From Prototyping to Allotyping. The invention of change of use and the crisis of building types

The chapter analyses the invention and the form of the discourse on building conversion as one particular instance of redefining what a technology is and how it operates. I describe a shift from expert defined closure to lay based openness and tinkering as a shift from prototyping to allotyping: Since the early 1970s, change of use and building conversion have become a central and fashionable discourse among architects and architectural theorists. Before the 1970s, buildings were understood as technologies, as ‘society made durable’. The notion of building type was central to link a building to a given use. A bank was a bank because architects applied existing templates, prototypes, to turn a building into a bank. In the 1970s, suddenly buildings became flexible – discursively, since building conversion always existed: ‘Building type’ no longer was a meaningful link between a building and its use. A bank should not stay a bank, but become a hotel, a theatre or a flat, in short: an allotype. The chapter elucidate this central shift in thinking about buildings and reflects on the special case of allotyping buildings and how it continues to vex thinking about buildings

Renal tubulointerstitial lesions in CBA/J mice.

Renal tubulointerstitial lesions (RTL) were observed with high frequency in CBA/J mice more than 2 months old. RTL were characterized by interstitial infiltrates of lymphocytes and macrophages in the corticomedullary zone. Multinucleated structures sometimes resembling giant cells were present, and there was destruction of tubules and tubular basement membranes in areas of infiltration. Glomeruli appeared normal. RTL were first seen in 12 to 22 CBA/J mice 2.5 to 3 months old. By the age of 7 to 9 months, 35 to 45 mice were affected, and all 24 mice 12 months old or older had RTL. CBA/J mice had these unique renal lesions whether they were purchased and examined immediately, were obtained as weanlings andreared in our quarters or those of another institution, or were fourth generation descendants of purchased breeders. The propensity to develop RTL has been present in this strain for at least 2 years. RTL were not observed in C57BL/6J mice housed for 14 months with affected animals or in a survey of CBA/HUmc, C57BL/6J, A/J, BALB/cJ, or C3H/HeJ mice. Immunofluorescent examination of CBA/J kidneys appears to rule out antitubular basement membrane autoantibodies or immune complexes in the pathogenesis of RTL

Murine lupus nephritis is accelerated by anti-glomerular basement membrane autoantibodies.

We have tested the effect of deposition of non-pathogenic amounts of induced anti-glomerular basement membrane (GBM) autoantibodies on the development of the spontaneous lupus nephritis of female (NZB x NZW) F1 (B x W) mice. Female and male B x W mice were immunized with rabbit renal tubular basement membrane in adjuvant at 2 months of age and their kidneys were examined 35 to 66 days later; control B x W mice were injected with adjuvant only or remained untreated. By immunofluorescent and histopathological criteria, only the 4-month-old female B x W mice with anti-GBM autoantibody deposits had an accelerated onset of lupus nephritis resembling the findings not seen until 6 to 8 months of age in unmanipulated mice. Thus potentially pathogenic amounts of immune complexes are present in young female B x W mice, but these do not deposit in glomeruli until much later in life. Evidently, the anti-GBM autoantibodies modified the glomerular milieu sufficiently to facilitate accelerated immune complex deposition