Coalition Strategies and Reduction of GHG Emissions

The Flexible Mechanisms articulated in the Kyoto Protocol provide a robust framework for emission reduction issue in a manner that is not just economically efficient, but is also pro-growth for trade. In the presence of liquid or illiquid markets, to attain higher value from the emission trading, we have shown that coalition strategies provide a pertinent alternative to production optimization measures which may not be feasible at times. The whole game is analyzed taking a resource based view of the strategic factor markets. We have also illustrated the measures needed to provide stability to the coalitions and hence the coalition strategies.coalition, strategy, game theory, emission, environment, resource based view, strategic factor market

Enhanced exercise and regenerative capacity in a mouse model that violates size constraints of oxidative muscle fibres

A central tenet of skeletal muscle biology is the existence of an inverse relationship between the oxidative fibre capacity and its size. However, robustness of this relationship is unknown. We show that superimposition of Estrogen-related receptor gamma (Erry) on the myostatin (Mtn) mouse null background (Mtn(-/-)Err gamma(Tg/+)) results in hypertrophic muscle with a high oxidative capacity thus violating the inverse relationship between fibre size and oxidative capacity. We also examined the canonical view that oxidative muscle phenotype positively correlate with Satellite cell number, the resident stem cells of skeletal muscle. Surprisingly, hypertrophic fibres from Mtn(-/-)Err gamma(Tg/+) mouse showed satellite cell deficit which unexpectedly did not affect muscle regeneration. These observations 1) challenge the concept of a constraint between fibre size and oxidative capacity and 2) indicate the important role of the microcirculation in the regenerative capacity of a muscle even when satellite cell numbers are reduced.Peer reviewe

A case control study of risk factors of coronary heart disease among patients admitted at tertiary hospital in western India

BackgroundCoronary heart disease (CHD) is a major cause of death in the world. In this study, various risk factors of CHD were explored.AimsTo find out association of CHD with its risk factors in Western India.Methods A 100 cases of first episode of Acute Coronary Syndrome (ACS) patients and 200 age and sex matched controls from medical wards of a government run tertiary care hospital were interviewed through modified WHO STEPS questionnaire along with physical examination and anthropometric measurements. Data was cleaned and analysed through SPSS.Results On bivariate analysis current smoking status [OR=2.906 (1.69–4.98)], BMI [OR=2.6492 (1.49–4.72)], waist circumference [OR=1.7051 (1.01–2.88)] and positive family history [OR=2.0457 (1.07–3.91)] were found to be significantly associated with ACS cases. On multivariate analysis, BMI [OR=2.612 (1.376–4.959)] and current smoking status [OR=3.005 (1.791–5.042)] were found to be significantly associated with ACS cases.ConclusionOut of conventional risk factors, BMI and current smoking status were the only risk factors which had positive association with CHD in this study

Exercise training attenuates the hypermuscular phenotype and restores skeletal muscle function in the myostatin null mouse

Myostatin regulates both muscle mass and muscle metabolism. The myostatin null (MSTN -/- ) mouse has a hypermuscular phenotype owing to both hypertrophy and hyperplasia of the myofibres. The enlarged muscles display a reliance on glycolysis for energy production; however, enlarged muscles that develop in the absence of myostatin have compromised force-generating capacity. Recent evidence has suggested that endurance exercise training increases the oxidative properties of muscle. Here, we aimed to identify key changes in the muscle phenotype of MSTN -/- mice that can be induced by training. To this end, we subjected MSTN -/- mice to two different forms of training, namely voluntary wheel running and swimming, and compared the response at the morphological, myocellular and molecular levels. We found that both regimes normalized changes of myostatin deficiency and restored muscle function. We showed that both exercise training regimes increased muscle capillary density and the expression of Ucp3, Cpt1α, Pdk4 and Errγ, key markers for oxidative metabolism. Cross-sectional area of hypertrophic myofibres from MSTN -/- mice decreased towards wild-type values in response to exercise and, in this context, Bnip3, a key autophagy-related gene, was upregulated. This reduction in myofibre size caused an increase of the nuclear-to-cytoplasmic ratio towards wild-type values. Importantly, both training regimes increased muscle force in MSTN -/- mice. We conclude that impaired skeletal muscle function in myostatin-deficient mice can be improved through endurance exercise-mediated remodelling of muscle fibre size and metabolic profile. © 2011 The Authors. Experimental Physiology © 2012 The Physiological Society