Are You Well Prepared for Long-term Care? – Assessing Financial Gaps in Private German Care Provision

The development of expenditure for care services is one of the most intensively debated topics in public. However, studies calculating financial provision gaps only focus on the macro-level implications for the compulsory care insurance. In contrast, this paper examines the individuals’ micro-level perspective. We use survey as well as regional and national statistical data to calculate expected individual costs of long-term care on a very detailed care arrangement and care level basis. Afterwards, we compare these costs with the individuals’ total wealth. In our most conservative policy scenario, our results show that about a third of statutorily insured individuals will have to face a financial care provision gap. Among homeowners, an even higher share will have to liquidate the main residence. The privately insured are affected to a somewhat lower extent. In both groups, the situation will become much more severe if the development of public transfers does not keep up with future increases of long-term care costs. Furthermore, regression analyses show that provision gaps are more frequent among statutorily insured individuals, females, and individuals in single households.Long-term care costs; care prevalence; life expectancy; provision gap

Oxidation protection of Mo-Si-B alloys by magnetron-sputtered coatings

Mo-Si-B alloys with melting temperature above 2000 °C are attractive high temperature materials offering significantly enhanced operating temperatures compared to those of the currently used Ni-based superalloys. However, their oxidation behavior is poor at temperatures below 1000 °C, suffering from evaporation of MoO3. Above 1000 °C oxidation is characterized by a transient state showing considerable mass loss followed by a steady state condition with reduced mass change. To mitigate this degradation by oxidation, application of coatings is an appropriate method ensuring the formation of slowly growing protective scales. The presentation summarizes recent results on overlay coatings that were deposited on coupons of a Mo-9Si-8B (in at.%) alloy using magnetron sputtering. A double layer design was applied: a 2 µm thick intermediate Mo5SiB2 layer to prevent interdiffusion and approximately 5 µm thick protective topcoats with different chemical compositions: Mo-45Si-25B, Mo-55Si-10B, Mo-29Si-15B, Mo-48Si-24Al, Mo-71Si-8Al (all in at.%). The amorphous as-deposited coatings were annealed in a vacuum furnace. In the boron containing Mo-Si topcoats, the MoSi2 and MoB phases formed as well as the Mo5Si3 phase in the Mo-29Si-15B coating. In the annealed Mo-48Si-24Al and Mo-71Si-8Al topcoats, the C40-Mo(Si,Al)2 and C11b-MoSi2 phases were observed, respectively. The oxidation behavior of the coated samples was investigated at 800, 1100 and 1300 °C under cyclic condition in laboratory air. The dwell time at high temperature was 10 or 20 h and the samples were tested for up to 10 cycles. Microstructural examinations of the coated samples were carried out using scanning electron microscopy, energy-dispersive X-ray spectroscopy, glow discharge optical emission spectroscopy and X-ray diffraction measurements. Please click Additional Files below to see the full abstract

Lifetime of environmental/thermal barrier coatings deposited on an Nb/Nb5Si3- based alloy with FeB-Modified M7Si6-based bond coat

To enhance the performance of aircraft engines, high temperature materials are required being capable to operate at temperatures significantly higher than the temperature limit of about 1150°C approached for Ni-based superalloys currently employed. Nb/Nb5Si3-based composites are promising candidates for turbine engine applications at temperatures up to 1300°C, exhibiting balanced mechanical properties and reduced density compared to Ni-based superalloys [1]. To use these composites in gas turbine combustion atmosphere, environmental/thermal barrier coatings (E/TBCs) are required to protect them against heat, degradation in flowing water vapour and chemical attack of calcium-magnesium-alumino-silicate (CMAS)

CtBP1-Mediated Membrane Fission Contributes to Effective Recycling of Synaptic Vesicles

Compensatory endocytosis of released synaptic vesicles (SVs) relies on coordinated signaling at the lipid-protein interface. Here, we address the synaptic function of C-terminal binding protein 1 (CtBP1), a ubiquitous regulator of gene expression and membrane trafficking in cultured hippocampal neurons. In the absence of CtBP1, synapses form in greater density and show changes in SV distribution and size. The increased basal neurotransmission and enhanced synaptic depression could be attributed to a higher vesicular release probability and a smaller fraction of release-competent SVs, respectively. Rescue experiments with specifically targeted constructs indicate that, while synaptogenesis and release probability are controlled by nuclear CtBP1, the efficient recycling of SVs relies on its synaptic expression. The ability of presynaptic CtBP1 to facilitate compensatory endocytosis depends on its membrane-fission activity and the activation of the lipid-metabolizing enzyme PLD1. Thus, CtBP1 regulates SV recycling by promoting a permissive lipid environment for compensatory endocytosis

New Platform Technology for Comprehensive Serological Diagnostics of Autoimmune Diseases

Antibody assessment is an essential part in the serological diagnosis of autoimmune diseases. However, different diagnostic strategies have been proposed for the work up of sera in particular from patients with systemic autoimmune rheumatic disease (SARD). In general, screening for SARD-associated antibodies by indirect immunofluorescence (IIF) is followed by confirmatory testing covering different assay techniques. Due to lacking automation, standardization, modern data management, and human bias in IIF screening, this two-stage approach has recently been challenged by multiplex techniques particularly in laboratories with high workload. However, detection of antinuclear antibodies by IIF is still recommended to be the gold standard method for antibody screening in sera from patients with suspected SARD. To address the limitations of IIF and to meet the demand for cost-efficient autoantibody screening, automated IIF methods employing novel pattern recognition algorithms for image analysis have been introduced recently. In this respect, the AKLIDES technology has been the first commercially available platform for automated interpretation of cell-based IIF testing and provides multiplexing by addressable microbead immunoassays for confirmatory testing. This paper gives an overview of recently published studies demonstrating the advantages of this new technology for SARD serology

Causal effect of plasminogen activator inhibitor type 1 on coronary heart disease

Background--Plasminogen activator inhibitor type 1 (PAI-1) plays an essential role in the fibrinolysis system and thrombosis. Population studies have reported that blood PAI-1 levels are associated with increased risk of coronary heart disease (CHD). However, it is unclear whether the association reflects a causal influence of PAI-1 on CHD risk. Methods and Results--To evaluate the association between PAI-1 and CHD, we applied a 3-step strategy. First, we investigated the observational association between PAI-1 and CHD incidence using a systematic review based on a literature search for PAI-1 and CHD studies. Second, we explored the causal association between PAI-1 and CHD using a Mendelian randomization approach using summary statistics from large genome-wide association studies. Finally, we explored the causal effect of PAI-1 on cardiovascular risk factors including metabolic and subclinical atherosclerosis measures. In the systematic meta-analysis, the highest quantile of blood PAI-1 level was associated with higher CHD risk comparing with the lowest quantile (odds ratio=2.17; 95% CI: 1.53, 3.07) in an age- and sex-adjusted model. The effect size was reduced in studies using a multivariable-adjusted model (odds ratio=1.46; 95% CI: 1.13, 1.88). The Mendelian randomization analyses suggested a causal effect of increased PAI-1 level on CHD risk (odds ratio=1.22 per unit increase of log-transformed PAI-1; 95% CI: 1.01, 1.47). In addition, we also detected a causal effect of PAI-1 on elevating blood glucose and high-density lipoprotein cholesterol. Conclusions--Our study indicates a causal effect of elevated PAI-1 level on CHD risk, which may be mediated by glucose dysfunction

New genetic loci link adipose and insulin biology to body fat distribution.

Body fat distribution is a heritable trait and a well-established predictor of adverse metabolic outcomes, independent of overall adiposity. To increase our understanding of the genetic basis of body fat distribution and its molecular links to cardiometabolic traits, here we conduct genome-wide association meta-analyses of traits related to waist and hip circumferences in up to 224,459 individuals. We identify 49 loci (33 new) associated with waist-to-hip ratio adjusted for body mass index (BMI), and an additional 19 loci newly associated with related waist and hip circumference measures (P < 5 × 10(-8)). In total, 20 of the 49 waist-to-hip ratio adjusted for BMI loci show significant sexual dimorphism, 19 of which display a stronger effect in women. The identified loci were enriched for genes expressed in adipose tissue and for putative regulatory elements in adipocytes. Pathway analyses implicated adipogenesis, angiogenesis, transcriptional regulation and insulin resistance as processes affecting fat distribution, providing insight into potential pathophysiological mechanisms

Genetic associations at 53 loci highlight cell types and biological pathways relevant for kidney function.

Reduced glomerular filtration rate defines chronic kidney disease and is associated with cardiovascular and all-cause mortality. We conducted a meta-analysis of genome-wide association studies for estimated glomerular filtration rate (eGFR), combining data across 133,413 individuals with replication in up to 42,166 individuals. We identify 24 new and confirm 29 previously identified loci. Of these 53 loci, 19 associate with eGFR among individuals with diabetes. Using bioinformatics, we show that identified genes at eGFR loci are enriched for expression in kidney tissues and in pathways relevant for kidney development and transmembrane transporter activity, kidney structure, and regulation of glucose metabolism. Chromatin state mapping and DNase I hypersensitivity analyses across adult tissues demonstrate preferential mapping of associated variants to regulatory regions in kidney but not extra-renal tissues. These findings suggest that genetic determinants of eGFR are mediated largely through direct effects within the kidney and highlight important cell types and biological pathways