Formation of the oxygen torus in the inner magnetosphere: Van Allen Probes observations

We study the formation process of an oxygen torus during the 12–15 November 2012 magnetic storm, using the magnetic field and plasma wave data obtained by Van Allen Probes. We estimate the local plasma mass density (ρL) and the local electron number density (neL) from the resonant frequencies of standing Alfvén waves and the upper hybrid resonance band. The average ion mass (M) can be calculated by M ∼ ρL/neL under the assumption of quasi-neutrality of plasma. During the storm recovery phase, both Probe A and Probe B observe the oxygen torus at L = 3.0–4.0 and L = 3.7–4.5, respectively, on the morning side. The oxygen torus has M = 4.5–8 amu and extends around the plasmapause that is identified at L∼3.2–3.9. We find that during the initial phase, M is 4–7 amu throughout the plasma trough and remains at ∼1 amu in the plasmasphere, implying that ionospheric O+ ions are supplied into the inner magnetosphere already in the initial phase of the magnetic storm. Numerical calculation under a decrease of the convection electric field reveals that some of thermal O+ ions distributed throughout the plasma trough are trapped within the expanded plasmasphere, whereas some of them drift around the plasmapause on the dawnside. This creates the oxygen torus spreading near the plasmapause, which is consistent with the Van Allen Probes observations. We conclude that the oxygen torus identified in this study favors the formation scenario of supplying O+ in the inner magnetosphere during the initial phase and subsequent drift during the recovery phase

Simulation of Van Allen probes plasmapause encounters

Abstract We use an E × B-driven plasmapause test particle (PTP) simulation to provide global contextual information for in situ measurements by the Van Allen Probes (Radiation Belt Storm Probes (RBSP)) during 15-20 January 2013. During 120 h of simulation time beginning on 15 January, geomagnetic activity produced three plumes. The third and largest simulated plume formed during enhanced convection on 17 January, and survived as a rotating, wrapped, residual plume for tens of hours. To validate the simulation, we compare its output with RBSP data. Virtual RBSP satellites recorded 28 virtual plasmapause encounters during 15-19 January. For 26 of 28 (92%) virtual crossings, there were corresponding actual RBSP encounters with plasmapause density gradients. The mean difference in encounter time between model and data is 36 min. The mean model-data difference in radial location is 0.40 ± 0.05 RE. The model-data agreement is better for strong convection than for quiet or weakly disturbed conditions. On 18 January, both RBSP spacecraft crossed a tenuous, detached plasma feature at approximately the same time and nightside location as a wrapped residual plume, predicted by the model to have formed 32 h earlier on 17 January. The agreement between simulation and data indicates that the model-provided global information is adequate to correctly interpret the RBSP density observations. Key Points Model nightside plasmapause encounters agree with observations to within 0.4 REBoth RBSP satellites crossed features consistent with a 32 h old residual plumeModel-provided global context is adequate to interpret in situ density data

The nonlinear relaxation time and quasideterministic-theory approaches to characterize the decay of unestable states

We present the relationship between nonlinear-relaxation-time (NLRT) and quasideterministic approaches to characterize the decay of an unstable state. The universal character of the NLRT is established. The theoretical results are applied to study the dynamical relaxation of the Landau model in one and n variables and also a laser model

Genetic and Expression Analysis of CASP7 Gene in a European Caucasian Population with Rheumatoid Arthritis

International audienceObjective. To study the possible role of the caspase 7 (CASP7) gene in susceptibility to rheumatoid arthritis (RA) in a European Caucasian population. Methods. CASP7 rs2227309 single nucleotide polymorphism (SNP) was genotyped in 197 French RA trio families and in 252 European RA families available for replication using Taqman allelic discrimination assay. Relative quantification of caspase 7 isoforms α and β mRNA expression was performed from whole blood in 25 unrelated patients with RA and in 15 healthy controls by real-time quantitative reverse transcription-polymerase chain reaction. The genetic analyses for association and linkage were performed using the comparison of allelic frequencies, the transmission disequilibrium test, and the genotype relative risk. Results. We observed, in the first sample, a significant association of rs2227309-AA genotype with RA [p = 0.03, odds ratio (OR) 2.11 (95% CI 1.0-4.6)]. The second sample did not show any significant association of the AA genotype with RA [p = 0.6, OR 0.87 (95% CI 0.4-1.8)]. When the 2 samples were combined, no significant association of the AA genotype [p = 0.3, OR 1.32 (95% CI 0.8-2.2)] was observed. CASP7 isoforms α and β mRNA were expressed in patients with RA at lower level than in healthy controls (-89%, p = 0.003 and -47%, p = 0.01; respectively). Conclusion. CASP7 rs2227309 SNP was not associated with RA in a European Caucasian population. Nevertheless, CASP7 isoforms α and β could have an involvement in the apoptosis process in RA. The Journal of Rheumatology Copyright © 2008. All rights reserved

Association between tumor necrosis factor receptor II and familial, but not sporadic, rheumatoid arthritis: Evidence for genetic heterogeneity

OBJECTIVE: Tumor necrosis factor alpha (TNFalpha) binds the receptors TNFRI and TNFRII. Results of genome scans have suggested that TNFR2 is a candidate rheumatoid arthritis (RA) locus. A case-control study in a UK Caucasian population has shown an association between a TNFR2 genotype (196R/R in exon 6) and familial, but not sporadic, RA. The present study was undertaken to test this association in the French Caucasian population. METHODS: To test for an association in sporadic RA, 100 families were genotyped for the 196M/R polymorphism and analyzed using the transmission disequilibrium test and haplotype relative risk. To test for an association in familial RA, RA index cases from 100 affected sibpair (ASP) families were genotyped for 196M/R. Linkage analysis was performed with 3 TNFR2 microsatellite markers. RESULTS: The TNFR2 196R/R genotype was not associated with sporadic RA (odds ratio [OR] 0.59, P = 0.72), but was associated with familial RA (OR 4.0, P = 0.026). The association was most marked in the context of TNFR2 "twin-like" RA sibs (affected sibs sharing both TNFR2 haplotypes) (OR 9.2, P = 0.0017). Linkage analysis results were consistent with the association; most of the TNFR2 linkage evidence was found in the subgroup of families with 196R/R ASP index cases. CONCLUSION: This study is the first to replicate evidence of the involvement of TNFR2 in RA genetic heterogeneity. Our data refine the initial hypothesis, to suggest that a TNFR2 recessive factor, in linkage disequilibrium with the 196R allele, plays a major role in a subset of families with multiple cases of RA

Association between Tumor Necrosis Factor Receptor II and Familial, but Not Sporadic, Rheumatoid Arthritis: Evidence for Genetic Heterogeneity

International audienceObjective. Tumor necrosis factor α (TNFα) binds the receptors TNFRI and TNFRII. Results of genome scans have suggested that TNFR2 is a candidate rheumatoid arthritis (RA) locus. A case-control study in a UK Caucasian population has shown an association between a TNFR2 genotype (196R/R in exon 6) and familial, but not sporadic, RA. The present study was undertaken to test this association in the French Caucasian population. Methods. To test for an association in sporadic RA, 100 families were genotyped for the 196M/R polymorphism and analyzed using the transmission disequilibrium test and haplotype relative risk. To test for an association in familial RA, RA index cases from 100 affected sibpair (ASP) families were genotyped for 196M/R. Linkage analysis was performed with 3 TNFR2 microsatellite markers. Results. The TNFR2 196R/R genotype was not associated with sporadic RA (odds ratio [OR] 0.59, P = 0.72), but was associated with familial RA (OR 4.0, P = 0.026). The association was most marked in the context of TNFR2 "twin-like" RA sibs (affected sibs sharing both TNFR2 haplotypes) (OR 9.2, P = 0.0017). Linkage analysis results were consistent with the association; most of the TNFR2 linkage evidence was found in the subgroup of families with 196R/R ASP index cases. Conclusion. This study is the first to replicate evidence of the involvement of TNFR2 in RA genetic heterogeneity. Our data refine the initial hypothesis, to suggest that a TNFR2 recessive factor, in linkage disequilibrium with the 196R allele, plays a major role in a subset of families with multiple cases of RA

Homologous Expression of Glycosylphosphatidylinositol-Anchored Glycoproteins in Trypanosoma cruzi

The surface coat of Trypanosoma cruzi is covered with glycosylphosphatidylinositol (GPI)-anchored glycoproteins (GAGPs) that contribute to parasite protection and to the establishment of a persistent infection in both the insect vector and the mammalian host. Multiple GAGPs that vary by amino acid sequence and/or posttranslational modifications are co-expressed on the parasite surface coat, hence curtailing structural/functional analyses on these molecules. Studies in our lab have indicated that GAGP-tagged variants expressed by transfected parasites undergo analogous posttranslational processing than endogenous ones and therefore constitute suitable tools to overcome these limitations. In this chapter, we detail the entire methodological pipeline for the efficient homologous expression of GAGPs in T. cruzi: from a simple strategy for the simultaneously cloning and tagging of the gene of interest to the biochemical validation of the parasite-expressed product.Fil: Balouz, Virginia. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas. - Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Biotecnológicas; ArgentinaFil: Mesias, Andrea Cecilia. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas. - Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Biotecnológicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Salta. Instituto de Patología Experimental. Universidad Nacional de Salta. Facultad de Ciencias de la Salud. Instituto de Patología Experimental; ArgentinaFil: Centeno Camean, Camila. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas. - Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Biotecnológicas; ArgentinaFil: Ducrey, Ivana. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas. - Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Biotecnológicas; ArgentinaFil: Lobo, Mabel Maite. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas. - Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Biotecnológicas; ArgentinaFil: Durante, Ignacio Miguel. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas. - Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Biotecnológicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Estudios de la Inmunidad Humoral Prof. Ricardo A. Margni. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Estudios de la Inmunidad Humoral Prof. Ricardo A. Margni; ArgentinaFil: Cánepa, Gaspar E.. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas. - Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Biotecnológicas; ArgentinaFil: Buscaglia, Carlos Andres. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas. - Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Biotecnológicas; ArgentinaFil: Camara, Maria de Los Milagros. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas. - Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Biotecnológicas; Argentin

Genetic and expression analysis of CASP7 gene in a European Caucasian population with rheumatoid arthritis

INTRODUCTION A candidate gene approach, in a large case-control association study in the Dutch population, has shown that a 480 kb block on chromosome 4q27 encompassing KIAA1109/Tenr/IL2/IL21 genes is associated with rheumatoid arthritis. Compared with case-control association studies, family-based studies have the added advantage of controlling potential differences in population structure. Therefore, our aim was to test this association in populations of European origin by using a family-based approach. METHODS: A total of 1,302 West European white individuals from 434 trio families were genotyped for the rs4505848, rs11732095, rs6822844, rs4492018 and rs1398553 polymorphisms using the TaqMan Allelic discrimination assay (Applied Biosystems). The genetic association analyses for each SNP and haplotype were performed using the Transmission Disequilibrium Test and the genotype relative risk. RESULTS: We observed evidence for association of the heterozygous rs4505848-AG genotype with rheumatoid arthritis (P = 0.04); however, no significance was found after Bonferroni correction. In concordance with previous findings in the Dutch population, we observed a trend of undertransmission for the rs6822844-T allele and rs6822844-GT genotype to rheumatoid arthritis patients. We further investigated the five SNP haplotypes of the KIAA1109/Tenr/IL2/IL21 gene region. We observed, as described in the Dutch population, a nonsignificant undertransmission of the AATGG haplotype to rheumatoid arthritis patients. CONCLUSIONS: Using a family-based study, we have provided a trend for the association of the KIAA1109/Tenr/IL2/IL21 gene region with rheumatoid arthritis in populations of European descent. Nevertheless, we failed to replicate a significant association of this region in our rheumatoid arthritis family sample. Further investigation of this region, including detection and testing of all variants, is required to confirm rheumatoid arthritis association