Lens magnification by CL0024+1654 in the U and R band

[ABRIDGED] We estimate the total mass distribution of the galaxy cluster CL0024+1654 from the measured source depletion due to lens magnification in the R band. Within a radius of 0.54Mpc/h, a total projected mass of (8.1+/-3.2)*10^14 M_sol/h (EdS) is measured, which corresponds to a mass- to-light ratio of M/L(B)=470+/-180. We compute the luminosity function of CL0024+1654 in order to estimate contamination of the background source counts from cluster galaxies. Three different magnification-based reconstruction methods are employed using both local and non-local techniques. We have modified the standard single power-law slope number count theory to incorporate a break and applied this to our observations. Fitting analytical magnification profiles of different cluster models to the observed number counts, we find that the cluster is best described either by a NFW model with scale radius r_s=334+/-191 kpc/h and normalisation kappa_s=0.23+/-0.08 or a power-law profile with slope xi=0.61+/-0.11, central surface mass density kappa_0=1.52+/-0.20 and assuming a core radius of r_core=35 kpc/h. The NFW model predicts that the cumulative projected mass contained within a radius R scales as M(<R)=2.9*10^14*(R/1')^[1.3-0.5lg (R/1')] M_sol/h. Finally, we have exploited the fact that flux magnification effectively enables us to probe deeper than the physical limiting magnitude of our observations in searching for a change of slope in the U band number counts. We rule out both a total flattening of the counts with a break up to U_AB<=26.6 and a change of slope, reported by some studies, from dlog N/dm=0.4->0.15 up to U_AB<=26.4 with 95% confidence.Comment: 19 pages, 12 figures, submitted to A&A. New version includes more robust U band break analysis and contamination estimates, plus new plot

Neutrino opacity in magnetised hot and dense nuclear matter

We study the neutrino interaction rates in hot matter at high densities in the presence of uniform magnetic field. The neutrino cross-sections involving both the charged current absorption and neutral current scattering reactions on baryons and leptons have been considered. We have in particular considered the interesting case when the magnetic field is strong enough to completely polarise the protons and electrons in supernovae and neutron stars. The opacity in such a situation is considerably modified and the cross-section develops anisotropy. This has implications for phenomenon invoked in the literature to explain the observed pulsar kicks.Comment: 22 latex pages and 7 postscript figure

Radial Oscillations of Neutron Stars in Strong Magnetic Fields

The eigen frequencies of radial pulsations of neutron stars are calculated in a strong magnetic field. At low densities we use the magnetic BPS equation of state(EOS) similar to that obtained by Lai and Shapiro while at high densities the EOS obtained from the relativistic nuclear mean field theory is taken and extended to include strong magnetic field. It is found that magnetised neutron stars support higher maximum mass where as the effect of magnetic field on radial stability for observed neutron star masses is minimal.Comment: latex2e file with five postscript figure

Molecular benchmarks of a SARS-CoV-2 epidemic.

To access publisher's full text version of this article, please click on the hyperlink in Additional Links field or click on the hyperlink at the top of the page marked DownloadA pressing concern in the SARS-CoV-2 epidemic and other viral outbreaks, is the extent to which the containment measures are halting the viral spread. A straightforward way to assess this is to tally the active cases and the recovered ones throughout the epidemic. Here, we show how epidemic control can be assessed with molecular information during a well characterized epidemic in Iceland. We demonstrate how the viral concentration decreased in those newly diagnosed as the epidemic transitioned from exponential growth phase to containment phase. The viral concentration in the cases identified in population screening decreased faster than in those symptomatic and considered at high risk and that were targeted by the healthcare system. The viral concentration persists in recovering individuals as we found that half of the cases are still positive after two weeks. We demonstrate that accumulation of mutations in SARS-CoV-2 genome can be exploited to track the rate of new viral generations throughout the different phases of the epidemic, where the accumulation of mutations decreases as the transmission rate decreases in the containment phase. Overall, the molecular signatures of SARS-CoV-2 infections contain valuable epidemiological information that can be used to assess the effectiveness of containment measures

Multiomics analysis of rheumatoid arthritis yields sequence variants that have large effects on risk of the seropositive subset

Funding Information: Funding The study was funded by NORDFORSK (grant agreement no. 90825, project NORA), the Swedish Research Council (2018-02803), the Swedish innovation Agency (Vinnova), Innovationsfonden and The Research Council of Norway, Region Stockholm-Karolinska Institutet and Region Västerbotten (ALF), the Danish Rheumatism Association (R194-A6956), the Swedish Brain Foundation, Nils and Bibbi Jensens Foundation, the Knut and Alice Wallenberg Foundation, Margaretha af Ugglas Foundation, the South-Eastern Heath Region of Norway, the Health Research Fund of Central Denmark Region, Region of Southern Denmark, the A.P. Moller Foundation for the Advancement of Medical Science, the Colitis-Crohn Foreningen, the Novo Nordisk Foundation (NNF15OC0016932), Aase og Ejnar Danielsens Fond, Beckett-Fonden, Augustinus Fonden, Knud and Edith Eriksens Mindefond, Laege Sofus Carl Emil Friis and Hustru Olga Doris Friis’ Legat, the Psoriasis Forskningsfonden, the University of Aarhus, the Danish Rheumatism Association (R194-A6956, A1923, A3037 and A3570 – www. gigtforeningen.dk), Region of Southern Denmark’s PhD Fund, 12/7725 (www.regionsyddanmark.dk) and the Department of Rheumatology, Frederiksberg Hospital (www.frederiksberghospital. dk). MoBa Genetics has been funded by the Research Council of Norway (#229624, #223273), South East and Western Norway Health Authorities, ERC AdG project SELECTionPREDISPOSED, Stiftelsen Kristian Gerhard Jebsen, Trond Mohn Foundation, the Novo Nordisk Foundation and the University of Bergen. KB and SB acknowledge the Novo Nordisk Foundation (grant NNF14CC0001). Funding Information: competing financial interests as employees. OAA is a consultant to HealthLytix. The following coauthors report the following but unrelated to the current report: Karolinska Institutet, with JA as principal investigator, has entered into agreements with the following entities, mainly but not exclusively for safety monitoring of rheumatology immunomodulators: Abbvie, BMS, Eli Lilly, Janssen, MSD, Pfizer, Roche, Samsung Bioepis and Sanofi, unrelated to the present study. SB has ownerships in Intomics A/S, Hoba Therapeutics Aps, Novo Nordisk A/S, Lundbeck A/S and managing board memberships in Proscion A/S and Intomics A/S. BG has received research grants from AbbVie, Bristol Myers-Squibb and Pfizer; OH has received research grants from AbbVie, Novartis and Pfizer, DVJ has received speaker and consultation fees from AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, Roche and UCB, AGL has received speaking and/or consulting fees from AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, Roche and UCB; and CT has received consulting fees from Roche, speaker fees from Abbvie, Bristol Myers-Squibb, Nordic Drugs, Pfizer and Roche, and an unrestricted grant from Bristol Myers-Squibb. Publisher Copyright: © Funding Information: Funding The study was funded by NORDFORSK (grant agreement no. 90825, project NORA), the Swedish Research Council (2018-02803), the Swedish innovation Agency (Vinnova), Innovationsfonden and The Research Council of Norway, Region Stockholm-Karolinska Institutet and Region Västerbotten (ALF), the Danish Rheumatism Association (R194-A6956), the Swedish Brain Foundation, Nils and Bibbi Jensens Foundation, the Knut and Alice Wallenberg Foundation, Margaretha af Ugglas Foundation, the South-Eastern Heath Region of Norway, the Health Research Fund of Central Denmark Region, Region of Southern Denmark, the A.P. Moller Foundation for the Advancement of Medical Science, the Colitis-Crohn Foreningen, the Novo Nordisk Foundation (NNF15OC0016932), Aase og Ejnar Danielsens Fond, Beckett-Fonden, Augustinus Fonden, Knud and Edith Eriksens Mindefond, Laege Sofus Carl Emil Friis and Hustru Olga Doris Friis’ Legat, the Psoriasis Forskningsfonden, the University of Aarhus, the Danish Rheumatism Association (R194-A6956, A1923, A3037 and A3570 – www. gigtforeningen.dk), Region of Southern Denmark’s PhD Fund, 12/7725 (www.regionsyddanmark.dk) and the Department of Rheumatology, Frederiksberg Hospital (www.frederiksberghospital. dk). MoBa Genetics has been funded by the Research Council of Norway (#229624, #223273), South East and Western Norway Health Authorities, ERC AdG project SELECTionPREDISPOSED, Stiftelsen Kristian Gerhard Jebsen, Trond Mohn Foundation, the Novo Nordisk Foundation and the University of Bergen. KB and SB acknowledge the Novo Nordisk Foundation (grant NNF14CC0001). Funding Information: competing financial interests as employees. OAA is a consultant to HealthLytix. The following coauthors report the following but unrelated to the current report: Karolinska Institutet, with JA as principal investigator, has entered into agreements with the following entities, mainly but not exclusively for safety monitoring of rheumatology immunomodulators: Abbvie, BMS, Eli Lilly, Janssen, MSD, Pfizer, Roche, Samsung Bioepis and Sanofi, unrelated to the present study. SB has ownerships in Intomics A/S, Hoba Therapeutics Aps, Novo Nordisk A/S, Lundbeck A/S and managing board memberships in Proscion A/S and Intomics A/S. BG has received research grants from AbbVie, Bristol Myers-Squibb and Pfizer; OH has received research grants from AbbVie, Novartis and Pfizer, DVJ has received speaker and consultation fees from AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, Roche and UCB, AGL has received speaking and/or consulting fees from AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, Roche and UCB; and CT has received consulting fees from Roche, speaker fees from Abbvie, Bristol Myers-Squibb, Nordic Drugs, Pfizer and Roche, and an unrestricted grant from Bristol Myers-Squibb. Publisher Copyright: ©Objectives To find causal genes for rheumatoid arthritis (RA) and its seropositive (RF and/or ACPA positive) and seronegative subsets. Methods We performed a genome-wide association study (GWAS) of 31 313 RA cases (68% seropositive) and ∼1 million controls from Northwestern Europe. We searched for causal genes outside the HLA-locus through effect on coding, mRNA expression in several tissues and/or levels of plasma proteins (SomaScan) and did network analysis (Qiagen). Results We found 25 sequence variants for RA overall, 33 for seropositive and 2 for seronegative RA, altogether 37 sequence variants at 34 non-HLA loci, of which 15 are novel. Genomic, transcriptomic and proteomic analysis of these yielded 25 causal genes in seropositive RA and additional two overall. Most encode proteins in the network of interferon-Alpha/beta and IL-12/23 that signal through the JAK/STAT-pathway. Highlighting those with largest effect on seropositive RA, a rare missense variant in STAT4 (rs140675301-A) that is independent of reported non-coding STAT4-variants, increases the risk of seropositive RA 2.27-fold (p=2.1×10-9), more than the rs2476601-A missense variant in PTPN22 (OR=1.59, p=1.3×10-160). STAT4 rs140675301-A replaces hydrophilic glutamic acid with hydrophobic valine (Glu128Val) in a conserved, surface-exposed loop. A stop-mutation (rs76428106-C) in FLT3 increases seropositive RA risk (OR=1.35, p=6.6×10-11). Independent missense variants in TYK2 (rs34536443-C, rs12720356-C, rs35018800-A, latter two novel) associate with decreased risk of seropositive RA (ORs=0.63-0.87, p=10-9-10-27) and decreased plasma levels of interferon-Alpha/beta receptor 1 that signals through TYK2/JAK1/STAT4. Conclusion Sequence variants pointing to causal genes in the JAK/STAT pathway have largest effect on seropositive RA, while associations with seronegative RA remain scarce.Peer reviewe

Lens magnification by CL0024+1654 in the and band

Peer reviewe

The added value of ECG-gating for the diagnosis of myocardial infarction using myocardial perfusion scintigraphy and artificial neural networks

To assess the value of ECG-gating for the diagnosis of myocardial infarction using myocardial perfusion scintigraphy (MPS) and an artificial neural network. A total of 422 patients referred for MPS were studied using a one day Tc-99m-tetrofosmin protocol. Adenosine stress combined with submaximal dynamic exercise was used. The images were interpreted by one of three experienced clinicians and these interpretations regarding the presence or absence of myocardial infarction were used as the standard. A fully automated method using artificial neural networks was compared with the clinical interpretation. Either perfusion data alone or a combination of perfusion and function from ECG-gated images were used as input to different artificial neural networks. After a training session, the two types of neural networks were evaluated in separate test groups using an eightfold cross-validation procedure. The neural networks trained with both perfusion and ECG-gated images had a 4-7% higher specificity compared with the corresponding networks using perfusion data only, in four of five segments compared at the same level of sensitivity. The greatest improvement in specificity, from 70% to 77%, was seen in the inferior segment. In the septal and lateral segments the specificity rose from 73% to 77% and from 81% to 85%, respectively. In the anterior segment, the increase in specificity from 93% to 94% by adding functional data was not significant. The addition of functional information from ECG-gated MPS is of value for the diagnosis of myocardial infarction using an automated method of interpreting myocardial perfusion images

Comorbidities in multiple myeloma and implications on survival: A population-based study.

To access publisher's full text version of this article click on the hyperlink belowHigh proportion of patients with multiple myeloma suffer from comorbidities which may alter clinical management. Therefore, our aims were to evaluate the prevalence of comorbidities and their impact on survival. We included patients diagnosed with multiple myeloma 1990-2013 in Sweden and all diagnoses from each patient from 1985. A total of 13 656 patients with multiple myeloma were included in the study, thereof 7404 (54%) had comorbidity at diagnosis. The risk of death was increased for those with one comorbidity at diagnosis compared to those without any comorbidity (hazard ratio = 1.19; 95% confidence interval:1.14-1.25); this risk was higher for those with two (1.38; 1.30-1.47) and three or more comorbidities (1.72; 1.62-1.83). Furthermore, the risk of death was increased in patients with prior history of cancer, arrhythmia, heart failure, diabetes mellitus, cerebrovascular disease, chronic lung disease, psychological disease, peptic ulcer, neurological disease, peripheral vascular disease, chronic kidney disease, dementia, and inflammatory bowel disease. This large study shows that over 50% of multiple myeloma patients have a comorbidity at diagnosis and survival decreased with increasing numbers of comorbidities. This emphasizes the importance of comorbidities when evaluating patients and deciding on treatment strategies for individuals with multiple myeloma. Keywords: comorbidities; multiple myeloma; survival.Research Fund of Landspitali, University Hospital of Iceland, The Nordic Cancer Union Icelandic Centre for Researc