Feminist epistemology meets the masculinity of marketing and consumer knowledge: a contemporary rendering of a decade-long debate

In this paper I outline possibilities for, and issues arising from, opposition towards the dominant ideologies and practices of marketing knowledge (Hirschman 1993) through an engagement with feminist epistemology (Longino 1991, Harding 1987). Feminist epistemology is a political branch of naturalised epistemology (Quine 1969) primarily concerned with critique of constructions of gender, gender norms and gendered interests within the production of knowledge (Anderson 1995) and with theorising, grounding and legitimating feminist knowledge making practices (Harding 1987). It is most often associated with the feminist critique of science, and with feminist science and technology studies (Haraway 1987, Wajman 1997). Feminist epistemology asks the question, ‘what is the nature of the feminist critical project as a way of knowing?’ (McLennan 1995:392). This paper outlines the basis of the feminist critique of knowledge generally, and as applied to marketing knowledge, offers description of the three main epistemological approaches to this question and suggestions for their application in practice. The paper progresses important work by consumer behaviour theorists (Bristor and Fischer 1993, Hirschman 1993) on the potentials of feminist ways of knowing for marketing and consumer behaviour by moving beyond the tripartite of feminist approaches outlined, and extending the discussion to take into account the development of situated knowledges theory (Haraway 1989, 1997), which has become so important in the decade since these papers were written. It joins ongoing conversations in consumer behaviour and marketing that share similar feminist concerns (Catterall et al 1997, 2000, 2005, Bettany and Woodruffe Burton 1999, 2005, and Hogg et al 1999, 2000) but in this contribution it takes a slightly tangential approach, seeing marketing knowledge in terms of its epistemic culture by using a model of masculinity in academic cultures from feminist theory (Wagner 1994) to help conceptualise it as such. The dominant masculine ideology of marketing knowledge both in execution (Penaloza 1994, Bristor and Fischer 1994, Fischer and Bristor 1993, Woodruffe 1996), and values (Hirschman 1993, Brown 2000, Desmond 1997) has been well documented over the past fifteen years. However, although the basis of this, how is it manifested and how a feminist informed marketing knowledge could be achieved, have been addressed somewhat in the literature (Bristor and Fischer 1993, Hogg, Bettany and Long 2000) an updated rendering is necessary which focuses specifically on epistemology and situates this discussion within a cultural framework. To do this I use the notions of cultural masculinity in academic disciplines developed by Wagner (1994) of ‘organisational egocentrism’, ‘fake collectivity’ and ‘de realisation’. With these, I raise important and specific issues around the notion of the masculinity of marketing knowledge, and then present an outline of feminist epistemologies to illustrate how different feminist approaches to knowledge would address these concerns.

Studies of the role of nf-κb in controlling osteoclast differentiation and bone loss

Increased osteoclast (OC) bone resorption and/or decreased osteoblast (OB) bone formation contribute to bone loss in osteoporosis and rheumatoid arthritis (RA). Findings of the basic and translational research presented in this thesis demonstrate a number of mechanisms by which cytokine-induced NF-κB activation controls bone resorption and formation: 1) Tumour necrosis factor-α (TNF) expands pool of OC precursors (OCPs) by promoting their proliferation through stimulation of the expression of macrophage colony stimulating factor (M-CSF) receptor, c-Fms, and switching M-CSF-induced resident (M2) to inflammatory (M1) macrophages with enhanced OC forming potential and increased production of inflammatory factors through induction of NF-κB RelB; 2) Similar to RANKL, TNF sequentially activates transcriptional factors NF-κB p50 and p52 followed by c-Fos and then NFATc1 to induce OC differentiation. However, TNF alone induces very limited OC differentiation. In contrast, it pre-activates OCPs to express cFos which cooperates with interleukin-1 (IL-1) produced by these OCPs in an autocrine mechanism by interacting with bone matrix to mediate the OC terminal differentiation and bone resorption from these pre-activated OCPs. 3) TNF-induced OC formation is independent of RANKL but it also induces NF-κB2 p100 to limit OC formation and bone resorption, and thus p100 deletion accelerates joint destruction and systemic bone loss in TNF-induced RA; 4) TNF receptor associated factor-3 (TRAF3) limits OC differentiation by negatively regulating non-canonical NF-κB activation and RANKL induces TRAF3 ubiquitination and lysosomal degradation to promote OC differentiation. Importantly, a lysosomal inhibitor that inhibits TRAF3 degradation prevents ovariectomy-induced bone loss; 5) RelB and Notch NICD bind RUNX2 to inhibit OB differentiation and RelB:p52 dimer association with NICD inhibit OB differentiation by enhancing the binding of RBPjκ to Hes1. These findings suggest that non-canonical NF- κB signaling could be targets to develop new therapies for RA or osteoporosis. For example 1) Agents that degrade TNF-induced RelB could block M1 macrophage differentiation to inhibit inflammation and joint destruction for the therapy of RA; 2)Agents that prevent p100 processing or TRAF3 degradation could inhibit bone resorption and also stimulate bone formation simultaneously for the therapy of osteoporosis.