Proton-irradiation-immune electronics implemented with two-dimensional charge-density-wave devices.

We demonstrate that charge-density-wave devices with quasi-two-dimensional 1T-TaS2 channels show remarkable immunity to bombardment with 1.8 MeV protons to a fluence of at least 1014 H+cm-2. The current-voltage characteristics of these devices do not change as a result of proton irradiation, in striking contrast to most conventional semiconductor devices or other two-dimensional devices. Only negligible changes are found in the low-frequency noise spectra. The radiation immunity of these "all-metallic" charge-density-wave devices is attributed to the quasi-2D nature of the electron transport in the nanoscale-thickness channel, high concentration of charge carriers in the utilized charge-density-wave phases, and two-dimensional device design. Such devices, capable of operating over a wide temperature range, can constitute a crucial segment of future electronics for space, particle accelerator and other radiation environments.

Brain iron accumulation exacerbates the pathogenesis of MPTP-induced Parkinson's disease.

Brain iron levels are significantly increased in Parkinson's disease (PD) and iron deposition is observed in the substantia nigra (SN) of PD patients. It is unclear whether iron overload is an initial cause of dopaminergic neuronal death or merely a byproduct that occurs in the SN of PD patients. In this study, ceruloplasmin knockout (CP-/-) mice and mice receiving an intracerebroventricular injection of ferric ammonium citrate (FAC) were selected as mouse models with high levels of brain iron. These mice were administered with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) by intraperitoneal injection. Their behavior and the dopaminergic neuron damage to their substantia nigra pars compacta (SNpc) were assessed. These findings suggest that the injection of FAC or the absence of the CP gene may exacerbate both the observed apoptosis of TH-positive neurons and the behavioral symptoms of the MPTP-treated mice. The intracerebroventricular injection of deferoxamine (DFO) significantly alleviated the neuronal damage caused by MPTP in CP-/- mice. Furthermore, our findings suggest that the increased nigral iron content exacerbates the oxidative stress levels, promoting apoptosis through the Bcl-2/Bax pathway and the activated caspase-3 pathway in the brain. Therefore, iron overload in the brain exacerbates dopaminergic neuronal death in SNpc and leads to the onset of PD.