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The millennium declaration ratified in 2000 by the 189 member states of the United Nations, committed rich and developing countries to work in partnership to achieve a set of critical development outcomes. Those commitments are embodied in the eight Millennium Development Goals (MDGs) for 2015, supported by 18 quantified targets and 60 indicators measuring progress since 1990. Progress has been uneven and many countries will not reach the targets set for 2015, but others have met or exceeded the targets, improving the lives of hundreds of millions of people. Standards of living vary substantially across the globe. Comparing income or consumption or poverty levels among countries requires a common unit of measurement. Exchange rates reflect the relative value of currencies as traded in the market. Purchasing power parities take into account differences in price levels. Both have important roles in measuring the size of economies. To measure differences in welfare, comparisons of income among economies should take into account differences in domestic price levels. Economic growth reduces poverty. As a result, fast-growing developing countries are closing the income gap with high-income economies. But growth must be sustained over the long term and the gains from economic growth must be shared to make lasting improvements in the wellbeing of all people. In addition to inequality of incomes, inequality of opportunities is a challenge facing most developing countries.

Published in association with Harper Collins, the completely revised and updated third edition of the Atlas of Global Development vividly illustrates the key development challenges facing our world today. 'This is an excellent, up-to-date source book which will be invaluable for students of, and staff teaching, higher levels of geography ... a clear, concise, easily-accessible and well-illustrated volume.' - Geographical Association, United Kingdom.

COMPLETELY REVISED AND UPDATED Published in association with Harper Collins, the completely revised and updated fourth edition of the Atlas of Global Development is a comprehensive guide to the most critical issues facing our changing world today. A visual guide to global issues -easy-to-read graphical presentation with every topic presented by colorful world maps, tables, graphs, and photographs Topics that are shaping our world - key development indicators, from poverty, population growth, and food production to climate change, foreign direct investment, and international trade The latest, authoritative statistics - from the World Bank?s World Development Indicators database The Atlas comes with an interactive companion online atlas, the new World Bank e-Atlas of Global Development, and new to this edition, a companion mobile app. 'This is an excellent, up-to-date source book which will be invaluable for students of, and staff teaching, higher levels of geography ... a clear, concise, easily-accessible and well-illustrated volume.' - Geographical Association, United Kingdom

The World Bank Atlas is changing its publication cycle. Beginning in 2004, the World Bank Atlas will publish in September each year. The World Bank Atlas (36th edition) is the edition following the World Bank Atlas 2003. The World Bank Atlas (36th edition) vividly illustrates the key development challenges in the world today. It provides easy-to read, colorful world maps, tables, and graphs highlighting key social, economic, and environmental data for 208 countries. Drawing on data from World Development Indicators, the Atlas brings to life cross-country comparisons of social indicators like life expectancy, infant mortality, safe water, population below the poverty line and energy efficiency, as well as basic economic indicators like income growth, income per person, private capital and aid flows.

Urban health indicator (UHI) tools provide evidence about the health impacts of the physical urban environment which can be used in built environment policy and decision-making. Where UHI tools provide data at the neighborhood (and lower) scale they can provide valuable information about health inequalities and environmental deprivation. This review performs a census of UHI tools and explores their nature and characteristics (including how they represent, simplify or address complex systems) to increase understanding of their potential use by municipal built environment policy and decision-makers. We searched seven bibliographic databases, four key journals and six practitioner websites and conducted Google searches between January 27, 2016 and February 24, 2016 for UHI tools. We extracted data from primary studies and online indicator systems. We included 198 documents which identified 145 UHI tools comprising 8006 indicators, from which we developed a taxonomy. Our taxonomy classifies the significant diversity of UHI tools with respect to topic, spatial scale, format, scope and purpose. The proportions of UHI tools which measure data at the neighborhood and lower scale, and present data via interactive maps, have both increased over time. This is particularly relevant to built environment policy and decision-makers, reflects growing analytical capability and offers the potential for improved understanding of the complexity of influences on urban health (an aspect noted as a particular challenge by some indicator producers). The relation between urban health indicators and health impacts attributable to modifiable environmental characteristics is often indirect. Furthermore, the use of UHI tools in policy and decision-making appears to be limited, thus raising questions about the continued development of such tools by multiple organisations duplicating scarce resources. Further research is needed to understand the requirements of built environment policy and decision-makers, public health professionals and local communities regarding the form and presentation of indicators which support their varied objectives.

Hypoactive BRAF mutants bind more tightly than wild type to the upstream regulator RAS, thus amplifying to amplify ERK signalling; tumours expressing these mutants require coexistent mechanisms for RAS activation to grow and are sensitive to their inhibition. Inactive BRAF mutants in cancer Mutant alleles of the kinase BRAF have been identified in human tumours, some of which have activated catalytic functions, whereas others have impaired or absent kinase activity. Here Neal Rosen and colleagues have characterized the less-understood hypoactive BRAF mutants. They find that these mutants bind more tightly to the upstream regulator RAS in order to amplify signalling and require coexistent mechanisms for RAS activation in the tumour in order to function. The mechanistic action of these hypoactive BRAF mutants is different to that of the activated mutants and dictates their sensitivity to therapeutic inhibitors of the pathway. Elsewhere in this issue, David Santamaria and colleagues show that kinase-inactive BRAF mutants can initiate the development of lung adenocarcinoma in mice. Approximately 200 BRAF mutant alleles have been identified in human tumours. Activating BRAF mutants cause feedback inhibition of GTP-bound RAS, are RAS-independent and signal either as active monomers (class 1) or constitutively active dimers (class 2) 1 . Here we characterize a third class of BRAF mutants—those that have impaired kinase activity or are kinase-dead. These mutants are sensitive to ERK-mediated feedback and their activation of signalling is RAS-dependent. The mutants bind more tightly than wild-type BRAF to RAS–GTP, and their binding to and activation of wild-type CRAF is enhanced, leading to increased ERK signalling. The model suggests that dysregulation of signalling by these mutants in tumours requires coexistent mechanisms for maintaining RAS activation despite ERK-dependent feedback. Consistent with this hypothesis, melanomas with these class 3 BRAF mutations also harbour RAS mutations or NF1 deletions. By contrast, in lung and colorectal cancers with class 3 BRAF mutants, RAS is typically activated by receptor tyrosine kinase signalling. These tumours are sensitive to the inhibition of RAS activation by inhibitors of receptor tyrosine kinases. We have thus defined three distinct functional classes of BRAF mutants in human tumours. The mutants activate ERK signalling by different mechanisms that dictate their sensitivity to therapeutic inhibitors of the pathway.

An artificial recombination locus, Polylox , that can generate hundreds of thousands of individual barcodes is used to trace the fates of haematopoietic stem cells in mice. Barcode tracking blood stem cells Transplantation-based assays of haematopoietic stem cells (HSCs) and progenitors isolated on the basis of the expression of their surface markers have inferred that the haematopoietic lineage follows a tree-like structure that starts from a long-term multipotent HSC at its base and splits into a few major branches. However, recent data question the existence of this structure, instead supporting the idea that the blood lineage is sustained by several fate-restricted progenitors. Hans-Reimer Rodewald and colleagues have developed a DNA recombination locus based on the Cre– loxP system that can tag single cells using several hundred thousand barcodes. They introduce the labelling in mouse embryos and track HSCs during their life. Surprisingly, the adult HSC compartment is a mosaic of HSC clones derived from embryos and contributes with different proportion to blood lineage, some multilineage and others of restricted fates, according to a pattern that is consistent within clones. However, they define an early split of fate between myeloid erythroid and lymphocyte development which agrees with the tree-like structure. Developmental deconvolution of complex organs and tissues at the level of individual cells remains challenging. Non-invasive genetic fate mapping 1 has been widely used, but the low number of distinct fluorescent marker proteins limits its resolution. Much higher numbers of cell markers have been generated using viral integration sites 2 , viral barcodes 3 , and strategies based on transposons 4 and CRISPR–Cas9 genome editing 5 ; however, temporal and tissue-specific induction of barcodes in situ has not been achieved. Here we report the development of an artificial DNA recombination locus (termed Polylox ) that enables broadly applicable endogenous barcoding based on the Cre– loxP recombination system 6 , 7 . Polylox recombination in situ reaches a practical diversity of several hundred thousand barcodes, allowing tagging of single cells. We have used this experimental system, combined with fate mapping, to assess haematopoietic stem cell (HSC) fates in vivo . Classical models of haematopoietic lineage specification assume a tree with few major branches. More recently, driven in part by the development of more efficient single-cell assays and improved transplantation efficiencies, different models have been proposed, in which unilineage priming may occur in mice and humans at the level of HSCs 8 , 9 , 10 . We have introduced barcodes into HSC progenitors in embryonic mice, and found that the adult HSC compartment is a mosaic of embryo-derived HSC clones, some of which are unexpectedly large. Most HSC clones gave rise to multilineage or oligolineage fates, arguing against unilineage priming, and suggesting coherent usage of the potential of cells in a clone. The spreading of barcodes, both after induction in embryos and in adult mice, revealed a basic split between common myeloid–erythroid development and common lymphocyte development, supporting the long-held but contested view of a tree-like haematopoietic structure.