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World culture theory seeks to explain the apparent educational convergence through a neo-institutionalist lens, seeing global rationalization in education as driven by the logic of science and the myth of progress. While critics have challenged these assumptions by focusing on local manifestations of world-level tendencies, such critique is comfortably accommodated within world culture theory. We approach the debate from a fresh perspective by examining its ideological foundations. We also highlight its shift from notions of myth and enactment toward advocacy for particular models, and we show that world culture theory can become normative, while obscuring our view of policy convergence. Finally, we critique the methods and evidence in world culture research. We argue that such research, while failing to support its own claims, actually produces world culture, as its assumptions and parameters create the very image of consensus and homogeneity that world culture theorists expect scholars to accept-in faith-as empirically grounded.

A nonapeptide epitope contained in the 65-kD species of heat shock protein of many mycobacterial species shares homology with a peptide on a mammalian cartilage link protein (1), with four of the amino acids identical. Structures containing this epitope, including proteoglycans extracted from human rheumatoid synovial effusions (2), induce proliferation ofan arthritogenic, rat T lymphocyte line (3) that has been subdivided into two clones, A2b and A2c, which, respectively, induce adjuvant arthritis or suppress the developing and established phases ofthis experimental model of autoimmunity (4, 5). Both clones proliferate in the presence of the epitope, as do T lymphocytes from some rheumatoid arthritis patients (6), but it is not established ifthe epitope plays a role in the pathogenesis of the arthritis. Administration of the recombinant (r) 65-kD shock protein antigen intraperitoneally did not induce arthritis in rats, but rendered such rats resistant to further attempts to induce arthritis with mycobacteria (1) or streptococcal cell walls (7). It is known, however, that adjuvant arthritis development requires the arthritogens to be administered in an oil vehicle by either the intradermal or subcutaneous routes (reviewed in reference 8), and that the peptidoglycan component of the mycobacterial cell wall is essential (8).Using high levels of the r65-kD protein in an oil vehicle, and even combining the protein with low levels of a synthetic, nonimmunogenic adjuvant, CP20961 (9), to mimic the peptidoglycan portion of mycobacteria, we have been unable to induce arthritis with the r65-kD shock protein, though the induction of resistance was confirmed. At high levels, the synthetic adjuvant CP20961, which is known to be arthritogenic (9), induced arthritis in rats rendered resistant to mycobacterial arthritis by the r65-kD shock protein. Type II collagen-induced arthritis also developed in r65-kD protein-pretreated rats. These results strongly suggest that the r65-kD shock protein produces an antigen-specific resistance to classical, mycobacterial adjuvant arthritis, since it is much less effective at inhibiting the arthritis induced by both CP20961 and type II collagen . Furthermore, the pathogenesis ofthe actual adjuvant arthritis does not appear to involve the 65-kD protein.

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The molecular identity of a gene which encodes the pore-forming subunit (alpha1G) of a member of the family of low-voltage-activated, T-type, voltage-dependent calcium channels has been described recently. Although northern mRNA analyses have shown alpha1G to be expressed predominantly in the brain, the detailed cellular distribution of this protein in the central nervous system (CNS) has not yet been reported. The current study describes the preparation of a subunit specific alpha1G riboprobe and antiserum which have been used in parallel in situ mRNA hybridization and immunohistochemical studies to localize alpha1G in the mature rat brain. Both alpha1G mRNA and protein were widely distributed throughout the brain, but variations were observed in the relative level of expression in discrete nuclei. Immunoreactivity for alpha1G was typically localized in both the soma and dendrites of many neurons. Whilst alpha1G protein and mRNA expression were often observed in cells known to exhibit T-type current activity, some was also noted in regions, e.g. cerebellar granule cells, in which T-type activity has not been described. These observations may reflect differences between the subcellular distribution of channels that can be identified by immunohistochemical methods compared with electrophysiological techniques.

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