Connectivity strategies to enhance the capacity of weight-bearing networks

The connectivity properties of a weight-bearing network are exploited to enhance it's capacity. We study a 2-d network of sites where the weight-bearing capacity of a given site depends on the capacities of the sites connected to it in the layers above. The network consists of clusters viz. a set of sites connected with each other with the largest such collection of sites being denoted as the maximal cluster. New connections are made between sites in successive layers using two distinct strategies. The key element of our strategies consists of adding as many disjoint clusters as possible to the sites on the trunk $T$ of the maximal cluster. The new networks can bear much higher weights than the original networks and have much lower failure rates. The first strategy leads to a greater enhancement of stability whereas the second leads to a greater enhancement of capacity compared to the original networks. The original network used here is a typical example of the branching hierarchical class. However the application of strategies similar to ours can yield useful results in other types of networks as well.Comment: 17 pages, 3 EPS files, 5 PS files, Phys. Rev. E (to appear

A model for cascading failures in complex networks

Large but rare cascades triggered by small initial shocks are present in most of the infrastructure networks. Here we present a simple model for cascading failures based on the dynamical redistribution of the flow on the network. We show that the breakdown of a single node is sufficient to collapse the efficiency of the entire system if the node is among the ones with largest load. This is particularly important for real-world networks with an highly hetereogeneous distribution of loads as the Internet and electrical power grids.Comment: 4 pages, 4 figure

How big is too big? Critical Shocks for Systemic Failure Cascades

External or internal shocks may lead to the collapse of a system consisting of many agents. If the shock hits only one agent initially and causes it to fail, this can induce a cascade of failures among neighoring agents. Several critical constellations determine whether this cascade remains finite or reaches the size of the system, i.e. leads to systemic risk. We investigate the critical parameters for such cascades in a simple model, where agents are characterized by an individual threshold \theta_i determining their capacity to handle a load \alpha\theta_i with 1-\alpha being their safety margin. If agents fail, they redistribute their load equally to K neighboring agents in a regular network. For three different threshold distributions P(\theta), we derive analytical results for the size of the cascade, X(t), which is regarded as a measure of systemic risk, and the time when it stops. We focus on two different regimes, (i) EEE, an external extreme event where the size of the shock is of the order of the total capacity of the network, and (ii) RIE, a random internal event where the size of the shock is of the order of the capacity of an agent. We find that even for large extreme events that exceed the capacity of the network finite cascades are still possible, if a power-law threshold distribution is assumed. On the other hand, even small random fluctuations may lead to full cascades if critical conditions are met. Most importantly, we demonstrate that the size of the "big" shock is not the problem, as the systemic risk only varies slightly for changes of 10 to 50 percent of the external shock. Systemic risk depends much more on ingredients such as the network topology, the safety margin and the threshold distribution, which gives hints on how to reduce systemic risk.Comment: 23 pages, 7 Figure

Cough due to ace inhibitors: A case control study using automated general practice data

Objectives: To determine the risk of coughing as an adverse reaction to ACE inhibitors under everyday circumstances in a large population, and to study whether this adverse effect was duration or dose dependent. Design: A population-based case-control study. Setting: Ten general practices of 14 Dutch general practitioners (GP), in which all consultations, morbidity and medical interventions, including drugs prescribed, were registered over the 18 month period from 1st September, 1992 to 1st March, 1994. Subjects: 1458 patients with incident coughing and up to four controls per case were obtained (total 4182 controls), matched for GP. All cases and controls were 20 years or older and had no record of respiratory infection, influenza, tuberculosis, asthma, chronic bronchitis, emphysema, congestive heart failure, sinusitis, laryngitis, haemoptysis or respiratory neoplasms during the study period. Results: Cases were 2.1-times more likely than controls to have been exposed to ACE inhibitors (95% CI 1.5-3.1), but after adjustment the odds ratio was 1.4 (95% CI 0.9-2.1). The crude odds ratio for captopril was 1.3 (95% CI 0.7-2.5), for enalapril 2.6 (95% CI 1.6-4.2) and for lisinopril 2.0 (95% CI 0.5-9.3). The adjusted odds ratio for captopril was 0.9 (95% CI 0.4-1.7), for enalapril 1.7 (95% CI 1.03-2.8) and for lisinopril 1.7 (95% CI 0.4-7.9). For patients who had been on ACE inhibitor treatment for no longer than 2 months the odds ratio was 4.8 (95% CI 1.7-13.3). The odds ratio declined to 2.0 (95% CI 1.1-3.8) for those who had taken an ACE inhibitor for 2-6 months, and to 1.6 (95% CI 0.9-2.7) for those on ACE-inhibitors for more than 6 months. Conclusion: The risk of coughing was increased twofold among ACE inhibitor users, but the odds ratios were no longer significant after controlling for several confounding factors. The risk of developing cough due to ACE-inhibitors declines with the duration of treatment, possibly due to depletion of susceptible persons

Progression of aortic calcification is associated with metacarpal bone loss during menopause: a population-based longitudinal study

offerosclerosis and osteoporosis are major causes of morbidity and mortality in postmenopausal women and have been suggested to be associated. No study has examined whether progression of atherosclerotic calcification is associated with bone loss. In the present study, we examined progression of aortic calcification, diagnosed by radiographic detection of calcified deposits in the abdominal aorta, in relation to metacarpal bone loss, as assessed by metacarpal radiogrammetry, during menopause. Initially premenopausal women (n=236), aged 45 to 57 years at baseline, were followed for 9 years. We additionally assessed the cross-sectional association between the extent of aortic calcification and metacarpal bone mass and density in 720 postmenopausal women. Twenty-five percent of women going through menopause showed progression of aortic calcification. The average loss of metacarpal bone mass among women with progression of aortic calcification was 3.2 mm(2), and their loss of metacarpal bone density was 7.2 mm(2) %, whereas in women without progression of aortic calcification, these losses were 2.0 mm(2) and 5.6 mm(2) %, respectively, adjusted for age and years of follow-up (P<0.05). Additional adjustment for age at menopause, body mass index, blood pressure, smoking, diabetes mellitus, and use of hormone replacement therapy, thiazide, and loop diuretics did not influence these results. In postmenopausal women, a graded inverse cross-sectional association between the extent of aortic calcification and metacarpal bone mass and density was found. In conclusion, our results indicate that progression of atherosclerotic calcification is associated with increased bone loss in women during menopause

Scale-free network on a vertical plane

A scale-free network is grown in the Euclidean space with a global directional bias. On a vertical plane, nodes are introduced at unit rate at randomly selected points and a node is allowed to be connected only to the subset of nodes which are below it using the attachment probability: $\pi_i(t) \sim k_i(t)\ell^{\alpha}$. Our numerical results indicate that the directed scale-free network for $\alpha=0$ belongs to a different universality class compared to the isotropic scale-free network. For $\alpha < \alpha_c$ the degree distribution is stretched exponential in general which takes a pure exponential form in the limit of $\alpha \to -\infty$. The link length distribution is calculated analytically for all values of $\alpha$.Comment: 4 pages, 4 figure

Subclinical hypothyroidism is an independent risk factor for atherosclerosis and myocardial infarction in elderly women: the Rotterdam Study

BACKGROUND: Overt hypothyroidism has been found to be associated with cardiovascular disease. Whether subclinical hypothyroidism and thyroid autoimmunity are also risk factors for cardiovascular disease is controversial. OBJECTIVE: To investigate whether subclinical hypothyroidism and thyroid autoimmunity are associated with aortic atherosclerosis and myocardial infarction in postmenopausal women. DESIGN: Population-based cross-sectional study. SETTING: A district of Rotterdam, The Netherlands. PARTICIPANTS: Random sample of 1149 women (mean age +/- SD, 69.0 +/- 7.5 years) participating in the Rotterdam Study. MEASUREMENTS: Data on thyroid status, aortic atherosclerosis, and history of myocardial infarction were obtained at baseline. Subclinical hypothyroidism was defined as an elevated thyroid-stimulating hormone level (>4.0 mU/L) and a normal serum free thyroxine level (11 to 25 pmol/L [0.9 to 1.9 ng/dL]). In tests for antibodies to thyroid peroxidase, a serum level greater than 10 IU/mL was considered a positive result. RESULTS: Subclinical hypothyroidism was present in 10.8% of participants and was associated with a greater age-adjusted prevalence of aortic atherosclerosis (odds ratio, 1.7 [95% CI, 1.1 to 2.6]) and myocardial infarction (odds ratio, 2.3 [CI, 1.3 to 4.0]). Additional adjustment for body mass index, total and high-density lipoprotein cholesterol level, blood pressure, and smoking status, as well as exclusion of women who took beta-blockers, did not affect these estimates. Associations were slightly stronger in women who had subclinical hypothyroidism and antibodies to thyroid peroxidase (odds ratio for aortic atherosclerosis, 1.9 [CI, 1.1 to 3.6]; odds ratio for myocardial infarction, 3.1 [CI, 1.5 to 6.3]). No association was found between thyroid autoimmunity itself an

From Network Structure to Dynamics and Back Again: Relating dynamical stability and connection topology in biological complex systems

The recent discovery of universal principles underlying many complex networks occurring across a wide range of length scales in the biological world has spurred physicists in trying to understand such features using techniques from statistical physics and non-linear dynamics. In this paper, we look at a few examples of biological networks to see how similar questions can come up in very different contexts. We review some of our recent work that looks at how network structure (e.g., its connection topology) can dictate the nature of its dynamics, and conversely, how dynamical considerations constrain the network structure. We also see how networks occurring in nature can evolve to modular configurations as a result of simultaneously trying to satisfy multiple structural and dynamical constraints. The resulting optimal networks possess hubs and have heterogeneous degree distribution similar to those seen in biological systems.Comment: 15 pages, 6 figures, to appear in Proceedings of "Dynamics On and Of Complex Networks", ECSS'07 Satellite Workshop, Dresden, Oct 1-5, 200