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,

No abstract

No abstract

The Policy Research Working Paper Series disseminates the findings of work in progress to encourage the exchange of ideas about development issues. An objective of the series is to get the findings out quickly, even if the presentations are less than fully polished. The papers carry the names of the authors and should be cited accordingly. The findings, interpretations, and conclusions expressed in this paper are entirely those of the authors. They do not necessarily represent the views of the International Bank for Reconstruction and Development/World Bank and its affiliated organizations, or those of the Executive Directors of the World Bank or the governments they represent.

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.

No abstract

We find that one-quarter of the world's consumption poor live in urban areas

In this work, we constructed a Collagen I-Matrigel composite extracellular matrix (ECM). The composite ECM was used to determine the influence of the local collagen fiber orientation on the collective intravasation ability of tumor cells. We found that the local fiber alignment enhanced cell-ECM interactions. Specifically, metastatic MDA-MB-231 breast cancer cells followed the local fiber alignment direction during the intravasation into rigid Matrigel (∼10 mg/mL protein concentration).M etastasis is a lethal milestone in cancer: Cells escape from the confinement of primary tumor sites (intravasation), invade tissues as well as the lymphatic and vascular systems, and finally colonize (extravasation) distant sites. It has been estimated that less than 1% of tumor cells undergo this process, but metastasis contributes to more than 90% of cancerrelated deaths (1, 2). Metastasis involves both genetic and epigenetic alternation of tumor cells, as well as external biochemical and biophysical microenvironments (3-5). Pathology studies suggest that metastatic tumor cells exhibit highly branched morphologies and distinct aligned registration with aligned extracellular matrix (ECM) during metastatic tumor progression (4, 5).We address three important questions concerning metastasis. (i) Can we build in vitro complex ECM structures with heterogeneously oriented collagen fibers and basement membrane components to mimic the cancer cell intravasation process? (ii) How does aligned collagen influence cell intravasation into/ through the basement membrane before entering vessels? (iii) After cell detachment from the primary tumor site, how does a heterogeneous ECM with a varying degree of local fiber alignment influence cell intravasation and subsequent penetration into the basement membrane during their intravasation process? The major obstacle to addressing these questions is the difficulty in constructing both an in vitro 3D microenvironment to mimic the above process and flexible controls of the environmental parameters, such as fiber orientations in a complex collagen/Matrigel composite, nutrition, oxygen, drug concentrations, etc.In breast cancer metastasis, cancer cells are believed to reorganize and progress through the interstitial ECM matrix, break through the basement membrane, and enter blood vessels or lymphatic capillaries (6-10). Fig. 1C presents a schematic illustration of the intravasation process in metastasis. Tumor-associated collagen signatures (TACS), basically environmentally elevated collagen density and collagen fiber reorganization, are used to stage mammary carcinoma tumor progression levels (6, 11-13). Fig. 1 presents hematoxylin/eosin (H&E)-stained biopsy slices of breast cancer imaged by second harmonic generation (SHG) under a two-photon confocal microscopy (A1R MP; Nikon) (detailed information provided in SI Appendix, SI Text) (6, 14, 15). Fig. 1 A, 1-3 shows the stained human invasive ductal carcinoma tumor at grade I. In the enlarged figures (Fig. 1 A, 2 and 3), the cells have well-defined bord...