Technology Advantage and Trade: Home Market Effects Revisited

According to conventional home market effects, free trade tends to shrink the market share for the smaller economy in the differentiated manufacturing goods, and in the extreme, leads to a complete hollowing out of the industry. In departing from the original Helpman-Krugman modeling assumptions behind the home market effects, we introduce technology differences between trading partners and prove that the home market effects will be offset and will even reverse if the small economy has better technology than the other country. We also prove that even with identical country size, the intra-industry trade addressed in the existing literature may not occur; it will occur only if the technology differential lies within a certain range that is positively affected by the level of transport cost.Home market Effects, Country Size, Technology Differential

Spectrometer‐free Optical Hydrogen Sensing Based on Fano‐like Spatial Distribution of Transmission in a Metal−Insulator−Metal Plasmonic Doppler Grating

Optical nanosensors are promising for hydrogen sensing because they are small, free from spark generation, and feasible for remote optical readout. Conventional optical nanosensors require broadband excitation and spectrometers, rendering the devices bulky and complex. An alternative is spatial intensity-based optical sensing, which only requires an imaging system and a smartly designed platform to report the spatial distribution of analytical optical signals. Here, a spatial intensity-based hydrogen sensing platform is presented based on Fano-like spatial distribution of the transmission in a Pd-Al2O3-Au metal-insulator-metal plasmonic Doppler grating (MIM-PDG). The MIM-PDG manifests the Fano resonance as an asymmetric spatial transmission intensity profile. The absorption of hydrogen changes the spatial Fano-like transmission profiles, which can be analyzed with a “spatial” Fano resonance model and the extracted Fano resonance parameters can be used to establish analytical calibration lines. While gratings sensitive to hydrogen absorption are suitable for hydrogen sensing, hydrogen insensitive gratings are also found, which provide an unperturbed reference signal and may find applications in nanophotonic devices that require a stable optical response under fluctuating hydrogen atmosphere. The MIM-PDG platform is a spectrometer-free and intensity-based optical sensor that requires only an imaging system, making it promising for cellphone-based optical sensing applications. © 2021 The Authors. Advanced Optical Materials published by Wiley-VCH GmbH

Down-regulation of the tumor suppressor miR-34a contributes to head and neck cancer by up-regulating the MET oncogene and modulating tumor immune evasion

BACKGROUND: MicroRNAs (miRs) have been shown to play an important role in tumorigenesis, including in head and neck squamous cell carcinoma (HNSCC). The miR-34 family is thought to play a role in tumor suppression, but the exact mechanism of their action in HNSCC is not well understood. Moreover, the impact of chromosomal changes and mutation status on miR-34a expression remains unknown. METHODS: Differential expression of miR-34a, MET, and genomic alterations were assessed in the Cancer Genome Atlas (TCGA) datasets as well as in primary HNSCC and adjacent normal tissue. The biological functions of miR-34a in HNSCC were investigated in samples derived from primary human tumors and HNSCC cell lines. The expression of MET was evaluated using immunohistochemistry, and the molecular interaction of miR-34a and MET were demonstrated by RNA pulldown, RNA immunoprecipitation, luciferase reporter assay, and rescue experiments. Lastly, locked nucleic acid (LNA) miRs in mouse xenograft models were used to evaluate the clinical relevance of miR-34a in HNSCC tumor growth and modulation of the tumor microenvironment in vivo. RESULTS: Chromosome arm 1p loss and P53 mutations are both associated with lower levels of miR-34a. In HNSCC, miR-34a acts as a tumor suppressor and physically interacts with and functionally targets the proto-oncogene MET. Our studies found that miR-34a suppresses HNSCC carcinogenesis, at least in part, by downregulating MET, consequently inhibiting HNSCC proliferation. Consistent with these findings, administration of LNA-miR-34a in an in vivo model of HNSCC leads to diminished HNSCC cell proliferation and tumor burden in vitro and in vivo, represses expression of genes involved in epithelial-mesenchymal transition, and negates the oncogenic effect of MET in mouse tumors. Consistently, LNA-miR-34a induced a decreased number of immunosuppressive PDL1-expressing tumor-associated macrophages in the tumor microenvironment. In HNSCC patient samples, higher levels of miR-34a are significantly associated with a higher frequency of Th1 cells and CD8 naive T cells. CONCLUSIONS: Our results demonstrate that miR-34a directly targets MET and maintains anti-tumor immune activity. We propose miR-34a as a potential new therapeutic approach for HNSCC