Two-dimensional spiral plasmonic structures have emerged as a versatile approach to generate near-field vortex fields with tunable topological charges. We demonstrate here a far-field approach to observe the chiral second-harmonic generation (SHG) at designated visible wavelengths from a single plasmonic vortex metalens. This metalens comprises an Archimedean spiral slit fabricated on atomically flat aluminum epitaxial film, which allows for precise tuning of plasmonic resonances and subsequent transfer of two-dimensional materials on top of the spiral slit. The nonlinear optical measurements show a giant SHG circular dichroism. Furthermore, we have achieved an enhanced chiral SHG conversion efficiency (about an order of magnitude greater than the bare aluminum lens) from monolayer tungsten disulfide (WS 2 )/aluminum metalens, which is designed at the C-exciton resonance of WS 2 . Since the C-exciton is not a valley exciton, the enhanced chiral SHG in this hybrid system originates from the plasmonic vortex field-enhanced SHG under the optical spin−orbit interaction.
Background/Aim: Epidermal growth factor receptor (EGFR), mothers against decapentaplegic homolog 7 (SMAD7) and transforming growth factor betta (TGFB) are crucial for colorectal cancer (CRC) tumorigenesis. This study investigated whether polymorphisms in EGFR, SMAD7, and TGFB are associated with CRC risk in patients with Lynch syndrome. Materials and Methods: Genotyping was performed using Sequenom iPLEX MassArray. Association between genetic polymorphisms and CRC was assessed using a weighted Cox proportional hazard model. Results: Patients carrying the AA genotype of EGFR rs2227983 had a significantly higher CRC risk than those carrying the G allele (HR=2.55,). The dominant model of SMAD7 rs12953717 (CT + TT genotypes) significantly increased CRC risk (HR=2.17, 95% CI=1.12-4.16) when compared to the wild-type CC genotype. Similarly, the GG genotype of TGFBR2 rs6785358 significantly increased the risk of CRC (HR=21.1, 95% CI=5.06-88.1) compared to the AA genotype. Conclusion: EGFR, SMAD7, and TGFBR2 are associated with CRC risk in patients with Lynch syndrome.Lynch syndrome is a cancer predisposition disorder caused by a germline mutation in one of the mismatch repair (MMR) genes (1). MMR genes encode proteins that prevent both mutation and cancer development (2). Loss of function in MMR proteins usually results in error-prone DNA replication and microsatellite instability (MSI) (3). Approximately 1 in 3,140 individuals harbors a germline mutation in MLH1 or MSH2 and are at a higher risk of colorectal cancer (CRC) and other cancers than the general population (4, 5). Moreover, these patients exhibit an earlier onset of CRC and other cancers compared to the general population (6, 7).Lichtenstein et al. estimated that 35% of inherited genetic factors are associated with CRC susceptibility (8). One of these genetic factors is the transforming growth factor beta (TGFB), whose mutations have been identified in colorectal tumors with MSI (9), a feature of Lynch syndrome. The TGFB signaling pathway is mediated via the TGFB receptor (TGFBR) or mothers against decapentaplegic homolog 7 (SMAD7) (9). Epidermal growth factor receptor (EGFR) inhibits TGFB signaling pathway through SMAD7 (10). Studies have reported that single nucleotide polymorphisms (SNPs) in EGFR, SMAD7, and TGFB are associated with cancer predisposition (11-13). More specifically, EGFR is involved in angiogenesis, metastasis, tumor invasion, and survival; TGFB plays a crucial role in cell proliferation, differentiation, and apoptosis, whereas SMAD7 is an 5983
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