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Abstract-This paper aims at finding fundamental design principles for hierarchical web caching. An analytical modeling technique is developed to characterize an uncooperative two-level hierarchical caching system where the least recently used (LRU) algorithm is locally run at each cache. With this modeling technique, we are able to identify a characteristic time for each cache, which plays a fundamental role in understanding the caching processes. In particular, a cache can be viewed roughly as a lowpass filter with its cutoff frequency equal to the inverse of the characteristic time. Documents with access frequencies lower than this cutoff frequency will have good chances to pass through the cache without cache hits. This viewpoint enables us to take any branch of the cache tree as a tandem of lowpass filters at different cutoff frequencies, which further results in the finding of two fundamental design principles. Finally, to demonstrate how to use the principles to guide the caching algorithm design, we propose a cooperative hierarchical web caching architecture based on these principles. The simulation study shows that the proposed cooperative architecture results in 50% saving of the cache resource compared with the traditional uncooperative hierarchical caching architecture.

Abstract-This paper aims at finding fundamental design principles for hierarchical web caching. An analytical modeling technique is developed to characterize an uncooperative twolevel hierarchical caching system where the least recently used (LRU) algorithm is locally run at each cache. With this modeling technique, we are able to identify a characteristic time for each cache, which plays a fundamental role in understanding the caching processes. In particular, a cache can be viewed roughly as a low-pass filter with its cutoff frequency equal to the inverse of the characteristic time. Documents with access frequencies lower than this cutoff frequency have good chances to pass through the cache without cache hits. This viewpoint enables us to take any branch of the cache tree as a tandem of low-pass filters at different cutoff frequencies, which further results in the finding of two fundamental design principles. Finally, to demonstrate how to use the principles to guide the caching algorithm design, we propose a cooperative hierarchical web caching architecture based on these principles. Both model-based and real trace simulation studies show that the proposed cooperative architecture results in more than 50% memory saving and substantial central processing unit (CPU) power saving for the management and update of cache entries compared with the traditional uncooperative hierarchical caching architecture.Index Terms-Cache replacement algorithms, hierarchical caching, least recently used (LRU), web caching.

No abstract

Exposure of Lead (Pb), a known neurotoxicant, can impair spatial learning and memory probably via impairing the hippocampal long-term potentiation (LTP) as well as hippocampal neuronal injury. Activation of hippocampal microglia also impairs spatial learning and memory. Thus, we raised the hypothesis that activation of microglia is involved in the Pb exposure induced hippocampal LTP impairment and neuronal injury. To test this hypothesis and clarify its underlying mechanisms, we investigated the Pb-exposure on the microglia activation, cytokine release, hippocampal LTP level as well as neuronal injury in in vivo or in vitro model. The changes of these parameters were also observed after pretreatment with minocycline, a microglia activation inhibitor. Long-term low dose Pb exposure (100 ppm for 8 weeks) caused significant reduction of LTP in acute slice preparations, meanwhile, such treatment also significantly increased hippocampal microglia activation as well as neuronal injury. In vitro Pb-exposure also induced significantly increase of microglia activation, up-regulate the release of cytokines including tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β) and inducible nitric oxide synthase (iNOS) in microglia culture alone as well as neuronal injury in the co-culture with hippocampal neurons. Inhibiting the microglia activation with minocycline significantly reversed the above-mentioned Pb-exposure induced changes. Our results showed that Pb can cause microglia activation, which can up-regulate the level of IL-1β, TNF-α and iNOS, these proinflammatory factors may cause hippocampal neuronal injury as well as LTP deficits.