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SUMMARY When dealing with node or link failures in software-defined networking (SDN), the network capability to establish an alternative path depends on controller reachability and on the round-trip times between controller and involved switches. Moreover, current SDN data plane abstractions for failure detection, such as OpenFlow “Fast-failover,” do not allow programmers to tweak switches' detection mechanism, thus leaving SDN operators relying on proprietary management interfaces (when available) to achieve guaranteed detection and recovery delays. We propose SPIDER, an OpenFlow-like pipeline design that provides (i) a detection mechanism based on switches' periodic link probing and (ii) fast reroute of traffic flows even in the case of distant failures, regardless of controller availability. SPIDER is based on stateful data plane abstractions such as OpenState or P4, and it offers guaranteed short (few milliseconds or less) failure detection and recovery delays, with a configurable trade-off between overhead and failover responsiveness. We present here the SPIDER pipeline design, behavioral model, and analysis on flow tables' memory impact. We also implemented and experimentally validated SPIDER using OpenState (an OpenFlow 1.3 extension for stateful packet processing) and P4, showing numerical results on its performance in terms of recovery latency and packet loss.

Cardiovascular disease represents the most common cause for the excess of morbidity and mortality found in end-stage renal disease (ESRD) and has prompted the exploration of multiple approaches to improve outcomes in these patients. Cardiovascular risk factors such as increased oxidative stress (OxSt) and inflammation are found in ESRD patients. A vitamin E-coated dialyzer using polysulfone membranes has been suggested to have positive effects on these factors. This 1-year study evaluated in 25 ESRD patients under chronic dialysis, the effects of a vitamin E-coated membrane (VitabranE ViE) "ex vivo" on mononuclear cells, OxSt, and inflammation-related biochemical and molecular biology markers using a molecular biology approach. p22(phox), heme oxygenase (HO)-1, plasminogen activator inhibitor (PAI)-1 protein level, and phosphorylated extracellular signal-regulated kinase (pERK)1/2 status were evaluated at the beginning of the study, after 6 months and after 12 months by Western blot analysis and oxidized low-density lipoprotein (OxLDL) plasma level by enzyme-linked immunosorbent assay, alongside vascular remodeling assessment as measured by carotid intima-media thickness (IMT) in a subgroup of nine randomly selected patients. p22(phox), PAI-1, OxLDL, and pERK all decreased with VitabranE use, while HO-1 increased. Carotid IMT did not increase. Treatment with VitabranE significantly decreases the expression of proteins and markers relevant to OxSt and inflammation tightly associated with cardiovascular disease, and it appears highly likely that VitabranE use will provide a benefit in terms of cardiovascular protection.