Intelligent reflecting surface (IRS) has emerged as a competitive solution to address blockage issues in millimeter wave (mmWave) and Terahertz (THz) communications due to its capability of reshaping wireless transmission environments. Nevertheless, obtaining the channel state information of IRS-assisted systems is quite challenging because of the passive characteristics of the IRS. In this paper, we consider the problem of beam training/alignment for IRS-assisted downlink mmWave/THz systems, where a multi-antenna base station (BS) with a hybrid structure serves a single-antenna user aided by IRS. By exploiting the inherent sparse structure of the BS-IRS-user cascade channel, the beam training problem is formulated as a joint sparse sensing and phaseless estimation problem, which involves devising a sparse sensing matrix and developing an efficient estimation algorithm to identify the best beam alignment from compressive phaseless measurements. Theoretical analysis reveals that the proposed method can identify the best alignment with only a modest amount of training overhead. Simulation results show that, for both line-of-sight (LOS) and NLOS scenarios, the proposed method obtains a significant performance improvement over existing state-of-art methods. Notably, it can achieve performance close to that of the exhaustive beam search scheme, while reducing the training overhead by 95%.
Background
Childhood-onset asthma is highly affected by genetic components. In recent years, many genome-wide association studies (GWAS) have reported a large group of genetic variants and susceptible genes associated with asthma-related phenotypes including childhood-onset asthma. However, the regulatory mechanisms of these genetic variants for childhood-onset asthma susceptibility remain largely unknown.
Methods
In the current investigation, we conducted a two-stage designed Sherlock-based integrative genomics analysis to explore the cis- and/or trans-regulatory effects of genome-wide SNPs on gene expression as well as childhood-onset asthma risk through incorporating a large-scale GWAS data (N = 314,633) and two independent expression quantitative trait loci (eQTL) datasets (N = 1890). Furthermore, we applied various bioinformatics analyses, including MAGMA gene-based analysis, pathway enrichment analysis, drug/disease-based enrichment analysis, computer-based permutation analysis, PPI network analysis, gene co-expression analysis and differential gene expression analysis, to prioritize susceptible genes associated with childhood-onset asthma.
Results
Based on comprehensive genomics analyses, we found 31 genes with multiple eSNPs to be convincing candidates for childhood-onset asthma risk; such as, PSMB9 (cis-rs4148882 and cis-rs2071534) and TAP2 (cis-rs9267798, cis-rs4148882, cis-rs241456, and trans-10,447,456). These 31 genes were functionally interacted with each other in our PPI network analysis. Our pathway enrichment analysis showed that numerous KEGG pathways including antigen processing and presentation, type I diabetes mellitus, and asthma were significantly enriched to involve in childhood-onset asthma risk. The co-expression patterns among 31 genes were remarkably altered according to asthma status, and 25 of 31 genes (25/31 = 80.65%) showed significantly or suggestively differential expression between asthma group and control group.
Conclusions
We provide strong evidence to highlight 31 candidate genes for childhood-onset asthma risk, and offer a new insight into the genetic pathogenesis of childhood-onset asthma.
A substantial percentage (8%) of all newly diagnosed cancer cases are in patients with previous tumours, with a similar trend in lung cancer. Cases of multiple primary lung cancer (MPLC) are increasing worldwide, due to improved diagnostic and surveillance mechanisms and the ageing population. Diagnosis of MPLC is complicated by difficulties in distinguishing it from lung cancer metastasis. Clinicopathological assessment, diagnosis and management have evolved, but remain severely limited by the lack of robust and dependable molecular markers for the differential diagnosis of metastasis and MPLC. This systematic review evaluates diagnostic criteria for MPLC, and the subsequent management and success rates. The incorporation of molecular biology techniques into the diagnostic process for MPLC is also discussed.
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