Canada's Stratford Festival 1953--1967 : Hegemony, commodity, institution

This thesis undertakes a critique of Canada's Stratford Festival as an institutional site of theatre production in the years 1953 through 1967. I propose to identify the major recurring "statements" of the institutional discourse; those statements which were circulated through various printed documents, including commentaries on the Festival and its work and the Festival's public relations material. The exercise of critique reveals that the Festival discourse became a hegemonic discourse, circulating a set of normative and prescriptive understandings as to what should constitute theatre and culture for Canada. The ideology dominating the discourse was that identified by Max Horkheimer and Theodor Adorno by the term the "culture industry." This ideology allowed for the autonomy of the Festival's productions to be eliminated, such that they functioned as commodities in which all capacity for critique has been abrogated.It will be shown that the Festival discourse privileged an aesthetic of spectacle and effect throughout these years, an aesthetic which implied a concept of cultural experiences as passive spectatorship and the easy consumption of effects; in short as commodity. In conjunction with this aesthetic, the discourse registered a concept of culture as affirmative--as an experience which affirms existing social relations in offering an apparent, if false, resolution or catharsis of conflict and of social inequality. When the Festival was identified as proof of Canada's cultural maturity and the focus of the nation's "life of the mind" these values were established as the nation's dominant cultural values. Moreover, this discursive portrayal of the Festival established it as Canada's foremost cultural commodity. And so the discourse simultaneously conveyed a concept of culture and of the Festival as commodities.By the 1960's the Festival was being identified as not simply a leading voice in Canadian culture, but as the institution on which the development of Canadian culture depended, thereby positioning the Festival as hegemonic. The Festival discourse thus articulated the Festival's central duality, its capacity to function as both cultural commodity and authority. The position of the Festival and its discourse as cultural authority ensured that it was the Festival concept of affirmative culture, marked by the displacement of the political, philosophical and existential role of culture, which dominated the discourse on theatre and the wider discourse of Canadian culture. In this respect the Festival failed to offer an active-critical experience which would counter the tendency towards the ethos of spectatorship and passivity which followed from the developing mass media

Charge Immobilization of Skeletal Muscle Na+ Channels: Role of Residues in the Inactivation Linker

We investigated structural determinants of fast inactivation and deactivation in sodium channels by comparing ionic flux and charge movement in skeletal muscle channels, using mutations of DIII-DIV linker charges. Charge altering and substituting mutations at K-1317, K-1318 depolarized the g(V) curve but hyperpolarized the h∞ curve. Charge reversal and substitution at this locus reduced the apparent voltage sensitivity of open- and closed-state fast inactivation. These effects were not observed with charge reversal at E-1314, E-1315. Mutations swapping or neutralizing the negative cluster at 1314, 1315 and the positive cluster at 1317, 1318 indicated that local interactions dictate the coupling of activation to fast inactivation. Gating charge was immobilized before channel entry into fast inactivation in hNaV1.4 but to a lesser extent in mutations at K-1317, K-1318. These results suggest that charge is preferentially immobilized in channels inactivating from the open state. Recovery of gating charge proceeded with a single, fast phase in the double mutation K-1317R, K-1318R. This mutation also partially uncoupled recovery from deactivation. Our findings indicate that charged residues near the fast inactivation “particle” allosterically interact with voltage sensors to control aspects of gating in sodium channels

Temperature Sensitive Defects in Paramyotonia Congenita Mutants R1448C and T1313M

The biophysical origins of paramyotonia congenita and its exacerbation in cold temperatures were examined. Human skeletal muscle voltage-gated sodium channels were expressed in Xenopus oocytes and macroscopic currents were recorded from cell-attached patches. Wild-type (hNaV1.4) channels were compared to two mutant channel isoforms, T1313M and R1448C. The voltage dependence and temperature sensitivity of activation, fast-inactivation onset and recovery, and deactivation were studied. Although activation and the onset of fast-inactivation were temperature sensitive in all three isoforms, and although these properties in mutant channels differed from those in wild-type channels, they did not account for cold-exacerbation. Deactivation, however, was disproportionately slower in R1448C, but not in T1313M, than in hNaV1.4. These defects may, at least in part, account for the clinical symptoms of paramyotonia congenita and its exacerbation by cold, and provide a basis for studies into the therapeutic alleviation of these symptoms

Influence of mutations affecting gonadotropin production or responsiveness on expression of inhibin subunit mRNA and protein in the mouse ovary

Measurement of inhibins A and B in the serum of normal cyclic rodents has implicated FSH in the regulation of these peptides within the ovary. To extend these observations we have used a panel of mutant mice carrying mutations which affect either the production of, or the ability to respond to, FSH and LH. As a consequence, the females are infertile and show different degrees of follicular development. The aim of this study was to measure inhibin gene transcription in the ovaries of these mutant females together with inhibin protein levels in ovaries and serum and to relate these to follicular development within the ovary. Comparison was made with a pool of normal/heterozygous females. In hpg females where lack of GnRH production results in the absence of gonadotropin synthesis, in FSHbeta knockout (FSHbetaKO) females where disruption of the gene encoding FSHbeta results in the absence of FSH production, and in FSH receptor knockout (FSHRKO) females which are unable to respond to circulating FSH, follicular development remains at the pre-antral stage in these three mutants. Only in the hpg females were common inhibin alpha subunit mRNA levels significantly lower than normal. In these three mutants, however, mRNA levels for both the betaA and betaB subunits were extremely low compared with normal mice. At the protein level, neither inhibin A nor B was detected in the serum of these three mutants; however inhibin B, albeit at very low levels, was detectable within the ovaries. These observations confirm a major role for FSH in the control of transcription of the RA and betaB genes but suggest that the constitutive transcription of the alpha subunit is less dependent on FSH. In contrast, in LH receptor knockout (LuRKO) female mice inhibin betaA subunit mRNA levels were similar to those measured in normal/heterozygous females but levels of inhibin alpha and betaB subunit mRNAs were significantly higher than in the normal group. This was reflected in significantly higher inhibin B protein levels in ovaries and serum. An inability to respond to LH combined with high circulating levels of FSH leads to a high proportion of antral follicles in LuRKO females, with granulosa cells constituting the major cell type within the ovary. The high percentage of antral granulosa cells is likely to account for the significantly higher levels of inhibin B production in these ovaries