State-of-the-art compact antennas rely on electromagnetic wave resonance, which leads to antenna sizes that are comparable to the electromagnetic wavelength. As a result, antennas typically have a size greater than one-tenth of the wavelength, and further miniaturization of antennas has been an open challenge for decades. Here we report on acoustically actuated nanomechanical magnetoelectric (ME) antennas with a suspended ferromagnetic/piezoelectric thin-film heterostructure. These ME antennas receive and transmit electromagnetic waves through the ME effect at their acoustic resonance frequencies. The bulk acoustic waves in ME antennas stimulate magnetization oscillations of the ferromagnetic thin film, which results in the radiation of electromagnetic waves. Vice versa, these antennas sense the magnetic fields of electromagnetic waves, giving a piezoelectric voltage output. The ME antennas (with sizes as small as one-thousandth of a wavelength) demonstrates 1–2 orders of magnitude miniaturization over state-of-the-art compact antennas without performance degradation. These ME antennas have potential implications for portable wireless communication systems.

Ultrathin plasmonic metasurfaces have proven their ability to control and manipulate light at unprecedented levels, leading to exciting optical functionalities and applications. Although to date metasurfaces have mainly been investigated from an electromagnetic perspective, their ultrathin nature may also provide novel and useful mechanical properties. Here we propose a thin piezoelectric plasmonic metasurface forming the resonant body of a nanomechanical resonator with simultaneously tailored optical and electromechanical properties. We experimentally demonstrate that it is possible to achieve high thermomechanical coupling between electromagnetic and mechanical resonances in a single ultrathin piezoelectric nanoplate. The combination of nanoplasmonic and piezoelectric resonances allows the proposed device to selectively detect long-wavelength infrared radiation with unprecedented electromechanical performance and thermal capabilities. These attributes lead to the demonstration of a fast, high-resolution, uncooled infrared detector with ∼80% absorption for an optimized spectral bandwidth centered around 8.8 μm.

Colorectal cancer (CRC) remains a major contributor to cancer-related mortality. LIN28A and LIN28B are highly related RNA-binding protein paralogs that regulate biogenesis of let-7 microRNAs and influence development, metabolism, tissue regeneration, and oncogenesis. Here we demonstrate that overexpression of either LIN28 paralog cooperates with the Wnt pathway to promote invasive intestinal adenocarcinoma in murine models. When LIN28 alone is induced genetically, half of the resulting tumors harbor Ctnnb1 (β-catenin) mutation. When overexpressed in Apc Min/+ mice, LIN28 accelerates tumor formation and enhances proliferation and invasiveness. In conditional genetic models, enforced expression of a LIN28-resistant form of the let-7 microRNA reduces LIN28-induced tumor burden, while silencing of LIN28 expression reduces tumor volume and increases tumor differentiation, indicating that LIN28 contributes to tumor maintenance. We detected aberrant expression of LIN28A and/or LIN28B in 38% of a large series of human CRC samples (n = 595), where LIN28 expression levels were associated with invasive tumor growth. Our late-stage CRC murine models and analysis of primary human tumors demonstrate prominent roles for both LIN28 paralogs in promoting CRC growth and progression and implicate the LIN28/let-7 pathway as a therapeutic target.

State-of-the-art sensors use active electronics to detect and discriminate light, sound, vibration and other signals. They consume power constantly, even when there is no relevant data to be detected, which limits their lifetime and results in high costs of deployment and maintenance for unattended sensor networks. Here we propose a device concept that fundamentally breaks this paradigm-the sensors remain dormant with near-zero power consumption until awakened by a specific physical signature associated with an event of interest. In particular, we demonstrate infrared digitizing sensors that consist of plasmonically enhanced micromechanical photoswitches (PMPs) that selectively harvest the impinging electromagnetic energy in design-defined spectral bands of interest, and use it to create mechanically a conducting channel between two electrical contacts, without the need for any additional power source. Our zero-power digitizing sensor prototypes produce a digitized output bit (that is, a large and sharp off-to-on state transition with an on/off conductance ratio >10 and subthreshold slope >9 dec nW) when exposed to infrared radiation in a specific narrow spectral band (∼900 nm bandwidth in the mid-infrared) with the intensity above a power threshold of only ∼500 nW, which is not achievable with any existing photoswitch technologies.

Colorectal cancer (CRC) is a common malignant tumor that affects people worldwide. Metagenomic analyses have shown an enrichment of Fusobacterium nucleatum (F. nucleatum) in colorectal carcinoma tissue; many studies have indicated that F. nucleatum is closely related to the colorectal carcinogenesis. In this review, we provide the latest information to reveal the related molecular mechanisms. The known virulence factors of F. nucleatum promote adhesion to intestinal epithelial cells via FadA and Fap2. Besides, Fap2 also binds to immune cells causing immunosuppression. Furthermore, F. nucleatum recruits tumor-infiltrating immune cells, thus yielding a pro-inflammatory microenvironment, which promotes colorectal neoplasia progression. F. nucleatum was also found to potentiate CRC development through toll-like receptor 2 (TLR2)/toll-like receptor 4 (TLR4) signaling and microRNA (miRNA)-21 expression. In addition, F. nucleatum increases CRC recurrence along with chemoresistance by mediating a molecular network of miRNA-18a*, miRNA-4802, and autophagy components. Moreover, viable F. nucleatum was detected in mouse xenografts of human primary colorectal adenocarcinomas through successive passages. These findings indicated that an increased number of F. nucleatum in the tissues is a biomarker for the diagnosis and prognosis of CRC, and the underlying molecular mechanism can probably provide a potential intervention treatment strategy for patients with F. nucleatum-associated CRC.

Autophagy promotes tumor progression downstream of oncogenic KRAS, yet also restrains inflammation and dysplasia through mechanisms that remain incompletely characterized. Understanding the basis of this paradox has important implications for the optimal targeting of autophagy in cancer. Using a mouse model of cerulein-induced pancreatitis, we found that loss of autophagy by deletion of Atg5 enhanced activation of the IκB kinase (IKK) related kinase TBK1 in vivo, associated with increased neutrophil and T cell infiltration and PD-L1 upregulation. Consistent with this observation, pharmacologic or genetic inhibition of autophagy in pancreatic ductal adenocarcinoma (PDAC) cells, including suppression of the autophagy receptors NDP52 or p62, prolonged TBK1 activation and increased expression of CCL5, IL6, and several other T-cell and neutrophil chemotactic cytokines in vitro. Defective autophagy also promoted PD-L1 upregulation, which is particularly pronounced downstream of IFNγ signaling and involves JAK pathway activation. Treatment with the TBK1/IKKε/JAK inhibitor CYT387 (also known as momelotinib) not only inhibits autophagy, but also suppresses this feedback inflammation and reduces PD-L1 expression, limiting KRAS-driven pancreatic dysplasia. These findings could contribute to the dual role of autophagy in oncogenesis and have important consequences for its therapeutic targeting.

Colorectal cancer (CRC) heritability has been estimated to be around 30%. However, mutations in the known CRC-susceptibility genes explain CRC risk in fewer than 10% of affected individuals. Germline mutations in DNA-repair genes (DRGs) have recently been reported in CRC, but their contribution to CRC risk is largely unknown. We evaluated the gene-level germline mutation enrichment of 40 DRGs in 680 unselected CRC individuals and 27,728 ancestry-matched cancer-free adults. Significant findings were then examined in independent cohorts of 1,661 unselected CRC individuals and 1,456 individuals with early-onset CRC. Of the 680 individuals in the discovery set, 31 (4.56%) individuals harbored germline pathogenic mutations in known CRC-susceptibility genes, and another 33 (4.85%) individuals had DRG mutations that have not been previously associated with CRC risk. Germline pathogenic mutations in ATM and PALB2 were enriched in both the discovery (OR = 2.81 and p = 0.035 for ATM and OR = 4.91 and p = 0.024 for PALB2) and validation (OR = 2.97 and adjusted p = 0.0013 for ATM and OR = 3.42 and adjusted p = 0.034 for PALB2) sets. Biallelic loss of ATM was evident in all individuals with matched tumor profiling. CRC individuals also had higher rates of actionable mutations in the HR pathway, which can substantially increase the risk of developing cancers other than CRC. Our analysis provides evidence for ATM and PALB2 as CRC-risk genes, underscoring the importance of the homologous recombination pathway in CRC. In addition, we identified frequent complete homologous recombination deficiency in CRC tumors, representing a unique opportunity to explore targeted therapeutic interventions such as poly-ADP ribose polymerase inhibitor (PARPi).

We report a highly sensitive NEMS DC/low frequency magnetic field sensor consisting of an AlN/ FeGaB resonator, with a DE effect-based sensing principle. Unlike previously reported magnetic field detection schemes, such as observing induced magnetoelectric voltage, or monitoring impedance, we designed a system to directly measure the reflected output voltage from the sensor as a function of magnetic field. The AlN/FeGaB resonator shows a resonance frequency shift of 3.19 MHz (1.44%), which leads to a high DC magnetic field sensitivity of 2.8 Hz/nT and a limit of detection of 800pT in an unshielded, room temperature and pressure, lab environment.