Breaking With Neoliberalization by Restricting The Housing Market:Novel Urban Policies and the Case of Hamburg

Hamburg currently exemplifies the departure from a straightforward neoliberal urban track. The city's neoliberal path only moved into full swing in the first decade of the 2000s. During this period, urban development was primarily subject to property market mechanismswith projects being granted to the highest bidderprompting effects such as rapidly rising rents, deepened social segregation and increased property-led displacement. Since 2009, however, the city's entrepreneurial urban policy encountered comprehensive resistance movements that eventually led to the rediscovery of a political will for a new housing policy and interventionist policy instruments. This article focuses on the turning point of neoliberal policies and examines the wider scope of the contemporary urban agenda in Hamburg. We first conceptualize potential limits of the neoliberal city in general and then discuss three momentous local policy experimentsthe International Building Exhibition, promising improvement without displacement'; the rediscovery of housing regulations through the Social Preservation Statute'; and the Alliance for Housing', aiming to tackle the housing shortage. We discuss these approaches as funding, regulation, and actor-based approaches to limiting the neoliberal city

Novel multiple sclerosis susceptibility loci implicated in epigenetic regulation.

We conducted a genome-wide association study (GWAS) on multiple sclerosis (MS) susceptibility in German cohorts with 4888 cases and 10,395 controls. In addition to associations within the major histocompatibility complex (MHC) region, 15 non-MHC loci reached genome-wide significance. Four of these loci are novel MS susceptibility loci. They map to the genes L3MBTL3, MAZ, ERG, and SHMT1. The lead variant at SHMT1 was replicated in an independent Sardinian cohort. Products of the genes L3MBTL3, MAZ, and ERG play important roles in immune cell regulation. SHMT1 encodes a serine hydroxymethyltransferase catalyzing the transfer of a carbon unit to the folate cycle. This reaction is required for regulation of methylation homeostasis, which is important for establishment and maintenance of epigenetic signatures. Our GWAS approach in a defined population with limited genetic substructure detected associations not found in larger, more heterogeneous cohorts, thus providing new clues regarding MS pathogenesis