The Swedish Housing Market: Structure, Policy Issues and Modeling

Contribution to the Metropolitan Study: 20 -- The project "Nested Dynamics of Metropolitan Processes and Policies" is a collaborative study within the project area Regional Issues at IIASA. The series of contributions is a means of conveying information between the collaborators in the network of the project. This paper reports on a penetrating investigation of the housing market in the Stockholm region. It is based on a sequence of interviews and discussions with various decision makers and managers whose actions form an important market system. The paper examines the details of the system structure with the objective of formulating a reliable model of transactions, regulations, investments, etc. The work on the model itself is currently underway and will also be presented in the near future. The approach undertaken by the authors is original in its careful treatment of such system properties which constitute deviations from a free market. Consequently, the paper provides an already tested guideline for the work on the housing sector in other metropolitan regions in the study. Recently, this type of work has been initiated in several of those regions. It is believed that this work may bring about a new generation of housing sector modeling and a renewal of the pertinent analyses

Helicobacter pylori VacA Toxin/Subunit p34: Targeting of an Anion Channel to the Inner Mitochondrial Membrane

The vacuolating toxin VacA, released by Helicobacter pylori, is an important virulence factor in the pathogenesis of gastritis and gastroduodenal ulcers. VacA contains two subunits: The p58 subunit mediates entry into target cells, and the p34 subunit mediates targeting to mitochondria and is essential for toxicity. In this study we found that targeting to mitochondria is dependent on a unique signal sequence of 32 uncharged amino acid residues at the p34 N-terminus. Mitochondrial import of p34 is mediated by the import receptor Tom20 and the import channel of the outer membrane TOM complex, leading to insertion of p34 into the mitochondrial inner membrane. p34 assembles in homo-hexamers of extraordinary high stability. CD spectra of the purified protein indicate a content of >40% β-strands, similar to pore-forming β-barrel proteins. p34 forms an anion channel with a conductivity of about 12 pS in 1.5 M KCl buffer. Oligomerization and channel formation are independent both of the 32 uncharged N-terminal residues and of the p58 subunit of the toxin. The conductivity is efficiently blocked by 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB), a reagent known to inhibit VacA-mediated apoptosis. We conclude that p34 essentially acts as a small pore-forming toxin, targeted to the mitochondrial inner membrane by a special hydrophobic N-terminal signal

Bacterial Porin Disrupts Mitochondrial Membrane Potential and Sensitizes Host Cells to Apoptosis

The bacterial PorB porin, an ATP-binding beta-barrel protein of pathogenic Neisseria gonorrhoeae, triggers host cell apoptosis by an unknown mechanism. PorB is targeted to and imported by host cell mitochondria, causing the breakdown of the mitochondrial membrane potential (Delta psi(m)). Here, we show that PorB induces the condensation of the mitochondrial matrix and the loss of cristae structures, sensitizing cells to the induction of apoptosis via signaling pathways activated by BH3-only proteins. PorB is imported into mitochondria through the general translocase TOM but, unexpectedly, is not recognized by the SAM sorting machinery, usually required for the assembly of beta-barrel proteins in the mitochondrial outer membrane. PorB integrates into the mitochondrial inner membrane, leading to the breakdown of Delta psi(m). The PorB channel is regulated by nucleotides and an isogenic PorB mutant defective in ATP-binding failed to induce Delta psi(m) loss and apoptosis, demonstrating that dissipation of Delta psi(m) is a requirement for cell death caused by neisserial infection

Bacterial porin disrupts mitochondrial membrane potential and sensitizes host cells to apoptosis

The bacterial PorB porin, an ATP-binding beta-barrel protein of pathogenic Neisseria gonorrhoeae, triggers host cell apoptosis by an unknown mechanism. PorB is targeted to and imported by host cell mitochondria, causing the breakdown of the mitochondrial membrane potential (delta psi m). Here, we show that PorB induces the condensation of the mitochondrial matrix and the loss of cristae structures, sensitizing cells to the induction of apoptosis via signaling pathways activated by BH3-only proteins. PorB is imported into mitochondria through the general translocase TOM but, unexpectedly, is not recognized by the SAM sorting machinery, usually required for the assembly of beta-barrel proteins in the mitochondrial outer membrane. PorB integrates into the mitochondrial inner membrane, leading to the breakdown of delta psi m. The PorB channel is regulated by nucleotides and an isogenic PorB mutant defective in ATP-binding failed to induce delta psi m loss and apoptosis, demonstrating that dissipation of delta psi m is a requirement for cell death caused by neisserial infection

Location and spatial clustering of artists

Surveys of artists' location choices show that they disproportionately reside in large cities. This paper introduces a model that attempts to explain this urban preference. The model includes four factors: access to other artists; access to consumer demand; access to service jobs; and housing affordability. These four factors are combined in a spatial equilibrium model. An equilibrium spatial distribution of artists is derived from the model and is correlated with the actual distribution among Swedish municipalities. Subsequently, the model is used for an econometric estimation of factor effects. The results show that access to other artists and local access to service jobs are important localization factors. Educated labor used as a proxy for consumer demand has a significant effect on artists' location choices. © 2013 Elsevier B.V

Complexity, scientific creativity and clustering

Industrial research investments and new product development have been the key factors behind economic growth in recent decades. They have also been the most important causes of the changing comparative advantages of regions and countries. An aim of this paper is to generate some theoretical insights into the mechanisms behind the spatial clustering of research-dependent production and the impact of the increasing complexity of products and production technologies. We claim that increases in product complexity in ICT, biomedicine and other high-tech industries necessitate closer co-operation with basic science and interdisciplinary research in universities. At the same time, statistics on the allocation of R&D investments between industry and universities show that in most countries the share going to university-based research is quite low. This is especially marked in the cases of South Korea and Japan. Policy conclusions are formulated. First, national governments should increase the support of scientific research, providing a better knowledge infrastructure of industrial R&D investments. Second, increasing scientific complexity implies more support for projects with secured scientific diversity and with a leadership that can integrate different fields of science. Third, there is a need for strategy of drastic increases of science and R&D investments in southern and eastern European in order to avoid further widening of the gap between slow and fast growth regions of Europe

Journal of Biological Chemistry

Chloroplasts and mitochondria are unique endosymbiotic cellular organelles surrounded by two membranes. Essential metabolic networking between these compartments and their hosting cells requires the exchange of a large number of biochemical pathway intermediates in a directed and coordinated fashion across their inner and outer envelope membranes. Here, we describe the identification and functional characterization of a highly specific, regulated solute channel in the outer envelope of chloroplasts, named OEP40. Loss of OEP40 function in Arabidopsis thaliana results in early flowering under cold temperature. The reconstituted recombinant OEP40 protein forms a high conductance β-barrel ion channel with subconductant states in planar lipid bilayers. The OEP40 channel is slightly cation-selective P(K+)/P(Cl−) ≈ 4:1 and rectifying (i⃗/i⃖ ≅ 2) with a slope conductance of Ḡ(max) ≅ 690 picosiemens. The OEP40 channel has a restriction zone diameter of ≅1.4 nm and is permeable for glucose, glucose 1-phosphate and glucose 6-phosphate, but not for maltose. Moreover, channel properties are regulated by trehalose 6-phosphate, which cannot permeate. Altogether, our results indicate that OEP40 is a “glucose-gate” in the outer envelope membrane of chloroplasts, facilitating selective metabolite exchange between chloroplasts and the surrounding cell