Experience with Restoration of Asia Pacific Network Failures from Taiwan Earthquake

We explain how network failures were caused by a natural disaster, describe the restoration steps that were taken, and present lessons learned from the recovery. At 21:26 on December 26th (UTC+9), 2006, there was a serious undersea earthquake off the coast of Taiwan, which measured 7.1 on the Richter scale. This earthquake caused significant damage to submarine cable systems. The resulting fiber cable failures shut down communications in several countries in the Asia Pacific networks. In the first post-earthquake recovery step, BGP routers detoured traffic along redundant backup paths, which provided poor quality connection. Subsequently, operators engineered traffic to improve the quality of recovered communication. To avoid filling narrow-bandwidth links with detoured traffic, the operators had to change the BGP routing policy. Despite the routing-level first aid, a few institutions could not be directly connected to the R&E network community because they had only a single link to the network. For these single-link networks, the commodity link was temporarily used for connectivity. Then, cable connection configurations at the switches were changed to provide high bandwidth and next-generation Internet service. From the whole restoration procedure, we learned that redundant BGP routing information is useful for recovering connectivity but not for providing available bandwidth for the re-routed traffic load and that collaboration between operators is valuable in solving traffic engineering issues such as poor-quality re-routing and lost connections of single-link networks

Itaconate ameliorates autoimmunity by modulating T cell imbalance via metabolic and epigenetic reprogramming

Dysregulation of T cell homeostasis is known to contribute to the immunopathology of autoimmune diseases. Here the authors show that itaconate impacts autoimmune pathology by altering T cells via modulation of metabolic and epigenetic programs. Dysregulation of Th17 and Treg cells contributes to the pathophysiology of many autoimmune diseases. Herein, we show that itaconate, an immunomodulatory metabolite, inhibits Th17 cell differentiation and promotes Treg cell differentiation by orchestrating metabolic and epigenetic reprogramming. Mechanistically, itaconate suppresses glycolysis and oxidative phosphorylation in Th17- and Treg-polarizing T cells. Following treatment with itaconate, the S-adenosyl-L-methionine/S-adenosylhomocysteine ratio and 2-hydroxyglutarate levels are decreased by inhibiting the synthetic enzyme activities in Th17 and Treg cells, respectively. Consequently, these metabolic changes are associated with altered chromatin accessibility of essential transcription factors and key gene expression in Th17 and Treg cell differentiation, including decreased ROR gamma t binding at the Il17a promoter. The adoptive transfer of itaconate-treated Th17-polarizing T cells ameliorates experimental autoimmune encephalomyelitis. These results indicate that itaconate is a crucial metabolic regulator for Th17/Treg cell balance and could be a potential therapeutic agent for autoimmune diseases