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We propose a targeted intervention protocol where recovery is restricted to individuals that have the least number of infected neighbours. Our recovery strategy is highly efficient on any kind of network, since epidemic outbreaks are minimal when compared to the baseline scenario of spontaneous recovery. In the case of spatially embedded networks, we find that an epidemic stays strongly spatially confined with a characteristic length scale undergoing a random walk. We demonstrate numerically and analytically that this dynamics leads to an epidemic spot with a flat surface structure and a radius that grows linearly with the spreading rate.

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We study the critical behavior of a general contagion model where nodes are either active (e.g., with opinion A, or functioning) or inactive (e.g., with opinion B, or damaged). The transitions between these two states are determined by (i) spontaneous transitions independent of the neighborhood, (ii) transitions induced by neighboring nodes, and (iii) spontaneous reverse transitions. The resulting dynamics is extremely rich including limit cycles and random phase switching. We derive a unifying mean-field theory. Specifically, we analytically show that the critical behavior of systems whose dynamics is governed by processes (i)-(iii) can only exhibit three distinct regimes: (a) uncorrelated spontaneous transition dynamics, (b) contact process dynamics, and (c) cusp catastrophes. This ends a long-standing debate on the universality classes of complex contagion dynamics in mean field and substantially deepens its mathematical understanding.

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Failure, damage spread and recovery crucially underlie many spatially embedded networked systems ranging from transportation structures to the human body. Here we study the interplay between spontaneous damage, induced failure and recovery in both embedded and non-embedded networks. In our model the network's components follow three realistic processes that capture these features: (i) spontaneous failure of a component independent of the neighborhood (internal failure), (ii) failure induced by failed neighboring nodes (external failure) and (iii) spontaneous recovery of a component. We identify a metastable domain in the global network phase diagram spanned by the model's control parameters where dramatic hysteresis effects and random switching between two coexisting states are observed. This dynamics depends on the characteristic link length of the embedded system. For the Euclidean lattice in particular, hysteresis and switching only occur in an extremely narrow region of the parameter space compared to random networks. We develop a unifying theory which links the dynamics of our model to contact processes. Our unifying framework may help to better understand controllability in spatially embedded and random networks where spontaneous recovery of components can mitigate spontaneous failure and damage spread in dynamical networks.

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We investigate the spread of an infection or other malfunction of cascading nature when a system component can recover only if it remains reachable from a functioning central component. We consider the susceptible-infected-susceptible model, typical of mathematical epidemiology, on a network. Infection spreads from infected to healthy nodes, with the addition that infected nodes can only recover when they remain connected to a predefined central node, through a path that contains only healthy nodes. In this system, clusters of infected nodes will absorb their noninfected interior because no path exists between the central node and encapsulated nodes. This gives rise to the simultaneous infection of multiple nodes. Interestingly, the system converges to only one of two stationary states: either the whole population is healthy or it becomes completely infected. This simultaneous cluster infection can give rise to discontinuous jumps of different sizes in the number of failed nodes. Larger jumps emerge at lower infection rates. The network topology has an important effect on the nature of the transition: we observed hysteresis for networks with dominating local interactions. Our model shows how local spread can abruptly turn uncontrollable when it disrupts connectivity at a larger spatial scale.

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Advances in mathematical epidemiology have led to a better understanding of the risks posed by epidemic spreading and informed strategies to contain disease spread. However, a challenge that has been overlooked is that, as a disease becomes more prevalent, it can limit the availability of the capital needed to effectively treat those who have fallen ill. Here we use a simple mathematical model to gain insight into the dynamics of an epidemic when the recovery of sick individuals depends on the availability of healing resources that are generated by the healthy population. We find that epidemics spiral out of control into "explosive" spread if the cost of recovery is above a critical cost. This can occur even when the disease would die out without the resource constraint. The onset of explosive epidemics is very sudden, exhibiting a discontinuous transition under very general assumptions. We find analytical expressions for the critical cost and the size of the explosive jump in infection levels in terms of the parameters that characterize the spreading process. Our model and results apply beyond epidemics to contagion dynamics that self-induce constraints on recovery, thereby amplifying the spreading process.

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At 10 Danish obstetrical departments, 116 residents (42 senior and 74 junior) participated in a study to assess inter-observer and regional variability in the description and evaluation of and clinical decision regarding 11 fetal heart rate patterns. The 11 traces included normal as well as pathological patterns, and normal as well as clinically asphyxiated babies. Five antepartum and six intrapartum patterns were included. A total of 1,276 descriptions and evaluations were obtained. The degree of agreement in description of fetal heart rate changes was high regarding the baseline and the presence of silent or sinusoidal pattern (87-94% on an arbitrary 0-100% scale), and low regarding the assessment of variability and type of deceleration (50-72%). The degree of agreement in interpreting heart rate patterns was 59% (on an arbitrary 0-100% scale). Senior residents generally interpreted the changes as indicative of less serious fetal stress than did their junior colleagues, explaining why junior residents 30% more frequently than their older colleagues found an indication for Cesarean section. Relatively low regional inter-observer agreement scores were primarily due to low agreement between departments, especially between departments far apart. It is concluded that we still need a scientific clarification of which specific heart rate changes are the best predictors of fetal stress. Artificial intelligence programs for interpreting fetal cardiotocograms and ECG signals constitute one promising prospect.

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