DEX: Self-Healing Expanders

We present a fully-distributed self-healing algorithm DEX, that maintains a constant degree expander network in a dynamic setting. To the best of our knowledge, our algorithm provides the first efficient distributed construction of expanders - whose expansion properties hold deterministically - that works even under an all-powerful adaptive adversary that controls the dynamic changes to the network (the adversary has unlimited computational power and knowledge of the entire network state, can decide which nodes join and leave and at what time, and knows the past random choices made by the algorithm). Previous distributed expander constructions typically provide only probabilistic guarantees on the network expansion which rapidly degrade in a dynamic setting, in particular, the expansion properties can degrade even more rapidly under adversarial insertions and deletions. Our algorithm provides efficient maintenance and incurs a low overhead per insertion/deletion by an adaptive adversary: only O(log n) rounds and O(log n) messages are needed with high probability (n is the number of nodes currently in the network). The algorithm requires only a constant number of topology changes. Moreover, our algorithm allows for an efficient implementation and maintenance of a distributed hash table (DHT) on top of DEX, with only a constant additional overhead. Our results are a step towards implementing efficient self-healing networks that have guaranteed properties (constant bounded degree and expansion) despite dynamic changes.

Report on the Remedying the Past, Healing for the Future Conference

DEX: self-healing expanders

The role of LL-37 in periodontal wound healing

Introduction: As a result of chronic inflammation during periodontal disease the junctional epithelium becomes micro-ulcerated. The inflammatory process is mediated by both bacterial and host cell products. Host defence peptides such as defensins, secretory leucocyte protease inhibitor (SLPI) and the sole human cathelicidin, LL-37, are secreted by both periodontal cells and neutrophils into gingival crevicular fluid (GCF). They have the ability to modulate the immune response in periodontitis and are thought to have a potential role in periodontal wound healing. Objectives: The aims of this study were to determine the role of LL-37 in the production of Interleukin (IL)-8, IL-6, hepatocyte growth factor (HGF) and basic-fibroblast growth factor (bFGF) by gingival fibroblasts. The role of LL-37 in modulating total matrix metalloproteinase (MMP) activity and expression of tissue inhibitors of metalloproteinase (TIMP)-1 and -2 by gingival fibroblasts was also investigated. Methods: Primary gingival fibroblasts were co-cultured with concentrations of LL-37 (1, 5 and 10µg/ml) for 24 hours and their supernatants tested for levels of IL-8 and IL-6, HGF, bFGF, TIMP-1 and TIMP-2 by ELISA. Rates of MMP turnover in the supernatants were tested by fluorogenic assay using fluorescence resonance energy transfer (FRET) peptide substrates. Cytotoxicity was measured by MTT assay. Statistical significance was measured using the independent t-test and p<0.05 was considered significant. Results: LL-37 significantly upregulated levels of IL-8, IL-6, HGF, bFGF and TIMP-1 (p<0.05) in a dose-dependent fashion. LL-37 significantly decreased the total MMP activity (p<0.05). None of the LL-37 concentrations tested were cytotoxic to gingival fibroblasts. Conclusion: These results indicate that LL-37 is involved in periodontal wound healing. LL-37 increased levels of proinflammatory cytokines and increased levels of growth factors involved in re-epithelialisation. LL-37 has the ability to regulate remodelling of the periodontium by controlling MMP overactivity both directly and by stimulating production of inhibitors by gingival fibroblasts.

Compact Routing Messages in Self-Healing Trees

Existing compact routing schemes, e.g., Thorup and Zwick [SPAA 2001] and Chechik [PODC 2013], often have no means to tolerate failures, once the system has been setup and started. This paper presents, to our knowledge, the first self-healing compact routing scheme. Besides, our schemes are developed for low memory nodes, i.e., nodes need only O(log2 n) memory, and are thus, compact schemes.
We introduce two algorithms of independent interest: The first is CompactFT, a novel compact version (using only O(log n) local memory) of the self-healing algorithm Forgiving Tree of Hayes et al. [PODC 2008]. The second algorithm (CompactFTZ) combines CompactFT with Thorup-Zwick’s treebased compact routing scheme [SPAA 2001] to produce a fully compact self-healing routing scheme. In the self-healing model, the adversary deletes nodes one at a time with the affected nodes self-healing locally by adding few edges. CompactFT recovers from each attack in only O(1) time and ∆ messages, with only +3 degree increase and O(log∆) graph diameter increase, over any sequence of deletions (∆ is the initial maximum degree).
Additionally, CompactFTZ guarantees delivery of a packet sent from sender s as long as the receiver has not been deleted, with only an additional O(y log ∆) latency, where y is the number of nodes that have been deleted on the path between s and t. If t has been deleted, s gets informed and the packet removed from the network.

Self-healing of cracks during ductile regime machining of silicon: Insights from molecular dynamics simulation

During nanoindentation and ductile-regime machining of silicon, a phenomenon known as “self-healing” takes place in that the microcracks, microfractures, and small spallings generated during the machining are filled by the plastically flowing ductile phase of silicon. However, this phenomenon has not been observed in simulation studies. In this work, using a long-range potential function, molecular dynamics simulation was used to provide an improved explanation of this mechanism. A unique phenomenon of brittle cracking was discovered, typically inclined at an angle of 45° to 55° to the cut surface, leading to the formation of periodic arrays of nanogrooves being filled by plastically flowing silicon during cutting. This observation is supported by the direct imaging. The simulated X-ray diffraction analysis proves that in contrast to experiments, Si-I to Si-II (beta tin) transformation during ductile-regime cutting is highly unlikely and solid-state amorphisation of silicon caused solely by the machining stress rather than the cutting temperature is the key to its brittle-ductile transition observed during the MD simulations