Conceptualizing a distributed, multi-scalar global public sphere through activist communication practices in the World Social Forum

This article contributes to debate about how to conceptualize the global public sphere. Drawing on media practice theory and ethnographic research on media activism in the World Social Forum, it shows how ‘global publics’ can be constituted through a diverse range of activist communication practices that complicate both conventional hierarchies of scale and contemporary theorizations of publics as personalized networks. It develops an understanding of the global public sphere as an emergent formation made up of multiple, interlinked publics at different scales and emphasizes the significance of collective communication spaces for actors at the margins of the global network society

Autophagy requires endoplasmic reticulum targeting of the PI3-kinase complex via Atg14L

Generation of PI3P in the normally PI3P-deficient ER membrane makes the organelle a platform for autophagosome formation

Climate Policy Networks in Australia: Dynamics of Failure and Possibility

Many high-income countries are committed to effective climate policy, yet remain heavily dependent on fossil fuel extraction. The contradiction between an intensifying climate crisis and continued policy failure generates new political alignments, constituencies, and agendas. A dialectical process of socio-ecological change opens-up, where the climate is "socialised" and society is "climatised". Australia is a high-income, high-emitting fossil fuel "superpower" with a thirty-year stretch of failing climate policy, and offers an exceptionally vivid illustration of this dynamic. The paper explores these themes through the rhetoric of participants in Australian climate policy networks. It is based on sustained involvement the field and a series of in-depth interviews with organisations that seek to influence Australian climate policy, across business associations, trade unions, environmental non-governmental organisations, government agencies, and think tanks. It finds extensive strategic reflection across these organisations, with moves to more collaboration and alliance-building to isolate the fossil fuel lobby, and efforts at creating new constituencies to advance decarbonisation "on the ground".Peer reviewe

AAV8-mediated sVEGFR2 and sVEGFR3 gene therapy combined with chemotherapy reduces the growth and microvasculature of human ovarian cancer and prolongs the survival in mice

Abstract Background: Vascular endothelial growth factors (VEGFs) are major regulators of intratumoral angiogenesis in ovarian cancer (OVCA). Overexpression of VEGFs is associated with increased tumor growth and metastatic tendency and VEGF-targeting therapies are thus considered as potential treatments for OVCA. Here, we examined the antiangiogenic and antitumoral effects on OVCA of adeno-associated virus 8 (AAV8)-mediated expression of soluble VEGF receptors (sVEGFRs) sVEGFR2 and sVEGFR3 together with paclitaxel and carboplatin chemotherapy. Materials and methods: Immunodeficient mice were inoculated with human OVCA cell line SKOV-3m. Development of tumors was confirmed with magnetic resonance imaging (MRI) and mice were treated with gene therapy and paclitaxel and carboplatin chemotherapy. The study groups included (I) non-treated control group, (II) blank control vector AAV8-CMV, (III) AAV8-CMV with chemotherapy, (IV) AAV8-sVEGFR2, (V) AAV8-sVEGFR3, (VI) AAV8-sVEGFR2 and AAV8-sVEGFR3, and (VII) AAV8-sVEGFR2 and AAV8-sVEGFR3 with chemotherapy. Antiangiogenic and antitumoral effects were evaluated with immunohistochemical stainings and serial MRI. Results: Reduced intratumoral angiogenesis was observed in all antiangiogenic gene therapy groups. The combined use of AAV8-sVEGFR2 and AAV8-sVEGFR3 with chemotherapy suppressed ascites fluid formation and tumor growth, thus improving the overall survival of mice. Antitumoral effect was mainly caused by AAV8-sVEGFR2 while the benefits of AAV8-sVEGFR3 and chemotherapy were less prominent. Conclusions: Combined use of the AAV8-sVEGFR2 and AAV8-sVEGFR3 with chemotherapy reduces intratumoral angiogenesis and tumor growth in OVCA mouse model. Results provide preclinical proof-of-concept for the use of soluble decoy VEGFRs and especially the AAV8-sVEGFR2 in the treatment of OVCA