Radially Polarized Second-Harmonic Generation from a Single-Element Nanoantenna via Dark Plasmon Coupling of Nonlinear Polarization

Controlling the process of second-harmonic (SH) generation at the nanoscale is important in photonic applications but remains challenging in nanophotonics. Herein, based on theoretical and experimental studies, we found that a cross-shaped single-element plasmonic nanoantenna resonating with bright and dark modes at the fundamental (excitation) and SH wavelengths, respectively, generates radially polarized ring-shaped SH radiations with axial symmetry by exciting the bright dipole mode with linearly polarized light. Mode expansion analysis of the generated SH radiation revealed that the radial polarization arises from a dark breathing mode in which coherent dipoles are radially distributed along the arms of the cross-shaped antenna. This study reveals that surface SH polarization generated by the electric near-field of the bright mode at the fundamental wavelength efficiently is coupled to the dark modes rather than the bright mode because its spatial distribution has the same symmetry as the dark modes. By engineering bright and dark modes at the fundamental and SH wavelengths, respectively, novel plasmonic nanodevices that simultaneously perform polarization control and efficient wavelength conversion are expected

Radially Polarized Second-Harmonic Generation from a Single-Element Nanoantenna via Dark Plasmon Coupling of Nonlinear Polarization

Controlling the process of second-harmonic (SH) generation at the nanoscale is important in photonic applications but remains challenging in nanophotonics. Herein, based on theoretical and experimental studies, we found that a cross-shaped single-element plasmonic nanoantenna resonating with bright and dark modes at the fundamental (excitation) and SH wavelengths, respectively, generates radially polarized ring-shaped SH radiations with axial symmetry by exciting the bright dipole mode with linearly polarized light. Mode expansion analysis of the generated SH radiation revealed that the radial polarization arises from a dark breathing mode in which coherent dipoles are radially distributed along the arms of the cross-shaped antenna. This study reveals that surface SH polarization generated by the electric near-field of the bright mode at the fundamental wavelength efficiently is coupled to the dark modes rather than the bright mode because its spatial distribution has the same symmetry as the dark modes. By engineering bright and dark modes at the fundamental and SH wavelengths, respectively, novel plasmonic nanodevices that simultaneously perform polarization control and efficient wavelength conversion are expected

Media 1: Simultaneous separation of polydisperse particles using an asymmetric nonperiodic optical stripe pattern

Originally published in Applied Optics on 10 March 2009 (ao-48-8-1543

Severe mitochondrial damage associated with low-dose radiation sensitivity in ATM- and NBS1-deficient cells

Low-dose radiation risks remain unclear owing to a lack of sufficient studies. We previously reported that low-dose, long-term fractionated radiation (FR) with 0.01 or 0.05 Gy/fraction for 31 d inflicts oxidative stress in human fibroblasts due to excess levels of mitochondrial reactive oxygen species (ROS). To identify the small effects of low-dose radiation, we investigated how mitochondria respond to low-dose radiation in radiosensitive human ataxia telangiectasia mutated (ATM)- and Nijmegen breakage syndrome (NBS)1-deficient cell lines compared with corresponding cell lines expressing ATM and NBS1. Consistent with previous results in normal fibroblasts, low-dose, long-term FR increased mitochondrial mass and caused accumulation of mitochondrial ROS in ATM- and NBS1-complemented cell lines. Excess mitochondrial ROS resulted in mitochondrial damage that was in turn recognized by Parkin, leading to mitochondrial autophagy (mitophagy). In contrast, ATM- and NBS1-deficient cells showed defective induction of mitophagy after low-dose, long-term FR, leading to accumulation of abnormal mitochondria; this was determined by mitochondrial fragmentation and decreased mitochondrial membrane potential. Consequently, apoptosis was induced in ATM- and NBS1-deficient cells after low-dose, long-term FR. Antioxidant N-acetyl-L-cysteine was effective as a radioprotective agent against mitochondrial damage induced by low-dose, long-term FR among all cell lines, including radiosensitive cell lines. In conclusion, we demonstrated that mitochondria are target organelles of low-dose radiation. Mitochondrial response influences radiation sensitivity in human cells. Our findings provide new insights into cancer risk estimation associated with low-dose radiation exposure.</p

Helical dichroism for hybridized quadrupole plasmon modes in twisted metal nanorods

Helical dichroism (HD), based on the interaction between chiral plasmonic nanostructures and light with orbital angular momentum (OAM), has attracted researchers in a wide range of fields from the viewpoint of fundamental physics and applications. However, the relation between the HD and the excited plasmon modes has been poorly understood in experiments. Because of the weak chiral interaction between the chiral structures and OAM light, the structure size had to be much larger than the incident light wavelength to obtain a sufficient HD signal in an experiment, resulting in a complex superposition of higher-order plasmon modes. Recently, we experimentally demonstrated that a twisted gold nanorod dimer, one of the simplest 3D chiral plasmonic structures, exhibits giant circular dichroism due to strong plasmon coupling between the nanorods, followed by the hybridization of dipole mode. In this study, we reveal that the HD of this nanorod dimer appears due to the hybridization of quadrupole plasmon mode rather than dipole mode. Furthermore, the measurement of the HD signal can be achieved by using the array of the twisted dimers. The dependence of the HD on the incident light wavelength exhibits that the HD sign changes around the quadrupole plasmon resonance, which is in good agreement with the simulation. These results open new avenues for the profound understanding of the light-matter interaction with respect to angular momentum

Figure S1 from Radiation-Induced Myofibroblasts Promote Tumor Growth via Mitochondrial ROS–Activated TGFβ Signaling

Induction of alpha-SMA after acute single radiation</p

Supplemental Figure Legends from Radiation-Induced Myofibroblasts Promote Tumor Growth via Mitochondrial ROS–Activated TGFβ Signaling

S1. The percentage of TIG-3 and MRC-5 cells with alpha-SMA staining exposed to indicated doses is shown in the graph. S2. Tumor volumes of HeLa, HeLa+MRC-5 0FR tumors, HeLa+MRC-5 0.05FR tumors, HeLa+MRC-5 NAC 0FR tumors, and HeLa+MRC-5 0.05FR tumors.</p

FIgure S2 from Radiation-Induced Myofibroblasts Promote Tumor Growth via Mitochondrial ROS–Activated TGFβ Signaling

Individual tumor measurements data</p

Systematic Protein Level Regulation via Degradation Machinery Induced by Genotoxic Drugs

In this study we monitored protein dynamics in response to cisplatin, 5-fluorouracil, and irinotecan with different concentrations and administration modes using “reverse-phase” protein arrays (RPPAs) in order to gain comprehensive insight into the protein dynamics induced by genotoxic drugs. Among 666 protein time-courses, 38% exhibited an increasing trend, 32% exhibited a steady decrease, and 30% fluctuated within 24 h after drug exposure. We analyzed almost 12,000 time-course pairs of protein levels based on the geometrical similarity by correlation distance (<i>dCor</i>). Twenty-two percent of the pairs showed <i>dCor</i> > 0.8, which indicates that each protein of the pair had similar dynamics. These trends were disrupted by a proteasome inhibitor, MG132, suggesting that the protein degradation system was activated in response to the drugs. Among the pairs with high <i>dCor</i>, the average <i>dCor</i> of pairs with apoptosis-related protein was significantly higher than those without, indicating that regulation of protein levels was induced by the drugs. These results suggest that the levels of numerous functionally distinct proteins may be regulated by common degradation machinery induced by genotoxic drugs

Quantitative Protein Network Monitoring in Response to DNA Damage

Conventional molecular biology techniques have identified a large number of cell signaling pathways; however, the importance of these pathways often varies, depending on factors such as treatment type, dose, time after treatment, and cell type. Here, we describe a technique using “reverse-phase” protein lysate microarrays (RPAs) to acquire multiple dimensions of information on protein dynamics in response to DNA damage. Whole-cell lysates from three cellular stress treatments (IR, UV, and ADR) were collected at four doses per treatment, and each, in turn, at 10 time points, resulting in a single-slide RPA consisting of 10 240 features, including replicates. The dynamic molecular profile of 18 unique protein species was compared to phenotypic fate by FACS analysis for corresponding stress conditions. Our initial quantitative results in this new platform confirmed that (1) there is clear stress dose–response effect in p53 protein and (2) a comparison of the rates of increase of p21 and Cyclin D3/p53-Ser15 in response to DNA damage may be associated with the pattern of DNA content. This method, offering a quantitative time-course monitoring of protein expression levels, can provide an experimental reference for developing mathematical models of cell signaling dynamics. Although the present study focuses on the DNA damage-repair pathway, the technique is generally useful to the study of protein signaling