The higher-end tail of the wealth distribution in India is studied using recently published lists of the wealth of richest Indians between the years 2002-4. The resulting rank distribution seems to imply a power-law tail for the wealth distribution, with a Pareto exponent between 0.81 and 0.92 (depending on the year under analysis). This provides a comparison with previous studies of wealth distribution, which have all been confined to Western advanced capitalist economies. We conclude with a discussion on the appropriateness of multiplicative stochastic process as a model for asset accumulation, the relation between the wealth and income distributions (we estimate the Pareto exponent for the latter to be around 1.5 for India), as well as possible sources of error in measuring the Pareto exponent for wealth.

Ventricular fibrillation (VF), the major reason behind sudden cardiac death, is turbulent cardiac electrical activity in which rapid, irregular disturbances in the spatiotemporal electrical activation of the heart makes it incapable of any concerted pumping action. Methods of controlling VF include electrical defibrillation as well as injected medication. Both methods yield results that are subject to chance. Electrical defibrillation, though widely used, involves subjecting the whole heart to massive, and often counterproductive, electrical shocks. We propose a defibrillation method that uses a very-low-amplitude shock (of order mV) applied for a brief duration (of order 100 ms) and over a coarse mesh of lines on our model ventricle. Our proposal is based on a detailed numerical study of a model for ventricular fibrillation [1].

Every sixth death in industrialized countries occurs because of cardiac arrhythmias such as ventricular tachycardia (VT) and ventricular fibrillation (VF). There is growing consensus that VT is associated with an unbroken spiral wave of electrical activation on cardiac tissue but VF with broken waves, spiral turbulence, spatiotemporal chaos and rapid, irregular activation. Thus spiral-wave activity in cardiac tissue has been studied extensively. Nevertheless, many aspects of such spiral dynamics remain elusive because of the intrinsically high-dimensional nature of the cardiac-dynamical system. In particular, the role of tissue heterogeneities in the stability of cardiac spiral waves is still being investigated. Experiments with conduction inhomogeneities in cardiac tissue yield a variety of results: some suggest that conduction inhomogeneities can eliminate VF partially or completely, leading to VT or quiescence, but others show that VF is unaffected by obstacles. We propose theoretically that this variety of results is a natural manifestation of a complex, fractal-like boundary that must separate the basins of the attractors associated, respectively, with spiral breakup and single spiral wave. We substantiate this with extensive numerical studies of Panfilov and Luo-Rudy I models, where we show that the suppression of spiral breakup depends sensitively on the position, size, and nature of the inhomogeneity.

Modular structure is ubiquitous among complex networks. We note that most such systems are subject to multiple structural and functional constraints, e.g., minimizing the average path length and the total number of links, while maximizing robustness against perturbations in node activity. We show that the optimal networks satisfying these three constraints are characterized by the existence of multiple subnetworks (modules) sparsely connected to each other. In addition, these modules have distinct hubs, resulting in an overall heterogeneous degree distribution.

To investigate the universality of the structure of interactions in different markets, we analyze the cross-correlation matrix C of stock price fluctuations in the National Stock Exchange (NSE) of India. We find that this emerging market exhibits strong correlations in the movement of stock prices compared to developed markets, such as the New York Stock Exchange (NYSE). This is shown to be due to the dominant influence of a common market mode on the stock prices. By comparison, interactions between related stocks, e.g., those belonging to the same business sector, are much weaker. This lack of distinct sector identity in emerging markets is explicitly shown by reconstructing the network of mutually interacting stocks. Spectral analysis of C for NSE reveals that, the few largest eigenvalues deviate from the bulk of the spectrum predicted by random matrix theory, but they are far fewer in number compared to, e.g., NYSE. We show this to be due to the relative weakness of intra-sector interactions between stocks, compared to the market mode, by modeling stock price dynamics with a two-factor model. Our results suggest that the emergence of an internal structure comprising multiple groups of strongly coupled components is a signature of market development.

One of the biggest challenges in biology is to understand how activity at the cellular level of neurons, as a result of their mutual interactions, leads to the observed behavior of an organism responding to a variety of environmental stimuli. Investigating the intermediate or mesoscopic level of organization in the nervous system is a vital step towards understanding how the integration of micro-level dynamics results in macro-level functioning. The coordination of many different co-occurring processes at this level underlies the command and control of overall network activity. In this paper, we have considered the somatic nervous system of the nematode Caenorhabditis elegans, for which the entire neuronal connectivity diagram is known. We focus on the organization of the system into modules, i.e., neuronal groups having relatively higher connection density compared to that of the overall network. We show that this mesoscopic feature cannot be explained exclusively in terms of considerations such as, optimizing for resource constraints (viz., total wiring cost) and communication efficiency (i.e., network path length). Even including information about the genetic relatedness of the cells cannot account for the observed modular structure. Comparison with other complex networks designed for efficient transport (of signals or resources) implies that neuronal networks form a distinct class. This suggests that the principal function of the network, viz., processing of sensory information resulting in appropriate motor response, may be playing a vital role in determining the connection topology. Using modular spectral analysis we make explicit the intimate relation between function and structure in the nervous system. This is further brought out by identifying functionally critical neurons purely on the basis of patterns of intra- and inter-modular connections. Our study reveals how the design of the nervous system reflects several constraints, including its key functional role as a processor of information.

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A series of mixed ligand ruthenium(II) complexes [Ru(pdto)(diimine)](ClO4)2/(PF6)2 1-3 and [Ru(bbdo)(diimine)](ClO4), 4-6, where pdto is 1,8-bis(pyrid-2-yl)-3,6-dithiooctane, bbdo is 1,8-bis(benzimidazol-2-yl)-3,6-dithiooctane and diimine is 1,10-phenanthroline (phen), dipyrido-[3,2-d:2',3'-f]-quinoxaline (dpq) and dipyrido[3,2-a:2',3'-c]phenazine (dppz), have been isolated and characterised by analytical and spectral methods. The complexes [Ru(pdto)(phen)](PF6)2 la, [Ru(pdto)(dpq)(Cl](PF6) 2a, [Ru(bbdo)(phen)](PF6)2 4a and [Ru(bbdo)(dpq)](ClO4)2 5 have been structurally characterized and their coordination geometries around ruthenium(II) are described as distorted octahedral. In la, 4a and 5 the two thioether sulfur and two py/bzim nitrogen atoms of the tetradentate pdto/bbdo ligand are folded around Ru(II) to give predominantly a "cis-alpha" configuration. (I)H NMR spectral data of the complexes support this configuration in solution. In [Ru(pdto)(dpq)Cl](PF6) 2a with a distorted octahedral coordination geometry, one of the two py nitrogens of pdto is not coordinated. The DNA binding constants (Kb: 2, 2.00 +/- 0.02 x 10(4) M(-1), s = 1.0; 3, 3.00 +/- 0.01 x 10(6) M(-1), s = 1.3) determined by absorption spectral titrations of the complexes with CT DNA reveal that 3 interacts with DNA more tightly than 2 through partial intercalation of the extended planar ring of coordinated dppz with the DNA base stack. The DNA binding affinities of the complexes increase with increase in the number of planar aromatic rings in the co-ligand, and on replacing both the py moieties in pdto complexes (1-3) by bzim moieties to give bbdo complexes (4-6). Upon interaction with CT DNA the complexes 1, 2, 5 and 6 show a decrease in anodic current in the cyclic voltammograms. On the other hand, interestingly, 3 and 4 show an increase in anodic current suggesting their involvement in electrocatalytic guanine oxidation. Interestingly, of all the complexes, only 6 alters the superhelicity of DNA upon binding with supercoiled pBR322 DNA. The cytotoxicities of the dppz complexes 3 and 6, which avidly bind to DNA, have been examined by screening them against cell lines of different cancer origins. It is noteworthy that 6 exhibits selectivity with higher cytotoxicity against the melanoma cancer cell line (A375) than other cell lines, potency approximately twice that of cisplatin and toxicity to normal cells 3 and 90 times less than cisplatin and adriamycin respectively.