The institutions of archaic post-modernity and their organizational and managerial consequences: The case of Portugal

The long march of modernization of the Western societies tends to be presented as following a regular sequence: societies and institutions were pre-modern, and then they were modernized, eventually becoming post-modern. Such teleology may provide an incomplete or distorted narrative of societal evolution in many parts of the world, even in the ‘post-modern heartland’ of Western Europe, with Portugal being a case in point. The concept of archaic post-modernity has been developed by a philosopher, José Gil, to show how Portuguese institutions and organizations combine elements of pre-modernity and post-modernity. The notion of an archaic post-modernity is advanced in order to provide an alternative account of the modernization process, which enriches discussion of the varieties of capitalism. Differences in historical experiences create singularities that may be considered in the analysis of culture, management and organization

2004, “Decreased sarcoplasmic reticulum activity in diabeticdb/db mouse heart

Although it is known that insulin-dependent (type 1) diabetes results in depressed contractile performance associated with diminished sarcoendoplasmic reticular Ca 2؉ -ATPase (SERCA2a) activity, findings in insulinresistant (type 2) diabetes suggest a less clear association. The db/db insulin-resistant mouse model exhibits decreased cardiac performance both in situ and in isolated ex vivo working hearts. In this study, contractile performance and calcium transients were measured in Langendorff-perfused hearts and isolated cardiac myocytes. Diabetic (db/db) mouse hearts demonstrated decreased rates of contraction, relaxation, and pressure development. Calcium transients from isolated myocytes revealed significantly lower diastolic and systolic levels of calcium in diabetic hearts. Furthermore, the decay rate of the calcium transient was significantly reduced in diabetic myocytes, suggesting a diminished capacity for cytosolic calcium removal not associated with a change in sodium-calcium exchanger activity. Calcium leakage from the sarcoplasmic reticulum (SR) measured using tetracaine was significantly increased in diabetic myocytes. Western blot analysis indicated only a small decrease in SERCA2a expression in diabetic mice, but a large increase in phospholamban expression. Expression of the ryanodine receptor did not differ between groups. In conclusion, the decreased contractile function observed in the db/db diabetic mouse model appears to be related to decreased calcium handling by the SR. Diabetes 53:3201-3208, 2004 H eart disease is the leading cause of death among diabetic patients. It has been recognized for a number of years that diabetes can impair myocardial performance independent of coronary artery disease or hypertension (1,2). Type 2 (noninsulin-dependent) diabetes is the most prevalent form of this disease, resulting from a combination of insulin resistance (resulting in hyperinsulinemia) and ultimately a failure of pancreatic ␤-cells to maintain adequate insulin secretion to overcome resistance (3,4). The etiology of type 2 diabetes is complex, arising from a mixture of genetic and environmental factors. In contrast, type 1 (insulin-dependent) diabetes is characterized by decreased insulin secretion and is readily reversed by insulin replacement. Although a number of studies have examined the effect of type 1 diabetes on contractile function in the heart, fewer such studies have been performed in type 2 diabetic models. The db/db mouse model of type 2 diabetes was originally isolated from the C57BLK6 strain Ͼ30 years ago (5). Disease development in this strain follows a distinct pattern. Outwardly, the mice are indistinguishable from their nondiabetic littermates until soon after weaning, when they show an accelerated gain in body mass. Initially, insulin secretion increases to overcome insulin resistance in the periphery to prevent hyperglycemia. By age 8 -12 weeks, the maximum extent of hyperinsulinemia is attained; hyperglycemia then develops when the insulin levels are no longer sufficient to counter the insulin resistance (6,7). In the diabetic state, these mice show a diminished capacity for cardiac power output in the isolated working heart preparation (8). This effect is age dependent with the onset of diabetes (9), an observation confirmed in vivo by echocardiography (10). Although this model shows some characteristics similar to type 1 diabetes, including altered metabolic substrate preference (11), it is not known how calcium handling is affected in this model. Alterations in myocyte calcium handling in type 1 diabetes have been well documented (12-14). The type 1 diabetic model is associated with a depression in contractile function underlined primarily by reduced sequestration of calcium into the sarcoplasmic reticulum (SR) as a result of decreased sarcoendoplasmic reticular Ca 2ϩ -ATPase (SERCA) pump activity. The decreased SERCA pump activity is the result of either a decreased expression of SERCA itself or an increase in the prevalence of its inhibitory protein phospholamban (PLN

Increased oxygen consumption and OXPHOS potential in superhealer mesenchymal stem cells

Abstract Background Cell-based therapies show promise in repairing cardiac tissue and improving contractile performance following a myocardial infarction. Despite this, ischemia-induced death of transplanted cells remains a major hurdle to the efficacy of treatment. ‘Superhealer’ MRL/MpJ mesenchymal stem cells (MRL-MSCs) have been reported to exhibit increased engraftment resulting in reduced infarct size and enhanced contractile function. This study determines whether intrinsic differences in mitochondrial oxidative phosphorylation (OXPHOS) assist in explaining the enhanced cellular survival and engraftment of MRL-MSCs. Findings Compared to wild type MSCs (WT-MSCs), mitochondria from intact MRL-MSCs exhibited an increase in routine respiration and maximal electron transport capacity by 2.0- and 3.5-fold, respectively. When routine oxygen utilization is expressed as a portion of maximal cellular oxygen flux, the MRL-MSCs have a greater spare respiratory capcity. Additionally, glutamate/malate succinate-supported oxygen consumption in permeabilized cells was elevated approximately 1.25- and 1.4-fold in the MRL-MSCs, respectively. Conclusion The results from intact and permeabilized MSCs indicate MRL-MSCs exhibit a greater reliance on and capacity for aerobic metabolism. The greater capacity for oxidative metabolism may provide a protective effect by increasing ATP synthesis per unit substrate and prevent glycolysis-mediated acidosis and subsequent cell death upon transplantation into the glucose-and oxygen-deprived environment of the infarcted heart.</p