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Flexible, pressure-sensitive composites can be prepared through the inclusion of electrically conductive particles as functional fillers into an elastomeric polymer matrix, which have been used for the applications of wearable devices for health monitoring and electronic skins. A key challenge associated with these composites is developing anisotropic pressure sensitivity while retaining their flexibility (or low filler content). Herein, we demonstrate a simple and scalable method for aligning anisotropic nickel-coated carbon fibers (NiCF) along with the thickness direction of a polymer matrix by applying a magnetic field. The aligning mechanisms and kinetics of NiCF in the polydimethylsiloxane (PDMS) precursor are revealed by in situ optical microscopy images while a magnetic field is applied. The aligned nickel-coated carbon fibers in the polymer effectively endow the composite films excellent pressure-sensitive performance. The pressure sensitivity of NiCF/PDMS composite films has been systematically studied and can be used for biological monitoring. We believe that this magnetic field assisted processing strategy provides a promising material solution for manufacturing fiber embedded polymer composites with enhanced pressure sensitivity, which is essential for future wearable health monitoring electronics and electronic skin.

Papillary thyroid carcinoma (PTC) is the main kind of thyroid carcinoma, most of which are diagnosed in women. MiR-21 has been reported to be upregulated in multiple cancers to effect tumor growth. However, the role of miR-21 in PTC development remains unclear. In this present study, miR-21 and VHL expressions in PTC tissues and cells were evaluated by RT-qPCR and/or western blot. MTT assay and transwell assay were employed to assess cell proliferative and invasive abilities, respectively. Luciferase reporter assay was carried out to identify the target of miR-21and explore its roles in PTC. MiR-21 was upregulated in PTC tissues and cells. Ectopic of miR-21 expression promoted cell proliferative and invasive abilities, while knockdown miR-21 suppressed these in TPC-1 and BCPAP cells. Overexpression of miR-21 predicted poor prognosis in PTC. What is more, luciferase reporter assays showed miR-21 can directly target VHL in PTC cells. Knockdown of miR-21 expression inhibited TPC-1 and BCPAP cell invasion-mediated EMT and proliferation through the PI3K/AKT pathway. In addition, VHL reverses partial function of miR-21 on PTC cell proliferation and invasion. MiR-21 can inhibit cell proliferation and invasion by regulated VHL in PTC cells. The newly identified miR-21/VHL axis might provide a novel insight into the pathogenesis and therapy of PTC.

As the predominant thyroid cancer, papillary thyroid cancer (PTC) accounts for 75‑85% of thyroid cancer cases. This research aimed to investigate transcriptomic changes and key genes in PTC. Using RNA‑sequencing technology, the transcriptional profiles of 5 thyroid tumor tissues and 5 adjacent normal tissues were obtained. The single nucleotide polymorphisms (SNPs) were identified by SAMtools software and then annotated by ANNOVAR software. After differentially expressed genes (DEGs) were selected by edgR software, they were further investigated by enrichment analysis, protein domain analysis, and protein‑protein interaction (PPI) network analysis. Additionally, the potential gene fusion events were predicted using FusionMap software. A total of 70,172 SNPs and 2,686 DEGs in the tumor tissues, as well as 83,869 SNPs in the normal tissues were identified. In the PPI network, fibronectin 1 (FN1; degree=31) and transforming growth factor β receptor 1 (TGFβR1; degree=22) had higher degrees. A total of 7 PPI pairs containing the non‑synonymous risk SNP loci in the interaction domains were identified. Particularly, the interaction domains involved in the interactions of FN1 and 5 other proteins (such as FN1‑tenascin C, TNC) had non‑synonymous risk SNP loci. Furthermore, 11 and 4 gene fusion events were identified in all of the tumor tissues and normal tissues, respectively. Additionally, the NK2 homeobox 1‑surfactant associated 3 (NKX2‑1‑SFTA3) gene fusion was identified in both tumor and normal tissues. These results indicated that TGFβR1 and the NKX2‑1‑SFTA3 gene fusion may be involved in PTC. Furthermore, FN1 and TNC containing the non‑synonymous risk SNP loci might serve a role in PTC by interacting with each other.

Interleukin-23 (IL-23) and IL-17 are involved in the pathogenesis of allergic rhinitis (AR). However, the roles of IL-23 and IL-17 in ovalbumin (OVA)-induced AR remain unclear. Therefore in this study we aim to investigate the precise roles of IL-23 and IL-17 in a mouse model of OVA-induced AR. We found that during OVA-induced AR, eosinophil and goblet cells in the nose were significantly decreased in IL-23-deficient, but not in IL-17-deficient mice. However, there was no difference in the serum IgE and IgG1 levels between IL-23-deficient or IL-17-deficient and wild-type mice. Moreover, IL-4 levels in lymph node cell culture supernatants were significantly decreased in IL-23-deficient, but not IL-17-deficient, compared with wild-type mice. Furthermore, OVA-induced AR developed similarly in wild-type mice transferred with either IL-23-deficient BM cells or wild-type BM cells. These findings suggest that IL-23, but not IL-17 is crucial for the development of OVA-induced AR, and IL-23 neutralization may be a potential approach for treatment of OVA-induced AR in humans.