Topics in Black American Philanthropy in the United States Since 1785

This document was part of the Multicultural Philanthropy Project, funded by the W.K. Kellogg Foundation. A series of fourteen guides examine the ways in which various gender, ethnic, cultural, religious and racial groups use their gifts of time, money, and talent. They reflect the ways giving and voluntarism are embedded in American life and challenge the notion that philanthropy is the exclusive province of elites. The guides include discussion topics, research questions, and literature overviews with annotated bibliographies. They were developed both to integrate the study of philanthropy into the curricula at colleges and universities, and to provide a tool to nonprofit professionals in the area of development and fundraising. Each volume provides background information on a selected community that will help practitioners work effectively with these groups. This guide documents the various ways in which blacks have practiced self-help starting with the formation in 1785 of the Free African Society, the first of many mutual aid societies established by free blacks in the United States. The author emphasizes the organizations and individuals who were significant to efforts to improve the black condition, while also analyzing the ideology that legitimized various philanthropic exercises. Colin Palmer considers both the successes and the failures and includes a look at those who sought to "redeem" Africa and Africans. The guide will be of particular use to those seeking to understand the long tradition of black philanthropy, self-help and other organizations, and how the history of these organizations reflects the struggles of a people to create and realize themselves. The guide may be used to identify sound building blocks for developing strategies for culturally sensitive and historically appropriate fundraising appeals. Information on key African American individuals and organizations is readily accessible

The transcription factor Zfx is required for tumorigenesis caused by Hedgehog pathway activation

The Hedgehog (Hh) signaling pathway regulates normal development and cell proliferation across the metazoa. Upon its aberrant activation, mammalian Hh signaling can also cause tumor formation. Hh-induced tumors can arise from different tissues and can be locally invasive but rarely metastatic or highly aggressive, as is the case with basal cell carcinoma (BCC) of the skin and the cerebellar tumor medulloblastoma (MB), respectively. Little is known about common cell-intrinsic factors that control the development of such diverse Hh-dependent tumors. The zinc-finger transcription factor Zfx is required for the self-renewal of several stem cell types in both mouse and human, but its role in malignant transformation remains controversial. We found that Zfx is variably required for the development of two distinct Hh-dependent tumors in vivo. Co-deletion of Zfx prevented BCC formation initiated by Hh pathway overactivation in the skin following deletion of the inhibitory receptor Ptch1. Co-deletion of Zfx also delayed development of Hh-dependent MB caused by Ptch1 deletion in vivo. In contrast, Zfx was dispensable for the development of the PTEN-dependent brain tumor glioblastoma, showing that a requirement for Zfx is not generalizable across all cancers. We used genome-wide expression and chromatin binding analysis in a human MB cell line to identify direct, evolutionarily conserved targets of Zfx. These targets included the Hh signal transducer Smoothened (Smo). Smo expression data from Zfx-deficient BCC and MB cells in vivo and in vitro suggest that Zfx may directly regulate Hh pathway activation in some cancers. We identified two additional conserved downstream targets of Zfx, Dis3L and Ube2j1, which were required for optimal growth of human MB cells in vitro. These results identify Zfx as a common cell-intrinsic regulator of diverse Hh-induced tumors. Further investigation of the requirement for Zfx and its conserved downstream target genes, such as Dis3L and Ube2j1, in in vivo models of Hh-dependent BCC and MB could lead to the identification of novel targetable molecules for therapies directed against these malignancies

Surface drag reduction and flow separation control in pelagic vertebrates, with implications for interpreting scale morphologies in fossil taxa

Living in water imposes severe constraints on the evolution of the vertebrate body. As a result of these constraints, numerous extant and extinct aquatic vertebrate groups evolved convergent osteological and soft-tissue adaptations. However, one important suite of adaptations is still poorly understood: dermal cover morphologies and how they influence surface fluid dynamics. This is especially true for fossil aquatic vertebrates where the soft tissue of the dermis is rarely preserved. Recent studies have suggested that the keeled scales of mosasaurids (pelagic lizards that lived during the Late Cretaceous) aided in surface frictional drag reduction in a manner analogous to the riblets on shark placoid scales. However, here we demonstrate that mosasaurid scales were over an order of magnitude too large to have this effect. More likely they increased the frictional drag of the body and may have played a role in controlling flow separation by acting as surface roughness that turbulated the boundary layer. Such a role could have reduced pressure drag and enhanced manoeuvrability. We caution those studying fossil aquatic vertebrates from positing the presence of surface drag reducing morphologies, because as we show herein, to be effective such features need to have a spacing of approximately 0.1?mm or less

Social cognition as causal inference: implications for common knowledge and autism

This chapter explores the idea that the need to establish common knowledge is one feature that makes social cognition stand apart in important ways from cognition in general. We develop this idea on the background of the claim that social cognition is nothing but a type of causal inference. We focus on autism as our test-case, and propose that a specific type of problem with common knowledge processing is implicated in challenges to social cognition in autism spectrum disorder (ASD). This problem has to do with the individual’s assessment of the reliability of messages that are passed between people as common knowledge emerges. The proposal is developed on the background of our own empirical studies and outlines different ways common knowledge might be comprised. We discuss what these issues may tell us about ASD, about the relation between social and non-social cognition, about social objects, and about the dynamics of social networks

The peroxisome proliferator activated receptor δ is required for the differentiation of THP-1 monocytic cells by phorbol ester

BACKGROUND: PPARδ (NR1C2) promotes lipid accumulation in human macrophages in vitro and has been implicated in the response of macrophages to vLDL. We have investigated the role of PPARδ in PMA-stimulated macrophage differentiation. The THP-1 monocytic cell line which displays macrophage like differentiation in response to phorbol esters was used as a model system. We manipulated the response to PMA using a potent synthetic agonist of PPARδ , compound F. THP-1 sub-lines that either over-expressed PPARδ protein, or expressed PPARδ anti-sense RNA were generated. We then explored the effects of these genetic modulations on the differentiation process. RESULTS: The PPARδ agonist, compound F, stimulated differentiation in the presence of sub-nanomolar concentrations of phorbol ester. Several markers of differentiation were induced by compound F in a synergistic fashion with phorbol ester, including CD68 and IL8. Over-expression of PPARδ also sensitised THP-1 cells to phorbol ester and correspondingly, inhibition of PPARδ by anti-sense RNA completely abolished this response. CONCLUSIONS: These data collectively demonstrate that PPARδ plays a fundamental role in mediating a subset of cellular effects of phorbol ester and supports observations from mouse knockout models that PPARδ is involved in macrophage-mediated inflammatory responses