In this paper, a broadband metamaterial absorber suitable for the S, C, and X bands is designed and manufactured. The absorber is made of FR-4 substrate, resonant metal structure, lumped resistance, and metal backplate, has a unit size of 0.11λL, and a total thickness of 0.084λL. The absorption principle of the absorber is analyzed using equivalent medium theory and parametric research. The calculation results show that the absorber achieves more than 90% broadband absorption (relative bandwidth of 130%) between 2.7 GHz and 12.7 GHz, has a good polarization angle and incidence angle insensitivity, uses electromagnetic resonance to explain its absorption characteristics, and experiments confirm that the absorber has good broadband absorption. The proposed absorber has higher absorption and simpler construction than the previously described broadband absorber, and it has the potential for practical applications in EMC, radar, and electromagnetic protection.

Dermatomyositis (DM), an inflammatory disorder, is often associated with interstitial lung disease (ILD). However, the underlying mechanism remains unclear. Our study performed RNA sequencing (RNA-seq) and integrative bioinformatics analysis of differentially expressed genes (DEGs) in patients with dermatomyositis-associated interstitial lung disease (DM-ILD) and healthy controls. A total of 2,018 DEGs were identified between DM-ILD and healthy blood samples. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis showed that DEGs were mainly involved in immune- and inflammatory-related biological processes and pathways. Disease ontology (DO) enrichment analysis identified 35 candidate key genes involved in both skin and lung diseases. Meanwhile, a total of 886 differentially expressed alternative splicing (AS) events were found between DM-ILD and healthy blood samples. After overlapping DEGs with differential AS genes, the plasminogen activator and urokinase receptor (PLAUR) involved in immune-related biological processes and complement and coagulation cascades was screened and identified as the most important gene associated with DM-ILD. The protein–protein interaction (PPI) network revealed that PLAUR had interactions with multiple candidate key genes. Moreover, we observed that there were significantly more neutrophils and less naive B cells in DM-ILD samples than in healthy samples. And the expression of PLAUR was significantly positively correlated with the abundance of neutrophils. Significant higher abundance of PLAUR in DM-ILD patients than healthy controls was validated by RT-qPCR. In conclusion, we identified PLAUR as an important player in regulating DM-ILD by neutrophil-associated immune response. These findings enrich our understanding, which may benefit DM-ILD patients.

Systemic lupus erythematosus (SLE) is a prototypical autoimmune disease, characterized by overactive inflammation and aberrant activation of lymphocytes. Chemokine C‑X‑C motif ligand 10 (CXCL10) has an important role in the initiation and deterioration of SLE. However, the expression levels of CXCL10 mRNA in T‑helper (Th) cells and B lymphocytes from SLE patients have remained elusive. In the present study, a Bioinformatics analysis of differentially expressed gene (DEG) profiles obtained from RNA sequencing data for three matched samples was performed to explore the hub genes, mainly through Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes and protein‑protein interaction analysis. Furthermore, the expression of CXCL10 in peripheral blood mononuclear cells (PBMCs), CD4+ Th cells and CD19+ B cells of 108 subjects, including 66 SLE patients and 42 healthy controls, was confirmed by reverse transcription‑quantitative PCR. In addition, 4 single‑nucleotide polymorphism (SNP) loci in the 3'‑untranslated region of CXCL10 were assessed using the Snapshot SNP genotyping assay. A total of 152 clustered DEGs mainly accumulated in immune‑associated GO terms and interferon‑associated pathways were identified. The expression of CXCL10, one of the central genes in the interaction network cluster (the degree of interaction, MCODE score=28.414), was 6.27‑fold higher in SLE patients compared with control patients. Furthermore, CXCL10 mRNA was confirmed to be elevated in PBMCs and CD19+ B cells of patients with SLE (P<0.001 for the two cell types). However, no significant difference in CD4+ T lymphocytes was present (P=0.881). In addition, no polymorphism was identified in four selected loci from the samples. Taken together, the present results demonstrated that CXCL10, one of the hub genes in the pathogenesis of SLE, is upregulated in PBMCs and B lymphocytes of patients with SLE, although none of the SNPs selected for analysis in the present study were identified to have any potential associations with SLE.

Mutations in and reduced expression of the ETS1 gene may be associated with systemic lupus erythematosus (SLE). Here, we report a replication study to investigate associations of eight ETS1 single-nucleotide polymorphisms in the 3′-untranslated region (3′-UTR) with SLE and their regulation of ETS1 expression in a study population. We found that the rs4937333 T allele was associated with a significantly increased risk of SLE (odds ratio: 1.800, 95% confidence interval: 1.02–3.157, P = 0.040) and with dramatically reduced levels of ETS1 in B cells from SLE subjects. Functionally, the rs4937333 T allele alters the binding affinity between miR-5003 and its ETS1 3′-UTR target, thus enhancing suppression of ETS1 expression. Furthermore, immunoglobulin M-secreting plasmacytes were significantly reduced among B cells with the rs4937333 C allele versus the T allele according to FACS and ELISA. Additionally, miR-5003 expression was higher in B cells than in T cells from SLE patients, and a negative correlation between miR-5003 and ETS1 was found, especially in B cells with the T allele. These findings suggest that the rs4937333 T allele is a risk factor for susceptibility to SLE in the studied population. The rs4937333 T allele may enhance the binding of miR-5003 to ETS1, which probably promotes the involvement of ETS1 in the differentiation of B cells into plasmacytes.

The purpose of this article is to improve the detection sensitivity and quantitative assessment of different levels of cerebral hemorrhage (CH), and a high-sensitivity and shielding-free rabbit brain magnetic induction phase shift (MIPS) scanner was developed and validated. First, a uniform rotating magnetic field generated by a birdcage coil was utilized instead of the divergent magnetic field for the first time, and the birdcage structure has inherent characteristics of shielding external interference. Furthermore, the primary field was canceled, and the axial and tangential magnetic field components of the secondary magnetic field were synchronously detected and then synthesized for the first time using a magnetron sensor coil and a circular solenoid coil. Specifically, a field-programmable gate array-based spectrometer was used to guarantee the two-channel signal of high-precision quadrature excitation for birdcage coil, signal acquisition, and data processing. Experimental results indicated that the phase shift difference decreases linearly with the volume increase of blood injection, and the average MIPS caused by a 3-mL blood injection of rabbit inner capsule hemorrhage was 2.709°, which was 7.7 times higher than that of the traditional single excitation coil and single receiving coil (single coil–coil) method. The results have proven that this scanner has high sensitivity, strong anti-interference ability, and potential to realize the quantitative detection of hematoma volume.