Autophagy, a main degradation pathway for maintaining cellular homeostasis, and redox homeostasis have recently been considered to play protective roles in neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. Increased levels of reactive oxygen species (ROS) in neurons can induce mitochondrial damage and protein aggregation, thereby resulting in neurodegeneration. Oxidative stress is one of the major activation signals for the induction of autophagy. Upon activation, autophagy can remove ROS, damaged mitochondria, and aggregated proteins from the cells. Thus, autophagy can be an effective strategy to maintain redox homeostasis in the brain. However, the interaction between redox homeostasis and autophagy is not clearly elucidated. In this review, we discuss recent studies on the relationship between redox homeostasis and autophagy associated with neurodegenerative diseases and propose that autophagy induction through pharmacological intervention or genetic activation might be a promising strategy to treat these disorders.

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TCAM-based payload inspection algorithms for detecting viruses and worms wasted much memory for storing redundant bytes, "don't care". The aim of our research was to eliminate the redundancy so as to store more rules in TCAM or reduce the area cost. To eliminate the redundancy, we devised Split-TCAM mechanism where a TCAM block is split into every byte. We simulated our Split-TCAM mechanism using Snort v2.8.5 [1]. Results indicated that the proposed mechanism could save the required size of memory to 37.4% and 27.7% on average when applying it to the R-TCAM and Jumping Window algorithm, respectively.

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