Adaptive Filters Revisited - RFI Mitigation in pulsar observations

Pulsar detection and timing experiments are applications where adaptive filters seem eminently suitable tools for radio-frequency-interference (RFI) mitigation. We describe a novel variant which works well in field trials of pulsar observations centred on an observing frequency of 675 MHz, a bandwidth of 64 MHz and with 2-bit sampling. Adaptive filters have generally received bad press for RFI mitigation in radio astronomical observations with their most serious drawback being a spectral echo of the RFI embedded in the filtered signals. Pulsar observations are intrinsically less sensitive to this as they operate in the (pulsar period) time domain. The field trials have allowed us to identify those issues which limit the effectiveness of the adaptive filter. We conclude that adaptive filters can significantly improve pulsar observations in the presence of RFI.Comment: Accepted for publication in Radio Scienc

Two-body Cabibbo-suppressed Decays of Charmed Baryons into Vector Mesons and into Photons

The heavy quark effective theory and the factorization approximation are used to treat the Cabibbo-suppressed decays of charmed baryons to vector mesons, $\Lambda_C\rightarrow p{\rho^0}, p\omega$, $\Xi_C^{+,0}\rightarrow\Sigma^{+,0}\phi, \Sigma^{+,0}{\rho^0}, \Sigma^{+,0}\omega$ and $\Xi_C^{0}\rightarrow\Lambda\phi, \Lambda\rho, \Lambda\omega$. The input from two recent experimental results on $\Lambda_C$ decays allows the estimation of the branching ratios for these modes, which turn out to be between $10^{-4}$ and $10^{-3}$. The long distance contribution of these transitions via vector meson dominance to the radiative weak processes $\Lambda_C\rightarrow p\gamma$, $\Xi_C\rightarrow\Sigma\gamma$ and $\Xi_C^0\rightarrow\Lambda\gamma$ leads to quite small branching ratios, $10^{-6}-10^{-9}$; the larger value holds if a sum rule between the coupling constants of the vector mesons is broken.Comment: 11 pages, latex, no figure

History of ZIKV infections in India and management of disease outbreaks

© 2007-2018 Frontiers Media S.A. All Rights Reserved. Zika virus (ZIKV) is an emerging arbovirus infection endemic in multiple countries spread from Asia, Africa to the Americas and Europe. Previously known to cause rare and fairly benign human infections, ZIKV has become a major international public health emergency after being linked to unexpected neurological complications, that includes fetal brain damage/death and microcephaly in babies born to infected mothers and Guillain-Barre syndrome (GBS) in adults. It appears that a single genetic mutation in the ZIKV genome, likely acquired during explosive ZIKV outbreak in French Polynesia (2013), made virus causing mild disease to target fetus brain. The Aedes mosquitoes are found to be the main carrier of ZIKV, passing the virus to humans. Originally isolated from patients in Africa in 1954 (African lineage), virus disseminated to Southeast Asia (Asian lineage), establishing new endemic foci, including one in India. Numerous cases of ZIKV infection have been reported in several locations in India and neighboring countries like Pakistan and Bangladesh since mid of the last century, suggesting that the virus reached this part of Asia soon after it was first discovered in Uganda in 1947. Although, the exact means by which ZIKV was introduced to India remains unknown, it appears that the ZIKV strain circulating in India possibly belongs to the "Asian lineage, " which has not yet been associated with microcephaly and other neurological disorders. However, there still exists a threat that the contemporary ZIKV virulent strain from South America, carrying a mutation can return to Asia, posing a potential crisis to newborns and adult patients. Currently there is no specific vaccine or antiviral medication to combat ZIKV infection, thus, vector control and continuous monitoring of potential ZIKV exposure is essential to prevent the devastating consequences similar to the ones experienced in Brazil. However, the major obstacle faced by Indian healthcare agencies is that most cases of ZIKV infection have been reported in rural areas that lack access to rapid diagnosis of infection. In this review, we attempt to present a comprehensive analysis of what is currently known about the ZIKV infection in India and the neighboring countries

Formation of CO2 on a carbonaceous surface: a quantum chemical study

The formation of CO2 in the gas phase and on a polyaromatic hydrocarbon surface (coronene) via three possible pathways is investigated with density functional theory. Calculations show that the coronene surface catalyses the formation of CO2 on model grain surfaces. The addition of O-3 to CO is activated by 2530 K in the gas phase. This barrier is lowered by 253 K for the Eley-Rideal mechanism and 952 K for the hot-atom mechanism on the surface of coronene. Alternative pathways for the formation of CO2 are the addition of O-3 to the HCO radical, followed by dissociation of the HCO2 intermediate. The O + HCO addition is barrierless in the gas phase and on the surface and is more than sufficiently exothermic to subsequently cleave the H-C bond. The third mechanism, OH + CO addition followed by H removal from the energized HOCO intermediate, has a gas-phase exit barrier that is 1160 K lower than the entrance barrier. On the coronene surface, however, both barriers are almost equal. Because the HOCO intermediate can also be stabilized by energy dissipation to the surface, it is anticipated that for the surface reaction the adsorbed HOCO could be a long-lived intermediate. In this case, the stabilized HOCO intermediate could react, in a barrierless manner, with a hydrogen atom to form H-2 + CO2, HCO2H, or H2O + CO

ZIKV infection regulates inflammasomes pathway for replication in monocytes

© 2017 The Author(s). ZIKV causes microcephaly by crossing the placental barrier, however, the mechanism of trans-placental dissemination of ZIKV remains unknown. Here, we sought to determine whether monocytes, which can cross tissue barriers, assist ZIKV dissemination to the fetus. We determined this by infecting monocytes with two strains of ZIKV: South American (PRVABC59) and Nigerian (IBH30656) and analyzing viral replication. We found that ZIKV infects and replicates in monocytes and macrophages, which results in the modulation of a large number of cellular genes. Analysis of these genes identified multiple pathways including inflammasome to be targeted by ZIKV, which was confirmed by analyzing the transcript levels of the proteins of inflammasome pathways, NLRP3, ASC, caspase 1, IL-1 and IL-18. Interestingly, IFNα and the IFN inducible gene, MxA were not enhanced, suggesting prevention of innate antiviral defense by ZIKV. Also, inhibition of inflammasome led to an increased transcriptional activity of IFNα, MxA and CXCL10. Based on these results we suggest that ZIKV transcription is regulated by inflammasomes

DNA Methylation Dynamics of Human Hematopoietic Stem Cell Differentiation

Hematopoietic stem cells give rise to all blood cells in a differentiation process that involves widespread epigenome remodeling. Here we present genome-wide reference maps of the associated DNA methylation dynamics. We used a meta-epigenomic approach that combines DNA methylation profiles across many small pools of cells and performed single-cell methylome sequencing to assess cell-to-cell heterogeneity. The resulting dataset identified characteristic differences between HSCs derived from fetal liver, cord blood, bone marrow, and peripheral blood. We also observed lineage-specific DNA methylation between myeloid and lymphoid progenitors, characterized immature multi-lymphoid progenitors, and detected progressive DNA methylation differences in maturing megakaryocytes. We linked these patterns to gene expression, histone modifications, and chromatin accessibility, and we used machine learning to derive a model of human hematopoietic differentiation directly from DNA methylation data. Our results contribute to a better understanding of human hematopoietic stem cell differentiation and provide a framework for studying blood-linked diseases.This work was funded by the BLUEPRINT project (European Union’s Seventh Framework Programme grant 282510), the NIHR Cambridge Biomedical Research Centre, and the Austrian Academy of Sciences. F.A.C. is supported by a Medical Research Council Clinical Training Fellowship (grant MR/K024043/1). F.H. is supported by a postdoctoral fellowship of the German Research Council (DFG; grant HA 7723/1-1). J.K. is supported by a DOC Fellowship of the Austrian Academy of Sciences. W.H.O. is supported by the NIHR, BHF (grants PG-0310-1002 and RG/09/12/28096), and NHS Blood and Transplant. E.L. is supported by a Wellcome Trust Sir Henry Dale Fellowship (grant 107630/Z/15/Z) and core support grant from the Wellcome Trust and MRC to the Wellcome Trust-Medical Research Council Cambridge Stem Cell Institute. M. Frontini is supported by the BHF Cambridge Centre of Excellence (grant RE/13/6/30180). C.B. is supported by a New Frontiers Group award of the Austrian Academy of Sciences and by a European Research Council (ERC) Starting Grant (European Union’s Horizon 2020 research and innovation program; grant 679146)