Synergistic Radiation Effects in PPD CMOS Image Sensors Induced by Neutron Displacement Damage and Gamma Ionization Damage.

The synergistic effects on the 0.18 µm PPD CISs induced by neutron displacement damage and gamma ionization damage are investigated. The typical characterizations of the CISs induced by the neutron displacement damage and gamma ionization damage are presented separately. The CISs are irradiated by reactor neutron beams up to 1 × 1011 n/cm2 (1 MeV neutron equivalent fluence) and 60Co γ-rays up to the total ionizing dose level of 200 krad(Si) with different sequential order. The experimental results show that the mean dark signal increase in the CISs induced by reactor neutron radiation has not been influenced by previous 60Co γ-ray radiation. However, the mean dark signal increase in the CISs induced by 60Co γ-ray radiation has been remarkably influenced by previous reactor neutron radiation. The synergistic effects on the PPD CISs are discussed by combining the experimental results and the TCAD simulation results of radiation damage.

Proton Radiation Effects on Dark Signal Distribution of PPD CMOS Image Sensors: Both TID and DDD Effects.

Four-transistor (T) pinned photodiode (PPD) CMOS image sensors (CISs) with four-megapixel resolution using 11µm pitch high dynamic range pixel were radiated with 3 MeV and 10MeV protons. The dark signal was measured pre- and post-radiation, with the dark signal post irradiation showing a remarkable increase. A theoretical method of dark signal distribution pre- and post-radiation is used to analyze the degradation mechanisms of the dark signal distribution. The theoretical results are in good agreement with experimental results. This research would provide a good understanding of the proton radiation effects on the CIS and make it possible to predict the dark signal distribution of the CIS under the complex proton radiation environments.

Simulation Study on the Defect Generation, Accumulation Mechanism and Mechanical Response of GaAs Nanowires under Heavy-Ion Irradiation.

Nanowire structures with high-density interfaces are considered to have higher radiation damage resistance properties compared to conventional bulk structures. In the present work, molecular dynamics (MD) is conducted to investigate the irradiation effects and mechanical response changes of GaAs nanowires (NWs) under heavy-ion irradiation. For this simulation, single-ion damage and high-dose ion injection are used to reveal defect generation and accumulation mechanisms. The presence of surface effects gives an advantage to defects in rapid accumulation but is also the main cause of dynamic annihilation of the surface. Overall, the defects exhibit a particular mechanism of rapid accumulation to saturation. Moreover, for the structural transformation of irradiated GaAs NWs, amorphization is the main mode. The main damage mechanism of NWs is sputtering, which also leads to erosion refinement at high doses. The high flux ions lead to a softening of the mechanical properties, which can be reflected by a reduction in yield strength and Young's modulus.

Upregulation of MicroRNA-34a Sensitizes Ovarian Cancer Cells to Resveratrol by Targeting Bcl-2.

PURPOSE: Resveratrol (REV), a natural compound found in red wine, exhibits antitumor activity in various cancers, including ovarian cancer (OC). However, its potential anti-tumor mechanisms in OC are not well characterized. Here, we tried to elucidate the underlying mechanisms of REV in OC cells. MATERIALS AND METHODS: The anti-proliferative effects of REV against OC cells were measured using CCK-8 assay. Apoptosis was measured using an Annexin V-FITC/PI apoptosis detection kit. The anti-metastasis effects of REV were evaluated by invasion assay and wound healing assay. The miRNA profiles in REV-treated cells were determined by microarray assay. RESULTS: Our results showed that REV treatment suppresses the proliferation, induces the apoptosis, and inhibits the invasion and migration of OV-90 and SKOV-3 cells. miR-34a was selected for further study due to its tumor suppressive roles in various human cancers. We found miR-34a overexpression enhanced the inhibitory effects of REV on OC cells, whereas miR-34a inhibition had the opposite effect in OC cells. In addition, we verified that BCL2, an anti-apoptotic gene, was found directly targeted by miR-34a. We also found that REV reduced the expression of Bcl-2 in OC cells. Further investigations revealed that overexpression of Bcl-2 significantly abolished the anti-tumor effects of REV on OC cells. CONCLUSION: Overall, these results demonstrated that REV exerts anti-cancer effects on OC cells through an miR-34a/Bcl-2 axis, highlighting the therapeutic potential of REV for treatment of OC.