How to Restore Long-term Prosperity in the United States and Overcome the Contained Depression of the 1990s

Special Report of the Institute

HIV-infected cells are major inducers of plasmacytoid dendritic cell interferon production, maturation, and migration

AbstractPlasmacytoid dendritic cells (PDC), natural type-1 interferon (IFN) producing cells, could play a role in the innate anti-HIV immune response. Previous reports indicated that PDC IFN production is induced by HIV. Our results show a more robust IFN induction when purified PDC (>95%) were exposed to HIV-infected cells. This effect was not observed with non-viable cells, DNA, and RNA extracted from infected cells, and viral proteins. The response was blocked by anti-CD4 and neutralizing anti-gp120 antibodies as well as soluble CD4. IFN induction by HIV-infected cells was also prevented by low-dose chloroquine, which inhibits endosomal acidification. PDC IFN release resulted in reduced HIV production by infected CD4+ cells, supporting an anti-HIV activity of PDC. Stimulated CD4+ cells induced PDC activation and maturation; markers for PDC migration (CCR7) were enhanced by HIV-infected CD4+ cells only. This latter finding could explain the decline in circulating PDC in HIV-infected individuals

Sonographically Guided Popliteus Tendon Sheath Injection

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/135538/1/jum2010295775.pd

The spread, treatment, and prevention of HIV-1: evolution of a global pandemic

The most up-to-date estimates demonstrate very heterogeneous spread of HIV-1, and more than 30 million people are now living with HIV-1 infection, most of them in sub-Saharan Africa. The efficiency of transmission of HIV-1 depends primarily on the concentration of the virus in the infectious host. Although treatment with antiviral agents has proven a very effective way to improve the health and survival of infected individuals, as we discuss here, the epidemic will continue to grow unless greatly improved prevention strategies can be developed and implemented. No prophylactic vaccine is on the horizon. However, several behavioral and structural strategies have made a difference — male circumcision provides substantial protection from sexually transmitted diseases, including HIV-1, and the application of antiretroviral agents for prevention holds great promise

Whose personal is more political? Experience in contemporary feminist politics

Whose personal is more political? This paper rethinks the role of experience in contemporary feminism, arguing that it can operate as a form of capital within abstracted and decontextualised debates which entrench existing power relations. Although experiential epistemologies are crucial to progressive feminist thought and action, in a neoliberal context in which the personal and emotional is commodified powerful groups can mobilise traumatic narratives to gain political advantage. Through case study analysis this paper shows how privileged feminists, speaking for others and sometimes for themselves, use experience to generate emotion and justify particular agendas, silencing critics who are often from more marginalised social positions. The use of the experiential as capital both reflects and perpetuates the neoliberal invisibilisation of structural dynamics: it situates all experiences as equal, and in the process fortifies existing inequalities. This competitive discursive field is polarising, and creates selective empathies through which we tend to discredit others¹ realities instead of engaging with their politics. However, I am not arguing for a renunciation of the politics of experience: instead, I ask that we resist its commodification and respect varied narratives while situating them in a structural frame

Neuroinflammation, Mast Cells, and Glia: Dangerous Liaisons

The perspective of neuroinflammation as an epiphenomenon following neuron damage is being replaced by the awareness of glia and their importance in neural functions and disorders. Systemic inflammation generates signals that communicate with the brain and leads to changes in metabolism and behavior, with microglia assuming a pro-inflammatory phenotype. Identification of potential peripheral-to-central cellular links is thus a critical step in designing effective therapeutics. Mast cells may fulfill such a role. These resident immune cells are found close to and within peripheral nerves and in brain parenchyma/meninges, where they exercise a key role in orchestrating the inflammatory process from initiation through chronic activation. Mast cells and glia engage in crosstalk that contributes to accelerate disease progression; such interactions become exaggerated with aging and increased cell sensitivity to stress. Emerging evidence for oligodendrocytes, independent of myelin and support of axonal integrity, points to their having strong immune functions, innate immune receptor expression, and production/response to chemokines and cytokines that modulate immune responses in the central nervous system while engaging in crosstalk with microglia and astrocytes. In this review, we summarize the findings related to our understanding of the biology and cellular signaling mechanisms of neuroinflammation, with emphasis on mast cell-glia interactions