Efficient free-space to on-chip coupling of THz-bandwidth pulses for biomolecule fingerprint sensing.

Wide bandwidth THz pulses can be used to record the distinctive spectral fingerprints related to the vibrational or rotational modes of polycrystalline biomolecules, and can be used to resolve the time-dependent dynamics of such systems. Waveguides, owing to their tight spatial confinement of the electromagnetic fields and the longer interaction distance, are promising platforms with which to study small volumes of such systems. The efficient input of sub-ps THz pulses into waveguides is challenging owing to the wide bandwidth of the THz signal. Here, we propose a sensing chip comprised of a pair of back-to-back Vivaldi antennas feeding into, and out from, a 90° bent slotline waveguide to overcome this problem. The effective operating bandwidth of the sensing chip ranges from 0.2 to 1.15 THz, and the free-space to on-chip coupling efficiency is as high as 51% at 0.44 THz. Over the entire band, the THz signal is ∼42 dB above the noise level at room temperature, with a peak of ∼73 dB above the noise. In order to demonstrate the use of the chip, we have measured the characteristic fingerprint of α-lactose monohydrate, and its sharp absorption peak at ∼0.53 THz was successfully observed, demonstrating the promise of our technique. The chip has the merits of efficient in-plane coupling, ultra-wide bandwidth, ease-of-integration, and simple fabrication. It has the potential for large-scale manufacture, and can be a strong candidate for integration into other THz light-matter interaction platforms.

Tunable bilayer dielectric metasurface via stacking magnetic mirrors.

Functional tunability, environmental adaptability, and easy fabrication are highly desired properties in metasurfaces. Here we provide a tunable bilayer metasurface composed of two stacked identical dielectric magnetic mirrors. The magnetic mirrors are excited by the interaction between the interference of multipoles of each cylinder and the lattice resonance of the periodic array, which exhibits nonlocal electric field enhancement near the interface and high reflection. We achieve the reversible conversion between high reflection and high transmission by manipulating the interlayer coupling near the interface between the two magnetic mirrors. Controlling the interlayer spacing leads to the controllable interlayer coupling and scattering of meta-atom. The magnetic mirror effect boosts the interlayer coupling when the interlayer spacing is small. Furthermore, the high transmission of the bilayer metasurface has good robustness due to the meta-atom with interlayer coupling can maintain scattering suppression against positional perturbation. This work provides a straightforward method to design tunable metasurface and sheds new light on high-performance optical switches applied in communication and sensing.

Emerging roles of activating transcription factor (ATF) family members in tumourigenesis and immunity: Implications in cancer immunotherapy.

Activating transcription factors, ATFs, are a group of bZIP transcription factors that act as homodimers or heterodimers with a range of other bZIP factors. In general, ATFs respond to extracellular signals, indicating their important roles in maintaining homeostasis. The ATF family includes ATF1, ATF2, ATF3, ATF4, ATF5, ATF6, and ATF7. Consistent with the diversity of cellular processes reported to be regulated by ATFs, the functions of ATFs are also diverse. ATFs play an important role in cell proliferation, apoptosis, differentiation and inflammation-related pathological processes. The expression and phosphorylation status of ATFs are also related to neurodegenerative diseases and polycystic kidney disease. Various miRNAs target ATFs to regulate cancer proliferation, apoptosis, autophagy, sensitivity and resistance to radiotherapy and chemotherapy. Moreover, ATFs are necessary to maintain cell redox homeostasis. Therefore, deepening our understanding of the regulation and function of ATFs will provide insights into the basic regulatory mechanisms that influence how cells integrate extracellular and intracellular signals into genomic responses through transcription factors. Under pathological conditions, especially in cancer biology and response to treatment, the characterization of ATF dysfunction is important for understanding how to therapeutically utilize ATF2 or other pathways controlled by transcription factors. In this review, we will demonstrate how ATF1, ATF2, ATF3, ATF4, ATF5, ATF6, and ATF7 function in promoting or suppressing cancer development and identify their roles in tumour immunotherapy.

The Apelin/APLNR system modulates tumor immune response by reshaping the tumor microenvironment.

Apelin is an endogenous ligand of the Apelin receptor (APLNR), a seven-transmembrane G protein-coupled receptor, which is widely distributed in human tissue. The Apelin/APLNR system is involved in regulating several physiological and pathological processes. The Apelin expression is increased in a variety of cancer and the Apelin/APLNR system could regulate the development of tumors through mediating autophagy, apoptosis, pyroptosis, and other biological processes to regulate tumor cell proliferation, migration, and invasion. The Apelin/APLNR system also participates in immune response and immune regulation through PI3K-Akt, ERK-MAPK, and other signal pathways. The latest research points out that there is a negative regulatory relationship between APLNR and immune checkpoint PD-L1. In this review, we outline the significance of the Apelin/APLNR signaling pathway in tumorigenesis and its immune regulation. These endeavors provide new insights into the translational application of Apelin/APLNR in cancer and may contribute to the promotion of more effective treatments for cancers.

Mitochondrial DNA in NLRP3 inflammasome activation.

As an intracellular polyprotein complex, the NLRP3 inflammasome is activated by NLRP3 perceiving pathogen-related molecular patterns, damage-related molecular patterns(DAMPs), which will result in the secretion of the caspase1-dependent pro-inflammatory cytokines IL1ß and IL18, and the cleavage of GSDMD-mediated pyroptosis. Therefore, inflammasome signaling is tightly regulated. Intracellular and extracellular mitochondria DNA (mtDNA) play different roles in activating the NLRP3 inflammasome. Intracellular mtDNA is easily oxidized and transferred to the cytoplasm, and directly binds to NLRP3 to activate NLRP3 inflammasome, the extracellular mtDNA is involved in the priming and activation of NLRP3 inflammasome as a DAMP; which is related to the occurrence and development of plentiful diseases. In this paper, we will discuss how mitochondrial DNA activates the NLRP3 inflammasome and how the process of activating NLRP3 inflammasome by mtDNA interacts with other NLRP3 inflammasome activation models.

Identification of potential biomarkers associated with immune infiltration in the esophageal carcinoma tumor microenvironment.

Tumor immune cell infiltration was significantly correlated with the progression and the effect of immunotherapy in cancers including esophageal carcinoma (ESCA). However, no biomarkers were identified which were associated with immune infiltration in ESCA. In the present study, a total of 128 common differentially expressed genes (DEGs) were identified between esophageal squamous cell carcinomas (ESCC) and esophageal adenocarcinomas (EAC). The results of gene ontology (GO) enrichment and Reactome pathway analysis displayed that the up-regulated DEGs were mainly involved in the regulation of extracellular matrix (ECM), while the down-regulated DEGs were mainly involved in the regulation of cornification and keratinocyte differentiation. The most significant module of up-regulated DEGs was selected by Molecular Complex Detection (MCODE). Top ten similar genes of COL1A2 were explored, then validation and the prognostic analysis of these genes displayed that COL1A2, COL1A1, COL3A1, ZNF469 and Periostin (POSTN) had the prognostic value which were up-regulated in ESCA. The expressions of COL1A2 and its four similar genes were mainly correlated with infiltrating levels of macrophages and dendritic cells (DCs) and showed strong correlations with diverse immune marker sets in ESCA. To summarize, COL1A2 and its four similar genes were identified as the potential biomarkers associated with immune infiltration in ESCA. These genes might be applied to immunotherapy for ESCA.