What is ‘post-race’ and what does it reveal about contemporary racisms?

ABSTRACT

In this paper, I will critically engage those aspects of Goldberg’s Are We All Postracial Yet that I found to be particularly generative for thinking about contemporary racisms. These foci include the place of post-racial mystification vis-à-vis liberal market capitalism, animalization and synchronic global relationalities. A case will be made for post-race being best understood in terms of how it both incorporates as well as exceeds the explanatory terrain already serviced by the concept of ‘Cultural Racism’ and/or ‘New Racism’. A unique connection to Chamayou’s recent Manhunts will also be advanced. I will read contemporary processes of post-racial animalization via Chamayou’s key contention that Power is always about who is to be the object of force, who shall do the enforcing and how is it to be enforced – a historically contingent force that results in particular technologies of classification, hunting, surveillance, internment, killing and fortification.     

Notes on theorizing racism and other things

ABSTRACT

In the spirit of ‘furthering debate and reflection’ in this response to Theories of Race and Ethnicity, we consider here the pertinence of the theme of resistance that occupies particular chapters within the collection and that has been central to key works within the wider race critical scholarship. Yet, when the larger field of contemporary race study is considered, we also note that other contiguous concerns – including capitalism, religion, nation, and war – are key factors in thinking through racism. Here, we further elaborate on how future theorizations of race and ethnicity must engage with these domains.     

Increased expression of poly(ADP-ribose) polymerase-1 contributes to caspase-independent myocyte cell death during heart failure

Poly(ADP-ribose) polymerase-1 (PARP-1) plays a pivotal role in regulating genome stability, cell cycle progression, and cell survival. However, overactivation of PARP has been shown to contribute to cell death and organ failure in various stress-related disease conditions. In this study, we examined the role of PARP in the development and progression of cardiac hypertrophy. We measured the expression of PARP in mouse hearts with physiological (swimming exercise) and pathological (aortic banding) cardiac hypertrophy as well as in human heart samples taken at the time of transplantation. PARP levels were elevated both in swimming and banded mice hearts and demonstrated a linear positive correlation with the degree of cardiac hypertrophy. A dramatic increase (4-fold) of PARP occurred in 6-wk banded mice, accompanied by apparent signs of ventricular dilation and myocyte cell death. PARP levels were also elevated (2- to 3-fold) in human hearts with end-stage heart failure compared with controls. However, we found no evidence of caspase-mediated PARP cleavage in either mouse or human failing hearts. Overexpression of PARP in primary cultures of cardiac myocytes led to suppression of gene expression and robust myocyte cell death. Furthermore, data obtained from the analysis of PARP knockout mice revealed that these hearts produce an attenuated hypertrophic response to aortic banding compared with controls. Together, these results demonstrate a role for PARP in the onset and progression of cardiac hypertrophy and suggest that some events related to cardiac hypertrophy growth and progression to heart failure are mediated by a PARP-dependent mechanism.     

G protein-coupled receptor kinase-2 is a novel regulator of collagen synthesis in adult human cardiac fibroblasts

Cardiac fibroblasts (CF) make up 60-70% of the total cell number in the heart and play a critical role in regulating normal myocardial function and in adverse remodeling following myocardial infarction and the transition to heart failure. Recent studies have shown that increased intracellular cAMP can inhibit CF transformation and collagen synthesis in adult rat CF; however, mechanisms by which cAMP production is regulated in CF have not been elucidated. We investigated the potential role of G protein-coupled receptor kinase-2 (GRK2) in modulating collagen synthesis by adult human CF isolated from normal and failing left ventricles. Baseline collagen synthesis was elevated in failing CF and was not inhibited by β-agonist stimulation in contrast to normal controls. β-adrenergic receptor (β-AR) signaling was markedly uncoupled in the failing CF, and expression and activity of GRK2 were increased 3-fold. Overexpression of GRK2 in normal CF recapitulated a heart failure phenotype with minimal inhibition of collagen synthesis following β-agonist stimulation. In contrast, knockdown of GRK2 expression in normal CF enhanced cAMP production and led to greater β-agonist-mediated inhibition of basal and TGFβ-stimulated collagen synthesis versus control. Inhibition of GRK2 activity in failing CF by expression of the GRK2 inhibitor, GRK2ct, or siRNA-mediated knockdown restored β-agonist-stimulated inhibition of collagen synthesis and decreased collagen synthesis in response to TGFβ stimulation. GRK2 appears to play a significant role in regulating collagen synthesis in adult human CF, and increased activity of this kinase may be an important mechanism of maladaptive ventricular remodeling as mediated by cardiac fibroblasts.     

Efficient feature selection and classification through ensemble method for network intrusion detection on cloud computing

Cluster Computing - Cloud computing is a preferred option for organizations around the globe, it offers scalable and internet-based computing resources as a flexible service. Security is a key...