8 research outputs found
The Politics of Exhaustion and the Externalization of British Border Control. An Articulation of a Strategy Designed to Deter, Control and Exclude
In response to contemporary forms of human mobility, there has been a continued hardening of borders seeking to deter, control and exclude certain groups of people from entering nation states in Europe, North America and Australasia. Within this context, a disconcerting evolution of new and increasingly sophisticated forms of border control measures have emerged, which often play out within bilateral arrangements of âexternalisedâ or âoffshoreâ border controls. Drawing on extensive firstâhand field research among displaced people in Calais, Paris and Brussels in 2016â2019, this paper argues that the externalization of the British border to France is contingent upon a harmful strategy, which can be understood as the âpolitics of exhaustion.â This is a raft of (micro) practices and methods strategically aimed to deter, control and exclude certain groups of people on the move who have been profiled as âundesirable,â with a detrimental (un)intended impact on human lives
Panobinostat Synergistically Enhances the Cytotoxic Effects of Cisplatin, Doxorubicin or Etoposide on High-Risk Neuroblastoma Cells
A regimen combining the Wee1 inhibitor AZD1775 with HDAC inhibitors targets human acute myeloid leukemia cells harboring various genetic mutations
VEGF signaling inhibitors: More pro-apoptotic than anti-angiogenic
The vascular endothelial growth factor (VEGF) family of polypeptide growth factors regulates a family of VEGF receptor (VEGFR) tyrosine kinases with pleiotropic downstream effects. Angiogenesis is the best known of these effects, but additional VEGF-dependent actions include increased vascular permeability, paracrine/autocrine growth factor release, enhancement of cell motility, and inhibition of apoptosis. In theory, therapeutic inhibition of angiogenesis should reduce tumor perfusion and thus increase tumor hypoxia and chemoresistance, but in clinical practice the VEGF antibody bevacizumab acts as a broad-spectrum chemosensitizer. Since VEGFR expression occurs in many tumor types, such chemosensitization is more readily explained by direct inhibition of tumor cell survival signals than by indirect stromal/vascular effects. The emerging model of anti-VEGF drug action being mediated primarily by tumoral (as distinct from endothelial) VEGFRs has clinically important implications for optimizing the anti-metastatic efficacy of this expanding drug class. © 2007 Springer Science+Business Media, LLC.link_to_subscribed_fulltex