Guiding-mode-assisted double-BICs in an all-dielectric metasurface.

The electromagnetically induced transparency (EIT) effect realized in a metasurface is potential for slow light applications for its extreme dispersion variation in the transparency window. Herein, we propose an all-dielectric metasurface to generate a double resonance-trapped quasi bound states in the continuum (BICs) in the form of EIT or Fano resonance through selectively exciting the guiding modes with the grating. The group delay of the EIT is effectively improved up to 2113 ps attributing to the ultrahigh Q-factor resonance carried by the resonance-trapped quasi-BIC. The coupled harmonic oscillator model and a full multipole decomposition are utilized to analyze the physical mechanism of EIT-based quasi-BIC. In addition, the BIC based on Fano and EIT resonance can simultaneously exist at different wavelengths. These findings provide a new feasible platform for slow light devices in the near-infrared region.

Rapid measurement and compensation method of eccentricity in automatic profile measurement of the ICF capsule.

In this paper, we propose a new measurement and compensation method for the eccentricity of the inertial confinement fusion (ICF) capsule, which combines computer vision and the laser differential confocal method to align the capsule in rotation measurement. This technique measures the eccentricity of the capsule by obtaining the sub-pixel profile with a moment-based algorithm, then performs the preliminary alignment by the two-dimensional adjustment. Next, we use the laser differential confocal sensor to measure the height data of the equatorial surface of the capsule by turning it around, then obtain and compensate the remaining eccentricity ultimately. This method is a non-contact, automatic, rapid, high-precision measurement and compensation technique of eccentricity for the capsule. Theoretical analyses and preliminary experiments indicate that the maximum measurement range of eccentricity of this proposed method is 1.8 mm for the capsule with a diameter of 1 mm, and it could eliminate the eccentricity to less than 0.5 µm in 30 s.

Radiosensitization of Non-Small Cell Lung Cancer Cells by Inhibition of TGF-ß1 Signaling With SB431542 Is Dependent on p53 Status.

Although medically inoperable patients with stage I non-small cell lung cancer cells (NSCLC) are often treated with stereotactic body radiation therapy, its efficacy can be compromised due to poor radiosensitivity of cancer cells. Inhibition of transforming growth factor-ß1 (TGF-ß1) using LY364947 and LY2109761 has been demonstrated to radiosensitize cancer cells such as breast cancer, glioblastoma, and lung cancer. Our previous results have demonstrated that another potent and selective inhibitor of TGF-ß1 receptor kinases, SB431542, could radiosensitize H460 cells both in vitro and in vivo. In the present study, we investigated whether SB431542 could radiosensitize other NSCLC cell lines, trying to explore the potential implication of this TGF-ß1 inhibitor in radiotherapy for NSCLC patients. The results showed that A549 cells were significantly radiosensitized by SB431542, whereas no radiosensitizing effect was observed in H1299 cells. Interestingly, both H460 and A549 cells have wild-type p53, while H1299 cells have deficient p53. To study whether the radiosensitizing effect of SB431542 was associated with p53 status of cancer cells, the p53 of H460 cells was silenced using shRNA transfection. Then it was found that the radiosensitizing effect of SB431542 on H460 cells was not observed in H460 cells with silenced p53. Moreover, X-irradiation caused rapid Smad2 activation in H460 and A549 cells but not in H1299 and H460 cells with silenced p53. The Smad2 activation postirradiation could be abolished by SB431542. This may explain the lack of radiosensitizing effect of SB431542 in H1299 and H460 cells with silenced p53. Thus, we concluded that the radiosensitizing effect of inhibition of TGF-ß1 signaling in NSCLC cells by SB431542 was p53 dependent, suggesting that using TGF-ß1 inhibitor in radiotherapy may be more complicated than previously thought and may need further investigation.

The key role of miR-21-regulated SOD2 in the medium-mediated bystander responses in human fibroblasts induced by α-irradiated keratinocytes.

Radiation-induced bystander effect (RIBE) is well accepted in the radiation research field by now, but the underlying molecular mechanisms for better understanding this phenomenon caused by intercellular communication and intracellular signal transduction are still incomplete. Although our previous study has demonstrated an important role of miR-21 of unirradiated bystander cells in RIBEs, the direct evidence for the hypothesis that RIBE is epigenetically regulated is still limited and how miR-21 mediates RIBEs is unknown. Reactive oxygen species (ROS) have been demonstrated to be involved in RIBEs, however, the roles of anti-oxidative stress system of cells in RIBEs are unclear. Using transwell insert co-culture system, we investigated medium-mediated bystander responses in WS1 human fibroblasts after co-culture with HaCaT keratinocytes traversed by α-particles. Results showed that the ROS levels in unirradiated bystander WS1 cells were significantly elevated after 30min of co-culture, and 53BP1 foci, a surrogate marker of DNA damage, were obviously induced after 3h of co-culture. This indicates the occurrence of oxidative stress and DNA damage in bystander WS1 cells after co-culture with irradiated keratinocytes. Furthermore, the expression of miR-21 was increased in bystander WS1 cells, downregulation of miR-21 eliminated the bystander responses, overexpression of miR-21 alone could induce bystander-like oxidative stress and DNA damage in WS1 cells. These data indicate an important mediating role of miR-21 in RIBEs. In addition, MnSOD or SOD2 in WS1 cells was involved in the bystander effects, overexpression of SOD2 abolished the bystander oxidative stress and DNA damage, indicating that SOD2 was critical to the induction of RIBEs. Moreover, we found that miR-21 regulated SOD2, suggesting that miR-21 might mediate bystander responses through its regulation on SOD2. In conclusion, this study revealed a profound role of miR-21-regulated SOD2 of unirradiated WS1 cells in bystander effects induced by α-irradiated HaCaT keratinocytes.

Radiation quality-dependence of bystander effect in unirradiated fibroblasts is associated with TGF-ß1-Smad2 pathway and miR-21 in irradiated keratinocytes.

Traditional radiation biology states that radiation causes damage only in cells traversed by ionizing radiation. But radiation-induced bystander effect (RIBE), which refers to the biological responses in unirradiated cells when the neighboring cells are exposed to radiation, challenged this old dogma and has become a new paradigm of this field. By nature, RIBEs are the consequences of intercellular communication between irradiated and unirradiated cells. However, there are still some important questions remain unanswered such as whether RIBE is dependent on radiation quality, what are the determining factors if so, etc. Using a transwell co-culture system, we found that HaCaT keratinocytes irradiated with α-particles but not X-rays could induce bystander micronucleus formation in unirradiated WS1 fibroblasts after co-culture. More importantly, the activation of TGF-ß1-Smad2 pathway and the consistent decrease of miR-21 level in α-irradiated HaCaT cells were essential to the micronucleus induction in bystander WS1 cells. On the other hand, X-irradiation did not induce bystander effect in unirradiated WS1 cells, accompanied by lack of Smad2 activation and consistent decrease of miR-21 in X-irradiated HaCaT cells. Taken together, these results suggest that the radiation quality-dependence of bystander effect may be associated with the TGF-ß1-Smad2 pathway and miR-21 in irradiated cells.