Results: The number of terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end-labelling (TUNEL)positive apoptotic nuclei in the DG increased and both Ki-67- and DCX-positive cells declined in a dose-dependent pattern, with fast neutrons or gamma-rays. In the hippocampus, which selleck inhibitor showed an apoptosis frequency between 2 and 8 per DG, the RBE of fast neutrons was approximately 1.9. Additionally,
the inhibitory effects of fast neutrons on the expression frequencies of Ki-67 (4-8) and DCX (8-32) were approximately 3.2 and 2.5 times, respectively, the effects of gamma-rays at the same dose.
Conclusions: Increased apoptotic cell death and decreased neurogenesis in the hippocampal DG were seen in a dose-dependent pattern after exposure to
fast neutrons and gamma- rays. In addition, the different rate of hippocampal neurogenesis between different radiation qualities may be an index of RBE.”
“Transmission electron microscopy (TEM) and ab initio calculations revealed that the Ni-Si reaction around 300 degrees C is significantly changed by adding Pt to Ni. TEM analysis clarified that NiSi2 was formed in a reaction between Ni thin film (similar to 1 nm) and Si substrate, while NiSi was formed when Pt was added to the Ni film. We also found that the Ni-adamantane structure, which acts Elacridar Transmembrane Transporters inhibitor as a precursor for NiSi2 formation around the reaction temperature, was formed in the former reaction but was significantly suppressed in the latter reaction.
Theoretical calculations indicated that Pt addition increased stress at the Ni-adamantane structure/Si-substrate interface. The increase in interface stress caused by Pt addition should raise the interface energy to suppress the Ni-adamantane structure formation, leading to NiSi2 formation being suppressed. (C) 2011 American Institute of Physics. [doi:10.1063/1.3560532]“
“Purpose: To determine alpha/beta (alpha/beta) values of arteriovenous malformations (AVM), meningiomas, acoustic neuromas (AN), and the optic chiasma using clinical data.
Methods and materials: Data of dose/fractionation schedules form the literature, iso-effective for a specific clinical outcome, were Acalabrutinib analysed using the Fraction Equivalent plot (FE) method and the Tucker method. Established safe dose/fractionation schedules for the optic chiasma were used to determine its alpha/beta value.
Results: With the FE plot method, an alpha/beta value of 3.76 Gray (Gy) (95% confidence level [CL]: 2.8-4.6 Gy) for meningiomas, 2.4 Gy (95% CL: 0.8-3.9 Gy) for acoustic neuroma, and 14.7 Gy (95% CL: 3.8-25.7 Gy) for arteriovenous malformations were determined. The respective alpha/beta values using the Tucker method were 3.3 Gy (95% CL: 2.2-6.8 Gy), 1.77 Gy (95% CL: 1.3-3.0 Gy) and -57 Gy (95% CL: -79.6 to -35.2 Gy). No meaningful alpha/beta values could be determined for the optic chiasma.