How to Defend a Network?

Modern economies rely heavily on their infrastructure networks. These networks face threats ranging from natural disasters to human attacks. As networks are pervasive, the investments needed to protect them are very large; this motivates the study of targeted defence. What are the ���key�� nodes to defend to maximize functionality of the network? What are the incentives of individual nodes to protect themselves in a networked environment and how do these incentives correspond to collective welfare? We provide a characterization of equilibrium attack and defence in terms of two classical concepts in graph theory ��� separators and transversals. We study the welfare costs of decentralized defence. We apply our results to the defence of the US Airport Network and the London Underground

How to Defend a Network?

Modern economies rely heavily on their infrastructure networks. These networks face threats ranging from natural disasters to human attacks. As networks are pervasive, the investments needed to protect them are very large; this motivates the study of targeted defence. What are the ���key�� nodes to defend to maximize functionality of the network? What are the incentives of individual nodes to protect themselves in a networked environment and how do these incentives correspond to collective welfare? We provide a characterization of equilibrium attack and defence in terms of two classical concepts in graph theory ��� separators and transversals. We study the welfare costs of decentralized defence. We apply our results to the defence of the US Airport Network and the London Underground

Contagion Risk and Network Design

Individuals derive bene ts from their connections, but these may, at the same time, transmit external threats. Individuals therefore invest in security to protect themselves. However, the incentives to invest in security depend on their network exposures. We study the problem of designing a network that provides the right individual incentives. Motivated by cybersecurity, we rst study the situation where the threat to the network comes from an intelligent adversary. We show that, by choosing the right topology, the designer can bound the welfare costs of decentralized protection. Both over-investment as well as under-investment can occur depending on the costs of security. At low costs, over-protection is important: this is addressed by discon- necting the network into two unequal components and sacri cing some nodes. At high costs, under-protection becomes salient: it is addressed by disconnecting the network into equal components. Motivated by epidemiology, we then turn to the study of random attacks. The over-protection problem is no longer present, whereas under-protection problems is mitigated in a diametrically opposite way: namely, by creating dense networks that expose the individuals to the risk of contagion

Conflict and Networks

Con flict remains a central element in human interaction. Networks - social, economic and infrastructure - are a defining feature of society. The two intersect in a wide range of empirical contexts. This motivates the recent interest in con flict and networks. The aim of the survey is to present the general themes, provide a survey of the nascent research and point to a number of interesting open questions

Conflict and Networks

Con flict remains a central element in human interaction. Networks - social, economic and infrastructure - are a defining feature of society. The two intersect in a wide range of empirical contexts. This motivates the recent interest in con flict and networks. The aim of the survey is to present the general themes, provide a survey of the nascent research and point to a number of interesting open questions

The Strategy of Conquest

This paper develops a theoretical framework for the study of war and conquest. The analysis highlights the role of three factors - the technology of war, resources, and contiguity network - in shaping the dynamics of appropriation and the formation of empires. The world of many kingdoms is characterized by incessant fighting. After an initial phase of uncertain and gradual growth, the expansion of the winning kingdom speeds up, and it grows rapidly through contiguous expansion. The size of the empire is limited by the connectivity of the network. These dynamics are consistent with the rise of the First Chinese Empire

HNF4A and GATA6 Loss Reveals Therapeutically Actionable Subtypes in Pancreatic Cancer.

Pancreatic ductal adenocarcinoma (PDAC) can be divided into transcriptomic subtypes with two broad lineages referred to as classical (pancreatic) and squamous. We find that these two subtypes are driven by distinct metabolic phenotypes. Loss of genes that drive endodermal lineage specification, HNF4A and GATA6, switch metabolic profiles from classical (pancreatic) to predominantly squamous, with glycogen synthase kinase 3 beta (GSK3β) a key regulator of glycolysis. Pharmacological inhibition of GSK3β results in selective sensitivity in the squamous subtype; however, a subset of these squamous patient-derived cell lines (PDCLs) acquires rapid drug tolerance. Using chromatin accessibility maps, we demonstrate that the squamous subtype can be further classified using chromatin accessibility to predict responsiveness and tolerance to GSK3β inhibitors. Our findings demonstrate that distinct patterns of chromatin accessibility can be used to identify patient subgroups that are indistinguishable by gene expression profiles, highlighting the utility of chromatin-based biomarkers for patient selection in the treatment of PDAC

HNF4A and GATA6 loss reveals therapeutically actionable subtypes in pancreatic cancer

Pancreatic ductal adenocarcinoma (PDAC) can be divided into transcriptomic subtypes with two broad lineages referred to as classical (pancreatic) and squamous. We find that these two subtypes are driven by distinct metabolic phenotypes. Loss of genes that drive endodermal lineage specification, HNF4A and GATA6, switch metabolic profiles from classical (pancreatic) to predominantly squamous, with glycogen synthase kinase 3 beta (GSK3β) a key regulator of glycolysis. Pharmacological inhibition of GSK3β results in selective sensitivity in the squamous subtype; however, a subset of these squamous patient-derived cell lines (PDCLs) acquires rapid drug tolerance. Using chromatin accessibility maps, we demonstrate that the squamous subtype can be further classified using chromatin accessibility to predict responsiveness and tolerance to GSK3β inhibitors. Our findings demonstrate that distinct patterns of chromatin accessibility can be used to identify patient subgroups that are indistinguishable by gene expression profiles, highlighting the utility of chromatin-based biomarkers for patient selection in the treatment of PDAC