Of Fair Markets and Distributive Justice

The authors argue that a free market paradigm facilitates wealth creation but does little to distribute that wealth in a just manner. In order to achieve the social goal of distributive justice, the concept of a fair market is introduced and explored. The authors then examine three drivers that can help improve the lives of all people, especially the poor: civil society, its institutions, and business. After exploring the roles these drivers might play in developing fair markets, we describe three enablers that serve as catalysts for change: the effects of globalization, the impact of technology, and the emergence of entrepreneurial activity. We conclude by making recommendations for establishing fair markets and provide exemplars of two firms that embody the arguments made in the article

Poverty Alleviation through Partnerships: A Road Less Travelled for Business, Governments & Entrepreneurs

While investigating the role of business and accepting that profitable partnerships are the primary solution for poverty alleviation, we voice certain concerns that we hope will extend the authors’ discourse in Alleviating Poverty through Profitable Partnerships. We present a model that we believe can serve as an effective framework for addressing these issues. We then establish the imperative of inclusive growth. Here, we engage with the necessity of formulating strategies that focus on the pace and, importantly, the pattern of economic growth, including its social and cultural dimensions. We also deliberate on the parameters of inclusive growth with the overriding objective of ensuring that multiple strata of society share the benefits of globalization. Turning to the critical role of institutions in promoting social welfare, we explore the impact of government policy vis-à-vis the leverage enjoyed by other social institutions. Despite the reality that state and private interests often operate at cross purposes, we argue that government must still be an integral part of the solution matrix. With direction from other social institutions, entrepreneurial forces can be unleashed to tackle endemic poverty prevalent in the base of the pyramid. We then provide an in-depth case study in which the availability of telecommunications in rural areas was utilized as a means to foster development and ensure inclusive growth. The conclusion examines lessons learned while operationalizing the model, and spells out the impact of our enablers at ground level

Synchronisation schemes for two dimensional discrete systems

In this work we consider two models of two dimensional discrete systems subjected to three different types of coupling and analyse systematically the performance of each in realising synchronised states.We find that linear coupling effectively introduce control of chaos along with synchronisation,while synchronised chaotic states are possible with an additive parametric coupling scheme both being equally relevant for specific applications.The basin leading to synchronisationin the initial value plane and the choice of parameter values for synchronisation in the parameter plane are isolatedin each case.Comment: 17 pages 8 figures. submitted to physica script

Andersen-Tawil Syndrome Presenting with Complete Heart Block

Andersen-Tawil syndrome (ATS) is a rare autosomal dominant neuromuscular disorder due to mutations in the KCNJ2 gene. The classical phenotype of ATS consists of a triad of periodic paralysis, cardiac conduction abnormalities and dysmorphic features. Episodes of either muscle weakness or cardiac arrhythmia may predominate however, and dysmorphic features may be subtle, masking the true breadth of the clinical presentation, and posing a diagnostic challenge. The severity of cardiac involvement varies but includes reports of life-threatening events or sudden cardiac death, usually attributed to ventricular tachyarrhythmias. We report the first case of advanced atrioventricular (AV) block in ATS and highlight clinical factors that may delay diagnosis

Myotonia in a patient with a mutation in an S4 arginine residue associated with hypokalaemic periodic paralysis and a concomitant synonymous CLCN1 mutation

The sarcolemmal voltage gated sodium channel NaV1.4 conducts the key depolarizing current that drives the upstroke of the skeletal muscle action potential. It contains four voltage-sensing domains (VSDs) that regulate the opening of the pore domain and ensuing permeation of sodium ions. Mutations that lead to increased NaV1.4 currents are found in patients with myotonia or hyperkalaemic periodic paralysis (HyperPP). Myotonia is also caused by mutations in the CLCN1gene that result in loss-of-function of the skeletal muscle chloride channel ClC-1. Mutations affecting arginine residues in the fourth transmembrane helix (S4) of the NaV1.4 VSDs can result in a leak current through the VSD and hypokalemic periodic paralysis (HypoPP), but these have hitherto not been associated with myotonia. We report a patient with an Nav1.4 S4 arginine mutation, R222Q, presenting with severe myotonia without fulminant paralytic episodes. Other mutations affecting the same residue, R222W and R222G, have been found in patients with HypoPP. We show that R222Q channels have enhanced activation, consistent with myotonia, but also conduct a leak current. The patient carries a concomitant synonymous CLCN1 variant that likely worsens the myotonia and potentially contributes to the amelioration of muscle paralysis. Our data show phenotypic variability for different mutations affecting the same S4 arginine that have implications for clinical therapy