Getting nowhere fast: a teleological conception of socio-technical acceleration

It has been frequently recognized that the perceived acceleration of life that has been experienced from the Industrial Revolution onward is engendered, at least in part, by an understanding of speed as an end in itself. There is no equilibrium to be reached – no perfect speed – and as such, social processes are increasingly driven not by rational ends, but by an indeterminate demand for acceleration that both defines and restricts the decisional possibilities of actors. In Aristotelian terms, this is a final cause – i.e. a teleology – of speed: it is not a defined end-point, but rather, a purposive aim that predicates the emergence of possibilities. By tracing this notion of telos from its beginnings in ancient Greece, through the ur-empiricism of Francis Bacon, and then to our present epoch, this paper seeks to tentatively examine the way in which such a teleology can be theoretically divorced from the idea of historical progress, arguing that the former is premised upon an untenable ontological privileging of becoming

Liquid networks and the metaphysics of flux: ontologies of flow in an age of speed and mobility

It is common for social theorists to utilize the metaphors of ‘flow’, ‘fluidity’, and ‘liquidity’ in order to substantiate the ways in which speed and mobility form the basis for a new kind of information or network society. Yet rarely have these concepts been sufficiently theorized in order to establish their relevance or appropriateness. This article contends that the notion of flow as utilized in social theory is profoundly metaphysical in nature, and needs to be judged as such. Beginning with a discussion of the accelerating timescape that characterizes the network society, it will then move on to examine three main issues with this ‘metaphysics of flux’. First, that the concept of flows unjustly privileges the process of becoming and, as a result, is unable to account for the materiality, substantiality, and agency of the objects being mobilized, and the contingency of their mediation. Second, that it posits the accelerating tendencies of capital as an ontological inevitability, thus discounting resistance to such forces. Finally, that it ignores the human faculty for reason and speculative thought in developing alternative means of political praxis. The solution, it will be argued, is not to abandon metaphysical accounts of the network society, but rather to challenge those accounts that, in exhibiting a crude empiricism, work to justify the status quo

Metformin:historical overview

Metformin (dimethylbiguanide) has become the preferred first-line oral blood glucose-lowering agent to manage type 2 diabetes. Its history is linked to Galega officinalis (also known as goat's rue), a traditional herbal medicine in Europe, found to be rich in guanidine, which, in 1918, was shown to lower blood glucose. Guanidine derivatives, including metformin, were synthesised and some (not metformin) were used to treat diabetes in the 1920s and 1930s but were discontinued due to toxicity and the increased availability of insulin. Metformin was rediscovered in the search for antimalarial agents in the 1940s and, during clinical tests, proved useful to treat influenza when it sometimes lowered blood glucose. This property was pursued by the French physician Jean Sterne, who first reported the use of metformin to treat diabetes in 1957. However, metformin received limited attention as it was less potent than other glucose-lowering biguanides (phenformin and buformin), which were generally discontinued in the late 1970s due to high risk of lactic acidosis. Metformin's future was precarious, its reputation tarnished by association with other biguanides despite evident differences. The ability of metformin to counter insulin resistance and address adult-onset hyperglycaemia without weight gain or increased risk of hypoglycaemia gradually gathered credence in Europe, and after intensive scrutiny metformin was introduced into the USA in 1995. Long-term cardiovascular benefits of metformin were identified by the UK Prospective Diabetes Study (UKPDS) in 1998, providing a new rationale to adopt metformin as initial therapy to manage hyperglycaemia in type 2 diabetes. Sixty years after its introduction in diabetes treatment, metformin has become the most prescribed glucose-lowering medicine worldwide with the potential for further therapeutic applications

An interleukin-17–mediated paracrine network promotes tumor resistance to anti-angiogenic therapy

Although angiogenesis inhibitors have provided substantial clinical benefit as cancer therapeutics, their use is limited by resistance to their therapeutic effects. While ample evidence indicates that such resistance can be influenced by the tumor microenvironment, the underlying mechanisms remain incompletely understood. Here, we have uncovered a paracrine signaling network between the adaptive and innate immune systems that is associated with resistance in multiple tumor models: lymphoma, lung and colon. Tumor-infiltrating T helper type 17 (T(H)17) cells and interleukin-17 (IL-17) induced the expression of granulocyte colony-stimulating factor (G-CSF) through nuclear factor κB (NF-κB) and extracellular-related kinase (ERK) signaling, leading to immature myeloid-cell mobilization and recruitment into the tumor microenvironment. The occurrence of T(H)17 cells and Bv8-positive granulocytes was also observed in clinical tumor specimens. Tumors resistant to treatment with antibodies to VEGF were rendered sensitive in IL-17 receptor (IL-17R)-knockout hosts deficient in T(H)17 effector function. Furthermore, pharmacological blockade of T(H)17 cell function sensitized resistant tumors to therapy with antibodies to VEGF. These findings indicate that IL-17 promotes tumor resistance to VEGF inhibition, suggesting that immunomodulatory strategies could improve the efficacy of anti-angiogenic therapy