The ability to slow down wave propagation in materials has attracted significant research interest. A successful solution will give rise to manageable enhanced wave-matter interaction, freewheeling phase engineering and spatial compression of wave signals. The existing methods are typically associated with constructing dispersive materials or structures with local resonators, thus resulting in unavoidable distortion of waveforms. Here we show that, with helical-structured acoustic metamaterials, it is now possible to implement dispersion-free sound deceleration. The helical-structured metamaterials present a non-dispersive high effective refractive index that is tunable through adjusting the helicity of structures, while the wavefront revolution plays a dominant role in reducing the group velocity. Finally, we numerically and experimentally demonstrate that the helical-structured metamaterials with designed inhomogeneous unit cells can turn a normally incident plane wave into a self-accelerating beam on the prescribed parabolic trajectory. The helicalstructured metamaterials will have profound impact to applications in explorations of slow wave physics.

No abstract

Triple-negative breast cancer (TNBC) represents a collection of malignant breast tumors that are often aggressive and have an increased risk of metastasis and relapse. Long non-coding RNAs are generally defined as RNA transcripts measuring 200 nucleotides or longer that do not encode for any protein. During the past decade, increasing evidence has shown that lncRNAs play important roles in oncogenesis and tumor suppression; however, the roles of lncRNAs in TNBC are poorly understood. To address this issue, we used Agilent human lncRNA microarray chips and bioinformatics tools, including Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG), to assess lncRNA expression in 3 pairs of TNBC tissues. A dysregulated lncRNA expression profile was identified by microarray and verified by qRT-PCR in 48 pairs of breast cancer subtype tissues. Metastasis is the major cause of cancer-related deaths, including those in TNBC, and the presence of dormant residual disseminated tumor cells (DTC) may be a key factor leading to metastasis. ANKRD30A, a potential target for breast cancer immunotherapy, is currently one of the most used DTC markers. Notably, we found the expression levels of the novel intergenic lncRNA LINC00993 to be associated with the expression levels of ANKRD30A. Furthermore, our qRT-PCR data indicated that the expression of LINC00993 was also associated with the expression of the estrogen receptor. In conclusion, our study identified a set of lncRNAs that were consistently aberrantly expressed in TNBC, and these dysregulated lncRNAs may be involved in the development and/or progression of TNBC.

Chemokine (C-X-C motif) ligand 1 (CXCL1), a member of the CXC chemokine family, has been reported to be a critical factor in inflammatory diseases and tumor progression; however, its functions and molecular mechanisms in estrogen receptor α (ER)-negative breast cancer (BC) remain largely unknown. The present study demonstrated that CXCL1 was upregulated in ER-negative BC tissues and cell lines compared with ER-positive tissues and cell lines. Treatment with recombinant human CXCL1 protein promoted ER-negative BC cell migration and invasion in a dose-dependent manner, and stimulated the activation of phosphorylated (p)- extracellular signal-regulated kinase (ERK)1/2, but not p-STAT3 or p-AKT. Conversely, knockdown of CXCL1 in BC cells attenuated these effects. Additionally, CXCL1 increased the expression of matrix metalloproteinase (MMP)2/9 via the ERK1/2 pathway. Inhibition of MEK1/2 by its antagonist U0126 reversed the effects of CXCL1 on MMP2/9 expression. Furthermore, immunohistochemical analysis revealed a strong positive association between CXCL1 and p-ERK1/2 expression levels in BC tissues. In conclusion, the present study demonstrated that CXCL1 is highly expressed in ER-negative BC, and stimulates BC cell migration and invasion via the ERK/MMP2/9 pathway. Therefore, CXCL1 may serve as a potential therapeutic target in ER-negative BC.