Explore the vast range of titles available.

Fifty years after Oscar Lewis's famous depiction of five Mexican families caught in a \"culture of poverty,\" Caroline Moser tells a very different story of five neighborhood women and their families strategically accumulating assets to escape poverty in the Ecuadoran city of Guayaquil. InOrdinary Families, Extraordinary Lives, Moser shows how a more sophisticated understanding of the complexities of asset accumulation as well as poverty itself can help counter inaccurate stereotypes about global poverty. It provides invaluable insight into strategies that may help people in developing countries improve their wellbeing. The similar socioeconomic characteristics and economic circumstances of the Guayaquil families in 1978, when Moser began her research, set the stage for a natural experiment. By 2004, these circumstances varied widely. Moser captures the causes and consequences of these developments through economic data, anthropological narrative, and personal photos. She then places this compelling story within the broader context of political, economic, and spatial changes in Guayaquil and Ecuador. Moser describes how households in a Third World urban slum relentlessly and systematically fought to accumulate human, social, and financial capital assets. Her longitudinal account of their odyssey captures long-term trends and changes in perception that are missed in snapshot assessments. Chapters in this holistic story cover diverse issues such as housing and infrastructure, community mobilization and political negotiation, employment, family dynamics, violence, and emigration.

Latin America is both the world's most urbanized fastest developing regions, where the links between social exclusion, inequality and violence are clearly visible. The banal, ubiquitous nature of drug crime, robbery, gang and intra-family violence destabilizes countries' economies and harms their people and social structures. Encounters with Violence & Crime in Latin America explores the meaning of violence and insecurity in nine towns and cities in Columbia and Guatemala to create a framework of how and why daily violence takes place at the community level. It uses pioneering new methods of participatory urban appraisal to ask local people about their own perceptions of violence as mediated by family, gender, ethnicity and age. It develops a typology which distinguishes between the political, social, and economic violence that afflicts communities, and which assesses the costs of consequences of violence in terms of community cohesion and social capital. This gives voice to those whose daily lives and dominated by widespread aggression, and provides important new insights for researchers and policy-makers.

Aims/hypothesisIn the context of diabetes, the health benefit of antioxidant treatment has been widely debated. In this study, we investigated the effect of antioxidant treatment during the development of insulin resistance and hyperphagia in obesity and partial lipodystrophy.MethodsWe studied the role of antioxidants in the regulation of insulin resistance using the tamoxifen-inducible fat-specific insulin receptor knockout (iFIRKO) mouse model, which allowed us to analyse the antioxidant’s effect in a time-resolved manner. In addition, leptin-deficient ob/ob mice were used as a hyperphagic, chronically obese and diabetic mouse model to validate the beneficial effect of antioxidants on metabolism.ResultsAcute induction of insulin receptor knockout in adipocytes changed the substrate preference to fat before induction of a diabetic phenotype including hyperinsulinaemia and hyperglycaemia. In healthy chow-fed animals as well as in morbidly obese mice, this diabetic phase could be reversed within a few weeks. Furthermore, after the induction of insulin receptor knockout in mature adipocytes, iFIRKO mice were protected from subsequent obesity development through high-fat diet feeding. By genetic tracing we show that the persistent fat mass loss in mice after insulin receptor knockout in adipocytes is not caused by the depletion of adipocytes. Treatment of iFIRKO mice with antioxidants postponed and reduced hyperglycaemia by increasing insulin sensitivity. In ob/ob mice, antioxidants rescued both hyperglycaemia and hyperphagia.Conclusions/interpretationWe conclude that fat mass reduction through insulin resistance in adipocytes is not reversible. Furthermore, it seems unlikely that adipocytes undergo apoptosis during the process of extreme lipolysis, as a consequence of insulin resistance. Antioxidants have a beneficial health effect not only during the acute phase of diabetes development, but also in a temporary fashion once chronic obesity and diabetes have been established.

Natural remedies are used as standalone treatments or complementary to modern medicine to control type 2 diabetes. In Palau, the traditional leaf decoction of Phaleria nisidai (PNe) is selected to treat hyperglycemia and its efficacy has been supported by a small clinical trial. As part of a reverse pharmacology approach, we here investigated the anti-diabetic potential of PNe and its bioactive compounds to alleviate insulin resistance in diet-induced obese, male mice. Dietary supplementation with PNe improves insulin sensitivity and promotes glucose uptake into adipose depots. In vitro, PNe triggers glucose disposal into murine and human adipocytes by upregulating Glut1 expression through PKC-ERK1/2 signaling. To identify active constituents in PNe, we conducted bioactivity-guided fractionations and deciphered genkwanin flavone glycosides as bioactive principles. Moreover, we demonstrate that the aglycone genkwanin (GE) improves insulin resistance to a comparable extent to the anti-diabetic drug, metformin. Our findings present GE as promising glucoregulatory phytochemical that facilitates glucose uptake into adipocytes, thereby reducing systemic glucose load and enhancing insulin sensitivity. Here the authors show that genkwanin glycosides from Phaleria nisida i leaf extract improve glucose homeostasis by enhancing glucose uptake into adipose tissue, with effects comparable to metformin in a study with male mice with obesity and insulin resistance.

The current obesity epidemic and high prevalence of metabolic diseases necessitate efficacious and safe treatments. Brown adipose tissue in this context is a promising target with the potential to increase energy expenditure, however no pharmacological treatments activating brown adipose tissue are currently available. Here, we identify AXL receptor tyrosine kinase as a regulator of adipose function. Pharmacological and genetic inhibition of AXL enhance thermogenic capacity of brown and white adipocytes, in vitro and in vivo. Mechanistically, these effects are mediated through inhibition of PI3K/AKT/PDE signaling pathway, resulting in induction of nuclear FOXO1 localization and increased intracellular cAMP levels via PDE3/4 inhibition and subsequent stimulation of the PKA-ATF2 pathway. In line with this, both constitutive Axl deletion as well as inducible adipocyte-specific Axl deletion protect animals from diet-induced obesity concomitant with increases in energy expenditure. Based on these data, we propose AXL receptor as a target for the treatment of obesity. Brown adipose tissue is a promising target for the treatment of obesity with the potential to increase energy expenditure. Here, the authors use pharmacological and genetic approaches to block AXL receptor activation and show that its inhibition enhances brown adipocyte functionality and thermogenesis, leading to weight loss and metabolic improvements in mice.

Activation of thermogenic brown and beige adipocytes is considered as a strategy to improve metabolic control. Here, we identify GPR180 as a receptor regulating brown and beige adipocyte function and whole-body glucose homeostasis, whose expression in humans is associated with improved metabolic control. We demonstrate that GPR180 is not a GPCR but a component of the TGFβ signalling pathway and regulates the activity of the TGFβ receptor complex through SMAD3 phosphorylation. In addition, using genetic and pharmacological tools, we provide evidence that GPR180 is required to manifest Collagen triple helix repeat containing 1 (CTHRC1) action to regulate brown and beige adipocyte activity and glucose homeostasis. In this work, we show that CTHRC1/GPR180 signalling integrates into the TGFβ signalling as an alternative axis to fine-tune and achieve low-grade activation of the pathway to prevent pathophysiological response while contributing to control of glucose and energy metabolism. Activation of thermogenic adipocytes is a strategy to combat metabolic diseases. Here the authors report that GPR180 is a component of TGFβ signalling that promotes thermogenic adipocyte function and mediates the metabolic effects of the adipocyte-secreted factor CTHRC1, and contributes to the regulation of glucose and energy metabolism.

The papers in this volume discuss the strategies adopted by people to accumulate assets through migration, housing investments, natural resources management, and informal businesses and consider how an asset-based social policy could enable those strategies or help them overcome the constraints of an unfavorable institutional environment.

Biomaterials development for bone repair is currently hindered by the lack of physiologically relevant testing systems. Here we describe the novel use of a bi-directional perfusion bioreactor to support the long term culture of human bone marrow stromal cells (BMSCs) differentiated on polylactic co-glycolic acid (PLGA). Primary human BMSCs were seeded onto porous PLGA scaffolds and cultured in static vs. perfusion culture conditions for 21 days in osteogenic vs. control media. PLGA scaffolds were osteoconductive, supporting a mature osteogenic phenotype as shown by the upregulation of Runx2 and the early osteocyte marker E11. Perfusion culture enhanced the expression of osteogenic genes Osteocalcin and Osteopontin. Extracellular matrix deposition and mineralisation were spatially regulated within PLGA scaffolds in a donor dependant manner. This, together with the observed upregulation of Collagen type X suggested an environment permissive for the study of differentiation pathways associated with both intramembranous and endochondral ossification routes of bone healing. This culture system offers a platform to assess BMSC behavior on candidate biomaterials under physiologically relevant conditions. Use of this system may improve our understanding of the environmental cues orchestrating BMSC differentiation and enable fine tuning of biomaterial design as we develop tissue-engineered strategies for bone regeneration.

The Beijing Platform for Action prioritised gender mainstreaming as the mechanism to achieve gender equality. A decade later, policy makers and practitioners are debating whether this has succeeded or failed. This article aims to contribute to this debate by reviewing progress made to date, through a review of gender mainstreaming policies in international development institutions. Categorising progress into three stages - adoption of terminology, putting a policy into place, and implementation - the article argues that while most institutions have put gender mainstreaming policies in place, implementation remains inconsistent. Most important of all, the outcomes and impact of the implementation of gender mainstreaming in terms of gender equality remain largely unknown, with implications for the next decade's strategies. Reprinted by permission of Oxfam GB