The Bauhaus and the Business School: Exploring Analogies, Resisting Imitation

We offer here a case history of one of the 20th century's most famous organizations: The Bauhaus. In mapping various tensions and contradictions running through the Bauhaus we endeavour to provide a richer texture to the debates on the future of the business school which have become increasingly prominent in the field of management and organization studies. While we explore possible analogies between the Bauhaus and today's business schools, it is this very exploration which we intend to scrutinize at the same time. Our objective is not to mine the Bauhaus as something that existed in the past and whose principles (whatever they are now deemed to be) we can shape into a convenient, handy tool for current management teaching. In looking closely at the Bauhaus example we also detect the pitfalls of tracing straightforward equivalence. Our piece is intended to revitalize the somewhat stale discourse on the future of the business school; it is not offered as a final, one-size-fits-all solution

Mutational spectrum of the CHAC gene in patients with chorea-acanthocytosis

Chorea-acanthocytosis (ChAc) is an autosomal recessive neurological disorder whose characteristic features include hyperkinetic movements and abnormal red blood cell morphology. Mutations in the CHAC gene on 9q21 were recently found to cause chorea-acanthocytosis. CHAC encodes a large, novel protein with a yeast homologue implicated in protein sorting. In this study, all 73 exons plus flanking intronic sequence in CHAC were screened for mutations by denaturing high-performance liquid chromatography in 43 probands with ChAc. We identified 57 different mutations, 54 of which have not previously been reported, in 39 probands. The novel mutations comprise 15 nonsense, 22 insertion/deletion, 15 splice-site and two missense mutations and are distributed throughout the CHAC gene. Three mutations were found in multiple families within this or our previous study. The preponderance of mutations that are predicted to cause absence of gene product is consistent with the recessive inheritance of this disease. The high proportion of splice-site mutations found is probably a reflection of the large number of exons that comprise the CHAC gene. The CHAC protein product, chorein, appears to have a certain tolerance to amino-acid substitutions since only two out of nine substitutions described here appear to be pathogeni