OpenFlow makes a network highly flexible and fast-evolving by separating control and data planes. The control plane thus becomes responsive to changes in topology and load balancing requirements. OpenFlow also offers a new approach to handle security threats accurately and responsively. Therefore, it is used as an innovative firewall that acts as a first-hop security to protect networks against malicious users. However, the firewall provided by OpenFlow suffers from Internet protocol version 6 (IPv6) fragmentation, which can be used to bypass the OpenFlow firewall. The OpenFlow firewall cannot identify the message payload unless the switch implements IPv6 fragment reassembly. This study tests the IPv6 fragmented packets that can evade the OpenFlow firewall, and proposes a new mechanism to guard against attacks carried out by malicious users to exploit IPv6 fragmentation loophole in OpenFlow networks. The proposed mechanism is evaluated in a simulated environment by using six scenarios, and results exhibit that the proposed mechanism effectively fixes the loophole and successfully prevents the abuse of IPv6 fragmentation in OpenFlow networks.
Autophagy is a critical process in the regulation of muscle mass, function and integrity. The molecular mechanisms regulating autophagy are complex and still partly understood. Here, we identify and characterize a novel FoxO-dependent gene, d230025d16rik which we named Mytho (Macroautophagy and YouTH Optimizer), as a regulator of autophagy and skeletal muscle integrity in vivo. Mytho is significantly up-regulated in various mouse models of skeletal muscle atrophy. Short term depletion of MYTHO in mice attenuates muscle atrophy caused by fasting, denervation, cancer cachexia and sepsis. While MYTHO overexpression is sufficient to trigger muscle atrophy, MYTHO knockdown results in a progressive increase in muscle mass associated with a sustained activation of the mTORC1 signaling pathway. Prolonged MYTHO knockdown is associated with severe myopathic features, including impaired autophagy, muscle weakness, myofiber degeneration, and extensive ultrastructural defects, such as accumulation of autophagic vacuoles and tubular aggregates. Inhibition of the mTORC1 signaling pathway in mice using rapamycin treatment attenuates the myopathic phenotype triggered by MYTHO knockdown. Skeletal muscles from human patients diagnosed with myotonic dystrophy type 1 (DM1) display reduced Mytho expression, activation of the mTORC1 signaling pathway and impaired autophagy, raising the possibility that low Mytho expression might contribute to the progression of the disease. We conclude that MYTHO is a key regulator of muscle autophagy and integrity.