No-go for Partially Massless Spin-2 Yang-Mills

There are various no-go results forbidding self-interactions for a single partially massless spin-2 field. Given the photon-like structure of the linear partially massless field, it is natural to ask whether a multiplet of such fields can interact under an internal Yang-Mills like extension of the partially massless symmetry. We give two arguments that such a partially massless Yang-Mills theory does not exist. The first is that there is no Yang-Mills like non-abelian deformation of the partially massless symmetry, and the second is that cubic vertices with the appropriate structure constants do not exist.Comment: 18 pages. v2 small corrections and ref

Die Kämpfe únd schláchten—the struggles and battles of innate-like effector T lymphocytes with microbes

The large majority of lymphocytes belong to the adaptive immune system, which are made up of B2 B cells and the αβ T cells; these are the effectors in an adaptive immune response. A multitudinous group of lymphoid lineage cells does not fit the conventional lymphocyte paradigm; it is the unconventional lymphocytes. Unconventional lymphocytes—here called innate/innate-like lymphocytes, include those that express rearranged antigen receptor genes and those that do not. Even though the innate/innate-like lymphocytes express rearranged, adaptive antigen-specific receptors, they behave like innate immune cells, which allows them to integrate sensory signals from the innate immune system and relay that umwelt to downstream innate and adaptive effector responses. Here, we review natural killer T cells and mucosal-associated invariant T cells—two prototypic innate-like T lymphocytes, which sense their local environment and relay that umwelt to downstream innate and adaptive effector cells to actuate an appropriate host response that confers immunity to infectious agents

Imaging and Imagining Taiwan: Identity representation and cultural politics

Since the 1990s the issue of identity has been one of the most prominent and hotly-debated topics in Taiwan Studies. A rich corpus of literature has been produced in various fields in the attempt to address this problematic issue, examining questions of Taiwanese identity from political, social and cultural perspectives. Imaging and Imagining Taiwan takes a fresh approach to this important topic, examining Taiwanese identity from a visual perspective and exploring the ways in which the island is presented and imagined. In contrast to those studies that seek to address the issue of identity from an essentialist position, Imaging and Imagining Taiwan offers a new contextualization of identity, investigating the ways in which Taiwan has been represented in films, fine art, advertising, sport, and social spaces at different periods in history. Covering a diverse range of topics, the book aims to capture the fluidity, changeability, fragmentation and dynamism of Taiwanese identity as an imaginary and encompassing whole. Through seven case studies the book focuses on the ways in which Taiwan is represented, how this relates to identity politics, and how the island is imaged and imagined visually, socially, and symbolically. The essays comprising this collection are grouped into three sections, each of which focuses on a particular approach to the topic of Taiwanese identity. The first of these —Colonial Representation —deals with colonial subjectivity and traumatic experience. The second, entitled Imaging Difference, examines cultural practices in film, TV advertisements and fine art, and explores the boundaries between the inside and the outside, the difference marked by the process of othering, and the anxiety and alienation of the excluded. The third section—Identity and Place—focuses on the relationship between identity and the social construction of place, and examines the role of place-making in the new Taiwanese nation-building process. Interrogating the complex issue of Taiwanese identity from various standpoints, the seven contributors write from a range of disciplinary backgrounds (Literature, History, Film Studies, Linguistics, Anthropology and Cultural Studies) and geographical contexts (Taiwan, Europe and America). This combination of fresh perspectives and a range of disciplinary approaches offers a set of diverse yet complementary insights into how Taiwan has been envisioned and imagined, and how the Taiwanese have positioned and identified themselves at different times. By combining different themes and disciplinary approaches together in one publication, Imaging and Imagining Taiwan brings both nuance and depth to the discussion of the representation of Taiwanese identity. The book articulates and examines the complexity of identity, avoiding essentialist approaches to the topic, instead illustrating identity's multi-faceted nature and dynamic messiness. Thus, the book argues, the politics of identity is not only a politics of representation, but also a politics of positioning, whereby identity is formulated both by the construction of sameness and the inscription of difference. The interdisciplinary approach adopted by this book makes the discussion of Taiwanese identity of interest to those both studying and working in a range of subject disciplines, not limited to Taiwan Studies, but also in History, Film, Linguistics, Literary Studies, Nationalism Studies, and Urban Studies

Interventions for Challenging Behaviours of Students with Autism Spectrum Disorders and Developmental Disabilities: A Synthesis Paper

This synthesis paper summarizes research literature addressing challenging be-haviours in children and youth with autism spectrum disorders and developmental disabilities in school settings. We conducted a comprehensive literature review to identify relevant peer-reviewed articles published between the years 2000 and 2011. The methodological quality of all studies was screened following a stan-dard quality assessment checklist. Intervention effects were assessed quantitatively. Results of quality analysis and intervention effectiveness were in-tegrated to identify interventions with strong support and evidence of effectiveness. We discuss results in terms of implications for intervention choice and implementation in school settings, limitations, and directions for future re-search

Opposing Regulation of the EGF Receptor: A Molecular Switch Controlling Cytomegalovirus Latency and Replication

Herpesviruses persist indefinitely in their host through complex and poorly defined interactions that mediate latent, chronic or productive states of infection. Human cytomegalovirus (CMV or HCMV), a ubiquitous β-herpesvirus, coordinates the expression of two viral genes, UL135 and UL138, which have opposing roles in regulating viral replication. UL135 promotes reactivation from latency and virus replication, in part, by overcoming replication-suppressive effects of UL138. The mechanism by which UL135 and UL138 oppose one another is not known. We identified viral and host proteins interacting with UL138 protein (pUL138) to begin to define the mechanisms by which pUL135 and pUL138 function. We show that pUL135 and pUL138 regulate the viral cycle by targeting that same receptor tyrosine kinase (RTK) epidermal growth factor receptor (EGFR). EGFR is a major homeostatic regulator involved in cellular proliferation, differentiation, and survival, making it an ideal target for viral manipulation during infection. pUL135 promotes internalization and turnover of EGFR from the cell surface, whereas pUL138 preserves surface expression and activation of EGFR. We show that activated EGFR is sequestered within the infection-induced, juxtanuclear viral assembly compartment and is unresponsive to stress. Intriguingly, these findings suggest that CMV insulates active EGFR in the cell and that pUL135 and pUL138 function to fine-tune EGFR levels at the cell surface to allow the infected cell to respond to extracellular cues. Consistent with the role of pUL135 in promoting replication, inhibition of EGFR or the downstream phosphoinositide 3-kinase (PI3K) favors reactivation from latency and replication. We propose a model whereby pUL135 and pUL138 together with EGFR comprise a molecular switch that regulates states of latency and replication in HCMV infection by regulating EGFR trafficking to fine tune EGFR signaling

Artemisinin-based combination therapy in pregnant women in Zambia: efficacy, safety and risk of recurrent malaria.

BACKGROUND: In Zambia, malaria is one of the leading causes of morbidity and mortality, especially among under five children and pregnant women. For the latter, the World Health Organization recommends the use of artemisinin-based combination therapy (ACT) in the second and third trimester of pregnancy. In a context of limited information on ACT, the safety and efficacy of three combinations, namely artemether-lumefantrine (AL), mefloquine-artesunate (MQAS) and dihydroartemisinin-piperaquine (DHAPQ) were assessed in pregnant women with malaria. METHODS: The trial was carried out between July 2010 and August 2013 in Nchelenge district, Luapula Province, an area of high transmission, as part of a multi-centre trial. Women in the second or third trimester of pregnancy and with malaria were recruited and randomized to one of the three study arms. Women were actively followed up for 63 days, and then at delivery and 1 year post-delivery. RESULTS: Nine hundred pregnant women were included, 300 per arm. PCR-adjusted treatment failure was 4.7% (12/258) (95% CI 2.7-8.0) for AL, 1.3% (3/235) (95% CI 0.4-3.7) for MQAS and 0.8% (2/236) (95% CI 0.2-3.0) for DHAPQ, with significant risk difference between AL and DHAPQ (p = 0.01) and between AL and MQAS (p = 0.03) treatments. Re-infections during follow up were more frequent in the AL (HR: 4.71; 95% CI 3.10-7.2; p < 0.01) and MQAS (HR: 1.59; 95% CI 1.02-2.46; p = 0.04) arms compared to the DHAPQ arm. PCR-adjusted treatment failure was significantly associated with women under 20 years [Hazard Ratio (HR) 5.35 (95% CI 1.07-26.73; p = 0.04)] and higher malaria parasite density [3.23 (95% CI 1.03-10.10; p = 0.04)], and still women under 20 years [1.78, (95% CI 1.26-2.52; p < 0.01)] had a significantly higher risk of re-infection. The three treatments were generally well tolerated. Dizziness, nausea, vomiting, headache and asthenia as adverse events (AEs) were more common in MQAS than in AL or DHAPQ (p < 0.001). Birth outcomes were not significantly different between treatment arms. CONCLUSION: As new infections can be prevented by a long acting partner drug to the artemisinins, DHAPQ should be preferred in places as Nchelenge district where transmission is intense while in areas of low transmission intensity AL or MQAS may be used

Nur77 controls tolerance induction, terminal differentiation, and effector functions in semi-invariant natural killer T cells

Semi-invariant natural killer T (iNKT) cells are self-reactive lymphocytes, yet how this lineage attains self-tolerance remains unknown. iNKT cells constitutively express high levels of Nr4a1-encoded Nur77, a transcription factor that integrates signal strength downstream of the T cell receptor (TCR) within activated thymocytes and peripheral T cells. The function of Nur77 in iNKT cells is unknown. Here we report that sustained Nur77 overexpression (Nur77^(tg)) in mouse thymocytes abrogates iNKT cell development. Introgression of a rearranged Vα14-Jα18 TCR-α chain gene into the Nur77^(tg) (Nur77^(tg);Vα14^(tg)) mouse rescued iNKT cell development up to the early precursor stage, stage 0. iNKT cells in bone marrow chimeras that reconstituted thymic cellularity developed beyond stage 0 precursors and yielded IL-4–producing NKT2 cell subset but not IFN-γ–producing NKT1 cell subset. Nonetheless, the developing thymic iNKT cells that emerged in these chimeras expressed the exhaustion marker PD1 and responded poorly to a strong glycolipid agonist. Thus, Nur77 integrates signals emanating from the TCR to control thymic iNKT cell tolerance induction, terminal differentiation, and effector functions

Nur77 controls tolerance induction, terminal differentiation, and effector functions in semi-invariant natural killer T cells

Semi-invariant natural killer T (iNKT) cells are self-reactive lymphocytes, yet how this lineage attains self-tolerance remains unknown. iNKT cells constitutively express high levels of Nr4a1-encoded Nur77, a transcription factor that integrates signal strength downstream of the T cell receptor (TCR) within activated thymocytes and peripheral T cells. The function of Nur77 in iNKT cells is unknown. Here we report that sustained Nur77 overexpression (Nur77^(tg)) in mouse thymocytes abrogates iNKT cell development. Introgression of a rearranged Vα14-Jα18 TCR-α chain gene into the Nur77^(tg) (Nur77^(tg);Vα14^(tg)) mouse rescued iNKT cell development up to the early precursor stage, stage 0. iNKT cells in bone marrow chimeras that reconstituted thymic cellularity developed beyond stage 0 precursors and yielded IL-4–producing NKT2 cell subset but not IFN-γ–producing NKT1 cell subset. Nonetheless, the developing thymic iNKT cells that emerged in these chimeras expressed the exhaustion marker PD1 and responded poorly to a strong glycolipid agonist. Thus, Nur77 integrates signals emanating from the TCR to control thymic iNKT cell tolerance induction, terminal differentiation, and effector functions