The Pinboard in Practice: A Study of Method through the Case of US Telemedicine, 1945-1980

In view of calls for sociology to engage more thoroughly with method and methodological innovation (Law, 2004; Savage and Burrows, 2007) this thesis presents an exploration of John Law’s (2002) ‘pinboard’ method. Grounded in the ontological and epistemological premises of post-Actor-Network Theory (post-ANT), the pinboard is an analytical method which attempts to engage with the ‘messiness’ of reality by articulating its complexity, diversity and non-coherence which are all typically erased in traditional narrative accounts. Law’s explication of the pinboard is imprecise, however, and even within the context of post-ANT literature it is a method which has seen very little use. Hence, in taking up the pinboard method this thesis works, firstly, to illustrate what the pinboard method might mean in practice and, secondly, to offer of it a critical discussion and evaluation. In doing this, the thesis works through a series of empirical case studies related to the early practice of ‘telemedicine’ in the US between roughly 1950 and 1980. Based upon both contemporary and recent documentary resources as well as a small number of interviews with early telemedicine researchers, these pinboards are contrasted with existing histories of early US telemedicine to produce a comparative illustration and discussion. On the basis of these case studies, it is argued that the pinboard can be successfully used to produce decentred, ‘messy’ accounts of ontologically complex realities as is argued by Law. As a result of both practical and conceptual issues, however, the pinboard nevertheless performs reductions and erasures of its own thereby rendering it complementary to narrative accounts rather than antithetical

Flipping a Phosphate Switch on Kinesin-II to Turn IFT Around

Cilia and flagella are assembled and maintained by the motor-driven, bidirectional traffic of large protein complexes in a process termed intraflagellar transport (IFT). In this issue of Developmental Cell, Liang et al. (2014) report that IFT is regulated in part by the phosphorylation status of the kinesin-II subunit FLA8/KIF3B