ABSTRACT
In 1963, the United Nations Educational, Scientific, and Cultural Organization (UNESCO) published the first volume of its long-awaited cultural and scientific history of mankind. First announced in 1948, the History of Mankind was envisioned as a comprehensive, universal human history, from the evolution of Homo sapiens to the middle of the twentieth century. This article uses editorial conflicts over the site of the cradle of the human species to explore the position of scientific knowledge in world history writing and to examine tensions between different national traditions of expertise at a moment of political and scientific transition.
Subject(s)
United Nations , Humans , UNESCO , Educational StatusABSTRACT
Today, the most powerful research technique available for assigning chronometric age to human cultural objects is radiocarbon dating. Developed in the United States in the late 1940s by an alumnus of the Manhattan Project, radiocarbon dating measures the decay of the radioactive isotope carbon-14 (C14) in organic material, and calculates the time elapsed since the materials were removed from the life cycle. This paper traces the interdisciplinary collaboration between archaeology and radiochemistry that led to the successful development of radiocarbon dating in the early 1950s, following the movement of people and ideas from Willard Libby's Chicago radiocarbon laboratory to museums, universities and government labs in the United States, Australia, Denmark and New Zealand. I show how radiocarbon research built on existing technologies and networks in atomic chemistry and physics but was deeply shaped by its original private philanthropic funders and archaeologist users, and ultimately remained to the side of many contemporaneous Cold War scientific and military projects.
ABSTRACT
OBJECTIVE: We examined the relationship between the expression of thrombospondin (TSP)1, an antiangiogenic factor and regulator of transforming growth factor-beta activity, obesity, adipose inflammation, and insulin resistance. RESEARCH DESIGN AND METHODS: TSP1 gene expression was quantified in subcutaneous adipose tissue (SAT) of 86 nondiabetic subjects covering a wide range of BMI and insulin sensitivity, from visceral adipose (VAT) and SAT from 14 surgical patients and from 38 subjects with impaired glucose tolerance randomized to receive either pioglitazone or metformin for 10 weeks. An adipocyte culture system was also used to assess the effects of pioglitazone and coculture with macrophages on TSP1 gene expression. RESULTS: TSP1 mRNA was significantly associated with obesity (BMI) and insulin resistance (low insulin sensitivity index). Relatively strong positive associations were seen with markers of inflammation, including CD68, macrophage chemoattractant protein-1, and plasminogen activator inhibitor (PAI)-1 mRNA (r >/= 0.46, P = 0.001 for each), that remained significant after controlling for BMI and S(i). However, TSP1 mRNA was preferentially expressed in adipocyte fraction, whereas inflammatory markers predominated in stromal vascular fraction. Coculture of adipocytes and macrophages augmented TSP1 gene expression and secretion from both cell types. Pioglitazone (not metformin) treatment resulted in a 54% decrease (P < 0.04) in adipose TSP gene expression, as did in vitro pioglitazone treatment of adipocytes. CONCLUSIONS: TSP1 is a true adipokine that is highly expressed in obese, insulin-resistant subjects; is highly correlated with adipose inflammation; and is decreased by pioglitazone. TSP1 is an important link between adipocytes and macrophage-driven adipose tissue inflammation and may mediate the elevation of PAI-1 that promotes a prothrombotic state.
