A new antenna concept for satellite communications

A novel antenna configuration of two reflecting surfaces and a phased array is examined for application to satellite communications and shown to be superior in every respect to earlier designs for service to the continental United States from synchronous orbit. The vignetting that afflicts other two reflector optical systems is eliminated by use of a reflecting field element. The remaining aberrations, predominantly coma, are isolated in the time delay distribution at the surface of the array and can be compensated by ordinary array techniques. The optics exhibits infinite bandwidth and the frequency range is limited only by the design of the array

Beyond Perfect phylogeny: Multisample Phylogeny reconstruction via ILP

Most of the evolutionary history reconstruction approaches are based on the infinite site assumption which is underlying the Perfect Phylogeny model. This is one of the most used models in cancer genomics. Recent results gives a strong evidence that recurrent and back mutations are present in the evolutionary history of tumors [19], thus showing that more general models then the Perfect phylogeny are required. To address this problem we propose a framework based on the notion of Incomplete Perfect Phylogeny. Our framework incorporates losing and gaining mutations, hence including the Dollo and the Camin-Sokal models, and is described with an Integer Linear Programming (ILP) formulation. Our approach generalizes the notion of persistent phylogeny [1] and the ILP approach [14, 15] proposed to solve the corresponding phylogeny reconstruction problem on character data. The final goal of our paper is to integrate our approach into an ILP formulation of the problem of reconstructing trees on mixed populations, where the input data consists of the fraction of cells in a set of samples that have a certain mutation. This is a fundamental problem in cancer genomics, where the goal is to study the evolutionary history of a tumor. An experimental analysis shows that our ILP approach is able to explain data that do not fit the perfect phylogeny assumption, thereby allowing (1) multiple losses and gains of mutations, and (2) a number of subpopulations that is smaller than the number of input mutations

Common Genetic Polymorphisms Influence Blood Biomarker Measurements in COPD

Implementing precision medicine for complex diseases such as chronic obstructive lung disease (COPD) will require extensive use of biomarkers and an in-depth understanding of how genetic, epigenetic, and environmental variations contribute to phenotypic diversity and disease progression. A meta-analysis from two large cohorts of current and former smokers with and without COPD [SPIROMICS (N = 750); COPDGene (N = 590)] was used to identify single nucleotide polymorphisms (SNPs) associated with measurement of 88 blood proteins (protein quantitative trait loci; pQTLs). PQTLs consistently replicated between the two cohorts. Features of pQTLs were compared to previously reported expression QTLs (eQTLs). Inference of causal relations of pQTL genotypes, biomarker measurements, and four clinical COPD phenotypes (airflow obstruction, emphysema, exacerbation history, and chronic bronchitis) were explored using conditional independence tests. We identified 527 highly significant (p 10% of measured variation in 13 protein biomarkers, with a single SNP (rs7041; p = 10−392) explaining 71%-75% of the measured variation in vitamin D binding protein (gene = GC). Some of these pQTLs [e.g., pQTLs for VDBP, sRAGE (gene = AGER), surfactant protein D (gene = SFTPD), and TNFRSF10C] have been previously associated with COPD phenotypes. Most pQTLs were local (cis), but distant (trans) pQTL SNPs in the ABO blood group locus were the top pQTL SNPs for five proteins. The inclusion of pQTL SNPs improved the clinical predictive value for the established association of sRAGE and emphysema, and the explanation of variance (R2) for emphysema improved from 0.3 to 0.4 when the pQTL SNP was included in the model along with clinical covariates. Causal modeling provided insight into specific pQTL-disease relationships for airflow obstruction and emphysema. In conclusion, given the frequency of highly significant local pQTLs, the large amount of variance potentially explained by pQTL, and the differences observed between pQTLs and eQTLs SNPs, we recommend that protein biomarker-disease association studies take into account the potential effect of common local SNPs and that pQTLs be integrated along with eQTLs to uncover disease mechanisms. Large-scale blood biomarker studies would also benefit from close attention to the ABO blood group