Catastrophic Cascade Research Articles

Catastrophic cascade of failures in interdependent networks

Complex networks have been studied intensively for a decade, but research still focuses on the limited case of a single, non-interacting network. Modern systems are coupled together and therefore should be modelled as interdependent networks. A fundamental property of interdependent networks is that failure of nodes in one network may lead to failure of dependent nodes in other networks. This may happen recursively and can lead to a cascade of failures. In fact, a failure of a very small fraction of nodes in one network may lead to the complete fragmentation of a system of several interdependent networks. A dramatic real-world example of a cascade of failures ('concurrent malfunction') is the electrical blackout that affected much of Italy on 28 September 2003: the shutdown of power stations directly led to the failure of nodes in the Internet communication network, which in turn caused further breakdown of power stations. Here we develop a framework for understanding the robustness of interacting networks subject to such cascading failures. We present exact analytical solutions for the critical fraction of nodes that, on removal, will lead to a failure cascade and to a complete fragmentation of two interdependent networks. Surprisingly, a broader degree distribution increases the vulnerability of interdependent networks to random failure, which is opposite to how a single network behaves. Our findings highlight the need to consider interdependent network properties in designing robust networks.

Alterations induced by ischemic preconditioning on secretory pathways Ca2+-ATPase (SPCA) gene expression and oxidative damage after global cerebral ischemia/reperfusion in rats.

Ischemic preconditioning (IPC) represents the phenomenon of CNC adaptation, which results in increased tolerance of CNS to lethal ischemia. Brain ischemia/reperfusion (IRI) initiates a catastrophic cascade in which many subcellular organelles play an important role. The Golgi apparatus, which is a part of secretory pathways (SP), represents the Ca(2+) store and regulates secretion of proteins for growth/reorganization of neuronal circuit by secretory Ca(2+)ATPases (SPCA1). The purpose of this study is to evaluate the effect of IRI and preconditioning on SPCA1 gene expression and oxidative damage after 4-vessel occlusion for 15 min and after being exposed to different reperfusion periods. Rats were preconditioned by 5 min of sub-lethal ischemia and 2 days later, 15 min of lethal ischemia was induced. Our experiments conclusively showed IRI-induced depression of SPCA activity and lipo- and protein oxidation in rat hippocampal membranes. IRI also activates the induction of SPCA1 gene expression in later reperfusion periods. IPC partially suppresses lipo- and protein oxidation in hippocampal membranes and leads to partiall rovery of the ischemic-induced depression of SPCA activity. In addition, IPC initiates earlier cellular response to the injury by the significant elevation of mRNA expression to 142% comparing to 1 h of corresponding reperfusion and to 11% comparing to 24 h of corresponding reperfusion, respectively. Similar patterns were observed on the translational level by Western blot analysis. Our results indicate the specific SPCA1 expression pattern in ischemic hippocampus. It also shows that the SPCA expression and the post-translational changes induced by ischemia are modulated by the IPC. This might serve to understand the molecular mechanisms involved in the structural integrity and function of the SP after ischemic challenge. It also suggests that there is a correlation of SPCA function with the role of SP in the response to pre-ischemic challenge.

Catastrophic Cascades: Extending Our Understanding of Urban Change and Dynamics

Catastrophic Cascades: Extending Our Understanding of Urban Change and Dynamics

Islet Glia, Neurons, and β Cells

Type 1 diabetes (T1D) is caused by autoimmune beta cell destruction. The early events triggering T1D and the forces that keep diabetic autoimmunity pancreas specific have been unclear. Our discovery that autoimmune islet destruction is not beta-cell-exclusive but includes cytotoxic T cell targeting of peri-islet glia, evoked the possibility that T1D pathogenesis may involve neuronal elements beyond beta cell/immune interactions. Recently, we have found that sensory afferent neurons are a critical component in prediabetes initiation, promoting islet inflammation through altered glucose homeostasis and progressive beta cell stress. These factors orchestrate a catastrophic cascade culminating in insulin insufficiency mediated by an autoimmune-prone host. This neuro-immuno-endocrinological triad explains diabetic inflammation as a consequence of local neuropeptide deficiency, leading to an innovative concept of disease pathogenesis with novel therapeutic implications.

Ischemic neuronal cell death and organellae damage

The brain is an organ that consumes much energy. This is partially due to the character of neurons; they possess excitable plasma membrane and a large amount of ATP is indispensable for maintaining ion gradient. Once neurons experience energy failure, calcium accumulates in the intracellular space as a result of disturbed ion homeostasis. This, in turn, activates many cellular processes, which culminate in cell death. In this cellular catastrophic cascade, many organelles play important roles. In addition to the plasma membrane, cytosol is the 'organelle' that first becomes exposed to the increased level of calcium. Many proteases, kinases and lipases are localized here, and are activated directly or indirectly by the ischemic insult. Some enzymes are pro-apoptotic ones, while others are anti-apoptotic. It was reported that neurons that would die later showed activated pro-apoptotic enzymes, but ones that would survive possessed activated anti-apoptotic molecules. Mitochondria is the organelle that plays the central role for intrinsic pathways of apoptosis. The release of cytochrome c from this organelle is the key step in apoptotic cascade in the ischemic neurons. However, the exact molecular mechanism of cytochrome c release remains uncertain. In addition, expression of genes essential for mitochondrial function changes in neurons after ischemia, which further indicates the crucial role of this organelle in cell death. Endoplasmic reticulum (ER) not only mediates proteins processing, but also regulates intracellular calcium homeostasis and cell death signal activation. Recent reports indicate that dysfunction of this organelle occurs at an early stage after ischemia and might be the initial step of apoptotic cascades in neurons. Golgi apparatus and lysosomes are organelles that are involved in apoptotic cell death in some situations. There have been no reports that demonstrated active role of these organelles in ischemic neuronal cell death. Further investigation would be desired about this issue. Nucleus is the organelle that contains genomic DNA. Many studies demonstrated DNA breakage in the neurons that would die later, but whether this is the cause or merely the result of the insult remains uncertain. If the more precise role of each organelle in neuronal cell death are disclosed, we should be able to think about new means of therapy for ischemic stroke.

The Heart of the Atlantic Constitution: International Economic Stability, 1919-1998

enough to be relevant in the more rarified, infinite dimensional context of beliefs and very general social choice rules. In the world, however, beliefs need not be convex. An individual may hold two conflicting views, assigning to each differing probabilities of truth, or indeed, as Keynes noted, may be completely uncertain. Because of the failure of convexity, the heart can fail continuity at certain configurations of beliefs. By analogy with dynamic systems, the failure of continuity is called a catastrophe. A cascade is precisely the catastrophic change from one heart configuration to a completely different one. This very simple notion of a catastrophic cascade is adapted from Zeeman’s earlier ideas. However, the extension of the idea that I have proposed is made in the attempt to include more general transformations than those considered by Zeeman. The abstract object that I call a heart may not, in fact, be an equilibrium, if by this we mean that it is associated with unchanging beliefs and constant behavior on the part of the members of the society. However, the heart is defined by certain boundaries in the domains of beliefs and actions. An important feature of the heart is that when the equilibrium or core is, in fact, nonempty, then the heart and core coincide. On the other hand, when the core is empty, then behavioral cycles are certainly possible inside the heart. In normal circumstances, such cycles need not prove destructive to fundamental belief coherence in the Constitution. By analogy with the notion of an economic core, I use the term core belief to refer to the set of collective beliefs that are mutually compatible within the community. Under the circumstance of a catastrophe, the core belief can become empty. The heart of the Constitution is the exceedingly complex pattern of beliefs and actions, all of which are individually rational with respect to empirical reality and tenable according to the philosophical attitudes of the members of the community. It is defined by certain barriers, or boundaries, to belief, cognition, and behavior. What I have termed the chaos hypothesis (my interpretation of Keynes’s key insight), I see as a device by Keynes to overcome a belief barrier that prevented an understanding of the Depression. Keynes’s insight made accessible a number of different possible hearts, one of which eventually came into focus in the period after World War II. The earlier discussion of the implementation of hegemonic internationalism was intended to show how this depended on core beliefs about the nature of the international system and of the necessity of Soviet containment held by