A Microeconometric Characterisation of Household Consumption Using Quantile Regression

The paper uses micro cross-section data from the GfK consumer panel for econometric demand analysis of private households in Germany. Contrary to most research which considered \average" behavior we extend this approach to consumer behavior for di®erent \intensities" of consumption. Our analytical tool is quantile regression which allows us to describe the conditional distribu- tion for any quantile including the (conditional) median representing \average" behavior. As an illustrative example we use the demand for beer and wine. The paper shows quite distinct patterns regarding price and income e®ects for di®erent goods which leads us to an extended characterization of household demand.econometric demand analysis, Engel curve, demand system, micro data

The geography of greenhouse gas emissions from within urban areas of Asia

This paper aims to advance two objectives: (1) identify and explore greenhouse gas emissions from urban areas in Asia at the regional level; and (2) explore covariates of urban greenhouse gas emissions. We use the Emissions Database for Global Atmospheric Research estimates for carbon dioxide, methane, nitrous oxide, and sulfur hexafluoride from 14 source activities for the year 2000, which are allocated on a 1/108 global grid. We extract emissions for 3535 urban extents all with populations over 50,000, accounting for approximately 91% of the region’s urban population. We use regression analysis to associate emissions with urban area and growth, economic, and biophysical characteristics. Our findings suggest that urban areas account for between 30 and 38% of total anthropogenic greenhouse gas emissions for the region and that emission per capita averages from urban areas are lower than those at the national level. Important covariates for total urban greenhouse gas emissions include population size, density and growth rate, income per capita, development status and elevation. This is a first and preliminary assessment of regional baseline trends using these data and this top-down analysis

The Role of Suburbia in the Attribution of Greenhouse Gas Emissions

The original goal of the research presented here was to quantify by world region, the contribution of urbanized areas to global greenhouse gas (GHG) emissions (EDGAR, 2011). Regressions on population density and growth rate, GDP, and heating/cooling degree days, as well as a row of other non-significant variables, show that the contribution of urban extents is between 38% and 49% of total emissions (Marcotullio et al., 2012). In spite of using very liberal definitions of urban extents (GRUMP, 2011) this is at the low end of academic estimates (Satterthwaite, 2008; WEO, 2008; Dhakal, 2010). It is no surprise that the relative weight of individual variables varies by world region and economic development. We were, however, very surprised to find that around the world, the highest levels of GHG emissions are in a belt 20-40 km around urban centres. This result is consistent using both traditional fixed-effects and spatial regression techniques, which will be discussed in detail in this paper. There are variations (e.g. the role of African suburbs is smaller than that of their Asian and European counterparts) but the signature prevails. We suggest that this has consequences for both planning and geography theory as well as for policy. In spite of globalization, we have very few local indicators that are so consistently the same across cultures, economic and physical regimes. On a practical level, our results are an urgent reminder that cities by and large are rather efficient constructs while the biggest impacts on minimizing GHG emissions can be achieved by optimizing suburban energy use and transport

Assessing Urban Greenhouse Gas Emissions in European Medium and Large Cities: Methodological Considerations

Policymakers need clear, consistent, and reliable information about the location of greenhouse gases and drivers of emitting activity in order to design appropriate mitigating strategies. At the urban scale, there have been challenges in developing consistent and reliable emissions inventories. This chapter examines selected methods to determine greenhouse gas emissions at the urban scale. We describe the various criteria considered when constructing an urban greenhouse gas protocol including the definition of urban, the gasses that are measured, the source they come from, the scope of analysis and how the measurements are undertaken. We then present results for European medium and large sized cities derived from alternative methodologies to demonstrate the range of results. Finally, we briefly discuss the policy implications of the various approaches

Workshop-Bericht "Journals in der Open-Access-Transformation"

In einem virtuellen Workshop diskutierten die fünf vom Bundesministerium für Bildung und Forschung (BMBF) geförderten Projekte B!SON, CODRIA, KOALA, OPTIMETA und Scholar-led Plus ihre Zwischenergebnisse mit der Fachöffentlichkeit

The coronary circulation in acute myocardial ischaemia/reperfusion injury - a target for cardioprotection

The coronary circulation is both culprit and victim of acute myocardial infarction. The rupture of an epicardial atherosclerotic plaque with superimposed thrombosis causes coronary occlusion, and this occlusion must be removed to induce reperfusion. However, ischaemia and reperfusion cause damage not only in cardiomyocytes but also in the coronary circulation, including microembolisation of debris and release of soluble factors from the culprit lesion, impairment of endothelial integrity with subsequently increased permeability and oedema formation, platelet activation and leukocyte adherence, erythrocyte stasis, a shift from vasodilation to vasoconstriction, and ultimately structural damage to the capillaries with eventual no-reflow, microvascular obstruction and intramyocardial haemorrhage. Therefore, the coronary circulation is a valid target for cardioprotection, beyond protection of the cardiomyocyte. Virtually all of the above deleterious endpoints have been demonstrated to be favourably influenced by one or the other mechanical or pharmacological cardioprotective intervention. However, no-reflow is still a serious complication of reperfused myocardial infarction and carries, independently from infarct size, an unfavourable prognosis. Microvascular obstruction and intramyocardial haemorrhage can be diagnosed by modern imaging technologies, but still await an effective therapy. The current review provides an overview of strategies to protect the coronary circulation from acute myocardial ischaemia/reperfusion injury. This article is part of a Cardiovascular Research Spotlight Issue entitled 'Cardioprotection Beyond the Cardiomyocyte', and emerged as part of the discussions of the European Union (EU)-CARDIOPROTECTION Cooperation in Science and Technology (COST) Action, CA16225

Cause-Specific Excess Mortality in Siblings of Patients Co-Infected with HIV and Hepatitis C Virus

BACKGROUND: Co-infection with hepatitis C in HIV-infected individuals is associated with 3- to 4-fold higher mortality among these patients' siblings, compared with siblings of mono-infected HIV-patients or population controls. This indicates that risk factors shared by family members partially account for the excess mortality of HIV/HCV-co-infected patients. We aimed to explore the causes of death contributing to the excess sibling mortality. METHODOLOGY AND PRINCIPAL FINDINGS: We retrieved causes of death from the Danish National Registry of Deaths and estimated cause-specific excess mortality rates (EMR) for siblings of HIV/HCV-co-infected individuals (n = 436) and siblings of HIV mono-infected individuals (n = 1837) compared with siblings of population controls (n = 281,221). Siblings of HIV/HCV-co-infected individuals had an all-cause EMR of 3.03 (95% CI, 1.56-4.50) per 1,000 person-years, compared with siblings of matched population controls. Substance abuse-related deaths contributed most to the elevated mortality among siblings [EMR = 2.25 (1.09-3.40)] followed by unnatural deaths [EMR = 0.67 (-0.05-1.39)]. No siblings of HIV/HCV co-infected patients had a liver-related diagnosis as underlying cause of death. Siblings of HIV-mono-infected individuals had an all-cause EMR of 0.60 (0.16-1.05) compared with siblings of controls. This modest excess mortality was due to deaths from an unknown cause [EMR = 0.28 (0.07-0.48)], deaths from substance abuse [EMR = 0.19 (-0.04-0.43)], and unnatural deaths [EMR = 0.18 (-0.06-0.42)]. CONCLUSIONS: HCV co-infection among HIV-infected patients was a strong marker for family-related mortality due to substance abuse and other unnatural causes. To reduce morbidity and mortality in HIV/HCV-co-infected patients, the advances in antiviral treatment of HCV should be accompanied by continued focus on interventions targeted at substance abuse-related risk factors

A novel rare CUBN variant and three additional genes identified in Europeans with and without diabetes : results from an exome-wide association study of albuminuria

Aims/hypothesisIdentifying rare coding variants associated with albuminuria may open new avenues for preventing chronic kidney disease and end-stage renal disease, which are highly prevalent in individuals with diabetes. Efforts to identify genetic susceptibility variants for albuminuria have so far been limited, with the majority of studies focusing on common variants.MethodsWe performed an exome-wide association study to identify coding variants in a two-stage (discovery and replication) approach. Data from 33,985 individuals of European ancestry (15,872 with and 18,113 without diabetes) and 2605 Greenlanders were included.ResultsWe identified a rare (minor allele frequency [MAF]: 0.8%) missense (A1690V) variant in CUBN (rs141640975, =0.27, p=1.3x10(-11)) associated with albuminuria as a continuous measure in the combined European meta-analysis. The presence of each rare allele of the variant was associated with a 6.4% increase in albuminuria. The rare CUBN variant had an effect that was three times stronger in individuals with type 2 diabetes compared with those without (p(interaction)=7.0x10(-4), with diabetes=0.69, without diabetes=0.20) in the discovery meta-analysis. Gene-aggregate tests based on rare and common variants identified three additional genes associated with albuminuria (HES1, CDC73 and GRM5) after multiple testing correction (p(Bonferroni)Peer reviewe