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Object detection models are at the core of various computer vision tasks and have shown excellent performance on public datasets, but they also inherit the disadvantage of neural networks that they are vulnerable to adversarial example attacks. Adversarial patches are specific forms of adversarial examples that, as shown in previous studies, can only make specific objects (such as pedestrians and traffic signs), but not all objects, disappear. In addition, a patch must be placed on every object to deceive the detector. To solve the above problems, we propose a location-independent adversarial patch generation method that can attack objects in the range to be detected with a single patch. By attacking the confidence loss of the object detector, we creatively assign a greater weight to the foreground region, which makes its confidence decrease faster and effectively guides the convergence direction of the adversarial patch in the training process. Furthermore, we glue the patches randomly on the images to make them less sensitive to location during patch training. Experimental results indicate that the patches generated using our proposed method are not restricted to specific areas of the image and provide a minimum recall of 29.5%. [ABSTRACT FROM AUTHOR]

The mechanisms underlying the neurotoxicology of endemic fluorosis still remain obscure. To explore lactate dehydrogenase (LDH) leakage, intracellular Ca2+ concentration ([Ca2+]i) and reactive oxygen species (ROS) production induced by fluoride, human neuroblastoma (SH-SY5Y) cells were incubated with sodium fluoride (NaF, 20, 40, 80 mg/L) for 24 h, with 40 mg/L NaF for 3, 6, 12, 18, 24 h, and N-acetyl- L-cysteine (NAC), ethyleneglycol-bis-(β-aminoethyl ether)- N, N, N′, N′-tetraacetic acid (EGTA), 1,2-bis( O-aminophenoxy)ethane- N, N, N′, N′-tetraacetic acid tetra(acetoxymethyl) ester (BAPTA-AM) alone or combined with fluoride (40 mg/L) respectively for 12 h in vitro. The results showed that the LDH levels in the 40 and 80 mg/L fluoride-treated groups were significantly higher than that of the control group (in the test level of 0.05, the difference were statistical significance). [Ca2+]i and ROS reached a peak at 3 h and 12 h respectively after exposure to 40 mg/L fluoride. Fluoride coincubated with NAC (antioxidant) dramatically decreased ROS and LDH levels compared with the fluoride only group (in the test level of 0.05, the difference were statistical significance). However, fluoride-induced increase in [Ca2+]i was not affected by NAC. BAPTA-AM (intracellular calcium chelator) markedly lowered fluoride-induced increase of [Ca2+]i, ROS and LDH levels while EGTA (extracellular calcium chelator) have no effects on them. These results indicate that fluoride-related Ca2+ release from the site of intracellular calcium storage causes the elevation of ROS contributing to the cytotoxicity in SH-SY5Y cells. © 2011 Wiley Periodicals, Inc. Environ Toxicol, 2013. [ABSTRACT FROM AUTHOR]

The mechanisms underlying the neurotoxicology of endemic fluorosis still remain obscure. To explore lactate dehydrogenase (LDH) leakage, intracellular Ca²⁺ concentration ([Ca²⁺]i ) and reactive oxygen species (ROS) production induced by fluoride, human neuroblastoma (SH-SY5Y) cells were incubated with sodium fluoride (NaF, 20, 40, 80 mg/L) for 24 h, with 40 mg/L NaF for 3, 6, 12, 18, 24 h, and N-acetyl-L-cysteine (NAC), ethyleneglycol-bis-(β-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA), 1,2-bis(O-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetra(acetoxymethyl) ester (BAPTA-AM) alone or combined with fluoride (40 mg/L) respectively for 12 h in vitro. The results showed that the LDH levels in the 40 and 80 mg/L fluoride-treated groups were significantly higher than that of the control group (in the test level of 0.05, the difference were statistical significance). [Ca²⁺]i and ROS reached a peak at 3 h and 12 h respectively after exposure to 40 mg/L fluoride. Fluoride coincubated with NAC (antioxidant) dramatically decreased ROS and LDH levels compared with the fluoride only group (in the test level of 0.05, the difference were statistical significance). However, fluoride-induced increase in [Ca²⁺]i was not affected by NAC. BAPTA-AM (intracellular calcium chelator) markedly lowered fluoride-induced increase of [Ca²⁺]i , ROS and LDH levels while EGTA (extracellular calcium chelator) have no effects on them. These results indicate that fluoride-related Ca²⁺ release from the site of intracellular calcium storage causes the elevation of ROS contributing to the cytotoxicity in SH-SY5Y cells., (Copyright © 2011 Wiley Periodicals, Inc.)

Objective: To explore the effects of PCB153 on DNA damage and DNA repair-related gene expressions induced by PBDE-47 in SH-SY5Y cells., Methods: SH-SY5Y cells were incubated with different concentrations of 1,5 and 10 micromol/L PBDE-47 or/and 5 micromol/L PCB153 and antioxidant n-acetyl cysteine (NAC 100 micromol/L) for 24h in vitro, percentage of DNA in the tail, olive tail moment, the mRNA expression levels of XRCC1 and XRCC3 were measured respectively., Results: PBDE-47 increased percentage of DNA in the tail and olive tail moment significantly at doses of 5 micromol/L and above in a concentration-dependent manner compared to the control (P < 0.05). The percentage of DNA in the tail and olive tail moment were significantly higher in cells treated by 5 micromol/L PBDE-47 + 5 micromol/L PCB153 and 10 micromol/L PBDE-47 + 5 micromol/L PCB153 groups compared to the corresponding doses of PBDE-47 groups or PCB153 group (P < 0.05). The percentage of DNA in the tail and olive tail moment of cells treated by the groups added NAC were obviously lower than that of their corresponding groups not added it (P < 0.05). The interactive action was observed between PBDE-47 and PCB153 at concentrations of 10 micromol/L PBDE-47 (F = 23.74, P < 0.01). Significant decreased XRCC1 mRNA expression were observed at 10 micromol/L PBDE-47, 5 micromol/L PBDE-47 + 5 micromol/L PCB153, and 10 micromol/L PBDE-47 + 5 micromol/L PCB153 groups while significant increased XRCC3 mRNA expression were observed at 10 micromol/L PBDE-47 and 10 micromol/L PBDE-47 + 5 micromol/L PCB153 compared to the control group (P < 0.05). XRCC1 mRNA expression in cells treated by 100 micromol/L NAC + 10 micromol/L PBDE-47 + 5 micromol/L PCB153 group was significantly higher than that in 10 micromol/L PBDE-47 + 5 micromol/L PCB153 group (P < 0.05). XRCC3 mRNA expression in cells treated by PBDE-47 antioxidant groups were significantly lower than that in their corresponding non-antioxidant groups (P < 0.05). Correlation analysis showed there was a negative relationship between DNA damage and XRCC1 mRNA expression while a positive relationship between DNA damage and XRCC3 mRNA expression (r1 = 0.74, r2 = 0.76, P < 0.05)., Conclusion: PBDE-47 can induce DNA damage, PBDE-47 combined with PCB153 may increase the effects on DNA damage in SH-SY5Y cells in vitro, oxidative stress may play a important role in DNA damage induced by PBDE-47.