It is important to know how aggregate economic growth index of poverty gives a measure of the rate of pro-poor or contraction was distributed according to initial levels growth consistent with the Watts index for the level of of living. In particular, to what extent can it be said that poverty. growth was "pro-poor?" There are problems with pastThe authors give examples using survey data for China methods of addressing this question, notably that the during the 1990s. Over 1990-99, the ordinary growth measures used are inconsistent with the properties that rate of household income per capita in China was 7 are considered desirable for a measure of the level of percent a year. The growth rate by quantile varied from poverty.3 percent for the poorest percentile to 11 percent for the Ravallion and Chen provide some new tools for richest, while the rate of pro-poor growth was around 4 assessing to what extent the aggregate growth process in percent. The pattern was reversed for a few years in the an economy is pro-poor. The key measurement tool is mid-1990s, when the rate of pro-poor growth rose to 10 the "growth incidence curve," which gives growth rates percent a year-above the ordinary growth rate of 8 by quantiles (such as percentiles) ranked by income.percent. Taking the area under this curve up to the headcount This paper-a product of Poverty, Development Research Group-is part of a larger effort in the group to improve the analytic tools used for monitoring poverty over time and studying the impacts of economywide changes. Copies of the paper are available free from the World Bank,

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The molecular mechanisms of angiogenesis in relation to adipose tissue metabolism remain poorly understood. Here, we show that exposure of mice to cold led to activation of angiogenesis in both white and brown adipose tissues. In the inguinal depot, cold exposure resulted in elevated expression levels of brown-fat-associated proteins, including uncoupling protein-1 (UCP1) and PGC-1alpha. Proangiogenic factors such as VEGF were upregulated, and endogenous angiogenesis inhibitors, including thrombospondin, were downregulated. In wild-type mice, the adipose tissues became hypoxic during cold exposure; in UCP1(-/-) mice, hypoxia did not occur, but, remarkably, the augmented angiogenesis was unaltered and was thus hypoxia independent. Intriguingly, VEGFR2 blockage abolished the cold-induced angiogenesis and significantly impaired nonshivering thermogenesis capacity. Unexpectedly, VEGFR1 blockage resulted in the opposite effects: increased adipose vascularity and nonshivering thermogenesis capacity. Our findings have conceptual implications concerning application of angiogenesis modulators for treatment of obesity and metabolic disorders.