Sociology’s missed opportunity: John Stuart-Glennie’s lost theory of the moral revolution, also known as the axial age

In 1873, 75 years before Karl Jaspers published his theory of the Axial Age in 1949, unknown to Jaspers and to contemporary scholars today, Scottish folklorist John Stuart Stuart-Glennie elaborated the first fully developed and nuanced theory of what he termed “the Moral Revolution” to characterize the historical shift emerging roughly around 600 BCE in a variety of civilizations, most notably ancient China, India, Judaism, and Greece, as part of a broader critical philosophy of history. He continued to write on the idea over decades in books and articles and also presented his ideas to the fledgling Sociological Society of London in 1905, which were published the following year in the volume Sociological Papers, Volume 2. This article discusses Stuart-Glennie’s ideas on the moral revolution in the context of his philosophy of history, including what he termed “panzooinism”; ideas with implications for contemporary debates in theory, comparative history, and sociology of religion. It shows why he should be acknowledged as the originator of the theory now known as the axial age, and also now be included as a significant sociologist in the movement toward the establishment of sociology

Energy and Effort

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Immunomodulatory monoclonal antibodies combined with peptide vaccination provide potent immunotherapy in an aggressive murine neuroblastoma model

PURPOSE: Neuroblastoma is one of the commonest extra-cranial tumors of childhood. The majority of patients present with metastatic disease for which outcome remains poor. Immunotherapy is an attractive therapeutic approach for this disease, and a number of neuroblastoma tumor antigens have been identified. Here we examine the therapeutic potential of combining immunomodulatory monoclonal antibodies (mAb) with peptide vaccination in murine neuroblastoma models. EXPERIMENTAL DESIGN: Neuroblastoma bearing mice were treated with mAb targeting 4-1BB, CD40 and CTLA-4 alone, or in combination with a peptide derived from the tumor antigen survivin (GWEDPPNDI). Survivin-specific immune response and therapeutic efficacy was assessed. RESULTS: In the Neuro2a model, treatment of established tumor with either anti-4-1BB, anti-CD40 or anti-CTLA-4 mAb results in tumor regression and long-term survival in 40-60% of mice. This is dependent on NK and CD8+ T cells and is associated with tumor CD8+ lymphocyte infiltrate. Successful therapy is achieved only if mAb is given to mice once tumors are established, suggesting dependence on sufficient tumor to provide antigen. In the more aggressive AgN2a and NXS2 models, single agent mAb therapy provides ineffective therapy. However if mAb (anti-CTLA-4) is given in conjunction with survivin peptide vaccination then 60% long term survival is achieved. This is associated with the generation of survivin-specific T cell immunity, which again is only demonstrated in the presence of tumor antigen. CONCLUSIONS: These data suggest the combination of antigen and co-stimulatory mAb may provide effective immunotherapy against neuroblastoma and may be of particular use in the minimal-residual disease setting