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This paper is an edited version of a conversation between Silvia Gherardi and Lynne Baxter at the Inaugural Distinguished Speaker Event of the Gender, Materialities, and Activism Network. We learn about the development of Professor Gherardi's interest in feminism, how it evolves and informs her wider work on organization studies and methodology, and how she supports community development while advancing her own work. Moreover, there is a perceptive reflection from Professor Gherardi uncovering what the article, as written text, loses compared to the multisensory verbal encounter taking place in virtual space. [ABSTRACT FROM AUTHOR]

Diagnostic encounters can be seen as complex socio‐material processes. Drawing on the new materialist ideas of Barad, we studied how an innovative technology became part of the intra‐actions between different human and non‐human materialities in a cervical cancer diagnostic process. While researching the development of a technology intended to improve cervical cancer detection, we carried out a series of observations of diagnostic encounters involving clinicians, patients and the device in a hospital. The intra‐actions between the different materialities had rhythmic properties, repeated activities and timings that varied in intensity, for example, movements, exchanged looks, and talk that helped co‐produce the diagnosis and maintain consent. Sadly, the device interfered with the rhythms, undermining the clinicians' desire to adopt it, despite it being more accurate at diagnosing ill health than previous assistive technologies. Studying rhythms as part of diagnostic encounters could help with the design and subsequent integration of novel technologies in healthcare, because they encompass relationships created by human and non‐human materialities. Importantly, highlighting the role of rhythms contributes another way diagnostic encounters are co‐produced between clinicians and patients, and how they can be disrupted, improving the understanding of how consent is maintained or lost. [ABSTRACT FROM AUTHOR]

Deep subcortical lesions (DSCL) of the brain, are present in ~60% of the ageing population, and are linked to cognitive decline and depression. DSCL are associated with demyelination, blood brain barrier (BBB) dysfunction, and microgliosis. Microglia are the main immune cell of the brain. Under physiological conditions microglia have a ramified morphology, and react to pathology with a change to a more rounded morphology as well as showing protein expression alterations. This study builds on previous characterisations of DSCL and radiologically ‘normal-appearing’ white matter (NAWM) by performing a detailed characterisation of a range of microglial markers in addition to markers of vascular integrity. The Cognitive Function and Ageing Study (CFAS) provided control white matter (WM), NAWM and DSCL human post mortem tissue for immunohistochemistry using microglial markers (Iba-1, CD68 and MHCII), a vascular basement membrane marker (collagen IV) and markers of BBB integrity (fibrinogen and aquaporin 4). The immunoreactive profile of CD68 increased in a stepwise manner from control WM to NAWM to DSCL. This correlated with a shift from small, ramified cells, to larger, more rounded microglia. While there was greater Iba-1 immunoreactivity in NAWM compared to controls, in DSCL, Iba-1 levels were reduced to control levels. A prominent feature of these DSCL was a population of Iba-1-/CD68+ microglia. There were increases in collagen IV, but no change in BBB integrity. Overall the study shows significant differences in the immunoreactive profile of microglial markers. Whether this is a cause or effect of lesion development remains to be elucidated. Identifying microglia subpopulations based on their morphology and molecular markers may ultimately help decipher their function and role in neurodegeneration. Furthermore, this study demonstrates that Iba-1 is not a pan-microglial marker, and that a combination of several microglial markers is required to fully characterise the microglial phenotype. [ABSTRACT FROM AUTHOR]

This paper examines the relationship between formal product development management tools and actual business processes in a world class company, NCR, Dundee, Scotland, U.K., whose manufactured products include significant associated computer software written and designed in-house. After providing some background to the company and the research project which has led to this paper, a detailed case study of the software design and development processes in NCR is presented. This is contrasted with the formal management approach NCR is endeavoring to follow. The authors identify some key inconsistencies between the two processes and consider the implications for improving the management of the concept generation process. Index Terms - New product development, qualitative methodology, software development.

We offer a method for enabling inclusive participation in group discussion: the five senses exercise used by clean language practitioners. The method helped a diverse set of participants with intersectional subject positions articulate their perspectives on feminism in a non-hierarchical way. We describe the basis for the method, the intentions of the session convenor and results from the session. Participants reflect on the method and the responses it evoked. The method is a way of honouring individual perspectives and experiences whilst building connections between people. We think the method is useful for facilitating diverse groups in contexts such as workshops, teaching and meetings at work where the convenor wants to build inclusion and fresh perspectives. [ABSTRACT FROM AUTHOR]

The mechanisms by which prostaglandin F2α (PGF2α) increases intracellular Ca2+ concentration [Ca2+]i in vascular smooth muscle remain unclear. We examined the role of store-, receptor- and voltage-operated Ca2+ influx pathways in rat intrapulmonary arteries (IPA) loaded with Fura PE-3. Low concentrations (0.01–1 μm) of PGF2α caused a transient followed by a plateau rise in [Ca2+]i. Both responses became maximal at 0.1 μm PGF2α. At higher concentrations of PGF2α, a further slower rise in [Ca2+]i was superimposed on the plateau. The [Ca2+]i response to 0.1 μm PGF2α was mimicked by the FP receptor agonist fluprostenol, whilst the effect of 10 μm PGF2α was mimicked by the TP receptor agonist U-46619. The plateau rise in [Ca2+]i in response to 0.1 μm PGF2α was insensitive to diltiazem, and was abolished in Ca2+-free physiological salt solution, and by pretreatment with La3+, 2-APB, thapsigargin or U-73122. The rises in [Ca2+]i in response to 10 μm PGF2α and 0.01 μm U-46619 were partially inhibited by diltiazem. The diltiazem-resistant components of both of these responses were inhibited by 2-APB and La3+ to an extent which was significantly less than that seen for the response to 0.1 μm PGF2α, and were also much less sensitive to U-73122. The U-46619 response was also relatively insensitive to thapsigargin. When Ca2+ was replaced with Sr2+, the sustained increase in the Fura PE-3 signal to 0.1 μm PGF2α was abolished, whereas 10 μm PGF2α and 0.05 μm U-46619 still caused substantial increases. These results suggest that low concentrations of PGF2α act via FP receptors to cause IP3-dependent Ca2+ release and store operated Ca2+ entry (SOCE). U-46619 and 10–100 μm PGF2α cause a TP receptor-mediated Ca2+ influx involving both L-type Ca2+ channels and a receptor operated pathway, which differs from SOCE in its susceptibility to La3+, 2-APB and thapsigargin, does not require phospholipase C activation, and is Sr2+ permeable. [ABSTRACT FROM AUTHOR]

1 The effect of the Cl channel blockers niflumic acid (NFA). 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB). 4.4′-diisothiocyanatostilbene-2.2′-disulfonic acid (DIDS). and anthracene-9-carboxylic acid (A-9-C), on Ca[sup2+] signalling in rat pulmonary artery smooth muscle cells was examined. Intracellular Ca[Sup2+] concentration (Ca[sup2+],) was monitored with either fura-2 or fluo-4, and caffeine was used to activate the ryanodine receptor, thereby releasing Ca[sup2+] from the sarcoplasmic reticulum (SR). 2 NFA and NPPB significantly increased basal [Ca[sup2+] ], and attenuated the caffeine-induced increase in [Ca[sup2 +],. These Cl[sup-] channel blockers also increased the half-time (t[sub1/2] ) to peak for the caffeine-induced [Ca[sup2+ ], transient. and slowed the removal of Ca[sup2+] from the cytosol following application of caffeine. Since DIDS and A-9-C were found to adversely affect furo-2 fluorescence, fluo-4 was used in monitor intracellular Ca[sup2+] in studies involving these Cl[sup-] channel blockers. Both DIDS and A-9-C increased basal fluo-4 fluorescence, indicating an increase in intracellular Ca[sup2+]. and while DIDS had no significant effect on the t[sub1/2] to peak for the caffeine-induced Ca[sup2+] transient, it was significantly increased by A-9-C. 3 In the absence of extracellular Ca[sup2+], NFA significantly increased basal [Ca[sup2+],. suggesting that the release of Ca[sup2+] from an intracellular store was responsible for the observed effect. 4 Depleting the SR with the combination of caffeine and cyclopiazonic acid prevented the increase in basal [Ca[sup2+]], induced by NFA. Additionally, incubating the cells with ryanodine also prevented the increase in basal [Ca[sup2+]], induced by NFA. 5 These data show that Cl[sup-] channel blockers have marked effects on Ca[sup2+]signalling in pulmonary artery smooth muscle cells. Furthermore, examination of the NFA-induced increase in [Ca[sup2+]], indicates that it is likely due to Ca[sup2+] release from an intracellular store, most probably the SR. [ABSTRACT FROM AUTHOR]