Neighborhood decline and the economic crisis : an introduction

Some of Maarten van Ham’s time on this project has received funding from the European Research Council under the European Union's Seventh Framework Programme (FP/2007-2013) / ERC Grant Agreement n. 615159 (ERC Consolidator Grant DEPRIVEDHOODS, Socio-spatial inequality, deprived neighbourhoods, and neighbourhood effects) and from the Marie Curie programme under the European Union's Seventh Framework Programme (FP/2007-2013) / Career Integration Grant n. PCIG10-GA-2011-303728 (CIG Grant NBHCHOICE, Neighbourhood choice, neighbourhood sorting, and neighbourhood effects), Platform31 (The Netherlands).Urban neighborhoods are still important in the lives of its residents. Therefore, it is important to find out how the recent global financial and economic crisis affects these neighborhoods. Which types of neighborhoods and which residents suffer more than others? This introduction provides an overview of the papers in this special feature that focus on this question. It concludes with the statement that governments should specifically pay attention to the poor neighborhoods and the people living there, because here the effects of the crisis are very prominent and in many cases probably long-lasting.PostprintPeer reviewe

Neighborhood Decline and the Economic Crisis

Neighborhood decline is a complex and multidimensional process. National and regional variation in economic and political structures (including variety in national welfare state arrangements), combined with differences in neighborhood history, development and population composition, makes it extremely difficult to identify a unilateral process of neighborhood decline over time. Some scholars have tried to develop all-encompassing models to explain neighborhood decline; others have studied more deeply the relevance of a limited number of factors and developments in processes of decline. The literature has paid little attention to the influence of economic development on neighborhood development, and surprisingly, few studies have focused on the effects of the economic crisis on urban neighborhoods. The recent global economic and financial crisis affected many European and North-American cities in terms of growing unemployment levels and rising poverty in concentrated areas. At the same time, urban investments such as urban restructuring and neighborhood improvement programs have decreased, or come to a halt altogether. By reviewing existing literature, this paper aims to contribute to an understanding of neighborhood decline in light of the economic crisis. By formulating ten hypotheses about the ways in which the economic crisis might interact with processes of neighborhood decline, this paper aims to push the debate on neighborhood decline forward and calls for more contextualized research on neighborhood change. We will highlight challenges for future research and point to factors that need to be taken into consideration in a post-crisis society

The Global Financial Crisis and neighborhood decline

The Global Financial Crisis (GFC), which started in 2008, has had a major impact on many Western European and North American countries. In the years preceding the crisis, many countries in the Global North experienced rising house prices, accompanied by an expansion of mortgage financing (Wachter, 2015). As the financial market has become increasingly global, the collapse of the subprime mortgage market and house price bubble in the United States (US) has had repercussions on a global scale (Martin, 2011). While there were significant differences between impacted countries in the timing and macroeconomic processes underlying the GFC, the characteristics of the subsequent economic recession have been similar: stagnating economic growth, a sovereign debt crisis, and rising unemployment (Aalbers, 2015). Many governments have responded to the declining economy and growing unemployment levels with the implementation of major budget cuts for social provisions (Peck, 2012). This has contributed to both relative and absolute growth in the number of economically disadvantaged households and has exacerbated poverty on both sides of the Atlantic. While the average income of the top 10% of the populations of OECD countries was essentially unaffected by the crisis, the average income of households in the lowest income decile experienced an annual decline of 2% between 2007 and 2010 (OECD, 2013a). In many countries, the GFC has also had a major impact on the housing market, evidenced by a large drop in home prices and declining sales of both existing and new-build housing (Van Der Heijden et al., 2011). Today, many countries are slowly recovering from the first shocks of the GFC and the economic recession that followed. However, in many Southern European countries, unemployment rates continue to be very high and, although unemployment is declining in places like the United States and Germany, long-term unemployment appears to be a persistent problem in many countries (OECD, 2014; Shierholz, 2014). Similarly, despite graudual stock market recoveries and some modest increases in house prices, repercussions from the GFC and economic recession persist in all countries. In many countries, the GFC has had predictable effects on the supply side of the housing market - the willingness of banks to lend money to prospective owners has generally declined. In some countries, investors in real estate became more selective, avoiding projects with too much risk; in the United States, in contrast, investors of another ilk have bought large numbers of foreclosed, real estate owned (REO) properties with the main goal of making a profit (e.g. Mallach, 2010b). Regeneration and restructuring initiatives have been put on hold throughout Western Europe (Boelhouwer & Priemus, 2014; Raco & Tasan-Kok, 2009; Schwartz, 2011). While some governments, such as the United Kingdom and the Netherlands, implemented stimulus programs to generate more (affordable) housing in the years after the crisis, recent budget cuts have put an end to these programs (Scanlon & Elsinga, 2014; Schwartz, 2011). The demand side of the housing market has also changed. Banks have tightened lending terms, making it more difficult for many households to obtain a mortgage (Goodman et al., 2015). As a result, there is more demand for private rentals and social or public housing. The GFC has affected employment on both sides of the Atlantic, in terms of either high unemployment levels or a shift toward more casualized labor contracts such as zero hour or temporary employment contracts (Aalbers, 2015; Puno & Thomas, 2010). This has led to financial strain and housing affordability problems for many households (JCHS, 2015). In the United States, households that are behind on their mortgage payments, and that are unable to obtain a mortgage modification with their lender, are faced with displacement due to foreclosure. This results in a large group of residents with badly damaged credit ratings who are in search of post-foreclosure housing in nearby areas (Martin, 2012). In other countries where the option of foreclosure is often not available, households that are unable to pay their rent or mortgage often have to move to cheaper dwellings and less attractive neighborhoods, while others have to stay put, because moving is too expensive or alternatives are not available, or because negative equity makes it impossible for them to move. All of these developments have contributed to rising inequality in the Global North, particularly in terms of income and housing (e.g. Immervoll et al., 2011; Bellman & Gerner, 2011). The GFC therefore raises questions about the future development of neighborhoods, especially because inequality tends to have specific spatial outcomes including increased segregation, increased spatial concentrations of low-income groups, and negative neighborhood effects (e.g., European Commission, 2010; Glaeser et al., 2009; Van Eijk, 2010; Zwiers & Koster, 2015). While there has been little research on the effects of the GFC at the neighborhood level, the evidence described above suggests that the effects are distributed unevenly across urban areas (Foster & Kleit, 2015;   Batson & Monnat, 2015). As households in the bottom income decile have experienced the sharpest drop in income, the effects of the GFC are likely to be felt most acutely in the most disadvantaged neighborhoods (see also Rugh & Massey, 2010; Thomas, 2013). In view of these concerns, this article sets out to identify factors that affect neighborhood decline in the aftermath of the GFC. Many economists have pointed to structural changes in national housing markets and to the changing role of states as important consequences of the GFC (e.g. Wachter, 2015), yet, few researchers analyze how these changes play out at the neighborhood level. Similarly, housing researchers have identified multiple drivers behind neighborhood decline, but many of them focus on within-neighborhood processes at the expense of developments at higher scale levels (Van Beckhoven et al., 2009). In this paper, we aim to bridge this gap by presenting 10 hypotheses on how changes at different geographical scales affect neighborhood decline. Our goal is not to create the next ideal-type model of neighborhood decline processes; rather, we seek to further the intellectual debate on neighborhood decline call for more research on the spatial consequences of the GFC, specifically on neighborhoods as an important territorial dimension of increasing inequality. Our hypotheses mainly pertain to the Global North. Although these countries have very different political, economic, and social structures, research on neighborhood change in different contexts in the Global North has often led to broadly similar findings. This suggests that many of the underlying processes of neighborhood change are comparable across countries. In the same vein, the increasingly global nature of financial and housing markets (Aalbers, 2015) yields similarities in the effects of the GFC and the economic recession between countries. However, the effects of the GFC are mediated by national policies, local (housing market) circumstances, and intra-neighborhood processes, meaning that the GFC has different outcomes in different places. The next section of this article presents a short discussion of definitions of neighborhoods and neighborhood decline. We then highlight important elements from existing studies to formulate 10 hypotheses about the effects of the GFC and the economic recession on neighborhood decline. These hypotheses are divided over three sections, each with a different geographical focus. The conclusion brings our arguments together and calls for more contextualized longitudinal research.&nbsp

Design and Control of a Lower Limb Exoskeleton for Robot-Assisted Gait Training

Robot-assisted rehabilitation of gait still faces many challenges, one of which is improving physical human-robot interaction. The use of pleated pneumatic artificial muscles to power a step rehabilitation robot has the potential to meet this challenge. This paper reports on the development of a gait rehabilitation exoskeleton with a knee joint powered by pleated pneumatic artificial muscles. It is intended as a platform for the evaluation of design and control concepts in view of improved physical human-robot interaction. The design was focused on the optimal dimensioning of the actuator configuration. Safety being the most important prerequisite, a proxy-based sliding mode controller (PSMC) was implemented as it combines accurate tracking during normal operation with a smooth, slow and safe recovery from large position errors. Treadmill walking experiments of a healthy subject wearing the powered exoskeleton show the potential of PSMC as a safe robot-in-charge control strategy for robot-assisted gait training

The prevalence of thyroid dysfunction and hyperprolactinemia in women with PCOS

Introduction: Ovulatory dysfunction is usually caused by an endocrine disorder, of which polycystic ovary syndrome (PCOS) is the most common cause. PCOS is usually associated with estrogen levels within the normal range and can be characterized by oligo-/anovulation resulting in decreased progesterone levels. It is suggested that decreased progesterone levels may lead to more autoimmune diseases in women with PCOS. In addition, it is often claimed that there is an association between hyperprolactinemia and PCOS. In this large well-phenotyped cohort of women with PCOS, we have studied the prevalence of thyroid dysfunction and hyperprolactinemia compared to controls, and compared this between the four PCOS phenotypes. Methods: This retrospective cross-sectional study contains data of 1429 women with PCOS and 299 women without PCOS. Main outcome measures included thyroid stimulating hormone (TSH), Free Thyroxine (FT4), and anti-thyroid peroxidase antibodies (TPOab) levels in serum, the prevalence of thyroid diseases and hyperprolactinemia. Results: The prevalence of thyroid disease in PCOS women was similar to that of controls (1.9% versus 2.7%; P = 0.39 for hypothyroidism and 0.5% versus 0%; P = 0.99 for hyperthyroidism). TSH levels were also similar (1.55 mIU/L versus 1.48 mIU/L; P = 0.54). FT4 levels were slightly elevated in the PCOS group, although within the normal range (18.1 pmol/L versus 17.7 pmol/L; P &lt; 0.05). The prevalence of positive TPOab was similar in both groups (5.7% versus 8.7%; P = 0.12). The prevalence of hyperprolactinemia was similarly not increased in women with PCOS (1.3%% versus 3%; P = 0.05). In a subanalysis of 235 women with PCOS and 235 age- and BMI-matched controls, we found no differences in thyroid dysfunction or hyperprolactinemia. In according to differences between PCOS phenotypes, only the prevalence of subclinical hypothyroidism was significantly higher in phenotype B (6.3%, n = 6) compared to the other phenotypes. Conclusion: Women with PCOS do not suffer from thyroid dysfunction more often than controls. Also, the prevalence of positive TPOab, being a marker for future risk of thyroid pathology, was similar in both groups. Furthermore, the prevalence of hyperprolactinemia was similar in women with PCOS compared to controls.</p

Immunohistochemical detection of somatostatin receptor subtypes sst1 and sst2A in human somatostatin receptor positive tumors

Although in situ hybridization has been used to examine the distribution of messenger RNA for somatostatin receptor subtypes (sst) in human tumors, the cellular localization of sst1 and sst2A receptors has not been reported. In this study, we describe the cellular localization of human sst1 and sst2A receptor proteins in both cryostat- and paraffin-embedded sections of 25 human tumor tissues using two recently developed polyclonal antibodies. Six somatostatin (SS) receptor (SSR) positive tumors (two gastrinomas, three carcinoids, one pheochromocytoma) and one SSR negative tumor (renal cell carcinoma), selected by positive and negative SSR autoradiography, respectively, were studied by both immunohistochemistry and Western blot analysis. The six SSR positive tumors expressed sst2A, while 4 of 5 expressed sst1 as well. The SSR negative tumor did not express either sst1 or sst2A. Western blot analysis of wheat germ agglutinin purified membrane proteins confirmed the presence of the sst1 and sst2A glycosylated receptors. The paraffin-embedded sections gave best information with respect to the subcellular localization. Sst1 immunoreactivity was observed both on the membrane and in the cytoplasm, while sst2A showed predominantly membrane-associated immunoreactivity. This subcellular distribution of sst1 or sst2A receptors was confirmed in paraffin-embedded sections of 8 additional intestinal carcinoids, 5 gastrinomas and 5 pheochromocytomas. Sst1 receptors were detected in 7 out of 8 carcinoids, in all gastrinomas, and in 4 out of 5 pheochromocytomas, while 6 out of 8 carcinoids, all gastrinomas, and 3 out of 5 pheochromocytomas expressed sst2A receptors. In conclusion, sst1 and sst2A receptors show a differential subcellular localization in human SSR positive tumors. The use of SSR subtype selective antibodies to detect the subcellular distribution of SSR subtypes in individual tumor cells is an important step forward to understand more about the pathophysiological role of the different SSR subtypes in human tumors

<i>C-elegans</i> model identifies genetic modifiers of alpha-synuclein inclusion formation during aging

Inclusions in the brain containing alpha-synuclein are the pathological hallmark of Parkinson's disease, but how these inclusions are formed and how this links to disease is poorly understood. We have developed a &lt;i&gt;C-elegans&lt;/i&gt; model that makes it possible to monitor, in living animals, the formation of alpha-synuclein inclusions. In worms of old age, inclusions contain aggregated alpha-synuclein, resembling a critical pathological feature. We used genome-wide RNA interference to identify processes involved in inclusion formation, and identified 80 genes that, when knocked down, resulted in a premature increase in the number of inclusions. Quality control and vesicle-trafficking genes expressed in the ER/Golgi complex and vesicular compartments were overrepresented, indicating a specific role for these processes in alpha-synuclein inclusion formation. Suppressors include aging-associated genes, such as sir-2.1/SIRT1 and lagr-1/LASS2. Altogether, our data suggest a link between alpha-synuclein inclusion formation and cellular aging, likely through an endomembrane-related mechanism. The processes and genes identified here present a framework for further study of the disease mechanism and provide candidate susceptibility genes and drug targets for Parkinson's disease and other alpha-synuclein related disorders

Tissue-specific suppression of thyroid hormone signaling in various mouse models of aging

DNA damage contributes to the process of aging, as underscored by premature aging syndromes caused by defective DNA repair. Thyroid state changes during aging, but underlying mechanisms remain elusive. Since thyroid hormone (TH) is a key regulator of metabolism, changes in TH signaling have widespread effects. Here, we reveal a significant common transcriptomic signature in livers from hypothyroid mice, DNA repair-deficient mice with severe (Csbm/m/Xpa-/-) or intermediate (Ercc1-/Δ-7) progeria and naturally aged mice. A strong induction of TH-inactivating deiodinase D3 and decrease of TH-activating D1 activities are observed in Csbm/m/Xpa-/- livers. Similar findings are noticed in Ercc1-/Δ-7, in naturally aged animals and in wild-type mice exposed to a chronic subtoxic dose of DNAdamaging agents. In contrast, TH signaling in muscle, heart and brain appears unaltered. These data show a strong suppression of TH signaling in specific peripheral organs in premature and normal aging, probably lowering metabolism, while other tissues appear to preserve metabolism. D3-mediated TH inactivation is unexpected, given its expression mainly in fetal tissues. Our studies highlight the importance of DNA damage as the underlying mechanism of changes in thyroid state. Tissue-specific regulation of deiodinase activities, ensuring diminished TH signaling, may contribute importantly to the protective metabolic response in aging