Cyber Deception Architecture: Covert Attack Reconnaissance Using a Safe SDN Approach

Significant valuable information can be determined by observing attackers in action. These observations provide significant insight into the attacker’s TTPs and motivations. It is challenging to continue observations when attackers breach operational networks. This paper describes a deception network methodology that redirects traffic from the compromised Operational Network (O-Net) to an identically configured Deception Network (D-Net) minimizing any further compromise of operational data and assets, while also allowing the tactics, techniques, and procedures of the attacker to be studied. To keep the adversary oblivious to the transfer from the O-Net to the D-Net, we employ a sophisticated and unique packet rewriting technique using Software Defined Networking (SDN) technology that builds on two other strategies. This paper discusses the foundational strategies and introduces a new strategy that improves behavior for our described scenarios. We then provide some preliminary test results and suggest topics for further research

Autophagosome formation is initiated at phosphatidylinositol synthase‐enriched ER subdomains

The autophagosome, a double‐membrane structure mediating degradation of cytoplasmic materials by macroautophagy, is formed in close proximity to the endoplasmic reticulum (ER). However, how the ER membrane is involved in autophagy initiation and to which membrane structures the autophagy‐initiation complex is localized have not been fully characterized. Here, we were able to biochemically analyze autophagic intermediate membranes and show that the autophagy‐initiation complex containing ULK and FIP200 first associates with the ER membrane. To further characterize the ER subdomain, we screened phospholipid biosynthetic enzymes and found that the autophagy‐initiation complex localizes to phosphatidylinositol synthase (PIS)‐enriched ER subdomains. Then, the initiation complex translocates to the ATG9A‐positive autophagosome precursors in a PI3P‐dependent manner. Depletion of phosphatidylinositol (PI) by targeting bacterial PI‐specific phospholipase C to the PIS domain impairs recruitment of downstream autophagy factors and autophagosome formation. These findings suggest that the autophagy‐initiation complex, the PIS‐enriched ER subdomain, and ATG9A vesicles together initiate autophagosome formation

Guest‐selective gate‐opening by pore engineering of two‐dimensional Kagomè lattice porous coordination polymers

Porous coordination polymers (PCPs) with pore decoration have been used as materials for excellent storage and separation functions. The cooperative properties of flexible PCPs can be utilized to achieve the separation of mixtures of gaseous molecules having highly similar properties. The key to efficient molecular recognition and separation lies in increasing the degrees of freedom of the structure without sacrificing the stability of the system. However, the mechanism study of such behavior is still scarce in the literature. Here, we focused on PCPs with two-dimensional Kagomè lattice structures and functionalized the pores with various alkoxy pendant groups; this facilitated systematic tuning of the pore aperture size, the interlayer spacing, as well as the interactions between the host and adsorbed molecules. The combination of characterization techniques allowed us to observe a unique deformation of the lattice upon gas sorption, allowing the separation of gas molecules with similar physicochemical properties, such as propane and propylene

酸化リン脂質選択的ホスホリパーゼを介したエポキシ化ω3脂肪酸の産生とその生理的意義

学位の種別: 課程博士審査委員会委員 : （主査）東京大学教授 新井 洋由, 東京大学教授 村田 茂穂, 東京大学准教授 垣内 力, 東京大学講師 河野 望, 東京大学講師 名黒 功University of Tokyo(東京大学

Dynamic physiological alpha-synuclein S129 phosphorylation is driven by neuronal activity

In Parkinson’s disease and other synucleinopathies, the elevation of α-synuclein phosphorylated at Serine129 (pS129) is a widely cited marker of pathology. However, the physiological role for pS129 has remained undefined. Here we use multiple approaches to show for the first time that pS129 functions as a physiological regulator of neuronal activity. Neuronal activity triggers a sustained increase of pS129 in cultured neurons (200% within 4 h). In accord, brain pS129 is elevated in environmentally enriched mice exhibiting enhanced long-term potentiation. Activity-dependent α-synuclein phosphorylation is S129-specific, reversible, confers no cytotoxicity, and accumulates at synapsin-containing presynaptic boutons. Mechanistically, our findings are consistent with a model in which neuronal stimulation enhances Plk2 kinase activity via a calcium/calcineurin pathway to counteract PP2A phosphatase activity for efficient phosphorylation of membrane-bound α-synuclein. Patch clamping of rat SNCA−/− neurons expressing exogenous wild-type or phospho-incompetent (S129A) α-synuclein suggests that pS129 fine-tunes the balance between excitatory and inhibitory neuronal currents. Consistently, our novel S129A knock-in (S129AKI) mice exhibit impaired hippocampal plasticity. The discovery of a key physiological function for pS129 has implications for understanding the role of α-synuclein in neurotransmission and adds nuance to the interpretation of pS129 as a synucleinopathy biomarker