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Can queer theory proceed without an allegiance to antinormativity? The introduction to this special issue establishes the value of this question by staging an encounter with the most widely held assumption in queer theory today: that the political value of the field lies in its antinormative commitments. The first section of this introduction demonstrates how profoundly the history of queer theorizing has been shaped by an antinormative sensibility, one that has organized the multiple and at times discordant itineraries of analysis that comprise the queer theoretical archive into a field-forming synthesis. In part 2, the authors offer a more studied consideration of the character of norms. By articulating the difference between a norm and the terms that often define it—domination, homogenization, exclusion, hegemony, identity, or more colloquially, the familiar, status quo, or routine—this section demonstrates the importance of renewing queer theoretical attention to the conceptual and political particularity of normativity as a distinct object of inquiry. The authors’ aim is not to dismiss the political agenda that antinormativity has come to represent for queer inquiry, but to channel some of the field’s energies toward analyzing the critical authority it now wields. This entails promoting scholarship that not only rethinks the meaning of norms, normalization, and the normal but that also imagines new ways to approach the politics of queer criticism altogether. In the final section, the authors describe the specific contribution of each of the volume’s essays to this endeavor.

This study described the development of the Social Skills Improvement System Social Emotional Learning Edition Rating Forms (SSIS SEL RF) for teachers, parents, and students. This new multirater assessment is a reconfiguration of the SSIS Rating Scales items inspired by the CASEL Social Emotional Competency framework. The internal structure and score reliability estimates were examined across three raters for a common sample of more than 200 individual children ages 3 to 18 years. Confirmatory factor analyses tested against the CASEL five-dimensional SEL theoretical model demonstrated adequate fit for the SSIS SEL Parent and Student RFs and mediocre fit of the Teacher RF. Internal consistency, test-retest, and interrater reliability estimates for scores on each of the SSIS SEL RFs all met or exceeded acceptable criteria. Thus, researchers and practitioners interested in measuring the social–emotional behavior of children ages 3 to 18 can expect reliable scores and structurally meaningful behavior content within the Collaborative on Academic Social Emotional Learning (CASEL) SEL competency framework. Limitations to the present findings and suggestions for future research conclude the report.

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Tamoxifen is widely used as an adjuvant therapy for patients with estrogen receptor (ERa)-positive tumors. However, the clinical benefit is often limited because of the emergence of drug resistance. In this study, overexpression of ribonucleotide reductase M2 (RRM2) in MCF-7 breast cancer cells resulted in a reduction in the effectiveness of tamoxifen, through downregulation of ERa66 and upregulation of the 36-kDa variant of ER (ERa36). We identified that NF-kB, HIF1a, and MAPK/JNK are the major pathways that are affected by RRM2 overexpression and result in increased NF-kB activity and increased protein levels of EGFR, HER2, IKKs, Bcl-2, RelB, and p50. RRM2-overexpressing cells also exhibited higher migratory and invasive properties. Through time-lapse microscopy and protein profiling studies of tamoxifen-treated MCF-7 and T-47D cells, we have identified that RRM2, along with other key proteins, is altered during the emergence of acquired tamoxifen resistance. Inhibition of RRM2 using siRRM2 or the ribonucleotide reductase (RR) inhibitor didox not only eradicated and effectively prevented the emergence of tamoxifen-resistant populations but also led to the reversal of many of the proteins altered during the process of acquired tamoxifen resistance. Because didox also appears to be a potent inhibitor of NF-kB activation, combining didox with tamoxifen treatment cooperatively reverses ER-a alterations and inhibits NF-kB activation. Finally, inhibition of RRM2 by didox reversed tamoxifenresistant in vivo tumor growth and decreased in vitro migratory and invasive properties, revealing a beneficial effect of combination therapy that includes RRM2 inhibition to delay or abrogate tamoxifen resistance.