Antarctic marine mammals and ocean acoustics

Marine mammals rely on sound and hearing as their primary means of communication and sensing their world. Concerns that anthropogenic sound in the ocean could infer their sensing, cause stress or even damage their hearing physically rose a controversial discussion and triggered a worldwide boost in marine bioacoustic research. Innovative acoustic technologies and field methods are required to provide a basis for carefully designed and technically challenging research projects on free-ranging marine mammals, especially under the harsh environmental conditions of polar regions. The Ocean Acoustics group within the Marine Observing Systems section endeavors multidisciplinary research of environmental scientists, geophysicists, oceanographers, physicists, physiologists, and biologists to investigate the need and scope of mitigation measures for the effects of man-generated sound in the ocean, develop acoustic census techniques, explore marine mammal responses to various anthropogenic sounds, and study the vocal behaviour and hearing physiology of Antarctic marine mammals

Exploiting technological synergies for future launch vehicles

Two launch vehicle concepts based on technologies available today or in a short term future in Western Europe are presented. The design of both launchers has the goal of exploiting synergies with current European programs to limit development and operational costs. Technologies of particular interest here are the high performance solid rocket motors with carbon-epoxy filament wound monolithic motor cases and the future high performance cryogenic expander cycle engine Vinci. The first concept dubbed ANGELA (A New GEneration LAuncher) is a study financed with funds of the German Ministry of Economics and managed by the DLR Space Administration. The project, which started in the summer of 2012 aims at designing a low cost versatile launcher able to place payloads between 2 and 5 tons into GTO. Three architectures have been considered during the first phase of the study. This phase was concluded in March 2013 with the preliminary stagings, which will be the starting point of more detailed analyses. The first architecture is made out of an H110 (stage with 110 tons of LOx/LH2) equipped with two Vulcain 2 engines with shortened nozzles and an H29 propelled by a Vinci engine. In addition the variation of the number of P36 solid rocket boosters allow to reach the entire range of payload performance. The second architecture differs from the first one only by the use of a new staged-combustion engine instead of two Vulcain 2 engines. The new engine, which should deliver 1800 kN in vacuum, allows a reduction of the size of the stages to H90-H24, enhanced with P34 boosters. The third and last architecture is a so called Multi PPH. The first stage is a bundle of 2 or 3 P120 solid rocket motors. The second stage is made out of one single P120, strictly similar to those used for the first stage. Finally the upper stage is an H23 equipped with a Vinci engine, the same as the two other architectures. The second launcher concept described in this paper is the small TSTO launch vehicle. It consists of a large solid rocket motor first stage P175 and a cryogenic upper stage propelled by the Vinci engine, H26. The preliminary design performed at DLR-SART considers two target performances. The light version of the small TSTO shall perform Galileo satellite replacement single launch missions to MTO corresponding to a payload performance of about 1400 kg in GTO. A heavy version of the launch vehicle shall be able to launch payloads up to 3000 kg in GTO. The performance increase for the heavy version is made possible by the addition of two pairs of P23 boosters, the second pair being ignited with a delay

REBOOKING MEETING ROOM WHEN MEETING ROOM BECOMES UNAVAILABLE

In organizations with multiple meeting rooms or conference rooms, meeting rooms can become unavailable after a meeting has already been scheduled in that room. The described system can respond to an indication that the meeting room is unavailable by finding another meeting room for the meeting that meets the requirements for the meeting. The system can notify the participants or attendees of the meeting of the new meeting room

Biomarkers for Non-Invasive Stratification of Coronary Artery Disease and Prognostic Impact on Long-Term Survival in Patients with Stable Coronary Heart Disease

Knowledge about cardiac and inflammatory biomarkers in patients with stable coronary artery disease (CAD) is limited. To address this, we analyzed 3072 patients (36% female) with a median follow-up of 10 years in the Leipzig LIFE Heart Study with suspected CAD with coronary angiography. Selected biomarkers included troponin T (hsTNT), N-terminal pro B-type natriuretic peptide (NT-proBNP), copeptin, C-reactive protein (hsCRP), and interleukin-6 (IL-6). Patients were stratified by CAD severity: CAD0 (no sclerosis), CAD1 (non-obstructive, i.e., stenosis < 50%), and CAD2 (one stenosis 50%). Group comparison (GC) included GC1: CAD0 + 1 vs. CAD2; GC2: CAD0 vs. CAD1 + 2. CAD0, CAD1, and CAD2 were apparent in 1271, 631, and 1170 patients, respectively. Adjusted for classical risk factors, hs-cTnT, NT-proBNP, and IL-6 differed significantly in both GC and hsCRP only in GC2. After multivariate analysis, hs-cTnT, NT-proBNP, and IL-6 remained significant in GC1. In GC2, hs-cTnT (p < 0.001) and copeptin (p = 0.014) reached significance. Ten-year survival in groups CAD0, CAD1, and CAD2 was 88.3%, 77.3%, and 72.4%. Incorporation of hs-cTnT, NT-proBNP, copeptin, and IL-6 improved risk prediction (p < 0.001). The studied cardiac and inflammatory biomarkers enable fast and precise non-invasive identification of mortality risk in CAD patients, allowing the tailoring of primary and secondary CAD prevention

The Human Blood Transcriptome in a Large Population Cohort and Its Relation to Aging and Health

Background: The blood transcriptome is expected to provide a detailed picture of an organism’s physiological state with potential outcomes for applications in medical diagnostics and molecular and epidemiological research.We here present the analysis of blood specimens of 3,388 adult individuals, together with phenotype characteristics such as disease history, medication status, lifestyle factors, and body mass index (BMI). The size and heterogeneity of this data challenges analytics in terms of dimension reduction, knowledge mining, feature extraction, and data integration. Methods: Self-organizing maps (SOM)-machine learning was applied to study transcriptional states on a population-wide scale. This method permits a detailed description and visualization of the molecular heterogeneity of transcriptomes and of their association with different phenotypic features. Results: The diversity of transcriptomes is described by personalized SOM-portraits, which specify the samples in terms of modules of co-expressed genes of different functional context. We identified two major blood transcriptome types where type 1 was found more in men, the elderly, and overweight people and it upregulated genes associated with inflammation and increased heme metabolism, while type 2 was predominantly found in women, younger, and normal weight participants and it was associated with activated immune responses, transcriptional, ribosomal, mitochondrial, and telomere-maintenance cell-functions. We find a striking overlap of signatures shared by multiple diseases, aging, and obesity driven by an underlying common pattern, which was associated with the immune response and the increase of inflammatory processes. Conclusions: Machine learning applications for large and heterogeneous omics data provide a holistic view on the diversity of the human blood transcriptome. It provides a tool for comparative analyses of transcriptional signatures and of associated phenotypes in population studies and medical applications

Integration of Genome-Wide SNP Data and Gene-Expression Profiles Reveals Six Novel Loci and Regulatory Mechanisms for Amino Acids and Acylcarnitines in Whole Blood

Profiling amino acids and acylcarnitines in whole blood spots is a powerful tool in the laboratory diagnosis of several inborn errors of metabolism. Emerging data suggests that altered blood levels of amino acids and acylcarnitines are also associated with common metabolic diseases in adults. Thus, the identification of common genetic determinants for blood metabolites might shed light on pathways contributing to human physiology and common diseases. We applied a targeted mass-spectrometry-based method to analyze whole blood concentrations of 96 amino acids, acylcarnitines and pathway associated metabolite ratios in a Central European cohort of 2, 107 adults and performed genome-wide association (GWA) to identify genetic modifiers of metabolite concentrations. We discovered and replicated six novel loci associated with blood levels of total acylcarnitine, arginine (both on chromosome 6;rs12210538, rs17657775),propionylcarnitine (chromosome 10;rs12779637),2-hydroxyisovalerylcarnitine (chromosome 21;rs1571700),stearoylcarnitine (chromosome 1;rs3811444),and aspartic acid traits (chromosome 8;rs750472). Based on an integrative analysis of expression quantitative trait loci in blood mononuclear cells and correlations between gene expressions and metabolite levels, we provide evidence for putative causative genes: SLC22A16 for total acylcarnitines, ARG1 for arginine, HLCS for 2-hydroxyisovalerylcarnitine, JAM3 for stearoylcarnitine via a trans-effect at chromosome 1, and PPP1R16A for aspartic acid traits. Further, we report replication and provide additional functional evidence for ten loci that have previously been published for metabolites measured in plasma, serum or urine. In conclusion, our integrative analysis of SNP, gene-expression and metabolite data points to novel genetic factors that may be involved in the regulation of human metabolism. At several loci, we provide evidence for metabolite regulation via gene-expression and observed overlaps with GWAS loci for common diseases. These results form a strong rationale for subsequent functional and disease-related studies

Association of MICA with rheumatoid arthritis independent of known HLA-DRB1 risk alleles in a family-based and a case control study

Introduction The gene MICA encodes the protein major histocompatibility complex class I polypeptide-related sequence A. It is expressed in synovium of patients with rheumatoid arthritis (RA) and its implication in autoimmunity is discussed. We analyzed the association of genetic variants of MICA with susceptibility to RA. Methods Initially, 300 French Caucasian individuals belonging to 100 RA trio families were studied. An additional 100 independent RA trio families and a German Caucasian case-control cohort (90/182 individuals) were available for replication. As MICA is situated in proximity to known risk alleles of the HLA-DRB1 locus, our analysis accounted for linkage disequilibrium either by analyzing the subgroup consisting of parents not carrying HLA-DRB1 risk alleles with transmission disequilibrium test (TDT) or by implementing a regression model including all available data. Analysis included a microsatellite polymorphism (GCT)n and single-nucleotide polymorphisms (SNPs) rs3763288 and rs1051794. Results In contrast to the other investigated polymorphisms, the non-synonymously coding SNP MICA-250 (rs1051794, Lys196Glu) was strongly associated in the first family cohort (TDT: P = 0.014; regression model: odds ratio [OR] 0.46, 95% confidence interval [CI] 0.25 to 0.82, P = 0.007). Although the replication family sample showed only a trend, combined family data remained consistent with the hypothesis of MICA-250 association independent from shared epitope (SE) alleles (TDT: P = 0.027; regression model: OR 0.56, 95% CI 0.38 to 0.83, P = 0.003). We also replicated the protective association of MICA-250A within a German Caucasian cohort (OR 0.31, 95% CI 0.1 to 0.7, P = 0.005; regression model: OR 0.6, 95% CI 0.37 to 0.96, P = 0.032). We showed complete linkage disequilibrium of MICA-250 (D' = 1, r2= 1) with the functional MICA variant rs1051792 (D' = 1, r2= 1). As rs1051792 confers differential allelic affinity of MICA to the receptor NKG2D, this provides a possible functional explanation for the observed association. Conclusions We present evidence for linkage and association of MICA-250 (rs1051794) with RA independent of known HLA-DRB1 risk alleles, suggesting MICA as an RA susceptibility gene. However, more studies within other populations are necessary to prove the general relevance of this polymorphism for RA