Languages of “National Socialism”: From Reactionary Apocalypse to Social Media Clickbait

In this article I examine language used to define, express, and exploit “NationalSocialism”. These different uses vary in time and purpose, and need to be understood in context. The Nazis did not create much of the language most closely associated with National Socialism, but their use of certain language, symbols, and images has been so firmly established that we immediately recognize them even when partially spoken or indirectly referenced. This easy recognition, combined with the emotional charge of anger and horror, lends itself to commercial and political exploitation. I discuss this with examples from scholarly publishing and current events, and also discuss possibilities for crowd manipulation made possible by political use of interactive social networks

Is Small Beautiful? The Position of Independent Scholarly Publishers in an Environment of Rapid Industry Consolidation

The publishing industry continues to consolidate, with large multinational publishers acquiring journals and other content from academic societies and independent publishers. This panel provided candid insights into the challenges facing smaller publishers, including how/why they continue to exist in a business environment increasingly dominated by large companies. The discussion examined the advantages that smaller, independent publishers enjoy and addressed their adaptation strategies, business planning (including open versus paid access models), strategic partnerships, technical infrastructure, production procedures, relationships with libraries, and the work needed to meet the evolving needs of library end users. The impact of industry consolidation on libraries, including that of the intermediaries between publishers and libraries, was also discussed. The panel included speakers from humanities, social science, and science publishers who provided a range of perspectives from across the disciplines

Human Non-neutralizing HIV-1 Envelope Monoclonal Antibodies Limit the Number of Founder Viruses during SHIV Mucosal Infection in Rhesus Macaques

HIV-1 mucosal transmission begins with virus or virus-infected cells moving through mucus across mucosal epithelium to infect CD4+ T cells. Although broadly neutralizing antibodies (bnAbs) are the type of HIV-1 antibodies that are most likely protective, they are not induced with current vaccine candidates. In contrast, antibodies that do not neutralize primary HIV-1 strains in the TZM-bl infection assay are readily induced by current vaccine candidates and have also been implicated as secondary correlates of decreased HIV-1 risk in the RV144 vaccine efficacy trial. Here, we have studied the capacity of anti-Env monoclonal antibodies (mAbs) against either the immunodominant region of gp41 (7B2 IgG1), the first constant region of gp120 (A32 IgG1), or the third variable loop (V3) of gp120 (CH22 IgG1) to modulate in vivo rectal mucosal transmission of a high-dose simian-human immunodeficiency virus (SHIV-BaL) in rhesus macaques. 7B2 IgG1 or A32 IgG1, each containing mutations to enhance Fc function, was administered passively to rhesus macaques but afforded no protection against productive clinical infection while the positive control antibody CH22 IgG1 prevented infection in 4 of 6 animals. Enumeration of transmitted/founder (T/F) viruses revealed that passive infusion of each of the three antibodies significantly reduced the number of T/F genomes. Thus, some antibodies that bind HIV-1 Env but fail to neutralize virus in traditional neutralization assays may limit the number of T/F viruses involved in transmission without leading to enhancement of viral infection. For one of these mAbs, gp41 mAb 7B2, we provide the first co-crystal structure in complex with a common cyclical loop motif demonstrated to be critical for infection by other retroviruses

Languages of “National Socialism”: From Reactionary Apocalypse to Social Media Clickbait

In this article I examine language used to define, express, and exploit “National Socialism”. These different uses vary in time and purpose, and need to be understood in context. The Nazis did not create much of the language most closely associated with National Socialism, but their use of certain language, symbols, and images has been so firmly established that we immediately recognize them even when partially spoken or indirectly referenced. This easy recognition, combined with the emotional charge of anger and horror, lends itself to commercial and political exploitation. I discuss this with examples from scholarly publishing and current events, and also discuss possibilities for crowd manipulation made possible by political use of interactive social networks

Contextual misreadings: The United States reception of Heidegger\u27s political thought

The thesis of this dissertation is that the political dimension of Martin Heidegger\u27s philosophical work has been widely misinterpreted in the United States, and that this misinterpretation has been caused by censorship, historical and political ignorance, and poor scholarship. This study reveals the extent to which Heidegger engaged in politically motivated editing of his work after the war, and shows how such edited German editions were used as a basis for many English translations of his work. It also shows that Heidegger suppressed the publication of some politically sensitive texts while he was alive, and that archival materials in different parts of Germany have been manipulated so as to protect Heidegger from critical scrutiny. Such practices have also been employed by (or in the service of) other philosophers who worked in Germany at the time; the manipulation of post-war editions of philosophical texts written in Germany between 1933-1945 seems to be a widespread phenomenon. To improve the US reader\u27s understanding of the historical context of Heidegger\u27s political thought, this study also relates Heidegger\u27s professional and political actions to those of all of the other 213 professors of philosophy who taught at a German university between 1933 and 1945. Heidegger\u27s political arguments are compared to those of the other philosophers who, as university Rectors, were in similar positions of political responsibility as Heidegger. The presentation of this new information allows the US reader to understand better the development of philosophy in Germany, and reveals the uniqueness of Heidegger\u27s philosophical commitment to a particular version of National Socialist ideology. Finally, this study identifies the main sources of interpretive error in the US reception of Heidegger\u27s political thought, and shows how philosophers can avoid such mistakes in the future

Regulation of STAT-Dependent Pathways by Growth Factors and Cytokines

Polypeptide growth factors and cytokines elicit their effects by activating specific cell-surface receptors, thereby initiating signaling cascades that culminate in the induction of specific subsets of genes. Initially identified as the primary mediators of interferon-dependent signaling, JAKs and STATs are now known to be utilized by many different extracellular signaling proteins. In this report we describe how JAK-STAT pathways transduce signals initiated by both cytokines and growth factors, focusing on how specificity is achieved through STAT-receptor interactions and on how receptor-associated kinases function in STAT activation. We also summarize current information on interactions between signaling pathways, particularly STAT-Ras cross-talk and the relative importance of these two pathways in regulating the transcription of target genes

A mutant cell line defective in response to double-stranded RNA and in regulating basal expression of interferon-stimulated genes

Although much progress has been made in identifying the signaling pathways that mediate the initial responses to interferons (IFNs), much less is known about how IFN-stimulated genes (ISGs) are kept quiescent in untreated cells, how the response is sustained after the initial induction, and how ISG expression is down-regulated, even in the continued presence of IFN. We have used the cell sorter to isolate mutant cells with constitutively high ISG expression. A recessive mutant, P2.1, has higher constitutive ISG levels than the parental U4C cells, which do not respond to any IFN. Unexpectedly, P2.1 cells also are deficient in the expression of ISGs in response to double-stranded RNA (dsRNA). Electrophoretic mobility-shift assays revealed that the defect is upstream of the activation of the transcription factors NFκB and IFN regulatory factor 1. Analysis of the pivotal dsRNA-dependent serine/threonine kinase PKR revealed that the wild-type kinase is present and is activated normally in response to dsRNA in P2.1 cells. Together, these data suggest that the defect in P2.1 cells is either downstream of PKR or in a component of a distinct pathway that is involved both in activating multiple transcription factors in response to dsRNA and in regulating the basal expression of ISGs

Characterization of β-R1, a Gene That Is Selectively Induced by Interferon β (IFN-β) Compared with IFN-α

We report preliminary characterization of a gene designated beta-R1, which is selectively expressed in response to interferon beta (IFN-beta) compared with IFN-alpha. In human astrocytoma cells, beta-R1 was induced to an equivalent extent by 10 IU/mL IFN-beta or 2500 IU/mL IFN-alpha2. To address the mechanism of this differential response, we analyzed induction of the beta-R1 gene in fibrosarcoma cells and derivative mutant cells lacking components required for signaling by type I IFNs. beta-R1 was readily induced by IFN-beta in the parental 2fTGH cell line, but not by recombinant IFN-alpha2, IFN-alpha Con1, or a mixture of IFN-alpha subtypes. IFN-alpha8 induced beta-R1 weakly. beta-R1 was not induced by IFN-beta in mutant cell lines U2A, U3A, U4A, and U6A, which lack, respectively, p48, STAT1, JAK1, and STAT2. U5A cells, which lack the Ifnar 2.2 component of the IFN-alpha and -beta receptor, also failed to express beta-R1. U1A cells are partially responsive to IFN-beta and IFN-alpha8 but lacked beta-R1 expression, indicating that TYK2 protein is essential for induction of this gene. Taken together, these results suggest that the expression of beta-R1 in response to type I IFN requires IFN-stimulated gene factor 3 plus an additional component, which is more efficiently formed on induction by IFN-beta compared with IFN-alpha