(In)justice and the blue economy

While the ocean space has long been ignored by social sciences, the past 15 years have witnessed an increased interest in the marine environment by scholars in Human Geography. The academic literature on the blue economy, almost non-existent a few years ago, is now burgeoning. The academic debate has offered some critical assessment of blue economy initiatives, but more needs to be done to address the true place of environmental protection within a blue economy, and to put people at the centre of concerns and analyses. Of particular concern, is the ambiguity of the blue economy concept and the confusion over its social and environmental sustainability, which can ultimately result in harmful practices. An important question is then how should social scientists in general and geographers, specifically, engage with these debates, and in particular how should the potential human and social costs of the blue economy be investigated and addressed while assuring justice and fairness? The papers presented here share the vision that environmental sustainability, justice and equality should be at the heart of the blue economy; not just conceptually, but practically too. The papers pursue efforts to identify blue economy risks and the mechanisms through which they occur; assess the place of inclusion and participation in a sustainable blue economy; define what blue economy policies should include to drive just and sustainable practices; and identify where the dominant understandings of the blue economy and its priorities are coming from. In other words, they put considerations of justice and broader cultural structures at the centre of their concerns and analysis. They also highlight the need to bypass geographical boundaries and gain insights from other disciplines and methodologies to grasp such an encompassing concept, and foster not just a blue economy with social justice, but a blue economy for social justice

Protein kinase Cθ is required for cardiomyocyte survival and cardiac remodeling

Protein kinase Cs (PKCs) constitute a family of serine/threonine kinases, which has distinguished and specific roles in regulating cardiac responses, including those associated with heart failure. We found that the PKCθ isoform is expressed at considerable levels in the cardiac muscle in mouse, and that it is rapidly activated after pressure overload. To investigate the role of PKCθ in cardiac remodeling, we used PKCθ−/− mice. In vivo analyses of PKCθ−/− hearts showed that the lack of PKCθ expression leads to left ventricular dilation and reduced function. Histological analyses showed a reduction in the number of cardiomyocytes, combined with hypertrophy of the remaining cardiomyocytes, cardiac fibrosis, myofibroblast hyper-proliferation and matrix deposition. We also observed p38 and JunK activation, known to promote cell death in response to stress, combined with upregulation of the fetal pattern of gene expression, considered to be a feature of the hemodynamically or metabolically stressed heart. In keeping with these observations, cultured PKCθ−/− cardiomyocytes were less viable than wild-type cardiomyocytes, and, unlike wild-type cardiomyocytes, underwent programmed cell death upon stimulation with α1-adrenergic agonists and hypoxia. Taken together, these results show that PKCθ maintains the correct structure and function of the heart by preventing cardiomyocyte cell death in response to work demand and to neuro-hormonal signals, to which heart cells are continuously exposed

Protein kinase C and cardiac dysfunction: a review

Heart failure (HF) is a physiological state in which cardiac output is insufficient to meet the needs of the body. It is a clinical syndrome characterized by impaired ability of the left ventricle to either fill or eject blood efficiently. HF is a disease of multiple aetiologies leading to progressive cardiac dysfunction and it is the leading cause of deaths in both developed and developing countries. HF is responsible for about 73,000 deaths in the UK each year. In the USA, HF affects 5.8 million people and 550,000 new cases are diagnosed annually. Cardiac remodelling (CD), which plays an important role in pathogenesis of HF, is viewed as stress response to an index event such as myocardial ischaemia or imposition of mechanical load leading to a series of structural and functional changes in the viable myocardium. Protein kinase C (PKC) isozymes are a family of serine/threonine kinases. PKC is a central enzyme in the regulation of growth, hypertrophy, and mediators of signal transduction pathways. In response to circulating hormones, activation of PKC triggers a multitude of intracellular events influencing multiple physiological processes in the heart, including heart rate, contraction, and relaxation. Recent research implicates PKC activation in the pathophysiology of a number of cardiovascular disease states. Few reports are available that examine PKC in normal and diseased human hearts. This review describes the structure, functions, and distribution of PKCs in the healthy and diseased heart with emphasis on the human heart and, also importantly, their regulation in heart failure

Cardioprotection induced by hydrogen sulfide preconditioning involves activation of ERK and PI3K/Akt pathways

10.1007/s00424-007-0321-4Pflugers Archiv European Journal of Physiology4554607-61