Potential for deep geological sequestration of CO2 in Switzerland: a first appraisal

Possibilities to sequester anthropogenic CO2 in deep geological formations are being investigated worldwide, but the potential within Switzerland has not yet been evaluated. This study presents a first-order appraisal based solely on geological criteria collated from the literature. The Swiss Molasse Basin (SMB) and the adjacent Folded Jura are the only realms of the country where CO2 could conceivably be stored in saline aquifers. Evaluation of geological criteria at the basin-wide scale shows that the SMB-Jura has moderate potential (score of 0.6 on a scale from 0 to 1) when compared to basins elsewhere. At the intrabasinal scale, inspection of the stratigraphy reveals four regional candidate aquifers that are sealed by suitable caprocks: top Basement plus basal Mesozoic sandstones, all sealed by the Anhydrite Group; Upper Muschelkalk sealed by the Gipskeuper; Hauptrogenstein sealed by the Effinger Member, and Upper Malm plus Lower Cretaceous sealed by the Lower Freshwater Molasse. Nine geological criteria are defined to evaluate the storage potential of these and other smaller scale candidates. A numerical scoring and weighting scheme allows the criteria to be assessed simultaneously, permitting the storage potential to be depicted using the 0-1 scale in contoured maps. Approximately 5,000km2 of the central SMB exhibits potentials between 0.6 and 0.96. The Fribourg-Olten-Luzern area is the most favoured owing to the presence of several sealed aquifers within the preferred 800-2,500m depth interval, and to its low seismicity, low geothermal gradient, low fault density, and long groundwater residence times. Smaller areas with good potential lie between Zürich and St. Gallen. In contrast, western Switzerland, the Jura and the southern SMB have markedly poorer potential. Considering only the portions of the aquifers with potential above 0.6, the theoretical, effective storage capacity of the basin is estimated to be 2,680 million tonnes of CO

The Swiss and Dutch Health Insurance Systems: Universal Coverage and Regulated Competitive Insurance Markets

Compares systems of universal insurance coverage based on individual mandates, consumer choice of health plans, and regulated insurance market competition in Switzerland and the Netherlands. Discusses insights and implications for U.S. reform efforts

The nanosyntax of spatial deixis

This paper provides a fine-grained morphosyntactic analysis of spatial deixis. We propose that the universal core of spatial deixis is a three-way contrast: Proximal close to speaker', Medial close to hearer', and Distal far from speaker and hearer'. This system arises from three features merged as heads in a single universal functional sequence: Dx(3) > Dx(2) > Dx(1). The hierarchy is understood in terms of superset-subset relations, such that Proximal [Dx(1)] is a subset of Medial [Dx(2) [Dx(1)]], which in turn is a subset of Distal [Dx(3) [Dx(2) [Dx(1)]]]. Evidence comes from patterns of syncretism and morphological containment in the demonstrative systems of a number of genetically diverse languages. Regarding syncretisms, languages can show a transparent three-way morphological contrast, or some sort of syncretism: Medial/Proximal vs. Distal, Distal/Medial vs. Proximal, or a totally syncretic Distal/Medial/Proximal (i.e. a neutral demonstrative). These syncretisms entail that the features responsible for the Proximal and Medial readings be adjacent and that the features responsible for the Distal and Medial readings be adjacent in the fseq. Regarding containment, we show that Proximal can be structurally contained within Medial and that Medial can be structurally contained within Distal, meaning that Medial structures are larger than Proximal structures, and that Distal structures are larger than Medial structures, confirming our hierarchy. We show that these facts are naturally accounted for by nanosyntactic principles of spellout. We end the paper by accounting for potential counterexamples and other issues

Decreased Circulating Endothelial Progenitor Cell Levels and Function in Patients with Nonalcoholic Fatty Liver Disease

OBJECTIVES: Nonalcoholic fatty liver disease (NAFLD) is associated with advanced atherosclerosis and a higher risk of cardiovascular disease. Increasing evidence suggests that injured endothelial monolayer is regenerated by circulating bone marrow derived-endothelial progenitor cells (EPCs), and levels of circulating EPCs reflect vascular repair capacity. However, the relation between NAFLD and EPC remains unclear. Here, we tested the hypothesis that patients with nonalcoholic fatty liver disease (NAFLD) might have decreased endothelial progenitor cell (EPC) levels and attenuated EPC function. METHODS AND RESULTS: A total of 312 consecutive patients undergoing elective coronary angiography because of suspected coronary artery disease were screened and received examinations of abdominal ultrasonography between July 2009 and November 2010. Finally, 34 patients with an ultrasonographic diagnosis of NAFLD, and 68 age- and sex-matched controls without NAFLD were enrolled. Flow cytometry with quantification of EPC markers (defined as CD34(+), CD34(+)KDR(+), and CD34(+)KDR(+)CD133(+)) in peripheral blood samples was used to assess circulating EPC numbers. The adhesive function, and migration, and tube formation capacities of EPCs were also determined in NAFLD patients and controls. Patients with NAFLD had a significantly higher incidence of metabolic syndrome, previous myocardial infarction, hyperuricemia, and higher waist circumference, body mass index, fasting glucose and triglyceride levels. In addition, patients with NAFLD had significantly decreased circulating EPC levels (all P<0.05), attenuated EPC functions, and enhanced systemic inflammation compared to controls. Multivariate logistic regression analysis showed that circulating EPC level (CD34(+)KDR(+) [cells/10(5) events]) was an independent reverse predictor of NAFLD (Odds ratio: 0.78; 95% confidence interval: 0.69-0.89, P<0.001). CONCLUSIONS: NAFLD patients have decreased circulating EPC numbers and functions than those without NAFLD, which may be one of the mechanisms to explain atherosclerotic disease progression and enhanced cardiovascular risk in patients with NAFLD

Estimating the Cost of Type 1 Diabetes in the U.S.: A Propensity Score Matching Method

Diabetes costs represent a large burden to both patients and the health care system. However, few studies that examine the economic consequences of diabetes have distinguished between the two major forms, type 1 and type 2 diabetes, despite differences in underlying pathologies. Combining the two diseases implies that there is no difference between the costs of type 1 and type 2 diabetes to a patient. In this study, we examine the costs of type 1 diabetes, which is often overlooked due to the larger population of type 2 patients, and compare them to the estimated costs of diabetes reported in the literature.Using a nationally representative dataset, we estimate yearly and lifetime medical and indirect costs of type 1 diabetes by implementing a matching method to compare a patient with type 1 diabetes to a similar individual without the disease. We find that each year type 1 diabetes costs this country $14.4 billion (11.5-17.3) in medical costs and lost income. In terms of lost income, type 1 patients incur a disproportionate share of type 1 and type 2 costs. Further, if the disease were eliminated by therapeutic intervention, an estimated$10.6 billion (7.2-14.0) incurred by a new cohort and $422.9 billion (327.2-519.4) incurred by the existing number of type 1 diabetic patients over their lifetime would be avoided.We find that the costs attributed to type 1 diabetes are disproportionately higher than the number of type 1 patients compared with type 2 patients, suggesting that combining the two diseases when estimating costs is not appropriate. This study and another recent contribution provides a necessary first step in estimating the substantial costs of type 1 diabetes on the U.S

Deadly liaisons: fatal attraction between CCN matricellular proteins and the tumor necrosis factor family of cytokines

Recent studies have revealed an unexpected synergism between two seemingly unrelated protein families: CCN matricellular proteins and the tumor necrosis factor (TNF) family of cytokines. CCN proteins are dynamically expressed at sites of injury repair and inflammation, where TNF cytokines are also expressed. Although TNFα is an apoptotic inducer in some cancer cells, it activates NFκB to promote survival and proliferation in normal cells, and its cytotoxicity requires inhibition of de novo protein synthesis or NFκB signaling. The presence of CCN1, CCN2, or CCN3 overrides this requirement and unmasks the apoptotic potential of TNFα, thus converting TNFα from a proliferation-promoting protein into an apoptotic inducer. These CCN proteins also enhance the cytotoxicity of other TNF cytokines, including LTα, FasL, and TRAIL. Mechanistically, CCNs function through integrin α6β1 and the heparan sulfate proteoglycan (HSPG) syndecan-4 to induce reactive oxygen species (ROS) accumulation, which is essential for apoptotic synergism. Mutant CCN1 proteins defective for binding α6β1-HSPGs are unable to induce ROS or apoptotic synergism with TNF cytokines. Further, knockin mice that express an α6β1-HSPG-binding defective CCN1 are blunted in TNFα- and Fas-mediated apoptosis, indicating that CCN1 is a physiologic regulator of these processes. These findings implicate CCN proteins as contextual regulators of the inflammatory response by dictating or enhancing the cytotoxicity of TNFα and related cytokines

The role of diet in the aetiopathogenesis of inflammatory bowel disease

Crohn’s disease and ulcerative colitis, collectively known as IBD, are chronic inflammatory disorders of the gastrointestinal tract. Although the aetiopathogenesis of IBD is largely unknown, it is widely thought that diet has a crucial role in the development and progression of IBD. Indeed, epidemiological and genetic association studies have identified a number of promising dietary and genetic risk factors for IBD. These preliminary studies have led to major interest in investigating the complex interaction between diet, host genetics, the gut microbiota and immune function in the pathogenesis of IBD. In this Review, we discuss the recent epidemiological, gene–environment interaction, microbiome and animal studies that have explored the relationship between diet and the risk of IBD. In addition, we highlight the limitations of these prior studies, in part by explaining their contradictory findings, and review future directions

Clay Mineral Diagenesis and Thermal History of the Thonex Well, Western Swiss Molasse Basin

Results are presented of a diagenetic study from the 1300 m thick Oligocene Molasse deposits penetrated by the Thônex geothermal exploration well (Geneva, Switzerland). The x-ray diffraction (XRD) studies of fine-grained rocks indicate the following diagenetic changes: a decrease of illite/smectite (US) expandability from approximately 90% to 30% with depth, a decrease of the amount of US in the clay mineral fraction, and the appearance of corrensite at depths >750 m. The transition from random US to ordered I/S occurs at the base of the Thônex well (1200 to 1300 m) and is associated with a coal rank of about 0.7% Rr (mean random vitrinite reflectance) corresponding to paleotemperatures of 110 to 115 °C Corrensite appears at a vitrinite reflectance value of 0.6% Rr and a corresponding paleotemperature of 100 °C. The amount of post-Molasse erosion is estimated to be approximately 2 km. Thermal history modeling of the Thônex well suggests maximum paleotemperatures of 80 to 115°C and an average paleogeothermal gradient of 27 °C/km during Late Miocene maximum burial conditions