Mitigation of GPS Multipath Using Polarization and Spatial Diversities

This paper presents a GPS multipath mitigation method using a dual circularly polarized antenna array and a multi-channel receiver. The method is based on the exploitation of both polarization and spatial diversity associated with a GPS signal and its multipath signals available at the receiver input. Conventional GPS antennas are right-hand circularly polarized (RHCP) to suppress multipath contributions to the input. This polarization-based discrimination of multipath signal cannot completely eliminate multipath induced GPS range measurement errors. We present an algorithm that performs spatial processing on the input from the left-hand circular polarized (LHCP) array with an increased relative strength of the multipath signal, thereby providing improved multipath angle of arrival (AOA) estimation. With the known multipath AOA and direct signal AOA (which can be obtained from almanac/ephemeris together with the antenna attitude or estimated in a separate process), we can then take advantage of the spatial diversity of the direct signal and multipath by applying null-steering to the RHCP array input. The paper presents the algorithm and simulation results for a uniform linear array receiving one direct signal and one multipath. Our preliminary studies showed that the multipath AOA estimator produces negligible error if the direct signal and multipath AOA are not close to each other (more than 5 degrees apart) and that the direct signal is not at low elevation. The results also suggested that longer time delay between the direct and multipath signal will increase multipath AOA estimation error but this increase is tolerable. Furthermore, we demonstrated that the multipath estimation improves with increasing spatial diversity for multipath and direct GPS signals even if the signal arrivals are close in time. Finally, we demonstrated that the multipath mitigation technique does produce an improved receiver correlator function which directly impacts the GPS code range measurement accurac

Phylogenetic Networks Do not Need to Be Complex: Using Fewer Reticulations to Represent Conflicting Clusters

Phylogenetic trees are widely used to display estimates of how groups of species evolved. Each phylogenetic tree can be seen as a collection of clusters, subgroups of the species that evolved from a common ancestor. When phylogenetic trees are obtained for several data sets (e.g. for different genes), then their clusters are often contradicting. Consequently, the set of all clusters of such a data set cannot be combined into a single phylogenetic tree. Phylogenetic networks are a generalization of phylogenetic trees that can be used to display more complex evolutionary histories, including reticulate events such as hybridizations, recombinations and horizontal gene transfers. Here we present the new CASS algorithm that can combine any set of clusters into a phylogenetic network. We show that the networks constructed by CASS are usually simpler than networks constructed by other available methods. Moreover, we show that CASS is guaranteed to produce a network with at most two reticulations per biconnected component, whenever such a network exists. We have implemented CASS and integrated it in the freely available Dendroscope software

Dehydro­brachylaenolide: an eudesmane-type sesquiterpene lactone

The three-ring eudesmanolide, C15H16O3, is a natural product isolated from Dicoma anomala Sond. (Asteraceae). The compound contains an endo–exo cross conjugated methyl­enecyclo­hexenone ring with an envelope conformation trans-fused with cyclo­hexane and trans-annelated with an α-methyl­ene γ-lactone. The absolute structure was assigned by optical rotation measurements compared to those from the synthetic compound with known stereochemistry. The crystal packing is consolidated by C—H⋯O interactions

Inactivation of the type I interferon pathway reveals long double‐stranded RNA ‐mediated RNA interference in mammalian cells

RNA interference (RNAi) elicited by long double-stranded (ds) or base-paired viral RNA constitutes the major mechanism of antiviral defence in plants and invertebrates. In contrast, it is controversial whether it acts in chordates. Rather, in vertebrates, viral RNAs induce a distinct defence system known as the interferon (IFN) response. Here, we tested the possibility that the IFN response masks or inhibits antiviral RNAi in mammalian cells. Consistent with that notion, we find that sequence-specific gene silencing can be triggered by long dsRNAs in differentiated mouse cells rendered deficient in components of the IFN pathway. This unveiled response is dependent on the canonical RNAi machinery and is lost upon treatment of IFN-responsive cells with type I IFN. Notably, transfection with long dsRNA specifically vaccinates IFN-deficient cells against infection with viruses bearing a homologous sequence. Thus, our data reveal that RNAi constitutes an ancient antiviral strategy conserved from plants to mammals that precedes but has not been superseded by vertebrate evolution of the IFN system

An embedding scheme for the Dirac equation

An embedding scheme is developed for the Dirac Hamiltonian H. Dividing space into regions I and II separated by surface S, an expression is derived for the expectation value of H which makes explicit reference to a trial function defined in I alone, with all details of region II replaced by an effective potential acting on S and which is related to the Green function of region II. Stationary solutions provide approximations to the eigenstates of H within I. The Green function for the embedded Hamiltonian is equal to the Green function for the entire system in region I. Application of the method is illustrated for the problem of a hydrogen atom in a spherical cavity and an Au(001)/Ag/Au(001) sandwich structure using basis sets that satisfy kinetic balance.Comment: 16 pages, 5 figure

Primary sequence and epigenetic determinants of in vivo occupancy of genomic DNA by GATA1

DNA sequence motifs and epigenetic modifications contribute to specific binding by a transcription factor, but the extent to which each feature determines occupancy in vivo is poorly understood. We addressed this question in erythroid cells by identifying DNA segments occupied by GATA1 and measuring the level of trimethylation of histone H3 lysine 27 (H3K27me3) and monomethylation of H3 lysine 4 (H3K4me1) along a 66 Mb region of mouse chromosome 7. While 91% of the GATA1-occupied segments contain the consensus binding-site motif WGATAR, only ∼0.7% of DNA segments with such a motif are occupied. Using a discriminative motif enumeration method, we identified additional motifs predictive of occupancy given the presence of WGATAR. The specific motif variant AGATAA and occurrence of multiple WGATAR motifs are both strong discriminators. Combining motifs to pair a WGATAR motif with a binding site motif for GATA1, EKLF or SP1 improves discriminative power. Epigenetic modifications are also strong determinants, with the factor-bound segments highly enriched for H3K4me1 and depleted of H3K27me3. Combining primary sequence and epigenetic determinants captures 52% of the GATA1-occupied DNA segments and substantially increases the specificity, to one out of seven segments with the required motif combination and epigenetic signals being bound

A prospective multicenter validation study for a novel angiography-derived physiological assessment software:Rationale and design of the radiographic imaging validation and evaluation for Angio-iFR (ReVEAL iFR) study

Background Angiography-derived physiological assessment of coronary lesions has emerged as an alternative to wire based assessment aiming at less-invasiveness and shorter procedural time as well as cost effectiveness in physiology-guided decision making. However, current available image-derived physiology software have limitations including the requirement of multiple projections and are time consuming. Methods/Design The ReVEAL iFR (Radiographic imaging Validation and EvALuation for Angio-iFR) trial is a multicenter, multicontinental, validation study which aims to validate the diagnostic accuracy of the Angio-iFR medical software device (Philips, San Diego, US) in patients undergoing angiography for Chronic Coronary Syndrome (CCS). The Angio-iFR will enable operators to predict both the iFR and FFR value within a few seconds from a single projection of cine angiography by using a lumped parameter fluid dynamics model. Approximately 440 patients with at least one de-novo 40% to 90% stenosis by visual angiographic assessment will be enrolled in the study. The primary endpoint is the sensitivity and specificity of the iFR and FFR for a given lesion compared to the corresponding invasive measures. The enrollment started in August 2019, and was completed in March 2021. Summary The Angio-iFR system has the potential of simplifying physiological evaluation of coronary stenosis compared with available systems, providing estimates of both FFR and iFR. The ReVEAL iFR study will investigate the predictive performance of the novel Angio-iFR software in CCS patients. Ultimately, based on its unique characteristics, the Angio-iFR system may contribute to improve adoption of functional coronary assessment and the workflow in the catheter laboratory

Molecular heterogeneity in AML/MDS patients with 3q21q26 rearrangements

Patients with 3q21q26 rearrangements seem to share similar clinicopathologic features and a common molecular mechanism, leading to myelodysplasia or acute myeloid leukemia (AML). The ectopic expression of EVI1 (3q26) has been implicated in the dysplasia that characterizes this subset of myeloid neoplasias. However, lack of EVI1 expression has been reported in several cases, and overexpression of EVI1 was detected in 9% of AML cases without 3q26 abnormalities. We report the molecular characterization of seven patients with inv(3)(q21q26), t(3;3)(q21;q26) or related abnormalities. EVI1 expression was detected in only one case, and thus ectopic expression of this gene failed to explain all of these cases. GATA2 (3q21) was found to be overexpressed in 5 of the 7 patients. GATA2 is highly expressed in stem cells, and its expression dramatically decreases when erythroid and megakaryocytic differentiation proceeds. No mutations in GATA1 were found in any patient, excluding loss of function of GATA1 as the cause of GATA2 overexpression. We report finding molecular heterogeneity in patients with 3q21q26 rearrangements in both breakpoints and in the expression pattern of the genes near these breakpoints. Our data suggest that a unique mechanism is not likely to be involved in 3q21q26 rearrangements

A Single cis Element Maintains Repression of the Key Developmental Regulator Gata2

In development, lineage-restricted transcription factors simultaneously promote differentiation while repressing alternative fates. Molecular dissection of this process has been challenging as transcription factor loci are regulated by many trans-acting factors functioning through dispersed cis elements. It is not understood whether these elements function collectively to confer transcriptional regulation, or individually to control specific aspects of activation or repression, such as initiation versus maintenance. Here, we have analyzed cis element regulation of the critical hematopoietic factor Gata2, which is expressed in early precursors and repressed as GATA-1 levels rise during terminal differentiation. We engineered mice lacking a single cis element −1.8 kb upstream of the Gata2 transcriptional start site. Although Gata2 is normally repressed in late-stage erythroblasts, the −1.8 kb mutation unexpectedly resulted in reactivated Gata2 transcription, blocked differentiation, and an aberrant lineage-specific gene expression pattern. Our findings demonstrate that the −1.8 kb site selectively maintains repression, confers a specific histone modification pattern and expels RNA Polymerase II from the locus. These studies reveal how an individual cis element establishes a normal developmental program via regulating specific steps in the mechanism by which a critical transcription factor is repressed