metabolism, augument lipid accumulation in the liver, and further contribute to the development of NAFLD, thereby revealing the detrimental effects associated with PCB exposure on animal growth and metabolism

Downregulation of Long Non-coding RNA FALEC Inhibits Gastric Cancer Cell Migration and Invasion Through Impairing ECM1 Expression by Exerting Its Enhancer-Like Function

Long non-coding RNAs (lncRNAs) have been shown to play important roles in many human diseases. However, their functions and mechanisms in tumorigenesis and development remain largely unknown. Here, we demonstrated that focally amplified lncRNA in epithelial cancer (FALEC) was upregulated and significantly correlated with lymph node metastasis, TNM stage in gastric cancer (GC). Further experiments revealed that FALEC knockdown significantly inhibited GC cells migration and invasion in vitro. Mechanistic investigations demonstrated that small interfering RNA-induced silencing of FALEC decreased expression of the nearby gene extracellular matrix protein 1 (ECM1) in cis. Additionally, ECM1 and FALEC expression were positively correlated, and high levels of ECM1 predicted shorter survival time in GC patients. Our results suggest that the downregulation of FALEC significantly inhibited the migration and invasion of GC cells through impairing ECM1 expression by exerting an enhancer-like function. Our work provides valuable information and a novel promising target for developing new therapeutic strategies in GC

Identification and Validation of METTL3-Related Molecules for Predicting Prognosis and Efficacy of Immunotherapy in Gastric Cancer Based on m6A Methylome and Transcriptome Sequencing Analysis

Abnormal N6-methyladenosine (m6A) modification levels caused by METTL3 have been identified to be a critical regulator in human cancers, and its roles in the immune microenvironment and the relationship between targeted therapy and immunotherapy sensitivity in gastric cancer (GC) remain poorly understood. In this study, we assessed the transcriptome-wide m6A methylation profile after METTL3 overexpression by m6A sequencing and RNA sequencing in BGC-823 cells. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed to analyze the function of core targets of METTL3. Eighteen methylation core molecules were identified in GC patients by combining transcriptome and methylome sequencing. GC patients can be separated into two subtypes based on the expression of 18 methylation core molecules. Furthermore, subgroup analysis showed that patients with different subtypes had a different OS, PFS, stage, grade, and TMB. Gene set enrichment analysis (GSEA) showed that immune-related pathways were enriched among subtype A. The ESTIMATE analysis suggested that the extent of infiltration of immune cells was different in two subtypes of GC patients. Tumor Immune Dysfunction and Exclusion (TIDE) and The Cancer Immunome Atlas (TCIA) database also showed that there were significant differences in the efficacy of immunotherapy among different types of GC patients. Altogether, our results reveal that METTL3-mediated m6A methylation modification is associated with the immune microenvironment and the effects of immunotherapy in GC patients. Our findings provide novel insights for clinicians in the diagnosis and optimal treatment of GC patients