Bridging rhetoric and practice: new perspectives on barriers to gendered change

Contains fulltext : 167537.pdf (publisher's version ) (Open Access)This article presents a new methodology, Gender Knowledge Contestation Analysis, and uses it to examine the processes under way when transformative gender equality policies, such as gender mainstreaming are implemented. Drawing on data gathered in the European Commission, the findings show the processes linking high-level rhetorical policy statements, strategic policies, and daily working practices. This analysis enables exploration of the mechanisms through which indifference to and nonawareness of gendered policy problems are collectively constituted and methods through which they can be challenged. Findings thus deepen our understanding of barriers to the implementation of gender mainstreaming and the steps required for its effective implementation.20 juli 201

Feminist Political Economy and its Explanatory Promise

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Does European Union Studies have a Gender Problem? Experiences from Researching Brexit

On International Women’s Day 2017, EU Vice-President Frans Timmermans and High Representative Federica Mogherini claimed, “the European Union stands by women in Europe and around the globe today, as it did at the time of its foundation.” Indeed, (gender) equality has long been used as a foundational narrative of the EU (MacRae 2010). If we take these claims seriously, then gender-sensitive analysis should have a central place within EU studies. So, why do (gender) equality and the insights of feminist scholarship remain largely marginal to the EU studies canon? And how has the United Kingdom’s decision to exit the EU (Brexit) amplified this marginalization? By drawing on our experiences of researching and writing about the gendered impact of Brexit, we draw attention to significant blind spots at the heart of our discipline. This analysis ultimately highlights disparities in focus that reproduce disciplinary hierarchie

Hepatitis C Virus Induced a Novel Apoptosis-Like Death of Pancreatic Beta Cells through a Caspase 3-Dependent Pathway

Epidemiological and experimental studies have suggested that Hepatitis C virus (HCV) infection is associated with the development of type 2 diabetes. Pancreatic beta cell failure is central to the progression of type 2 diabetes. Using virus infection system, we investigate the influence of HCV infection on the fate of the insulinoma cell line, MIN6. Our experiments demonstrate that the HCV virion itself is indispensable and has a dose- and time-dependent cytopathic effect on the cells. HCV infection inhibits cell proliferation and induces death of MIN6 cells with apoptotic characteristics, including cell surface exposure of phosphatidylserine, decreased mitochondrial membrane potential, activation of caspase 3 and poly (ADP-ribose) polymerase, and DNA fragmentation in the nucleus. However, the fact that HCV-infected cells exhibit a dilated, low-density nucleus with intact plasma and nuclear membrane indicates that a novel apoptosis-like death occurs. HCV infection also causes endoplasmic reticulum (ER) stress. Further, HCV RNA replication was detected in MIN6 cells, although the infection efficiency is very low and no progeny virus particle generates. Taken together, our data suggest that HCV infection induces death of pancreatic beta cells through an ER stress-involved, caspase 3-dependent, special pathway

Pioglitazone and sulfonylureas: effectively treating type 2 diabetes

Type 2 diabetes is characterised by a gradual decline in glycaemic control and progression from oral glucose-lowering monotherapy to combination therapy and exogenous insulin therapy. Functional decline of the insulin-secreting β-cells is largely responsible for the deterioration in glycaemic control. Preservation of β-cell functionality, in addition to maintaining glycaemic control and reducing insulin resistance, is now regarded as a key target for long-term management strategies. Early, aggressive intervention with combination therapy is emerging as a valid approach to optimise long-term outcomes and combining agents with differing modes of action and secondary effect profiles should prove valuable. Sulfonylureas and thiazolidinediones exert their glucose-lowering effect through differing mechanisms of action – the sulfonylureas by stimulating insulin secretion, whereas the thiazolidinediones are insulin sensitisers. Both agents offer excellent improvements in glycaemic control when given as monotherapy or in combination. The thiazolidinediones protect β-cell structural and functional integrity and functionality and complement the sulfonylureas by inducing and maintaining improvements in insulin resistance, the abnormal lipid profile associated with type 2 diabetes and other cardiovascular risk factors. Thus, there is a strong rationale to support the addition of thiazolidinediones to sulfonylureas as a treatment option for type 2 diabetes. This combination may be particularly effective in the early stages of the disease when β-cell function is at its highest, allowing maximal benefit to be obtained from the insulin secretion-promoting abilities of the sulfonylureas and the β-cell-protective effects of the thiazolidinediones