‘Re-reading Raphael Samuel: Politics, Personality and Performance’

For British historian Raphael Samuel, history and politics were inextricable. Best known as the founder of the history workshop movement, the controversial historian took his stance on the democratisation of history-making, becoming an outspoken advocate for public history. Despite making a significant contribution to contemporary historiography, he remains a neglected, even disparaged, figure. This paper contends that the most significant aspect of Samuel’s historical work was not one or other theory of history or argument about the past but his entire way of being an historian. Samuel embodied as much as expressed his ideas, consciously using his personality as a powerful political tool. It is further argued that conventional approaches to intellectual history, focusing on textual outputs, do not fully recognise the significance of performative modes of thinking. Theoretical approaches to performance as identity offer important insight here but can be too schematic in their view of applied and enacted thought. A biographical approach, by contrast, provides the intimate perspective necessary to fully appreciate the fluidity and complexity of such a personality. The paper first situates Samuel in the context of his earlier life, focusing on how and why he created such a public persona and how he adapted it in response to changing circumstances. It then considers the implications and effectiveness of this persona by assessing how it was perceived and narrated by others, acknowledging, in the process, why different groups engaged with and interpreted it differently

Setting the Stage: Performing Politics in Theatres of Memory

The British historian Raphael Samuel is best known as a founding figure in the first British New Left and the driving force behind the history workshop movement which set out to democratise history-making in post Britain. Whilst the workshop has attracted attention for its radical pedagogical practice, Samuel’s distinctive approach to the writing of history has been less acknowledged. This paper contends that Theatres of Memory (1994), Samuel’s only sole-authored book published in his lifetime, both articulates and performs its author’s activist, participatory politics. If the workshop was intended to turn the formality of the historical conference or seminar on its head, Theatres applied the same subversive spirit to that icon of professional scholarship: the monograph. Written in the wake of and in response to the post-war fragmentation of the political left, Samuel sought a means of escaping the ideological and epistemological impasse that had arisen between factions. Rather than taking a stance on ‘people’s history’, Theatres recognised, and advocated for, history making as a common social activity. By making participation its core principle, it reconstituted socialism as an ethics of practice, an adjective rather than a noun, that could accommodate many variations. Drawing on a dramaturgical analysis to illuminate its dynamics of action, this article examines how the book enacted this participatory politics through a range of compositional techniques aimed at stimulating active readership. In doing so, it demonstrated, rather than described, a blueprint for the historian’s role in an expanding, pluralist, historical culture

The ACTTION-APS-AAPM Pain Taxonomy (AAAPT) Multidimensional Approach to Classifying Acute Pain Conditions.

Objective: With the increasing societal awareness of the prevalence and impact of acute pain, there is a need to develop an acute pain classification system that both reflects contemporary mechanistic insights and helps guide future research and treatment. Existing classifications of acute pain conditions are limiting, with a predominant focus on the sensory experience (e.g., pain intensity) and pharmacologic consumption. Consequently, there is a need to more broadly characterize and classify the multidimensional experience of acute pain. Setting: Consensus report following expert panel involving the Analgesic, Anesthetic, and Addiction Clinical Trial Translations, Innovations, Opportunities, and Networks (ACTTION), American Pain Society (APS), and American Academy of Pain Medicine (AAPM). Methods: As a complement to a taxonomy recently developed for chronic pain, the ACTTION public-private partnership with the US Food and Drug Administration, the APS, and the AAPM convened a consensus meeting of experts to develop an acute pain taxonomy using prevailing evidence. Key issues pertaining to the distinct nature of acute pain are presented followed by the agreed-upon taxonomy. The ACTTION-APS-AAPM Acute Pain Taxonomy will include the following dimensions: 1) core criteria, 2) common features, 3) modulating factors, 4) impact/functional consequences, and 5) putative pathophysiologic pain mechanisms. Future efforts will consist of working groups utilizing this taxonomy to develop diagnostic criteria for a comprehensive set of acute pain conditions. Perspective: The ACTTION-APS-AAPM Acute Pain Taxonomy (AAAPT) is a multidimensional acute pain classification system designed to classify acute pain along the following dimensions: 1) core criteria, 2) common features, 3) modulating factors, 4) impact/functional consequences, and 5) putative pathophysiologic pain mechanisms. Conclusions: Significant numbers of patients still suffer from significant acute pain, despite the advent of modern multimodal analgesic strategies. Mismanaged acute pain has a broad societal impact as significant numbers of patients may progress to suffer from chronic pain. An acute pain taxonomy provides a much-needed standardization of clinical diagnostic criteria, which benefits clinical care, research, education, and public policy. For the purposes of the present taxonomy, acute pain is considered to last up to seven days, with prolongation to 30 days being common. The current understanding of acute pain mechanisms poorly differentiates between acute and chronic pain and is often insufficient to distinguish among many types of acute pain conditions. Given the usefulness of the AAPT multidimensional framework, the AAAPT undertook a similar approach to organizing various acute pain conditions

Abstract A39: H3K9 methyltransferases G9a/Glp link the chromatin regulation of lung adenocarcinoma tumor propagating cells and lung bronchiolaveolar stem cells

Abstract Proper epigenetic control of transcription is essential for stem cell homeostasis and is frequently disrupted in cancer, but this has not been well investigated in lung biology or lung disease. We determined to test if lung stem cells and lung cancer stem cell-like tumor propagating cells (TPCs) shared mechanisms of chromatin regulation and if these contributed to the TPC cell fate. We have previously demonstrated that the stem cell marker Sca-1 enriches for mouse bronchioalveolar stem cells (BASCs) and cancer stem celll-like lung adenocarcinoma cells with enhanced metastatic and tumor propagation abilities (TPCs). A FACS screen of lung adenocarcinoma cell lines revealed that UNC0638, an inhibitor of H3K9me1/2 methyltransferases G9a and Glp enriches for high Sca-1 expressing, TPC-like cells. Gene expression analysis of primary adenocarcinomas shows that G9a/Glp are down-regulated in Sca-1+ metastatic TPCs. Furthermore, analysis of 400+ early stage patient lung adenocarcinomas reveals that low G9a expression and high expression of KDM3A, an H3K9me1/2 demethylase, significantly correlate with worse survival (P=0.008, P=0.002). This implies that dysregulation of H3K9me1/2 is also a significant factor in human disease. Depletion of G9a throughout tumorigenesis causes significant increases in tumor burden and in a Lox-stop-Lox-Kras; p53-flox mouse model of lung adenocarcinoma. Tumors generated with a Cre/shG9a lentivirus had a significantly higher tumor burden, tumor grade (P&amp;lt;0.0001) than those with a control Cre/shLuciferase virus, and gave rise to significantly more metastases (47% vs 0%, P=0.0035). FACS Analysis demonstrated that the shG9a tumors had a significantly expanded Sca-1+ CD24+ TPC fraction (27.7% vs 15.6%, P=0.019), and shG9a Metastases were even further enriched in TPCs (63.5% + 8.3%). This suggests that G9a depletion drives tumor cells towards the more tumorigenic TPC cell fate and this may be responsible for the greatly accelerated disease progression in these mice. H3K9me1/2 also regulates the behavior of lung stem cells. G9a/Glp inhibition of BASCs or alveolar type 2 cells in 3D co-culture assays increases both Sca-1+ cells and undifferentiated organoids, and significantly decreases alveolar-lineage organoids (P&amp;lt;0.0005). BASC cultures also show increases in bronchiolar-lineage organoids (P&amp;lt;0.0005), implying that cell fate decisions may regulated by H3K9me1/2. These findings demonstrate that common means of epigenetic regulation exist between mouse lung stem cells and lung TPCs, and suggests that lung TPCs may adopt these whilst promoting disease progression. Determining the precise mechanisms of this regulation will be important for our understanding of lung biology and disease, with potential implications for the diagnosis and treatment of human adenocarcinoma. Citation Format: Samuel P. Rowbotham, Carla F. Kim. H3K9 methyltransferases G9a/Glp link the chromatin regulation of lung adenocarcinoma tumor propagating cells and lung bronchiolaveolar stem cells. [abstract]. In: Proceedings of the AACR Special Conference on Chromatin and Epigenetics in Cancer; Sep 24-27, 2015; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2016;76(2 Suppl):Abstract nr A39.</jats:p